Osteoporosis Clinical Guidelines for Prevention, Diagnosis, and Management Editors Sarah H. Gueldner, DSN, RN, FAAN, FGSA, FNAP, FAGHE Theresa N. Grabo, PhD, APRN, BC, CRNP Eric D. Newman, MD David R. Cooper, MD, AAOS
.EW 9ORK
Osteoporosis
Sarah H. Gueldner, DSN, RN, FAAN, FGSA, FNAP, FAGHE, presently serves as the Garvin Visiting Professor of Nursing at Case Western Reserve University and is professor of nursing and fellow in the Institute of Primary and Preventative Health Care at Binghamton University, in Binghamton, New York, She holds a bachelor’s degree in nursing from the University of Tennessee College of Nursing in Memphis, a masters degree in nursing from Emory University, and a doctor of science in nursing from the University of Alabama in Birmingham, where she was named medical center graduate fellow. Dr. Gueldner served as senior research scientist at the University of Georgia Gerontology Center, and served as the principal investigator of a federally funded study that examined the benefits of exercise in nursing home residents. She presently heads a 5-year study profiling the prevalence of osteoporosis in rural women, and a doubleblind clinical trial to test interventions that support smoking cessation to improve bone health. She lists more than 100 publications, including 53 articles in referred journals, 7 books, and 39 chapters, and is a fellow in the American Academy of Nursing, the National Academies of Practice, the Gerontological Society of America, and the Association of Gerontology in Higher Education.
Theresa N. Grabo, PhD, APRN, BC, CRNP, is associate professor of nursing and director of graduate programs and fellow in the Institute of Primary and Preventative Health Care at Binghamton University, in Binghamton, New York. She holds a bachelor of science in nursing degree from the State University of New York at Buffalo, a master of nursing degree and family nurse practitioner certificate from Binghamton University, a master of public administration from Marywood University in Scranton, Pennsylvania, and a PhD from the University of Pennsylvania in Philadelphia, where she served as a fellow in the Summer Nursing Research Institute, International Center of Research for Women, Children, and Families at the University of Pennsylvania School of Nursing. She is presently co-investigator on a National Institute of Nursing Research grant investigating ways to improve heart healthy behaviors among rural women. She is an advanced practice registered nurse, board certified in family health nursing, with over 20 years experience as a certified nurse practitioner providing care to women and practices at Valley Gyn Specialists in Luzerne, Pennsylvania.
Eric D. Newman, MD, received his bachelor of arts degree in biology from Johns Hopkins University, and his medical degree from the Pennsylvania State University College of Medicine in Hershey, Pennsylvania, where he was the recipient of a National Institutes of Health (NIH) research grant. He completed an internal medicine residency at the University of North Carolina (Chapel Hill) and a rheumatology fellowship at Geisinger Medical Center in Danville, Pennsylvania. He has been on staff at Geisinger since 1988 and has served as director of rheumatology, vice-chairman of the Division of Medicine, and director of the Clinical Trials Office for the Geisinger Health Care System. He developed and maintains the Rheumatology Diagnosis, Treatment, and Outcomes Database, with information on 30,000 patients, encompassing over 220,000 clinic visits. He played an integral role in the design and implementation of the Geisinger Osteoporosis Disease Management Program, which has received three national awards and generated 12 peer-reviewed publications. In this role he developed and directs the Geisinger Mobile DXA Program, which performs 3,500 DXAs yearly in outlying areas of Pennsylvania.
David R. Cooper, MD, AAOS, received his Bachelor of Arts degree at Binghamton University in Binghamton, New York, and his medical degree at the Thomas Jefferson University Medical School, followed by an orthopedic residency in Philadelphia. He is the director of The Knee Center in Wilkes-Barre, Pennsylvania, and has personally performed over 6,000 arthroscopies and 500 knee replacements in his career. He is an adjunct professor at Kings College in Wilkes-Barre, and at the Decker School of Nursing at Binghamton University in Binghamton, New York. He is also the attending orthopedic surgeon at the Pocono Raceway for the NASCAR events each year. In addition to his clinical practice, Dr. Cooper lectures and teaches nationwide, including presentations at the national conference of the American Bar Association and the LRP Publications, national workers’ compensation program. He is the recipient of the Professional Education Seminars, Inc., Excellence in Teaching Award.
Copyright © 2008 Springer Publishing Company, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of Springer Publishing Company, LLC. Springer Publishing Company, LLC 11 West 42nd Street New York, NY 10036 www.springerpub.com Acquisitions Editor: Sally J. Barhydt Project Manager: Carol Cain Cover design: Joanne E. Honigman Composition: Apex Publishing, LLC 07 08 09 10/ 5 4 3 2 1 Library of Congress Cataloging-in-Publication Data Osteoporosis : clinical guidelines for prevention, diagnosis, and management / [edited by] Sarah H. Gueldner . . . [et al.]. p. cm. Includes bibliographical references and index. ISBN-13: 978-0-8261-0276-8 (alk. paper) ISBN-10: 0-8261-0276-X (alk. paper) 1. Osteoporosis—Prevention. 2. Osteoporosis—Diagnosis. 3. Osteoporosis—Treatment. I. Gueldner, Sarah Hall. [DNLM: 1. Osteoporosis—therapy. 2. Fractures, Bone—prevention & control. 3. Health Promotion. 4. Osteoporosis—diagnosis. WE 250 O851185 2008] RC931.O73O7725 2008 616.7'16—dc22 2007022459 Printed in the United States of America by Malloy Incorporated.
This book is dedicated to the elimination of osteoporotic fractures within our own and future generations.
Contents
Contributors xi Foreword xiii Preface xv Acknowledgments xvii
1
Introduction and Overview 1
Sarah H. Gueldner, Theresa N. Grabo, Eric D. Newman, and David R. Cooper
The Problem 1
The Science 1
Transferring Knowledge to Practice 2
The Clinical Mandate 2
Children: An Overlooked At-Risk Group 2
The System Mandate 3
The Purpose of This Book 3
Summary 5
Part 1: Prevalence, Risk Factors, and Pathogenesis
2
Demographic Perspectives: The Magnitude of Concern 9
Janice Penrod, Annabelle M. Smith, Susan Terwilliger, and Sarah H. Gueldner
Introduction 9
Prevalence 10
Fractures 11
Lifetime Fracture Risks 11
Global Perspectives 12
Consequences of Osteoporosis 13
ix
Contents
3
Future Projections 16
The Pathogenesis of Osteoporosis 19
Sheri A. Stucke, Bernadette M. Lombardi, Sarah H. Gueldner, and Theresa N. Grabo
Introduction 19
Bone Physiology 20
Conclusion 28
Part 2: Clinical Management
4
Diagnostic Tests and Interpretation 33
William T. Ayoub
Introduction 33
Bone Mineral Density Testing 33
Guidelines for Interpretation 35
Clinical Utility 38
Markers of Bone Turnover 39
Secondary Cause Evaluation 40
5
Pharmacological Management 47
Theresa N. Grabo and Daniel S. Longyhore
Bisphosphonate Therapy 48
Parathyroid Hormone Therapy (PTH) 52
Estrogen Therapy 53
Bioidentical Hormones 57
Selective Estrogen Receptor Modulators (SERMs) 59
Calcitonin (Salmon) Therapy 64
Combination Antiresorptive Therapy 66
Calcium and Vitamin D 67
Vitamin D 69
Integrative Therapies 72
Pain Management 73
Conclusion 76
6
Surgical Management of Fractures 83
Eric Seybold, Heather Hazlett, and David R. Cooper
Complications of Osteoporosis 83
Contents
xi
Hip Fractures 84
Vertebral Compression Fractures 88
Wrist Fractures 97
Prevention 99
Conclusion 99
Part 3: Nonpharmacological Management
7
Diet and Bone Health 103
Helen Smiciklas-Wright and Catherine E. Wright
The Effect of Calcium on Peak Bone Mass 104
Does Calcium Intake Minimize Bone Loss and Reduce Fractures? 104
Recommended Calcium Intakes 105
The Calcium Paradox 106
Food Sources of Calcium 106
Vitamin D 107
Sources of Vitamin D 108
Recommended Vitamin D Intakes 109
How Much Calcium and Vitamin D Is Available in Foods and Supplements? 109
Is It Possible to Consume Too Much Calcium and Vitamin D? 109
Total Diet 110
Nutritional Recommendations 112
Summary 113
8
Exercise Mandate: Preventative and Restorative 117
Renée M. Hakim and Janet Ramos Grabo
Preventative 118
Restorative 127
General Considerations 132
Summary 133
9
Osteoporosis and Fall Prevention 141
Roberta A. Newton
Elements of a Fall Prevention Program 143
HEROS© Fall Prevention Program for Community Dwelling Older Adults 148
xii
Contents
10
Maintaining Independence and Quality of Life 153
Marlene Joy Morgan
Client-Centered Approach 154
Setting Goals for Lifestyle Redesign 155
Integrating Interdisciplinary Assessments 155
Common Problems Affecting Independence and Quality of Life 159
Lifestyle Redesign for Living With Osteoporosis 161
Successful Lifestyle Redesign—Outcomes and Prognosis 164
Summary 164
Part 4: Prevention Strategies
11 Maximizing Peak Bone Mass in Children, Adolescents, and Young Adults: A Public Health Priority 169
Leann M. Lesperance
Nutrition 170
Physical Activity 173
Medications 174
Medical Conditions 175
Prevention Programs 177
12 A Model for Improving Access to Osteoporosis Care: The Geisinger Health System Mobile DXA Program 181
Eric D. Newman
Osteoporosis Testing 181
Heel Ultrasound—A Helpful but Incomplete Solution 182
Mobile DXA—Providing the Gold-Standard Test at the Convenience of the Patient’s Primary Care Physician’s Office 183
Mobile DXA—Conclusions and Future Directions 185
13 A Model for Community Outreach: Cooperative Extension Osteoporosis Prevention and Screening Programs 187
Marilyn A. Corbin, Jane Trainor, Chin-Fang Liu, and Sarah H. Gueldner
Introduction 187
About cooperative Extension 188
Creating Health: Osteoporosis 190
Other Program Examples 192
Summary 198
Contents
xiii 14
Health Policy and Insurance Reimbursement 201
Geraldine R. Avidano Britton, Katherine Kaby Anselmi, and Laura Pascucci
Policy Makers and Stakeholders 202
Reimbursement: Federal 208
Policy and Reimbursement: Individual States in the United States 209
Policy Development: Case Studies 214
Summary 216
15
Emerging Approaches in the Prevention of Osteoporosis 219
Carolyn S. Pierce, Guruprasad Madhavan, and Kenneth J. McLeod
Introduction 219
Bone Adaptation and Fluid Flow 220
Fluid Flow in Humans 221
Skeletal Muscle Pump Stimulation and Bone Health 224
Concluding Remarks 228
Acknowledgments 229
Appendix A Resources and Related Links 235
Federal Government 235
State Government 238
Nongovernment 239
Appendix B Diagnoses That Support Medical Necessity for Bone Densitometry for Reimbursement 241 Index 247
Contributors
Katherine Kaby Anselmi, FNP, WHNP, PhD, Esquire
Assistant Professor College of Nursing and Health Professions Drexel University Philadelphia, Pennsylvania Former Staff Attorney, Barbara J. Hart Justice Center A project of the Women’s Resource Center Scranton, Pennsylvania William T. Ayoub, MD, FACP, FACR
Geisinger Health System State College, Pennsylvania Geraldine R. Avidano Britton, PhD, RN, FNP
Research Assistant Professor Decker School of Nursing Binghamton University Binghamton, New York Chin-Fang Liu, PhD, RN
Professional Registered Nurse Department of Nursing Kaohsiung Medical University Chung-Ho Memorial Hospital Kaohsiung City, Taiwan Marilyn A. Corbin, PhD
Associate Director, State Program Leader for Children, Youth, and Families, and Professor Penn State Cooperative Extension Pennsylvania State University University Park, Pennsylvania
Janet Ramos Grabo, MPT
Physical Therapist Center Manager for NovaCare Stratford, New Jersey Renée M. Hakim, PT, PhD, NCS
Certified Neurology Clinical Specialist Associate Professor and Director Department of Physical Therapy University of Scranton Scranton, Pennsylvania Heather Hazlett, RPA
Physician Assistant Orthopedic Associates PC Binghamton, New York Leann M. Lesperance, MD, PhD, FAAP
Research Assistant Professor Department of Bioengineering Thomas J. Watson School of Engineering and Applied Sciences Binghamton University Department of Pediatrics, Binghamton Clinical Campus Upstate Medical University Department of Pediatrics, United Health Services Hospitals Binghamton, New York Bernadette M. Lombardi, MS, RN
PhD Candidate, Decker School of Nursing Binghamton University Binghamton, New York
xv
xvi Daniel S. Longyhore, PharmD, BCPS
Nesbitt College of Pharmacy and Nursing Wilkes University Clinical Pharmacist Wyoming Valley Family Practice Residency Wilkes-Barre, Pennsylvania Guruprasad Madhavan, MS
Clinical Science and Engineering Research Center and Department of Bioengineering Thomas J. Watson School of Engineering and Applied Science State University of New York Binghamton, New York Kenneth J. McLeod, PhD
Professor and Chair Department of Bioengineering Thomas J. Watson School of Engineering and Applied Science Innovative Technologies Complex Binghamton University Binghamton, New York Marlene Joy Morgan, EdD, OTR/L
Assistant Professor Department of Occupational Therapy University of Scranton Scranton, Pennsylvania Roberta A. Newton, PhD, FGSA
Professor, Department of Physical Therapy College of Health Professions Associate Director, Institute on Aging Temple University Philadelphia, Pennsylvania Laura Pascucci, CC-P
Compliance Specialist Our Lady of Lourdes Memorial Hospital, Inc. Binghamton, New York Janice Penrod, PhD, RN
Professor in Charge of Graduate Programs and Assistant Professor of Nursing College of Health and Human Development Assistant Professor of Humanities College of Medicine
Contributors
Pennsylvania State University State College, Pennsylvania Carolyn S. Pierce, DSN, RN
Assistant Professor Decker School of Nursing Clinical Science and Engineering Research Center and Department of Bioengineering Binghamton University Binghamton, New York Eric Seybold, MD
Board Certified Orthopedic Surgeon Orthopedic Associates, PC Binghamton, New York Helen Smiciklas-Wright, PhD
Professor of Nutrition Pennsylvania State University State College, Pennsylvania Annabelle M. Smith, PhD(c), RN
School of Nursing Pennsylvania State University State College, Pennsylvania Sheri A. Stucke, PhD, RN, FNP
Assistant Professor Department of Physiologic Nursing University of Nevada at Las Vegas Las Vegas, Nevada Susan Terwilliger, EdD(c), RN, PNP
Clinical Lecturer Decker School of Nursing Binghamton University Binghamton, New York Jane Trainor, EdD, RN
Clinical Professor School of Nursing—Harrisburg Pennsylvania State University Harrisburg, Pennsylvania Catherine E. Wright, MPH
Epidemiologist Science Writing Consultant Pittsburgh, Pennsylvania
Foreword
T
his highly informative book fills a critical gap in the health care literature. Written by a team of key clinicians and researchers within the fields of medicine, nursing, nutrition, exercise physiology, physical therapy, and health care policy, the book is a comprehensive handbook of evidencebased clinical guidelines for the diagnosis and treatment of osteoporosis. It is specifically designed for frontline health care providers, who are in the best position to detect the presence of osteoporosis early and institute treatment in time to prevent its devastating fractures. The authors also acknowledge the disease and its sequelae as a global problem that will continue to exceed epidemic proportions in the rapidly aging population unless preventive measures are instituted now. The authors provide compelling statistics profiling the prevalence and impact of osteoporosis on individuals, their families, and society. The book also presents the most current information about the defining pathology of osteoporosis, including a detailed description of the complex process of bone remodeling and a discussion of risk factors that cue primary care providers to rule out osteoporosis. The diagnostic and treatment protocols are particularly thorough, providing exceptional ready-to-hand reference materials for busy clinicians; the appendixes point the reader to an extensive listing of additional relevant organizations and online resources. Given that the presenting symptom of osteoporosis is still most often a fracture, the chapter outlining the surgical repair of common fractures is a valuable resource for frontline health care providers as they prepare their clients with fractures for surgical referral and the ensuing period of postoperative rehabilitation. The vivid descriptions and illustrations of the specific surgical procedures are also instructive to those who provide rehabilitative follow-up care after the surgical procedure has been performed. The chapter on health care policy is authored collaboratively by a nurse attorney, a nurse practitioner, and a reimbursement specialist. It deals with the bottom line of how to document services within the codes of public payment systems so that preventive and treatment services are available to all who need them. But the book goes beyond the diagnosis and treatment of osteoporosis. It also includes a discussion of the national and global mandate for community-based educational programs that support lifestyle choices to prevent osteoporosis, starting with helping children achieve their maximum potential bone mass. A particularly innovative community outreach model featuring a mobile unit equipped with a full-body dual
xvii
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Foreword
energy X-ray absorptiometry (DXA) machine is described in detail and presented for its use in facilitating early diagnosis for individuals who live in remote regions. The authors’ practical and in-depth insights challenge the complacency that has too long been the norm and offer new ways of confronting this silent but unwelcome intruder. Our research on osteoporosis is finally yielding the diagnostic and treatment options needed to eliminate osteoporosis in future generations. This book translates emerging findings in a way that will inform and mobilize the health care community toward this increasingly realistic goal. It provides a roadmap of detailed clinical protocols that will arm frontline clinicians from across disciplines with the information they need to significantly reduce the prevalence and impact of osteoporosis at the grassroots level. May L. Wykle, PhD, RN, FAAN, FGSA, FAGHE Dean and Cellar Professor of Nursing Frances Payne Bolton School of Nursing Director, University Center on Aging and Health Case Western Reserve University
Preface
O
steoporosis is a major global health problem that is increasing dramatically as the population ages. The World Health Organization (WHO) estimates that 70 million people worldwide have osteoporosis. Hip fractures are the most severe consequence of osteoporosis and are associated with lengthy hospital admissions, difficulty in performing activities of daily life, nursing home placement, and a high rate of mortality. The annual worldwide incidence of hip fracture is 1.5 million, a number projected to grow to 2.6 million by 2025 and to 4.5 million by 2050. The economic burden of osteoporotic fractures on society is immense. Each year in the United States, osteoporotic fractures result in more than 500,000 hospitalizations, 800,000 emergency room visits, 2.6 million physician’s office visits, and the placement of nearly 180,000 individuals in nursing homes. It is estimated that each hip fracture represents approximately $40,000 in total medical costs. But the impact of osteoporosis on the personal lives of the patients and their families is even greater. One in five persons who sustain hip fracture end up in a nursing home, and 20% of them die before a year has passed. Two-thirds of the individuals who sustain hip fracture never return to their prefracture level of function, and many lose their ability to walk, even if they were ambulatory before their fracture occurred. The primary purpose of this book is to address this now preventable health problem by giving busy clinicians the heightened awareness and knowledge they need to reduce osteoporotic fractures in present generations through early diagnosis and treatment and to prevent osteoporosis in future generations. The book is written as a handbook for frontline nurses, physicians, and other clinicians, who on a daily basis see individuals who have osteoporosis or are at risk for low bone density. They are in the best position to identify and teach those at risk early and to institute treatment in time to prevent fractures. The WHO has declared 2002–2011 as the Decade of the Bone and Joint, uniting nations throughout the world in the commitment of energy and resources to accelerate progress in bone health and prevention of fractures. Keeping in mind this global context, the chapters in this book offer quick reference information about the prevalence and impact of osteoporosis, its signature pathology, and factors that place individuals at risk for developing osteoporosis. Comprehensive but concise clinical protocols are provided, and state-of-the-art diagnostic measures, pharmacological and nonpharmaceutical
xix
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Preface
therapies, and prevention-based community education strategies are described. One chapter is devoted to surgical repair following vertebral and hip fractures, including the preparation and support of the patient and the family before and during surgery and during the ensuing lengthy rehabilitation process. Attention is also given to important related issues such as dietary requirements, exercise, fall prevention, quality of life, and independence issues. Encouraging information is also provided about emerging technological developments that may enhance our ability to detect and treat osteoporosis even earlier. But access and cost remain formidable issues in the detection of osteoporosis and the prevention of fractures, particularly for underserved and underinsured populations. Our policy and finance specialists address these issues, including Medicaid and insurance reimbursement, in their chapter. They have compiled a comprehensive list of reimbursement codes for diagnostic and treatment procedures to help practitioners apply for and obtain reimbursement for osteoporosis screening and management. Even more importantly, the editors and contributors hope that this book will have a significant impact on dispelling the insidious but still prevalent mind-set, even among clinicians, that osteoporosis and fractures are an inevitable part of aging. Specifically, we hope the book will raise the consciousness of health-related professionals about the mandate for widespread educational programs for the public, beginning with children of both genders and their parents, to eliminate osteoporosis as a public health problem in future generations. In summary, although osteoporosis is a devastating public health problem that affects all strata of the global community, there is a sound body of research findings indicating that osteoporotic fractures can be eliminated. And in recent years, pharmaceutical companies have stepped up to the challenge and are developing a sophisticated portfolio of new and improved products that can stop bone loss and build bone density. Data-based risk assessment protocols have proven to be reliable, and bone-scanning technologies are becoming increasingly portable and available to measure bone density with high accuracy, even among outlying populations. Simple but powerful bone healthy life choices are also well documented, and almost everyone in developed countries has now been exposed to the teachings that exercise, adequate calcium, and vitamin D are critical to building and maintaining strong bones. But we must not let up in our efforts. If together we apply what we already know in our practice, we can spare millions of elders in our country and around the world from the shattering experience of vertebral and hip fractures. We ask that you help us achieve this goal by applying the spirit of commitment and information provided in this book with those you see every day in your practice. Sarah H. Gueldner Theresa N. Grabo Eric D. Newman David R. Cooper
Acknowledgments
T
he editors would like to acknowledge and express appreciation to the many individuals and affiliating academic and practice institutions that have contributed to their vision and support to the development and completion of this book. In particular, we would like to thank the team of researchers and clinicians from across disciplines who have provided the high quality and relevant evidence-based information in the chapters. We would also express our deep appreciation to our respective institutional affiliations for their substantial support in terms of both their positive corporate energy and the technical assistance that they have made available to the project. Specifically, they include the Decker School of Nursing and the Bioengineering Department at Binghamton University, in Binghamton, New York; the Frances Payne Bolton School of Nursing at Case Western Reserve University in Cleveland, Ohio; The Knee Center in Wilkes-Barre, Pennsylvania; the Geisinger Health System based in Danville, Pennsylvania, and Valley GYN Specialists in Luzerne, Pennsylvania. Thanks also to artistic illustrators Stan Kaufman and Michael Cameron for their meticulous assistance in creating illustrations to clarify points made in the text, and to Guruprasad Madhavan, Ellen Madison, Jeffery Peake, Janice Pecen, Nick Plavac, Caron Baldwin, Ivy Ko, and Michael and Bernadette Lombardi for their unusually willing and capable technological support, often on short notice. Others who provided essential editorial assistance include Sally Barhydt and Katherine Tengco at Springer Publishing, Carol Cain and others at APEX Publishing, Dr. Marion Kennedy, Susan Forbush, and Meredith Lynn Cooper. We would also take this opportunity to express our appreciation to the Crane Fund for Widows and Children and the Binghamton University Research Foundation for their support of our community based research initiatives that provided the impetus for this book. Finally, we extend our utmost appreciation to the editors and support staff at Springer Publishing Company for their careful critique and polishing of our work, and for taking it to production. We believe they have once again brought out the best in us. And finally, we would like to thank the courageous individuals, including our own family members and friends, who have sustained fractures and grown stooped in their later years; it is they who have provided the personal inspiration for the book. We offer this quick reference guide to front line clinicians, who are in the best position to detect osteoporosis early and institute treatment measures in time to prevent its devastating fractures. Even more importantly, the editors and authors hope that this book will have a significant impact in dispelling the insidious but still prevalent mind set, even among clinicians, that osteoporosis and fractures are an inevitable part of aging. We hope the book will serve as an impetus to raise the awareness of health related professionals to the mandate for widespread educational programs, beginning with our children and their parents, to eliminate osteoporosis as a public health problem within future generations. Please help us achieve these goals. Sarah Gueldner, Theresa Grabo, Eric Newman, and David Cooper
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Introduction and Overview
The incidence and prevalence of musculoskeletal pain and disability in older people in all parts of the world should be considered as a matter of urgency. (World Health Organization, The Burden of Musculoskeletal Conditions at the Start of the New Millennium: Report of a Scientific Group )
The Problem
O
1
Sarah H. Gueldner Theresa N. Grabo Eric D. Newman David R. Cooper
steoporosis, leaving behind its devastating wake of fractures, is a major global health concern. And like other chronic diseases that disproportionately affect the elderly, the prevalence of osteoporosis and associated fractures is projected to increase markedly as the population ages. The most devastating consequence of osteoporosis is fracture. In the United States, 1 in 2 two women and 1 in every 5 men over 50 years of age experience an osteoporotic fracture during their lives, and more women die from the aftereffects of osteoporotic fractures than from cancer of the ovaries, cervix, and uterus together. Likewise, the economic burden of osteoporosis on society is sobering.
The Science For years it was assumed that osteoporosis was an inevitable part of aging, and that little could be done. But the state of the art is improving. With recent advances in diagnostic and treatment modalities, it has become clear that it
2
Osteoporosis
should no longer be regarded as an untreatable disease. Research in the area of bone disorders has accelerated markedly, providing both the medical community and the public with a more detailed understanding of factors that promote bone health or cause bone disease and fractures. Advances in scientific knowledge have also revealed much about the pathology, prevention, diagnosis, and treatment of osteoporosis and have shown that osteoporosis can someday be prevented in the majority of individuals and identified early and treated effectively in those who do develop it.
Transferring Knowledge to Practice The next critical step in the quest to stop osteoporosis is to transfer the knowledge gained from prevalence data and research findings to the practice of clinicians and the lifestyles of the general public. By focusing on prevention and lifestyle changes as well as early diagnosis and appropriate treatment, Americans and their fellow global citizens can avoid much of the impact of osteoporosis. Health care professionals play a critical role in promoting and supporting these lifestyle choices, and in identifying and treating those at risk early enough to prevent fractures.
The Clinical Mandate Improved methods of routine screening now allow frontline clinicians to diagnose more patients and to diagnose them earlier, significantly slowing the progression of their osteoporosis. But preventing the disease in the first place is paramount to the ultimate management goals. Systematic national and global effort must be directed toward educating the world’s public about the importance of lifestyle habits from childhood through old age. It is imperative that an algorithm be developed and instituted worldwide to support lifestyle changes and early diagnosis of osteoporosis in time to prevent fractures if at all possible. It has been shown that low bone mass is a function of failing to achieve adequate peak bone mass during childhood and adolescence, and/or the occurrence of a high rate of bone loss during times of vulnerability, as seen during menopause and advancing age. Generic and lifestyle variables (i.e., nutrition, exercise, smoking), chronic disease, and exposure to drugs (such as steroids) known to be associated with rapid bone loss also affect rate of bone loss, superimposed on the influences of age, including menopause.
Children: An Overlooked At-Risk Group Until recently, little attention was given by the primary health care community to the achievement of maximum bone mass in children during their bone development years. Fortunately, that window of opportunity for prevention is gaining considerably more attention. The National Bone Health campaign, Powerful Bones, is a national campaign to promote optimal bone health in girls 9–12 years old to help reduce their risk of
Introduction and Overview
3
osteoporosis later in life, and healthy bone awareness programs that stress diet and physical activity are increasingly being implemented in elementary schools.
The System Mandate Individuals and health professionals acting alone cannot make enough of a difference. A coordinated public health approach is the most promising strategy for eliminating osteoporosis in coming generations. However, faced with other pressing health problems such as AIDS, tuberculosis, and malaria, osteoporosis has been relegated to a low priority in most countries. Thus, the persistent challenge is once and for all to erase the lingering misperception that osteoporosis and fractures are inevitable conditions of growing old, and that nothing can be done to prevent them. Toward that purpose, the World Health Organization (WHO), in collaboration with national and international organizations concerned with bone health, has taken the lead in uniting nations around the world in the commitment of effort and resources to improve bone health and prevent fractures. America’s response to that global charge is outlined in the surgeon general’s report of 2004 on bone health and osteoporosis, drafted by more than 100 experts in the field. The report provides state-of-the-science information about bone health and illustrates the large burden that osteoporosis places on our nation and its citizens. The report is intended to alert both the public and the medical community to the importance of bone health, including its impact on overall health and well-being, and the need to take action to prevent, assess, and treat bone disease throughout life. The primary message of the report is that the bone health status of Americans can be improved, and that prevention of bone disease, particularly osteoporosis, begins at birth and is a lifelong challenge.
The Purpose of This Book Addressing the rapidly increasing prevalence and global impact of osteoporosis, the purpose of this book is to translate research findings related to osteoporosis into concise clinical guidelines for frontline clinicians, who are in a position to make the biggest difference in the future trajectory of the disease. The book is organized around four content areas: (1) prevalence, risk factors, and pathogenesis; (2) clinical management; (3) nonpharmacologic considerations; and (4) prevention strategies. Part I of the book, composed of two chapters, profiles the prevalence, risk factors, and pathogenesis of osteoporosis. Chapter 2 provides an overview of the prevalence of osteoporosis, highlighting its exponentially growing impact on the aging global society. Chapter 3 describes the underlying pathogenesis of osteoporosis, with a detailed discussion of bone remodeling. Part II of the book, composed of three chapters, provides a detailed discussion of clinical topics germane to the diagnosis and clinical management of individuals with osteoporosis. Chapter 4, written by a physician-hematologist with many years of experience in osteoporosis, profiles diagnostic tests and interpretation, outlining the steps necessary to arrive at a confirmatory differential diagnosis. This chapter also discusses specific characteristics of clinical presentation across gender and
4
Osteoporosis
life span and offers data-based protocols for obtaining individual and family history. Chapter 5, contributed by faculty in pharmacology and practice, outlines treatment imperatives, including presently available and future pharmacologic prevention and treatment options. Chapter 6, coauthored collaboratively by two orthopedic surgeons and a physician’s assistant, features the latest information about surgical procedures and perioperative management for the best treatment and rehabilitation outcomes following hip, vertebral, or wrist fracture. Each of the four chapters in part III describes nonpharmacologic approaches important to the prevention or management of osteoporosis. Chapter 7, written by a professor of nutrition and a public health epidemiologist, provides an overview of nutritional considerations. Chapters 8 and 9, authored by experts in physical therapy, speak to the exercise mandate and the critical aspect of fall prevention. Chapter 10, authored by an occupational therapist, offers protocols that address the personal experience of living with osteoporosis, including maximum functional rehabilitation and psychological adjustment to characteristic body changes. All the chapters in part IV are directed specifically at steps that need to be taken if we are to eliminate osteoporosis in coming generations. Addressing the irretrievable opportunity to achieve maximum bone mass during childhood and young adult years, chapter 11 is devoted to ways of reaching young girls and boys who are presently building their peak bone mass. The chapter also highlights the potential of school-based health centers as a readily available venue for fostering bone healthy lifestyles in elementary and middle grade children. Chapters 12 and 13 feature two successful large-scale community osteoporosis education and screening programs designed to enable physician groups and other clinicians to reach even the most remote populations. Chapter 12, addressing the barrier to access, describes an innovative screening and diagnostic program using two DXAequipped mobile vans that are operated by the rural-based Geisinger Health System and travel throughout their outpost clinic network. Each year this mobile program screens more than 3,000 persons in outlying areas of Pennsylvania, and one-third of those screened are found to have low bone density. Remarkably, the program sustains itself financially. Chapter 13 describes Creating Health: Osteoporosis, an impressive statewide education and heel-screening program that is disseminated to every county in conjunction with the state-wide network of the Pennsylvania State University Extension Program. The public broadcasting system associated with the extension program enhances the production and delivery of appealing high-quality sound bites to a wide regional audience. Stand Tall Pennsylvania, a successful partnership model for the delivery of a screening and education program to people who live in remote areas of Pennsylvania, is also described. Chapter 14, written jointly by a nurse lawyer, a nurse practitioner, and a Medicare specialist, provides invaluable information about the role that health policy and insurance reimbursement play in the prevention and management of osteoporosis. The chapter provides detailed how-to information for obtaining reimbursement for procedures related to the diagnosis and management of osteoporosis. Finally, encouraging information is presented in chapter 15 about innovative nonpharmacological bioengineering theories and technologies under development that hold promise for increasing our ability to detect and treat osteoporosis in time to reduce
Introduction and Overview
5
and better manage its unwelcome sequelae. Perhaps the best-known such innovation is a vibrating platform device that resembles a bathroom scale that sits on the floor and delivers a high-frequency, low-magnitude (30Hz) mechanical signal (perceived as a gentle vibration) to the femur and spine of the standing human. It is thought by its developers to boost bone mass by increasing lower limb circulation, thus improving the delivery of essential nutrients and minerals to the bones. The device has been tested in children with disabling conditions, postmenopausal women, U.S. Army recruits, and most recently NASA astronauts, who are known to lose bone mass while in the weightless environment of space. In animal models, the intervention has been shown to inhibit disuse osteopenia. This chapter is written collaboratively by bioengineering and nursing faculty at Binghamton University, where the research project is based. The comprehensive appendix A provided at the back of the book includes access information for a number of important documents that have utility for clinicians as they incorporate best practices into their management of persons who have or are at risk for osteoporosis. The 2004 surgeon general’s report, Bone Health and Osteoporosis, prepared by the U.S. Department of Health and Human Services under the direction of the Office of the Surgeon General, represents perhaps the most definitive document available on this topic and served as a primary source for much of the information in this book. The full document is not provided in the appendix, but the NIH Resource Center provides free single copies of this publication to individuals who request it by faxing 1-202-293-2356. Appendix B is a listing of the diagnoses that support the medical necessity for bone densitometry studies, thus facilitating the reimbursement process.
Summary Osteoporosis is a severe public health problem that affects all strata of the global community. The good news is that healthy women and men 50–65 years of age still have time to engage in osteoporosis-preventing behaviors to reduce bone loss and eventual height loss. It is imperative that research efforts be continued and expanded to develop additional effective treatment measures with fewer unpleasant side effects, and that both professionals and the general public become better informed about lifestyles that support bone health. Professional and community education programs are beginning to have an impact in teaching primary care providers and the clients that they serve about the importance of early diagnosis of osteoporosis and the timely institution of treatment. But for best results, more awareness and education efforts need to also be directed toward the young girls and boys who are presently building their peak bone mass, for it is only through their generation and following generations that osteoporosis can be eliminated. Osteoporosis is a lifelong condition that manifests itself in old age, and the best treatment is to engage in bone healthy lifestyles from childhood on. Applying what is already known about prevention, assessment of risk factors, diagnosis, and treatment has led to marked improvements in bone health status. It is the intent of this book to place that stateof-the-science information at the fingertips of primary health care providers and other health-related professionals, to hasten the achievement of that goal.
1
Prevalence, Risk Factors, and Pathogenesis
Demographic Perspectives: The Magnitude of Concern
The silent epidemic of osteoporosis has been challenged. We are now beginning to appreciate the magnitude of this disorder in our world populations. (R. L. Wolf, “Epidemiology: The Magnitude of Concern” )
Introduction
T
2
Janice Penrod Annabelle M. Smith Susan Terwilliger Sarah H. Gueldner
he prevalence of osteoporosis is typically determined using a classification system suggested in 1994 by an expert panel of the World Health Organization (WHO) (Kanis, 1994; World Health Organization [WHO], 2003). The classification system is based on measurements of the bone mineral density (BMD) of women. A woman’s actual BMD is assessed and then compared to the average peak BMD of a healthy young adult White female reference group. The woman’s deviation from this average (statistical mean) is then calculated in standardized units (i.e., standard deviations or SDs). Women are considered to have a normal BMD if their score falls within 1 SD of the mean. Those whose BMD score falls within 1 to 2 SDs below the mean are classified as having osteopenia, a condition in which the bone loss is not severe enough to warrant classification as osteoporosis. The classification of osteoporosis is given to those whose BMD score is greater than (or equal to) 2.5 SDs below the mean. Women who have a history of fragility fractures and a BMD score greater than or equal to 2.5 SDs below the mean are classified as having severe or established osteoporosis. It is important to take into account the fact that this classification system, though commonly used, has significant limitations for estimating prevalence across diverse international populations. The applicability of the WHO criteria to groups other than White women is not exact. Current recommendations are to use a White female
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Osteoporosis
reference population for all groups (Radiological Devices FDA Panel Meeting Summary, 1999), although the appropriate cutoff values for osteoporosis and osteopenia in men and other racial and ethnic groups are still under investigation. In addition, the prevalence of osteoporosis may be underestimated when only a single BMD site (e.g., the hip) is used, since an individual with normal BMD at one site may have low BMD at another site (e.g., the spine, wrist). The prevalence of osteoporosis is expected to be higher if a number of skeletal sites are assessed simultaneously (Melton, Atkinson, O’Connor, O’Fallon, & Riggs, 1998). These limitations are important when trying to estimate the prevalence rates of osteoporosis in a given population, especially from a global perspective. Since available estimates are based on these measurements, the authors acknowledge the possibility of variances in the prevalence statistics presented below. Likewise, despite advances in the accurate measurement and interpretation of BMD, it is recognized that the numbers of individuals tested for and diagnosed as having osteoporosis may be underestimated.
Prevalence Using the WHO definition based on bone density measurement, it is estimated that there are roughly 10 million Americans over the age of 50 with osteoporosis of the hip, and 34 million others with osteopenia of the hip (National Osteoporosis Foundation [NOF], 2002; U.S. Department of Health and Human Services [USDHHS], 2004). Using the WHO criteria for osteopenia and osteoporosis, Looker et al. (1997) reported the prevalence of low femoral bone density in a sample of 14,646 men and women who participated in the Third National Health and Nutritional Examination Survey (NHANES III). The reference population was 382 White men and 409 White women, 20 to 29 years of age. According to the WHO criteria, osteoporosis under age 50 was rare. However, 13% to 18% of women aged 50 or older had osteoporosis, and another 37% to 50% had osteopenia. At the time of this report, those figures translate to 4 to 6 million women with osteoporosis and 13 to 17 million with low bone mass (osteopenia). Further predictions based on the NHANES III study were made for the year 2002 and beyond (NOF, 2002), with a reported expectation that by the year 2002, 7.8 million women and 2.3 million men over age 50 would have osteoporosis, and 21.8 million women and 11.8 million men over age 50 would have osteopenia. The prevalence of osteoporosis in the United States is highest among White women (Hispanic or non-Hispanic). The NHANES III report estimated that 15% of White women met the criteria for osteoporosis (Mirza & Prestwood, 2004). Similar numbers were seen in the Hispanic population; however, the prevalence among African American women was only half as great as was seen in the White and Hispanic populations. The National Osteoporosis Foundation (NOF) estimates that 55% of all Americans aged 50 and older in the year 2002 had either osteoporosis or osteopenia (low bone mass). Based on the 2000 Census, prevalence estimates increased to 52 million women and men for the year 2010, and to 61 million in 2020 (NOF, 2002). In the United Kingdom, it is estimated that 23% of women aged 50 years or more are osteoporotic, with increases proportional to age (Upton, 2005). The percentages of Swedish women who have osteoporosis range from 7% of women 50–59 years of
Demographic Perspectives
11
age to 36% for those 80–89 years. The prevalence of osteoporosis is higher for women in Norway than anywhere else in Europe. Estimates of prevalence among African American women are that it is about half that of White women (Mirza & Prestwood, 2004). Asian and White non-Hispanic women have the lowest BMDs throughout life, and African American women have the highest. Mexican American women have bone densities that are intermediate between the two groups. Limited data suggest that Japanese and Native American women attain a peak BMD that is lower than for White non-Hispanic women (National Institutes of Health, 2000). In 2002, it was estimated that 44 million people in the United States have osteoporosis, with 68% being women and 32% being men (Gueldner, Britton, & Stucke, 2006; NOF, 2002), providing confirmatory evidence that osteoporosis affects both genders, and that the numbers of individuals with the disease are on the rise. It is estimated that the number of persons with osteoporosis/osteopenia will increase to 52 million by year 2010, and to 61 million by year 2020.
Fractures Fracture is the most significant consequence of osteoporosis. Although osteoporosis can affect any bone in the body, the most typical sites of fractures related to osteoporosis are the hip, spine, and wrist (NOF, 2006). Of the 1.5 million fractures that occur in the United States each year, 20% occur at the hip, 50% in the spine, and 30% at the wrist and other sites. The annual worldwide incidence of fracture was estimated to be 1.29 million in l990, and is projected to grow to 2.6 million by 2025 and to 4.5 million by 2050 (WHO, 2003). The highest fracture rates are reported from northern Europe, the northern part of the United States, and among Southeast Asian populations, with the lowest rate from African countries. The risk of hip fracture among Norwegians is four times that of southern Europeans and double that of Americans. It is of note that the differences in incidence of hip fractures between countries are greater than the differences between genders (Chang, Center, Nguyen, & Eisman, 2004; WHO, 2003). Fracture site is also age related. For individuals in their 50s, wrist fractures are most common. Individuals in their 60s are more likely to sustain fractures of the vertebrae of the spine, and by the time an individual reaches the 70s, the hip becomes the most common site of osteoporotic fracture (Cooper, Campion, & Melton, 1992). The rates of all three types of fracture increase with age, but the increased risk with aging is most pronounced for hip fractures (Kenny, Joseph, Taxel, & Prestwood, 2003; Melton, 1996).
Lifetime Fracture Risks Considering the lifetime fracture risk for each site, women have about an 18% chance of hip fracture, a 16% chance of vertebral fracture, and a 16% chance of wrist fracture (Melton, Chrischilles, Cooper, Lane, & Riggs, 1992). Again, age-related changes are prominent; by age 50, White women have about a 40% chance of fracturing their hip, spine, or wrist in their remaining lifetime (Cummings & Melton, 2002). This statistic equates to a 4 out
12
Table
2.1
Osteoporosis
2002 Prevalence of Osteoporosis and Low Bone Mass for the Top 10 States, With Estimated Prevalence for 2010 and 2020 State California Florida New York Texas Pennsylvania Ohio Michigan New Jersey North Carolina Virginia
2002
2010
2020
4,297,500 3,014,600 2,831,400 2,748,500 2,216,300 1,889,200 1,509,300 1,323,200 1,273,300 1,058,100
5,246,600 3,772,400 3,123,200 3,444,300 2,490,200 2,156,500 1,731,000 1,512,800 1,594,100 1,295,700
6,542,700 4,715,900 3,424,500 4,152,600 2,728,300 2,365,500 1,898,600 1,710,800 1,937,000 1,541,200
Note. From “Tables in National Osteoporosis Foundation,” 2002, in America’s Bone Health: The State of Osteoporosis and Low Bone Mass in Our Nation (Washington, DC: National Osteoporosis Foundation), pp. 17–25.
of 10 lifetime risk for significant fracture and a 1 out of 6 lifetime risk for hip fracture for every woman over the age of 50. These risks are equal to the combined risks of developing breast, uterine, and ovarian cancer in the remaining years of life (NOF, 2002). For men, the estimated lifetime fracture risk is about 13% after age 50 (Cauley, 2002; Cummings & Melton, 2002). The site-specific fracture risks are 6% for the hip, 5% for the spine, and 3% for the wrist. However, even though men age 50 and beyond have a lower lifetime risk for osteoporotic fracture than women, the risk for developing a fracture is almost as great as the risk of developing other conditions common to this age group, such as prostate cancer (Cauley, 2002). The lifetime risk for a White male, based on an age-adjusted incidence rate, is 16.3% (National Cancer Institute, 2006). The most abundant data available for non-Whites in the United States are related to fractures of the hip. Fang, Freeman, Jeganathan, and Alderman (2004) conducted a study in New York City from 1988 to 2002 in which hospitalization rates for male and female non-Hispanic Whites, Blacks, Hispanics, and Asians over age 50 were tracked. The results showed that the risk of a hip fracture in the three ethno-cultural subgroups was approximately one-third to one-half less than that of Whites. A listing of the top 10 states, by prevalence and estimate increase, is provided in Table 2.1.
Global Perspectives The WHO has reported that in 1990, 1.66 million hip fractures occurred around the world (WHO, 2003). Johnell and Kanis (2004) estimated slightly fewer fractures (1.3 million) for the same year, with the most fractures (52.5%) occurring in North America, Japan, Australia, and western Europe, and the least (0.5%) in sub-Saharan Africa. The highest rates of hip fracture have been found to occur in Scandinavia (Woolf & Pfleger,
Demographic Perspectives
13
2003), with 5-year mortality rates in Sweden following hip fracture reaching 59%, and 72% after fracture of the spine ( Johnell et al., 2004). When considering the geographic distribution of osteoporosis and related fractures, deficiencies in vitamin D cannot be ignored. Vitamin D deficiency may predispose individuals to developing osteoporosis and, subsequently, to suffering osteoporotic fracture. Individuals living north of 42 degrees north latitude (the established northern border for optimal ultraviolet B (UVB) synthesis of vitamin D; Higdon, 2004), such as those included in the Scandinavian region, are at risk for vitamin D deficiencies. Similarly, individuals who cover their bodies or are darker skinned are also at risk for vitamin D deficiencies. A study of Lebanese men and women (both people of dark pigmentation and people who practice veiling) reported a 68.1% vitamin deficiency in this population, with the deficiency being more prevalent in women than men (Ghassan et al., 2004).
Consequences of Osteoporosis Mortality Of the three most common sites of osteoporotic fractures, hip fracture poses the most significant insult to the health status of an individual. Increased mortality risk with hip fracture is related to comorbidities such as strokes or chronic lung diseases (Browner, Pressman, Nevitt, & Cummings, 1996), poor health prior to the fracture (Richmond, Aharonoff, Zuckerman, & Koval, 2003), and complications that arise secondary to medical/surgical treatment of the fracture. Excess mortality occurring after a hip fracture, compared with that expected in the population, is estimated to be 12% to 35% higher. A person’s age, race, gender (Center, Nguyen, Schneider, Sambrook, & Eisman, 1999; Ismail et al, 1998; Jacobsen et al., 1992), health, and functional status (Browner et al., 1996; Magaziner et al., 1997) contribute to the survival outcome following hip fractures. The greatest excess mortality typically occurs within the first year ( Jacobsen et al., 1992), with one study reporting a death rate of 20% in the first year following hip fracture (Leibson, Tosteson, Gabriel, Ransom, & Melton, 2002). In the same study it was shown that the risk of mortality was four times greater during the first 3 months following the fracture. Men appear to have a poorer prognosis postfracture than do women (Center et al., 1999). A large prospective study demonstrated that men had poorer survival outcomes than women for hip, vertebra, and other major (e.g., pelvic, rib) and minor (e.g., distal arm and leg) fractures (Center et al., 1999). In general, African Americans fare relatively worse than their White counterparts ( Jacobsen et al., 1992) in terms of mortality following hip fracture.
Morbidity Morbidity, the term used to denote living with the sustained effects of a health disturbance, is of great concern for persons who suffer a fracture. For most, the effects of the event are sustained. Reports from the Established Populations for Epidemiologic Studies of the Elderly (EPESE) confirm that 40%–79% do not regain their prefracture
14
Osteoporosis
walking status within a year after hip fracture, and fewer than 50% ever recover their prefracture ability to perform physical activities of daily living such as eating, dressing, grooming, or bathing (Greendale & Barrett-Connor, 2001). Further, nearly 1 in 5 persons who sustain a hip fracture will end up in a nursing home, and 20% will die before a year has passed (Leibson et al., 2002). One study showed that more than half of the men who suffer a hip fracture are discharged to a nursing home, and that 79% of these men who survive at 1 year will reside in nursing homes or intermediate care facilities (Poor, Atkinson, Lewallen, O’Fallon, & Melton, 1995). By comparison, 19% of women who suffer a hip fracture will require the services of a long-term care facility (Chrischilles, Butler, Davis, & Wallace, 1991). In a study of members of a fairly healthy population sustaining a new hip fracture and then being discharged to their own homes, gait and balance were assessed 2 months after the fracture and then patients were followed for the next 2 years (Fox et al., 1998). Both poor balance and poor gait were associated with more admissions to nursing homes (20% and 17% increases in odds, respectively); however, poor balance, but not gait, resulted in more hospitalizations and increased mortality rates (a 17% increase with each unit decrease in balance score) following the fracture. Another study found that after adjustments for possible confounders, including comorbid conditions, women with hip fractures were significantly more likely to report difficulty performing 11 out of 15 different tasks, including mobility tasks (e.g., walking two or three blocks), higherfunctioning tasks (e.g., light housework, preparing meals), and basic self-care tasks (e.g., bathing, dressing) (Hochberg et al., 1998). Thus, hip fracture presents long-term negative effects for those who survive the initial threat to health. In vertebral fractures, morbidity is a profound concern. Osteoporotic fractures of the spine result in an unnatural, pronounced curvature of the spine (i.e., kyphosis) and loss of height. These spinal fractures are often called crush fractures—a term that captures the collapse of the vertebral column onto itself. As the spine loses structural support, the rib cage moves downward. In some cases, the rib cage eventually comes to rest on the iliac crests. This downward shift of the body’s structural support pushes internal organs downward and forward from the thorax toward the abdomen, accentuating an abdominal protuberance. These structural changes produce concomitant morbidity: height loss, back pain, abdominal fullness, and inhibited breathing patterns. Nevitt et al. (1998) reported the results from a large prospective study of 7,223 older White women who had spine X-rays at baseline, and at a follow-up examination an average of 3.7 years later as part of their participation in the Study of Osteoporotic Fractures (SOF). Compared to women without a spine fracture at baseline, those with at least one new vertebral fracture were more likely to have increased back pain and back disability. Among women who already had a fracture at baseline, those with a new incident fracture had a substantial increase in back pain and functional limitations as well. Many of these problems subsequently affect other health patterns. For example, kyphosis is associated with diminished function, especially in mobility tasks like walking and climbing stairs (Ryan & Fried, 1997). Abdominal fullness is often related to early satiety (a term referring to early satisfaction and fullness upon eating), which over time may result in weight loss. Kyphotic changes in posture lead to more shallow respirations, which have implications should the person affected require surgery or anesthesia. Over time, severe kyphosis may even lead to chronic lung disease.
Demographic Perspectives
15
The impact of vertebral deformities may be worse for men than for women (Burger et al., 1997; Matthis, Weber, O’Neill, & Raspe, 1998). A large study of 15,570 European men and women showed that the associations between vertebral deformities and negative health outcomes (presence and intensity of back pain, functional capacity, and overall subjective health) were stronger in men than women (Matthis et al., 1998). Similarly, in another prospective study conducted in Rotterdam, the Netherlands, stronger associations were found between severe deformities and detrimental health outcomes in men than in women (Burger et al., 1997). Even wrist fracture poses morbidity concerns. Colles’ fractures can result in longterm inability to perform household tasks or personal hygiene. Though the impact on function tends to be underestimated, these fractures may have serious lasting effects on everyday life (USDHHS, 2004). It is also important to note that while the consequences of wrist fractures are generally not as serious as those of hip and spinal fractures on presentation, they have great clinical importance as a predictor of future hip fractures. The risk of hip fracture after a wrist fracture is increased 1.4-fold in U.S. women, 1.5-fold in Swedish women, and 1.8-fold in Danish women. Wrist fracture is an even stronger predictor of hip fracture in men; U.S. men who had a wrist fracture were found to be 2.3 times more likely to sustain a hip fracture, and Swedish men with a wrist fracture were 2.8 times more likely to sustain a hip fracture. From a psychological perspective, postfracture morbidity poses a threat to the overall quality of life. Several factors discussed above contribute to perceived losses in functional, social, and psychological well-being. For example, limited mobility and functional capabilities, pain, and loss of independence are often direct effects of fracture. Deformity, produced as osteoporotic changes invade the spine, is difficult for many to accept. Fear of falling and of subsequent fractures may also pose psychological concerns. In a survey conducted by the NOF, 89% of the women who had sustained an osteoporotic fracture said they were afraid of breaking another bone, 80% feared losing their independence, 80% feared they would not be able to perform their daily activities, and 68% were afraid that they would have to go to a nursing home if they had another fracture. As noted before, approximately half of the individuals who sustain hip fractures never walk independently again, even if they were ambulatory before their fracture (USDHHS, 2004). Such morbidities should not be underattended in the effort to reduce the toll of osteoporosis on the public’s health. Nor is the effect of postfracture morbidity limited to the individual—the effect ripples into the social structures of the adult with osteoporosis. Loss of independence leads to new family roles and responsibilities. Chronic care, offered informally within the family and coordinated with formal caregivers, has its own set of demands and burdens that extend into the network of family and community, and ultimately into society at large. The human and monetary costs of treatment and rehabilitation following fracture are often shared among family members and are partially assumed by public providers. Osteoporosis reaches into the lives and pockets of us all.
Costs The monetary costs associated with osteoporotic fractures are sobering. In l995, osteoporosis resulted in 423,000 hospital admissions, 800,000 emergency room visits, 180,000 nursing home admissions, and 2.5 million physician’s office visits. In the United States alone, the annual direct cost for medical care associated with osteoporotic fractures was
16
Osteoporosis
estimated to be between $12.2 and $17.9 billion in 2002, with each hip fracture costing $40,000 in medical costs (Tosteson, 1999). Spinal fractures are considerably less problematic in terms of cost, with only 10% requiring hospitalization and fewer than 2% being admitted to a nursing home. However, they account for 66,000 physician’s office visits and at least 45,000 hospital admissions each year (USDHHS, 2004). Since most of these fractures occur among older adults who are no longer employed, these figures are not heavily weighted by loss of wages. Rather, the costs are associated with direct care services: inpatient care (62%), nursing home care (28%), and outpatient service (10%). Hip fractures account for about 63% of these costs, while fractures at other sites consume the remaining 37% (Ray, Chan, & Thamer, 1997). Given that 75% of all hip, spine, and distal forearm fractures occur in persons 65 years and older, a large portion of the direct costs is borne by society, in the form of social reimbursement programs (Gueldner, Grabo, Britton, Pierce, & Lombardi, 2007). Even the group least susceptible to fracture, non-White men, required $174 million in osteoporosis care in 1995. The significant contribution of nonhip fractures in men and non-White groups to health care expenditures dispels any lingering misconceptions that the impact of osteoporosis is limited to hip fractures among older White women.
Future Projections Global graying has become a commonplace reality—the population is living longer, and the proportion of old people within the population is growing. The fastest-growing segment of the population is the oldest-old (i.e., those age 85 years or more). Consider the ramifications of these demographic trends on the incidence of osteoporosis and fracture (both highly associated with increasing age). Global demographic changes are expected to dramatically increase the prevalence of osteoporosis. By 2050, it is estimated, the number of individuals age 65 and older will be nearly 1.55 billion worldwide. The increase among this population could result in an almost 4-fold increase in the number of hip fractures worldwide (Cooper et al., 1992). That projection equates to a growth from 1.66 million fractures (worldwide) in 1990 to 6.26 million fractures in 2050. The most significant increase in hip fracture rates is expected to occur in third world countries, particularly in Asia ( Johnell & Kanis, 2004). Currently, Asia accounts for approximately 30% of global hip fractures. By 2050, it is expected to account for more than 50% of all hip fractures (Ellfors, 1998). It is imperative that due consideration be given to the collective impact of these fractures on the individual, the family, the community, and society. Osteoporotic fractures represent a phenomenal concern that demands our utmost attention if we are to avert the predicted rapidly increasing trend. Osteoporosis presents a major public health concern. Arresting this preventable disorder must be a major focus of global preventive efforts in this century.
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Burger, H., Van Daele, P. L., Grashuis, K., Hofman, A., Grobbee, D. E., Schutte, et al. (1997). Vertebral deformities and functional impairment in men and women. Journal of Bone and Mineral Research, 12, 152–157. Cauley, J. A. (2002). The determinants of fracture in men. Journal of Musculoskeletal and Neurological Interactions, 2(3), 220–221. Center, J. R., Nguyen, T. V., Schneider, D., Sambrook, P. N., & Eisman, J. A. (1999). Mortality after all major types of osteoporotic fracture in men and women: An observational study. Lancet, 353, 878–882. Chang, K., Center, J., Nguyen, T., & Eisman, J. (2004). Incidence of hip and other osteoporotic fractures in elderly men and women: Dubbo Osteoporosis Epidemiology Study. Journal of Bone and Mineral Research, 19(4), 532–536. Chrischilles, E. A., Butler, C. D., Davis, C. S., & Wallace, R. B. (1991). A model of lifetime osteoporosis impact. Archives of Internal Medicine, 151(10), 2026–2032. Cooper, C., Campion, G., & Melton, L. J., III. (1992). Hip fractures in the elderly: A world-wide projection. Osteoporosis International, 2(6), 285–289. Cummings, S. R., & Melton, L. J., III. (2002). Epidemiology and outcomes of osteoporotic fractures. Lancet, 18(359), 1761–1767. Ellfors, L. (1998). Are osteoporotic fractures due to osteoporosis? Impacts of a frailty pandemic in an aging world. Aging: Clinical and Experimental Research, 10, 191–204. Fang, J., Freeman, R., Jeganathan, R., & Alderman, M. H. (2004). Variations in hip fracture hospitalization rates among different race/ethnicity groups in New York City. Ethnicity and Disease, 14(2), 280–284. Fox, K. M., Hawkes, W. G., Hebel, J. R., Felsenthal, G., Clark, M., Zimmerman, S. E., et al. (1998). Mobility after hip fracture predicts health outcome. Journal of the American Geriatrics Society, 46, 169–173. Ghassan, M., Alexandre, N., Joseph, W., Fadj, H., Georges, F., Joseph, H., et al. (2004). Osteoporosis a disease for all; in Lebanon. Clinical Calcium, 14(9), 116–122. Greendale, G. A., & Barrett-Connor, E. (2001). Outcomes of osteoporotic fractures. In R. Marcus, D. Feldman, & J. Kelsey (Eds.), Osteoporosis (Vol. 1, 2nd ed., pp. 819–829). San Diego: Academic Press. Gueldner, S. H., Britton, G., & Stucke J. (2006). Osteoporosis. In J. Fitzpatrick & M. Wallace (Eds.), Encyclopedia of nursing research. New York: Springer Publishing. Gueldner, S. H., Grabo, T. N., Britton, G. A., Pierce, C., & Lombardi, B. (2007). Osteoporosis and aging related bone disorders. In J. Birren (Ed.), Encyclopedia of gerontology. Oxford, England: Elsevier. Higdon, J. The Linus Pauling Institute Micronutrient Information Center. (2004). Vitamin D. Retrieved October 17, 2005, from http://lpi.oregonstate.edu/infocenter/vitamins/vitaminD/ Hochberg, M. C., Williamson, J., Skinner, E. A., Guralnik, J., Kasper, J. D., & Fried, L. P. (1998). The prevalence and impact of self-reported hip fracture in elderly community-dwelling women: The Women’s Heath and Aging Study. Osteoporosis International, 8, 385–389. Ismail. A. A., O’Neill, T. W., Cooper, C., Finn, J. D., Bhalla, A. K., Cannata, J. B., et al. (1998). Mortality associated with vertebral deformity in men and women: Results from the European Prospective Osteoporosis Study (EPOS). Osteoporosis International, 8, 291–297. Jacobsen, S. J., Goldberg, J., Miles, T. P., Brody, J. A., Stiers, W., & Rimm, A. A. (1992). Race and sex differences in mortality following fracture of the hip. American Journal of Public Health, 82, 1147–1150. Johnell, O., & Kanis, J. A. (2004). An estimate of the worldwide prevalence, mortality and disability associated with hip fracture. Osteoporosis International, 15, 897–902. Johnell, O., Kanis, J. A., Oden, A., Sernbo, I., Redlund-Johnell, I., Petterson, C., et al. (2004). Mortality after osteoporotic fractures. Osteoporosis International, 15, 38–42. Kanis, J. A. (1994). Osteoporosis and its consequences. In R. Marcus (Ed.), Osteoporosis (pp. 1–20). Cambridge, MA: Blackwell Science. Kenny, A. M., Joseph, C., Taxel, P., & Prestwood, K. M. (2003). Osteoporosis in older men and women. Connecticut Medicine, 67(8), 481–486. Leibson, C. L., Tosteson, A. N., Gabriel, S. E., Ransom, J. E., & Melton L. J. (2002). Mortality, disability, and nursing home use for persons with and without hip fracture: A population-based study. Journal of the American Geriatrics Society, 50(10), 1644–1650. Looker, A. C., Orwoll, E. S., Johnston, C. C., Jr., Lindsay, R. L., Whaner, H. W., Dunn, W. L., et al. (1997). Prevalence of low femoral bone density in older US adults from NHANES III. Journal of Bone and Mineral Research, 12, 1761–1768.
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Osteoporosis Magaziner, J., Lydick, E., Hawkes, W., Fox, K. M., Zimmerman, S. I., Epstein, R. S., et al. (1997). Excess mortality attributable to hip fracture in white women aged 70 years and older. American Journal of Public Health, 87, 1630–1636. Matthis, C., Weber, U., O’Neill, T. W., & Raspe, H. (1998). Health impact associated with vertebral deformities: Results from the European Vertebral Osteoporosis Study (EVOS). Osteoporosis International, 8, 364–372. Melton, L. J., III. (1996). Epidemiology of hip fractures: Implications of the exponential increase with age. Bone, 18, 121S–125S. Melton, L. J., III, Atkinson, E. J., O’Connor, M. K., O’Fallon, W. M., & Riggs, B. L. (1998). Bone density and fracture risk in men. Journal of Bone and Mineral Research, 13, 1915–1923. Melton, L. J., III, Chrischilles, E. A., Cooper, C., Lane, A. W., & Riggs, B. L. (1992). Perspective: How many women have osteoporosis? Journal of Bone and Mineral Research, 7, 1005–1010. Mirza, F. S., & Prestwood, K. M. (2004). Bone health and aging: implications for menopause. Endocrinology and Metabolism Clinics of North America, 33, 741–759. National Cancer Institute. (2006). SEER cancer statistics review 1975–2002. Retrieved June 28, 2006, from http://seer.cancer.gov/statfacts/html/prost.html National Institutes of Health. (2000). Osteoporosis prevention, diagnosis, and therapy. NIH Consensus Statement, 17(1), 1–52. National Osteoporosis Foundation. (2002). America’s bone health: The state of osteoporosis and low bone mass in our nation. Washington, DC: National Osteoporosis Foundation. National Osteoporosis Foundation. (2006). Osteoporosis: What is it? Retrieved June 28, 2006, from http://www.nof.org/osteoporosis/index.htm Nevitt, M. C., Ettinger, B., Black, D. M., Stone, K., Jamal, S. A., Ensrud, K., et al. (1998). The association of radiographically detected vertebral fractures with back pain and function: A prospective study. Annals of Internal Medicine, 128, 793–800. Poor, G., Atkinson, E. J., Lewallen, D. G., O’Fallon, W. M., & Melton, L. J., III. (1995). Age-related hip fractures in men: Clinical spectrum and short-term outcomes. Osteoporosis International, 5, 419–426. Radiological Devices Panel Meeting Summary. (1999, May 17). Retrieved from www.fda.gov/cdrh/ rdp.html Ray, N. F., Chan, J. K., & Thamer, M. (1997). Medical expenditures for the treatment of osteoporotic fractures in the US in 1995: Report from the National Osteoporosis Foundation. Journal of Bone and Mineral Research, 12, 24–35. Richmond, J., Aharonoff, G. B., Zuckerman, J. D., & Koval, K. J. (2003). Mortality risk after hip fracture. Journal of Orthopedic Trauma, 17(8)(Suppl.), S2–S5. Ryan, S. D., & Fried, L. P. (1997). The impact of kyphosis on daily functioning. Journal of the American Geriatrics Society, 45, 1479–1486. Tosteson, A.N.A. (1999). Economic impact of fractures. In E. S. Orwoll (Ed.), Osteoporosis in men: The effects of gender on skeletal health (pp. 15–27). San Diego: Academic Press. Upton, J. (2005). The osteoporosis nurse initiative: Past, present, and future. Retrieved July 1, 2005, from http://web4.epnet.com/DeliveryPrintSave.asp?tb=1&_ug=sid+C19B3F46–7D5F4E8A-B08 U.S. Department of Health and Human Services. (2004). Bone health and osteoporosis: A report of the surgeon general. Public Health Service, Office of the Surgeon General, Rockville, MD. Retrieved from http://www.surgeongeneral.gov/library/bonehealth/ Wolf, R. L., Penrod, J. & Cauley, J. A. (2000). Epidemiology: The magnitude of concern. In S. H. Gueldner, M. S. Burke, & H. Smiciklas-Wright (Eds.), Preventing and managing osteoporosis (p. 5). New York: Springer Publishing Company. Woolf, A. D., & Pfleger, B. (2003, September). Burden of major musculoskeletal conditions. Bulletin of the World Health Organization, 81(9), 646–656. World Health Organization. (2003). Prevention and management of osteoporosis. Technical Support Series, no. 921. Geneva, Switzerland: Author.
The Pathogenesis of Osteoporosis
Osteoporosis, regardless of etiology, always represents enhanced bone resorption, relative to formation. Thus, insights into the pathogenesis of this disease, and progress in its prevention and/or cure, depend upon understanding the mechanisms by which bone is degraded. (S. L. Teitelbaum, M. M. Tondravi, and P. Ross, “Osteoclast Biology” )
Introduction
F
3
Sheri A. Stucke Bernadette M. Lombardi Sarah H. Gueldner Theresa N. Grabo
or clinicians to be able to detect and treat this silent disease, an understanding of the pathophysiology of osteoporosis is critical. Osteoporosis is primarily a skeletal disorder, usually not diagnosed until an osteoporotic fracture occurs. But by the time a fracture occurs, the pathology has been in progress for a long time. We must learn how to recognize the pathology in time to institute treatment to prevent fractures. The human skeleton, comprised of approximately 206 bones, fulfills a variety of functions: Bones give shape and form to the body, support the body’s weight, protect vital organs, serve as a storage area for minerals such as calcium and phosphorus, provide stem cells from bone marrow for healing and cell growth, and work in concert with the muscular system to assist the body with movement (Black, Topping, Durham, Farquharson, & Fraser, 2000; Orthovita, 2006). Perhaps because of its hard texture, bone is commonly thought of as an inactive tissue. However, it is actually a dynamic tissue in which the cells are involved in extensive interactions with one another, and with hematopoietic (blood-forming) and stromal (connective-tissue) cells in the bone marrow. These interactions are particularly prominent in maintaining bone mass.
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Osteoporosis
Bone Physiology There are two types of bone, cancellous (also called trabecular) bone, which accounts for approximately 20% of the total bone mass, and cortical bone, which accounts for the other 80% of bone mass (American Medical Association [AMA], 2006). Cancellous bone is formed by an interconnected structure of latticework and is the more delicate type of bone. It is porous and is often referred to as the spongy inner structure of the bone. Because it is more metabolically active and has a larger surface area, cancellous bone is more susceptible to bone loss and fracture. Cancellous bone is located primarily at the ends of the long bones (such as the head of the femur and distal end of the ulna and radius, where osteoporotic fractures often occur) and is the main type of bone, comprising the flat bones such as the sternum, the pelvis, and the 33 vertebrae (Rosen, Verault, Steffens, Cheleuitte, & Glowacki, 1997). Cortical bone is the more dense type of bone that surrounds the cancellous bone to form the outer, more durable layer bearing the majority of the body’s weight. Cortical bone is located primarily in the middle section of the long bones of the body, including the tibia, fibula, femur, radius, ulna, and humerus. In addition to providing strength, cortical bone provides sites for attachment of tendons and muscles (U.S. Department of Health and Human Services [USDHHS], 2004).
At the Cellular Level The distinctive firm fabric of the bone is a unique deposit of living cells embedded in a three-dimensional structure of extra-cellular matrix that has been stabilized by calcification (Marcus, Feldman, & Kelsey, l996). Invasion by blood vessels brings in nutrients and the cells that carry out the functions of the bone, including repair and maintenance of mass. At the cellular level, bone is made up of three types of specialized bone cells (osteoblasts, osteocytes, and osteoclasts) that interact with a variety of minerals, proteins, hormones, water, and other molecules to nourish the bone, and to continually remove old or worn bone tissue and replace it with new bone in a process called remodeling, which is described in the next section. Both the osteoblasts and the osteocytes are derived from not yet differentiated precursor cells that can also be stimulated to become muscle, fat, or cartilage but under the right conditions can differentiate to form new bone cells. During the remodeling process, osteoblasts lay down orderly layers of bone that add strength to the matrix. Some of the osteoblasts are buried in the matrix as it is being produced, becoming osteocytes (bone cells). Other osteoblasts remain as thin bone cells that cover the surface of the bone, called lining cells (Figure 3.1). Osteocytes are connected to each other and to the surface of osteoblasts by a network of small threadlike extensions, and are involved in conveying nutrition and information throughout the bone (USDHHS, 2004). Osteoclasts, on the other hand, are the cells that remove old or damaged bone by dissolving the mineral and breaking down the matrix in a process called bone resorption. Under normal conditions, the functions of the osteoblasts and osteoclasts are coupled, with signals from one affecting the other (Manalagas, Jilka, Bellido, O’Brian, & Parfitt, 1996), to maintain the balance between bone breakdown and new bone formation (Figure 3.2). Osteoporosis results from an imbalance between bone resorption and formation, in which case bone resorption significantly exceeds bone formation. The body begins to lose bone
The Pathogenesis of Osteoporosis
21
Figure
3.1
Bone remodeling. Note: The sequence of activation, resorption, reversal, and formation is illustrated here. The activation step depends on cells of the osteoblast lineage, either on the surface of the bone or in the marrow, acting on blood cell precursors (hematopoietic cells) to form bone-resorbing osteoclasts. The resorption process may take place under a layer of lining cells as shown here. After a brief reversal phase, the osteoblasts begin to lay down new bone. Some of the osteoblasts remain inside the bone and are converted to osteocytes, which are connected to each other and to the surface osteoblasts. The resorption phases last only a few weeks, but the formation phase is much slower, taking several months to complete, as multiple layers of new bone are formed by successive waves of osteoblasts.
more rapidly, leaving the bones weaker and more susceptible to fracture (Figure 3.3). Since osteoclasts are the principal resorptive cells of the bone, virtually all successful treatment to date targets osteoclastic bone resorption (Teitelbaum, Tondravi, & Ross, l996).
Remodeling The skeleton is continually being renovated and replaced through the process of remodeling (see Figure 3.1). This process occurs to maintain maximal bone mineral density, in addition to repairing any damage that has occurred to the bones, including micro “cracks” or outright fractures (National Institutes of Health [NIH] Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy, 2001). Bone loss occurs when the osteoclasts produce an unusually deep resorption space, or when the osteoblasts fail to completely refill the cavity created during resorption (Oursler, Landers, Riggs, & Spelsberg, 1993). The remodeling process takes place at discrete locations near the surface of the bones, just underneath the thin lining cells (Figure 3.1). As described
22
Osteoporosis
Figure
3.2
How osteoclasts are formed. Note: The interaction between cells of the osteoblastic lineage and the osteoclast lineage is illustrated here. The osteoblastic cells produce several proteins that regulate osteoblast formation and activity. One is a macrophagecolony-stimulating factor (M-CSF), which acts on its receptor to increase the number of precursors available to form osteoclasts. The osteoclasts also produce a protein called a receptor activator of nuclear factor kappa B ligand (RANKL), which can bind to a receptor on the osteoclast precursors (RANK) and stimulate them to develop into fully differentiated osteoclasts. The RANKL/RANK interaction also increases osteoclast activity. Finally the osteoblastic cells can produce osteoprotegerin (OPG), a protein that can be secreted outside the cell and then bind RANKL and prevent it from interacting with RANK, thus blocking the formation and acitivation of osteoclasts. Hormones and local factors such as parathyroid hormone (PTH), calcitriol or 1,25 dihydroxy D (1,25D), prostaglandin F2 (PGF2) and Interleukin-1 (IL-1) are shown in this figure as acting on the osteoblastic cells to increase production of RANKL, and decrease production of OPG. The balance between RANKL and OPG production determines how fast bone breaks down.
earlier, two classes of cells participate in the remodeling process: osteoclasts, which break down and remove old bone matrix, and osteoblasts, which synthesize new bone matrix (Hughes & Boyce, 1997). The removal and replacement of bone in the remodeling cycle occurs in a carefully orchestrated sequence that involves four phases: activation, resorption, a period of reversal, and bone formation (Figure 3.1). Signaling the start of the activation stage, the cells of the osteoblast lineage act on blood cell precursors (i.e., hematopoietic cells) to produce more bone-resorbing osteoclasts. Then, during the resorption stage, the new army of osteoclasts removes worn or damaged bone by dissolving the mineral and breaking down the matrix, leaving small cavities in the surface of the bone (Simon, 2005). After a period of quiescence (called reversal), the osteoblasts then appear in increased numbers and repair the bone by filling the recently excavated cavities with new bone. During this process, some of the osteoblasts remain inside the bone tissue and are converted to actual bone cells (osteocytes). Once the new bone has been mineralized, the remodeling
The Pathogenesis of Osteoporosis
23
Figure
3.3
Normal vs. osteoporotic bone. Note: These pictures, called scanning electron micrographs, are from biopsies of a normal and an osteoporotic patient. The normal bone shows a pattern of strong interconnected plates of bone. Much of this bone is lost in osteoporosis and the remaining bone has a weaker rod-like structure. Moreover, some of the rods are completely disconnected. These bits of disconnected bone may be measured as bone mass but contribute nothing to bone strength. Source: Reproduced from the Journal of Bone and Mineral Research, 7, pp. 16–21, with permission from the American Society for Bone and Mineral Research.
process in that particular area of bone is complete. The resorption phase lasts only a few weeks, but the formation phase may take several months to complete, as layer after layer of new bone is created by the osteoblasts. Bone remodeling continues throughout adulthood, with each remodeling process lasting 6–9 months. During the adult lifetime, the bone is replaced about every 10 years. It is important to note that the bone is in a weakened state while it is undergoing the remodeling process and is more susceptible to fracture at that time (AMA, 2006; USDHHS, 2004). This remodeling process is necessary to maintain bone strength and occurs on all bone surfaces (Simon, 2005). Prior to adulthood, bone formation occurs at a higher rate than bone resorption, facilitating bone growth. The adult bone mass is thought to be genetically predetermined and when it is reached (by the late 20s to mid-30s), bone formation and resorption achieve an equal balance, so that the bone structure remains stable. Osteoporosis results from an imbalance between bone resorption and formation, in which bone resorption significantly exceeds bone formation. The body begins to lose bone tissue more rapidly, leaving the bones weaker and more susceptible to fracture. A dramatic period of bone loss occurs in some women around the time of menopause, and a similar pattern is seen in men at a slightly older age, linking the loss of bone to decreased androgens in both genders (USDHHS, 2004). The mechanism of resorption can also supply needed phosphorus and calcium when there is a deficiency in the diet, or for the extra needs of the developing fetus during pregnancy or the infant through lactation. Conversely, when the calcium and phosphorus supplies are sufficient, the formation phase of remodeling can absorb these minerals and replenish their storage in the bone (USDHHS, 2004).
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Osteoporosis
Nutrition Bones need nutritional essentials such as calcium, vitamin D, and phosphorus to build tissue; these minerals are normally obtained from one’s diet. Under normal conditions, a portion of the dietary calcium ingested is absorbed into the blood, with the remaining calcium being excreted via the intestinal tract. When a person does not ingest enough calcium and/or phosphorus, the body’s regulating hormones respond by removing these minerals from the bones for use in other essential functions in the body. But when this process continues to occur again and again over time, the bones become weakened (USDHHS, 2004). A complex system of regulatory hormones helps to maintain adequate supplies of the needed minerals in a variety of situations. These hormones act not only on bone but also on other tissues, such as the intestine and the kidney, to regulate the supply of the needed elements (USDHHS, 2004). These mechanisms rely on an intricate network of biologic messenger molecules, which will be discussed in the following sections.
Effects of Estrogen and Testosterone on Bone Two hormones that are particularly important in the formation of bone are estrogen and testosterone. There is a consensus that the early and most pronounced effect of estrogen on bone remodeling is a decrease in the amount of bone resorption (USDHHS, 2004). Estrogen is also known to have a variety of effects on the proliferation and synthesis of enzymes and bone matrix proteins by osteoblast-like cells through a process mediated by complex biomolecular biologic signals and mechanisms. It is estimated that women lose about 50% of their cancellous bone and about 35% of their cortical bone over their lifetime (Riggs et al., 1981). It is still not clear how much of this bone loss is due to estrogen deficiency and how much is due to age and environmentally related processes, but it is estimated that 25% of cancellous bone loss and 15% of cortical bone loss is due to estrogen deficiency (Lindsay, 1990). Estrogen acts on both osteoclasts and osteoblasts to inhibit bone breakdown at all stages in life, but in some instances it may also stimulate bone formation (USDHHS, 2004, p. 28). At the time of menopause there is a decrease in estrogen associated with rapid bone loss. Testosterone stimulates muscle growth, which encourages bone formation by placing stress on the bone, and also produces estrogen as a by product of its action. There is now a consensus that testosterone is important to bone health in both men and women (USDHHS, 2004).
Estrogen Receptors Estrogens mediate their receptor-dependent effects by diffusing through the plasma membrane of the cells and then binding to specific high-affinity estrogen receptors (ERs) in the target cell. The activated complex then translocates to the nucleus of the target cell and binds to chromatin at a specific region of the DNA called the hormone response element. The hormone response element then stimulates or inhibits specific genes, resulting in the synthesis of specific proteins. This generation of intracellular proteins causes the activation of a cascade of events leading to cell growth and differentiation. The ERs play a key role in mediating the cellular effects of estradiol on cell
The Pathogenesis of Osteoporosis
25
growth and differentiation (Phillips, Chalbas, & Rochefort, 1993; Rosselli, Reinhart, Imthurn, Keller, & Dubey, 2000).
Biologic Messenger Molecules Oseoblastic and osteoclastic functions and bone metabolism are regulated by numerous systemic and local factors, including the following: Systemic factors involved in calcium homeostasis. Local factors influencing bone cell function. Cytokines and colony-stimulating factors associated with the regulation of osteoclast development. Growth regulator factors that stimulate osteoblastic proliferation and differentiation from progenitor cells. A summary of mediating molecules is provided in Table 3.1.
Calcium-Regulating Hormones Parathyroid hormone (PTH), calcitriol, and calcitonin are calcium-regulating hormones that play an important role in producing healthy bones. PTH helps maintain the level of calcium, in addition to stimulating both resorption and formation of bone. Specifically, PTH assists with the movement of calcium from the bones to the bloodstream, but when too much PTH production occurs, hyperparathyroidism develops, and this can lead to accelerated bone loss. Biologically active calcitriol (1,25-dihydroxy vitamin D3) is made from activated cholecalciferol. Its function is to stimulate the intestines to facilitate the absorption of calcium and phosphorus. Calcitonin is produced by the thyroid gland and blocks bone breakdown by inactivating osteoclasts. Calcitonin is also important in maintaining bone development and regulating blood calcium levels in early development (USDHHS, 2004). Growth factors and cytokines are thought to be the mediators of the complex intercellular chemical communication between osteoblasts and osteoclasts that regulates bone resorption. Likewise, the increased production of bone-forming osteoblasts is thought to be linked to bone resorption by the release of growth factors from the bone matrix during the resorptive process (Jilka, 1998). There is evidence that osteoblast and osteoclast formation is controlled by the same set of factors, such as Interleukin 6 (IL-6)-type cytokines.
Cytokine Regulation by Estrogen The cellular hallmark of osteopenia caused by estrogen deficiency is an increase in bone remodeling, and it is proposed that cytokines mediate the acceleration of bone loss following menopause. The mediating cytokines include the following: 1 . TRANCE/RANKL/OPGL: this term refers to a cytokine that was inde-
pendently cloned by several laboratories and named the tumor necrosis factor–related, activation-induced cytokine (TRANCE), receptor activator of NFkB ligand (RANKL), or osteoprotegerin ligand (OPGL) (Jilka, 1998);
Table
Hormones and Growth Factors Regulating Bone Formation
3.1
Factor
Target cells and tissue
Effect
Parathyroid hormone (PTH)
Kidney and bone
Calcitonin (Produced by thyroid gland) Calcitriol (1,25-dihydroxy vitamin D3)
Bone osteoclasts
Stimulates the production of vitamin D (1,25D) and helps move calcium from bones to bloodstream Inhibits resorptive action of osteoclasts; lowers circulating calcium concentrations Stimulates collagen, osteopontin, osteocalcin synthesis; stimulates differentiation; increases circulating calcium concentrations Stimulates activity of osteoclasts Stimulates calcium retention Stimulates calcium absorption
Bone osteoblasts
Bone osteoclasts Kidney Intestine
Estrogen
Bone
Testosterone
Muscle, bone
Prostaglandins
Osteoclasts
Bone morphogenic protein
Mesenchyme
Transforming growth factor (TGF-B) Interleukins (IL-1, IL-3, IL-6, IL-11) Tumor necrosis factor (TNF-a); granulocytemacrophage-stimulatingfactor (GMCSF)
Osteoblasts, chondrocytes Bone marrow, osteoclasts Osteoclasts
Leukemic inhibitory factor
Osteoblasts, osteoclasts
Stimulates formation of calcitonin receptors, inhibiting resorption; may also stimulate bone formation Stimulates muscle growth, placing stress on the bone, increasing bone formation Stimulate resorption and formation Stimulates cartilage protein and bone matrix formation; stimulates replication Stimulates differentiation Stimulate osteoclast formation Stimulates bone resorption
Stimulates osteoblast and osteoclast formation in marrow
The Pathogenesis of Osteoporosis
2. 3. 4. 5.
27
the macrophage-colony stimulating factor (M-CSF); the granulocyte/monocyte-colony stimulating factor (GM-CSF); Interleukin 1 (IL-1); and Interleukin 6 (IL6).
Interleukens IL-1, IL-6, and TNF (the tumor necrosis factor) mediate the effects of estrogen deficiency on osteoclast number IL-1 and TNF, produced by monocytes and macrophages as well as by the systemic hormones PTH and 1,25-dihydroxy vitamin D3 [1,25(OH)2D3], and stimulate osteoclast differentiation by increasing the synthesis of mediating cytokines.
Regulation of Bone Loss It has been shown that IL-6 is an essential mediator of bone loss caused by estrogen deficiency, and that inherited or acquired disorders of testicular function, as well as congenital male hypogonadism, are also associated with bone loss (Jilka, l998). In the case of congenital male hypogonadism, bone mass can be increased with the administration of testosterone. It has also been established that castration in men causes increased bone resorption and bone loss. Research findings suggest that the cellular and molecular mechanisms that progress to bone loss due to androgen deficiency in the male are similar and may be identical to the mechanisms that underlie the bone loss caused by estrogen deficiency in the female. It is of note that IL-6 is an essential pathogenic factor in bone loss caused by both androgen and estrogen deficiencies (Bellido et al., 1995).
Lifestyle Factors Affecting Bone Loss Lifestyle factors also have a significant impact on bone health. While the size and shape of bones are principally predetermined by genetics, other modifiable factors, including physical activity and diet, are also important to bone health. It is known that physical activity can increase bone mass by increasing muscle mass, thus placing additional stress on bones. Individuals who are obese and those with high muscle mass tend to have a higher bone mass, whereas individuals who develop osteoporosis are more likely to be thin with less muscle mass (Simon, 2005). Other lifestyle habits, such as smoking and excessive use of alcohol, also represent modifiable lifestyle risk factors.
Concerns Related to Environmental Toxins Research by Wang, Shen, Li, and Agrawal (2002) has shown that it is not just changes in mineral content or mineral density that are important in evaluating the propensity of bone to fracture; equally important are changes in the organic nature of the bony matrix. These findings raise questions about how toxic environmental chemicals such as antiestrogenic dioxins (TCDDs) and polychlorobiphenyls (PCBs) may affect bone. It is known that antiestrogen molecules bind to the estrogen receptor to block its action, by preventing it from being available for estrogen or by blocking the receptor sites for further action. Animal studies have confirmed that exposure to PCBs and TCDDs interferes with bone growth, and that it weakens the mechanical strength of bone (Jamsa, Viluksela, Tuomisto, Tuomisto, & Tuukkanen, 2001; Juberg, 2000; McLachlan, 2001). Because PCBs are particularly stable environmental pollutants that bio-accumulate, their widespread presence
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Osteoporosis
in the environment and persistence in the body pose a serious and relevant concern in terms of bone health. Exposure to PCBs most often occurs by ingesting contaminated food, inhaling contaminated air, eating fish from PCB-contaminated waters, or coming in contact with other sources that we may not yet be aware of. Future studies are needed to address the effects of dioxins and other environmental contaminants on bone.
Conclusion In conclusion, our understanding of the pathology underlying osteoporosis is complex and still not fully known. But we already have the knowledge to detect its presence in time to institute treatment to prevent many devastating osteoporotic fractures. And in many cases, we know how to prevent osteoporosis. It is imperative that we apply the knowledge we already have, to reduce the impact of osteoporosis on global society.
REFERENCES American Medical Association. (2006). Osteoporosis management. Pathophysiology of osteoporosis. Retrieved July 2, 2006, from http://www.ama-cmeonline.com/osteo_mgmt/module03/ 01cme/02.htm Bellido, T., Jilka, R. L., Boyce, B. F., Girasole, G. G., Groxmeyer, H., Dalrymple, S. A., et al. (1995). Regulation of Interleukin-6, osteoclastogenesis and bone mass by androgens: The role of the androgen receptor. Journal of Clinical Investigation, 95, 2886–2895. Black, A., Topping, J., Durham, B., Farquharson, R., & Fraser, W. (2000). A detailed assessment of alterations in bone turnover, calcium homeostasis, and bone density in normal pregnancy. Journal of Bone and Mineral Research, 15, 557–563. Hughes, D. E., & Boyce, B. F. (1997). Apoptosis in bone physiology and disease. Journal of Clinical Pathology, 50, 132–137. Jamsa, T., Viluksela, M., Tuomisto, J. T., Tuomisto, J., & Tuukkanen, J. (2001). Effects of 2,3,7,8Tetrachlorodibenzo-p-Dioxin on bone in two rat strains with different aryl hydrocarbon receptor structures. Journal of Bone and Mineral Research, 16, 1812–1820. Jilka, R. L. (1998). Cytokine, bone, remodeling, and estrogen deficiency: A 1998 update. Bone, 23, 75–81. Juberg, R. J. (2000). An evaluation of endocrine modulators: implications for human health. Ecotoxicology and Environmental Safety, 45, 93–105. Lindsay, R. (1990). Overview of prevention strategies. In C. C. Overgaard (Ed.), Third international symposium on osteoporosis (pp. 945–947). Aalborg, Denmark: Handelstrykkeriet Aalgorg ApS. Manalagas, S. C., Jilka, R. L., Bellido, T., O’Brian, C. A., & Parfitt, A. M. (1996). Interleukin-6-type cytokines and their receptors. In J. P. Bilezikian, L. G. Raisz, & G. A. Rodan (Eds.), Principles of bone biology (pp. 701–713). San Diego: Academic Press. Marcus, R., Feldman, D., & Kelsey, J. (1996). Osteoporosis. New York: Academic Press. McLachlan, J. A. (2001). Environmental signaling: What embryos and evolution teach? us about endocrine disrupting chemicals. Endocrinology Review, 22, 319–341. National Institutes of Health Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy. (2001). Osteoporosis prevention, diagnosis, and therapy. The Journal of the American Medical Association, 285, 785–795. Orthovita. 2006. Bone health and repair. Retrieved August 5, 2006, from http://www.orthovita.com/ patient_info/bonehealth.html Oursler, M. J., Landers, J. P., Riggs, B. L., & Spelsberg, T. C. (1993). Estrogen effects on osteoblasts and osteoclasts. Annals of Medicine, 25, 361–371. Phillips, A., Chalbos, D., & Rochefort, H. (1993). Estradiol increases and antiestrogens antagonize the growth factor induced activator protein –I activity in MCF-7 cells without affecting c-fos and c-fos synthesis. Journal of Biological Chemistry, 268, 14103–14108.
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Reinhart, K. C., Dubey, R. K., Keller, P. J., Imthurn, B., & Rosselli, M. (1999). Xenoestrogens and phytoestrogens induce the synthesis of leukemia inhibitory factor by human and bovine oviduct. Molecular Human Reproduction, 5, 899–907. Riggs, B. L., Wahner, H. W., Dunn, W. L., Mazess, R. B., Offord, K. P., & Melton, L. J., III. (1981). Differential changes in bone mineral density of the appendicular skeleton with aging: relationship to spinal osteoporosis. Journal of Clinical Investigation. 67, 328–335. Rosen, C. J., Verault, D., Steffens, C., Cheleuitte, D., & Glowacki, J. (1997). Effects of age and estrogen status on the skeletal IGF regulatory system: Studies with human marrow. Endocrine, 7, 77–80. Rosselli, M., Reinhart, K., Imthurn, B., Keller, P. J., & Dubey, R. K. (2000). Cellular and biochemical mechanisms by which environmental oestrogens influence reproductive function. Human Reproduction Update, 6, 332–350. Simon, L. S. (2005). Osteoporosis. Clinics in Geriatric Medicine, 21, 603–629. Teitelbaum, S. L., Tondravi, M. M., & Ross, P. (1996). Osteoclast biology. In R. Marcus, D. Feldman, & J. Kelsey (Eds.), Osteoporosis (p. 61). New York: Academic Press. U.S. Department of Health and Human Services. (2004). Bone health and osteoporosis: A report of the surgeon general. Public Health Service, Office of the Surgeon General, Rockville, MD. Retrieved August 22, 2006, from http://www.surgeongeneral.gov/library/bonehealth/ Wang, X., Shen, X., Li, X., & Agrawal, C. M. (2002). Age-related changes in the collagen network and the toughness of bone. Bone, 31, 961–967.
2
Clinical Management
Diagnostic Tests and Interpretation
Much of the burden of bone disease can potentially be avoided if at-risk individuals are identified and appropriate interventions (both preventive and therapeutic) are made in a timely manner. (U.S. Department of Health and Human Services, Bone Health and Osteoporosis )
Introduction
4
William T. Ayoub
steoporosis is our most common metabolic bone disease. It has been defined as “a skeletal disorder characterized by compromised bone strength predisposing to an increased risk of fracture” (NIH Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy, 2001). Fractures produce significant morbidity and mortality, as well as a tremendous economic burden for our health care system (U.S. Department of Health and Human Services [USDHHS], 2004). Since osteoporosis is often clinically silent, it is imperative that we make a concerted effort to identify patients who are at risk for fracture. By doing this effectively, we can determine who should be treated with medication shown to decrease fracture risk and thus reduce morbidity and mortality. Studies have shown that effective screening of an at-risk population can result in a decreased incidence of fracture (Kern et al., 2005; Newman, Ayoub, Starkey, Diehl, & Wood, 2003).
O
Bone Mineral Density Testing Any individual patient’s risk of a fracture is dependent upon a variety of factors. First, the patient’s propensity to fall is an extremely important risk factor for
34
Osteoporosis
fracture (Tinetti, 2003). This issue will be discussed elsewhere in this text. Second, bone strength is another important determinant of fracture risk. Bone strength is related to bone mineral density (BMD) as well as other properties of bone that are often termed “bone quality” (Watts, 2002). Bone quality is a manifestation of the architecture (bone geometry, microarchitecture, trabecular thickness, trabecular connectivity, cortical thickness, and cortical porosity) and matrix and mineralization properties. In clinical practice, these various determinants of bone quality are not generally measurable and therefore cannot help the clinician predict fracture risk. Therefore, the cornerstone of evaluation is the measurement of BMD. BMD correlates highly with fracture risk and allows the clinician to determine the need for pharmacological interventions (Bates, Black, & Cummings, 2002; Bonnick, 2004; Cummings, Bates, & Black, 2002). Measurement of BMD can also help to monitor the response to therapy. Various techniques are used to measure BMD (Bonnick, 2004). Some of the earliest techniques to assess bone density included qualitative spinal morphometry and the Singh index. These studies utilized standard X-rays and attempted to grade the degree of bone loss by relying on the appearance of the trabecular patterns within the vertebral body or the proximal femur. These techniques proved to be highly subjective and did not necessarily correlate with dual photon absorptiometry. Photon absorptiometry techniques became available in the mid-1960s. Single photon absorptiometry was the first method employed. This involved passing a single energy photon beam from a radioactive source through a peripheral bone such as a radius or calcaneus. Bone density was estimated based on the degree of attenuation of this X-ray beam. Later, dual photon absorptiometry became available. This technique used photons with distinct photoelectric peaks from a radioactive source that were attenuated differently by soft tissue and bone. Bone density could therefore be more accurately estimated despite varying amounts of soft tissue. This allowed the study of axial sites such as the hip and spine. Dual energy X-ray absorptiometry (DXA) has become the most commonly used method to measure BMD (Bonnick, 2004). This technique involves an X-ray tube that generates photon beams of two different energy levels. The difference in attenuation of the two photon beams as they pass through the region of interest (ROI) allows this technology to differentiate bone from soft tissue. DXA measures both bone mineral content (BMC, in grams) and area (in cm2). By dividing bone mineral content by area, one obtains an “areal” BMD (g/cm2). This value can be converted to a T-score, which is calculated by subtracting the mean BMD of a young adult reference population from the patient’s BMD and then dividing by the standard deviation of the young adult population. Therefore, a T-score compares the patient to a gender-matched, young, healthy control population. This comparison is most often used for diagnostic purposes as noted later. Similarly, a Z-score can be derived by subtracting the mean BMD of an age- and sex-matched reference population from the patient’s BMD and dividing by the standard deviation of the reference population. Thus, a Z-score compares the patient to an age- and gender-matched population. This comparison is useful in certain situations. The Z-score is often reported in premenopausal women, men under the age of 50, and children. When the value is low, it is also a clue that a secondary cause of osteoporosis may be present. Central DXA units measure BMD at the lumbar spine, proximal femur, and distal forearm. These regions of interest correlate with the common areas affected by osteoporotic fracture.
Diagnostic Tests and Interpretation
35
Vertebra fracture assessment (VFA) has been an added feature to central DXA units (Ferrar, Jiang, Adams, & Eastell, 2005). VFA produces a lateral image of the thoracic and lumbar vertebrae. These images are reviewed visually and also measured in a morphometric fashion to determine if there are prevalent vertebral deformities. The presence and severity of vertebral fractures are determined by using the semiquantitative assessment criteria developed by Genant and colleagues (Genant, Wu, van Kuijk, & Nevitt, 1993). Vertebral fractures are common and are often not recognized clinically, with only about a third of vertebral fractures found on radiographs coming to clinical attention (Cooper, O’Neill, & Silman, 1993). VFA produces an image (taken at the time of the DXA scan) that is easy to obtain and adds very little radiation. The finding of a vertebral deformity allows the densitometrist to place the patient at a high risk for future fracture regardless of the BMD values. VFA is indicated when there is a documented height loss of greater than 2 cm, a historical height loss of greater than 4 cm, a history of a fracture after the age of 50, chronic use of glucocorticoids, or a history suggestive of vertebral fracture not documented by prior radiographic studies (Binkley et al., 2006). Quantitative computed tomography (QCT) is another method used to measure spinal bone density. It provides a three-dimensional, or volumetric, measurement with a spatial separation of trabecular from cortical bone. This technology is not as widely used as DXA because of the expense and higher radiation dosage. Quantitative ultrasonography (QUS) is another technique that has been used to predict fracture risk. QUS is commonly used at the calcaneus (heel). It does not measure bone mineral content or density directly but instead measures the transmission of ultrasound, including broadband ultrasound attenuation (BUA), speed of sound (SOS), and the combined quantitative ultrasound index (QUI). This technology is more portable and less expensive than central DXA units.
Guidelines for Interpretation The International Society for Clinical Densitometry (ISCD) has published official positions and guidelines for bone densitometry (Binkley et al., 2006; Hans et al., 2006; Leslie et al., 2006; Shepherd et al., 2006; Vokes et al., 2006). Since this is a rapidly evolving field, the ISCD has updated these positions on a yearly basis, and the reader should review the latest recommendations for the most updated version (International Society for Clinical Densitometry [ISCD], 2005). The 2005 official positions of the ISCD are available on the ISCD Web site (ISCD, 2005). Some of the important highlights in the official positions are as follows: 1. The reference data base for T-scores will now use a uniform White (non-race-
adjusted) normative database for men and women of all ethnic groups. This statement is limited to the United States. The rationale for this guideline stems from difficulties in defining ethnicity, along with multiethnic fracture data suggesting similar relative risks among various ethnic groups (Miller et al., 2002). 2 . Osteoporosis may be diagnosed in postmenopausal women and in men over the age of 50 if the T-score of the lumbar spine, total hip, or femoral neck is 2.5 or less. In patients with hyperparathyroidism, or if the above-mentioned
36
Osteoporosis
3.
4.
5.
6.
7.
sites cannot be measured or interpreted, the 33% radius site may be utilized to make the diagnosis. Other sites such as Ward’s area should not be used for diagnosis as they may significantly after the diagnostic category assigned to a patient without truly reflecting the known distribution of the disease. The spinal ROI should include L1 through L4. Vertebrae may be eliminated if there are structural changes or artifacts. If only one vertebra remains after excluding others, the diagnosis should be based on a different skeletal site. A distinction is made between diagnostic classification and the use of BMD for fracture risk assessment. Any well-validated technique can be used for fracture risk assessment. As seen below, combining BMD values with clinical risk factors allows for better determination of fracture risk. T-scores are reported in postmenopausal women and men age 50 and older. Z-scores are preferred in premenopausal women and men younger than the age of 50. This is particularly important in children. Serial BMD testing can be used to monitor the response to therapy. For those with an increased or stable bone density, it is felt that therapy is adequate, while a nonresponsive therapy would be suggested by finding a loss of bone density that exceeds the least significant change (LSC). Precision assessment should be calculated for each technologist.
Serial BMD testing allows one to determine changes in BMD over time. This may be important as the clinician monitors the response to therapy. When possible, it is recommended that the same unit be used for serial studies. The interpreting physician should compare BMD values as opposed to T-scores when performing serial studies. Each bone densitometry center should have the technologist perform a precision assessment (Shepherd et al., 2006). The precision assessment determines how well the technologist is able to replicate a study. This assessment produces an LSC, which would be expressed in an absolute value (g/cm2) with a 95% confidence level. This allows the interpreting physician to determine whether a repeat BMD has actually changed or whether the difference is merely within the range of the technologist’s and equipment’s error. Use of the LSC gives one the ability to determine when the next DXA scan should be performed. Most densitometry centers would have an LSC in the range of 3%–5%. One would consider repeating the DXA scan in a period of time in which a treatment would be expected to change BMD to an extent greater than the LSC. From a practical standpoint, initiating an antiresportive agent may allow an improvement of 2%–3% per year (depending on the ROI). Thus, repeating a DXA scan in 2 years after initiation of therapy may allow for proper interpretation of the results. Alternatively, in a situation such as treatment with high-dose corticosteroids, BMD could fall 5% or more within a year. In that situation, a DXA scan may be repeated in 1 year. The World Health Organization (WHO) has defined osteoporosis as a T-score below −2.5, while defining osteopenia as a T-score between −1.0 and −2.5, and normal as a T-score above −1.0 (World Health Organization [WHO], 1994; also Kanis, Melton, Christiansen, Johnston, & Khaltaev, 1994). This is an operational definition that allows researchers and clinicians to classify degrees of low bone density within populations. From a practical clinical standpoint, however, this definition lacks the ability to make decisions regarding fracture risk and treatment thresholds. The National Osteoporosis
Diagnostic Tests and Interpretation
37
Risk Assessment (NORA) study cohort of nearly 150,000 postmenopausal women showed that 82% of those with fractures had T-scores greater than −2.5 (Siris et al., 2004). Additionally, the Study of Osteoporotic Fractures showed that 54% of postmenopausal women with incident hip fractures did not have an osteoporotic T-score at the hip on the baseline DXA (Wainwright et al., 2005). Therefore, relying purely on WHO criteria to determine future fractures is inadequate. There have been attempts made to combine BMD values with clinical risk factors to allow clinicians to determine when to intervene with treatment modalities. The National Osteoporosis Foundation (NOF) has developed recommendations for treatment, which have been widely adopted by many physicians who interpret BMD studies (“Osteoporos: Review of the Evidence,” 1998). The NOF suggests that one should consider pharmacological treatment for individuals with a T-score below −2.0, regardless of risk factors, and below −1.5 in the presence of one or more of the major risk factors. The major risk factors are listed in Table 4.1. This guideline has been adopted and operationalized by many health care organizations and systems. Additionally, the American College of Rheumatology has recommended treatment in patients taking chronic oral corticosteroids if the T-score is less than -1.0 (“Recommendations for the Prevention and Treatment,” 2001). This recommendation is not based upon any controlled trial, but given the rapid loss of bone and the increased propensity to fracture at a higher BMD, this guideline seems quite appropriate. Fracture risk may be expressed in a variety of fashions. Absolute risk (AR) is the probability of a fracture over a specific period of time (for instance, 10 years). Meanwhile, relative risk (RR) is the ratio of absolute risks of two populations. RR tends to overestimate fracture risk in some populations and underestimate it in others. For example, a 50-year-old woman and an 80-year-old woman with identical T-scores will have the same RR for fracture compared to an age-matched population with a normal BMD. However, the AR over a 10-year period of time is much higher in the 80-year-old than in the 50-year-old. The WHO is presently attempting to define a cost utility analysis that will combine results from the BMD with clinical risk factors for fracture (Kanis, Borgstrom, et al., 2005; Kanis, Oden, et al., 2001). WHO is also attempting to use BMD and clinical risk factors to determine a 10-year absolute risk of fracture. This work may eventually set the standard for pharmacological therapy. Until that methodology is available and widely used, many suggest that the NOF approach should be used.
Table
4.1
National Osteoporosis Foundation Guidelines for Treatment • • •
T-score is less than –2.0 T-score is less than –1.5 with a major risk factor Major risk factors i. Personal history of fracture ii. Family history of fracture iii. Current cigarette smoker iv. Weight less than 127 pounds
38
Osteoporosis
Clinical Utility As with every piece of technology, we need to determine the most effective and efficient use of BMD testing. A number of organizations (the American Association of Clinical Endocrinologists [AACE], ISCD, National Institutes of Health [NIH], NOF, North American Menopause Society [NAMS], Institute for Clinical Systems Improvement [ICSI], and United States Preventive Services Task Force [USPSTF]) have recommended the need to screen certain high-risk groups (Binkley, Bilzikian, Kendler, Leib, Lewiecki, & Petak, 2006; Hodgson, Watts, Bilezikian, Clarke, Gray, Harris et al., 2003; ICSI, 2006; ISCD, 2005; Kern, Powe, Levine, Fitzpatrick, Harris, Robbins et al., 2005; NAMS, 2002; NOF, 2003; USDHHS, 2004).The published guidelines are slightly different among the various organizations but tend to agree on most recommendations. A listing of potential indications for BMD testing is found in Table 4.2. It is generally accepted that BMD testing is recommended for all women over the age of 65. In this age group, approximately 45% of screened patients are found to be at high risk according to NOF criteria. This group includes those patients who are not only at a higher absolute risk for fracture but also most likely to respond to pharmacological treatments (Newman et al., 2003). For younger postmenopausal women, BMD testing has been recommended in patients who have other major risk factors as noted above. Some organizations would limit this to women over the age of 60 (US Preventire Services Task Force, 2002). In younger postmenopausal women, a substantial number will be identified as at a high relative risk according to NOF criteria. Their 10-year absolute risk, however, will not be as high as that of the older postmenopausal group. Patients taking chronic corticosteroid therapy are another important group in which BMD testing can be quite useful. It is well established that chronic use of oral corticosteroids leads to decreased BMD and increased incidence of fractures (Haugeberg, Uhlig, Falch, Halse, & Kvien, 2000; Hooyman, Melton, Nelson, O’Fallon, & Riggs, 1984). Chronic use has been arbitrarily defined as taking the equivalent of 7.5mg of prednisone daily for 3 months. However, a number of studies have shown that lower doses of corticosteroids are associated with decreased bone density and increased fracture risk (Laan et al., 1993; Van Staa, Leufkens, Abenhaim, Zhang, & Cooper, 2000). Bone loss can occur rapidly after the initiation of oral glucocorticoids in a dose-dependent fashion. Within the first
Table
4.2
Groups That Should Be Tested With DXA • • • • • • •
All women over the age of 65 Postmenopausal women with major risk factors All individuals over the age of 50 who suffer an osteoporotic fracture All individuals who are taking long-term corticosteroids Men with hypogonadal conditions Men over the age of 70 Patients with diseases associated with bone loss and fracture
AQ3
Diagnostic Tests and Interpretation
Q3
39
6 months to 1 year, one can lose up to 20% of bone in patients taking high-dose corticosteroids. The rate of bone loss tends to lessen after 1 year and the bone loss effects can partially reverse after discontinuation of corticosteroids. The health care system tends to fall short in the evaluation and treatment of patients taking glucocorticoids (Solomon, Katz, La Tourette, & Coblyn, 2004). Other high-risk groups include any adult who presents with a fracture of the hip, vertebrae, or wrist (Cooper, Atkinson, O’Fallon, & Melton, 1992; Klotzbuecher, Ross, Landsman, Abbot, & Berger, 2000; Lindsay et al., 2001). There can be a 5-fold increase in vertebral fracture risk when a vertebral fracture is found at baseline (Klotzbuecher et al., 2000). This value may rise to a 12-fold increase when there are two vertebral fractures at baseline (Klotzbuecher et al., 2000). A number of investigators have shown that this high-risk group is infrequently evaluated for osteoporosis or treated with medication that could reduce future fractures (Andrade et al., 2003; Feldstein, Nichols, et al., 2003; Harrington, Broy, Derosa, Licata, & Shewman, 2002; Kamel, Hussain, Tariq, Perry, & Morley, 2000; Kiebzak et al., 2002; Smith, Ross, & Ahern, 2001; Solomon, Finkelstein, Katz, Morgun, & Avorn, 2003). A number of investigators have shown that less than 20% of patients hospitalized with hip fracture are ever evaluated for bone density. Additionally, less than 10% are ever treated with antiresorptive agents to prevent future fractures. A large health care system reviewed over 70,000 patients who had suffered over 2,800 fractures and found that only 8.4% of the women and 1.5% of the men had been BMD tested within 2 years of the fracture (Feldstein, Elmer, Orwell, Herson, & Hillier, 2003). The ISCD has also recommended DXA testing for men over the age of 70 (Shepherd et al., 2006). Although that recommendation has not been made by other organizations, it does appear clear that some men are at a much higher risk for future fracture. This includes men who are hypogonadal or taking chronic corticosteroid therapy. Those men that have been treated with orchiectomy or antiandrogen therapy for prostate cancer are at a particularly high risk for bone loss and subsequent fracture (Shahinian, Kuo, Freeman, & Goodwin, 2005).
Markers of Bone Turnover Bone is a dynamic organ that is constantly being remodeled (Eastell & Bainbridge, 2003; Fohr, Woitage, & Seibel, 2003). Bone resorption is initiated by osteoclasts. These cells attach to the bone surface and secrete hydrolytic enzymes that resorb bone. This releases a variety of bone minerals and fragments of collagen. Collagen is digested, and various fragments are excreted in the urine. This includes deoxypyridinoline (DPD) and peptide-bound alpha I to alpha II N-telopeptide (NTX) cross-links. The peptide-bound NTX can be measured in the urine and serum by an immunoassay termed Osteomark®. Bone formation is initiated by osteoblasts, which synthesize type I collagen and other proteins to form osteoid, which is the organic substrate upon which mineralization occurs. Osteoblasts express alkaline phosphatase on their cell membranes, and consequently bone-specific alkaline phosphatase (BSAP) reflects the cellular activity of osteoblasts. Osteoblasts also form osteocalcin, which can also be measured in the serum
40
Osteoporosis
Table
Bone Turnover Markers
4.3
•
Measures of osteoblast function i. Alkaline phosphatase (AP): a membrane-bound enzyme found in bone, liver, intestine, spleen, kidney, and placenta. The bone alkaline phosphatase (BAP) is more specific for bone and reflects cellular activity of osteoblasts. ii. Osteocalcin (OC): a hydroxyapatite binding protein synthesized by osteoblasts. A specific marker of osteoblast function, but heterogeneity of OC fragments in serum limits clinical usefulness. Significant diurnal variations.
•
Measures of osteoclast function i. Hydroxyproline (OHP): This reflects breakdown of collagen in bone, cartilage, and skin. It may also reflect dietary intake of collagen. ii. Collagen crosslinks: These reflect bone resorption but not dietary intake. They tend to be specific markers of bone resorption. These include the following: 1. N-telopeptide (NTX) measured in the urine and in serum by an immunoassay termed Osteomark 2. C-telopeptide (CTX) measured in serum by an immunoassay termed Crosslaps 3. Deoxypyridinoline (DPD)
and is a reflection of osteoblastic synthesis. A listing of some common markers of bone turnover are found in Table 4.3. In most cases of postmenopausal osteoporosis, bone loss is due to an increase in bone resorption with an inadequate increase in bone formation. This would result in elevated markers of bone resorption such as the urinary NTX. Some studies have shown a significant correlation of markers of bone turnover and subsequent rates of bone loss (Bauer et al., 1999; Chaki et al., 2000; Chestnut, Bell, & Clark, 1997; Ross & Knowlton, 1998). There have also been studies correlating bone turnover markers with an increased risk of hip fracture and a greater fracture reduction when taking antiresorptive agents (Bauer et al., 2004; Bauer et al., 2006; Seibel, Naganathan, Barton, & Grauer, 2004; Van Daele et al., 1996). Women with the highest bone turnover have been shown to gain the most BMD from antiresorptive therapy (Chestnut et al., 1997). The clinical utility of routine measurements of bone markers is unclear. Some have suggested that elevated bone turnover markers could predict which patients will respond to the initiation of antiresorptive therapy. Additionally, some have suggested that measurements of antiresorptive markers are useful to monitor the efficacy of and adherence to an antiresorptive agent. By measuring bone turnover markers 6 months after antiresorptive therapy, one could determine compliance and drug efficacy if urinary NTX or CTX decreased by 30%–50%. Alternatively, some have suggested that the routine measurement of bone turnover markers is not necessary.
Secondary Cause Evaluation As a diagnosis of osteoporosis is made, one needs to consider the possibility of secondary causes producing low bone density (Fitzpatrick, 2002). Primary osteoporosis is defined
Diagnostic Tests and Interpretation
41
as the bone loss that occurs during the normal aging process, while secondary osteoporosis reflects bone loss that is a result of another clinical problem. Obviously, it is important to determine secondary causes, since these conditions may be treated in a different manner. The numerous secondary causes of osteoporosis are reviewed elsewhere in this text, with some of the more common causes listed in Table 4.4. It is estimated that up to 20%–30% of postmenopausal women may have a secondary cause of osteoporosis, while the value may be 50% in men. A complete history and a physical examination are the first steps in the evaluation of potential secondary causes for osteoporosis. The history is especially important since
Table
Secondary Causes of Osteoporosis
4.4
•
Pharmacotherapy i. Glucocorticoids ii. Thyroid overreplacement iii. Anticonvulsants (phenytoin, phenobarbital) iv. Lithium, aluminum v. Heparin (long-term) vi. Drugs producing hypogonadism (aromatase inhibitors, antimetabolite chemotherapy, depo-medroxyprogesterone, gonadotropin-releasing hormone agonists)
•
Endocrine disorders i. Cushing syndrome ii. Hyperparathyroidism iii. Hypogonadism iv. Hyperthyroidism
•
Gastrointestinal disorders i. Alcohol-related diseases ii. Malabsorption syndromes iii. Eating disorders iv. Celiac disease v. Inflammatory bowel diseases vi. Chronic liver diseases vii. Gastrectomy
•
Genetic diseases i. Osteogenesis imperfecta ii. Hypophosphatasia
•
Miscellaneous causes i. Organ transplant ii. Rheumatoid arthritis iii. Neurological diseases iv. Spinal cord injury v. Multiple sclerosis vi. Prolonged bed rest vii. Multiple myeloma viii. Marrow infiltrative diseases
42
Osteoporosis
there are a number of clues that may help to explain low bone density. Obviously, one of the most common secondary causes of osteoporosis is the use of oral glucocorticoids. Other pharmacotherapy must also be considered, such as the use of thyroid hormone at high dosages, anticonvulsants (especially phenytoin and phenobarbital), lithium, longterm heparin, and drugs that produce hypogonadism (such as aromatase inhibitors, depo-medroxyprogesterone, and gonadotropin-releasing hormone agonists). Other items within the history that would be important to ascertain include a history of eating disorders, symptoms of hypogonadism in a male, gastrointestinal symptoms suggestive of malabsorption, alcohol excess, smoking, and the presence of a connective tissue disease. The physical examination might also assist in finding clues to a variety of endocrine, gastrointestinal, and inflammatory arthropathies. Several laboratory studies may also be useful in determining secondary causes of osteoporosis. Over the past several years, vitamin D deficiency has been shown to be a very common laboratory finding. Studies have shown that in patients with a vitamin D deficiency, supplementation is associated with improved bone density and a reduced risk of falls (Bischoff-Ferrari et al., 2004; Shea et al., 2002). It is felt that the serum 25-hydroxy vitamin D level should be at least 30ng/ml, since levels lower than this value are associated with elevated parathyroid hormone levels. Since vitamin D deficiency is so common, it appears wise to obtain a 25-hydroxy vitamin D level in any patient who is being considered for therapy with a pharmacological agent. Other appropriate laboratory studies would include a parathyroid hormone level, serum calcium, alkaline phosphatase, serum protein electrophoresis, a complete blood count, serum creatinine, and a testosterone level (in men). These studies would help to rule out the possibility of conditions such as hyperparathyroidism, hypogonadism, multiple myeloma, and renal insufficiency. Additional laboratory studies would be indicated if there are clues within the history and physical examination related to any of the secondary causes of osteoporosis. See Table 4.5 for a listing of common laboratory tests that may be used to evaluate secondary causes of osteoporosis. Secondary causes should be considered in all patients diagnosed with osteoporosis, and certainly the history and physical examination should always focus on the various possibilities. Complete laboratory testing in all patients is not likely a cost-effective
Table
4.5
Tests That Should Be Considered When Evaluating Secondary Causes of Osteoporosis • History and physical examination • 25-OH vitamin D • Serum calcium • Serum phosphorus, alkaline phosphatase, creatinine • Parathyroid hormone • Thyroid function tests • Serum protein electrophoresis • Serum testosterone (in men)
Diagnostic Tests and Interpretation
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approach. Since vitamin D deficiency is quite common, this test is often recommended. Certainly, in all men or if the patient’s Z-score (age-matched control) is less than 1.0, one might have a higher index of suspicion for a secondary cause and, in those cases, a thorough laboratory evaluation should be considered.
REFERENCES American College of Rheumatology Ad Hoc Committee on Glucocorticoid-Induced Osteoporosis. (2001). Recommendations for the prevention and treatment of glucocorticoid-induced osteoporosis. Arthritis Rheum, 44, 1496-1503. Andrade, S. E., Majumdar, S. R., Chan, K. A., Buist, D. S., Go, A. S., Goodman, M., et al. (2003). Low frequency of treatment of osteoporosis among postmenopausal women following a fracture. Archives of Internal Medicine, 163(17), 2052–2057. Bates, D. W., Black, D. M., & Cummings, S. R. (2002). Clinical use of bone densitometry. Journal of the American Medical Association 288, 1898–1900. Bauer, D. C., Black, D. M., Garnero, P., Hochberg, M., Ott, S., Orloff, J., et al. (2004). Change in bone turnover and hip, non-spine, and vertebral fracture in alendronate-treated women: The fracture intervention trial. Journal of Bone Mineral Research, 19, 1250. Bauer, D. C., Garnero, P., Hochberg, M. C., Santora, A., Delmas, P., Ewing, S. K., et al. (2006). Pretreatment levels of bone turnover and the antifracture efficacy of alendronate: The fracture intervention trial. Journal of Bone Mineral Research, 21, 292. Bauer, D. C., Sklarin, P. M., Stone, K. L., Black, D. M., Nevitt, M. C., Ensrud, K. E., et al. (1999). Biochemical markers of bone turnover and prediction of hip bone loss in older women: The study of osteoporotic fractures. Journal of Bone Mineral Research, 14, 1404. Binkley, N., Bilezikian, J. P., Kendler, D. L., Leib, E. S., Lewiecki, E. M., & Petak, S. M. (2006). Official positions of the International Society for Clinical Densitometry. Journal of Clinical Densitometry, 9, 4–14. Bischoff-Ferrari, H. A., Dawson-Hughes, B., Willett, W. C., Staehelin, H. B., Bazemore, M. G., Zee, R. Y., et al. (2004). Effects of vitamin D on falls: A meta-analysis. Journal of the American Medical Association, 291, 1999–2006. Bonnick, S. L. (2004). Bone densitometry in clinical practice. Totowa, NJ: Humana Press. Chaki, O., Yoshikata, I., Kikuchi, R., Nakayama, M., Uchiyama, Y., Hirahara, F., et al. (2000). The predictive value of biochemical markers of bone turnover for bone mineral density in postmenopausal Japanese women. Journal of Bone Mineral Research, 15, 1537. Chestnut, C. H., III, Bell, N. H., & Clark, G. S. (1997). Hormone replacement therapy in postmenopausal women: Urinary N-telopeptide of type I collagen monitors therapeutic effect and predicts response of bone mineral density. American Journal of Medicine, 102, 29. Cooper, C., Atkinson, E. J., O’Fallon, W. M., & Melton, L. J, III. (1992). Incidence of clinically diagnosed vertebral fractures: a population-based study in Rochester, Minnesota, 1985–1989. Journal of Bone Mineral Research, 7, 221. Cooper, C., O’Neill, T., & Silman, A. (1993). The epidemiology of vertebral fractures. European Vertebral Osteoporosis Study Group. Bone, 14(Suppl. 2), S89–S97. Cummings, S. R., Bates, D., & Black, D. M. (2002). Clinical use of bone densitometry. Journal of the American Medical Association, 288, 1889–1897. Eastell, R., & Bainbridge, P. R. (2003). Bone turnover markers. In E. S. Orwell & M. Bliziotes (Eds.), Osteoporosis: Pathophysiology and clinical management (pp. 185–197). Totowa, NJ: Humana Press. Feldstein, A., Elmer, P. J., Orwell, E., Herson, M., & Hillier, T. (2003). Bone mineral density measurement and treatment for osteoporosis in older individuals with fractures. Archives of Internal Medicine, 163, 2165–2172. Feldstein, A. C., Nichols, G. A., Elmer, P. J., Smith, D. H., Aickin, M., & Herson, M. (2003). Older women with fractures: Patients falling through the cracks of guideline recommended osteoporosis screening and treatment. Journal of Bone Joint Surgery of America, 85A(12), 2294–2302. Ferrar, L., Jiang, G., Adams, J., & Eastell, R. (2005). Identification of vertebral fractures: An update. Osteoporosis International, 16, 717. Fitzpatrick, L. A. (2002). Secondary causes of osteoporosis. Mayo Clinical Proceedings, 77, 453–468.
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Osteoporosis Fohr, B., Woitage, H. W., & Seibel, M. J. (2003). Molecular markers of bone turnover. In E. S. Orwell & M. Bliziotes (Eds.), Osteoporosis: Pathophysiology and clinical management (pp. 163–184). Totowa, NJ: Humana Press. Genant, H. K., Wu, C. Y., van Kuijk, C., & Nevitt, M. C. (1993). Vertebral fracture assessment using a semiquantitative technique. Journal of Bone Mineral Research, 8, 1137–1148. Hans, D. H., Downs, R. W., Jr., Duboeuf, F., Greenspan, S., Jankowski, L. G., Kiebzak, G. M., et al. (2006). Skeletal sites for osteoporosis diagnosis: The 2005 ISCD official positions. Journal of Clinical Densitometry, 9, 15–21. Harrington, J. T., Broy, S. B., Derosa, A. M., Licata, A. A., & Shewman, D. A. (2002). Hip fracture patients are not treated for osteoporosis: A call to action. Arthritis and Rheumatitis, 47, 651–654. Haugeberg, G., Uhlig, T., Falch, J. A., Halse, J. I., & Kvien, T. K. (2000). Bone mineral density and frequency of osteoporosis in female patients with rheumatoid arthritis. Arthritis and Rheumatitis, 43, 522–530. Hodgson, S. F., Watts, N. B., Bilezikian, J. P., Clarke, B. L., Gray, T. K., Harris, D. W., et al. (2003). American Association of Clinical Endocrinologists medical guidelines for clinical practice for the prevention and treatment of postmenopausal osteoporosis: 2001 edition, with selected updates for 2003. Endocrine Practice, 9, 544. Hooyman, J. R., Melton, L. J., III, Nelson, A. M., O’Fallon, W. M., & Riggs, B. L. (1984). Fractures after rheumatoid arthritis: A population based study. Arthritis and Rheumatitis, 27, 1353–1361. Retrieved July 27, 2006, from www.icsi.org Institute for Clinical Systems Improvement [ICSI] (2007). Diagnosis and treatment of osteoporosis. Retrieved July 9, 2007, from http://www.icsi.org/guidelines_and_more/guidelines__order_ sets__protocols/womens_health/osteoporosis/osteoporosis__diagnosis_and treatment_of.html International Society for Clinical Densitometry. (2005). Official positions. Retrieved July 17, 2006, from http://www.iscd.org/Visitors/positions/OfficialPositionsText.cfm Kamel, H. K., Hussain, M. S., Tariq, S., Perry, H. M., & Morley, J. E. (2000). Failure to diagnose and treat osteoporosis in elderly patients hospitalized with hip fracture. American Journal of Medicine, 109, 326–328. Kanis, J. A., Borgstrom, F., De Laet, C., Johansson, H., Johnell, O., Jonnson, B., et al. (2005). Assessment of fracture risk. Osteoporosis International, 16, 581. Kanis, J. A., Melton, L. J., III, Christiansen, C., Johnston, C. C., & Khaltaev, N. (1994). The diagnosis of osteoporosis. Journal of Bone Mineral Research, 9, 1137–1141. Kanis, J. A., Oden, A., Johnell, O., Jonsson, B., de Laet, C., & Dawson, A. (2001). The burden of osteoporotic fractures: A method for setting intervention thresholds. Osteoporosis International, 12, 417. Kern, L. M., Powe, N. R., Levine, M. A., Fitzpatrick, A. L., Harris, T. B., Robbins, J., et al. (2005). Association between screening for osteoporosis and the incidence of hip fracture. Annals of Internal Medicine, 142, 173–181. Kiebzak, G. M., Beinart, G. A., Perser, K., Ambrose, C. G., Siff, S. J., & Heggeness, M. H. (2002). Undertreatment of osteoporosis in men with hip fracture. Archives of Internal Medicine, 162, 2217–2222. Klotzbuecher, C. M., Ross, P. D., Landsman, P. B., Abbot, T. A., III, & Berger, M. (2000). Patients with prior fractures have an increased risk of future fractures: A summary of the literature and statistical synthesis. Journal of Bone Mineral Research, 15, 721. Laan, R.F.J., Van Riel, P.L.C.M., Van de Putte, L.B.A., van Erning, L. J., van’t Hof, M. A., & Lemmens, J. A. (1993). Low-dose prednisone induces rapid reversible axial bone loss in patients with rheumatoid arthritis: A randomized controlled trial. Annals of Internal Medicine, 119, 963–968. Leslie, W. D., Adler, R. A., El-Hajj Fuleihan, G., Hodsman, A. B., Kendler, D. L., McClung, M., et al. (2006). Application of the 1994 WHO classification to populations other than postmenopausal Caucasian women: The 2005 ISCD official positions. Journal of Clinical Densitometry, 9, 22–30. Lindsay, M. R., Silverman, S. L., Cooper, C., Hanley, D. A., Barton, I., Broy, S. B., et al. (2001). Risk of new vertebral fracture in the year following fracture. Journal of the American Medical Association, 285, 320–323. Miller, P. D., Siris, E. S., Barrett-Conner, E., Faulkner, K. G., Wehren, L. E., Abbott, T. A., et al. (2002). Prediction of fracture risk in postmenopausal White women with peripheral bone densitometry: Evidence from the National Osteoporosis Risk Assessment. Journal of Bone Mineral Research, 17, 2222–2230.
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Newman, E. D., Ayoub, W. T., Starkey, R. H., Diehl, J. M., & Wood, G. C. (2003). Osteoporosis disease management in a rural health care population: Hip fracture reduction and reduced costs in postmenopausal women after 5 years. Osteoporosis International, 14, 146–151. National Institutes of Health Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy. (2001). Osteoporsis prevention, diagnosis, and therapy. The Journal of the American Medical Association 285, 785–789. Osteoporosis: Review of the evidence for prevention, diagnosis and treatment and cost-effectiveness analysis. (1998). Osteoporosis International, 8(Suppl. 14), S7. Ross, P. D., & Knowlton, W. (2000). Rapid bone loss is associated with increased levels of biochemical markers. Journal of Bone Mineral Research, 13, 297. Seibel, M. J., Naganathan, V., Barton, I., & Grauer, A. (2004). Relationship between pretreatment bone resorption and vertebral fracture incidence in postmenopausal osteoporotic women treated with risedronate. Journal of Bone Mineral Research, 19, 323. Shahinian, V. B., Kuo, Y. F., Freeman, J. L., & Goodwin, J. S. (2005). Risk of fracture after androgen deprivation for prostate cancer. New England Journal of Medicine, 352, 154–164. Shea, B., Wells, G., Cranney, A., Zytaruk, N., Robinson, B., Griffith, L., et al. (2002). Meta-analysis of calcium supplementation for the prevention of postmenopausal osteoporosis. Endocrine Review, 23, 552–559. Shepherd, J. A., Lu, Y., Wilson, K., Fuerst, T., Genant, H., Hangartner, T. N., et al. (2006). Crosscalibration and minimum precision standards for Dual-Energy X-ray Absorptiometry: The 2005 ISCD official positions. Journal of Clinical Densitometry, 9, 31–36. Siris, E. S., Chen, Y. T., Abbott, T. A., Barrett-Connor, E., Miller, P. D., Wehren, L. E., et al. (2004). Bone mineral density thresholds for pharmacological intervention to prevent fractures. Archives of Internal Medicine, 164, 1108. Smith, M. D., Ross, W., & Ahern, M. J. (2001). Missing a therapeutic window of opportunity: An audit of patients attending a tertiary teaching hospital with potentially osteoporotic hip and wrist fractures. Journal of Rheumatology, 28, 2504–2508. Solomon, D. H., Finkelstein, J. S., Katz, J. N., Morgun, H., & Avorn, J. (2003). Underuse of osteoporosis medications in elderly patients with fractures. American Journal of Medicine, 115, 398–400. Solomon, D. H., Katz, J. N., La Tourette, A. M., & Coblyn, J. S. (2004). Multifaceted intervention to improve rheumatologists’ management of glucocorticoid-induced osteoporosis. Arthritis Care and Research, 51, 383–387. Tinetti, M. E. (2003). Preventing falls in elderly persons. New England Journal of Medicine, 348, 4249. U.S. Department of Health and Human Services. (2004). Bone health and osteoporosis: A report of the surgeon general. Public Health Service, Office of the Surgeon General, Rockville, MD. Retrieved on August 27, 2007 from http://www.surgeongeneral.gov/library/bonehealth/ U. S. Preventive Services Task Force [USPSTF] (2002). Screening for osteoporosis in postmenopausal women: Recommendations and rationale. Annals of Internal Medicine, 137, 526–528. Van Daele, P. L., Seibel, M. J., Burger, H., Hofman, A., Grobbee, D. E., van Leeuwen, J. P., et al. (1996). Case-control analysis of bone resorption markers, disability, and hip fracture risk: The Rotterdam study. Bone Mineral Journal, 312, 482. Van Staa, T. P., Leufkens, H.G.M., Abenhaim, L., Zhang, B., & Cooper, C. (2000). Use of oral corticosteroids and risk of fracture. Journal of Bone Mineral Research, 15, 993–1000. Vokes, T., Bachman, D., Baim, S., Binkley, N., Broy, S., Ferrar, L., et al. (2006). Vertebral fracture assessment: The 2005 ISCD official positions. Journal of Clinical Densitometry, 9, 37–46. Wainwright, S. A., Marshall, L. M., Ensrud, K. E., Cauleu, J. A., Black, D. M., Hillier, T. A., et al. (2005). Hip fracture in women without osteoporosis. Journal of Clinical Endocrinology Metabolism, 90, 2787. Watts, N. B. (2002). Bone quality: Getting closer to a definition. Journal of Bone Mineral Research, 17, 1148. World Health Organization. (1994). Assessment of fracture risk and its application to screening for postmenopausal women. Geneva, Switzerland: World Health Organization.
Pharmacological Management
Osteoporosis is not an inevitable part of ageing; it is preventable. So it is vital that all of us, of all ages, start taking care of our bones now, before it is too late. (Camilla, Duchess of Cornwall )
O
5
steoporosis is both a preventable and a treatable disease. Important advances have been made in the ability to prevent and treat fractures in the last decade, particularly in people with skeletal fragility (U.S. Department of Health and Human Services [USDHHS], 2004). There are a number of effective, well-tolerated therapies that may significantly reduce a person’s risk, in addition to lifestyle changes such as improved diet and increased exercise. The four major goals in the treatment of osteoporosis are (1) to prevent fracture, (2) to stabilize bone mass or achieve increased bone mass, (3) to relieve symptoms of fractures and skeletal deformity, and (4) to maximize physical function (Hodgson et al., 2003). The U.S. surgeon general has recommended a three-level pyramidal approach to treatment in order to achieve these goals (USDHHS, 2004):
Theresa N. Grabo Daniel S. Longyhore
Lifestyle changes form the base of the prevention and management pyramid, including adequate calcium and vitamin D intake, physical activity, and fall prevention. The second level includes assessing and treating secondary causes. The third level includes pharmacological interventions to improve bone density and reduce the risk of fracture (USDHHS, 2004). The purpose of this chapter is to present the current pharmacotherapeutic interventions used to prevent and treat osteoporosis. Pain management will also be addressed. A number of pharmacologic treatments are available for the prevention and/or treatment
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of postmenopausal osteoporosis based on their capability to increase bone mineral density (BMD) and to decrease the risk of fracture (Delaney, 2006). Current U.S. Food and Drug Administration (FDA)-approved pharmacotherapeutics include bisphosphonates, calcitonin (salmon), parathyroid hormone, risedronate, estrogen plus progestin or estrogen alone, and calcium and vitamin D.
Bisphosphonate Therapy Bisphosphonates are a pyrophosphate analogue and much less susceptible to hydrolysis from stomach acids than their predecessors, the inorganic pyrophosphates (Crandall, 2001). Their primary mechanism of action is inhibition of osteoclast activity and resorption of bone, thereby slowing deterioration and allowing osteoblast activity to slightly increase BMD. Bisphosphonate therapy should be considered first-line therapy for the treatment of osteoporosis, in conjunction with lifestyle modifications and appropriate doses of calcium plus vitamin D. As well, bisphosphonates are effective, have convenient dosing schedules, and a relatively safe adverse event profile. Their limitation is only their strict dosing procedures, as patients must remain upright and avoid sustenance before and 30 minutes or more after dosing. Alendronate (Fosamax®), risedronate (Actonel®), and ibandronate (Boniva®) are second- and third-generation bisphosphonates and are currently approved by the FDA for the prevention and treatment of postmenopausal osteoporosis (Merck & Co., 2006; Procter & Gamble Pharmaceuticals, 2006; Roche Laboratories Inc., 2006). Alendronate is also approved for the treatment of corticosteroid-induced osteoporosis, Paget’s disease, malignant hypercalcemia, and osteoporosis in Crohn’s disease (Merck & Co., 2006). Risedronate is also approved for the treatment and prevention of corticosteroidinduced osteoporosis (Procter & Gamble Pharmaceuticals, 2006). As some of the pivotal clinical trials are followed out to 10 years or more, the use of bisphosphonates for extended periods of time is questioned. Recently, Black et al., evaluated the prolonged use of bisphosphonates (5 versus 10 years) in the Fosamax Intervention Trial Extension and found that continuing bisphosphonates out to 10 years provided only a minimal, but statistically significant beneficial effect on bone mineral density (BMD). Black, Schwartz, et al. 2007, Colón-Emeric, 2006).
Mechanism of Action/Kinetics Bisphosphonates’ primary mechanism of action is inhibition of osteoclast activity on the surface of the bone. The bisphosphonates also inhibit osteoclast activity on the surface of the bone as well as inhibit the recruitment of osteoclasts to bone, decrease osteoclast life span, cause osteoclast apoptosis (a genetically determined process of cell self-destruction), and alter bone to slow or delay its resorption (Friedman, 2006; Licata, 2005). The bisphosphonates have a high affinity for bone, specifically those sites being prepared for resorption. There is a relatively low systemic concentration and any drug that is not deposited in the bone tissue is excreted rapidly in the urine. Also, this medication class has very limited absorption and less than 1% of the oral dose is absorbed systemically due to its decreased oral bioavailability, drug absorption is further lowered
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beyond its already limited degree when taken with or around mealtimes. Therefore, bisphosphonate dosing is recommended first thing in the morning with 8 ounces of water. The patient must then wait 30 minutes (alendronate or risedronate) or 60 minutes (ibandronate) before any food or beverage consumption, to allow the drug to reach maximal systemic concentration (Licata, 2005; Merck & Co., 2006; Procter & Gamble Pharmaceuticals, 2006; Roche Laboratories Inc., 2006).
Efficacy Vertebral Fractures Several clinical investigations have evaluated the use of bisphosphonates for primary and secondary prevention of vertebral fractures in postmenopausal women. BMDS of patients treated with a bisphosphonate are consistently increased to greater than the densities of those not taking a bisphosphonate. Increases in the lumbar spine can range from 5% to 8%, with some investigators finding a sustained increase of 13.7% up to 10 years later with alendronate 10 mg daily (Bone et al., 2004; O’Connell & Seaton, 2005). Alendronate is the most established of the three available approved oral bisphosphonates for the treatment of postmenopausal osteoporosis. Approved in 1995, its clinical efficacy for primary and secondary prevention of vertebral fractures set the stage for current osteoporosis treatment. The first major investigation was conducted by Liberman et al. (1995) in 994 postmenopausal women with a T-score of –2.5 or lower, regardless of history of fracture. The findings concluded that there was an overall 48% relative risk reduction in patients taking alendronate. The relative risk reduction for patients with and without a history of vertebral fractures was 30% and 50%, respectively. These findings were later validated further with the Fracture Intervention Trials (FITs), which evaluated alendronate’s benefit in patients with (FIT1) and without (FIT2) a history of vertebral fractures. The results were similar, with relative risk reductions of 47% and 45%, respectively (Black et al., 1996; Cummings et al., 1998). Interestingly, when Cummings et al. (1998) evaluated the benefit of alendronate in patients with a history of osteopenia without a vertebral fracture (T-score –1.0 to –2.5) they did not find a significant difference in fractures between their pharmacologic intervention and placebo. The researchers did find a significant difference between BMDs, but this difference did not translate into difference in fractures. Later studies also discovered that a once-weekly dose of alendronate 70 mg was comparable in efficacy to alendronate 10 mg daily (Schnitzer et al., 2000). Given this finding and the above information, alendronate 10 mg daily or alendronate 70 mg weekly is an effective agent for primary and secondary prevention of fractures secondary to osteoporosis. Most patients with osteopenia will not need alendronate 5 mg daily or 35 mg weekly for prevention of fracture, as appropriate calcium plus vitamin D supplementation may be sufficient. Risedronate showed much of the same beneficial clinical data as its predecessor in its major clinical investigations (Harris et al., 1999; Reginster et al., 2000). These trials, deemed the Vertebral Efficacy with Risedronate Therapy (VERT) trials, showed a 65% and 61% relative risk reduction in new vertebral fractures at 1 year, and a 41% and 49% reduction at 3 years of follow-up. These numbers were essentially equal to those of alendronate, making risedronate an acceptable alternative. Risedronate is also available in a
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once-weekly dosing of 35 mg that has proven just as efficacious as the 5 mg daily dose (Brown et al., 2002). The newest oral bisphosphonate, ibandronate, has been marketed in a 2.5 mg oncedaily dose as well as in a 150 mg once-monthly dose. Various monthly dosing regimens were compared to the original daily dose using multiple doses and dosing schemes. In the end, all monthly regimens were proven “noninferior” to daily dosing, with 150 mg monthly producing a significant increase in overall BMD over daily dosing (3.9% vs. 4.9%). However, the daily-dosing regimen of ibandronate is the only formulation with fracture prevention data (Chesnut et al., 2004; Felsenberg et al., 2005; Miller et al., 2005). Zoledronic acid (Zometa®, Reclast®) is a bisphosphonate originally prescribed for hyperclacemia of malignancy or Paget’s disease and is being studied for treatment of patients with osteoporosis. A 5mg annual infusion has been shown to reduce morphometric vertebral fractures by 70% (10.9 vs. 3.3%, HR 0.30, 95%CI 0.24–0.38) over a 36 month period. This new dosage form proves to be an interesting approach to osteoporosis therapy as it avoids the gastrointestinal adverse events reported with the oral formulations. However, in the major clinical study looking at zoledronic acid infusions for preventing fractures, patients were more likely to experience pyrexia, myalgias, influenza-like symptoms, headache, and arthralgias, occurring most often after the initial infusion. Surprisingly, the most concerning adverse event was “serious” atrial fibrillation, occurring in 2.4% of the zoledroninc acid population (versus 1.9% in placebo). (Black, Delmas, et al., 2007, Novartis Pharmaceuticals Corp., 2007).
Nonvertebral Fractures The bisphosphonate class is one of the few medications for decreasing nonvertebral fracture risks. Unlike the selective estrogen receptor modulators (SERMs) and intranasal calcitonin, the oral bisphosphonates alendronate and risedronate may be used effectively in patients for primary and secondary nonvertebral fracture prevention. Ibandronate has yet to prove its efficacy for preventing nonvertebral fractures (Rosen, 2005). It is this efficacy data that further supports the use of these agents as first-line therapy in postmenopausal osteoporosis, in conjunction with adequate calcium plus vitamin D supplementation. As discussed earlier, the FIT1 and FIT2 trials evaluated the use of alendronate in the primary and secondary prevention of fractures in postmenopausal women (Black et al., 1996; Cummings et al., 1998). The results for nonvertebral fractures in these trials were not as compelling as those for vertebral fractures, though a significant improvement was seen in the FIT1 trial. As well, Pols et al. (1999) found a significant difference in nonvertebral fracture rates in patients with a T-score of less than –2.0 who were taking alendronate 10 mg. Fracture relative risk reductions were reported by the FIT1 and Fosamax International Study Trial Group (FOSIT) (Pols et al., 1999) trials as 51% and 47% in the hip and nonvertebrae, respectively. Recently, a meta-analysis by Papapoulos et al. (2005) evaluated alendronate’s efficacy in hip fractures in postmenopausal women and found a 55% overall risk reduction in new fractures. Like alendronate, risedronate has proven its clinical efficacy for the prevention of primary and secondary nonvertebral fractures in postmenopausal women. In the Hip Intervention Program (HIP) trial, a relative risk reduction of 36% was found
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in women taking alendronate 5 mg when compared to women taking only placebo (McClung et al., 2001). The same efficacy for hip fractures can be seen with Deal’s work (2002), though some controversy exists over the results. Overall, patients experienced a significant 28% risk reduction for hip fractures, though a subgroup analysis showed that this benefit was not seen in patients aged 70 to 79 without a history of vertebral fractures. Currently, conclusive data is not available for ibandronate’s efficacy in nonvertebral fractures. Daily and intermittent dosing of ibandronate was compared to placebo for 3 years in order to evaluate its effect on nonvertebral fractures. At the trial’s end, there was a negligible, nonsignificant decrease in nonvertebral fracture rates (9.1%, 8.9%, and 8.2%, respectively) (Chesnut, Skag, et al., 2004). Given this information, ibandronate currently cannot be recommended for the prevention of nonvertebral fractures.
Administration and Adverse Events Bisphosphonates are highly polar compounds and have very limited gastrointestinal absorption after oral administration. Even under the best dosing conditions, on an empty stomach 2 hours before meals, the oral bioavailability of bisphosphonates is usually less than 1% and is drastically reduced when administered with a meal. Given this limited absorption, the oral bisphosphonates have specific dosing instructions that patients must follow. Patients should be instructed to take their dose first thing in the morning before eating or drinking anything for the day. They should take the tablet with 6–8 ounces of water and then refrain from eating and drinking for at least another 30 minutes for alendronate and risedronate, 60 minutes for ibandronate. The oral solution of alendronate (Fosamax®) should be followed by at least 2 ounces (a quarter of a cup) of water. Patients should also avoid taking any other medications. During this time, patients should also remain sitting or standing upright. They should avoid being in a supine position, for this may prolong esophageal exposure to the drug and increase changes of topical irritation and adverse reactions. In most cases, it is easy to counsel patients to take the dose immediately upon rising in the morning and then ready themselves for the day by performing hygienic activities and dressing. This procedure should be followed with each dose, be it daily, weekly, or monthly. As stated above, there is not a significant difference between dosing regimens, and patients should participate in the regimen that is most appropriate, given their propensity for medication adherence (and fracture risk). Many patients may prefer the onceweekly dosing schedule to the daily regimen, given the burden of the dosing rituals on a daily basis of taking the bisphosphonate with 8 ounces of plain water 30 minutes before any other medication, liquid, or food is consumed, and remaining upright. Less frequent dosing regimens may allow regeneration of drug-related damage of the stomach mucosa, though providers should evaluate for medication adherence problems due to forgotten doses. The side effect profiles of each oral bisphosphonate are comparable regardless of agent or dosing regimen. Abdominal pain, dyspepsia, and nausea appear to be the most prevalent gastrointestinal complaints of patients taking oral bisphosphonates, though these rates do not differ greatly from those of placebo. Back pain was also a highly reported adverse event among the bisphosphonates. Recently, bisphosphonate osteochemonecrosis has become the adverse event of attention for patients taking injectable
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and perhaps rarely oral bisphosphonates (Hellstein & Marek, 2004, 2005). Patients with these complaints should be evaluated by their providers to discuss the risks versus benefits of continuing therapy. Patients should also avoid taking bisphosphonates with products containing aluminum, calcium, and magnesium, as these products will decrease the absorption of the bisphosphonate from the gastrointestinal tract. It is important to note that while calcium is a critical component to the effectiveness of osteoporosis therapy, it should not be taken at the same time as a bisphosphonate, since bisphosphonate effectiveness decreases if calcium is taken within 30 minutes.
Parathyroid Hormone Therapy (PTH) The parathyroid gland was one of the last major human organs to be discovered (Holick, 2005). Its role, to secrete parathyroid hormone and regulate calcium and 1,25-dihydroxy vitamin D, is one of the few that facilitate osteoblast activity rather than preventing osteoclast activity (O’Connell et al., 2005). The recombinant human parathyroid hormone, teriparatide (Forteo®), is currently the only available agent in this class of medication. It is administered as a once-daily injection and is approved for use for up to 24 months. The FDA issued a black box warning for the medication because of an increased incidence of osteosarcoma in rats receiving doses at 3 to 60 times higher exposure than humans (Eli Lilly & Company, 2004). Although its exact placement in the paradigm of osteoporosis treatment has not been fully worked out, teriparatide may be an agent to consider in patients at very high risk of future vertebral fracture or patients who have failed to benefit from bisphosphonate therapy. After a course of teriparatide for up to 24 months, consideration should be given to adding a bisphosphonate to reduce the loss of bone density that may follow its cessation.
Mechanism of Action/Kinetics Parathyroid hormone functions to regulate bone metabolism, facilitate resorption of calcium and phosphate in the renal tubule, and control gastrointestinal calcium absorption, and increase 1,25-dihydroxy vitamin D (Eli Lilly & Company, 2004). Recently, parathyroid hormone receptors have been found on osteoblasts, better describing its anabolic properties and ability to catabolize bone metabolism (Holick, 2005). After subcutaneous administration, the drug is 95% bioavailable and has a half-life of approximately 1 hour (Eli Lilly & Company, 2004).
Efficacy Vertebral Fractures Various clinical investigations support bone mineral density improvements when teriparatide is used with or without antiresorptive agents. Monotherapy or combining teriparatide with hormone replacement therapy or selective estrogen receptor reuptake modulators increased bone mineral densities in the spine from 6% to 15% (Deal et al., 2005; Orwoll et al., 2003; Ste-Marie, Schwartz, Hossain, Desaiah, & Gaich, 2006). These
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benefits have been reported to be sustained out to 30 months after discontinuation of treatment (Prince et al., 2005). The addition of bisphosphonate therapy after 12 months of teriparatide (consecutive therapy) increased BMD minimally, though the changes were still better than teriparatide alone. Also, combining teriparatide with a bisphosphonate for the duration of treatment was beneficial, but still less so than the consecutive therapy (Black et al., 2005; Ettinger, San, Crans, & Pavo, 2004; Finkelstein et al., 2003). Teriparatide also has beneficial data surrounding fracture prevention in both men and women. Men using teriparatide 20 mcg daily experienced a reported 83% reduction in moderate to severe fracture risk (Kaufman et al., 2005). Women using teriparatide 20 mcg daily experienced a reported 65% reduction in new vertebral fractures (Neer et al., 2001).
Nonvertebral Fractures Teriparatide’s benefits are also present in increasing hip bone mineral density and preventing fractures when used alone or in combination (as above). Total hip and femoral neck BMDs increased as much as 5% with its use (Deal et al., 2005; McClung et al., 2005; Ste-Marie et al., 2006). Nonvertebral fractures were not significantly increased and were decreased by 53% in patients using teriparatide as compared to those using a placebo (Gallagher, Genant, Crans, Vargas, & Krege, 2005; Neer et al., 2001).
Administration and Adverse Events Teriparatide is administered as a daily subcutaneous injection. It is available as a 28-day, prefilled pen delivery device. Each administration provides the patient with a 20 mcg dose. The manufacturer suggests that patients should receive their first dose of teriparatide sitting or lying down because the drug may cause orthostatic hypotension. Patients should rotate injection sites along the abdominal belt line and thighs. Adverse events associated with the medication previously mentioned include osteosarcoma in rats (in particular, baby rats). To date there are no published reports of osteosarcoma in humans receiving teriparatide, and osteosarcoma has never been associated with hyperparathyroidism (where there is chronic elevation of parathyroid hormone). Other adverse events include injection-site reactions such as injection pain, erythema, itching, and urticaria. Patients using teriparatide may also report an increased incidence of leg cramps, dizziness, or paresthesias. Metabolic changes may include hyper- or hypocalcemia, hyperuricemia, or hypoparathyroidism (Eli Lilly & Company, 2004). A major limiting factor with teriparatide is cost—approximately 10 times the cost of bisphosphonate therapy.
Estrogen Therapy Estrogen is an essential hormone that is important throughout life for bone development in both men and women. Unlike the bisphosphonate drugs discussed earlier, estrogen acts primarily on reproductive and nonreproductive tissues in the body. Consequently,
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Osteoporosis
the use of exogenous estrogen hormone treatment for the prevention and treatment of osteoporosis must be weighed against the ways in which the form and dose of estrogen might affect other tissues in the body. Therefore, of particular importance is consideration of the risk: benefit ratio and whether there are risks that might restrict use (USDHHS, 2004).
Mechanism of Action/Kinetics Estrogens are available as naturally occurring hormones or as synthetic steroidal and nonsteroidal compounds with estrogenic action. Estrogens are secreted primarily by the ovaries, and also by the adrenals, corpus luteum, placenta, and testes. They regulate the growth and function of the female sex organs and the appearance of female secondary sex characteristics (McEvoy et al., 2006). Estrogen is effective in inhibiting bone resorption and increasing BMD by binding to estrogen receptors on bone and blocking the production of specific cytokines that increase the number of osteoclasts and prolong their life span (Ettinger, Pressman, & Silver, 1999). Estrogens are secreted at varying rates throughout the menstrual cycle, and during menopause, ovarian secretion of estrogens falls off at varying rates. The secretion of the ovarian hormones estradiol and progesterone is regulated by control mechanisms along the hypothalamic–pituitary– target organ axis. Rising levels of estrogen and progesterone stimulate the hypothalamus to secrete gonadotropin-releasing hormone (GnRH), which travels via the portal system to the anterior pituitary. GnRH regulates the synthesis, storage, and secretion of the gonadotropins, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) from the anterior pituitary. FSH and LH are responsible for follicular development (ovarian cycle) and sequential changes in the endometrium (uterine cycle) as well as the production of estrogen (primarily in the form of estradiol) and progesterone by the corpus luteum (McEvoy et al., 2006). The human body produces three estrogens: estradiol E2, estrone E1, and estriol E3. Of these, estradiol is the most potent of the estrogens produced by the ovary. Estrone, a metabolite of estradiol, is considerably less potent, and estriol, a further metabolite of estradiol, is very weak. There are several types of estrogen prescribed in the United States and Europe. These pharmaceuticals are given in a variety of prescription strengths and forms. Of the three estrogens, estrone is the form of estrogen present in women after menopause and is available as tablets under the brand name Ogen®. Until the recent report of the Women’s Health Initiative (WHI), the most commonly prescribed estrogen in the United States was Premarin®, a conjugated estrogen that is a mixture of estrone and other estrogens. Estradiol is the form of estrogen naturally present in premenopausal women. It is available as tablets (Estrace®), as transdermal patches (Estraderm®), or as vaginal creams (Estrace®, Estring®, Femring®) and vaginal tablets (Vagifem®). Estriol is a weaker form of estrogen produced by the breakdown of other forms of estrogen; it is most commonly used in Europe under the brand name Estriol and thought not to cause cancer. In the United States, estriol can be made by a compounding pharmacist (Gulli, 2002). Table 5.1 lists the estrogens approved for the prevention of osteoporosis in postmenopausal women (Nurse Practitioners’ Prescribing Reference, 2006). Currently, hormone therapy is not approved by the FDA for the treatment of osteoporosis, presumably because the fracture data required for the approval
55
Pharmacological Management
Table
5.1
Approved Estrogens for the Prevention of Osteoporosis in Postmenopausal Women Product *Estrace® estradiol *Ogen (USDHHS, 2004) estrone sodium as estropipate *Ortho-est® estropipate *Premarin® conjugated equine estrogens *Alora® (transdermal) estradiol *Estroderm® (transdermal) estradiol *Vivelle® (transdermal) estradiol *Vivelle Dot ® (transdermal) estradiol *Climara® (transdermal) estradiol
*Menostar® (transdermal) estradiol Esclim® (transdermal) estradiol
Estrogel® (topical gel) estradiol Estrosorb® (emulsion) estradiol
Dosage 0.5 mg, 1 mg, or 2 mg; tabs daily 0.625 mg, 1.25 mg, 2.5 mg; tabs daily 0.75 mg, 1.5 mg; tabs; daily 0.3 mg, 0.45 mg, 0.625 mg, 0.9 mg, 1.25 mg, 2.5 mg daily 0.025 mg/d, 0.05 mg/d, 0.075 mg/d, 0.1 mg/d Patch applied biweekly 0.05 mg/d, 0.1 mg /d Patch applied biweekly 0.05 mg/d, 0.1 mg Patch applied biweekly 0.025 mg/d, 0.0375 mg/d, 0.05 mg/d, 0.075 mg/d, 0.1 mg/d Patch applied biweekly 0.025 mg/d, 0.0375 mg/d, 0.05 mg/d, 0.06 mg/d, 0.075 mg/d, 0.1 mg/d Patch applied weekly 0.014 mg/d patch applied Patch applied biweekly 0.025 mg/d, 0.0375 mg/d, 0.05 mg/d, 0.075 mg/d, 0.1 mg/d Patch applied biweekly 1.25 mg pump once qd
Cautions (all estrogens) Undiagnosed abnormal genital bleeding Known or suspected breast cancer Known or suspected estrogen-dependent neoplasia Venous thromboembolism or pulmonary embolism or past history Active or recent (within past year) arterial thrombolic disease (e.g., stroke, myocardial infarction) Porphyria Liver disease or impairment Hypersensitivity to estrogens or any ingredient in the formulation Suspected or known pregnancy
1.74 g/pouch; 2 pouches qd
*FDA-approved estrogens for the prevention of osteoporosis in postmenopausal women. From Nurse Practitioners’ Prescribing Reference,® NPPR, 2006; McEvoy et al., 2006. Note. Estrogen must be combined with a progestin/progesterone either cyclically or continuous in women with an intact uterus.
process were never submitted (Grass & Dawson-Hughes, 2006). Women with an intact uterus should use estrogen combined with a progestin or progesterone either cyclically or continuously to prevent endometrial hyperplasia, which can lead to endometrial cancer if atypical cells are present.
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Osteoporosis
Efficacy Vertebral-Nonvertebral Fractures The favorable impact of hormone therapy (HT), including estrogen and combination therapy (estrogen + progestin), on BMD has been supported by the results of randomized, placebo-controlled trials, including the Postmenopausal Estrogen/Progestin Interventions (PEPI) trial (Writing Group for the Postmenopausal Estrogen/Progestin Interventions, 1996) and the Women’s Health, Osteoporosis, Progestin, Estrogen (HOPE) study (Lindsay, Gallagher, Kleerekoper, & Pickar, 2002). These studies and a meta-analysis conducted by Wells et al. (2002) found that postmenopausal HT had a consistent and positive result on BMD at the forearm (3%–4.5%), spine (3.5%–7%), and hip (2%–4%). According to these studies, BMD increased in the first year of HT. Different formulations of conjugated estrogen (CEE/Premarin®, as well as estradiol) and combination therapy were included in both the PEPI trial and the meta-analysis, and no significant differences were found in the effects of different formulations of estrogen on bone density (USDHHS, 2004). The effect of HT on fracture rates is more limited in the research literature. Kiel, Felson, Anderson, Wilson, and Moskowitz (1987) and Cauley et al. (1995) all found that there are fewer fractures in women who received HT over the long term. In order to fill the research gap, Torgerson and Bell-Syer conducted a systematic review of all randomized trials of HT that reported or collected vertebral fracture data. Their meta-analysis demonstrated that HT reduced nonvertebral fractures by 27% (Torgerson & Bell-Syer, 2001a) and produced an overall 33% reduction in vertebral factures (Torgerson & Bell-Syer, 2001b). The WHI conducted two separate randomized clinical trials to evaluate the effect of postmenopausal HT on decreasing the risk of cardiovascular disease. In addition, the results have provided information on other chronic diseases including fractures. In the first trial, women with an intact uterus received an estrogen-progestin combination, Prempro® 2.5 mg (E+P, 0.625 mg conjugated equine estrogen [CEE], and 2.5 mg medroxyprogesterone [MPA], daily) (Rossouw et al., 2002), and the second trial evaluated the effect of estrogen alone, Premarin® (CEE, 0.625 mg), in women who have undergone hysterectomies (Anderson et al., 2004). The WHI estrogen-plus-progestin study is the first large randomized clinical trial that confirmed that combined postmenopausal hormone therapy, specifically, Prempro® 2.5 mg, reduces the risk of fractures at the wrist, hip, and vertebrae (Cauley et al, 2003). Vertebral and hip and other fractures were decreased by at least one-third in both of the trials, and total fractures fell by 24%–30%. The results of these two large clinical trials are consistent with observational studies of postmenopausal women using HT and trials evaluating the outcome of HT on BMD (USDHHS, 2004). While the WHI set forth apparent benefits of HT in the prevention of postmenopausal bone loss and the reduction of bone turnover, these positive effects must be weighed against the higher rates of breast cancer, stroke, deep vein thrombosis, and cognitive impairment that were found among those receiving combined, continuous HT (E+P) for the 5.2 years of the study. Postmenopausal women receiving estrogen alone did not experience an increase in breast cancer risk based on 6.6 years of use (Anderson et al., 2004; Rossouw et al., 2002). In addition, no clear cardiovascular benefit of HT was demonstrated in the WHI trials (USDHHS, 2004).
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Based on the current evidence regarding the safety of the long-term use of HT, this treatment should be reserved for women unable to tolerate nonestrogen therapy. The FDA (U.S. Food and Drug Administration, 2004) recommends that HT only be used for the shortest amount of time at the lowest possible doses required to accomplish treatment goals. Research evidence has shown that lower doses of CEE alone, or CEE/MPA, 0.3 mg/1.5 mg daily, significantly increased spine and hip BMD from baseline within 2 years of therapy (Lindsay et al., 2002) and that low-dose estradiol also preserves bone (Prestwood, Kenny, Kleppinger, & Kulldorff, 2003). While HT is effective for the prevention of postmenopausal osteoporosis, there is general consensus that it should only be offered to women who are at increased risk for osteoporosis and are unable to tolerate nonestrogen medications (USDHHS, 2004). The current recommendations are that estrogens and progestins be used at the lowest doses for the shortest period of time needed to reach treatment goals (U.S. Food and Drug Administration, 2004). Estrogen or combination hormones (E+P) in lower doses can help to maintain bone density. The Women’s HOPE study, the first large, randomized placebo-controlled trial to evaluate BMD with lower doses of CEE and CEE/MPA, found that doses as low as 0.3 mg daily of CEE or the combination significantly increased spine and hip BMD from baseline within 2 years of therapy (Lindsay et al., 2002). Prestwood et al. (2003) also showed that low-dose estrogen preserved bone. They found that in postmenopausal women, taking a dosage of 0.25 mg daily of 17-estradiol for 3 years increased bone density of the hip, spine, and total body and reduced bone turnover. However, larger long-term trials are needed to support the lasting benefits of low-dose HT on bone health. Currently, the long-term effects of various doses, formulations (including estrogens or progesterone), and modes of administration (e.g., transdermal, vaginal administration) on bone and other tissues have been not been sufficiently studied to support their long-term effectiveness and safety (USDHHS, 2004).
Administration and Adverse Events Estrogens can be administered orally, intravaginally, transdermally, parenterally, and by topical application of a gel or emulsion to the skin. Estrogen is usually taken in a continuous daily dosage regimen or in a cyclic regimen. Cyclically administered estrogen is usually taken once daily for 3 weeks followed by 1 week off the drug, or once daily for 23 days followed by 5 days without the drug. Dosage is individualized according to the condition being treated, and the tolerance and therapeutic response of the patient (McEvoy et al., 2006).
Bioidentical Hormones In addition to conventional or traditional HT, discussed above, a brief discussion of bioidentical hormone therapy (BHRT), sometimes called natural hormone therapy (NHRT), is offered. These hormones are not the same as phytoestrogens, also referred to as natural estrogen-like products, which will be discussed under integrative therapies. Bioidentical hormones refer to hormones that have the same molecular structure as those made by the human body and are isomolecular and indistinguishable from each other.
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Osteoporosis
By definition, bioidentical hormones are plant derived and bioidentical to endogenous hormones. The prescription for BHRT is written by a licensed health care provider and made up by a compounding pharmacist to treat symptoms of perimenopause, menopause, and hormonal imbalance. The dosage, formulation, and administration are individualized to balance each woman’s hormone profile to manage symptoms of menopause and maintain health (Ahlgrimm & Kells, 2003; Smith, 2003; Wright & Morgenthaler, 1997). Salivary and blood spot hormone tests, in addition to symptoms, are used to guide the provider in achieving hormone balance (Ahlgrimm & Kells, 2003). There has been an increased interest in bioidentical or natural hormones since the WHI clinical trial report was released in 2002, noting greater harm than benefit from the use of combined CEE plus a progestin. These findings resulted in a precipitous decrease in the use of estrogen and progestin and a critical reexamination of menopausal HT and triggered greater interest in other approaches to managing menopausal symptoms, including the use of bioidentical hormones (Stefanick, 2005). Bioidentical hormones include estrogens estrone (E1), estradiol (E2), and estriol (E3), progesterone, testosterone, dehydroepiandrosterone (DHEA), and pregnenolone. Bioidentical hormones are prepared from either beta sitosterol extracted from the soybean or from diosgenin extracted from the Mexican wild yam root. Bioidentical hormones can be administered in various forms, including oral (capsules, drops, sublingual), transdermal/topical, vaginal, rectal, and pellet implants. In addition, estradiol (Estrase®) and micronized progesterone (Prometrium®) are considered bioidentical hormones and are found in synthetically produced hormones. Examples of individually compounded estrogens include Biestrogen (Biest), which is made up of estriol 80%, a weaker estrogen, and estradiol 20%, a more potent estrogen, expressed on a milligram-per-milligram basis. A similar preparation, Triestrogen (Triest), contains the three estrogens, estriol 80%, estradiol 10%, and estrone 10%. These hormones are pharmaceutical grade and are not commercially marketed but must be compounded in a pharmacy. In the United States, estrone and estradiol are commercially marketed, but estriol is not. Micronized progesterone is also compounded and prescribed singly or in combination with estrogen and or testosterone (Ahlgrimm & Kells, 2003; Smith, 2003; Wright & Morgenthaler, 1997).
Table
5.2
International Names for Evista® Brand name Bonmax Celvista Evista® Loxar Loxifen Optruma
Raxeto
Country where approved for use India Thailand United States, Hong Kong, Indonesia, Israel, Korea, Malaysia, Philippines, Singapore, Taiwan Uruguay Paraguay Austria, Belgium, Bulgaria, Czech Republic, Denmark, England, Finland, France, Germany, Greece, Guatemala, Hungary, Ireland, Italy, Netherlands, Norway, Poland, Portugal, Russia, Slovenia, Spain, Sweden, Switzerland, Turkey Argentina
Note. From Mosby’s Drug Consult, 16th ed., 2006.
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Proponents of BHRT assert that these hormones are better tolerated and are safer alternatives than synthetic manufactured hormones. However, the FDA recommends that the labeling of bioidentical hormones include a statement that there is no evidence these hormones are safer than synthetic products. Regrettably, few observational studies or clinical trials have been conducted comparing synthetic HT with BHRT (Stefanick, 2005). BHRT has not been approved by the FDA for the prevention or treatment of osteoporosis. Currently participants are being recruited for a double-blind, placebocontrolled pilot study comparing bioidentical hormones to low-dose Prempro®. The purpose of this study is to try to gather information about safety when bioidentical hormones are used during early menopause.
Selective Estrogen Receptor Modulators (SERMs) Raloxifene hydrochloride (Evista®) is a nonsteroidal benzothiophene derivative with mixed estrogen agonist or antagonist activity in specific tissues. Raloxifene belongs to the class of compounds known as SERMs (McEvoy et al., 2006). The biological actions of SERMs are principally mediated via binding to estrogen receptors. This binding results in the activation of specific estrogenic pathways and the blockade of others (“Raloxifene Hydrochloride,” 2006). Thus, raloxifene acts like estrogen to prevent bone loss and improve lipid profiles but also has the potential to block some estrogen effects, such as those that lead to breast and endometrial cancer. It increases the risk of deep vein thrombosis (DVT) compared to placebo and does not block the vasomotor symptoms seen with menopause, which may limit compliance with therapy in postmenopausal women. The effects on bone seen with the administration of SERMs appear to be less than with the use of estrogen therapy (Lexi-Comp Online, 2006). Table 5.2 lists the international brand names for raloxifene where it is approved for use in various countries. Tamoxifen, another SERM, is primarily used for the prevention of breast cancer, but it is not approved for the prevention and treatment of osteoporosis. Limited data on the effects of tamoxifen on bone turnover have shown that it maintains or improves BMD in postmenopausal women but causes bone loss in premenopausal women (Powles, Hickish, Kanis, Tidy, & Ashley, 1996). Newer SERMs are under development and may provide more benefit to the bones, heart, and breast tissue. They may also decrease vasomotor symptoms and have a positive effect on cholesterol (USDHHS, 2004). These newer SERMs include lasofoxifen, under development by Ligand and Pfizer. Now in phase III trials, it provides an improved effect on BMD and fracture reduction, and has cardiovascular benefits as well. Wyeth and Ligand are developing a new SERM, known as TSE-424, a combination bazedoxifene and conjugated estrogen (Premarin). Phase III clinical trials comparing TSE-424 to placebo and to raloxifene for the treatment of osteoporosis in postmenopausal women are in progress. Phase II clinical trials of SERM 3339, developed by Aventis for the treatment of osteoporosis, are in progress (Liebman, 2002). Raloxifene is the only SERM that has been approved by the FDA for osteoporosis prevention (LexiComp Online, 2006).
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Osteoporosis
A clinical trial that was designed to compare raloxifene with tamoxifen in reducing the incidence of breast cancer in postmenopausal women at increased risk for the disease demonstrated that both drugs reduced breast cancer risk by 50% for postmenopausal women. Additionally, the raloxifene group had 36% fewer uterine cancers and 29% fewer blood clots than the tamoxifen group (National Cancer Institute, 2006).
Mechanism of Action/Kinetics Raloxifene differs pharmacologically and chemically from naturally occurring estrogens, synthetic steroidal and nonsteroidal compounds with estrogenic activity, and antiestrogen agents (e.g., clomiphene, tamoxifen, toremifene). Raloxifene exhibits estrogen agonist activity on bone and circulating lipoproteins, but estrogen antagonist activity on breast and uterine tissue. As with estrogen replacement, the principal pharmacologic action of raloxifene is to decrease the rate of bone resorption, consequently slowing the rate of bone loss in postmenopausal women (McEvoy et al., 2006). In addition, raloxifene decreases total LDL cholesterol but usually does not affect HDL cholesterol or triglycerides (Mosby Drug Consult, 2006). Approximately 60% of raloxifene is rapidly absorbed from the gastrointestinal (GI) tract after an oral dose; however, its absolute bioavailability as an unchanged drug is only 2%, due to extensive first-pass effect metabolized to glucuronide conjugates. Taking it with a high-fat meal increases the absorption but does not substantially lead to clinically meaningful changes in systemic exposure; therefore, raloxifene can be taken without regard to meals and has a half-life of 27.7–32.5 hours. The usual dosage for the prevention of osteoporosis in postmenopausal women is 60 mg daily, but no additional benefit is gained from administering higher doses. The onset of action is 8 weeks from the commencement of taking the drug. Raloxifene’s use in invasive breast cancer risk reduction (investigational use) is 60 mg per day for 5 years (Lexi-Comp Online, 2006).
Efficacy Vertebral Data related to the fracture protection of raloxifene in postmenopausal women with osteoporosis come from the Multiple Outcomes of Raloxifene Evaluation (MORE) study, a large, 3-year, randomized, placebo-controlled, double-blind, multinational osteoporosis treatment trial (Ettinger, Black, et al., 1999). The incidence of new vertebral fracture was the primary end point in this trial. The results show that raloxifene increased spine BMD by 2.3% and hip BMD by approximately 2.5% after 3 years of use (Ettinger, Black, et al., 1999). About a 50% reduction in spine fractures was observed, but there was no effect on hip or other nonvertebral fractures (Cranney et al., 2002; Ettinger, Black, et al., 1999). A post hoc analysis of the MORE study found a 68% vertebral fracture reduction after 1 year of raloxifene 60 mg/d in the overall study population and a 66% reduction in women with known vertebral fracture at baseline (Maricic et al., 2002). In a 1-year extension of the MORE trial, women who remained on therapy for at least 4 years had a 36% vertebral fracture reduction in the overall study population,
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with a 34% reduction in women with at least 1 prevalent fracture at baseline (Delmas et al., 2002). The reduction in vertebral fracture in older postmenopausal women is raloxifene’s primary clinical benefit, particularly if some vertebral fractures are present at baseline; however, bone turnover can return to its prior condition, resulting in bone loss after raloxifene is stopped (USDHHS, 2004).
Nonvertebral Fractures Findings from the MORE study show that raloxifene did not significantly decrease the 3-year risk of hip or overall nonvertebral fractures in the overall population receiving raloxifene 60 mg per day and 120 mg per day (Ettinger, Black, et al., 1999).
Administration and Adverse Events Raloxifene is available in a 60 mg film-coated tablet for oral administration once daily at any time of day without regard to meals. It should be stopped around 72 hours prior to and during prolonged immobilization, such as surgery requiring restricted activity or extended travel by air or land, owing to serious adverse events due to venous thromboembolic disease (similar to the reported risk of HT) (Lexi-Comp Online, 2006). For prevention of thromboembolic events, antiembolism stockings and compression stockings are recommended. Raloxifene also causes significantly more mild to moderate adverse effects such as leg cramps and hot flashes compared with placebo, but considerably less vaginal bleeding than estrogen-progestin combination therapy. Contraindications: Prolonged immobilization (e.g., postoperative recovery, prolonged bed rest) or active thromboembolic condition. Side effects: Increased risk of thromboembolism, pulmonary embolism, and superficial thrombophlebitis, vasomotor symptoms (hot flashes), flu-like symptoms (these disappear with continued use), gastrointestinal upset, vaginitis, and urinary tract infection. Drug interactions: Cholestyramine (Questran®) and ampicillin decrease raloxifene absorption/blood levels. Raloxifene the potential to interact with other highly protein-bound drugs by increasing the effects of either drug. Caution is recommended with coadministration of highly protein-bound drugs, warfarin, clofibrate, indomethacin, naproxen, ibuprofen, diazepam, phenytoin, tamoxifen, or lidocaine (Lexi-Comp Online, 2006, Mosby’s Drug Consult, 2006). The MORE study reported that the majority of adverse events were mild or moderate. The most common serious event related to raloxifene treatment was venous thromboembolism. Women receiving raloxifene had an increased risk of venous thromboembolus as compared with women receiving a placebo (Ettinger, Black, et al., 1999). Raloxifene is administered in the geriatric population at the usual adult dose. There are no gender differences; however, the influence of race has not been conclusively determined. Studies in patients with renal insufficiency were not conducted, since only negligible amounts of raloxifene are excreted in urine. Raloxifene and metabolite concentrations in women enrolled in the osteoporosis treatment and prevention trials with
5.3
Ibandronate
Risedronate
Agent Bisphosphonates Alendronate
Boniva 2.5 mg, 150 mg, 1mg/mL (3 mL prefilled syringe)
Actonel + Calcium (35 mg/1250 mg)
Fosamax 7 0mg/75 ml solution Actonel 5 mg, 35 mg, 75 mg
Fosamax +D (70 mg/2,800 IU or 70 mg/5,000 IU)
Fosamax 5 mg, 10 mg, 35 mg, 70 mg
Brand name / Formulation
Gastrointestinal abdominal pain colitis diarrhea Musculoskeletal osteonecrosis of the jaw arthralgias (rare with oral bisphosphonates) Neurologic headache
Osteopenia Oral: 5 mg daily or 3 5 mg weekly
• Inhibit osteoclast activity on the surface of the bone • Inhibit recruitment of osteoclasts to bone • Alter bone to slow or delay its resorption Osteoporosis / Osteopenia Oral: 5 mg daily 35 mg weekly or 75 mg on 2 consecutive days monthly Osteoporosis Oral: 2.5 mg daily or 150 mg monthly Injection: 3 mg IV every 3 months
Osteoporosis Oral: 10 mg daily or 70 mg weekly
Adverse events
Dosing
Mechanism of action
Table Pharmacological Management of Osteoporosis
Forteo 750 mcg injection
Miacalcin 200 units/ activation
Various doses and formulations
Evista 60 mg
• Increased intestinal calcium absorption • Increased calcium and phosphate resorption by the bone • increased tubular calcium resorption in the presence of inhibited tubular phosphate resorption
• Excreted in response to serum hypercalcemia • Directly inhibits and depresses osteoclast function
• Inhibits bone resorption • Reduces biochemical markers of bone turnover to the premenopausal range • Inhibits bone resorption • Preserves or increases bone mass
Injection: 20 mg SC once daily for up to 2 years
Dizziness Leg cramps Osteosarcoma in rats
Rhinitis Back pain Nausea Vomiting
increased risk of venous thromboembolism Nausea Breast tenderness Menstrual flow
Dosing varies by product
Intranasal: 1 spray in alternating nostrils, daily Injection: 100 IU IM or SC every other day
increased risk of venous thromboembolism return of hot flashes
Oral: 60 mg daily
Note. From information in R. K. Klasco, ed., DRUGDEX® System, Internet database, Thomson Micromedex. Updated periodically. Retrieved August 28, 2006, from http://slhwebappsvr.slhn.org:81/hcs/librarian/PFPUI/Ms4kXLJ1XoHuvh
Parathyroid hormone Teriparatide
Calcitonin Calcitonin
Estrogen
SERM/Estrogen Raloxifene
64
Table
5.4
Osteoporosis
Pharmaceutical Agents: A Comparison of Their Efficacy in Vertebral and Nonvertebral Fractures Agent Alendronate
Risedronate Ibandronate Raloxifene
Estrogen
Vertebral fracture Primary Prevention 30%–47% relative risk reduction Secondary Prevention 45%–50% relative risk reduction 41%–49% relative risk reduction in new fractures 50%–62% relative risk reduction in new fractures
Nonvertebral fracture 47%–55% relative risk reduction in new fractures
64% relative risk reduction in new fractures, 60 mg daily; 57% 120 mg daily 33% reduction in new fractures
Not significantly affected
36% relative risk reduction in new fractures Not significantly affected
27% reduction in new fractures
Calcitonin
Primary Prevention 33% reduction in new fractures Secondary Prevention 36% reduction in recurrent fractures
Unable to report statistical significance
Teriparatide
65%–83% reduction in patients with a moderate to severe fracture risk
53% reduction in fracture
Note. Adapted with permission from Umland, E. M. (2006) Guidelines for pharmacists: Interpreting the medical evidence for bisphosphonates in postmenopausal osteoporosis U.S. Pharmacist. Retrieved July 9, 2007, from http://www.uspharmacist.com/index.asp?page=ce/105219/default.htm
an estimated creatinine clearance as low as 21 ml/min are similar to the concentrations in women with normal creatinine clearance. Raloxifene was examined following a single dose in Child-Pugh Class A patients with cirrhosis and total serum bilirubin ranging from 0.6–2.0 mg/dl, and plasma raloxifene concentrations were about 2.5 times higher than in controls and correlated with bilirubin concentrations. The safety and efficacy of raloxifene have not been further evaluated in patients with hepatic insufficiency. Table 5.3 provides a summary of the pharmaceutical agents used in the management of osteoporosis, and Table 5.4 presents a comparison of their efficacy in vertebral and nonvertebral fractures.
Calcitonin (Salmon) Therapy Calcitonin (Miacalcin®) is an endogenous hormone secreted by the thyroid’s parafollicular gland in mammals. In the treatment of osteoporosis, calcitonin derived from a salmon’s ultimobranchial gland is utilized, due to its greater potency and prolonged duration of action when compared to mammalian calcitonin (Novartis Pharmaceutical Corp., 2003). It was first formulated as an injection, to be administered on an everyother-day basis. Most recently, a daily nasal spray formulation was added as a dose
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65
delivery system. In clinical trials of women treated out to 5 years, intranasal calcitonin has demonstrated limited benefit in secondary vertebral fracture prevention (Chesnut et al., 2000). Calcitonin (salmon) is not an appropriate first-line agent for the treatment of osteoporosis. It should be considered as a second- or third-line agent in patients with intolerance to bisphosphonate therapy or patients who are unable to use bisphosphonates due to physiologic functional limitations. Calcitonin has reported analgesic effects in patients with Paget’s disease or bone metastases and provides minimal support to help with pain in patients with osteoporosis (Thomson Micromedex, 2006).
Mechanism of Action/Kinetics While the mechanism of action of calcitonin on bone has not been fully explicated, its use causes a decrease in bone resorption through direct osteoclastic inhibition and decreased life span of other circulating osteoclasts. Upon nasal administration, calcitonin is taken up rapidly into systemic circulation and approximately 3% of this dose is bioavailable (as compared to intravenous administration). It cannot be administered orally, as the product is destroyed by gastric acids. The peak concentration of the drug occurs in 20 (intravenous) to 35 (nasal) minutes, with an approximately 43-minute half-life (Novartis Pharmaceutical Corp., 2003; Thomson Micromedex, 2006).
Efficacy Vertebral Fractures There is sparse clinical evidence for the use of calcitonin (salmon) in vertebral fractures. Various clinical trials report an increase in lumbar spine BMD by 1% to 7% in patients using intranasal calcitonin for at least 12 months (Downs et al., 2000; Tiras, Noyan, Yildiz, & Biberoglu, 2000; Toth et al., 2005; Trovas, Lyritis, Galanos, Raptou, & Constantelou, 2002). Two clinical investigations provided evidence of calcitonin’s benefit in decreasing new vertebral fractures in patients with osteoporosis significantly over placebo (Dursun, Dursun, & Yalcin, 2001; Ishida & Kawai, 2004). In addition, the soundest evidence supporting calcitonin’s use in preventing fractures in osteoporosis was provided by the PROOF study (Chesnut et al., 2000). Researchers reported a 33% reduction in new vertebral fractures in patients using 200 IU calcitonin (salmon) daily over placebo. Patients with a previous history of fracture experienced a 36% reduction. This was the only effective dose in the trial for vertebral fracture, as both 100 IU and 400 IU yielded insignificant reductions in new vertebral fractures.
Nonvertebral Fractures Evidence for the use of calcitonin (salmon) in patients to prevent nonvertebral fractures is minimal. BMD in patients using calcitonin (salmon) increased by a maximum of 3% during the studies and did not show a significant change in risk of nonvertebral fractures (Chesnut et al., 2000; Downs et al., 2000; Huusko et al., 2002; Tiras et al., 2000; Toth et al., 2005; Trovas et al., 2002). Authors have reported a significant decrease in nonvertebral fractures in the group receiving 100 IU intranasally versus 200 IU and 400 IU doses.
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However, authors also point out that the study did not meet its statistical power and the evidence-based conclusion is not as sound as was anticipated (Hamdy et al., 2005).
Analgesic Effect The use of calcitonin (salmon) for pain associated with osteoporotic fractures is a unique feature of the medicine. Several clinical investigations have evaluated calcitonin’s effect on perception of pain and functionality with positive results. While a majority of the data involves injectable or rectal administration, Pontiroli et al. (1994) showed similar efficacy between the injectable and intranasal dosages. Patients with vertebral crush fracture reported a significant decrease in spinal pain and experienced earlier mobilization and earlier ability to sit, stand, and walk when using 200 IU intranasal calcitonin (salmon) daily (Lyritis et al., 1997). Patients randomized to placebo remained bed bound for almost the entire duration of the study.
Administration and Adverse Events Patients using intranasal calcitonin (salmon) should be educated to alternate the nostril in which they administer the medication on a daily basis. The medication is generally well tolerated without significant reporting of adverse events.
Combination Antiresorptive Therapy Bisphosphonates, HT, and SERMs are all classified as antiresorptive drugs; however, they operate through different mechanisms of action, suggesting that if used in combination they could have an additive effect. Bone et al. (2000) compared the use of two antiresorptive therapies together to a similar use of estrogen and alendronate alone in postmenopausal women with a hysterectomy over a 2-year period. Women receiving combination therapy had around an 8% increase in BMD at the spine, compared to 6% in women taking alendronate or estrogen. Similar results were reported in BMD at the hip, while combination therapy demonstrated a 1%–2% greater increase in BMD than either therapy alone. No additional unexpected side effects were seen in women in the combination therapy group. A study by Greenspan, Resnick, and Parker (2003) of women age 65 and older also reported that using alendronate and HT together resulted in greater increases in BMD at the spine and hip than did treatment with either drug alone. However, a study by Eviö, Tiitinen, Laitinen, Ylikorkala, and Välimäki (2004) did not support the findings of earlier studies; rather, these investigators found that treating elderly osteoporotic women with combination therapy of alendronate and HRT did not provide any additional advantage over either treatment alone. The use of risedronate in combination with HT for 1 year has also been studied and has been shown to increase BMD at the hip but not the spine (Harris et al., 2001). Johnell et al. (2002), in another short-term study using combination therapy of alendronate and raloxifene, also found a greater increase in hip BMD than in women taking either drug alone. In this study, women taking alendronate alone had a considerably higher BMD
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of the spine and hip than those taking raloxifene alone. A study by Greenspan et al. (2003) also found that women who took combination therapy or alendronate alone maintained BMD of the spine and hip following discontinuation of therapy, while women who gained bone during 2 years on HT lost their BMD gains at the spine and hip during the year after therapy was stopped. Because of the economic burden of multiple drug therapies, because of the greater risk for more side effects, and because trials reported in the literature did not study fracture risk, combination therapy is not generally recommended as first-line therapy. It is generally reserved for individuals of the following types: (1) those who have suffered a fracture while on a single drug, (2) those who have an extremely low BMD and a history of multiple fractures, and (3) those with a very low BMD who continue to lose more bone mass while being treated with a single drug (USDHHS, 2004). Combining an antiresorptive agent with an anabolic agent is discussed under parathyroid hormone therapy.
Calcium and Vitamin D Calcium is a mineral that accounts for 1% to 2% of the adult human body weight and plays a vital role in the development and maintenance of a healthy skeleton. Most of the body calcium (99%) is found in bones and teeth, providing mechanical rigidity. The rest of the calcium in the body is found in blood, intracellular fluid, muscle, and other tissues where it plays a role in other body functions. Calcium mainly exists in bone in the form of hydroxyapatite (Ca)10 (PO4)6(OH)2, and bone mineral is approximately 40% of bone weight (Institute of Medicine [IOM], 1997). Vitamin D (calciferol) is vital for bone health because it assists in the absorption and utilization of calcium. The major source of vitamin D is sunlight, which the human body absorbs by exposure to sunlight through the conversion of precursors in the skin to active vitamin D. Consumption of adequate levels of calcium and vitamin D throughout life and appropriate physical activity are essential to bone health (USDHHS, 2004). The skeleton also serves as a calcium reserve, and bone tissue is resorbed from the skeleton when the exogenous supply is inadequate to maintain serum calcium at a constant level. However, using skeletal calcium over the long term to meet this need leads to
Table
Calcium Recommendations
5.5
800 mg daily: children ages 1 to 10 1,000 mg daily: males, premenopausal women, and postmenopausal women receiving estrogen 1,200 mg daily: teenagers and young adults ages 11 to 24 1,500 mg daily: postmenopausal women not receiving estrogen 1,200 mg to 1500 mg daily: pregnant and nursing mothers Total daily intake of calcium should not exceed 2,000 mg
Note. National Institutes of Health(NIH) Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy. Osteoporosis prevention, diagnosis, and therapy. Journal of the American Medical Association, 285, 785–795, 2001.
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osteoporosis (Nieves, 2003). National nutrition surveys have shown that most Americans are not getting adequate calcium in their diets; in fact, the average diet contains merely 600 mg of calcium daily. While several organizations have established appropriate intakes of calcium and vitamin D, most experts support the recommendations made by the National Institutes of Health (NIH) Consensus Development Panel on Optimal Calcium Intake (NIH, 1994). According to their recommendations, postmenopausal women desiring to reduce the risk of osteoporosis should consume 1,000–1,500 mg of elemental calcium and 400–800 IU of vitamin D daily. The recommended calcium intake for postmenopausal women is 1,000–1,500 mg per day in two or more doses (since it cannot be effectively
Table
Adverse Reactions to Calcium
5.6
Calcium Carbonate: generally well tolerated, 1–10% Central nervous system: headache Endocrine and metabolic: hypercalcemia (anorexia, nausea, vomiting, constipation, headache, drowsiness, lethargy, muscle weakness, coma, polyuria, thirst); metabolic alkalosis; milk-alkali syndrome with very high, chronic dosing and/or renal failure (nausea, vomiting, headache, disorientation); hypophosphatemia Gastrointestinal: constipation, diarrhea, nausea, vomiting, anorexia, rebound hyperacidity, abdominal pain, flatulence, dry mouth Genitourinary: renal stones, renal dysfunction, renal failure
Calcium Citrate: frequency not defined Central nervous system: headache Endocrine and metabolic: hypophosphatemia, hypercalcemia: mild (calcium >10.5 mg/dL) asymptomatic or cause in anorexia, nausea, vomiting, and constipation; more severe (calcium >12 mg/dL) is manifested in confusion, delirium, stupor, and coma Gastrointestinal: nausea, vomiting, anorexia, constipation, abdominal pain, thirst
Note. From Lexi-Comp Online, 2006; MD Consult Online 2006..
Table
Calcium Drug Interactions
5.7
Calcium carbonate and Calcium citrate Calcium channel blockers (eg., verapamil): Effects may be reduced; monitor response. Levothyroxine: Calcium carbonate (and maybe other calcium salts) may decrease T4 absorption; separate dose of calcium from levothyroxine by a minimum of 4 hours. Polystyrene sulfonate: Potassium-binding ability is lessened; do not use concurrently. Tetracycline, atenolol (and possibly other beta-blockers): Iron, quinolone antibiotics, alendronate, sodium fluoride, and zinc absorption is considerably reduced; administer at different times. Thiazide diuretics: Can produce hypercalcemia; monitor response. Could potentiate digoxin toxicity. Milk-alkali syndrome and hypercalcemia can result from high doses of calcium with thiazide diuretics.
Note. From Lexi-Comp Online, 2006; MD Consult Online, 2006.
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absorbed in larger doses) through dietary calcium sources and/or supplements (e.g., calcium carbonate, calcium citrate, other calcium salts) and vitamin D 400–800 IU per day (IOM, 1997; NIH, 1994; Physician’s Guide to Prevention, 2003; WHI, 2006). The total calcium intake should not exceed 2,500 mg per day. Exceeding the recommended daily calcium intake offers no health benefit and may be harmful because of the risk of hypocalcaemia and hypercalciuria. While the threshold for calcium toxicity is high, the National Academy of Sciences does not recommend regularly taking more than 2,500 mg per day (IOM, 1997). Table 5.5 reflects the current calcium recommendations. Table 5.6 lists the adverse reactions to commonly used calcium preparations, and Table 5.7 presents drug interactions with calcium. There are a number of calcium salts readily available on the market (e.g., calcium citrate, calcium carbonate, calcium gluconate, oyster shell, and others) and many more commercial formulations (e.g., Tums, Caltrate, Citracal, Os-Cal 500, etc.) (Levenson & Bockman 1994). Calcium supplements are recommended if the patient is unable to ingest adequate amounts of dietary calcium. The two most common calcium supplements are calcium citrate and calcium carbonate. The highest amount of elemental calcium available among calcium formulations is calcium carbonate, with 40% elemental calcium. Calcium carbonate requires an acidic environment to maximize absorption capacity and should be taken with food (NIH, 1994). Calcium citrate may be taken without regard to food, but contains less elemental calcium (21%) (Heller, Stewart, Haynes, & Pak, 1999). Calcium citrate may be useful for patients taking histamine H2-receptor antagonists or proton-pump inhibitors and those with achlorhydria (Follin & Hansen, 2003). For a discussion of dietary sources of calcium, see chapter 7.
Vitamin D Vitamin D is essential for calcium absorption and bone mineralization. Vitamin D is synthesized in the skin by exposure to sunlight, or it may be taken in the form of a supplement. However, vitamin D is not synthesized by the skin of older individuals as well as by younger individuals; also some areas of the country do not receive sufficient sunlight in the winter, thereby promoting vitamin D deficiency. Some food sources contain vitamin D, such as fortified milk that contains 100 international units (IU) per cup (USDHHS, 2004), and fatty fish and fish oils as in cod, tuna, and shark (Hamdy et al., 2005). Since many individuals do not get enough vitamin D through sunlight or diet, recommendations for supplementation are set at a level designed to be adequate for individuals lacking sun exposure or food sources. Measuring serum 25-hydroxy vitamin D(3) 25-OHD(3) assists in determining adequate levels of vitamin D. Populations such as nursing home residents, hospitalized patients, and adults with hip fractures have been shown to experience a high prevalence of vitamin D insufficiency, presumably due to lack of sunlight exposure (Thomas et al., 1998). Vitamin D levels commonly decline in older adults, and consequently the requirement for vitamin D increases with age. A metaanalysis by Bischoff-Ferrari et al. (2005) found that 700-800 IU/daily vitamin D reduced hip fracture risk in elderly individuals by 25%. These results point out the need for additional calcium supplementation in individuals receiving vitamin D for
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the prevention of hip fractures. In a study designed to extend the findings of BischoffFerrari et al., found that oral vitamin D appears to decrease the risk of hip fractures only when calcium supplementation is added (Boonen, S., et al., 2007.) As with calcium, excessive amounts of vitamin D can be harmful to the skeleton. Vitamin D (400 IU/dose) is found in many calcium supplements and multiple vitamins; vitamin D can be taken in combination with these supplements or as a separate supplement (USDHHS, 2004). Vitamin D is a fat-soluble vitamin that can be stored in the body; therefore, excess vitamin D can be toxic, resulting in hypercalcemia, kidney failure, and calcification of soft tissue (IOM, 1997). As a result, a tolerable upper limit for the dietary intake of vitamin D of 2,000 IU per day has been established by the Institute of Medicine (IOM). Higher doses of vitamin D are required to treat individuals who are vitamin D insufficient (having low levels of vitamin D in the blood) or deficient (having very low levels of vitamin D in the blood). Secondary hyperparathyroidism can result from vitamin D deficiency with normal levels of blood calcium. Osteomalacia or rickets can result from severe cases. The optimal range for 25-OHD(3) is higher than the “normal” ranges established by clinical laboratories, because these ranges come from a population that includes individuals with suboptimal levels. The recommended treatment is vitamin D supplementation of 50,000 IU once a week for up to 3 months with follow-up blood tests of vitamin D, calcium, and PTH levels (Pettifor, 2003). Additional information about recommended requirements and dietary sources of vitamin D is provided in chapter 7.
Mechanism of Action/Kinetics Calcium functions as an antiresorptive agent like the bisphosphonates; however, its mechanism of action is not the same. On the cellular level, calcium is involved in several important processes such as blood clotting, nerve transmission, and muscle contraction. Calcium is also involved in the regulation of the release and storage of neurotransmitters and hormones, in the uptake and binding of amino acids, and in the absorption of vitamin B12 (cyanocobalamin) and gastrin secretion (Hospital Formulary Service [AHFS], 2006). A small amount of the total body calcium is also found in muscles, blood, extracellular fluid, and other tissues, where it plays a part in mediating vascular contraction and vasodilatation, muscular contraction, nerve transmission, and glandular secretion (Hospital Formulary Service [AHFS], 2006). The calcium level in the blood is protected via the PTH–vitamin D axis. Any drop in the blood level of calcium prompts an increase in PTH levels causing short-term bone remodeling, and vitamin D activation can result in an increase in calcium absorption in the gut and calcium resorption in the kidney (Morgan, 2001). Calcium is mobilized from the skeleton to maintain a normal blood calcium level if intake is insufficient. Along with being a substrate for bone mineralization, calcium also exerts an inhibitory effect on bone remodeling through suppression of circulating parathyroid hormone (Physician’s Guide to Prevention, 2003). Consuming adequate levels of calcium and vitamin D throughout life and engaging in appropriate physical activity are essential to bone health (USDHHS, 2004). In addition, calcium neutralizes gastric acidity.
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The absorption of calcium is from the GI tract by active transport and passive diffusion in the duodenum and proximal jejunum, and to a lesser extent in the more distal portions of the small intestine. Oral bioavailability from calcium supplements depends on intestinal pH, the presence or absence of food, and the dose. Calcium supplements are never completely absorbed from the small intestine. The degree of absorption depends on several factors, including (1) stable, ionized form; (2) acidic intestinal pH for ionization of calcium; (3) vitamin D in its activated form; and (4) estrogen (Hospital Formulary Service [AHFS], 2006). Studies indicate that in adults, only about 30% of calcium intake is actually absorbed by the body (IOM, 1997).) Some calcium is excreted from the body into the intestine, resulting in an even lower net absorption (Heaney & Abrams, 2004). The elderly actually absorb less dietary calcium because their intestines are no longer as responsive to the action of 25OHD(3) (Heaney, Recker, Stegman, & Moy, 1989). Increasing overall calcium intake and maintaining adequate levels of vitamin D can overcome poor absorption of calcium (USDHHS, 2004). Vitamin D is essential for calcium absorption, and recent studies have found that absorption effectiveness increases with improving vitamin D status up to serum 25OHD(3) levels of approximately 80 nmol/L (32 ng/mL) (Heaney, Dowell, Hale, & Bendich, 2003). Many studies report that postmenopausal women tend to have average serum 25-OHD(3) values of 50 to 55 nmol/L (20 to 22 ng/mL) and are consequently not absorbing the calcium they consume with the best efficiency. Osteoporotic fractures are reduced when serum 25-OHD(3) is raised to near 80 nmol/L (Heaney, 2005).
Efficacy Vertebral and Nonvertebral Fractures A study was conducted by the WHI (2006) to determine whether calcium/vitamin D supplements reduce the risk of colorectal cancer and the frequency of hip and other bone fractures in postmenopausal women. A sample of 36,282 postmenopausal women aged 50–79 who were enrolled in the WHI clinical trial was randomized into one of two study groups. One group received 1,000 mg of elemental calcium as calcium carbonate and 400 IU of vitamin D daily; the second group took a placebo for an average period of 7 years. Researchers found that calcium and vitamin D supplementation registered a modest but significant improvement on hip bone density but had no significant effect on the rate of hip fractures. The report indicates that calcium and vitamin D decrease the incidence of hip fracture more in older women than in younger women, which would be expected. Although calcium is usually not thought to be harmful, researchers found a 17% increase in nephrolithiasis in the women using the supplements (Jackson et al., 2006). In 1997, the IOM carried out a major review of the bone-related nutrients and developed evidence-based recommendations for calcium and vitamin D intake. Their purpose was to determine the level of nutrient intake for normal, healthy individuals that would prevent the development of a chronic state of deficiency related to that nutrient. Of the nutrients that affect bone health, calcium has been underscored as a major public health concern today, not only because it is an essential nutrient for bone, but also because national surveys show that individuals’ intake of calcium is significantly below the levels recommended for optimal bone health (USDHHS, 2004). Calcium supplements should
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be taken with meals in divided doses, with only 500 mg of elemental calcium taken at a time, since only a small percentage of the oral calcium supplement is absorbed with higher doses. In addition, vitamin D is necessary for the intestinal absorption of calcium. As the majority of women age, serum concentrations of 25-OHD(3) decrease, requiring vitamin D supplementation (Dawson-Hughes, Harris, Krall, & Dallal, 1997; Grass & Dawson-Hughes, 2006).
Administration and Adverse Events Calcium carbonate (Caltrate) contains 600 mg of calcium and 200 IU of vitamin D per tablet, and is administered one tablet twice daily in divided doses with food. Calcium citrate (Citracal) contains calcium 630 mg per two caplets (315 mg each caplet) and vitamin D 400 IU per two caplets (200 IU each caplet), and is administered one to two caplets twice daily in divided doses with or without food. Calcium is usually well tolerated. Table 5.6 lists the adverse reactions to the two most common calcium formulations, and Table 5.7 presents common drug interactions.
Integrative Therapies In light of the research findings in 2002 from the Writing Group for the Women’s Health Initiative Investigators, alternatives to HT for preventing and treating osteoporosis have received increased attention. Discussed earlier are bioidentical hormones, which are different from phytoestrogens. It is important to mention that although phytoestrogens have actions similar to those of estrogen, they are not true estrogens as produced by the human body. Bioidentical hormones are also derived from plants, but they have the same chemical structure as the body’s natural hormones after conversion to the human form by chemical synthesis carried out in the laboratory, and they require a prescription by a licensed provider. Recently, phytoestrogens (promoted as “natural” estrogen-like products) have been gaining popularity, due to the health benefits they claim to offer, and because of their wide range of availability in both foods and supplements. Phytoestrogens are naturally occurring plant compounds that have properties similar to those of estradiol (National Institutes of Health [NIH], 2005). Phytoestrogens are made up of more than 20 compounds and can be found in more than 300 plants such as fruits, herbs, and grains. However, phytoestrogens are not stored in the body, can be easily broken down
Table
Dietary Sources of Phytoestrogens
5.8
Isoflavones (genistein, daidzein, glycitein, and equol) Lignans (enterolactone and enterodiol)
Coumestans (coumestrol)
Primarily found in soy beans and soy products, chickpeas, and other legumes Found in oilseeds (primarily flaxseed), cereal bran, legumes, and alcohol (beer and bourbon) Found in alfalfa and clover
Note. From National Institutes of Health Osteoporosis and Related Bone Diseases National Resource Center, 2005.
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and eliminated, and have weaker effects than most estrogens. Isoflavones, lignans, and coumestans make up the three main classes of dietary phytoestrogens. Dietary sources of phytoestrogens are listed in Table 5.8. The majority of food sources containing these compounds usually include more than one class of phytoestrogens (NIH, 2005b). Observational studies have discovered a lower prevalence of hip fracture, breast cancer, and heart disease rates among people living in places like Southeast Asia, where diets traditionally are high in phytoestrogens. Much interest has been generated in the United States regarding the health benefits of phytoestrogens as a result of these studies. A great deal of the evidence related to the potential role of phytoestrogens in bone health is based on animal studies. Actually, soybean protein, soy isoflavones, genistein, daidzein, and coumestrol have all been shown to have a protective effect on bone in animals whose ovaries had been surgically removed. However, the evidence is conflicting in humans. Studies demonstrate that persons who live in Hong Kong, China, and Japan, where dietary phytoestrogen intakes are high, experience lower rates of hip fracture when compared to White populations. A number of studies have examined the effects of soy isoflavones on bone health; however, the results have been mixed, ranging from a modest effect to no effect. It is difficult to fully evaluate the impact of these compounds on bone health, since most of these studies have serious limitations, including short duration and small sample size (NIH, 2005b). In postmenopausal women, ipriflavone, a synthetic isoflavone, has shown some promise in its ability to preserve bone. However, a 3-year study of over 400 postmenopausal women found that ipriflavone did not prevent bone loss. According to some studies, phytoestrogens, unlike estrogen, do not appear to increase the risk of breast or uterine cancer. This finding suggests that they may function more like SERMs such as raloxifene and tamoxifen than as actual estrogens. Conversely, other studies show that high isoflavone levels have been linked to an increased risk of breast cancer. Currently, the NIH is supporting research looking at the safety of phytoestrogens and their potential role in the skeletal health of postmenopausal women (NIH, 2005b). A 1-year, placebo-controlled, randomized trial examined the effect of isoflavoneenriched soy extracts on bone loss in 203 Chinese postmenopausal women within the first 10 years postmenopause. Researchers found a mild, but statistically significant, effect of daily supplementation of soy-derived isoflavones in attenuating bone mineral content (BMC) loss at the trochanter, intertrochanter, and total hip (Chen, Ho, Lam, Ho, & Woo, 2003). Since currently available evidence concerning phytoestrogens is contradictory and incomplete, additional studies are needed to further evaluate the safety and effects of phytoestrogens (NIH, 2005b).
Pain Management Pain has been reported in up to 62% of female patients with osteoporosis (Roberto, 2004). There are various pain origins for osteoporosis, including concurrent degenerative disk disease, osteoarthritis, and vertebral fracture. Before introducing measures for pain management, patients’ pain should be evaluated for a drug-induced cause as opposed to a physiologic cause. Bisphosphonates are the agent of choice for most individuals with osteoporosis, though as many as 26% of patients taking these agents experience some sort of back or bone pain (Merck & Co., 2006; Procter & Gamble Pharmaceuticals, 2006;
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Table
5.9
Osteoporosis
Pain Management of Osteoporosis Agent Nonaspirin analgesic Acetaminophen
Daily dosing regimen
Maximum daily dose
500 mg every 4 hours as needed 1,000 mg every 6 hours as needed
4 grams daily
Nonsteroidal antiinflammatory drugs (NSAIDs) Ibuprofen 400 mg every 4 hours as needed Naproxen 500 mg every 12 hours Indomethacin 25 to 50 mg three times daily 75 mg (extended release) once to twice daily Opioid combinations Hydrocodone/APAP One 5/500 mg tablet every 4 hours as needed NOTE: There are varying dose combinations of hydrocodone/ APAP, and each should be evaluated for a maximum dose based on the daily maximum acetaminophen use. Hydrocodone/ibuprofen One 5/200 mg tablet every 4 hours as needed Oxycodone/APAP One 5/325 mg tablet every 4 hours as needed NOTE: There are varying dose combinations of oxycodone/ APAP, and each should be evaluated for a maximum dose based on the daily maximum acetaminophen use. Opiate analgesics Morphine Starting 15 mg every 12 hours scheduled Oxycodone Starting 10 mg every 12 hours scheduled Fentanyl Starting 25 mcg/hr every 72 hours in opiate-naïve patients
3,200 mg daily 1,500 mg daily 200 mg daily
Eight 5/500 tablets daily
Five 7.5/200 tablets daily 12 tablets daily
Patient tolerance Patient tolerance Patient tolerance
Note. Adapted from Thomson Micromedex, 2006.
Roche Laboratories Inc., 2006). If the bisphosphonate is the suspected cause of the pain, discontinuing it and evaluating for resolution of pain should be considered. If a patient’s pain does not subside, then analgesic and anti-inflammatory therapy may be warranted. Outside of oral and nonpharmacologic measures, surgical vertebroplasty or kyphoplasty procedures may also be considered, as outlined in this chapter (also see chapter 6).
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Table
International Names for Fosamax®
5.10
Brand name
Aldrox Alenato Alend Alnax Alovell Arendal Armol Bifemelan Bifosa Bonapex Defixal Endronax Eucalen Fixopan Fosalan Fosamax®
Fosmin Fosval Marvil MaxiBone MaxiBone 70 Neobon Osdron Osdronat Oseotenk Osficar Oslene Osteofar Osteofos Osteopor Osteosan Osteovan Osticalcin Porosal Tibolene Voroste
Country where approved for use
Chile Argentina Korea Paraguay Indonesia Peru Colombia Colombia India Egypt Costa Rica, Dominican Republic, El Salvador, Guatemala, Nicaragua, Panama Brazil Colombia Ecuador Israel United States, Argentina, Austria, Belgium, Brazil, Bulgaria, Canada, Chile, Costa Rica, Czech Republic, Denmark, Ecuador, Egypt, El Salvador, England, France, Germany, Guatemala, Honduras, Hong Kong, Hungary, Indonesia, Ireland, Italy, Korea, Malaysia, Mexico, Netherlands, Nicaragua, Norway, Panama, Peru, Philippines, Poland, Singapore, South Africa, Spain, Sweden, Switzerland, Taiwan, Thailand Peru Paraguay Peru, Paraguey Israel Israel Colombia Brazil Colombia Argentina Colombia Indonesia Indonesia Hong Kong Uruguay Chile Costa Rica Colombia Venezuela Colombia Indonesia Indonesia
Note. From Mosby’s Drug Consult, 16th ed., 2006 (St. Louis, MO: Mosby).
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Analgesics and Nonsteroidal Anti-inflammatory Drugs (NSAIDs) Analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs) have an important role in the treatment of pain associated with osteoporosis. However, these agents should be used cautiously in the postmenopausal (older) osteoporotic population. Patients using analgesics and NSAIDs regularly, or in higher than needed doses, may be more likely to develop gastrointestinal ulcers, renal insufficiency, or hepatotoxicity, or worsen cardiovascular status secondary to overuse. Table 5.9 lists available NSAIDs and analgesics for managing pain in patients with osteoporosis. Combination opioids (opiate plus NSAID or acetaminophen) may be considered in patients who do not respond to simple analgesics. These agents are beneficial in pain management but provide a potential for overuse of analgesic medication. In cases where patients require large doses of combination opioids to control osteoporotic pain, a switch to opioid alone should be considered. Patients will still receive the analgesic effect, but without the increased risk for gastrointestinal bleeding and other adverse side effects. Caution should be used, though, as some research suggests that patients using opioid analgesics may be at a higher risk for vertebral fractures, potentially secondary to falls related to opioids use (Vestergaard, Rejnmark, & Mosekilde, 2006). Patients should be continually assessed for fall risks as well, and for increased need for pain control and titration of maintenance medication.
Vertebroplasty and Kyphoplasty Vertebroplasty Recommendations from the National Osteoporosis Foundation (NOF) state that vertebroplasty should be reserved for those patients unable to achieve adequate pain control, after vertebral fracture, on traditional pharmacologic and nonpharmacologic therapies (Bonner et al., 2003). Emerging data regarding the use of vertebroplasty shows an initial benefit, especially in patients with pain due to a vertebral fracture, but long-term outcome data are still awaited (Muto, 2005).
Kyphoplasty The recommendations for vertebroplasty are generally applicable to kyphoplasty. Currently, there are no head-to-head trials for kyphoplasty in pain management versus vertebroplasty or medicinal therapies. Researchers state that this interventional therapy could lend to decreased hospital stays after a vertebral fracture as well, and more immediate pain relief in the patient (Masala, Fiori, Massari, & Simonetti, 2005). Further discussion of vertebroplasty and kyphoplasty is provided in chapter 6.
Conclusion The research supports proper nutrition and lifestyle as having a positive effect on bone health and shows that pharmacotherapy along with these can slow the rate of bone loss
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and also build new bone (USDHHS, 2004). The most thoroughly researched pharmaceutical treatments currently available for the prevention and treatment of osteoporosis are the bisphosphonates: alendronate, (Fosamax®), risedronate (Actonel®), and ibandronate (Boniva®). In planning intervention strategies, one needs to consider the unique features of each person, taking into account dosing and fracture risk. Table 5.10 lists the international brand names for Fosamax® where the drug is approved for use in various countries.
REFERENCES Ahlgrimm, M., & Kells, J. M. (2003). The HRT solution: Optimizing your hormonal potential. New York: Avery. Anderson, G. L., Limacher, M., Assaf, A. R., Bassford, T., Beresford, S. A., Black, H., et al. (2004). Women’s Health Initiative Steering Committee. Effects of conjugated equine estrogen in postmenopausal women with hysterectomy: The Women’s Health Initiative randomized controlled trial. Journal of the American Medical Association, 291(14), 1701–7012. Bischoff-Ferrari, H. A., Willett, W. C., Wong, J. B., Giovannucci, E., Dietrich, T., Dawson-Hughes, B. (2005). Fracture prevention with vitamin D supplementation: a meta-analysis of randomized controlled trials. Journal of the American Medical Association, 293, 2257–2264. Black, D. M., Bilezikian, J. P., Ensrud, K. E., Greenspan, S. L., Palermo, L., Hue, T., et al. (2005). One year of alendronate after one year of parathyroid hormone (1–84) for osteoporosis. New England Journal of Medicine, 353, 555–565. Black, D. M., Cummings, S. R., Karpf, D. B., Cauley, J. A., Thompson, D. E., Nevitt, M. C., et al. (1996). Randomised trial of effect of alendronate on risk of fracture in women with existing vertebral fractures. Fracture Intervention Trial Research Group. Lancet, 348, 1535–1541. Black, D. M., Delmas, P. D., Eastell R., Reid, I. R., Boonen, S., Cauley, J. A., et al. (2007). Once Yearly Zoledronic Acid for the Treatment of Postmenopausal Osteoporosis. HORIZON Pivotal Fracture Trial. New England Journal of Medicine, 356, 1809–1822. Bone, H. G., Greenspan, S. L., McKeever, C., Bell, N., Davidson, M., Downs, R. W., et al. (2000). Alendronate and estrogen effects in postmenopausal women with low bone mineral density. Alendronate/Estrogen Study Group. Journal of Clinical Endocrinology and Metabolism, 85(2), 720–726. Black, D. M., Schwartz, A.V., Esrund, K. E., Cauley, J. A. Levis, S., Quandt, S. A., et al. (2006). Effects of Continuing or Stopping Alendronate After 5 Years. The Fracture Intervention Trial Long Term Extension. Journal of the American Medical Associate, 296, 2927 – 2938. Bone, H. G., Hosking, D., Devogelaer, J. P., Tucci, J. R., Emkey, R. D., Tonino, R. P., et al. (2004). Ten years’ experience with alendronate for osteoporosis in postmenopausal women. New England Journal of Medicine, 350, 1189–1199. Bonner, F. J., Jr., Sinaki, M., Grabois, M., Shipp, K. M., Lane, J. M., Lindsay, R., et al. (2003). Health professional’s guide to rehabilitation of the patient with osteoporosis. Osteoporosis International, 14(Suppl 2), S1–22. Boonen, S., Lips, P., Bouillon, R., Bischoff-Ferrari, H. A., Vanderschueren, D. and Haentjens. P. (2007). Need for Additional Calcium to Reduce the Risk of Hip Fracture with Vitamin D Supplementation: Evidence from a Comparative Metaanalysis of Randomized Controlled Trials. Journal of Clinical Endocrinology and Metabolism 92, 1415–1423. Brown, J. P., Kendler, D. L., McClung, M. R., Emkey, R. D., Adachi, J. D., Bolognese, M. A., et al. (2002). The efficacy and tolerability of risedronate once a week for the treatment of postmenopausal osteoporosis. Calcified Tissue International, 71, 103–111. Cauley, J. A., Robbins, J., Chen, Z., Cummings, S. R., Jackson, R. D., LaCroix, A. Z., et al. (2003), Women’s Health Initiative Investigators. Effects of estrogen plus progestin on risk of fracture and bone mineral density: The Women’s Health Initiative randomized trial. Journal of the American Medical Association, 290(13), 1729–1738. Cauley, J. A., Seeley, D. G., Ensrud, K., Ettinger, B., Black, D., & Cummings, S. R. (1995). Estrogen replacement therapy and fractures in older women. Study of osteoporotic fractures research group. Annals of Internal Medicine, 122(1), 9–16.
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Osteoporosis Chen, Y. M., Ho, S. C., Lam, S. S., Ho, S. S., & Woo, J. L. (2003). Soy isoflavones have a favorable effect on bone loss in Chinese postmenopausal women with lower bone mass: A double-blind, randomized, controlled trial. Journal of Clinical Endocrinology and Metabolism, 88(10), 4740–4747. Chesnut, C. H., III, Silverman, S., Andriano, K., Genant, H., Gimona, A., Harris, S., et al. (2000). A randomized trial of nasal spray salmon calcitonin in postmenopausal women with established osteoporosis: The prevent recurrence of osteoporotic fractures study. PROOF Study Group. American Journal of Medicine, 109, 267–276. Chesnut, C. H., III, Skag, A., Christiansen, C., Recker, R., Stakkestad, J. A., Hoiseth, A., et al. (2004). Effects of oral ibandronate administered daily or intermittently on fracture risk in postmenopausal osteoporosis. Journal of Bone and Mineral Research, 19, 1241–1249. Colón-Emeric, C. S. (2006). 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Effect of calcium and vitamin D supplementation on bone density in men and women 65 years of age or older. New England Journal of Medicine, 337, 670–676. Deal, C. L. (2002). Risedronate prevents hip fractures, but who should get therapy? Cleveland Clinic Journal of Medicine, 69, 964, 968–6. Deal, C., Omizo, M., Schwartz, E. N., Eriksen, E. F., Cantor, P., Wang, J., et al. (2005). Combination teriparatide and raloxifene therapy for postmenopausal osteoporosis: Results from a 6-month double-blind placebo-controlled trial. Journal of Bone and Mineral Research, 20, 1905–1911. Delmas, P. D., Ensrud, K. E., Adachi, J. D., Harper, K. D., Sarkar, S., Gennari, C., et al. (2002). Multiple outcomes of raloxifene evaluation investigators. Efficacy of raloxifene on vertebral fracture risk reduction in postmenopausal women with osteoporosis: Four-year results from a randomized clinical trial. Journal of Clinical Endocrinology and Metabolism, 87(8), 3609–3617. Downs, R. W., Jr., Bell, N. H., Ettinger, M. P., Walsh, B. W., Favus, M. J., Mako, B., et al. (2000). Comparison of alendronate and intranasal calcitonin for treatment of osteoporosis in postmenopausal women. Journal of Clinical Endocrinology and Metabolism, 85, 1783–1788. Dursun, N., Dursun, E., & Yalcin, S. (2001). Comparison of alendronate, calcitonin and calcium treatments in postmenopausal osteoporosis. International Journal of Clinical Practice, 55, 505–509. Eli Lilly & Company. (2004). Forteo package insert. Pamphlet. Ettinger, B., Black, D. M., Mitlak, B. H., Knickerbocker, R. K., Nickelsen, T., Genant, H., et al. (1999). Reduction of vertebral fracture risk in postmenopausal women with osteoporosis treated with raloxifene: Results from a 3-year randomized clinical trial. Multiple outcomes of raloxifene evaluation (MORE) investigators. Journal of the American Medical Association, 282(7), 637–645. Ettinger, B., Pressman, A., & Silver, P. (1999). Effect of age on reasons for initiation and discontinuation of hormone therapy. Menopause, 6, 282–289. Ettinger, B., San, M. J., Crans, G., & Pavo, I. (2004). Differential effects of teriparatide on BMD after treatment with raloxifene or alendronate. Journal of Bone and Mineral Research, 19, 745–751. Eviö, S., Tiitinen, A., Laitinen, K. Ylikorkala, O., & Välimäki, M. J. (2004). Effects of alendronate and hormone replacement therapy, alone and in combination, on bone mass and markers of bone turnover in elderly women with osteoporosis. Journal of Clinical Endocrinology and Metabolism, 9(2), 626–631. Retrieved June 6, 2006, from http://home.mdconsult.com/das/journal/ view/60741976_2/N/14417862?sid=501437962&source=MI&SEQNO=1 Felsenberg, D., Miller, P., Armbrecht, G., Wilson, K., Schimmer, R. C., & Papapoulos, S. E. (2005). Oral ibandronate significantly reduces the risk of vertebral fractures of greater severity after 1, 2, and 3 years in postmenopausal women with osteoporosis. Bone, 37, 651–654. Finkelstein, J. S., Hayes, A., Hunzelman, J. L., Wyland, J. J., Lee, H., & Neer, R. M. (2003). The effects of parathyroid hormone, alendronate, or both in men with osteoporosis. New England Journal of Medicine, 349, 1216–1226.
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Follin, S. L., & Hansen, L. B. (2003). Current approaches to the prevention and treatment of postmenopausal osteoporosis. American Journal of Health-System Pharmacy, 60(9), 883, 901. Retrieved June 6, 2006, from http://www.medscape.com/viewarticle/453035 Friedman, P. A. (2006). Agents affecting mineral ion homeostasis and bone turnover. In L. L. Brunton, J. S. Lazo, & K. L. Parker (Eds.), The pharmacological basis of therapeutics (11th ed., pp. 1647– 1678). New York: McGraw-Hill Medical Publishing Division. Gallagher, J. C., Genant, H. K., Crans, G. G., Vargas, S. J., & Krege, J. H. (2005). Teriparatide reduces the fracture risk associated with increasing number and severity of osteoporotic fractures. Journal of Clinical Endocrinology and Metabolism, 90, 1583–1587. Grass, M., & Dawson-Hughes, B. (2006). Preventing osteoporosis-related fractures: An overview. American Journal of Medicine 119, S3–S11. Retrieved June 6, 2006, from http://home.mdconsult. com/das/journal/view/59590408–2/N/16114469?sid=491704938&source=MI&SEQNO=2 Greenspan, S. L., Resnick, N. M., & Parker, R. A. (2003). Combination therapy with hormone replacement and alendronate for prevention of bone loss in elderly women: A randomized controlled trial. Journal of the American Medical Association, 289(19), 2525–2533. Gulli, L. (2002). Hormone replacement therapy. In Jacqueline L. Longe (Ed.), Gale Encyclopedia of Medicine (Vol. 3, 2nd ed., pp. 1668–1673). Detroit: Gale. Retrieved June 6, 2006, from Gale Virtual Reference Library via Thomson Gale:
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Osteoporosis Jackson, R. D., LaCroix, A. Z., Gass, M., Wallace, R. B., Robbins, J., Lewis, C. E., et al. (2006). Calcium plus vitamin D supplementation and the risk of fractures. New England Journal of Medicine, 354(7), 669–683. Johnell, O., Scheek, W. H., Lu,Y., Reginster, J. Y., Need, A. G., & Seeman, E. (2002). Additive effects of raloxifene and alendronate on bone density and biochemical markers of bone remodeling in postmenopausal women with osteoporosis. Journal of Clinical Endocrinology and Metabolism, 87(3), 985–992. Kaufman, J. M., Orwoll, E., Goemaere, S., San, M. J., Hossain, A., Dalsky, G. P., et al. (2005). Teriparatide effects on vertebral fractures and bone mineral density in men with osteoporosis: treatment and discontinuation of therapy. Osteoporosis International, 16, 510–516. Kiel, D. P., Felson, D. T., Anderson, J. J., Wilson, P. W, & Moskowitz, M. A. (1987). Hip fracture and the use of estrogens in postmenopausal women. The Framingham study. New England Journal of Medicine, 317(19), 1169–1174. Levenson, D. I., & Bockman, R. S. (1994). A review of calcium preparations. Nutrition Review, 52, 221–232. Lexi-Comp Online. (2006). Retrieved June 6, 2006 from http://online.lexi.com/crlsql/servlet/crlonline Liberman, U. A., Weiss, S. R., Broll, J., Minne, H. W., Quan, H., Bell, N. H., et al. (1995). Effect of oral alendronate on bone mineral density and the incidence of fractures in postmenopausal osteoporosis. New England Journal of Medicine, 333, 1437–1444. Licata, A. A. (2005). Discovery, clinical development, and therapeutic uses of bisphosphonates. Annals of Pharmacotherapy, 39, 668–677. Liebman, M. (2002). Awakening the silent osteoporosis market. Medical market and media (pp. 1–6). Retrieved May 1, 2006, from http://www.micromri.com/OnlineDocs/osteoporosismkt.pdf Lindsay, R., Gallagher, J. C., Kleerekoper, M., & Pickar, J. H. (2002). Effect of lower doses of conjugated equine estrogens with and without medroxyprogesterone acetate on bone in early postmenopausal women. Journal of the American Medical Association, 287(20), 2668–2676. Lyritis, G. P., Paspati, I., Karachalios, T., Ioakimidis, D., Skarantavos, G., & Lyritis, P. G. (1997). Pain relief from nasal salmon calcitonin in osteoporotic vertebral crush fractures. A double blind, placebo-controlled clinical study. Acta orthopaedica Scandinavica, 275(Suppl.), 112–114. Maricic, M., Adachi, J. D., Sarkar, S., Wu, W., Wong, M., & Harper, K. D. (2002). Early effects of raloxifene on clinical vertebral fractures at 12 months in postmenopausal women with osteoporosis. Archives of Internal Medicine 162(10), 1140–1143. Masala, S., Fiori, R., Massari, F., & Simonetti, G. (2005). Kyphoplasty: Indications, contraindications and technique. Radiologia Medica (Turin), 110, 97–105. McClung, M. R., Geusens, P., Miller, P. D., Zippel, H., Bensen, W. G., Roux, C., et al. (2001). Effect of risedronate on the risk of hip fracture in elderly women. Hip Intervention Program Study Group. New England Journal of Medicine, 344, 333–340. McClung, M. R., San, M. J., Miller, P. D., Civitelli, R., Bandeira, F., Omizo, M., et al. (2005). Opposite bone remodeling effects of teriparatide and alendronate in increasing bone mass. Archives of Internal Medicine, 165, 1762–1768. McEvoy, G., Snow, E., Kester, L., Litvac, K., Miller, J., Welsh, O., et al. (Eds.). (2006). American Hospital Formulary Service (AHFS): Drug information 2006 (p. 3047). Bethesda, MD: American Society of Health-System Pharmacists. MDConsult® online service provided by Elsevier Inc. Retrieved May 1, 2006 from http://www. mdconsult.com/das/pharm/lookup/76560179-2?type=alldrugs Merck & Co. (2006). Fosamax package insert. Pamphlet. Miller, P. D., McClung, M. R., Macovei, L., Stakkestad, J. A., Luckey, M., Bonvoisin, B., et al. (2005). Monthly oral ibandronate therapy in postmenopausal osteoporosis: 1-year results from the MOBILE study. Journal of Bone and Mineral Research, 20, 1315–1322. Morgan, S. L. (2001). Calcium and vitamin D in osteoporosis. Rheumatic Disease Clinics of North America, 27(1), 101–103. Retrieved January 2, 2006, from http://home.mdconsult.com/das/ journal/view/59709867–2/N/11547756?sid = 492855525&source = MI&SEQNO = 7 Mosby’s drug consult (16th ed.). (2006). St. Louis, MO: Mosby. Muto, M., Muto, E., Izzo, R., Diano, A. A., Lavanga, A., & Di, F. U. (2005). Vertebroplasty in the treatment of back pain. Radiologia Medica (Turin), 109, 208–219. National Cancer Institute. (2006). The study of tamoxifen and raloxifene. Retrieved May 28, 2006, from http://www.cancer.gov.star National Institutes of Health Consensus Development Panel on Optimal Calcium Intake. (1994). Optimal calcium intake. Journal of the American Medical Association, 272, 1942–1948.
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National Institutes of Health Osteoporosis and Related Bone Diseases National Resource Center. (2005a). Retrieved June 6, 2006, from http://www.niams.nih.gov/bone/ National Institutes of Health Osteoporosis and Related Bone Diseases National Resource Center (2005b). Phytoestrogens and bone health. Retrieved January 2, 2006, from http://www.niams.nih. gov/bone/hi/bone_phyto.pdf National Osteoporosis Foundation (2003). Physician’s guide to prevention and treatment of osteoporosis. [Electronic Version]. Retrieved January 2, 2006, from http://www.nof.org/physguide/index.html Neer, R. M., Arnaud, C. D., Zanchetta, J. R., Prince, R., Gaich, G. A., Reginster, J. Y. et al. (2001). Effect of parathyroid hormone (1–34) on fractures and bone mineral density in postmenopausal women with osteoporosis. New England Journal of Medicine, 344, 1434–1441. Nieves, J. W. (2003). Calcium, vitamin D, and nutrition in elderly adults. Clinical Geriatric Medicine, 19, 321–325. Novartis Pharmaceutical Corp. (2003). Miacalcin package insert. Pamphlet. Novartis Pharmaceutical Corp. (2007). Zorneta and Reclast package insert. Pamphlet. Nurse Practitioners’ Prescribing Reference®. (2007, Spring). Prescribing Reference, 287. O’Connell, M. B., & Seaton, T. L. (2005). Osteoporosis and osteomalacia. In J. T. DiPiro, R. L. Talbert, G. C. Yee, G. R. Matzke, B. G. Wells, & L. M. Posey (Eds.), Phamacotherapy: A pathophysiologic approach (6th ed., pp. 1645–1669). New York: McGraw-Hill Medical Publishing Division. Orwoll, E. S., Scheele, W. H., Paul, S., Adami, S., Syversen, U., ez-Perez, A., et al. (2003). The effect of teriparatide [human parathyroid hormone (1–34)] therapy on bone density in men with osteoporosis. Journal of Bone and Mineral Research, 18, 9–17. Papapoulos, S. E., Quandt, S. A., Liberman, U. A., Hochberg, M. C., & Thompson, D. E. (2005). Meta-analysis of the efficacy of alendronate for the prevention of hip fractures in postmenopausal women. Osteoporosis International, 16, 468–474. Pettifor, J. M. (2003). Nutritional and drug-induced rickets and osteomalacia. In M. J. Favus (Ed), Primer on the metabolic bone diseases and disorders of mineral metabolism (5th ed., pp. 399–407). Washington, DC: American Society for Bone and Mineral Research. Pols, H. A., Felsenberg, D., Hanley, D. A., Stepan, J., Munoz-Torres, M., Wilkin, T. J., et al. (1999). Multinational, placebo-controlled, randomized trial of the effects of alendronate on bone density and fracture risk in postmenopausal women with low bone mass: Results of the FOSIT study. Fosamax International Trial Study Group. Osteoporosis International, 9, 461–468. Pontiroli, A. E., Pajetta, E., Scaglia, L., Rubinacci, A., Resmini, G., Arrigoni, M., et al. (1994). Analgesic effect of intranasal and intramuscular salmon calcitonin in post-menopausal osteoporosis: A double-blind, double-placebo study. Aging (Milan), 6, 459–463. Powles, T. J., Hickish, T., Kanis, J. A., Tidy, A., & Ashley S (1996). The effect of tamoxifen on lumbar bone mineral density in pre- and postmenopausal women. Journal of Clinical Oncology, 14, 78–84 Prestwood, K. M., Kenny, A. M., Kleppinger, A, & Kulldorff. M., (2003).Ultralow-dose micronized 17-estradiol and bone density and bone metabolism in older women: A randomized controlled trial. Journal of the American Medical Association, 290, 1042–1048. Prince, R., Sipos, A., Hossain, A., Syversen, U., Ish-Shalom, S., Marcinowska, E., et al. (2005). Sustained nonvertebral fragility fracture risk reduction after discontinuation of teriparatide treatment. Journal of Bone and Mineral Research, 20, 1507–1513. Procter & Gamble Pharmaceuticals. (2006). Actonel package insert. Pamphlet. Raloxifene Hydrochloride. (2006). Mosby’s Drug Consult. Retrieved August 3, 2006, from http:// home.mdconsult.com/das/drug/view/62368678–4/1/3370/top?sid=516660094&summaryres ults=true&SEQNO=1 Reginster, J., Minne, H. W., Sorensen, O. H., Hooper, M., Roux, C., Brandi, M. L., et al. (2000). Randomized trial of the effects of risedronate on vertebral fractures in women with established postmenopausal osteoporosis. Vertebral Efficacy with Risedronate Therapy (VERT) Study Group. Osteoporosis International, 11, 83–91. Roberto, K. A. (2004). Care practices and quality of life of rural older women with osteoporosis. Journal of American Medical Women’s Association, 59, 295–301. Roche Laboratories Inc. (2006). Boniva package insert. Pamphlet. Rosen, C. J. (2005). Clinical practice. Postmenopausal osteoporosis. New England Journal of Medicine, 353, 595–603. Rossouw, J. E., Anderson, G. L, Prentice, R. L., LaCroix, A. Z., Kooperberg, C., Stefanick, M. L., et al. (2002). Risks and benefits of estrogen plus progestin in healthy postmenopausal women: Principal results from the Women’s Health Initiative randomized controlled trial. American Journal of Medicine, 288(3), 321–233.
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Osteoporosis Schnitzer, T., Bone, H. G., Crepaldi, G., Adami, S., McClung, M., Kiel, D., et al. (2000). Therapeutic equivalence of alendronate 70 mg once-weekly and alendronate 10 mg daily in the treatment of osteoporosis. Alendronate Once-Weekly Study Group. Aging (Milan), 12, 1–12. Smith, P. W. (2003). HRT: The answers. A concise guide for solving the hormone replacement therapy puzzle. Long Island City, NY: Hatherleigh Press. Stefanick, M. L. (2005). Estrogens and progestins: Background and history, trends in use, and guidelines and regimens approved by the US Food and Drug Administration. Journal of American Medicine, 118(12, Suppl. 2), 64–73. Ste-Marie, L. G., Schwartz, S. L., Hossain, A., Desaiah, D., & Gaich, G. A. (2006). Effect of teriparatide [rhPTH(1–34)] on BMD when given to postmenopausal women receiving hormone replacement therapy. Journal of Bone and Mineral Research, 21, 283–291. Thomas, M. K., Lloyd-Jones, D. M., Thadhani R., Shaw, A., C., Deraska, D. J., Kitch, B. T., et al. (1998). Hypovitaminosis D in medical inpatients. New England Journal of Medicine, 338(12), 777–783. Thomson Micromedex. (2006). DRUGDEX® System. Thomson Micromedex Retrieved August 28, 2006, from http://slhwebappsvr.org:81/hcs/librarian/PFPUI/Ms4kXLJ1X.Hurh Tiras, M. B., Noyan, V., Yildiz, A., & Biberoglu, K. (2000). Comparison of different treatment modalities for postmenopausal patients with osteopenia: hormone replacement therapy, calcitonin and clodronate. Climacteric, 3, 92–101. Torgerson, D. J., & Bell-Syer, S. E. (2001a). Hormone replacement therapy and prevention of nonvertebral fractures: A meta-analysis of randomized trials. Journal of the American Medical Association, 285(22), 2891–2897. Torgerson, D. J., & Bell-Syer, S. E. (2001b). Hormone replacement therapy and prevention of vertebral fractures: A meta-analysis of randomized trials. BMC Musculoskeletal Disorders, 2(1), 7–10. Toth, E., Csupor, E., Meszaros, S., Ferencz, V., Nemeth, L., McCloskey, E. V., et al. (2005). The effect of intranasal salmon calcitonin therapy on bone mineral density in idiopathic male osteoporosis without vertebral fractures—An open label study. Bone, 36, 47–51. Trovas, G. P., Lyritis, G. P., Galanos, A., Raptou, P., & Constantelou, E. (2002). A randomized trial of nasal spray salmon calcitonin in men with idiopathic osteoporosis: Effects on bone mineral density and bone markers. Journal of Bone and Mineral Research, 17, 521–527. Umland, E. M. (2006). Guidelines for pharmacists: Interpreting the medical evidence for bisphosphonates in postmenopausal osteoporosis. U.S. Pharmacist. Retrieved July 9, 2007, from http://www. uspharmacist.com/index.asp?page=ce/105219/default.htm U.S. Department of Health and Human Services. (2004). Bone health and osteoporosis: A report of the surgeon general. Public Health Service, Office of the Surgeon General, Rockville, MD. Retrieved June 6, 2006 from http://www.surgeongeneral.gov/library/bonehealth/ U.S. Food and Drug and Administration. (2004). Menopause and hormones. Retrieved June 6, 2006, from http://www.fda.gov/womens/menopause/mht-FS.html Vestergaard, P., Rejnmark, L., & Mosekilde, L. (2006). Fracture risk associated with the use of morphine and opiates. Journal of Internal Medicine, 260, 76–87. Wells, G., Tugwell, P., Shea, B., Guyatt, G., Peterson, J., Zytaruk, N., et al. (2002). Meta-analyses of therapies for postmenopausal osteoporosis. V. Meta-analysis of the efficacy of hormone replacement therapy in treating and preventing osteoporosis in postmenopausal women. Endocrine Reviews, 23(4), 529–539. Women’s Health Initiative. (2006). Calcium/vitamin D supplementation study. Retrieved June 25, 2006, from http://www.nhlbi.nih.gov/whi/recommend.htm Wright, J. V., & Morgenthaler, J. (1997). Natural hormone replacement. Petaluma, CA: Smart Publications. Writing Group for the Postmenopausal Estrogen/Progestin Interventions (1996). Effects of hormone therapy on bone mineral density: Results from the postmenopausal estrogen/progestin interventions (PEPI) trial. Journal of the American Medical Association, 276(17), 1389–1396. Writing Group for the Women’s Health Initiative Investigators. (2002). Risks and benefits of estrogen plus progestin in healthy postmenopausal women: Principal results from the Women’s Health Initiative Randomized Controlled Trial. Journal of the American Medical Association, 288(3), 321–333.
Surgical Management of Fractures
It is fractures that define the devastating consequences of osteoporosis. (S. Gueldner)
Complications of Osteoporosis
T
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Eric Seybold Heather Hazlett David R. Cooper
he most significant complication of osteoporosis is a fracture, and while fractures may occur at many sites, they most commonly occur in the hip, spine, and wrist. Associated clinical complications include pain, disability, deformity, postural changes associated with vertebral compression fractures, and deconditioning secondary to physical inactivity (U.S. Department of Health & Human Services [USDHHS], 2004; World Health Organization [WHO], 2003). Most often fractures associated with osteoporosis are often referred to as “fragility fractures,” because they result from low-level trauma that would not cause normal bone to fracture. In the United States alone, osteoporosis is responsible for over 1.5 million fractures annually, including 300,000 hip fractures and 250,000 wrist fractures. Vertebral fractures account for the majority of osteoporotic fractures at 700,000, while fractures at other sites total more than 300,000 (WrongDiagnosis.com, 2006). Simple activities such as bending over to pick up a piece of paper or sneezing can cause a fracture in a patient with osteoporosis. Fractures associated with osteoporosis have a high predilection in females and are compounded by the patient’s age. While vertebral fracture is the most common type of osteoporotic fracture, hip fractures have a particularly high morbidity and mortality rate. They are more common in females than the combined risk of breast, uterine, and cervical cancer. One out of six women will suffer a hip fracture during her lifetime (Women’s Health Initiative [WHI], n.d.).
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It is estimated that one-fifth of the number of women suffering a hip fracture are likely to die within one year as a result of secondary postoperative complications (such as pulmonary embolism). While the incidence of hip fractures is more common in women, the one-year mortality rate is about twice as high in men (AMA, 2004). Two-thirds of patients suffering a hip fracture cannot return to their previous level of function. Basic activities of daily living (ADLs) become a challenge, forcing more than 50% of patients suffering a hip fracture to need long-term nursing care (AMA, 2004). This dependent care is usually provided to patients in the form of home health care, or in a nursing facility with a skilled nursing or assisted-living level of care. Given their serious and usually more acute clinical impact, hip fractures will be discussed first.
Hip Fractures Fracturing a hip is a major concern in many older people, in that it makes it difficult for the individual to perform necessary ADLs and limits independence, and secondary complications may even lead to death. Hip fractures may occur at any age but are more common in the aging population. Aging results in loss of bone density, increasing the risk of fracture related to osteoporosis. Hospitalizations associated with hip fractures tend to occur in patients over 65 years of age (Mayo Clinic, 2006). It is estimated that the health care costs related to osteoporotic fractures total $10 to $15 billion annually (WrongDiagnosis.com, 2006). “One in every two women and one in every four men age 50 and older will experience an osteoporosis-related fracture in their lifetime” (National Oesteoporosis Foundation [NOF], 2003). Surgical repair of hip fractures is almost always recommended, and is usually very effective; however, recovery requires patience and time. The future health of the patient often directly correlates with the postoperative outcome and mobility.
Types of Hip Fractures The two most common sites of hip fractures are the femoral neck (subcapital) and the intertrochanteric region (Figures 6.1). The femoral neck is at the proximal end of the femur, in the narrowed area just below the head of the femur. The trochanteric region extends from the greater trochanter, the large lateral prominence in the proximal femur to the lesser trochanter, a smaller prominence on the medial side of the femur. To a lesser degree, some fragility fractures may occur below the trochanteric region, and are known as subtrochanteric fractures, or even lower in the femoral shaft. The majority of hip fractures occur from a fall but can be the result of normal activities such as getting out of a chair or walking down stairs. Common signs and symptoms of hip fractures include the following: Severe pain in the groin or hip Shortening of the affected extremity Swelling, bruising, or stiffness in the hip area Inability to bear weight on the injured side Internal or external rotation of the affected extremity
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Figure
6.1
Common Procedures for repair of hip fractures.
Some patients may suffer from an impacted hip fracture with which they are capable of ambulating, but often will suffer from groin pain or increased pain with passive internal or external rotation of their hip. In a patient with any or all of these symptoms, an X-ray of the affected hip and femur is warranted to rule out a fracture. If a fracture is unable to be confirmed on X-ray in a patient with a painful hip, an MRI or CT scan should be considered. Studies have proven that MRIs are more effective in the identification of occult hip fractures than CT scans, thus allowing earlier treatment and decrease in length of hospitalization (National Center for Biotechnology Information [NCBI], 2006). Bone scans also prove useful in the identification of hip fractures that are undetectable on plain radiograph; however, the results are not considered accurate if the test is performed within the first 48 hours after the injury.
Treatment of Hip Fractures Once a hip fracture has been diagnosed, surgery is almost always the recommended course of treatment. Surgery eliminates movement of the broken bones, provides pain relief, and allows for early mobilization of the patient, which can decrease associated
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postoperative risks and complications. A complete physical examination is important in the treatment of hip fractures, to identify the patient’s comorbidities. Good communication between the orthopedic surgeon and the patient’s primary care physician is important in the overall pre- and postoperative management of the patient. Nonsurgical treatment may need to be considered in patients with whom the risk of surgery is greater than the risk associated with nonoperative management. If a serious illness precludes surgical treatment, alternative nonsurgical treatments for hip fractures include bed rest and traction. However, the provider must also consider the increased risk of nonoperative treatment, including skin breakdown, deep vein thrombosis, pneumonia, and pulmonary embolus from chronic bed rest. For example, an 85-year-old female’s status after a fall with a right hip fracture and acute myocardial infarction is at increased cardiac risk, and therefore her physicians may suggest postponement of surgery until the cardiac risk is reduced. The patient may be treated with traction of the right lower extremity, but if her pain is controlled she may also be allowed out of bed to sit in a chair, bearing no weight on the affected side, without cause for concern. Common procedures for repairing hip fractures are illustrated in Figures 6.1 and 6.2. Nondisplaced femoral neck fractures require the least invasive surgical procedure, called percutaneous pinning, also formerly known as Knowles pinning. Nondisplaced fracture means that the ends of the bones are still adequately aligned but must be stabilized to decrease pain and movement at the fracture site, thus allowing the bones to heal. Percutaneous pinning can be performed under general or regional anesthesia and has even been performed under local anesthesia with sedation. The incision is usually less than 3 inches in length and is over the lateral aspect of the hip distal to the greater trochanter. Two or three 7.4 mm diameter screws are placed across the fracture site into the femoral head to prevent movement of the fracture and rotation of the femoral head. Weight-bearing restrictions are usually ordered for 4–6 weeks after surgery in patients with a percutaneous pinning. A hip hemiarthroplasty is the recommended treatment for displaced femoral neck fractures. A displaced fracture refers to a fracture in which the ends of the bones are not in anatomic alignment. A hemiarthroplasty procedure involves replacing the femoral head with a metal prosthesis (see Figure 6.2) (Mayo Clinic, 2006). Some surgeons may choose to perform a total hip arthroplasty (replacement) for the treatment of a displaced femoral neck fracture in patients with significant arthritis of the hip. A total hip replacement includes replacement of the acetabulum or socket as well as the femoral head (Mayo Clinic, 2006). Hemiarthroplasties require general or regional anesthesia and an incision approximately 6–8 inches in length. Surgical time is estimated at 45–60 minutes. The prosthesis can be secured in the femur with cement or it may be press fitted. In patients with osteoporosis, surgeons will often opt to cement the prosthesis, due to poor bone quality. The cement is called polymethylmethacrylate (PMMA) (Rasul, 2005). Press fit prosthesis depends upon interdigitation or bony ingrowths to be successful. The primary advantage in treating a femoral neck fracture with a hemiarthroplasty is resolution of pain and early mobilization. Weight-bearing restrictions are not usually considered necessary in patients following a cemented hemiarthroplasty. Patients with a hip replacement or hemiarthroplasty are at increased risk of hip dislocation postoperatively; however, hemiarthroplasty treatment has a lower incidence of dislocation than total hip replacement. The risk of dislocation is greatest in the first 8–12 weeks after surgery. The surgical approach for hip replacement varies according
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to the surgeon’s preference. An anterior approach is less invasive and spares the hip musculature, whereas the posterior approach involves detachment of the posterior hip rotators and mobilization of the gluteus medius muscle. The anterior approach has a lesser incidence of postoperative dislocation but involves working in closer proximity to the large neurovascular structures of the leg. Preventative measures to decrease the risk of dislocation in patients with the posterior approach include three standard hip precautions: avoidance of crossing the affected extremity past midline, avoidance of hip flexion greater than 90 degrees, and avoidance of pivoting on the surgical extremity (Rasul, 2005). Open reduction internal fixation (Figures 6.1 and 6.2) is most commonly recommended for patients with an intertrochanteric hip fracture. This procedure can include fixation with an intramedullary rod (not depicted in the figures), or a hip compression screw and an external side plate. Intramedullary fixation is more frequently chosen if the fracture contains a subtrochanteric component. Fixation with a hip compression screw involves placing a metal screw across the fracture and attaching it to a metal plate that lies parallel to the lateral side of the femur. The plate is then secured with additional metal screws. This procedure is sometimes referred to as a dynamic hip screw because as the bone heals the screw and plate can slide, allowing the fracture to compress, so the bone can grow together (Mayo Clinic, 2006). This surgical procedure can be performed under general or regional anesthesia and is typically 30–45 minutes in length. The incision is over the lateral thigh and is on average 6–8 inches long. Weight-bearing restrictions are dependent upon the patient’s bone quality and the security of the hardware fixation. Perioperative complications of hip fractures include but are not limited to further fracture, myocardial infarction, pulmonary emboli, deep vein thrombosis (DVT), pneumonia, wound and urinary tract infection, bedsores, neurovascular injury such as foot drop, leg-length discrepancy, and sometimes even death. General standards exist for the prevention of some of these complications. Anticoagulation should be started within 24 hours after surgery to reduce the risk of DVT. The most common anticoagulants include Coumadin®, aspirin, Lovenox®, Arixtra®, and Heparin®. In addition to pharmacologic agents, mechanical devices such as antiembolism stockings and sequential compression devices (SCDs) are available to help in the prevention of postoperative DVT. Antibiotics administered up to 30 minutes prior to incision time and continued for 24 hours postoperatively may also reduce the risk of infection. One to two grams of intravenous Cefazolin® is recommended prior to induction and should continue every 8 hours for 24 hours postoperatively. If the patient is penicillin allergic, Clindamycin® is the recommended alternative (Duke Orthopaedics, n.d.). Incentive spirometry should be encouraged every hour while the patient is awake, in order to minimize the risk of atelectisis and pneumonia. Physiotherapy is a key contributor to the patient’s postoperative recovery. Early ambulation is essential in helping return patients to their previous level of function and decrease the risk of postoperative complications, which include skin breakdown, DVT, pneumonia, and overall deconditioning.
Rehabilitation of Hip Fractures All patients can benefit from physical and occupational therapy after a hip fracture. This is initiated in the hospital and likely continues for 1–2 months after discharge. Some patients sail through rehabilitation in the hospital with flying colors and are able to go
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home with minimal assistance. These are usually younger patients with fewer medical issues. However, many patients require temporary placement in a facility that can continue to offer them therapy and rebuild their strength until they are able to go home safely and function independently. Still others will need permanent placement in an adult care facility at either a skilled nursing or assisted-living level.
Vertebral Compression Fractures Vertebral compression fractures are a significant source of morbidity and mortality for patients with osteoporosis. Such fractures are not a problem confined to just the elderly. It is estimated that over 700,000 fractures occur annually in the Unites States alone. Vertebral compression fractures occur in 25% of women over 50 years of age and 40% of those aged 80–85 years. Approximately 60% of these fractures are clinically silent— often diagnosed on routine chest X-rays or tests performed for reasons other than back pain. The majority of clinically apparent vertebral compression fractures are secondary to relatively minor trauma applied to an already compromised spinal structure. Often, patients may not recall any specific inciting event at all but merely present to the practitioner with a sudden increase in back pain. Other times, patients can identify a specific date and time when their back pain became severe—although they still may not be able to identify an associated event. Nevertheless, both scenarios should raise suspicion for compression fractures. Unlike the pain from slowly progressive degenerative changes, the pain from compression fractures can be localized to a specific level by the patient. The greatest risk factor for compression fractures is underlying osteoporosis or some other underlying pathological process. Multiple myelomas or metastatic carcinomas are two common disease processes that will result in decreased bone mass of the vertebral column. The purpose of this section is to review the clinical pathology of vertebral compression fractures as well as various treatment options.
Anatomy of the Spinal Column and Vertebral Compression Fractures The human vertebral column consists of 24 load-bearing vertebral bodies separated from each other by intervening discs. The functional unit of the spine consists of two adjacent vertebral bodies and the intervening disc space between them. The discs themselves consist of type-distinct layers—a tough annular outer layer known as the annulus fibrosus and a soft gelatinous inner layer known as the nucleus pulposus. Each disc has firm fibrous attachments to the endplates of each vertebral body that it separates. These firm attachment points provide mechanical and structural stability to the anterior portion of the spinal column. The spinal column consists of anterior and posterior columns of support. The anterior column consists of the vertebral body itself and the discs; the remaining lamina, ligaments, facet joints, and spinous processes comprise the posterior column (Figure 6.2). Mechanical stability of the spine is provided by the interaction of posterior and anterior longitudinal ligaments, as well as the anterior attachment of the discs to each vertebral endplate and the interlocking facet joints (Figure 6.3b). The stability of the spinal column relies on the maintenance of these relationships. Injury or compromise of any one
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Figure
6.2
Anatomical features of the spinal column: a) Anterior and posterior columns of the spine; b) Facet joint.
of these structures can render the spine “unstable,” which, loosely defined, means that the spine can no longer maintain its integrity under normal physiologic loads. The profile (side view) of the spinal column consists of relative cervical lordosis (extension) followed by thoracic kyphosis (flexion) and then ultimately lumbar lordosis again. This changing contour results in a spinal column that is well “balanced,” meaning neither too flexed nor too extended. The net result of a well balanced (normal) spine is efficient shock absorption, muscle function, and economical load distribution of the head and trunk on the central axis of the body. The classic compensatory postural changes that occur after untreated vertebral compression fractures are shown in Figure 6.3. The vertebral bodies have both cortical or dense bone making up most of the posterior structures and cancellous or soft bone making up most of the anterior structure (i.e., the vertebral body itself). In the upright position, 80% of the weight-bearing load travels through the anterior portion of the vertebral body—directly through the body itself—while 20% of the load is carried by the posterior structures of the spinal column (posterior longitudinal ligament, facet joints, and spinous process and lamina) (Figure 6.4). Many dynamic forces can act upon the spinal column and each distinct force vector can produce distinct types of injury pattern. A forced flexion (bending
Figure
6.3
The compensatory changes that occur with posture after untreated compression fractures.
Figure
6.4
Normal load distribution within the vertebral column.
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movement) across the spine, such as a rapid deceleration injury, will primarily injure the anterior column, whereas a forced hyperextension (backward bending movement) can injure both the anterior and posterior columns. Vertebral compression fractures in elderly osteoporotic patients are primarily the result of low-energy flexion injuries, and are therefore typically stable injuries. This does not mean, however, that they are not a cause of significant pain and morbidity. This designation merely implies that catastrophic neurologic injury secondary to catastrophic collapse of the vertebral column is rarely associated with these simple types of compression fractures. As the vertebral body loses its height it assumes a wedge-type appearance (Figure 6.5). The net result is that the spine loses its normal contour and assumes a relatively kyphotic posture (hunchback). Ultimately, as the fractured bone heals, it heals in a collapsed state—which is permanent. This unbalanced posture places an additional load anterior to the spine, since the center of gravity has moved anteriorly (Figure 6.6). This shift in the center of gravity puts an excessive load on the remaining vertebral bodies, increasing the risk of another fracture. Because of the altered dynamics of the spine, the incidence of a subsequent compression fracture within 1 year of the initial fracture is approximately 19.2%. It also increases the net amount of oxygen consumed in a normal stance and leads to muscle fatigue and pain when a patient tries to maintain upright posture or ambulate. Overall, kyphosis results in extreme inefficiency in standing upright; that is why many patients assume relatively sedentary lifestyles. In addition, it has been reported that one thoracic compression fracture will reduce pulmonary vital capacity by 9%. Many patients with chronic lung diseases, such as Chronic Obstructive Pulmonary Disease (COPD), have severe osteoporosis secondary to chronic steroid use. Their pulmonary capacity is already compromised. A decreased vital capacity of 9% in these patients has much more far-reaching implications than in an otherwise healthy person. These patients are at much higher risk for mortality with every compression
Figure
6.5
Wedge-shaped appearance of fractured vertebral body.
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Figure
6.6
When a vertebra is fractured, the center of gravity (CG) moves away from the normal spine axis, resulting in an increased load on the vertebral bodies.
fracture. The estimates are that one untreated vertebral compression fractures leads to a 23% increase in mortality in women over 65 yrs of age when compared to age-matched controls (Barr, Barr, Lemely, & McCann, 2000).
Diagnosing Vertebral Compression Fractures Patients with compression fractures often present to the physician’s office or the emergency room with a sudden increase in back pain. Clinically silent compression fractures typically occur in the upper thoracic spine, where the vertebral body size is smaller and the amount of load borne by the vertebral body is relatively low. In the lumbar spine, however, the presence of compression fractures is rarely silent. Any elderly patient presenting with back pain deserves complete X-ray evaluation of the affected area. Negative X-rays do not exclude a fracture. There is clinical evidence to suggest that fragility fractures (such as compression fractures) can present with prefracture pain. Often microscopic fractures or subtle decreases in vertebral height may not be seen on a standard radiograph. Without previous X-rays for comparison, it is very difficult to differentiate acute versus chronic compression fractures. Therefore, if a patient continues to complain of significant pain despite inconclusive plain films, an MRI is ideal for identifying acute compression fractures as well as other underlying conditions such as pathologic bone marrow replacement, neurologic compression, and metastatic tumors. If a patient cannot tolerate an MRI (i.e., if the patient has a pacemaker), then a total body bone scan can also determine the age of a compression fracture. A CT scan is helpful in assessing fracture acuity and pattern, but its accuracy can depend on the number of slices taken per level and the angle of the gantry at the time of the scan (Figures 6.7a, 6.7b).
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Figure
6.7a
Nuclear bone scans of L1 compression fracture.
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Figure
6.7b
Compression fractures seen on CT scan.
Treatment Options Once a fracture has been accurately diagnosed, the treatment options need to be discussed clearly with the patient and the family. If it is determined that a fracture is not acute, or that it has healed, then it is no longer a source of pain. One must then look for additional sources of pain. Muscular pain and fatigue will be a normal consequence of an unbalanced spine. By the time this condition occurs, there is very little if anything that can be safely done except for palliative pain management. The low back pain this population experiences may be multifactorial (i.e., muscular, neurologic, mechanical, arthritic) and must be clearly distinguished from acute fracture pain. The treatment options for vertebral fractures have improved greatly over the past decade. Traditionally, only supportive medical care was available. This often consisted of bed rest, hospitalization if the pain was severe, narcotic analgesics, and poorly tolerated bracing. The recovery could take anywhere from 1 to 3 months depending on the size and location of the fracture(s). Unfortunately, in the elderly population, prolonged recumbency or use of narcotic analgesics is associated with other poorly tolerated consequences such as skin breakdown, decreased appetite, pneumonia, altered mental and constipation status, and additional falls. Often, the pain and disability from a fracture will precipitate a significant and permanent decline in the quality of life. Open surgical treatment of compression fractures is fraught with complications. Because the morbidity of traditional open spine surgery with hardware implantation (screws and rods) and fusion has serious associated risks, this option is rarely exercised. Only in extreme cases of neurologic deterioration is such an endeavor considered. The major problems associated with fusion surgery to stabilize the spine fall into two main categories. First, this typically aged population is often in frail health, which means that any significant undertaking involving prolonged anesthesia, blood loss, and open surgery can lead to a high rate of mortality in these patients, who may already have significantly
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compromised cardiovascular and pulmonary reserves. In addition, from a mechanical standpoint, obtaining surgical fixation in the osteoporotic spine with traditional screws and rods and cages is tenuous at best. The underlying bone is so osteoporotic that it will not be able to support the stress of surgical implants, thus leading to failure of fixation and surgical complications.
Vertebroplasty and Kyphoplasty Recently, minimally invasive and very effective treatment options have emerged for treating these fractures. Vertebroplasty and kyphoplasty have surfaced as the “gold standard” options for acutely painful compression fractures (Ledlie & Renfro, 2006). The purpose behind each technique is to immediately increase the strength of the fractured vertebral body via intraosseous injection of methylmethacrylate—otherwise known as bone cement. Methylmethacrylate has been used in orthopedic surgery for many decades as a form of glue fixation for hip and knee implants. It has an excellent track record for secure fixation with relatively few adverse effects on the local bone biology. Vertebroplasty was first developed in the late 1980s. Traditionally it involves the percutaneous injection of liquid PMMA into an acutely fractured vertebral body in an awake or sedated patient. Within a few minutes the polymer hardens and the strength of the fractured vertebral body is permanently restored. Initially performed by intervention radiologists, the procedure has become increasingly popular among other specialists. Studies show a dramatic and immediate reduction in fracture pain and low morbidity. The procedure is performed under strict radiographic guidance. Potential drawbacks have been cited. Often the injection of the liquid polymer requires high pressure to achieve equal distribution within the vertebral body. This complication may result in extravasations (leaking) of the cement into unwanted areas. Such complications as neurologic injury or pulmonary emboli have been cited—fortunately, the incidence of these serious events is quite low. Another potential drawback of vertebroplasty is that it does nothing to correct the deformity of the fractured vertebral body. Often the fractured body has collapsed into a position of kyphosis (as discussed earlier), which if left in the collapsed state results in an overall change in the center of gravity of the spinal column and ultimately an unbalanced spine. The consequences of an unbalanced spine have already been explained. Nevertheless, vertebroplasty does offer a relatively safe and immediate reduction in fracture pain without the associated risks of traditional open surgical stabilization. Several years ago, the procedure termed kyphoplasty was introduced. The premise behind kyphoplasty is similar to that behind vertebroplasty, in that it involves the percutaneous injection of liquid PMMA into an acutely broken and painful vertebral body. However, kyphoplasty involves the use of an inflatable bone tamp or balloon technology to achieve fracture reduction (Figures 6.8a, 6.8b). The patient is brought to the operation room or fluoroscopy suite and placed in the prone position. Then, a percutaneous cannula is placed into the vertebral body (Figure 6.9). Through that cannula, a nylon balloon is inserted. The balloon is then slowly inflated, essentially serving as an internal expander of the bone, in a manner similar to angioplasty. The end result is that the collapsed vertebral body is “inflated,” often restoring the height to prefracture levels. The balloon is removed; the PMMA is injected under very low pressure and fills the space created by the balloon. Once the cement hardens (in just a few minutes)
Figure
6.8a
Kyphex inflatable balloon.
Figure
6.8b
Diagram of insertion.
Figure
6.9 Balloon insertion
Balloon inflation
Illustration of repair of fractured vertebrae using kyphoplasty procedure.
Fracture reduced, balloon removed
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the procedure is complete. Usually a single-level kyphoplasty can be completed in less than 30 minutes. Two distinct advantages of kyphoplasty are that it restores the vertebral height and decreases the likelihood of cement extravasations, since the cement flows under low pressure into a previously made space. The clinical results are excellent. The majority of patients report a 90% improvement within the first week (Lieberman, Dudeney, & Reinhardt, 2001; Phillips et al., 2003; Voggenreiter, 2005). Often a dramatic reduction in pain is felt within the first 24 hours of the procedure and the spine can be restored to its balanced position. Aftercare is minimal. Since the PMMA is solid within a few minutes, most patients are discharged home within 24 hours of admission and are allowed to return to their prefracture activities immediately, significantly reducing the complications associated with a sedentary lifestyle.
Wrist Fractures The wrist is the third most common location for an osteoporotic-related fracture. The wrist joint is composed of two long bones in the forearm, the radius and the ulna, connecting to several smaller bones in the hand, known as carpal bones. In the event that a patient sustains a wrist fracture, it often includes both the radius and the ulna. The primary mechanism of injury is a fall on an extended wrist (Figure 6.10). This type of injury commonly results in a fracture of the distal radius and ulna, with dorsal angulation of the distal fragments (commonly referred to as a Colles’ fracture). If an individual falls with the wrist in flexion, causing a volar angulation of the distal radius and ulna, it is termed a Smith’s fracture. Colles’ fractures tend to occur more frequently in postmenopausal women (U.S. News and World Report—Best Health, 2005) and osteopenic or osteoporotic bone. X-rays confirm the diagnosis of a wrist fracture.
Treatment of Wrist Fractures Treatment of wrist fractures correlates with the severity of the injury. If the bones have remained in fairly good alignment, then often a splint or a cast is all that is needed to immobilize the wrist. The cast may need to extend above the elbow to ensure complete immobilization of the wrist. However, if the bones are not lined up appropriately, they must be realigned; this is called a reduction. This procedure can be accomplished in several different ways, depending on the nature of the fracture and the physician’s recommendations. One option includes giving the patient a sedative in the emergency room (called conscious sedation) and performing a closed reduction and application of a splint or cast. A closed reduction means realignment of the bones without making an incision. If the reduction is successful, the patient is followed closely over the next 1–2 weeks with X-rays in the doctor’s office. If the bones slip or an adequate reduction was not able to be achieved in the emergency room, an operation is indicated to reposition them. In the operating room, general anesthesia can be administered with muscle relaxation. If the reduction is considered to be stable, a cast splint is usually applied. However, if subsequent X-rays show that the closed reduction is no longer satisfactory, pins can be used to help hold the bones in place. This procedure is called a closed reduction with
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Figure
6.10
Wrist fractures.
percutaneous pinning, since the pins puncture the skin and drill into bone. Occasionally an incision must be made to achieve an adequate reduction, and additional hardware may be used to hold the bone fragments in place. This procedure is called an open reduction with internal fixation. A plate is placed on the bone and held with screws. The plate can be placed on either the volar or dorsal side of the bone. The last option for treatment of a wrist fracture is an external fixation device. This metal frame is anchored in the bone with screws and fastened together to hold the bones in place. An external fixator can be the primary form of immobilization, or it may be a temporary means of stabilizing the fracture until internal fixation can be carried out after a few weeks. This is beneficial if the patient has sustained significant trauma to the skin and the risk of making an incision is judged to be too great. Preexisting skin wounds increase the patient’s susceptibility to infection if an operation is carried out though them. Percutaneous pins are a temporary fixation, and are always removed at 3–6 weeks. They can usually be removed in the office. Internal fixation is often not removed but may be in certain circumstances. Common reasons to remove hardware are infection, chronic irritation, or risk of growth complications in children and adolescents.
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An open fracture occurs when the bone punctures the skin from inside out. In the event that a patient sustains an open fracture, the recommendation is to take the patient to the operating room for irrigation of the open wound and appropriate reduction and stabilization of the fracture. The chances of infection are greatly reduced if treatment can be initiated within the first 6–8 hours. These patients are at a higher risk of infection. Postoperative treatment remains the same as in closed fractures.
Rehabilitation of Wrist Fractures Joints become very stiff after any period of immobilization. Therapy is very important in helping patients achieve maximum use of their affected extremity once the immobilizing agent is removed. Even though casts are used, the fingers and the thumb are left free to move. It is imperative that the patient should actively move the digits so as to prevent contracture and loss of hand function. Casts are usually removed after 6–8 weeks. If internal fixation was used and the fixation is secure, therapy can begin as early as 2–4 weeks postfracture. Occupational therapy is usually encouraged since such therapists specialize in injuries of the upper extremities.
Prevention Educating patients about a bone healthy lifestyle is the key to preventing osteoporoticrelated fractures. Patients need to know that they can help themselves decrease their risk of fractures by addressing their osteoporosis. Proper diet and exercise can improve bone quality and balance. Patients also can decrease the risk of fracture by minimizing their fall risk. Throw rugs, electric cords, and loose items should not be left out. They are a tripping hazard. If balance is a concern, an assistive device should be used to steady the gait. In addition, it is also important for clinicians to be aware that all patients who have sustained a low-impact fracture should have a bone mineral density (BMD) test to assess their risk of future fractures and to determine their need for medication. However, the literature indicates that primary care providers usually do not order a BMD test, even after a fracture has occurred (Feldstein et al., 2003; Solomon, Finkelstein, Katz, Mogun, & Avorn, 2003).
Conclusion Continued research is needed in both the treatment and the prevention of painful osteoporotic fractures. It is not only the acute phase of the fracture that is of concern to patients and their families but also the long-term consequences of untreated fractures that heal in a collapsed position. Through continued efforts by the health care community, it is now possible to significantly reduce both the incidence and the impact of these fractures.
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REFERENCES American Medical Association. (2004). State of the art management of osteoporosis. In An AMA continuing medical education program for primary care physicians, 10–12. Barr, J. D., Barr, M. S., Lemely, T. J., & McCann, R. M. (2000). Percutaneous vertebroplasty for pain, relief, and spinal stabilization. Spine, 25, 923–928. Duke Orthopaedics. (n.d.). Antibiotic prophylaxis. Wheeless’ textbook of orthopaedics. Retrieved September 4, 2006, from http://www.wheelessonline.com/ortho/antibiotic_prophylaxis Feldstein, A. C., Nichols, G. A., Elmer, P. J., Smith, D. H., Aickin, M., & Herson, M. (2003). Older women with fractures: Patients falling through the cracks of guideline-recommended osteoporosis screening and treatment. Journal of Bone Joint Surgery of America, 12, 2294–2302. Ledlie, J., & Renfro, M. (2006). Kyphoplasty treatment of vertebral fractures: 2-year outcomes show sustained benefits. Spine, 31, 57–64. Lieberman, I. H., Dudeney, S., & Reinhardt, M. K. (2001). Initial outcome and efficacy of “kyphoplasty” in the treatment of painful osteoporotic compression fractures. Spine, 26, 1631–1638. Mayo Clinic. (2006, January 9). Hip fracture. Retrieved September 2, 2006, from http://www. mayoclinic.com/print/hip-fracture/ds00185/dsection+all&method+print National Oesteoporosis Foundation. (2006, September 4). Physician’s Guide to Prevention and Diagnosis of Osteoporosis. Retrieved September 4, 2006, from http://www.nof.org/ Phillips, F., Ho, E., Campbell-Hupp, M., NcNally, T., Todd, F., Wetzel, F., et al. (2003). Early radiographic and clinical results of balloon kyphoplasty for the treatment of osteoporotic vertebral compression fractures. Spine, 28, 2260–2265. Rasul, A. T., Jr. (2005, September 14). Total joint replacement rehabilitation. Retrieved September 4, 2006, from http://www.emedicine.com/pmr/topic221.htm Solomon, D. H., Finkelstein, J. S., Katz, J. N., Mogun, H., & Avorn, J. (2003). Underuse of osteoporosis medications in elderly patients with fractures. American Journal of Medicine, 115(5), 398–400. U.S. News and World Report—Best Health (2005, July 7). Wrist fractures. Retrieved September 4, 2006, from http://www.usnews.com/usnews/health/bones/osteoporosis/osteo.treat.wristfrac.htm U.S. Department of Health and Human Services. (2004). Bone health and osteoporosis: A report of the surgeon general. Public Health Service, Office of the Surgeon General, Rockville, MD. Retrieved from http://www.surgeongeneral.gov/library/bonehealth Voggenreiter, G. (2005). Balloon kyphoplasty is effective in the deformity correction of osteoporotic vertebral compression fractures. Spine, 30, 2806–2812 Women’s Health Initiative. (n.d.). Why WHI. Retrieved September 2, 2006, from http://www.nhlbi. nih.gov/whi/whywhi.htm World Health Organization [WHO] Scientific Group. (2003). Prevention and Management of Osteoporosis: A report of a WHO Scientific Group. Geneva, Switzerland: World Health Organization, WHO Technical report, 921. WrongDiagnosis.com. (2006, August 2). Complications of osteoporosis. Retrieved September 2, 2006, from http://www.wrongdiagnosis.com/o/osteoporosis/complic.htm
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Diet and Bone Health
Good nutrition—from birth to old age—cannot be overemphasized in the promotion of good bone health. (Matzko, “Preventing Osteoporosis” )
T
he purpose of this chapter is to do the following: 1. Explain why calcium
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Helen Smiciklas-Wright Catherine E. Wright
and vitamin D are essential for bone health 2 . Present recommended intakes of calcium and vitamin D throughout the life cycle 3 . Review the potential influences of selected nutrients and other food components on bone health 4 . Describe food patterns and nutritional supplement options that support bone health
Nutrition is one of several factors that can be modified to reduce osteoporosis risk. The following issues are basic to understanding nutrition and bone status: Life cycle: Osteoporosis has been described as a pediatric disease with a geriatric outcome (Kitchin & Morgan, 2003). Nutritional intake throughout life supports bone health. Several studies have shown that undernutrition during fetal development can modify bone mineral density and adult bone size (Harvey & Cooper, 2004). Total diet: Calcium and vitamin D have received most of the attention directed to diet and bone health, but there are continuing questions about their benefits for bone health. Moreover, many other nutrients and food components
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can affect bone status (Tucker, 2003). This chapter will present evidence for the roles of calcium and vitamin D. It will also address the importance of total diet and give recommendations for both food and supplement sources. Calcium is the most abundant mineral in bone, and over 98% of total body calcium is found in bone. Bone serves as the storage site for calcium. Putting this statistic in perspective, R. P. Heaney (2003) wrote that “we walk on our calcium reserve” (p. 913). Given the association between calcium and bone, it is reasonable to assume that dietary calcium will affect the risk of osteoporosis. The challenge has been to understand the role of calcium at different stages of the life cycle and to determine how much is adequate for bone health (Weaver, 2001).
The Effect of Calcium on Peak Bone Mass Peak bone mass (i.e., the amount of bone predominantly acquired by young adulthood) is a significant determinant of future fracture risk. About 70%–80% of the peak bone mass that can be achieved is genetically determined. Calcium intake is an important determinant of the remaining 20%–30% of variation in bone mass. Eastell and Lambert (2002) reviewed studies showing that calcium does indeed affect peak bone mass. The effect appears to be greater in children during periods of rapid bone growth (i.e., prepuberty and early puberty). Early studies seemed to indicate that the beneficial effect of calcium supplementation on bone mass lasted only while patients were taking supplements, and then disappeared when supplementation ended. However, recent studies have shown that supplementation even for 1 year can provide a longer term effect on bone mineral density (Dodiuk-Gad, Rozen, Rennert, Rennert, & Ish-Shalom, 2005). Most of the studies reviewed by Eastell and Lambert (2002) involved calcium supplements. Few studies have looked at food calcium and bone mass in children, but recently, Fiorita and colleagues reported that total dietary calcium intake by girls at ages 7 and 9 years was positively associated with bone mineral content at age 11 (Fiorita, Smiciklas-Wright, Mitchell, & Birch, in press).
Does Calcium Intake Minimize Bone Loss and Reduce Fractures? The results of studies of the relationship between calcium intake, bone loss, and fracture risk have been contradictory. However, several investigators have reviewed the effect of calcium during young and middle adulthood (Anderson & Rondano, 1996; Welten, Kemper, Post, & van Staveren, 1995), and the overall findings indicate that calcium has a beneficial effect in maintaining bone mass and reducing bone loss. The beneficial effect of calcium in reducing bone loss and fracture risk is more pronounced in later postmenopausal years rather than in the early postmenopausal period. The largest benefits are seen when calcium is added to the diets of women whose baseline intake is low. R. P. Heaney (2003) attributes the added benefit of higher calcium intake in older adults to a decreased ability to adapt to low calcium intakes.
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Further evidence for the benefits of calcium comes from studies showing that calcium was beneficial for women who were on hormone replacement therapy. The combined effect of calcium and estrogen was two or three times greater than the effect of estrogen alone in maintaining bone mass (Nieves, Komar, Cosman, & Lindsay, 1998). Dawson-Hughes and her colleagues showed that calcium and vitamin D supplements given to older subjects reduced bone loss and nonvertebral fractures (Dawson-Hughes, Harris, Krall, & Dallal, 1997). However, the efficacy of calcium and vitamin D supplements for reducing fractures was challenged in a study of more than 30,000 postmenopausal women who were enrolled in the Women’s Health Initiative (WHI) clinical trial (Jackson et al., 2006). Women were assigned to receive 1000 mg of calcium carbonate with 400 International Units (IU) of vitamin D or placebo; fractures were ascertained for an average follow-up of 7 years. The supplements did diminish hip bone loss but did not reduce hip fracture. This is not, however, a definitive study. The vitamin D dose may not have been high enough. Calcium and vitamin D supplements other than those prescribed were allowed in both groups. Women who were most faithful in taking the supplements did experience a decreased risk of hip fractures.
Recommended Calcium Intakes Recommended intakes for calcium are shown in Table 7.1. The recommendations are based on estimates of average calcium intakes by groups of healthy people.
Table
7.1
Recommended Intakes for Calcium and Vitamin D Life stage 1 –3 yrs. 4 – 8 yrs. 9 –18 yrs. 19 –50 yrs. 51 –70 yrs. >70 yrs.
Calcium (mg/day) 500 800 1300 1000 1200 1200
Vitamin D (μg/day [IU]) 5 (200) 5 (200) 5 (200) 5 (200) 10 (400) 15 (600)
Note. From Institute of Medicine, 1997.
Average calcium intake from food in the United States is approximately: 900 mg for adolescents 700 mg for adults 60 years and older Source: Ervin, Wang, Wright, & Kennedy-Stephenson, 2004. Average vitamin D intake from food in the United States is approximately as follows: 6–7 IU for children and adolescents 5.5–6 IU for men 19 years or older 4–4.5 IU for women 19 years and older Source: Moore et al., 2004.
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Most people in the United States consume far less calcium than the recommended amounts. This is particularly true for adolescents and older adults, two age groups with high recommended intakes (Ervin, Wang, Wright, & Kennedy-Stephenson, 2004). Women generally consume lower energy diets than men and are more likely to be well below the recommended calcium intakes. People with poor appetites and those who reduce energy intake to achieve weight loss are at particular risk of inadequate calcium intake.
The Calcium Paradox Recommended intakes for calcium set for the United States and Canada are higher (Institute of Medicine, 1997) than recommendations in other countries (Stear, 2000). However, people in some geographical areas with low calcium intakes, such as Japan, have a low incidence of osteoporotic fractures. In contrast, some populations such as those in Scandinavian countries, where average calcium intakes are high, have a high incidence of osteoporosis. There are many possible explanations for this apparent paradox: Life expectancies—the longer life expectancies of people in developed countries may lead to a greater risk of osteoporosis; Differential reporting—osteoporosis rates may simply be underrepresented in some areas; Genetic differences; Physical activity patterns; Bone architecture; and Other dietary factors—calcium intake alone is not the only nutritional factor associated with bone health.
Food Sources of Calcium Calcium is found in varying amounts in a wide range of foods (Table 7.2). Dairy products generally contribute about half of the calcium to American diets (Moore, Murphy, Keast, & Holick, 2004; Weaver, 2001). Calcium in milk is readily absorbed because milk is fortified with vitamin D, which facilitates calcium absorption. Lower fat milks contain more calcium than regular milk because some nonfat milk products are added to replace the fat. Cottage cheese has traditionally been considered a relatively poor dairy source of calcium because calcium is lost during production. However, some cottage cheese products are fortified with calcium. Canned salmon with bones, sardines, and mackerel are excellent sources of calcium. There are good sources of calcium in some vegetables, such as kale and Chinese cabbage, with lesser amounts in broccoli, green beans, and acorn squash. Spinach is a good source but contains oxalic acid, which binds the calcium in spinach and interferes with its absorption. Phytic acid in dried peas and beans can also decrease calcium absorption.
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Table
Approximate Amount of Calcium in Food
7.2
Amount
Nonfat milk Whole milk Milk, Ca fortified Yogurt Dry skim milk Cheddar, other hard cheeses Parmesan, grated Ice cream Cottage cheese Cottage cheese, Ca fortified
Calcium (mg)
Amount Nondairy ½ c. ½ c. ½ c. ½ c. ½ c. ½ c.
Calcium (mg)
Dairy 1 c. 1 c. 1 c. 1 c. ¼ c. 1 oz
415 315 500 300 210 150
Sardines, canned Salmon, canned Mackerel, canned Chinese cabbage Kale, cooked Broccoli
2 T. ½ c. ½ c. ½ c.
150 85 70 200
Beans, lima, kidney, navy Baked beans Orange Orange juice, Ca fortified
½ c. ½ c. 1 ½ c.
40 75 50 140
Almonds, blanched Tofu, firm processed with Ca Cereal, super-fortified Oatmeal, instant
1 oz ¼ c.
25 65
½ c. 1 pkg.
90 240 240 80 90 50
170 165
Note. For nutrient values in foods, refer to the U.S. Department of Agriculture’s Nutrient Database (2006), retrieved August 16, 2006 from http://www.nal.usda.gov/fnic/cgi-bin/nut_search.pl
As more and more calcium-fortified foods are produced, the number of good calcium sources increases. Currently, some manufacturers produce calcium-fortified rice, prune juice, pasta, waffles, and other foods.
Vitamin D Evidence is increasing for the many health benefits of vitamin D. Vitamin D deficiency increases the risk of some cancers, type 1 diabetes, cardiovascular disease, and autoimmune diseases, as well as osteoporosis (Calvo, Whiting, & Barton, 2005; Holick, 2004). While there is ongoing discussion about the recommended daily requirement for vitamin D, the Institute of Medicine (1997) recommends 5 micrograms (µg/day) for children and adults through 50 years of age, 10 µg for adults 51–70 years of age, and 15 µg for adults over 70 years of age (Table 7.1). Vitamin D is critical for bone health. It is necessary for the adequate absorption of both calcium and phosphorus, the bone-hardening minerals (Holick, 2004). Vitamin D has other functions that are essential for maintaining blood calcium levels and for bone health. It can act with bone-cell-building components to support bone status (Heaney, R. R., Carey, & Harkness, 2005). Vitamin D and calcium act as a team and function most effectively when the appropriate dose of vitamin D is coupled with calcium.
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Vitamin D is a fat-soluble vitamin that is deposited in body fat stores. Many obese persons are vitamin D–deficient because the vitamin is held in the large body fat pool and is not available for metabolic activity.
Sources of Vitamin D Sunlight Vitamin D is not, in the true sense of the word, a vitamin; that is, it does not need to be supplied by dietary sources. It exists in the epidermis layer of the skin as a previtamin, which is converted to vitamin D(3) upon exposure to light (Holick, 2004). In northern latitudes, during the summer months, 10 to 15 minutes of sun exposure two or three times per week should be sufficient to ensure adequate production of vitamin D in children and young adults. The amount of vitamin D produced in the skin is affected by several factors including skin pigmentation, distance from the equator, use of sunscreens, and age (Heaney R. R., et al., 2005). Older adults produce less vitamin D than young adults exposed to the same amount of sunlight. Furthermore, older adults often spend less time outdoors and thus have less exposure to sunlight than children and young adults. Nursing home residents are at particular risk of vitamin D deficiency (Kinyamu, Gallagher, Balhorn, & Petranick, 1997). Additionally, fear of skin cancer may cause older adults to be particularly conscientious about applying sunscreen, which hinders vitamin D production. Sunscreen with a sun protection factor (SPF) of 8 or above almost completely blocks the production of vitamin D.
Diet Vitamin D can be obtained from food sources but is not widely present in the food supply. The major natural sources are some fatty fish (see Table 7.3) and fish oils. While
Table
7.3
*
Approximate Amount of Vitamin D in Food Food Milk, all types Salmon Sardines Tuna Cod liver oil Cereal + D Orange juice + D Egg
Amount 1 c. (8 oz) 3 oz 3 oz 3 oz 1 tsp 1 c. 6 oz 1 whole
40 International Units (IU) = 1 microgram (µg).
Vitamin D (IU*) 100 425 425 200 450 40 75 20
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other animal foods, such as milk, eggs, and butter, contain some vitamin D, it is generally difficult to get the recommended amounts from unfortified foods. Some countries have mandatory fortification of milk. In the United States and Canada, milk is the only food that is routinely fortified with vitamin D. About half of the vitamin D intake from food is from dairy products. Most milk sold in North America is fortified to provide 100 IU per 8 ounces. Other products, such as breakfast cereals and orange juice, may also be vitamin D fortified.
Recommended Vitamin D Intakes The recommended intakes for vitamin D in the United States and Canada are shown in Table 7.1. The recommendations are expressed in two units: micrograms µg and IU. The higher recommendations for adults 50 to 70 years and for those 71 years or older are based on information about sunlight exposure, metabolism of vitamin D, and risk of skeletal fractures (Institute of Medicine, 1997). Higher vitamin D doses in combination with calcium have been shown to reduce fracture risk (Chapuy et al., 1992). Many teenagers and adults fail to consume adequate amounts of vitamin D from food. Less than 10% of adults 51 to 70 years old and 2% of those 71 years or older met the recommended intakes from food alone. Females, both teenagers and adults, reported the lowest vitamin D intakes in the Third National Health and Nutrition Examination Survey, 1994–1996 (Moore et al., 2004).
How Much Calcium and Vitamin D Is Available in Foods and Supplements? The amount of calcium and vitamin D is shown on the “Nutrition Facts” label for foods and the “Supplement Facts” label for supplements. However, interpreting the labels requires some information that is not on the label. The calcium content is listed as a percentage of daily value (DV). The DV for calcium is currently set at 1,000 mg; the DV for vitamin D is currently set at 400 IU. For example, a food product that provides 15% DV for calcium would contain 150 mg of calcium. A product that provides 25% DV for vitamin D would contain 100 IU of vitamin D.
Is It Possible to Consume Too Much Calcium and Vitamin D? Both calcium and vitamin D can cause health risks when consumed in very high amounts. The Institute of Medicine of the National Academy of Science (Institute of Medicine,
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1997) recently set upper limits (ULs) for both calcium and vitamin D for persons 1 year old and older: UL for calcium = 2,500 mg/day; UL for vitamin D = 50 µg (2,000 IU)/day. The potential risks of a high calcium intake are decreased absorption of other minerals, such as iron and zinc, that can compete for absorption sites with calcium, and the formation of kidney stones. The potential risk of an excessive vitamin D intake is damage to target tissues such as those of the central nervous system, which can result in severe depression, nausea, and anorexia. It is unlikely that people would consume toxic levels of calcium and vitamin D from traditional food sources. However, with the increasing availability of supplements and fortified foods, it may be important to monitor intakes of these nutrients.
Total Diet Energy intake, many nutrients, and other dietary components can affect bone health. Several excellent reviews of total diet needs and bone health have been published (Dowd, 2001; Ilich & Kerstetter, 2000; Tucker, 2003). A few of the many dietary components that influence bone health are presented here.
Energy Very low energy intakes and low body weight are associated with higher osteoporotic risk. The 2004 surgeon general’s report on bone health reviewed studies reporting that very low body weight may limit peak bone mass. Low body weight and weight loss in older women are associated with reduced bone mass and increased fracture risk (U.S. Department of Health and Human Services [USDHHS], 2004). Persons with reduced appetites and those who diet frequently or have eating disorders are at risk for impaired bone health.
Protein Protein plays a paradoxical role in bone health. Both low and high protein intakes may have a detrimental effect on bone status (Kerstetter, O’Brien, & Insogna, 2003). Several epidemiological studies show that individuals with low-protein diets have lower bone mineral densities and greater losses in bone density. An increased risk of hip fracture has been reported for women consuming the lowest amounts of protein. Protein may function in several ways to reduce fracture risk. Protein deficiency alters muscle function as well as impairing bone health (Rizzoli, Ammann, Chevalley, & Bonjour, 2001). Hip fracture patients provided with protein supplements show improved clinical outcomes. Concern about high protein intakes comes from many studies, carried out over many years, that show that urinary calcium excretion increases as protein intake increases (Heaney, R. P., 1993), leading to inadequate calcium retention. There is no simple answer to the question, “Does high protein intake adversely affect bone?” It really does depend on the amount of calcium consumed and other dietary components that can buffer some of the consequences of a high protein diet. Meat, fish, and cheese produce high potential
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renal acid loads (Tucker, 2003). However, vegetables, fruits, milk, and yogurts produce renal alkaline loads that buffer renal acid loads and promote calcium retention. This is one of many arguments for a varied diet with adequate servings from each of the food groups.
Other Nutrients Many nutrients are involved in bone health. Bone tissue is complex and dynamic with various hormones and enzymes regulating its metabolism. Therefore, it is not surprising that there are many possible roles for nutrients. Generally nutrients act in one of the following ways: Direct effect on bone structure and metabolism Effect on calcium absorption, metabolism, excretion Some nutrients directly affect bone structure (i.e., mineral matrix, collagen, and bone metabolism). These include phosphorus, zinc, magnesium, iron, vitamin K, vitamin B12, vitamin A, and fatty acids. Nutrients function indirectly in many ways to affect calcium status. Some, such as magnesium, potassium, and phytoestrogens, contribute to an alkaline environment promoting urinary calcium retention. Phytoestrogens are compounds that mimic the action of estrogen. They occur in many plant products, including cereals, seeds, vegetables, legumes, nuts, and fruits. Soy isoflavones are phytoestrogens that have been studied as potential adjuncts to or replacements for hormone replacement therapy. Higher intakes of soy isoflavones have been associated with increased bone mineral density and decreased bone loss. Relatively high doses (i.e., the consumption of several soy-containing foods per day) may be necessary to achieve bone effects (Setchell, 1998).
Caffeine High caffeine consumption has been suggested as a risk factor for osteoporosis. Various physiological mechanisms have been proposed to account for the risk. Unfortunately, studies of caffeine consumption as a potential risk factor have been contradictory. Overall, the evidence suggests that a daily caffeine intake equivalent to about two to three servings of brewed coffee may increase bone loss, particularly among postmenopausal women with low calcium intakes (Harris & Dawson-Hughes, 1994).
Alcohol A moderate alcohol intake appears to be positively associated with bone mineral density. There are likely several explanations for the protective effects, including the presence of antioxidants and other compounds in alcoholic drinks. However, heavy drinkers are at risk for bone loss and fractures. Poor nutrition, malabsorption of nutrients, and a direct “attack” on the bone-forming osteoblasts may contribute to bone loss. The North American Menopause Society (2002) recommends that postmenopausal women should not drink more than seven drinks a week (a drink is one beer, 4 oz of wine, or 1 oz of liquor).
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Nutritional Recommendations Diet Some years ago, Heaney published a paper entitled “Food: What a Surprise!” (Heaney, R. P. 1996), which described how a diet with an appropriate energy intake and a variety of foods can provide nutrients for bone health. Key foods in the diet are low-fat dairy products and fruits and vegetables. Dairy products are the major source of calcium in Western diets. Milk provides a good source of many nutrients. Diets low in dairy products are often low in many nutrients. Per capita consumption of milk has declined in the past 25 years. Many people prefer the taste of other beverages to that of milk or choose noncaloric beverages for weight control. Lactose intolerance is a major reason why many people avoid dairy products. Lactose intolerance occurs in people who have insufficient levels of the intestinal enzyme lactase to break down lactose, the principal carbohydrate in milk. Lactose that is not well digested can undergo microbial fermentation. The consequent gastrointestinal symptoms (i.e., bloating, cramps, pain, and diarrhea) may be mild or severe. Many people who have symptoms of lactose intolerance can tolerate small amounts of dairy products without experiencing gastrointestinal discomfort ( Jarvis & Miller, 2002). Solid products, such as cheese, may be better tolerated because of delayed gastric emptying time. Yogurts with active cultures and hard cheeses have lower lactose contents. Drinking milk with other foods or adding chocolate to milk may also improve lactose tolerance. Lactose-reduced milks are also available but are more expensive than regular milk. A number of studies have demonstrated an association between fruit and vegetable intake and bone health (New, 2004; Prynne et al., 2006). Fruits and vegetables contain many nutrients and phytochemicals that contribute to bone health. They also reduce the acid load and increase an alkaline environment, thereby reducing urinary calcium excretion. Studies are underway to assess the role of fruits and vegetables on bone health. Encouraging an increased intake of fruits and vegetables is likely to have many health-related benefits (Lanham-New, 2006).
Supplements Calcium and vitamin D are available as single nutrient supplements, as components of multinutrient supplements, or as calcium plus vitamin D supplements, with or without other nutrients (e.g., vitamin K, phosphate).
Calcium supplements are not a sole alternative to food sources that also provide other nutrients.
Calcium supplements are available as a number of salt forms, which can differ in their elemental calcium content (ranging from 200 to 600 mg calcium) as well as their
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solubility and cost (Kass-Wolff, 2004). The most common and generally least expensive form of calcium is calcium carbonate. Calcium carbonate contains the highest amount of calcium per tablet of any salt. Calcium carbonate supplements are best taken with meals to increase calcium absorption in an acid environment. Calcium citrate supplements have less calcium but may be better for older people with reduced stomach acidity (i.e., achlorhydia). They are also recommended for patients taking acid blockers. All calcium supplements should be taken in several small doses throughout the day for the most efficient calcium absorption. To maximize absorption, doses of less than 500 mg at a time are recommended. Some people complain that calcium supplements cause gas, constipation, bloating, or gastric irritation. Physicians may recommend trying another type of supplement to relieve the symptoms. Adequate fluid and fiber intake may help to alleviate symptoms. Vitamin D supplements also vary in doses from 100 to 400 IU. Supplements provide an added 2 to 3 µg (approximately 80 to 120 IU) to the vitamin D intakes of American adults (Calvo et al., 2005). Even with supplement use, total vitamin D intakes are generally below recommendations.
Summary There is a persuasive body of evidence that nutritional factors play significant roles in the development and maintenance of bone strength. Calcium and vitamin D have been the most extensively studied nutritional factors and appear to be important in bone health throughout life. Other dietary factors, energy, protein, micronutrients, and phytoestrogens can all have significant roles to play in reducing osteoporotic risk. Dietary recommendations encourage a varied diet with adequate intakes of low-fat dairy products and fruits and vegetables.
REFERENCES Anderson, J. J., & Rondano, P. A. (1996). Peak bone mass development of females: Can young adult women improve their peak bone mass? Journal of the American College of Nutrition, 15, 570–574. Calvo, M. S., Whiting, S. J., & Barton, C. N. (2005). Vitamin D intake: A global perspective of current status. Journal of Nutrition, 135, 310–316. Chapuy, M. C., Arlot, M. E., DuBoeuf, F., Brun, J., Crouzet, B., Arnaud, S. et al. (1992). Vitamin D3 and calcium to prevent hip fractures in elderly women. New England Journal of Medicine, 327, 1637–1642. Dawson-Hughes, B., Harris, S. S., Krall, E. A., & Dallal, G. E. (1997). Effect of calcium and vitamin D supplementation on bone density in men and women 65 years of age or older. New England Journal of Medicine, 337, 670–676. Dodiuk-Gad, R. P., Rozen, G. S., Rennert, G., Rennert, H. S., & Ish-Shalom, S. (2005). Sustained effect of short-term calcium supplementation on bone mass in adolescent girls with low calcium intake. American Journal of Clinical Nutrition, 81, 168–174. Dowd, R. (2001). Role of calcium, vitamin D, and other nutrients in the prevention and treatment of osteoporosis. Nursing Clinics of North America, 3, 417–431. Eastell, R., & Lambert, H. (2002). Diet and healthy bones. Calcified Tissue International, 70, 400–404. Ervin, R. B., Wang, C.-H., Wright, J. D., & Kennedy-Stephenson, W. (2004). Dietary intake of selected minerals for the United States population. Advance data, from vital and health statistics (No. 341). Hyattsville, MD: National Center for Health Statistics.
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Osteoporosis Fiorita, L. M., Smiciklas-Wright, H., Mitchell, D. C., & Birch, L. L. (in press). Dairy intake and bone mineral content during middle childhood. Journal of Nutrition. Harris, S. S., & Dawson-Hughes, B. (1994). Caffeine and bone loss in healthy postmenopausal women. American Journal of Clinical Nutrition, 60, 573–578. Harvey, N., & Cooper, C. (2004). The developing origins of osteoporotic fractures. Journal of the British Menopause Society, 10, 14–15, 29. Heaney, R. P. (1993). Protein intake and the calcium economy. Journal of the American Dietetic Association, 93, 125–160. Heaney, R. P. (1996). Food: What a surprise! American Journal of Clinical Nutrition, 64, 791–792. Heaney, R. P. (2003). Long-latent deficiency disease: Insights from calcium and vitamin D. American Journal of Clinical Nutrition, 78, 912–919. Heaney, R. R., Carey, R., & Harkness, L. (2005). Roles of Vitamin D, n-3 polyunsaturated fatty acid, and soy isoflavones in bone health. Journal of the American Dietetic Association, 105, 1700–1702. Holick, M. F. (2004). Vitamin D: Importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis. American Journal of Clinical Nutrition, 79, 362–371. Ilich, J. Z., & Kerstetter, J. E. (2000). Nutrition in bone health revisited. Journal of the American College of Nutrition, 19, 715–737. Institute of Medicine. (1997). Dietary reference intakes for calcium, phosphorus, magnesium, vitamin D, and fluoride. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Food and Nutrition Board. Washington, DC: National Academy Press. Jackson, R. D., LaCroix, A. Z., Gass, M., Wallace, R. B., Robbins, J., Lewis, C. F. et al. (2006). Calcium plus vitamin D supplementation and the risk of fractures. New England Journal of Medicine, 354, 669–683. Jarvis, J. K., & Miller, G. D. (2002). Overcoming the barrier of lactose intolerance to reduce health disparities. Journal of the National Medical Association, 94, 55–66. Kass-Wolff, J. H. (2004). Calcium in women: Healthy bones and much more. Journal of Obstetrical Gynecology of Neonatal Nursing, 33, 21–33. Kerstetter, J. E., O’Brien, K. O., & Insogna, K. L. (2003). Low protein intake: The impact on calcium and bone homeostasis in humans. Journal of Nutrition, 133, 855S–861S. Kinyamu, H. K., Gallagher, J. C., Balhorn, K. E., & Petranick, K. M. (1997). Serum vitamin D metabolism and calcium absorption in normal young and elderly free-living women and in women living in nursing homes. American Journal of Clinical Nutrition, 65, 790–797. Kitchin, B., & Morgan, S. (2003). Nutritional considerations in osteoporosis. Current Opinions in Rheumatology, 15, 476–480. Lanham-New, S. A. (2006). Fruit and vegetables: The unexpected natural answer to the question of osteoporosis prevention? American Journal of Clinical Nutrition, 83, 1254–1255. Matzko, M. (2002). Preventing osteoporosis: Lifelong nutrition and exercise habits are the most powerful weapons. ADVANCE for Nurse Practitioners, 10, 41–43, 76. Moore, C., Murphy, M. M., Keast, D. R., & Holick, M. F. (2004). Vitamin D intake in the United States. Journal of the American Dietetic Association, 104, 980–983. New, S. A. (2004). Intake of fruit and vegetables: Implications for bone health. Proceedings of the Nutrition Society, 62, 889–899. Nieves, J. W., Komar, L., Cosman, F., & Lindsay, R. (1998). Calcium potentiates the effect of estrogen and calcitonin on bone mass: Review and analysis. American Journal of Clinical Nutrition, 67, 18–24. North American Menopause Society. (2002). Management of postmenopausal osteoporosis: Position statement. Journal of the North American Menopause Society, 9, 84–101. Prynne, C. J., Mishra, G. D., O’Connell, M. A., Muniz, G., Laskey, M. A., Yan, L. et al. (2006). Fruit and vegetable intakes and bone mineral status: A cross-sectional study in 5 age and sex cohorts. American Journal of Clinical Nutrition, 83, 1420–1428. Rizzoli, R., Ammann, P., Chevalley, T., & Bonjour, J.-P. (2001). Protein intake and bone disorders in the elderly. Joint Bone Spine, 68, 383–392. Setchell, K. D. (1998). Phytoestrogens: The biochemistry, physiology, and implications for human health. American Journal of Clinical Nutrition, 68, 1333S–1346S. Stear, S. (2000). The role of diet in reducing the risk of osteoporosis. Community Nurse, 6(10), S7–S8. Tucker, K. L. (2003). Dietary intake and bone status with aging. Current Pharmaceutical Design, 9, 2687–2704.
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U.S. Department of Health and Human Services. (2004). Bone health and osteoporosis: A report of the surgeon general. Public Health Service, Office of the Surgeon General, Rockville, MD. Retrieved August 17, 2005, from http://www.surgeongeneral.gov/library/bonehealth/ Weaver, C. (2006). Calcium. In B. A. Bowman & P. M. Russell (Eds.), Present knowledge in nutrition (9th ed.). Washington, DC: International Life Sciences Institute, pp. 273–282. Welten, D. C., Kemper, H. C., Post, G. B., & van Staveren, W. A. (1995). A meta-analysis of the effect of calcium intake on bone mass in young and middle aged females and males. Journal of Nutrition, 125, 2802–2813.
Exercise Mandate: Preventative and Restorative
Exercise—Giving up a half-hour (one sitcom) of TV every day is all it takes. (Rankin, “Exercise: A Prescription for Osteoporosis?”)
T
8
he importance of sustained exercise over time cannot be overemphasized in the prevention and management of osteoporosis. Based on a growing body of evidence over the past several years, exercise has been supported as a means of maintaining good health in individuals of all ages, as well as preventing many diseases of the maturing adult. It is now possible to detect bone disease early, as well as to predict those individuals who are at a higher risk for developing bone disease and fractures. Exercise as a means of prevention and treatment of osteoporosis is extensively documented (Bassey, Rothwell, Littlewood, & Pye, 1998; Beverly, Rider, Evans, & Smith, 1989; Cussler et al., 2003; Heinonen et al., 1996; Kerr, Ackland, Maslen, Morton, & Prince, 2001; Kohrt, Ehsani, & Birge 1997; Snow, Shaw, Winters, & Witzke, 2000; Warden, Fuchs, & Turner, 2004; Winter & Snow, 2000). The effects of immobilization, bed rest, and spinal cord injury, as well as other skeletal unloading, can increase bone loss (Beck & Snow, 2003). These results in terms of bone loss can be taken to reflect the likely results for an aging adult with a sedentary lifestyle. The ability of exercise to improve bone strength through bone loading has been analyzed primarily through the use of bone mineral density (BMD) scans. Dual energy X-ray absorptiometry (DXA) is the standard method of measuring BMD in clinical and research settings. BMD describes the amount of mineral measured per unit area or volume of bone tissue (Kahn et. al., 2001; Kohrt, Bloomfield, Little, Nelson, & Yingling, 2004). Many factors that may affect BMD, such as nutrition, hormonal effects, and medications, are discussed in other chapters. Highlighted in this chapter
Renée M. Hakim Janet Ramos Grabo
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are recommendations relevant to exercise prescription in order to most greatly improve BMD across the lifespan, from both a preventative and a restorative perspective.
Preventative Risk Reduction for Fractures The goal of exercise should not only be to increase BMD but also to reduce the risk of fractures that occur with greater frequency in individuals with low bone mass. The mortality rate in the first year following hip fracture is 15%–20% (Schurch et al., 1996). It is estimated that the incidence of hip fractures will double to 2.6 million by the year 2025, with a greater increase in men than in women (Gullberg, Johnell, & Kanis, 1997). Because 90% of hip and 50% of spine fractures are associated with a fall, exercise should aim to improve peak bone mass, minimize bone loss in adulthood, and reduce the risk of falling (Beck & Snow, 2003). Exercise consideration should begin in childhood, because peak bone mineral accrual rate within a 2-year span of pubertal years is consistent with 26% of adult total body bone mineral (Bailey, 1997). The most commonly studied areas for changes in BMD are the hip, spine, forearm, and calcaneous (heel) (U.S. Department of Health and Human Services [USDHHS], 2004). Exercise may cause small gains in BMD and bone mineral content (BMC), while resulting in large improvements in bone strength because new bone formation is localized to the bone surfaces where there was the greatest mechanical stress (Robling, Burr, & Turner, 2001, 2002; Turner & Robling, 2005). The issue of how to overload a bone has been studied in varying forms. Breakthrough research by Hert, Liskova, and Landa (1971) established that bone tissue responds best to dynamic rather than static loading. Dynamic loading creates fluid movement in bone’s lacunar-canalicular network, which in turn generates shear stresses on the plasma membranes of resident osteocytes, bone lining cells, and osteoblasts. Bone cells are highly sensitive to fluid shear stresses. Therefore, high-impact exercises that produce high rates of deformation of the bone matrix are an effective application of mechanical forces (Turner & Robling, 2005). BMD is the most commonly used predictor for risk analysis of fractures (Beck & Snow, 2003); however, it should be noted that a general increase in strength, balance, and flexibility can be measures of decreased risk as well (USDHHS, 2004). A 12-week home-based trunk-strengthening exercise program developed by Chien, Yang, and Tsau (2005) was found to improve the quality of life of osteoporotic and osteopenic postmenopausal women. Twenty-eight postmenopausal women (mean age 60.3 ± 9.3 years) diagnosed with osteoporosis or osteopenia without fracture history were recruited and randomly assigned to exercise (n = 14) and control groups (n = 14). The study aimed to improve trunk strength, spinal range of motion, velocity, and quality of life (QOL), as well as to decrease disability (i.e., as measured by the Oswestry Disability Questionnaire [ ODQ ]). The 12-week exercise program included three sessions every day using an instructional booklet, after the initial instructional session. Exercises were selected by a physical therapist based on an individual’s abilities. The control
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group participants were asked to maintain their current lifestyle and diet. Statistically significant improvements were demonstrated in spinal range of motion (ROM) and motion velocity for the exercise group ( p < .05). Trunk flexor and extensor strength increased after exercise training ( p < .05) and the ODQ scores were improved ( p <.05) for the exercise group, while the controls showed no significant change. Although the sample size was small, exercise program adherence was over 90%, and none of the exercise group participants complained of discomfort during the strengthening period (Chien et al., 2005).
Life Span Considerations Exercise for children has recently been brought to the attention of the nation. While the growing rate of obesity in children has promoted this emphasis on exercise, studies have shown that increased activity in prepubertal years promotes greater maintenance of bone density in adults (Bakker, Twisk, Van Mechelen, Roos, & Kemper, 2003; Campbell et al., 1997; Kelley, 1998; Ulrich, Georgiou, Gillis, & Snow, 1999; Vainionpaa, Korpelainen, Leppaluoto, & Jamsa, 2005; Wolff, Van Croonenborg, Kemper, Kostense, & Twisk, 1999). During development, the bone surfaces are covered with a greater proportion of active osteoblasts than after skeletal maturity. Periosteal expansion occurs predominantly during this time. The addition of bone through exercise to the periosteal surface improves the bending and torsional strength of the bone. Resorption of bone from the periosteal surface is extremely rare in an adult; usually it is the trabecular, endocortical, and haversian bone surfaces that undergo remodeling. Therefore, the periosteal bone will remain intact and may reduce the fracture risk in adulthood (Karlsson et al., 2002; National Institutes of Health [NIH], 2000; Turner et al., 2005; Vainionpaa et al., 2005; Wallace & Cumming, 2000). Most of these findings are based on studies with children that were performed during school programs and lasted 7–20 months (Fuchs, Bauer, & Snow 2001; Kohrt, et al., 2004; MacKelvie, Khan, Petit, Janssen, & Mckay, 2003; MacKelvie, Khan, Petit, Moran, & Mckay, 2002; Mckay et al., 2000; Morris, Naughton, Gibbs, Carlson, & Wark, 1997; Petit et al., 2002). Research suggests that exercise has its greatest long-term effects when initiated in the prepubertal years, but less is understood about its effect during the peripubertal years (Beck & Snow, 2003). The effect of exercise on BMD is specific to the joint that receives the greatest load and can be diminished when the load no longer exists. Randomized, controlled trials have shown that training-induced changes in bone mass are maintained for 7 months to 3.5 years following the cessation of training (Braith, Mills, Welsch, Keller, & Pollock, 1996; Burr, 1998; Kohrt et al., 2004). Childhood behavior such as jumping and other weight-bearing activities that overload the skeleton are found to increase hip and spine BMC and BMD in prepubescent children, and this increase is maintained even after unloading of the joint has occurred (Beck & Snow, 2003; Bradney et al., 1998; Fuchs et al., 2001; Fuchs & Snow, 2002). During activities such as gymnastics, ground reaction forces can reach 6–8 times body weight, and even 10–15 times body weight with certain maneuvers. Ground reaction forces during walking or running are 1–2 times body weight (Kohrt et al., 2004; Mcnitt-Gray, 1993). One study by Morris et al. (1997) added weight lifting to high-impact loading exercises and found greater increases in the bone mass of the hip, spine, and total
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body. Maximizing peak bone mass in children and adolescents is discussed further in chapter 11. After the age of 40, regardless of sex or ethnicity, bone mass decreases approximately 0.5% per year (Kohrt et al., 2004). The greatest challenge is determining how to best influence BMD in those individuals found to be at risk for osteoporosis. An article by Drinkwater and McCloy (1994) recommended the implementation of five principles when planning an exercise program to increase bone mass: (1) specificity, (2) overload, (3) reversibility, (4) initial values, and (5) diminishing returns. That is, an exercise protocol should be designed to include the following: loading of the target bone, overloading the bone to stimulate it, awareness of bone loss when loading ceases, initial bone mass prior to overload, and the observation that early bone responses are more marked than ongoing responses. Randomized prospective and population-based studies of premenopausal women have shown positive results with regard to the effects of exercise on BMD (Bassey & Ramsdale, 1994; Friedlander, Genant, Sadowsky, Byll, & Gluer, 1995; Heinonen et al., 1996; Lohman et al., 1995; Snow-Harter, Bouxsein, Lewis, Carter, & Marcus, 1992; Vainionpaa et al., 2005). During early menopause, there is an accelerated bone loss due to ovarian changes; however, low-volume, high-resistance strength training and highimpact aerobics have been found to maintain BMD at the spine, hip, and calcaneous (Engelke et al., 2006). Preserving bone health in men is becoming more important as their life expectancy continues to increase. Research on osteoporosis in men is not as abundant as on osteoporosis in women because the fracture risk in men does not increase until the age of 80 or above (Cummings & Melton, 2002; Kohrt et al., 2004). A meta-analysis of exercise studies using male subjects concluded that exercise can improve or maintain BMD (Kelley, Kelley, & Tran, 2000). Studies of moderate- to high-resistance training in older men found improved BMD, especially at the femur (Braith et al., 1996; Maddalozzo & Snow, 2000; McCartney, Hicks, Martin, & Webber 1995; Menkes et al., 1993; Yarasheski, Campbell, & Kohrt, 1997). Most findings were much the same as those regarding the changes in BMD found in women with the same types of exercise programs (Kohrt et al., 2004). For older adults, exercise can increase muscle mass and strength in frail individuals, even those over 90 years of age (NIH, 2000). Evidence suggests that exercise can also improve function, decrease loss of independence, and therefore enhance the quality of life of elderly persons (USDHHS, 2004). Randomized clinical trials have shown exercise to reduce the risk of falls by as much as 25% (NIH, 2000).
Bone Loss and Skeletal Loading While it is known that unloading the skeleton can initiate bone loss, little is known about the need for rest during skeletal loading. A study by Umemura, Ishiko, Yamauchi, Masashi, and Mashiko (1997) conducted on animals showed that bone cells become desensitized to prolonged mechanical stimulation. After 24 hours of rest, 98% of bone mechanosensitivity returns. The potential for exercise to be beneficial increases when the exercise is divided into two short sessions separated by 8 hours. However, further division into three sessions with 4 hours rest did not further improve the results. Therefore, it appears more beneficial to shorten each exercise session rather than decrease the number of sessions, when trying to reduce exercise time (Turner & Robling, 2003; Turner & Robling, 2005). It
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requires 3–4 months for one remodeling cycle to complete the sequence of bone resorption, formation, and mineralization. A minimum of 6–8 months is necessary to achieve a measurable bone mass change (Kohrt et al., 2004; Mundy, 1999).
Exercise Recommendations—Preventative Numerous studies have been conducted on the effects of various exercise protocols on bone strength for subjects of both genders across the lifespan. There are recommendations available from the American College of Sports Medicine (ACSM), the surgeon general (USDHHS, 2004), and the National Institutes of Health (NIH), as well as several metaanalyses, systematic reviews, and clinical practice guidelines (CPGs). With respect to exercise prescription, these sources of evidence can be summarized to provide suggestions for the physical activity component of a preventative approach to osteoporosis management. In children, there are several types of exercises that can be used to augment bone mineral accrual. Gymnastics, plyometrics, and jumping activities, as well as moderate resistance training, are suggested (American College of Sports Medicine [ACSM], 1998a; Brown & Josse, 2002; USDHHS, 2004). Most sports that children participate in, such as baseball, basketball, and soccer, are associated with improved BMD (Brown & Josse, 2002). Nonimpact exercises (such as swimming) are of little benefit with respect to improving BMD (Brown & Josse, 2002; Cassell, Benedict, & Specker, 1996; Courteix et al., 1998). High-intensity forces at less than 60% of one repetition maximum (RM), at least 3 days per week, for 10–20 minutes twice a day should be included (Kohrt et al., 2004). In adulthood, the goal is to preserve bone health. Tennis, stair climbing, jogging, or other weight-bearing endurance activities that involve jumping, such as volleyball and basketball, are recommended, in addition to resistance training (USDHHS, 2004; Brown & Josse, 2002). The ACSM (1998a) suggests moderate to high bone-loading forces 3–5 times per week, with resistance exercise 2–3 times per week. A combination of these activities for 30–60 minutes per day will target all muscle groups (Kohrt et al., 2004). Special consideration has been given to adult female populations in relation to menopause. In a systematic review of studies aimed at the prevention of osteoporosis through the effects of exercise on BMD in postmenopausal women, the Cochrane review (Shea et al., 2004) subdivided the programs into three groups: (1) aerobic exercise, (2) muscle strengthening with machines, and (3) walking at different speeds. The aerobic exercise group, which consisted of calisthenics, fitness and muscular strengthening, exercise with elastic or with weights, and a little walking, showed effects in the lumbar spine but not at the hip. The resistance group showed significant effects at both the lumbar spine and the hip. The walking group was shown to have significant effects only at the level of the backbone (Shea et al., 2004). Premenopausal and postmenopausal women have also been included in studies that examined the effects of exercise in addition to the influence of hormone replacement therapies. Some studies have indicated that walking and jogging were more effective in increasing bone mass than nonimpact resistance training (Kohrt et al., 1997; Warden et al., 2004). Others showed the effectiveness of resistance training in improving BMD (Beverly et al., 1989; Cussler et al., 2003; Kerr et al., 2001; Nelson et al., 1994; Warden et al., 2004). Studies that focused on moderate load exercises have found no significant changes in BMD in the older adult (Greensdale et al., 2000; Shaw & Snow, 1998; Uusi-Rasi et al., 2003; Warden et al., 2004).
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For older adults, physical activity should be aimed at improving muscle strength in order to reduce falls. The surgeon general (USDHHS, 2004) suggests resistance training and aerobic exercise. Balance training is also an essential part of risk reduction. Weight-bearing activities that improve postural stability, such as Tai Chi, are also recommended (NIH, 2000). In order to maintain the benefits of exercise, 30–45 minutes, 3 times per week, for at least 3 months is advised (USDHHS, 2004). Exercise programs are also recommended for the frail elderly. Physical activity as health permits will preserve skeletal integrity and should include weight-bearing endurance and resistance training. Activities should also be designed to improve balance and prevent falls (Kohrt et al., 2004). Certain activities should be avoided when an individual has already sustained a fracture. Rehabilitation following fractures is discussed later in this chapter. Refer to Table 8.1 for a summary of recommendations across the life span. Table 8.2 provides a review of recent literature, describing some of the specific exercise protocols used and the findings in relation to impact on BMD.
Table
Evidence-Based Exercise Recommendations for Targeted Groups Across the Life Span to Prevent Osteoporosis
8.1
Exercise recommendations Target groups Chil• dren
Adults
Type Gymnastics, plyometrics, jumping activities, moderate resistance traininga, b, c, d, e, f, g
• Tennis, stair climbing, jogging, volleyball, basketball (jumping), resistance traininga, h, i
Elderly • Weight-bearing endurance exercises, and resistive traininga • Balance and postural stability exercises to prevent fallsb, c, h, i, j
•
•
Intensity High impact (at less than 60% of 1 RM*)a Moderate to high impacta
• As health permits to preserve skeletal integrityb, c, h, i, j
•
Frequency/duration 3 days per week, 10–20 minutes twice a daya
•
3–5 times per week (activities)a • 2–3 times per week (resistance training )a • A combination of both, 30–60 minutes per daya •
30–45 minutes, 3 times per week for at least 3 monthsb, c • Maintain active daily lifestyleb, c, h, i, j
*
repetition maximum
a
American College of Sports Medicine, 1998a; bU.S. Department of Health and Human Services, 2004; cShea et al., 2004; Bradney et al., 1998; eCourteix et al., 1998; fKarlsson et al., 2002; gCourteix et al., 1998; hKohrt, Bloomfield, Little, Nelson, & Yingling, 2004; iMcCartney, Hicks, Martin, & Webber, 1995; jEngelke, Kemmler, Lauber, Beeskow, Pintag, & Kalender, 2005. d
8.2
Table
Setting: clinical vs. home/ control
Low-volume/ high-impact program for postmenopausal women b
Setting: clinical vs. control
Type of program High-impact program for premenopausal womena
•
•
•
•
•
137 postmenopausal women (average = 55) Randomized into exercise group (n = 48) or control group (n = 30) Inclusion criteria: osteopenia at the lumbar spine or total proximal femur (–1 >DXA T-score > –2.5 SD)
Participants 120 premenopausal women (age 35–40 years) randomized into exercise (n = 39) and control (n = 41) groups No baseline group differences in weight, height, calcium intake, menarcheal age, exercise frequency, and activity level
Home/Control Group: • 2 home training sessions per week, 25 minutes each
Exercise Group: • 2 group sessions per week 60–70 minutes each
Control Group: • Usual activities
Intensity Exercise Group: • Training sessions 3 times a week for 12 months with a physical therapist • 60 minutes total with 10 minutes warm-up and cool-down; 40 minutes high-impact training; Plus daily home program (10 minutes)
At 6 months: jumping phase introduced including: rope skipping, 4 sets of 15 simple multidirectional jumps;
Exercise Group: First 3 months: warm-up; gradually increased walking and running; running games added (at 70%–80% HRmax); increasing amount of high-impact aerobics concluded the sequence for 20 minutes
Control Group: No prescribed exercise
High-impact exercise: step patterns, stamping, jumping, running, walking 3 months later 10 cm step 6 months later 2–3 steps Progression: higher j umps & drops added; plus 10-minute daily home program of similar patterns of exercise
Intervention details Exercise Group: Warm-up: walking, running in place, with/without arm movements/knee bends
•
•
•
•
(Continued)
Significant decreases ( p < .001) in pain frequency and intensity in the spine in the exercise group and increased in the control group, while no betweengroup differences were detected in the main joints Low-volume/high-intensity exercise program successful in maintaining BMD at the spine ( p <.001), hip ( p <.001),
Outcomes Exercise group demonstrated significant increase in femoral neck BMD ( p = .003), intertrochanteric BMD ( p = .029), total femoral BMD (p = .006), and L1 BMD ( p = .002) and calcaneal broadband ultrasound attenuation ( p = .015) No significant differences between or within groups in the distal forearm, or L2–4
Specific Examples of Exercise Protocols Used for Preventive Osteoporosis Management
8.2
Table
Type of program
Participants
Intensity
Home/ Control Group: 20–25 minute sessions twice per week; rope skipping, isometric and belt exercises, as well as stretchingd
At 7 months training: two high-intensity cycles (12 weeks each) and a 5 week regeneration period of constant intensity (50% 1 RM) and volume (13 exercises, 2 sets and 20 repetitions); second part of strength training: isometric exercises and exercises with elastic belts, dumbbells, and weighted vests; 2–4 sets of bench presses; one arm dumbbell rowing, and squats with weighted vests and boxes, performed parallel to the high-intensity machine training; 1–2 sets of passive stretching at 30 seconds for each major muscle group, before and after the strength sequence and during the rest periods
Intervention details strength training: with machines for all major muscle groups, 2 sets of 20 repetitions at 50% 1 repetition maximum (RM)
Outcomes and calcaneous ( p < .001), but not at the forearm
Specific Examples of Exercise Protocols Used for Preventive Osteoporosis Management (continued)
Setting: clinical vs. home
Exercise training (added to ongoing hormone replacement therapy/ HRT) in frail elderly women c
•
•
•
•
28 frail elderly women aged 75– 87 on HRT, who remained on HRT for the duration of the study Randomized into supervised (n = 14) and home exercise/placebo (n = 14) groups Inclusion criteria: mild to moderate physical frailty, based on peak endurance power of 11 to 18 mL/ kg/min, modified physical performance test score of 18–32, and difficulty or needed assistance with at least one activity of daily living (ADL) Exclusion criteria: existing medical condition that contraindicated exercise, HRT, Home/Control Group: • low impact exercise performed 2–3 times a week, plus a monthly exercise class
Exercise Group: • 3 exercise sessions per week, lasting 90–120 minutes; progressive highimpact program: 36 sessions in each of 3 phases completed prior to progressing to next phase
Phase 3: endurance exercises added to a core of phase 1 and 2 exercises including:
Phase 2: added progressive high-impact intensity training to a core of phase 1 exercises; resistance program: squats, leg press, knee extension, knee flexion, seated row, upright row, bench press, biceps curl, and triceps extension; 1RM was determined; weight lifting: 1–2 sets of 8–12 repetitions at 65% of 1 RM; volume increased to 2–3 sets of 6–8 repetitions at 75%–85% of 1 RM
Exercise Group: Phase 1: 22 exercises to improve flexibility, balance, coordination, and a modest degree of strength
Both groups were supplemented with calcium and vitamin D
•
•
•
•
(Continued)
Significant changes in BMD at the lumbar spine ( p = .048) in women who performed the exercise program, who were already on HRT; other sites not statistically significant Strong trend toward large increases of total body BMD in response to the exercise program ( p = .058) Significantly improved muscle strength at 9% –30% ( p < .05), which may reduce the risk for falls Significantly decreased body weight ( p = .018), while not recommended, was due to a decrease in fat mass, which in the elderly can contribute to functional disability (weight –2.2 ± 0.3 kg; and fat mass –2.7 ± 0.4 kg)
8.2
Table
a
or could influence bone loss; diagnosis of cancer within 5 years; thromboembolic disease; use of boneacting drugs in the previous year; and sensory or cognitive impairment
Participants
Intensity
Home/ Control Group: Consisted of 9 of the 22 phase 1 exercises; provided a low level of physical activity (not expected to produce any effect on BMD); exercises performed 2–3 times a week, plus a monthly exercise class
walking, cycling, and rowing; goal to exercise 15 minutes at 65%–75% of peak heart rate and progress rapidly to 30 minutes of exercise; four 5-minute intervals at 85%–90% of peak heart rate added after 4–6 weeks; combined with 3–4 minutes of low-intensity exercise
Intervention Details
Vainionpaa, Korpelainen, Leppaluoto, & Jamsa, 2004; bEngelke 2006; cVillareal et al., 2003; dKemmler et al. 2004.
Type of Program
Outcomes
Specific Examples of Exercise Protocols Used for Preventive Osteoporosis Management (continued)
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Restorative Despite the recent effort to improve prevention of osteoporosis, the problem of fractures among older adults remains. As previously noted, the most commonly researched sites for osteoporotic fracture are the hip, spine, and wrist (USDHHS 2004). Typically, the most disabling location for fracture occurs at the hip (NIH, 2000). Hip fractures occur most commonly in elderly females (90% 65 or older and 75% female) (Ingemarsson, Frandin, Mellstrom, & Moller, 2003). Hip fractures are associated with functional decline and high mortality rates of 10% to 28% at 6 months (Keene, Parker, & Pryor, 1993; Magaziner et al., 2000). Fewer than half of patients with hip fractures regain their prefracture status (Marotolli, Berkman, & Cooney, 1992). In contrast, approximately two-thirds of spine fractures go undiagnosed because there is little or no pain, or the pain is attributed to one of the many other causes of back pain (Johnell et al., 2002). However, spine fractures that are identified typically cause increasing levels of spinal deformity and pain, often resulting in progressive functional decline. The magnitude of individual loss, social consequences, and costs resulting from these injuries has promoted the development of new strategies for postsurgical care following osteoporotic fractures (as described elsewhere in this book). With respect to hip fractures, treatment following injury is typically multidisciplinary. The health care team commonly includes the orthopaedic surgeon, medical specialists (e.g., geriatricians, physiatrists), primary care physicians, nurses, physical and occupational therapists, nutritionists, and social workers. Whenever possible, the acute hospital care should be guided by the use of evidence-based clinical care pathways that utilize standardized evaluation and management approaches. This approach should also extend across the entire continuum of care whenever possible; from the acute care hospital into the subacute, rehabilitation, or skilled nursing facility, or into home health (USDHHS, 2004). Effective communication across health care settings by the health care providers is also important to effective clinical management (Morris & Zuckerman, 2002). Following medical management of the fracture, rehabilitative therapy is initiated with the primary goal to restore functional ability in a variety of settings as noted above. There are several approaches to rehabilitation following fracture, such as specialized geriatric orthopaedic rehabilitation units (GORUs), geriatric hip fracture programs (GHFPs), and early supported discharge programs (ESDPs), as well as the of use of clinical pathways or a combination of programs. According to a systematic review of geriatric rehabilitation following fracture in older adults by Cameron et al. (2000), GHFPs and ESDPs are probably cost-effective, because they appear to shorten the average length of hospital stay and are associated with significantly increased rates of return to previous residential status. GORUs are unlikely to be cost-effective, but some more frail patients may benefit with respect to reduced readmission rates and need for nursing home placement. There is weak evidence that use of formal clinical pathways may be advantageous (Cameron et al., 2000).
Exercise Recommendations—Restorative Hip Fractures The majority of patients with hip fractures should be encouraged to become mobile by the first or second postoperative day. Early mobility can help prevent secondary
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complications associated with prolonged bed rest, such as muscle atrophy, blot clots in the legs or lungs, skin breakdown, and overall deconditioning (USDHHS, 2004). In the acute care hospital, rehabilitation focuses on early mobility skills, such as transferring in and out of bed and walking with an assistive device, while maintaining any postsurgical precautions prescribed by the surgeon. Because the inpatient hospital stay is typically 2–3 days after surgery, most patients require transfer to a rehabilitation facility. During the inpatient rehabilitation stay, the clinical management focuses on general conditioning, strengthening exercises, and walking ability on different terrains and with decreasing levels of assistance (USDHHS, 2004). The degree to which the patient progresses depends upon the type of surgery and implanted device, as well as the prefracture physical condition and comorbidities of the patient. Approximately 85% of patients continue to use an assistive device for walking at 6 months after the fracture (Marotolli et al., 1992). Following discharge to the home or to another assisted-living facility, rehabilitation is typically continued on site or at an outpatient facility. The focus of therapy among the more frail patients is predominantly to minimize the risk of falling and optimize functional outcomes. The Chartered Society of Physiotherapy (CSP) clinical practice guidelines (1999) recommend that exercise training start at a very low intensity using low-impact exercises. Strength training should use very short levers or body resistance. All exercise programs should be progressive in terms of intensity and impact (ACSM, 1998b; Chartered Society of Physiotherapy [CSP], 1999).
Spine Fractures It is not uncommon for patients to have prolonged pain and functional limitations following spine fractures (USDHHS, 2004). Clinical management of spine fractures typically focuses on pain control and progressive levels of physical activity. Recent advances in surgical procedures, such as vertebroplasty and kyphoplasty, have the potential to stabilize spine fractures, prevent further collapse, and provide effective pain relief (Evans et al., 2003; Liberman, Dudeney, Reinhardt, & Bell, 2001). Following medical management of spine fractures, pain control is a high priority. During the acute rehabilitation phase, bed rest should be intermittent, interspersed with 30–60-minute periods of erect sitting, standing, and walking, and limited to 4 days or less in duration (USDHHS, 2004). Instruction in proper body mechanics and posture is essential. Patients should be taught to properly position themselves while sitting, standing, or lying down and to move safely when lifting, dressing, and doing housework. The maintenance of good posture should be stressed in order to reduce loads on the fracture and minimize pain. The short-term use of a back brace/orthosis is recommended when trunk weakness and/or pain prevent a patient from maintaining an upright posture (CSP, 1999; USDHHS, 2004). In addition, modification of activities or the use of caregiver assistance should be encouraged to reduce the risk of a new spine fracture (Bonner et al., 2003). During the subacute rehabilitation phase, walking should be encouraged, even in frail individuals. A gradual progression starting at 2–3 minutes and working up to 20 or more minutes can be achieved by adding a few minutes to walking sessions each week (USDHHS, 2004). If walking is limited because of pain, the use of a rolling walker
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(which allows pushing rather than lifting) may help the patient stay active during recovery, thus preventing further loss of strength and bone mass. In cases when a back brace is used, weaning from the device as muscle strength and endurance improve will maximize recovery. However, in some patients with chronic pain and deformity, continued use of a flexible support device may be helpful in reducing pain and improving function (Pfeifer, Begerow, & Minne, 2004). Throughout rehabilitation, exercise should be an important component to address strength, range of motion, and balance. Active ROM exercises should be continued throughout recovery, but resistance training should not be initiated or resumed until the fracture has healed (in approximately 8–12 weeks; USDHHS, 2004) Because the risk of recurrent spine fracture is high, patients should be instructed to avoid exercises and activities that put high loads on the spine, such as forward bending or twisting the trunk (USDHHS, 2004). Exercises and activities performed with good spinal alignment and low to moderate amounts of weight should be gradually increased, with the goals of regaining strength and promoting maintenance of bone mass. Abdominal strengthening (by tightening stomach muscles without moving the back) is safe and important to reducing loads on the low back. Spinal extension exercise (moving the trunk backward) within a moderate range is safe and can improve posture and may help prevent new spine fractures (Sinaki et al., 2002). Home-based exercises should be encouraged to increase physical activity and improve outcomes following spinal fracture. Papaioannou et al. (2003) studied postmenopausal women aged 60 years or older with symptomatic osteoporosis-related vertebral fractures (within the past 3 months) who participated in a 6-month home exercise program. The program included stretching, strength training, and aerobic exercise such as walking; these were described and illustrated in a manual and were completed for 60 minutes on 3 days each week. The authors found significant improvements in the quality of life in the domains of symptoms ( p = .03), emotion ( p = .01), and leisure ( p = .03) at 6 months, as well as improved balance ( p < .05) over 12 months as compared with a control group.
Wrist Fractures During the healing of a wrist fracture, clinical management should include early mobilization of the hand, elbow, and shoulder; arm elevation; and control of swelling. Rehabilitation of the wrist begins after the cast, brace, or surgical metal is removed. Progressive exercises typically include active and passive ROM exercises and resistance training for the wrist and grip, as well as functional training. A systematic review of rehabilitation for distal radius fractures in adults by Handoll, Madhok, and Howe (2002) found weak evidence (secondary to methodological flaws) in support of formal rehabilitation programs, passive mobilization, and whirlpool/hydrotherapy. A small number of patients may suffer from sympathetic dystrophy (i.e., complex regional pain syndrome) after wrist fracture, which results in swelling, weakness, and chronic pain at the wrist, thereby limiting recovery (USDHHS, 2004). Although most patients return to an adequate level of functioning following wrist fracture, many experience persistent loss of ROM at the wrist (USDHHS, 2004). For all of the targeted rehabilitation populations described above, balance activities should be included to improve safety and reduce fall risk. The exercise program should
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be accompanied by an assessment of fall risk and a reduction of modifiable fall risk factors as outlined elsewhere in this book. Modalities may also be an effective component of treatment for patients in need of pain management in any of the targeted groups. Hydrotherapy programs may be more tolerable than exercise on land, as the buoyancy provided by the water allows greater ease of movement with less pain. Aquatic exercise is also a very useful modality to build confidence in frail patients and those with a fear of falling (CSP, 1999). Transcutaneous electrical nerve stimulation (TENS) has been shown to be effective in some patients with chronic pain conditions (Gadsby, Bennett, & Flowerdew, 1995; Scottish Intercollegiate Guidelines Network [SIGN], 2003). TENS should be considered as a modality for patients with intractable pain, especially those with chronic back pain and recent vertebral fractures (CSP, 1999). In addition, applied heat has several possible benefits, such as reducing muscle spasms, increasing local blood flow, and stimulating an analgesic effect (Minor & Sanford, 1993). Patients should be instructed on how to use heat therapy safely at home to relieve pain symptoms (CSP, 1999). Relaxation techniques can also be used to help reduce muscle tension and anxiety (Takagi, 1992). For an overview of the rehabilitative management of targeted populations, refer to Table 8.3.
Table
8.3
Evidence-Based Restorative Exercise Recommendations for Targeted Groups Following Osteoporotic Fractures Target groups Patients status post (s/p) hip fracture
Patients s/p spine fracture
Exercise recommendations • Acute/hospital setting: Early mobility skills, such as transferring in and out of bed and walking with an assistive devicea • Inpatient rehabilitation setting: General conditioning, strengthening exercises, and walking ability on different terrains and with decreasing levels of assistancea • Home/assisted living facility or outpatient setting: Minimize the risk of falling and optimize functional outcomesa Acute phase: • Intermittent bed rest, interspersed with 30–60 minute periods of erect sitting, standing, and walking, and limited to 4 days or less in durationa • Instruction in proper body mechanics and posture; short-term use of a back brace/orthosisa, b
•
•
•
•
• • • •
Precautions Maintain any postsurgical precautions (e.g., ROM guidelines, weight-bearing status)a Start exercise training at a very low intensity using low-impact exercisesb Strengthening exercise should use very short levers or body resistance (not weights)b Progress all exercise programs in terms of intensity and impactb, c
Provide pain control as a high prioritya Advise gradual progression of physical activitya, b Promote proper body mechanics and posturea, b Modify activities or use caregiver assistance to reduce the risk of a new spine fractured
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Table
(Continued)
8.3
Target Groups
Exercise recommendations Include exercise addressing strength, range of motion, and balance performed with good spinal alignmenta, b • Continue active range of motion exercise throughout recoverya •
Subacute phase: • Progress activity level; walking program, even in frail individuals: starting at 2–3 minutes and working up to 20 or more minutesa • Low to moderate amounts of weight should be gradually increased; include abdominal strengthening and spinal extension exercisef • Modalities as indicated for pain management (e.g., aquatics, TENS, heat)b • Home exercise following discharge: stretching, strength training and aerobics (walking), 60 minutes on 3 days per weekg Patients s/p wrist fracture
•
•
•
a
During healing of the fracture: early mobilization of the hand, elbow and shoulder, arm elevation, and control of swellinga, h After the cast, brace or surgical metal is removed: progressive exercises including active and passive range of motion exercises and resistance training for the wrist and gripa Use of modalities such as hydrotherapyh
•
•
•
•
•
Precautions Do not initiate resistance training until the fracture has healed (in approximately 8–12 weeks)a Avoid exercises and activities that put high loads on the spine, such as forward bending or twisting the trunka If walking is limited because of pain, encourage use of a rolling walker (which allows pushing rather than lifting)a, b Wean from back brace to prevent dependency on device (some patients with chronic pain and deformity prefer continued use of a flexible support device to help reduce pain and improve function)e
Monitor for sympathetic dystrophy (i.e., complex regional pain syndrome): swelling, weakness, and chronic pain at the wrista
U.S. Department of Health and Human Services, 2004; bChartered Society of Physiotherapy, 1999; American College of Sports Medicine, 1998b; dBonner et al., 2003; ePfeifer, Begerow, & Minne, 2004; f Sinaki et al., 2002; gPapaioannou et al., 2003; hHandoll, Madhok, & Howe, 2002. c
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General Considerations Exercise Safety One of the concerns with regard to initiating any kind of exercise program is the risk of injury. A study by Hagberg et al. (2001) raised the possibility that an exercise intensity that is too high may negatively affect bone formation. It is possible that vigorous exercise that is performed repeatedly could lead to an accumulation of microdamage to the bone (USDHHS, 2004). Decreases in bone mass, trabecular thinning, and structural properties in response to very intense or excessive exercise have been observed in growing animals (Forwood & Burr, 1993; Iwamoto, Yeh, & Aloia, 1999; Kohrt et al., 2004; Notomi et al., 2001; Yingling, Davies, & Silva, 2001). However, no specific data to this effect have been clinically documented in humans, and therefore the topic needs to be further researched. It should be noted that in every one of the preventative studies outlined previously there were no injuries documented as a result of the training programs. Even during the high-intensity program developed by Engelke et al. (2005), pain reports did not increase. The authors attribute this response to a slow progression of exercise intensity and impact during the first months, not maximizing the number of repetitions at a given load, interrupting heavy-loading periods, and varying the intensity and volume within the heavyloading periods. The risk of injury from high-impact exercise in healthy premenopausal women is minor, and therefore this type of exercise can be considered an appropriate prevention tool (Engelke et al., 2006). In general, high-impact exercise is inappropriate and unsafe if an individual suffers from joint disease or pelvic floor dysfunction; if the exercise cannot be performed with the correct technique; or if the design of the program is not based on sound exercise principles and individual needs or precautions (CSP, 1999). For restorative purposes, all exercise programs should start at an easy level and be progressive in terms of intensity and impact. All precautions imposed as part of medical management (e.g., ROM guidelines and weight-bearing status) should be adhered to strictly when indicated. To safely address the targeted rehabilitation populations, the following activities should be avoided: high-impact exercises, trunk forward bending (flexion), trunk twisting (rotation) with any loading, and lifting (CSP, 1999).
Education and Exercise Adherence One of the greatest challenges in both the preventative and rehabilitative management of individuals with respect to osteoporosis is promoting exercise as a lifelong habit. Individuals must be instructed on how to exercise safely and avoid potential risks. Both the benefits and barriers to participating in a regular exercise regimen should be addressed. Additionally, a program must be established that meets the needs of the participants. Peer support and self-management techniques may be helpful (Owen, Lee, & Sedgwick, 1987). Many individuals may enjoy participating in exercise groups at leisure facilities and sports centers. Health care providers should forge relationships with local leisure and sport facilities (and possibly contribute to the training of fitness instructors) in order to promote the continuation of safe and effective exercise opportunities for the targeted groups outside of health care settings (CSP, 1999). However, some people may not like exercising in a group and should be encouraged to adopt an active lifestyle that includes exercising at home.
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In order to provide a framework for program development, theories of health behavior, such as the Health Belief Model (Becker, 1974), Social Cognitive Theory (Bandura, 1986), and Stages of Change (Prochaska & DiClemente, 1983), help to identify the targets for change and the methods for accomplishing these changes. Theory-driven health promotion and education programs are more likely to be effective in promoting lifestyle changes, particularly when the goal is to form a lifelong habit of regular exercise. A description of health behavior theory and application are beyond the scope of this chapter. A resource such as the text by Glanz, Lewis, and Rimer (1997) is recommended. With respect to program convenience, a follow-up study by Kerschan et al. (1998) examined adherence to a standard, nonprogressive exercise program carried out in the home. They found a 36% adherence level after 7.7 years. Most individuals were not willing to spend a large amount of time on prevention; therefore the authors of the Erlangen Fitness Osteoporosis Prevention Study (EFOPS) stated that their subjects’ time was used most effectively by using a low to moderate training volume (<3 hours/week), with a moderate to high intensity. Because adherence to supervised sessions was moderately low, 1–2 hours of high-impact exercise plus two home-based exercise sessions appeared sufficient for benefits to occur (Engelke et al., 2006). Aerobic and step exercises are popular, and appear to be sound options (Vainionpaa et al., 2005). Based on personal preference, many individuals self-prescribe a regimen of walking as therapy and as a means of promoting general well-being. Adherence to this type of program would likely be greater than most, since it can easily be incorporated into the daily routine of activities (Brooke-Wavell, Jones, Hardman, Tsuritani, & Yamada, 2001). In a meta-analysis of studies related to walking in postmenopausal women and men aged 50 years and older by Palombaro (2005), it was shown that there was a positive effect on increasing BMD in the lumbar spine ( p<.03). However, there was no significant effect on the calcaneous and femur (Hartori et al., 1993; Martin & Notelovitz, 1993). The amount of increase in BMD at these skeletal sites does not support the use of walking-only programs as a means to maintain or increase BMD (Palombaro, 2005). While walking alone to affect BMD may not be optimal, women who reported walking at least 4 hours per week had a 41% lower risk of hip fracture compared with sedentary women or those who walked less than 1 hour per week (Burr, 1998; Nichols, Sanborn, & Love, 2001). Studies have consistently shown that women with low-activity-level lifestyles have a higher incidence of fractures than those who maintain high activity levels (Chapurlat, Bauer, Nevitt, Stone, & Cummings, 2003; Cummings et al., 1995; Feskanich, Willett, & Colditz, 2002; Hoidrup et al., 2001; Warden et al., 2004). A successful exercise program, especially for older adults, should build on individuals’ previous habits, tapping any existing skills. Most importantly, exercise must be perceived as personally rewarding. Health care providers can encourage exercise as a means of escaping from physical dependency, earning respect from significant others, and gaining personal fulfillment (CSP, 1999).
Summary Exercise as prevention of osteoporosis should begin at an early age. It has been found that the prepubertal years are the most crucial years to affect periosteal expansion (Karlsson
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et al., 2002; NIH 2005; Turner & Robling 2005; Vainionpaa et al., 2005; Wallace & Cumming, 2000). Promoting exercise and high-impact activities in children will instill in them the importance of maintaining bone strength. For the adult male and premenopausal woman at risk for osteoporosis, high-impact exercise varied with resistance and endurance training can improve BMD and muscle strength and prevent the decline of balance and flexibility that may occur with the natural aging process. Individuals at high risk for fractures and those who have been diagnosed with osteoporosis would do well in a supervised exercise program designed to maintain BMD and prevent falls (USDHHS, 2004). Prescribed exercise is also an essential component of rehabilitative management for those who sustain osteoporotic fractures. All exercise programs should begin at an easy level and be progressive in terms of intensity and impact (ACSM, 1998a; USDHHS, 2004). Precautions should be taken to avoid high-impact activities, and to maintain the restrictions indicated by the physician or any existing comorbidities (USDHHS, 2004). The primary goals are to restore functional ability and reduce the likelihood of recurrent injury. All exercise programs should begin with supervision. Not every individual’s needs will be the same, and individuals will require personalized yet comprehensive exercise programs. Adherence will remain a concern with regard to any type of program; therefore, it is essential that the importance of prevention be enforced by clinicians and families alike. It is also vital to our society that we continue to explore the effectiveness of these programs in order to best provide quality care.
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Kerr, D., Ackland, T., Maslen, B., Morton, A., & Prince, R. (2001). Resistance training over 2 years increases bone mass in calcium-replete postmenopausal women. Journal of Bone and Mineral Research, 16, 175–181. Kerschan, K., Alacamlioglu, Y., Kollmitzer, J., Wober, C., Kaider, A., Hartard, M., et al. (1998). Functional impact of unvarying exercise program in women after menopause. American Journal of Physical Medicine and Rehabilitation, 77, 326–332. Kohrt, W. M., Bloomfield, S. A., Little, K. D., Nelson, M. E., & Yingling, V. R. (2004). Physical activity and bone health. Medicine and Science in Sports and Exercise, 27, 1985–1996. Kohrt, W. M., Ehsani, A. A., & Birge, S. J. (1997). Effects of exercise involving predominantly either joint reaction or ground reaction forces on bone mineral density on older women. Journal of Bone and Mineral Research, 12, 1253–1261. Liberman, I. H., Dudeney, S., Reinhardt, M. K., & Bell, G. (2001). Initial outcome and efficacy of “kyphoplasty” in the treatment of painful osteoporotic vertebral compression fractures. Spine, 26(14), 1631–1638. Lohman, T., Going, S., Pamenter, R., Hall, M., Boyden, T., Houtkooper, L., et al. (1995). Effects of resistance training on regional and total bone mineral density in premenopausal women: A randomized prospective study. Journal of Bone and Mineral Research, 10, 1015–1024. MacKelvie, K. J., Khan, K. M., Petit, M. A., Janssen, P. A., & Mckay, H. A. (2003). A school-based exercise intervention elicits substantial bone health benefits: A 2-year randomized controlled trial in girls. Pediatrics, 112, e447. MacKelvie, K. J., Khan, K. M., Petit, M. A., Moran, O., & Mckay, H. A. (2002). Bone mineral response to a 7-month randomized controlled, school-based jumping intervention in 121 prepubertal boys: Associations with ethnicity and body mass index. Journal of Bone and Mineral Research, 17, 834– 844. Maddolazzo, G. F., & Snow, C. M. (2000). High intensity resistance training: Effects on bone in older men and women. Calcified Tissue International, 66, 399–404. Magaziner, J., Hawkes, W., Hebel, J. R., Zimmerman, S. I., Fox, K. M., Dolan, M., et al. (2000). Recovery from hip fracture in eight areas of function. Journal of Gerontology Series A: Biological Sciences and Medical Sciences, 55, M498–M507. Marotolli, R. A., Berkman, L. F., & Cooney, L. M. (1992). Decline in physical function following hip fracture. Journal of the American Geriatrics Society, 40, 861–866. Martin, D., & Notelovitz, M. (1993). Effects of aerobic training on bone mineral density of postmenopausal women. Journal of Bone and Mineral Research, 8, 931–936. McCartney, N., Hicks, A. L., Martin, J. L., & Webber, C. E. (1995). Long-term resistance training in the elderly: effects on dynamic strength, exercise capacity, muscle, and bone. Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 50, B97–B104. Mckay, H. A., Schultz, W., Prior, J. C., Barr, S. I., Khan, K. M., & Petit, M. A. (2000). Augmented trochanteric BMD after modified physical education classes: A randomized school-based exercise intervention study in prepubescent and early pubescent children. Journal of Pediatrics, 136, 156–162. Mcnitt-Gray, J. L. (1993). Kinetics of the lower extremities during drop landings from three heights. Journal of Biomechanics, 26, 1037–1046. Menkes, A., Mazel, S., Redmond, R. A., Koffler, K., Libanati, C. R., Gundberg, C. M., et al. (1993). Strength training increases regional BMD and bone remodeling in middle-aged and older men. Journal of Applied Physiology, 74, 2478–2484. Minor, M. A., & Sanford, M. V. (1993). Physical interventions in the management of pain in arthritis. Arthritis Care Research, 6(4), 197–206. Morris, A. H., & Zuckerman, J. D. (2002). AAOS Council of Health Policy and Practice, USA. American Academy of Orthopaedic Surgeons. National Consensus Conference on Improving the Continuum of Care for Patients with Hip Fracture. Journal of Bone and Joint Surgery, 84(4), 670–674. Morris, F. L., Naughton, G. A., Gibbs, J. L., Carlson, J. S., & Wark, J. D. (1997). Prospective tenmonth exercise intervention in premenarcheal girls: Positive effects on bone and lean mass. Journal of Bone and Mineral Research, 12, 1453–1462. Mundy, G. R. (1999). Bone remodeling. In M. J. Favus (Ed.), Primer on the metabolic bone diseases and disorders of mineral metabolism (pp. 30–38). Philadelphia: Lippincott Williams & Wilkins. National Institutes of Health. (2001). Osteoporosis prevention, diagnosis, and therapy. NIH Consensus Statement online, 17(1), 1–36, March 27–29, 2000. Retrieved from http://consensus.nih. gov/2000/2000Osteoporosis111html.htm
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Ulrich, C. M., Georgiou, C. C., Gillis, D. E., & Snow, C. M. (1999). Life-time physical activity is associated with bone mineral density in premenopausal women. Journal of Women’s Health, 8, 365–375. Umemura, Y., Ishiko, T., Yamauchi, T., Masashi, K., & Mashiko, S. (1997). Five jumps per day increase bone mass and breaking force in rats. Journal of Bone and Mineral Research, 12, 1480–1485. U.S. Department of Health and Human Services. (2004). Bone health and osteoporosis: A report of the surgeon general. Public Health Service, Office of the Surgeon General, Rockville, MD. Retrieved from http://www.surgeongeneral.gov/library/bonehealth/ Uusi-Rasi, K., Kannus, P., Cheng, S., Sievanen, H., Pasanen, M., Heinonen, A., et al. (2003). Effect of alendronate and exercise on bone and physical performance of postmenopausal women: A randomized controlled trial. Bone, 33, 132–143. Vainionpaa, A., Korpelainen, R., Leppaluoto, J., & Jamsa, T. (2005). Effects of high-impact exercise on bone mineral density: A randomized controlled trial in premenopausal women. Osteoporosis International, 16, 191–197. Villareal, D. T, Binder, E. F., Yarasheski, K. E., Williams, D. B., Brown, M., Sinacore, D. R., et al. (2003). Effects of exercise training added to ongoing hormone replacement therapy on bone mineral density in frail elderly women. Journal of the American Geriatrics Society, 51(7), 985–990. Wallace, B. A., & Cumming, R. G. (2000). Systematic review of randomized trials of the effect of exercise on bone mass in pre- and postmenopausal women. Calcified Tissue International, 7, 10–18. Warden, S. J., Fuchs, R. K., & Turner, C. H. (2004). Steps for targeting exercise toward the skeleton to increase bone strength. European Journal of Physical Medicine, 40, 223–232. Winter, K. M., & Snow, C. M. (2000). Detraining reverses positive effects of exercise on the musculoskeletal system of premenopausal women. Journal of Bone and Mineral Research, 15, 2495–2503. Wolff, I., Van Croonenborg, J. J., Kemper, H. C., Kostense, P. J., & Twisk, J. W. (1999). The effect of exercise training programs on bone mass: A meta-analysis of published controlled trials in preand postmenopausal women. Osteoporosis International, 9(1), 1–12. Yarasheski, K. E., Campbell, J. A., & Kohrt, W. M. (1997). Effect of resistance exercise and growth hormone on bone density in older men. Clinical Endocrinology, 47, 223–229. Yingling, V. R., Davies, S., & Silva, M. J. (2001). The effects of repetitive physiologic loading on bone turnover and mechanical properties in adult female and male rats. Calcified Tissue International, 68, 235–239.
Osteoporosis and Fall Prevention
Approximately 30% of adults over 65 years of age and 40% of adults over age 75 years experience at least one fall annually. (M. E. Tinetti, M. Speechley, and S. Ginter, “Risk Factors for Falls Among Elderly Persons” )
F
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alls in the home environment are the leading cause of nonfatal unintentional injury and of death in older adults. For example, approximately 49% of home-injury deaths are due to falls in adults aged 60–69 years; and 66% of home-injury deaths are due to falls in adults 70 years and older (Runyan et al., 2005). These falls and their consequent injuries are associated with enormous health care costs, personal costs as evidenced by functional decline, erosion in the quality of life, and loss of independent living. Approximately 30% of people over 65 years of age and living in the community fall each year. Although less than 1 fall in 10 results in a fracture, one-fifth of fall incidents require medical attention (Rubenstein & Josephson, 2002). Between 1990 and 2000, the Centers for Disease Control (Centers for Disease Control and Prevention, 2001) reported a 94% (from 6,601 to 12,837) increase in the number of older adults over the age of 65 years who died as a result of falling. Incidence rates for falling range from 0.2 to 0.8 per person annually for community-dwelling older adults, to 2.9 to 3.6 for individuals residing in long-term care facilities (Rubenstein & Josephson, 2002; Rubenstein, Josephson, & Osterweil, 1994; Stevens, 2003). Falls tend to occur within the first few weeks after entering a nursing home. The reasons sited for these fall-related incidences include the unfamiliar environment, medications, the current diagnosis(es), the acuteness of the current diagnosis(es), and immobility or inactivity due to sitting for long periods or being confined to bed.
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Falls and their secondary consequences result in the increased use of substantial medical resources to cover emergency, operative, and rehabilitative services. In 1996, acute care costs for hip fractures in 250,000 older adults exceeded $10 billion. The number of hip fractures is expected to increase to over 500,000 per year by 2040, which will cost over $32 billion annually, further burdening Medicare and Medicaid programs (Cummings, Rubin, & Black, 1990). Hip fracture survivors have a 10%–15% decreased life expectancy and quality of life. Over half of the older adults who sustain hip fractures that require hospitalization cannot return home or live independently. One-third of these individuals will die within a year following the fall (Nevitt, Cummings, & the Study of Osteoporotic Fractures Research Group, 1992). Hip fractures cause the highest morbidity and mortality rates, most particularly in women with osteoporosis (Vanness & Tosteson, 2005). In addition to hip fractures, distal forearm or wrist fractures are also common (Gregg, Pereira, & Caspersen, 2000). Kelsey, Browner, Seeley, Nevitt, and Cummings (1992) postulated that women who are in good health and active, and who have good neuromuscular function but low bone density, tend to sustain distal forearm fractures during falls. Consequently, women who are less healthy and less active, and who have lower neuromuscular functioning and low bone density, are more likely to sustain proximal humerus (upper arm) fractures. Falls produce more than physical consequences, including a sometimes immobilizing fear of falling. This fear, obviously, is prevalent in older adults with osteoporosis. Fear of falling can lead to a loss of self-confidence in performing routine activities of daily living (ADL) and to social isolation (Friedman, Munoz, West, Rubin, & Fried, 2002). Individuals who self-report a fear of falling concurrent with a decrease in activity level are significantly more inclined to be socially isolated and less willing to talk to family or others about falls and are at greater risk of falling. The cause of falling is multifactorial (Newton, 2003; Rubenstein & Josephson, 2002). Individuals with osteoporosis may have a progressive kyphotic posture, which alters the biochemical alignment of the body by shifting the center of gravity forward. To maintain the head in an upright position, increased compensation by the neck occurs. However, other factors need to be considered in addition to postural alignment and low bone density. Risk factors for falls also include the following: a history of falling, previous fractures, taking four or more medications, visual impairments, lower extremity weakness, balance and gait impairments, and neurologic impairments. Environmental factors such as carpeting, obstacles, and lighting also play a prominent role in falls and fallrelated injuries. Although many of the falls among community-dwelling older adults occur in and around the home, the data are equivocal as to whether or not more falls and injuries occur inside or outside the home. It is important for health care professionals to provide fall prevention programs to cohorts of older adults independent of their current living status (i.e., community, residential facility, nursing home, and hospital). Special emphasis is placed on those individuals who have or are predisposed to osteoporosis. The following six principles need to be considered when developing a fall prevention program: 1 . What causes a fall in one individual may not necessarily cause a fall in another
individual. 2 . Falls can lead to a fear of falling as well as a fear of the inability to get back up after a fall has occurred.
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3 . Inactivity is a fall risk behavior. Inactivity includes the spectrum from pro-
longed bed rest to an inactive lifestyle. Older persons with a history of falls with fractures or osteoporosis may almost automatically choose a less active lifestyle in order to avoid falling. However, inactivity leads to a loss of selfconfidence and an increased fall risk. 4 . Deficits in physiologic factors such as muscle and skeletal strength, balance, and gait are associated with an increased risk for falling. The risk of falls increases with the number of physiologic risk factors, the number of medications, and the number of functional impairments. These factors are not only important to identify in terms of fall risk and potential fall-related injuries, but they are also important to consider when preventing or reducing the impact of a fall. 5 . A fall prevention program should include a screening component, an education component, and an activity component. 6 . Some older adults may not be committed to making the recommended changes in their lifestyle or home environment for a variety of social, cultural, financial, or personal reasons. Generally, fall prevention programs have been custom designed for specific settings. Therefore, no single reliable and valid model for a fall prevention program exists. The elements of a fall prevention program are listed in the section that follows. These elements include a self-report of those factors that may contribute to falls, a balance screen, an educational and activity component, and a follow-up component. The general elements of a program are outlined below and elaborated in an example program: the HEROS© Fall Prevention Program for Community Dwelling Older Adults (Newton, 1998, 2004). The purpose of any fall prevention program is to inform and motivate older adults to make necessary adaptations to their lifestyles and home environments to reduce the risk for falls. No program can guarantee a reduction in falls if the information is not perceived by the elders as relevant, or if participants do not actively take part in reducing their risks.
Elements of a Fall Prevention Program Fall Risk Assessment and Balance Screen A quick assessment can determine if referral to other health care professionals is needed. Items to consider include the following.
Fall History Determine the circumstances surrounding one fall or repeated falls. Determining fall history can be as simple as asking if the older adult has fallen within the past month or 6 months, or may be more comprehensive, logging the fall(s) in terms of the time of day, the activity surrounding the fall, and the location of the fall (i.e., inside or outside the house).
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Fear of Falling Index A simple question is to ask the individual to determine if any reduction in activities has occurred due to a fear of falling. More detailed assessments determine the confidence an individual has in performing routine activities. Two measures are the Falls Efficacy Scale (Tinetti, Richman, & Powell, 1990) and the Activities-Specific Balance Confidence (ABC) Scale (Powell & Myers, 1995).
Health Status Self-report of the person’s perception of his/her health comprises a simple question: “How do you perceive your health?” The rating is excellent, good, fair, or poor.
Medical History It is important to assess the individual’s medical history related to any chronic or acute conditions that might contribute to falls. Particular attention should be directed to musculoskeletal disorders, neurologic disorders, vision, cardiovascular status, cognitive status, and sensation. In addition, the number of medications is ascertained, including prescribed and over-the-counter medications. The use of a mobility aid such as a cane or walker is also noted.
Measure of Physical Performance and Ability to Accomplish Activities of Daily Living Examples of test batteries that actually measure the functional ability to perform specific physical activities include the following: The Established Populations for Epidemiology Studies of the Elderly (EPESE) battery tests balance, walking, and strength (Guralnik et al., 1994). The Performance Activities of Daily Living (PADL) battery simulates activities of daily living (Kuriansky & Gurland, 1976). The Physical Disability Index includes range of motion, strength, balance, and mobility and is designed for nursing home residents or frail individuals (Gerety et al., 1993). The Physical Performance Test includes manual abilities, strength, balance, and mobility (Reuben & Sie, 1990). The Physical Performance and Mobility Examination tests mobility and walking. It is designed for hospitalized patients (Winograd et al., 1994). Balance assessments. Several easy-to-administer and reliable balance assessments are indicated below. Many of these assessments are located online in the HEROS© Fall Prevention Program for Community Dwelling Older Adults manual (Newton, 1998, 2004). The Multi-Directional Reach Test (MDRT) (Newton, 2001) measures limits of stability by having the person reach in the forward, right, and left directions and lean backward. This test is a modification of the Forward Reach (Duncan, Weiner, Chandler, & Studenski, 1990), which only measures reach in the forward direction.
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Timed Up and Go (TUG) times the individual getting up from a chair, walking 10 feet, and returning to the original seated position (Podsiadlo & Richardson, 1991). The Performance Oriented Mobility Assessment (POMA) assesses balance and gait (Tinetti, 1986). The Berg Balance Test assesses balance performance during functional tasks (Berg, Wood-Dauphinee, Williams, & Gayton, 1989). A scoring sheet is seen in Exhibit 9.1 (Barhameen & Newton, 2003). The Gait Stability Ratio (GSR) (Cromwell & Newton, 2004) measures the number of steps per meter and is a measure of stability during walking. The ratio is obtained by counting the number of steps and timing the individual walking at a steady pace for 20 feet. The GSR = cadence (steps/meter) ÷ velocity (meters/second).
Exhibit
9.1
Instructions: I am going to ask you some questions about how confident you feel when you are doing certain activities. You are to rate your answer on a scale of 0 to 100. A zero means that you are not confident performing the task, and 100 means that you are extremely confident performing the activity. If you say you do not do the activity, please complete the question as if you had to do the activity. 0 10 20 30 40 50 60 70 80 90 100% No Confidence ____________________________________Completely Confident How confident are you that you will not lose your balance or become unsteady when you.......Score 1. ______ ….walk inside your house. 2. ______ ….walk up and down stairs inside your house. 3. ______ ….bend over and pick up a slipper from the front of a closet floor. 4. ______ ….reach for a small can off a shelf at eye level. 5. ______ ….stand on your tiptoes and reach for something above your head. 6. ______ ….stand on a chair and reach for something. 7. ______ ….sweep the floor. 8. ______ ….walk outside the house to a car parked in the driveway. 9. ______ ….get into or out of a car. 10. ______ ….walk across a parking lot to a mall. 11. ______ ….walk up or down a ramp. 12. ______ ….walk in a crowed mall where people rapidly walk toward you and pass you by. 13. ______ ….are bumped into as you walk through the mall. 14. ______ ….step onto or off of an escalator while holding onto a railing. 15. ______ ….step onto or off an escalator while holding onto parcels in such a way that you cannot hold onto the railing. 16. ______ ….walk outside on icy sidewalks.
Berg Balance Test Scoring Sheet
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Education and Activity When addressing modifications to lifestyle or the environment, considerations should include cultural factors, financial factors, relevance to older adults, and willingness of individuals to change their habits. Several rather than many suggestions should be recommended so as not to overwhelm or frustrate the older adult. Group participation to identify fall risk behavior and ways to modify these behaviors is one strategy to engage older adults in the learning process. Generally, older adults are more willing to change the environment than to change themselves.
Modifications to One’s Lifestyle Suggestions include the following: Wear appropriate clothing and shoes. For example, long bathrobes cause tripping and going barefoot or in stocking feet may result in a slip or trip. Participate in activities. Generally older adults should participate in some form of activity for at least 30 minutes a day. Activities include low-impact exercises, dancing, gardening, walking, Tai Chi, and other social or physical activities that fit into the lifestyle of the individual. Specific exercises for individuals with osteoporosis are discussed in chapter 8 (Henderson, White, & Eisman, 1998; Prior, Farr, Chow, & Faulkner, 1996). Eat in a healthy fashion. Nutrition is discussed in chapter 7.
How to Get Up From the Floor Older adults need a strategy to get up once a fall has occurred. The strategy may be yelling for help, crawling to a telephone, or getting up alone (see Table 9.1).
Modifications to the Environment Making the living space safe can best be achieved by providing a room-by-room assessment or addressing commonalties (lighting, flooring, obstacles, and stairs). Environmental modification also includes the exterior environment. The same factors are assessed: lighting, the walking surface, obstacles, and stairs. Recommendations for environmental modifications should take into account financial constraints.
Identify Resources Once modifications are recommended, it is helpful to provide information regarding the location of resources. These resources may include retired older persons with skills to help other seniors, projects by vocational schools or professional organizations, local agencies that provide health care or social services, health or social service professionals, and computer searches on the Web. Finally, gifts to give the older adult include help aids (e.g. grabbers, a portable telephone, a flashlight, and night-lights).
Follow-up A follow-up program is extremely helpful to answer questions older adults may have regarding points covered in the educational program, or to identify sources of assistance
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9.1
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Teaching Community-Dwelling Older Adults to Get Up From the Floor The following is a general scripted instruction sheet for helping older adults to get up from the floor after a fall. Personal experience or other hints are encouraged to make the talk appropriate to the audience. Many older adults have a fear of falling and have a great fear of being unable to get up once a fall has occurred. It is important that older persons know how to get up from the floor. It is particularly important for those individuals who live alone. The longer a person remains on the floor following a fall, the greater the chances for secondary complications resulting from lying there. It is a given that everyone falls. Before the person attempts to get up, determine if someone is available to assist. If the person is living with someone, it is better to call for assistance, even if it means waking the person up. The fall may have caused an injury, or badly shaken the person. In all cases the key is to move slowly, remain calm, and run through the mind the next step in getting up. First, the person should check to see if anything is broken; that is, does the bone feel broken, or does it just really hurt a lot? Generally, broken bones are associated with severe pain. If the person is living alone and believes that something was broken, he/she needs to move on the floor to reach a telephone. This should be done slowly. Ask the audience how they would get up from the floor if they have fallen. If the floor is clean (always bring a floor covering), lie down and have the group problem-solve how you would get up. This way they see the demonstration as well as being actively involved by providing hints (I find that most groups like this and will provide additional hints). The steps include moving along the floor to a sturdy chair that will not move or the sofa or some other fixed support (not a bathroom sink because it could pull away from the wall). You can move by pulling yourself along, crawling, or scooting. Get into a side-sitting position. Once in this position, pause a second to get your bearings (orient yourself and catch your breath). Kneel with the support of the chair, sofa, etc. Once in this position, pause a second to get your bearings (orient yourself and catch your breath). Use the stronger knee to push yourself onto the chair or sofa. Putting the forearms on the chair or sofa seat also helps to provide some leverage. Once in this position, pause a second to get your bearings (orient yourself and catch your breath). It is important to emphasize doing this slowly, and not impulsively just because you are embarrassed that a fall occurred. Once sitting in a chair or on the sofa, take time to calm down, catch your breath, and decide the next course of action. That is, do you need to call a friend, neighbor, relative, the ambulance, or 911 for help? Do you just need to talk to someone for assurance? For those individuals who may be reluctant to learn to get up because of fear, anxiety, or do not feel that they have the physical capability to get up, then other strategies are needed. For example, some individuals may be able to afford some type of alarm system. For all people, recommend a buddy system, that is, have someone call at least once a day. Also, recommend placing the telephone within easy reach and not attached to a kitchen wall where one has to stand to use it. Have a relative give the person a portable telephone for a birthday or other holiday present. (Reprinted slightly adapted with permission, from R. A Newton, Fall Prevention Project, 1998).
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to correct environmental hazards. In addition, the follow-up session provides an opportunity to determine whether or not the individual is compliant, and to develop an appropriate revision of strategies if the individual is found to not be compliant.
HEROS© Fall Prevention Program for Community Dwelling Older Adults The program described below is an example of a specific fall prevention program that was developed using the information provided above. The HEROS© Fall Prevention Program for Community Dwelling Older Adults can be modified based on the discipline of the participating health care professionals, the time available for such a program, and the needs of the community receiving the program. Additionally, the program can be modified for use in other settings and with other cohorts of older adults. The HEROS© Fall Prevention Program can be translated for those older adults whose first language is not English. The self-assessment portion can be read to the older adult who has visual or reading impairments. The following are components of the HEROS© Fall Prevention Program developed by the author (Newton, 1998, 2004).
Fall Risk Assessment 1 . Do you _____ live alone or _____with others? 2 . Have you fallen in the past month or past 6 months? _____ 3 . In the past 5 years, have you fallen and broken a bone? _____
If so where? _____ 4 . Medical history: Check or circle all those that apply to you.
_____ Number of medications [it is ideal to have individuals show the presenter the medications that they take] _____ Use of a mobility aid _____none _____cane _____walker _____ Heart problems (hypertension, heart attack, or other heart problems, peripheral vascular disease) _____ Respiratory problems (difficulty breathing, emphysema, allergies) _____ Visual problems (wearing glasses: bifocals, trifocals, progressive lenses; glaucoma or other visual impairments) _____ Hearing problems (difficulty hearing, wearing a hearing aid) _____ Poor sensation (feeling) in the feet _____ Musculoskeletal problems (arthritis, osteoporosis, muscle cramps) _____ Diabetes _____ Dizziness or an unsteady feeling 5. How do you rate your health? _____ Excellent _____Good _____ Fair _____
Poor 6. Do you have a fear of falling? If so has the fear changed your activity level
(lifestyle)? _____ Not afraid
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_____ Afraid but have not changed my activity level (lifestyle) _____ Afraid and have changed my activity (lifestyle)
Balance Assessment 1. Multi-Directional Reach Test 2. Timed Up and Go 3. Standing in typical stance, and with feet together, in semi-tandem, and in tan-
dem 4 . A spotter assists with all balance testing. As time permits, the Berg Balance
Test or other balance tests can be administered.
Education 1 . Discuss modification of lifestyle. Items can include those listed below. Time is
permitted for discussion. Wash glasses when brushing teeth so both are clean. Wear appropriate shoes and clothing. Refrain from sharing medications. “Brown bag” all medications and take them to the pharmacist or primary physician to check for drug interactions or to check for and dispose of those medications that are no longer required. 2. Demonstrate how to get up after a fall. Include group discussion so partici-
pants can explain how they would get up. 3. Discuss environmental risk factors:
Individuals should have someone change light bulbs that are burned out or replace the light bulbs with a higher wattage. Presenter should provide a checklist of no more than 10 items for environmental change. The checklist ranges from tasks that are easily accomplished and without cost to tasks that are more costly and require a repairman. Identify local resources to help with repairs, donations.
Activities Discuss with the group those activities that are appropriate for individuals with osteoporosis. Activities range from low-impact exercises to walking, Tai Chi, square dancing, dancing, social activities, and so on.
Other Activities Pass out fall prevention brochures, and other relevant brochures. A drawing for a prize for participation can motivate older adults to participate. Prizes could include a health aid or other item related to safety and prevention.
Follow-Up One month after the program the health care professional can meet with the group to discuss their accomplishments and to complete a questionnaire. The questionnaire includes items such as falls in the past month as well as the benefits of the program. The items
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on the checklist can be modified into a questionnaire to determine the benefits of the fall prevention program in terms of modifications made to the individual’s lifestyle or home environment. The three examples that follow attempt to determine if the modification was made, and if not, whether this was due to the relevance of the item, or due to financial constraints, or due to the fact that the individual is not yet willing to make a change.
YES
NO
_____ _____ _____ _____ _____
_____ _____ _____ _____ _____
YES
NO
_____ _____ _____ _____ _____ _____
_____ _____ _____ _____ _____ _____
YES
NO
_____ _____ _____
_____ _____ _____
I installed grab bars. I already had them. They cost too much. No one could install them. I do not think they are necessary.
I have been doing the low-impact activities at home. I do not find these activities helpful. I would prefer to do my normal routine activity such as walking. The low-impact activities interfere with my daily routine. I lost the sheet. I will start doing them tomorrow.
Have you fallen in the past month? If yes, did you find the information on getting up helpful? If no, did you find the information on getting up helpful?
In summary, falls can be reduced by a conscious effort on the part of all health care professionals and older adults, perhaps with the help of their families and/or friends. Fall prevention programs can be implemented in nursing homes or as a part of community activity programs. If an older adult can reduce the risk of falls, then the quality of life for that individual will be greatly improved. And if health care professionals, individually or across disciplines, can institute fall prevention programs in their facilities and in their communities, then the number of falls and fall-related injuries will significantly decrease. Thus, older adults can enjoy a healthier and better quality of life as they move into the twenty-first century.
REFERENCES Barhameen, A. Y., & Newton, R. A. (2003). Berg Balance Test scoring made easy: The BBT score sheet. Journal of Gerontologic Physical Therapy, 26, 50. Berg, K., Wood-Dauphinee, S., Williams, J., & Gayton, D. (1989). Measuring balance in the elderly: Preliminary development of an instrument. Physiotherapy Canada, 41, 304–311. Centers for Disease Control and Prevention. National Center for Injury Prevention and Control. (2001). Web-based injury statistics query and reporting system. Atlanta, GA: Author. Cromwell, R. L., & Newton, R. A. (2004). Relationship between balance and gait stability in healthy older adults. Journal of Aging and Physical Activity, 12, 90–100. Cummings, S. R., Rubin, S. M., & Black, D. (1990). The future of hip fractures in the United States: Numbers, costs, and potential effects of postmemopausal estrogen. Clinical Orthopaedics and Related Research, 252, 163–166.
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Duncan, P. W., Weiner, D. K., Chandler, J., & Studenski, S. (1990). Functional reach: A new clinical measure of balance. Journal of Gerontology, 45, M192–M197. Friedman, S. M., Munoz, B., West, S. K., Rubin, G. S., & Fried, L. P. (2002). Falls and fear of falling: which comes first? A longitudinal prediction model suggests strategies for primary and secondary prevention. Journal of the American Geriatrics Society, 50, 1329–1335. Gerety, M. B., Mulrow, C. D., Tuley, M. R., Hazuda, H. P., Lichtenstein, M. J., Bohannon, R., et al. (1993). Development and validation of a physical performance instrument for the functionally impaired: The physical disability index (PDI). Journal of Gerontology, 48, M33–M38. Gregg, E. W., Pereira, M. A., & Caspersen, C. J. (2000). Physical activity, falls, and fractures among older adults: A review of the epidemiologic evidence. Journal of the American Geriatrics Society, 48, 883–893. Guralnik, J. M., Simonsick, E. M., Ferrucci, L. Glynn, R. J., Berkman, L. F., Blazer, D. G., et al. (1994). A short physical performance battery assessing lower extremity function: Association with self-reported disability and prediction of mortality and nursing home admission. Journal of Gerontology, 49, M85–M94. Henderson, N. K., White, C. P., & Eisman, J. A. (1998). The roles of exercise and fall risk reduction in the prevention of osteoporosis. Endocrine and Metabolism Clinics of North America, 27, 369–387. Kelsey, J. L., Browner, W. S., Seeley, D. G., Nevitt, M. C., & Cummings, S. R. (1992). Risk factors for fractures of the distal forearm and proximal humerus: The study of osteoporotic fractures research group. American Journal of Epidemiology, 135, 477–489. Kuriansky, J., & Gurland, B. J. (1976). The performance test of activities of daily living. International Journal of Aging and Human Development, 7, 343–352. Nevitt, M., Cummings, S. R., and the Study of Osteoporotic Fractures Research Group. (1993). Type of fall and risk of hip and wrist fractures: The study of osteoporotic fractures. Journal of the American Geriatrics Society, 41, 1226–1234. Newton, R. A. (1998, 2004). HEROS© Reducing falls and serious injuries, training program manual. Retrieved August 13, 2007 from www.temple.edu/older_adult Newton, R. A. (2001). Multi-Directional Reach Test: A practical measure for limits of stability in older adults. Journal of Gerontology, 56, M1–M5. Newton, R. A. (2003). Balance and falls among older people. Generations, 27, 27–31. Podsiadlo, D., & Richardson, S. (1991). The timed “Up & Go”: A test of basic functional mobility for frail elderly persons. Journal of the American Geriatrics Society, 38, 142–148. Powell, L. E., & Myers, A. M. (1995). The activities-specific balance confidence (ABC) scale. Journal of Gerontology, 50A, M28–M34. Prior, J. C., Farr, S. I., Chow, R., & Faulkner, R. A. (1996). Physical activity as therapy for osteoporosis. Canadian Medical Association Journal, 155, 940–944. Reuben, D., & Sie, A. (1990). An objective measure of physical function of elderly patients: The physical performance test. Journal of the American Geriatrics Society, 38, 1105–1112. Rubenstein, L. Z., & Josephson, K. R. (2002). The epidemiology of falls and syncope. Clinics in Geriatric Medicine, 18, 141–158. Rubenstein, L. Z., Josephson, K. R., & Osterweil, D. (1994). Falls and fall prevention in the nursing home. Clinics in Geriatric Medicine, 12, 881–902. Runyan, C. W., Casteel, C., Perkis, D., Black, C., Marshall, S. W., Johnson, R. M., et al. (2005). Unintentional injuries in the home in the United States. Part I: Mortality. American Journal of Preventive Medicine, 28, 73–79. Stevens, J. A. (2003). Falls among older adults: Public health impact and prevention strategies. Generations, 26, 7–14. Tinetti, M. E. (1986). Performance-oriented assessment of mobility problems in elderly patients. Journal of the American Geriatrics Society, 34, 119–126. Tinetti, M. E., Richman, D., & Powell, L. (1990). Falls efficacy as a measure of fear of falling. Journal of Gerontology, 45, P239–P243. Tinetti, M. E., Speechley, M., & Ginter, S. (1998). Risk factors for falls among elderly persons living in the community. New England Journal of Medicine, 319, 1701–1707. Vanness, D. J., & Tosteson, N. A. (2005). Estimating the opportunity costs of osteoporosis in the United States. Topics in Geriatric Rehabilitation, 21, 4–16. Winograd, C. H., Lemsky, C. M., Nevitt, M. C., Nordstrom, T. M., Steward, A. L., Miller, C. J., et al. (1994). Development of a physical performance and mobility examination. Journal of the American Geriatrics Society, 42, 742–749.
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Fractures pose significant long-term changes in the lives of those with osteoporosis. For many, life is irrevocably changed after the incidence of even one fracture; almost half do not regain their premorbid abilities to perform activities of daily living. (J. Penrod, “Living with Osteoporosis”)
10
steoporosis is a condition that is known to result in the bones becoming porous, brittle, and vulnerable to fracture (Tamparo & Lewis, 2005). The disorder results in skeletal weakness (Damijanov, 2000). Persons living with osteoporosis may experience difficulty with maintaining independence in self-care. Independence in work and leisure may also be impacted. Psychosocial problems such as diminished self-concept or depression may develop. These factors, singly or in combination, may seriously impact the quality of life. The process of maintaining maximum independence and living a life of good quality will require that the client and the health care professional collaborate to develop and implement a dynamic treatment plan that is continuously revised and updated. Living with a chronic condition frequently requires clients to take a close look at their life and identify opportunities for positive change. One way to look at this process is to think of it as “lifestyle redesign.” Lifestyle redesign involves taking an inventory of all the aspects of life that may be impacted by osteoporosis and redesigning and rebalancing the components to create a plan that will promote maximum longterm independence and a satisfying quality of life (Hasselkus, 2002; Mandel, Jackson, Zemke, Nelson, & Clark, 1999).
O
Marlene Joy Morgan
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Client-Centered Approach While each person who is living with osteoporosis may experience a common set of symptoms, the effect of the disease impacts each life in a unique way. Each of us has designed a life that revolves around roles and activities that define us. Important first steps in working with any client are as follows: (1) to determine the roles and activities that are important to the client; (2) to identify those roles and activities that are at risk because of osteoporosis; and (3) to develop a dynamic plan of lifestyle redesign that will facilitate long-term independence and maximize the quality of life. Roles are clusters of interest and activities that give structure and meaning to life (Kielhofner, 2004). The names of roles such as parent, homemaker, volunteer, worker, and friend help to describe and identify important components of the life of each individual. The health care professional may engage the client in an interview and incorporate an assessment tool such as a role checklist to assist the client in identifying those roles in danger of being impacted by osteoporosis (Oakley, Kielhofner, Barris, & Reichler, 1986). Specifically, the completion of a role checklist provides insight into the roles that the client engages in, how important each is to the client, and how roles have changed over time. Table 10.1 provides a summary of examples of life roles. In addition to roles, the life of each client may be examined with respect to the specific activity patterns that he or she engages in. Activities may include activities of daily living (ADLs) such as self-care, dressing, bathing, eating, and grooming, and instrumental activities of daily living (IADLs) such as home maintenance and yard work, work, or leisure (AOTA, 2002). A useful step may be the development of an activity configuration. Simply stated, an activity configuration is a carefully crafted and written description of how an individual spends time (Yerxa & Locker, 1990). The use of an assessment specifically designed to identify activities that are important to the individual is warranted. Gregory (1983) describes a scale that assesses the degree of interest and participation in a variety of activities. In completing the Activity Index and Meaningfulness Scale, the client responds to 23 items designed to illuminate key activities and interests (Gregory, 1983). Baum and Edwards (2001) developed an
Table
10.1
Life Roles The life roles of an individual may include the following: – Parent – Worker – Homemaker – Student – Friend – Volunteer – Sibling – Grandparent – Caregiver – Religious participant
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activity card sort in which the client examines and sorts cards. The final placement of the cards documents participation or lack of participation in self-care, leisure, and social activities. Completion of a role checklist and an activity configuration, in conjunction with a gently probing interview, will provide the health care professional with important background information about the client’s history, skills, interests, and values.
Setting Goals for Lifestyle Redesign Armed with information from a role checklist and an activity configuration, the client and health care professional are ready to establish goals and a plan for lifestyle redesign. An assessment tool such as the Canadian Occupational Performance Measure (COPM) can be utilized to provide a structure for this process (Law et al., 1994). The COPM is an individualized measure designed to detect changes in a client’s selfperception of his or her performance over time (Law et al., 1994). The COPM is an interview-based assessment that solicits information from the client in the areas of selfcare, productivity, and leisure. Self-care includes personal care, functional mobility, and community management. Productivity includes paid or unpaid work, and leisure includes quiet recreation, active recreation, and socialization. Specifically, the client is asked to identify how he feels that his current condition (in this case osteoporosis) may impact his self-care, productivity, and leisure. The interviewer notes the client’s responses until a comprehensive list is generated in each category. The health professional and client then revisit the categories and the client rates the importance of each concern on a scale from 1 to 10 (when 10 = “extremely important” and 1 = “not important at all”). The client is also asked to rate, for each, his current level of performance (10 = “able to do it extremely well” and 1 = “not able to do it at all”) and level of current satisfaction with performance (10 = “extremely satisfied” and 1 = “not satisfied at all”) (Law et al., 1994). The scoring system for the COPM uses the client’s responses with regard to level of importance, performance, and level of satisfaction to develop a prioritized list of goals that will form the foundation for intervention and lifestyle redesign. This process focuses the goal setting and subsequent treatment planning on those areas and problems that are of primary concern to the client. The health care professional may not fully agree with the client’s list, but that is the core of client-centered care!
Integrating Interdisciplinary Assessments Information from a role checklist, an activity configuration, and the COPM provides a global perspective on the roles, activities, skill, interests, and values of the client living with osteoporosis. This information needs to be supplemented with the results of specific assessments that test for range of motion, muscle strength, postural control and balance, readiness for change, and depression. Outlines for assessing each of these attributes are offered below.
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Range of Motion Detailed measurements of range of motion (ROM), both active (AROM) and passive (PROM), can be completed by a physical or occupational therapist (Norkin, 1995). Range of motion is measured clinically using goniometry. Goniometry involves measuring the angle created by the bones at the joints. These angles are measured using a goniometer, a tool for clinical measurement that has three parts: a fulcrum, a stationary arm, and a movable arm. The goniometer measures angles from 0° to 180° (Norkin, 1995). In completing a goniometry assessment, the stable arm aligns with the immovable part of the limb, the fulcrum is placed over the joint, and the movable arm is placed on the part of the limb that is moving. For example, to measure knee flexion, the stable arm aligns over the thigh (in line with the greater trochanter of the femur), the fulcrum is placed over the joint (or lateral epicondyle of the femur), and the movable arm is aligned with the leg (or lateral malleolus). The client begins with the knee straight (in full extension) and bends it as much as possible (into flexion). The average motion at the knee is 0°–135°. Each joint in the body has a ROM that can be described as average or normal. A comprehensive ROM assessment will record the motion in the spine, neck, shoulder, elbow, forearm, wrist, thumb, fingers, hip, knee, ankle, and foot (Norkin, 1995). ROM, as measured by goniometry, provides valuable data regarding functional motion. Functional reach, functional ambulation, and the ability to bend, twist, stand, and lift are often impeded by osteoporosis. The development of bony deformities and/ or decrease in muscle strength may also impact functional motion. Current and subsequent ROM assessments allow the health care professional to track significant changes in ROM.
Muscle Strength Muscle strength is evaluated using the Manual Muscle Test (MMT) (Hislop & Montgomery, 1995). The MMT is a clinical examination that is scored on a 5-point scale. The scale is composed of both objective and subjective factors. The objective factors include the degree to which the patient can complete the available range of motion and move against gravity, and whether he/she can hold this position against a resistance applied by the examiner. The subjective judgment is based on the examiner’s knowing how much resistance to give and how much resistance the patient can tolerate (Hislop & Montgomery, 1995). At the extremes, a grade of 5 on the MMT indicates that the client is able to move through a full range of motion against gravity and maximum resistance applied by the examiner, and 0 indicates that the client is unable to move and there is no evidence of a contraction in the muscle (Kendall & McCreary, 1993). Performance on the MMT provides an overall picture of the client’s strength. It is important that clinicians be aware that muscle strength and subsequent endurance may be seriously compromised by osteoporosis. A combination of bony changes, skeletal deformity, and sedentary lifestyle may converge, resulting in diminished muscle strength.
Postural Control and Balance Assessment of postural control and balance in most settings is completed as one component of a comprehensive physical therapy and occupational therapy assessment ( Jacobs & Jacobs, 2004). Balance and control are assessed in both sitting and standing. Both static
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Table
Changes in Motor Control Associated With Osteoporosis
10.2
– – – – – –
Table
10.3
157
At risk for vertebral crush fracture at T8 or below, secondary to back flexion, heavy lifting, or weak back extensor muscles Decreased stability Decreased posture control and balance Decreased range of lumbar extension Decreased respiratory function secondary to severe kyphosis Back pain
Skeletal Changes Associated With Osteoporosis – – – – – – –
Dorsal kyphosis in the thoracic region Lordosis in the cervical region Loss of height Decreased bone strength Changes in posture Risk for hip fractures at the femoral neck associated with falling Risk for wrist fracture associated with falling
and dynamic balance and control are addressed. To assess sitting balance and control, the client sits at the edge of a chair or mat. The therapist notes whether the client is able to maintain stable sitting without using his or her hands for support. Next the therapist assesses dynamic balance. The examiner asks the client to move and observes whether balance and control are maintained. Finally, the therapist challenges the client’s sitting balance, by gently pushing, and records the client’s ability to meet the challenge without using his or her arms for support. Balance and control are tested in standing by following a similar sequence of steps. The ability to maintain balance in both sitting and standing without using the arms for support is an important skill ( Jacobs & Jacobs, 2004). ROM limitations, muscle weakness, and skeletal deformities may alter the client’s center of gravity and ability to react when balance is challenged. Problems with postural control and balance present fall risks for clients with osteoporosis. Table 10.2 presents a summary of the changes in motor control frequently associated with osteoporosis, and Table 10.3 summarizes common skeletal changes.
Psychosocial Assessment Assessment of self-concept, coping skills, readiness for change, and depression provides specific insights into the psychosocial status of an individual.
Self-Concept For many individuals, self-concept and sense of worth may be tied to physical beauty and/or level of independence. For this reason, the health care professional must be aware of the reaction that the client is expressing as a result of living with osteoporosis.
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The development of skeletal deformities, limitation of leisure pursuits, feelings of isolation, or difficulty maintaining a home or sustaining a prior level of performance at work may all result in a diminished self-concept in a client with osteoporosis (Christiansen, 2000; Lo & Zemke, 1997).
Coping Skills Each person has a set of skills that he or she has used successfully throughout life to confront challenges and problems. A probing interview will reveal the strategies that have been used by a client in the past. For instance, the interviewer might say, “Can you tell me about a time that was difficult for you, and how you managed to get around the problem?” and so on. The client, in conjunction with the health care professional, can help to determine if past coping skills will be adequate to the long-term challenges of living with a chronic disease such as osteoporosis (Christiansen, 2000).
Readiness for Change Because the successful treatment for a chronic condition such as osteoporosis frequently involves lifestyle change, it is important for the heath care professional to assess the client’s readiness to both plan for and implement change. One approach to addressing readiness for change is the transtheoretical model (TTM) (Prochaska, Redding, & Evers, 1997). The TTM enables the health care provider to analyze and also predict change in behaviors. The TTM identifies five stages of change: precontemplation (the client is not considering any health related behavior change in the next 6 months); contemplation (the client is considering the pros and cons of change); preparation (the client is ready and receptive to beginning an action-oriented program); action (the client engages in the change behavior); and maintenance (the client continues to demonstrate specific healthrelated change) (Prochaska et al., 1997). For persons living with osteoporosis, change may range from utilizing adaptive equipment for self-care to seeking the assistance of a caregiver to complete heavy housework. Developing a set of strategies that will not be implemented by the client is a hollow victory in terms of facilitating maximum independence and quality of life.
Depression In the presence of any chronic illness, the health care professional must be alert to the possibility of depression developing. Depression, disability, and chronic illness may form a vicious cycle. For some individuals, chronic illness can bring on bouts of depression, which, in turn, can lead to a rundown physical condition that interferes with successful treatment of the chronic condition. Individuals diagnosed with chronic illnesses such as osteoporosis must adjust to the demands of the illness itself, as well as to the treatments for their condition. The illness may affect people’s mobility and independence and change the way they live, how they see themselves, and how they relate to others. For this reason, a certain amount of sadness or despair is normal. In some cases, a chronic illness may actually cause depression, which, though treatable, is a serious medical condition by itself (Sullivan, 1990). The client and key members of his or her support system should be aware of the signs that may indicate depression. Common signs of
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depression include a depressed or sad mood, a decreased interest in activity, feelings of excessive guilt or worthlessness, apathy or lack of motivation, changes in sleep, appetite, weight, energy, or sexual desire, and a decline in attention or concentration or memory. At its extreme, depression may trigger thoughts of death or suicide. Persons living with osteoporosis may feel and act old because of changes in appearance. They may withdraw from social contact or avoid certain situations secondary to fear of falling. As the ability to complete IADLs and ADLs diminishes, they may become more dependent on family and friends to assume the role of caregivers. Any of these unwelcome consequences may lead to the onset of depression. A formal assessment such as the Beck Depression Inventory or the Geriatric Depression Scale may be utilized. The Beck Depression Inventory (Beck, 1967) consists of 21 items. In a self-report format, the client reveals attitudes and symptoms of depression (Groth-Marnat, 1990). The Geriatric Depression Scale (Yesavage et al., 1983) consists of 15 items with yes or no answer options, with a score of 5 or more suggesting possible depression. A formal assessment in combination with probing interviews and clinical observations will allow the health care professional to intervene, should depression be suspected (Groth-Marnat, 1990).
Home Environment An on-site assessment of the client’s home may be indicated, specifically if issues of changes in motor control, postural control, or balance surface. Couches and chairs in the home should be evaluated to see how easily the client can sit and come to a standing position. Higher, firmer, seats and seat backs coupled with study arms provide the easiest and safest support for sitting and standing. Bed height should be high enough to allow easy movement into and out of the bed. If the client is found to be using furniture to provide support when walking, the furniture should be heavy and/or secured to the wall. Grab bars installed in the bathroom will provide for safe and efficient toilet, shower, and tub transfers. A large nonskid mat should be placed in the bottom of the tub and shower (a mat that is large enough to cover the entire bottom of the tub and shower). Areas of tile or linoleum flooring should be examined to see if their surfaces are nonskid. Storage areas in the bedrooms, bathroom, and kitchen should be examined and arranged to provide easy access to frequently used items with the least amount of bending, twisting, or lifting. If the client uses a mobility device, such as a cane or walker, general accessibility to all areas of the home should be evaluated.
Common Problems Affecting Independence and Quality of Life A background understanding of the etiology and progression of osteoporosis, coupled with a knowledge of clinical assessments designed to identify potential deficits, allows the health care professional to anticipate problems that may affect independence and quality of life. Clients with osteoporosis may be at risk for specific problems in ADL, IADL, leisure, and work. Accompanying changes in self-concept, coping skills, willingness to accept change, and depression may compound the physical picture.
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Activities of Daily Living Clients living with osteoporosis may experience difficulty with ADL because of skeletal changes. The combination of limited ROM, decreased muscle strength, and skeletal deformity may limit functional reach. Reaching for and hanging clothes in a closet, reaching for dishes or glasses from the kitchen shelf, bathing, washing, dressing, or transferring from one surface to another may also be difficult. Some clients with osteoporosis experience sleep disturbances. These may be the result of decreased respiratory function (Tamparo & Lewis, 2005). Respiratory function may be compromised as the result of kyphosis and lordosis (Tamparo & Lewis, 2005). The presence of skeletal deformity may also limit a client’s positioning options. Inability to get comfortable and find a restful position may contribute to poor quality sleep. Sleep disturbance is one factor that contributes to fatigue in this population. In addition to contributing to sleep disturbances, the presence of kyphosis or lordosis may lead to difficulty finding clothing. Popular sizes and styles of clothing may no longer fit properly. Shopping for and selecting stylish, well-fitting clothing that is easy to put on and take off may pose a challenge. For women, waists and hemlines often need to be shortened in front and extended in the back. Another common complaint from clients with osteoporosis is increased fatigue. Completing their morning routine, bathing, dressing, grooming, and eating, may exceed their energy stores. Each of the foundational problems discussed previously, decreased ROM, decreased strength, the presence of skeletal deformity, and lack of sleep may contribute to an overall feeling of malaise.
Instrumental Activities of Daily Living IADLs such as light housework, heavy housework, cooking, lawn care, and home maintenance may present specific challenges to clients living with osteoporosis. Instrumental activities of daily living that require lifting or carrying heavy loads may be of concern because of the danger of exacerbating pain or increasing the risk of fracture, particularly in the vertebrae, or perhaps may cause individuals to topple forward or backward. Reduced sitting and standing tolerance secondary to pain, fatigue, or skeletal deformity may significantly limit engagement in activities such as lawn care, shoveling snow, or completing minor home repairs that require extended periods of standing or sitting for task completion. Likewise, persons with osteoporosis should be cautioned not to climb ladders or step stools.
Leisure A balanced lifestyle requires the pursuit of leisure interests. For some persons living with osteoporosis, the leisure pursuits that they have engaged in throughout life may need to be reexamined. Persons who have enjoyed a lifetime of sports or outdoor activities may be encouraged to identify leisure interests that can be engaged in while sitting or in a modified way. Decreased ROM, decreased strength, skeletal deformity, and increased fatigue may combine to diminish the pleasure that was formerly found in leisure pursuits.
Work While the most common profile of a client with osteoporosis is a woman who is over 50 years old, many clients living with this disease may still be in the workforce and want
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to remain there. All job classifications may be impacted. For instance, jobs that require work tasks to be completed in a sitting position may be compromised by reduced sitting tolerance secondary to skeletal deformity. Those jobs (such as stocking shelves) that require lifting or carrying heavy loads may be of concern because of the danger of exacerbating pain or increasing the risk of vertebral fracture.
Lifestyle Redesign for Living With Osteoporosis Facilitating and maintaining independence and quality of life while living with a chronic condition such as osteoporosis requires a dynamic approach that balances remediation, prevention, and compensation strategies. Remediation strategies are implemented in an attempt to fix or remediate problems that a client currently encounters. Prevention strategies are used to limit further complications. Compensation strategies are adaptations made to an activity that allow the client to work around a complication and continue being independent in a chosen task. Using the information gleaned from evaluating roles, activities, and interests, in combination with the results of the battery of assessments of component skills (ROM, strength, balance, posture, coping skills, self-concept, and depression), the health care professional matches prevention, remediation, and compensation techniques and designs a comprehensive set of goals and treatment strategies designed to preserve and promote maximum independence and quality of life.
Remediation Strategies Remediation strategies are designed to improve or remediate the negative effects of osteoporosis. The health professional is encouraged to consider the following points in designing a comprehensive treatment approach: • Encourage the client to engage in graded, progressive exercises to increase joint
motion. Most especially encourage hyperextending the back by gently raising the hands over the head. • Encourage the use of good body mechanics and positioning while performing any physical activity. • Encourage weight-bearing activities, such as walking and social dancing, that maintain/increase strength in the muscles around the hip. • Encourage a decrease in pain by promoting better posture and an increased (to tolerance) level of physical activity.
Prevention Strategies Prevention strategies are designed to limit further complications. Recognizing that osteoporosis is a chronic condition and working actively to prevent its impact on independence and quality of life, the heath care professional may incorporate the following precautions into a comprehensive plan: Instruct on safety procedures, including the use of grab bars and handrails. Fractures of the hip and radius may occur even from a minor fall.
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Eliminate hazards on the floor, such as throw rugs and extension cords. Stress the importance of adequate lighting in areas where the client will be walking. If the client uses a mobility aid (such as a walker or cane), make sure that the client is instructed in and can demonstrate proper use. Provide instruction on basic body mechanics, especially proper lifting and carrying, to avoid back strain or undue pressure on the vertebrae. Assist the client with establishing a schedule of activities that provides alternating cycles of activity and rest. Recommend physical activity to tolerance. Increased physical activity reduces the feeling of being old. Encourage creative crafts, music, drama, and dance to enhance self-concept. If withdrawal has occurred, encourage the person to reestablish contacts or make new contacts with community members who may also need more physical activity. Remind the client to try not to sleep in the fetal position. Explore with the client home management activities that can be performed safely and at the same time satisfy the need for physical activity. Dusting, washing and folding clothes, hanging clothes, and light vacuuming may be good choices. Explore with the client leisure activities that may substitute for more aggressive sports. Nature walks, shopping, visits to galleries or museums, and garden tours may safely satisfy a need for physical activity. Waist-high container gardens may also offer a meaningful leisure activity.
Compensation Strategies Compensation strategies are designed to allow the client to continue to be independent and productive while living with a chronic illness. In terms of osteoporosis specifically, clients may benefit from the use of adaptive equipment and the incorporation of energy conservation and joint protection techniques into the daily routine (Gerber, et al., 1987; Mathiowetz, Matuska, & Murphy, 2001; Steed & Mulligan, 2004; Young, 1991). Again, recognizing the fact that osteoporosis is a chronic condition and recognizing its potential impact on independence and quality of life, the health care professional may incorporate the following compensation techniques into a comprehensive plan: • Provide self-help devices that will facilitate safe performance of ADLs. Table 10.4
provides a short list of devices that compensate for decreased functional reach and promote safe transfers and mobility. Self-help devices can be purchased from medical equipment companies or many full-service drug stores. • Select furniture that will provide good support for the back and neck and solid arm rests to facilitate sitting and standing. • Instruct the client in principles of energy conservation and encourage the client to problem-solve strategies for incorporating energy conservation into the daily routine. Table 10.5 provides a list of energy conservation principles. • If appropriate, instruct in principles of joint protection (for selected joints based on an analysis of the activity) and encourage the client to problem-solve strategies for incorporating joint protection into the daily routine. A list of joint protection techniques is provided in Table 10.6.
Table
10.4
Table
10.5
Recommended Self-Help Devices Long-handled reacher Long-handled sponge Long-handled shoe horn Sock aid Raised toilet seat Tub or shower bench or chair Properly positioned grab bars Remote control device for lighting
Principles of Energy Conservation -
Table
10.6
Set priorities and do those tasks that are most important or necessary first. Schedule and complete tasks over a period of time. . . . DO NOT ATTEMPT TO DO EVERYTHING AT ONCE! Take frequent rest breaks to balance rest and activity. Sit instead of standing whenever possible. Use relaxation techniques to decrease anxiety and stress. Lead a balanced lifestyle with time for leisure and spiritual enrichment. Work slowly to save energy instead of rushing. Work at a comfortable pace. If you need assistance with a task, do the portion of a task that is enjoyable and let someone else do the rest!
Joint Protection -
Distribute weight evenly over joints if possible. Place more stress on larger joints. Avoid static holding for long periods of time. Avoid lifting excess weight. Use adaptive equipment (such as jar openers and levered door handles) to protect joints if possible. Raise seats to make sitting and standing easier. Avoid doing repetitious activities (such as weeding the garden) for long periods of time. Stop and rest your joints.
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Successful Lifestyle Redesign—Outcomes and Prognosis While the specifics of maintaining the maximum level of independence and quality of life while living with osteoporosis will be individual and somewhat different for each client, the health care professional can use the following set of outcomes to judge the relative success of a treatment program. As a result of a successful treatment program and lifestyle redesign that incorporates a dynamic balance of prevention, remediation, and compensation strategies, the client will do the following: Use adaptive equipment to perform ADLs and IADLs that would otherwise lead to back strain or excessive body flexion. Maintain postural control and balance. Demonstrate knowledge of safety issues and take preemptive action to reduce the risk of injury. Maintain or increase the level of physical activity that is associated with mild to moderate weight bearing. Maintain a component of leisure activities that are enjoyable and fulfilling. Adjust cycles of activity and rest to increase physical activity but not pain. Be able to maintain meaningful relationships, negotiate for assistance, and act as a personal advocate.
Summary Living with osteoporosis poses a substantial challenge to persons who have it, as well as to the health care professionals charged with providing help. By beginning with a foundational understanding of the roles and activities that are important to the client, the health care team can begin to predict the impact that osteoporosis may have on the individual. With knowledge and insight related to the symptoms and expected course of the disease and its major complications, the team can assess the specific ongoing impact of osteoporosis on key areas of function such as Rom, strength, balance and postural control, self-concept, coping skills, and depression. By developing a set of client-centered goals, the team guarantees that the proposed treatment will be client centered. By implementing a dynamic combination of prevention, remediation, and compensation strategies, the health care team can ensure that every effort is being made to facilitate maximum independence and quality of life for clients living with osteoporosis.
REFERENCES American Occupational Therapy Association (AOTA). (2002). Occupational therapy practice framework: Domain and process. Bethesda, MD: Author. Baum, C., & Edwards, D. (2001). Activity card sort. St. Louis, MO: Washington University School of Medicine. Beck, A. (1967). Depression: Clinical, experimental and clinical aspects. New York: Harper & Row. Christiansen, C. (2000). Identity, personal projects and happiness: Self construction in everyday action. Journal of Occupational Science, 7(3), 98 –107.
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Damijanov, I. (2000). Pathology for the health related professions (2nd ed.). Philadelphia: W B. Saunders. Gerber, L., Furst, G., Shulman, B., Smith, C., Thornton, B., Liang, M., et al. (1987). Patient education program to teach energy conservation behaviors to patients with rheumatoid arthritis: A pilot study. Archives of Physical Medicine and Rehabilitation, 68(7), 442–445. Gregory, M. (1983). Occupational behavior and lifestyle satisfaction among retirees. American Journal of Occupational Therapy, 37, 548 –553. Groth-Marnat, G. (1990). The handbook of psychological assessment (2nd ed.). New York: John Wiley & Sons. Hasselkus, B. (2002). The meaning of everyday occupation. Thorofare, NJ: Slack. Hislop, H., & Montgomery, J. (1995). Daniels and Worthingham muscle testing: Techniques of manual examination (6th ed.). Philadelphia: W. B. Saunders. Jacobs, K., & Jacobs, L. (2004). Quick reference dictionary for occupational therapy (4th ed., pp. 418 – 419). Thorofare, NJ: Slack, Inc. Kendall, F., & McCreary, E. (1993). Muscle testing and function (4th ed.). Baltimore: Williams and Wilkins. Kielhofner, G. (2004). Conceptual foundations for occupational therapy (3rd ed.). Philadelphia: F. A. Davis. Law, M., Baptiste, S., Carswell, A., McColl, M., Polatajko, H., & Pollock, N. (1991). Canadian occupational performance measure. Toronto: CAOT Publishers. Lo, J., & Zemke, R. (1997). The relationship between affective experience during daily occupations and subjective well being measures: A pilot study. Occupational Therapy in Mental Health 13(3), 1–21. Magaziner, J., Simonsick, E. M., Kashner, M., Hebel, J. R., & Kenzora, J. E. (1990). Predictors of functional recovery one year following hospital discharge for hip fracture: A prospective study. Journal of Gerontology, Medical Sciences, 45, M101–M107. Mandel, D., Jackson, J., Zemke, R., Nelson, L., & Clark, F. (1999). Lifestyle redesign: Implementing the well elderly study. Bethesda, MD: AOTA. Mathiowetz, V., Matuska, K., & Murphy, M. (2001). Efficacy of an energy conservation course for persons with multiple sclerosis. Archives of Physical Medicine and Rehabilitation, 82(4), 449–456. Norkin, C. (1995). Measurement of joint motion: A guide to goniometry. Philadelphia: F. A. Davis. Oakley, F., Kielhofner, G., Barris, R., & Reichler, R. (1986). The role checklist: Development and empirical assessment of reliability. Occupational Therapy Journal of Research, 5, 157–170. Penrod, J. (2000). Living with osteoporosis: The personal experience. In S. H. Gueldner, M. S. Burke, & H. Smiciklas-Wright (Eds.), Preventing and managing osteoporosis (pp. 17–24). New York: Springer Publishing. Prochhaska, J., Redding, C., & Evers, K. (1997). The transtheoretical model and stages of change. In K. Glanz, F. Lewis, & B. Timmer (Eds.), Health behavior and health education, theory, research and practice (2nd ed., pp. 63–91). San Francisco: Jossey-Bass. Steed, L., & Mulligan, K. (2004). Self-management interventions for chronic illness. Lancet, 36, 1523–1537. Sullivan, K. (1990). Depression and chronic illness. Journal of Clinical Psychology, 51, 3 –11. Tamparo, C., & Lewis, M. (2005). Diseases of the human body (4th ed.). Philadelphia: F. A. Davis. Yerxa, E., & Locker, S. (1990). Quality of time use by adults with spinal cord injury. American Journal of Occupational Therapy, 44(4), 318–326. Yesavage, J., Brink, T. L., Rose, T., Lum, O., Huang, V., Adey, M., et al. (1983). Development and validation of a geriatric depression screening scale: A preliminary report. Journal of Psychiatric Research, 17, 37– 49. Young, G. (1991). Energy conservation, occupational therapy, and the treatment of post-polio sequelae. Orthopedics 14(11), 1233 –1239.
4
Prevention Strategies
Maximizing Peak Bone Mass in Children, Adolescents, and Young Adults: A Public Health Priority
The period from infancy through adolescence is critical for building bones and developing healthful bone habits that help an individual to maintain a robust skeleton throughout life. . . . Health care professionals who are involved in the health maintenance of infants, children, and adolescents have an opportunity to positively influence bone health for the rest of their patient’s [sic ] lives. (U.S. Department of Health and Human Services, Bone Health and Osteoporosis: A Report of the Surgeon General )
I
11
Leann M. Lesperance
n 2004, the first-ever surgeon general’s report on bone health and osteoporosis was released (U.S. Department of Health and Human Services [USDHHS], 2004), as part of a coordinated public health effort to improve the bone health status of Americans. Not surprisingly, it includes recommendations for children, adolescents, and young adults. When bones are not well cared for during the early years of life, they may end up being thin and weak later in life, which means a higher risk for bone fractures. In other words, unhealthy choices and bad habits during childhood can lead to osteoporosis. Children of all ages (and their parents and health care providers) need to know about osteoporosis and take steps to prevent it. What can children, adolescents, and young adults do to care for their bones so that they will be strong and healthy throughout adulthood? Many researchers are addressing this and related questions. While the risk factors for developing osteoporosis in childhood are not yet completely understood, there is enough evidence to suggest that some can be modified during these early years. This chapter will review current recommendations from the surgeon general and other experts regarding strategies for the prevention of osteoporosis during childhood
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and adolescence. As with adults, nutrition and physical activity may play the biggest role in preventing osteoporosis. What foods children and teens eat and drink (or not) and what exercise they do (or do not do) may affect the health of their bones during their early years and later in life. For some children, medications and medical conditions also influence bone health.
Nutrition Bone is living tissue that increases in length, weight (mass), mineral content (density), and strength during childhood and adolescence. Most people reach their peak bone mass by age 30, and this is the strongest their bones will ever be. Starting out with stronger bones is thought to decrease the risk for developing osteoporosis later in life. The first 2 years of life and the early adolescent years are particularly important times for building bones. The amount of bone mineral gained during adolescence typically equals the amount lost throughout the rest of adult life (Bailey, Martin, McKay, Whiting, & Mirwald, 2000). It is critically important that children and teens get all the nutrients they need for optimal bone growth and development, including adequate calcium and vitamin D.
Calcium Calcium, in the presence of vitamin D and other essential nutrients (see chapter 7), is the mineral that makes bones dense and strong. Many studies have looked at the relationship between bone health and calcium intake (in foods and supplements) during childhood and adolescence. The results have been mixed, presumably due to variations in study design and confounding factors, and controversy regarding this issue persists. Several authors have attempted to clarify the situation. Wosje and Specker (2000) performed a meta-analysis of pediatric calcium supplementation trials and reported increased bone mineral density in adolescents who took supplements. However, these gains were most apparent in children who started with a low calcium intake and did not persist when the supplements were stopped. Lanou, Berkow, and Barnard (2005) examined the results of 58 studies of children and young adults and concluded that there was insufficient evidence to support nutrition guidelines promoting calcium intake. However, many of the individual studies did in fact show a modest positive effect, and Lanou, Berkow, and Barnard’s negative conclusion was refuted by several nutrition experts. A more recent clinical report issued by the Committee on Nutrition for the American Academy of Pediatrics encourages adequate calcium intake during childhood and adolescence as a strategy to promote bone health and possibly prevent osteoporosis (Greer, Krebs, & the Committee on Nutrition, 2006). The surgeon general’s report (USDHHS, 2004) also maintains that adequate calcium intake during these early years is critical for bone health. At this time, long-term studies on the relationship between calcium consumption during childhood and adolescence and bone density in adulthood are not available. Nevertheless, most experts agree that the evidence points toward long-lasting benefits from an adequate calcium intake throughout childhood and adolescence. Furthermore, habits established during childhood are more likely to persist into adulthood. In addition, calcium-rich foods tend to contain other important nutrients and, as such, are an important part of a healthy diet.
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How much calcium should a child get? The exact amount necessary for optimal growth and lifelong strong bones depends on many factors, including age, sex, ethnic background, and other foods in the diet. An estimate of the amount required is given by the Dietary Reference Intake (DRI) values, previously known as the Recommended Dietary Allowance (RDA), from the National Academy of Sciences’ Institute of Medicine (Table 11.1). These values are meant to be used as a general nutritional guideline. Some experts think children actually should be getting even higher amounts of calcium to reach maximum bone density. Except for the first year of life, however, many children do not get the recommended amounts of calcium. Most infants get enough calcium each day because they drink breast milk and/or infant formula, both excellent sources of calcium. The calcium in breast milk is more easily absorbed (more bioavailable), so the concentration of calcium in formula is higher. After the first year of life, the percentage of children who get the recommended amount of calcium declines dramatically. While 80% of toddlers (ages 1 to 2) achieve their recommended daily intake of calcium, only 50% of 3- to 5-year-olds still get enough calcium. That number drops even further among school age children. By ages 9 to 18, when the DRI for calcium is highest, only about 1 in 10 females and 1 in 3 males get the recommended amount of calcium (U.S. Department of Agriculture [USDA], 1997). The average actual calcium intake for teenage females is only two-thirds of the recommended amount (Ervin, Wang, Wright, & Kennedy-Stephenson, 2004). Milk remains the principal dietary source of calcium in the United States (Subar, KrebsSmith, Cook, & Kahle, 1998). Although toddlers are notoriously picky eaters, most of them get enough calcium because they drink at least two glasses of milk a day, getting 300 mg of calcium with each 8-ounce glass. However, older children increasingly are replacing milk with other beverages, most often sugar-sweetened drinks and fruit juice (Calvadini, SiegaRiz, & Popkin, 2000). Between 1977 and 1996, the consumption of sugar-sweetened beverages by children and adolescents aged 6 to 17 years increased approximately 40%, while milk consumption decreased by 30% to 40% among children and adolescents, respectively (Nielsen & Popkin, 2003). More than 50% of school age children consume at least some soda daily; 20% of adolescent males consume four or more servings daily (Gleason & Suitor, 2001). Some researchers have further suggested an association between carbonated
Table
11.1
Dietary Reference Intake (DRI)—Estimate of Amount Required Each Day Age 0 to 6 months old 6 to 12 months old 1 to 3 years old 4 to 8 years old 9 to 18 years old 19 to 50 years old
1
DRI for Calcium1
DRI for Vitamin D
210 mg 270 mg 500 mg 800 mg 1300 mg 1000 mg
200 IU 200 IU 200 IU 200 IU 200 IU
From Food and Nutrition Board of the National Academy of Sciences’ Institute of Medicine, 2001.
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beverage consumption, especially of cola, and bone fractures, possibly due to high levels of phosphoric acid in the cola, which may increase bone resorption (Wyshak, 2000). Some children avoid drinking milk because they are lactose intolerant. Fortunately, low-lactose and lactose-free milk now are available, as well as lactose-free ice cream and other dairy products. Other children, especially adolescent females, limit their intake of dairy products because they are concerned about dietary fat intake, although lower fat versions are available that contain as much (and sometimes more) calcium. Children and adolescents who are allergic to cow’s milk protein or who follow strictly vegetarian (vegan) diets can get enough calcium from nondairy sources. High levels of calcium can be found in a number of plant foods, including spinach, kale, turnip greens, broccoli, and almonds. Calcium is added to certain breads, cereals, and juices and also is found in tofu and soy milk. In a prospective study of 14- to 16-year-old girls drinking about two cups of calcium-fortified soy milk per day for a year, the bone mineral density and content of the hip was significantly increased in comparison with controls (Ho et al., 2005). Health care providers should take steps to make sure that children and adolescents are getting enough calcium: Ask questions about calcium intake at every well child visit, if possible, but especially at 2 or 3 years of age, after the child is no longer drinking human milk or infant formula; at 8 or 9 years of age, before the onset of puberty; and during early adolescence, when peak accumulation of calcium occurs. Encourage 2–3 age-appropriate servings per day of dairy products or equivalent calcium-containing foods or beverages (3–4 servings per day for adolescents). Give patients information regarding the calcium content of various foods, especially those patients whose calcium intake seems inadequate. Know that calcium-fortified soy milk and other nondairy foods are an option for children who cannot drink (due to allergy or intolerance) or do not choose to drink cow’s milk. Recommend calcium supplements for children and adolescents who do not get enough calcium in their diet. The most commonly available products contain calcium carbonate and calcium citrate. Avoid any calcium supplements that come from bone meal, oyster shell, or dolomite, because these may contain toxic ingredients like lead. For maximum absorption, take calcium supplements between meals, do not take more than 500 mg at once, and do not take iron supplements at the same time. Work initially to limit consumption of soft drinks at school, and ultimately to eliminate sweetened drinks in schools altogether (American Academy of Pediatrics [AAP], 2004).
Vitamin D In order to use calcium properly, children need to have enough vitamin D. The body can make its own vitamin D in the skin with exposure to sunlight. However, to decrease
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the risk of skin cancer, infants under 6 months of age should stay out of direct sunlight. When outside, children should regularly use sunscreen, which markedly decreases vitamin D production in the skin. Therefore, it is difficult to know whether children are making enough vitamin D. Severe vitamin D deficiency in children can cause rickets, a disease in which bone is not mineralized properly. The National Academy of Sciences recommends 200 IU per day to prevent vitamin D deficiency. High levels of vitamin D are found naturally in only a few foods, such as cod liver oil, salmon, tuna, and sardines; and these tend not to be popular with children. Egg yolks also contain vitamin D, but at much lower levels. Human milk contains relatively low levels of vitamin D. Today, vitamin D is added to infant formula and milk, including most brands of fortified soy milk. Infants who drink at least 500 mL (approximately 16 ounces or 2 cups) of formula and children who drink at least 500 mL of fortified milk usually get enough vitamin D in their diet (Gartner, Greer, & the Section on Breastfeeding and Committee on Nutrition, 2003). However, vitamin D generally is not added to other dairy products, such as cheese, yogurt, and ice cream. The following will help ensure adequate vitamin D intake: Babies who are exclusively breast fed should be given a supplement of 200 IU per day of vitamin D drops, especially babies in northern climates and during winter months, and babies with darker skin. Supplementation should begin within the first 2 months of life. Supplements no longer are recommended once the baby is drinking at least 500 mL per day of vitamin D–fortified formula or milk. Children and adolescents who do not drink at least 500 mL per day of vitamin D–fortified milk should take a supplement of 200 IU of vitamin D (the amount contained in most multivitamins).
Physical Activity Weight-bearing exercise, such as running or jumping, is thought to play an important part in reaching peak bone mass. In fact, some research suggests that regular weightbearing exercise influences peak bone mass more than dietary calcium intake (Welten et al., 1994). This type of exercise works bones and muscles against gravity, causing bones to build more cells and become stronger. Children who are more physically active tend to have increased bone densities. In one study, a high-impact, circuit-based, jumping intervention (10 minutes, 3 times per week) implemented over 2 consecutive years resulted in increased bone mineral content in pubertal girls compared with age-matched controls (MacKelvie, Khan, Petit, Janssen, & McKay, 2003). In another study, nonelite prepubertal dancers had greater bone mineral content than controls (Matthews et al., 2006), 1 and 2 years after peak height velocity was attained. Follow-up studies are needed to determine whether these bony changes persist. Other studies on older elite female dancers and gymnasts suggest that bone mineral density may remain higher in adulthood due to exercise in childhood (Bass et al., 1998; Khan et al., 1998). Not exercising may have the opposite effect. In a study of young adult women, Ho and Kung (2005) found that physical inactivity was associated with a three-fold risk of lower bone mineral density.
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Physical activity or sports participation should start before puberty and continue into adulthood (Vicente-Rodriguez, 2006). Exercising at a younger age may have a greater impact than exercising later. For example, Kannus et al. (1995) studied bone mineral content in the arms of female tennis and squash players and showed that the bone content was much greater in the dominant arm. However, the difference between the arms was two times greater in women who started playing before puberty. On the other hand, too much of a good thing can be harmful. Adolescent females who exercise so much that their menstrual periods stop (amenorrhea) are at increased risk for osteoporosis due to decreased estrogen levels. Regular physical activity has many health benefits, including weight control, stress reduction, and increased aerobic capacity. To help prevent osteoporosis and promote overall health and well-being, health care providers should do the following: Encourage regular exercise, especially weight-bearing exercise such as running and jumping, for all children and adolescents. Set a goal of 30 to 60 minutes of physical activity every day. Remind parents to set a good example for their children by getting regular exercise themselves. Suggest that children and adolescents limit their television, computer, and video game time to 1–2 hours per day. Watch for signs of overtraining or excessive exercise.
Medications Some medications commonly used by children, adolescents, and young adults can have a negative effect on bones. These include corticosteroids, antiepileptics, and immunosuppressive agents. Corticosteroids are used frequently to treat children with asthma, and also children with inflammatory disorders such as rheumatoid arthritis, lupus, and inflammatory bowel disease. The long-term effects of these medications on bone health in children have not been well described. However, studies in adults show that even small doses of oral glucocorticoids (as little as 2.5–7.5 mg of prednisone or equivalent daily) increased the risk of fractures (Van Staa, Leufkens, & Cooper, 2002). Fewer long-term studies are available on the effects of inhaled steroids, which have been in use for a relatively short period of time (Allen et al., 2003). Since they are absorbed from the lungs into the bloodstream, they have the potential to adversely affect bone, especially when used at higher doses or for long periods of time. Prospective studies found a short-term reduction in growth velocity in children using an inhaled corticosteroid, although target height was usually achieved (Mortimer, Harrison, & Tattersfield, 2005). Medications used to control seizures, in particular diphenylhydantoin, phenobarbital, carbamazine, and sodium valproate, can cause bone loss (Stein & Shane, 2003). Deleterious effects on bone health appear to be more likely for individuals who are on high doses or on more than one of these medications, who have been on these medications for many years, who are simultaneously taking other medications that raise liver enzymes, or who also have additional risk factors, such as nutritional deficiencies or other chronic illnesses.
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Some immunosuppressant agents also can cause bone disease. High doses of cyclosporine A and tacrolimus, which are often used in conjunction with steroids to prevent rejection after organ transplantation, can cause a severe form of osteoporosis (Cohen & Shance, 2003). Methotrexate, used to treat cancer and inflammatory diseases such as Crohn’s disease and rheumatoid arthritis, may also cause bone loss. Health care providers must be aware of medications that can affect bone health, and precautions that should be taken when patients are on these medications: Whenever systemic or inhaled steroids are prescribed, possible decreased bone density and reduced growth velocity must be taken into consideration. If steroids are necessary, the lowest dose required to control symptoms should be used, for the shortest time possible, in order to minimize any effects on bone health. Glucocorticoids should be given locally whenever possible. In a child with asthma, for example, choose inhaled steroids over oral steroids. If antiepileptics are necessary, they should be tapered as tolerated to the lowest possible dose. Children and adolescents on any medications known to have negative effects on bone health should be monitored. Counsel them about the importance of good nutrition and regular physical activity. A bone density test should be performed on young adults taking oral glucocorticoids, antiepileptics, immunosuppressants, or other medications that can result in bone loss.
Medical Conditions Certain medical conditions can affect bone health, either directly or indirectly, and put children and adolescents at risk for skeletal problems, including osteoporosis. Several rare conditions, such as osteogenesis imperfecta, chondrodysplasia, idiopathic juvenile osteoporosis, and fibrous dysplasia, affect the bones directly. Prematurity is another condition that directly affects bone health. Since the fetal skeleton acquires most of its calcium in the last trimester, premature babies have lower bone mass than full-term babies. They need additional supplementation of calcium, vitamin D, phosphorus, and protein until they build up their bone mass, which can take up to 5 years (Schanler, 2001). Childhood fractures, especially those that result from minimal trauma or repeated fractures, may be markers for low peak bone mass and persistent bone fragility (Ferrari, Chevalley, Bonjour, & Rizzoli, 2006). More commonly, medical conditions affect the bones indirectly. Celiac disease, inflammatory bowel disease, cystic fibrosis, and other gastrointestinal diseases can make it hard for the body to absorb nutrients from the intestines. Cerebral palsy and other musculoskeletal problems cause limited weight bearing, leading to loss of bone density. Estrogen and testosterone are essential for optimal bone development, and deficiency of these hormones leads to low peak bone mass (Riggs, Khosla, & Melton, 2002). This can be seen in adolescents with Turner’s or Klinefelter’s syndrome, cancer, or other
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chronic illnesses that interfere with the onset of puberty. Delayed puberty can be constitutional but also can be seen in adolescent females who exercise too much or eat too little. In a study of young adult women, late menarche (onset beyond 14 years) was associated with more than twice the risk of having low hipbone mineral density (Ho & Kung, 2005). In that study, low body weight also was predictive of low bone mineral density. Delayed puberty in adolescent males also may affect adult bone mineral density (Kindblom et al., 2006). Excessive exercise, emotional stress, and low body weight can cause oligomenorrhea (infrequent menstrual cycles) or amenorrhea (absent menstrual cycles). The complications of amenorrhea may include failure to achieve peak bone mass, bone loss, and increased risk of stress fractures. Anorexia nervosa has a significant impact on bone health, because the severe calorie restriction and resultant weight loss cause both hormonal imbalance and nutritional deficiencies. Furthermore, anorexia nervosa tends to occur during adolescence, a critical time for increasing bone mineral density. Adolescent females with anorexia nervosa are at high risk for reduced peak bone mass (Soyka et al., 2002). Amenorrhea combined with disordered eating should raise concern for the female athlete triad, a serious syndrome comprising disordered eating, amenorrhea, and osteopenia. Early identification and treatment of this condition may help to decrease the consequences (Waldrop, 2005). Survivors of childhood cancer have been shown to be at particular risk of bone disease (Kaste, 2004). Fortunately, regular physical activity seemed to help develop and preserve normal bone mineral density in survivors of acute lymphoblastic leukemia ( Jarfelt, Fors, Lannering, & Bjarnason, 2006) and may help with other cancers. Health care providers can limit the impact of these medical conditions on bone health: For all children, adolescents, and young adults, carefully review family histories and medical histories for any indications of medical conditions that may impact bone health. Monitor any children and adolescents with medical conditions known to affect bone health. Counsel them about the importance of good nutrition and regular physical activity. Premature babies who are being breast fed need supplemental calcium, vitamin D, phosphorus, and protein to meet their nutritional needs. Premature babies who are not being breast fed should receive formula that is specially designed for their needs. Ask adolescent and young adults about the onset and regularity of menses. Late menarche (beyond age 14) or amenorrhea lasting longer than 3 months (regardless of the cause) warrants further investigation. Measure height and weight at all health maintenance visits. Refer any child or adolescent with poor growth to a specialist. Since adolescents tend to visit health care providers infrequently, measure adolescent females’ weight at every visit. Weight loss or decreased weight percentiles should prompt questions about disordered eating. Referral to a specialist (usually an endocrinologist, nephrologist, or rheumatologist) is indicated.
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Prevention Programs Successful attempts are being made to increase children’s knowledge about bone health and osteoporosis. Since children spend most of their day in school, many of these programs are developed and implemented through schools. For example, in the Better Bones Buddies educational program, school children ages 9 to 15 improved their knowledge of osteoporosis and reported increased calcium consumption (Schrader, Blue, & Horner, 2005). Schools offer many opportunities to teach children bone healthy habits. A multifaceted approach aimed at osteoporosis prevention can be developed using the Centers for Disease Control and Prevention (CDC) coordinated school health model. This would include the following: Health services—School nurses and school-based health centers provide access and/or referral to primary health care services and can promote the prevention strategies outlined above and regularly assess for risk factors. Health education—A K–12 curriculum can include lessons about the importance of bone health and ways to achieve it. Physical education—A K–12 curriculum can promote lifelong physical activity, including weight-bearing exercise to help prevent osteoporosis. Nutrition services—Calcium-rich, low-fat meals, snacks, and beverages can be offered. Sugar-sweetened beverages should be discouraged. Healthy school environment—This may include safe playground equipment and limited or no soda-vending machines. Health promotion for staff—Opportunities for staff to improve their bone health should be offered. Family/community involvement—Programs can be developed to educate parents and community members about the importance of students’ and their own bone health. Counseling, psychological, and social services—Programs aimed at improving students’ mental, emotional, and social health may increase students’ desire to develop lifelong bone healthy habits. School-based health centers, in particular, have been shown to improve the health and well-being of children by making health care services more accessible to all, regardless of ability to pay (Kisker & Brown, 1996; Terwilliger, 1994). They are found in elementary, middle, and high schools, in rural, suburban, and urban schools, and particularly in schools with a high proportion of students living at or below the poverty level. Fortunately, there is increasing state support for these programs. Two states have initiated cooperative extension programs that focus specifically on children (Calcium, It’s Not Just Milk, Nevada) and adolescents ( Jump Start Your Bones©, Rutgers, New Jersey). Each of these programs is discussed further in chapter 13.
REFERENCES Allen, D. B., Bielory, L., Derendorf, H., Dluhy, R., Colice, G. L., & Szefler, S. J. (2003). Inhaled corticosteroids: Past lessons and future issues. Journal of Allergy and Clinical Immunology, 112, S1–S40.
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Osteoporosis American Academy of Pediatrics, Committee on Nutrition. (2004). Soft drinks in schools. Pediatrics, 113, 152–154. Bailey, D. A., Martin, A. D., McKay, H. A., Whiting, S., & Mirwald, R. (2000). Calcium accretion in girls and boys during puberty: A longitudinal analysis. Journal of Bone and Mineral Research, 15(11), 2245–2250. Bass, S., Pearce, G., Hendrich, E., Delmas, P., Bradney, M., Harding, A., et al. (1998). Exercise before puberty may confer residual benefits in bone density in adulthood: Studies in active prepubertal and retired gymnasts. Journal of Bone and Mineral Research, 13(3), 500–507. Calvadini, C., Siega-Riz, A. M., & Popkin, B. M. (2000). US adolescent food intake trends from 1965 to 1996. Archives of Disease in Childhood, 83, 18–24. Cohen, A., & Shance, E. (2003). Osteoporosis after solid organ and bone marrow transplantation. Osteoporosis International, 14, 617–630. Ervin, R. B., Wang, C. Y., Wright, J. D., & Kennedy-Stephenson, J. (2004). Dietary intake of selected minerals for the United States population: 1999–2000. Advance data from vital and health statistics (No. 34). Hyattsville, MD: National Center for Health Statistics. Ferrari, S. L., Chevalley, T., Bonjour, J. P., & Rizzoli, R. (2006). Childhood fractures are associated with decreased bone mass gain during puberty: An early marker of persistent bone fragility? Journal of Bone and Mineral Research, 21(4), 501–507. Gartner, L. M., Greer, F. R., and the Section on Breastfeeding and Committee on Nutrition. (2003). Prevention of rickets and vitamin D deficiency: new guidelines for vitamin D intake. Pediatrics, 111, 908–910. Gleason, P., & Suitor, C. (2001). Children’s diets in the mid-1990s: Dietary intake and its relationship with school meal participation. Alexandria, VA: U.S. Department of Agriculture, Food and Nutrition Service, Office of Analysis, Nutrition, and Evaluation. Available at://www.fns.usda.gov/oane/ menu/published/cnp/files/childiet.pdf. Greer, F. R., Krebs, N. F., and the Committee on Nutrition. (2006). Optimizing bone health and calcium intakes of infants, children, and adolescents. Pediatrics, 117, 578–585. Ho, A. Y., & Kung, A. W. (2005). Determinants of peak bone mineral density and bone area in young women. Journal of Bone and Mineral Metabolism, 23, 470–475. Ho, S. C., Guldan, G. S., Woo, J., Yu, R., Tse, M. M., Sham, A., & Cheng, J. (2005). A prospective study of the effects of 1-year calcium-fortified soy milk supplementation on dietary calcium intake and bone health in Chinese adolescent girls aged 14 to 16. Osteoporosis International, 16(12), 1907–1916. Jarfelt, M., Fors, H., Lannering, B., & Bjarnason, R. (2006). Bone mineral density and bone turnover in young adult survivors of childhood acute lymphoblastic leukaemia. European Journal of Endocrinology, 154(2), 303–309. Kannus, P., Haapasalo, H., Sankelo, M., Sievanen, H., Pasanen, M., Heinonen, A., et al. (1995). Effect of starting age of physical activity on bone mass in the dominant arm of tennis and squash players. Annals of Internal Medicine, 123, 27–31. Kaste, S. C. (2004). Bone-mineral density deficits from childhood cancer and its therapy: A review of at-risk patient cohorts and available imaging methods. Pediatric Radiology, 34(5), 373–378. Khan, K. M., Bennell, K. L., Hopper, J. L., Nowson, C., Sherwin, A. J., Flicker, L., et al. (1998). Self-reported ballet classes undertaken at age 10–12 and hip bone mineral density. Osteoporosis International, 8, 165–173. Kindblom, J. M., Lorentzon, M., Norjavaara, E., Hellqvist, A., Nilsson, S., Mellstrom, D., et al. (2006). Pubertal timing predicts previous fractures and BMD in young adult men: The GOOD study. Journal of Bone and Mineral Research, 21(5), 790–795. Kisker, E. E., & Brown, R. S. (1996). Do school-based health centers improve adolescents’ access to health care, health status, and risk-taking behavior? Journal of Adolescent Health, 18(5), 335–343. Lanou, A. J., Berkow, S. E., & Barnard, N. D. (2005). Calcium, dairy products, and bone health in children and young adults: a reevaluation of the evidence. Pediatrics, 115, 736–743. MacKelvie, K. J., Khan, K. M., Petit, M. A., Janssen, P. A., & McKay, H. A. (2003). A school-based exercise intervention elicits substantial bone health benefits: A 2-year randomized controlled trial in girls. Pediatrics, 112, e447–e452. Matthews, B. L., Bennell, K. L., McKay, H. A., Khan, K. M., Baxter-Jones, A. D., Mirwald, R. L., et al. (2006). Dancing for bone health: A 3-year longitudinal study of bone mineral accrual across puberty in female non-elite dancers and controls. Osteoporosis International, 17(7), 1043–1054. Mortimer, K. J., Harrison, T. W., & Tattersfield, A. E. (2005). Effects of inhaled corticosteroids on bone. Annals of Allergy, Asthma and Immunology, 94, 15–21.
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Nielsen, S. J., & Popkin, B. M. (2003). Patterns and trends in food portion sizes, 1977–1998. Journal of the American Medical Association, 289, 450–453. Riggs, B. L., Khosla, S., & Melton, L. J., III. (2002). Sex steroids and the construction and conservation of the adult skeleton. Endocrine Reviews, 23(2), 279–302. Schanler, R. J. (2001). The use of human milk for premature infants. Pediatric Clinics of North America, 48(1), 207–219. Schrader, S. L., Blue, R., & Horner, A. (2005). Better Bone Buddies: An osteoporosis prevention program. Journal of School Nursing, 21, 106–114. Soyka, L. A., Misra, M., Frendhman, A., Miller, K. K., Grinspoon, S., Schoenfeld, D. A., et al. (2002). Abnormal bone mineral accrual in adolescent girls with anorexia nervosa. Journal of Clinical Endocrinology and Metabolism, 87(9), 4177–4185. Stein, E., & Shane, E. (2003). Secondary osteoporosis. Endocrinology and Metabolism Clinics of North America, 32(1), 115–134. Subar, A. F., Krebs-Smith, S. M., Cook, A., & Kahle, L. L. (1998). Dietary sources of nutrients among US children, 1989–1991. Pediatrics, 102, 913–923. Terwilliger, S. H. (1994). Early access to health care services through a rural school-based health center. Journal of School Health, 64(7), 284–289. U.S. Department of Agriculture, Agricultural Research Service. (1997). Data tables: Results from USDA’s 1994–96 continuing survey of food intakes by individuals and 1994–96 diet and knowledge survey. Retrieved June 27, 2006 from www.ars.usda.gov/services/docs.htm?docid=7760 U.S. Department of Health and Human Services. (2004). Bone health and osteoporosis: A report of the surgeon general. Public Health Service, Office of the Surgeon General, Rockville, MD. Van Staa, T. P., Leufkens, H. G. M., & Cooper, C. (2002). The epidemiology of corticosteroid-induced osteoporosis: a meta-analysis. Osteoporosis International, 13(10), 777–787. Vicente-Rodriguez, G. (2006). How does exercise affect bone development during growth? Sports Medicine, 36(7), 561–569. Waldrop, J. (2005). Early identification and intervention for female athlete triad. Journal of Pediatric Health Care, 19(4), 213–220. Welten, D. C., Kemper, H. C., Post, G. B., Mechelen, W., Twisk, J., Lips, P., et al. (1994). Weightbearing activity during youth is a more important factor for peak bone mass than calcium intake. Journal of Bone and Mineral Research, 9, 1089–1096. Wosje, K. S., & Specker, B. L. (2000). Role of calcium in bone health during childhood. Nutrition Reviews, 58(9), 253–268. Wyshak, G. (2000). Teenaged girls, carbonated beverage consumption, and bone fractures. Archives of Pediatric and Adolescent Medicine, 154, 610–613.
A Model for Improving Access to Osteoporosis Care: The Geisinger Health System Mobile DXA Program
I
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n order to better serve its mostly rural population, Geisinger Health System, located in the heart of central Pennsylvania, outfitted two vans with full body dual X-ray absorptiometry (DXA) units, and these vans travel to remote locations in central Pennsylvania to provide screenings. The vans are very popular with the communities they serve and have become financially self-supporting. The vans travel more than 17,000 miles each year to screen people who live in outlying areas. More than 16,000 persons have been screened using the mobile units in the 5½ years since the program began; over one third of those screened were found to have low bone density. Details of the implementation and evaluation of the model are described in the paragraphs below.
Eric D. Newman
Osteoporosis Testing Osteoporosis is a highly prevalent disease that is significantly underdiagnosed. The complications of osteoporosis include fracture (with resultant pain and loss of function) as well as death. Treatment has been shown to decrease fracture risk by about 50% using currently available medicines. Thus diagnosing osteoporosis and assessing fracture risk are paramount. Although bone strength may be the most important determinant of fracture risk, it is a bone property that cannot be adequately measured in humans. The best test today for predicting fracture risk is assessment of bone density. Currently, the National
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Osteoporosis Foundation (NOF) (2002) and the surgeon general (U.S. Department of Health and Human Services, 2004) recommend routine bone density testing in all women over the age of 65. However, the most reliable technology for obtaining bone mineral density measures (DXA) is not readily transportable, which often poses a barrier to access for persons who live in nonurban areas.
Heel Ultrasound—A Helpful but Incomplete Solution The two technologies most frequently used for bone density testing are heel ultrasound (HUS) and DXA. HUS uses change in speed of sound and waveform attenuation to create a number that correlates with bone density. A T-score is created by comparing this extrapolated value to a normative database, and this value has been shown to predict fracture risk at the hip and spine. While DXA testing is considered the gold-standard fracture risk assessment tool, HUS does have some advantages, including portability, no radiation, and low cost. This makes it an appealing technology for patients as well as primary care offices. As part of the Geisinger Health System Osteoporosis Disease Management Program (Newman, Ayoub, Stachey, Diehl, & Wood, 2003), we developed a highly successful partnership with our primary care colleagues using HUS technology. We trained the support staff in the primary care offices to operate the HUS machine, trained their physicians to interpret the results, provided a complete reporting package (interpretation, education, and documentation), transported the machine to their offices on a prescheduled basis, and allowed them to bill for the study as appropriate. In return, we asked for them to highlight osteoporosis as an important issue for their patients. Over 10,000 HUS studies have been performed within this program. The major disadvantage to HUS is that a significant proportion of patients will need a DXA in addition, for two reasons: indeterminate results and a need for ongoing monitoring of low bone density or treatment effectiveness. HUS results can be categorized as low risk, high risk, and indeterminate risk. Low risk actually means that if a follow-up DXA is done, the chances of finding a T-score at the hip or spine that would suggest treatment are very low. (Bone loss occurs at different sites at different rates, necessitating a “low risk” T-score using HUS as > 0.0 or > –0.5. At this level it is unlikely that a follow-up DXA would show a result where treatment would be considered.) High risk means that the T-score is low enough, and hence fracture risk is high enough, that a prescription medication should be considered. However, a follow-up DXA should be considered if monitoring is desired (HUS has not been shown to be effective in monitoring response to therapy). Indeterminate risk means that it is unclear if the patient’s risk is high or low, and a follow-up DXA should be done at the clinically relevant sites (spine and hip) to best predict fracture risk in that patient. Using this paradigm, virtually all patients with high risk and indeterminate risk values should proceed with DXA testing. In our program, 65% of all patients receiving HUS were recommended for a DXA follow-up. Unfortunately, follow-up DXA scans were not accomplished in the majority of these cases, in large part because of lack of access to DXA technology in our rural setting.
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Mobile DXA—Providing the Gold-Standard Test at the Convenience of the Patient’s Primary Care Physician’s Office In an effort to complement our HUS program and improve the diagnosis and treatment of osteoporosis in our rural setting, we designed a mobile osteoporosis unit to house a Hologic Discovery–C Bone Densitometer (a type of DXA) inside a specially configured 30-foot van (see Figures 12.1 and 12.2) (Newman et al., 2004). The unit was designed to be comfortable, fully computerized, and efficient. The front of the unit has seats for the driver and the technologist. The mid-section houses the patient entrance into the vehicle (two steps with a safety handrail), a couch, and a patient education area. The computer workstation is oriented so that the technologist can see the patient on the DXA table through a windowed pass-through. The rear of the van houses the DXA, in a section that is 9 feet long by 8 feet wide. The DXA unit measures spine/hip/forearm bone mineral density and performs vertebral fracture assessment (VFA). The unit can be operated alone with a generator, or with a 220-volt shoreline cord. The Mobile DXA Program began in November 2001. Staffing includes 1.5 DXA technologist and 1.5 driver positions. Services are provided to 18 primary care physician (PCP) sites throughout central Pennsylvania. Sites are as far away as 2 hours from
Figure
12.1
Mobile DXA van: Exterior view (top), patient seating and education area (bottom left), workstation (bottom middle), and scanning area (bottom right).
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Figure
12.2
Layout of mobile DXA: Scanning area (in rear), technologist workstation area (middle), and patient seating and educational area (in front).
the home base in Danville, Pennsylvania. All mobile DXA technologists and physician readers are International Society of Clinical Densitometry (ISCD) certified. Mobile DXA testing is carried out as follows. Patients are mailed and complete a prestudy questionnaire. The study is performed at the PCP site parking lot. Upon check-in, the driver escorts the patients to the van and assists them with any questionnaire problems. The DXA and VFA are performed as per our health system DXA/VFA protocol by the mobile DXA technologist, and then patients receive osteoporosis education and complete a satisfaction questionnaire. At the conclusion, they are escorted safely out of the van by the driver. The physician readers interpret the DXA and VFA, and the results are sent electronically to the ordering physician within 48 hours. Utilizing our electronic medical record (EMR) and intranet, we developed electronic tools and processes to improve our mobile DXA services, including smart tools to improve the ease of DXA ordering by physicians, DXA templates to enhance reporting consistency, wireless transmission of VFA images to improve turnaround time, an EMR-based callback system based on DXA results, and daily wireless offsite backup of DXA/VFA results to ensure data integrity. The mobile DXA service is offered 5–6 days per week and has been well received by both patients and referring physicians. The mobile DXA vans travel over 17,000 miles per year. Over 16,000 DXAs and 7,800 VFAs have been performed over the 5½ years since the program’s inception. Volumes have increased dramatically and now exceed those of all nonmobile DXA sites in our system (Table 12.1 provides data on the first 4 fiscal years). A formal mobile DXA programmatic analysis was done on the first 7,368 patients (Newman, Olenginski, Perruquet, Hummel, & Hummer, 2005). The patient population studied by mobile DXA has a mean age of 65.1 ± 10.8 years. One-third of patients had a T-score below –2.0, placing them at high risk of future fracture and making them candidates for prescription therapy according to NOF and Geisinger osteoporosis guidelines (Newman, Ayoub, Starkey, Diehl, & Wood, 2003). Of the 2,155 patients studied by VFA, 463 (21.5%) had a prevalent vertebral fracture. At PCP sites without onsite DXA services, only 15.4% of the 8,578 women over 65 had a DXA performed over a 2-year period. At the PCP sites with mobile DXA services, however, 23.3% of the 9,470 women over 65 received a DXA scan over the same time period, and several sites exceeded 40%.
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Table
12.1
Mobile DXA Volumes Compared to Nonmobile Sites for the First Four Fiscal Years
Fiscal year 2001–2002 2002–2003 2003–2004 2004–2005
Number of mobile DXAs 979 2,128 2,432 2,910
Number of DXAs per nonmobile site 2,189 2,199 2,311 2,318
The Mobile DXA Program is financially self-supportive. Monthly expenses, including salary/benefits for DXA technologists and drivers, fuel, maintenance, and vehicle/DXA depreciation (calculated over 4 years), total $10,300 per month. Profitability is achieved by performing at least 75 studies per month. A subanalysis was performed on the first 500 patients studied (Newman et al., 2004). Patient satisfaction questionnaires (potential scores ranging from A+ to F) showed a score of A or A+ for convenience, education, comfort, and ease of appointment in 98.5% of returns. In addition, by utilizing mobile DXA instead of the fixed sites in our health care system, the mean travel time saved was 70.5 ± 1.7 minutes per patient. About 60% of patients saved more than 1 hour, and 7% of patients saved more than 2 hours of travel time.
Mobile DXA—Conclusions and Future Directions By utilizing a highly motivated care team, electronic tools, and efficient process methodologies, our Mobile DXA Program efficiently delivers high-quality, high-output care. The program is service oriented and sustainable, and it improves access to technology for an older, high-risk population with low bone density and prevalent vertebral fractures. Because the highly successful Mobile DXA Program had reached maximal capacity, a second mobile DXA unit has been constructed and put into service (February 2006). This new unit is built on a truck chassis to provide greater stability and easier maneuverability, and is 4 feet shorter, enabling more access to smaller parking lots. The new design still has sufficient interior room for patient comfort. The high-visibility white mobile DXA vehicle has become so well recognized in central Pennsylvania that passersby often walk up to the mobile DXA van door, knock, and inquire whether they can “have their bones checked.” Access and accessibility don’t get any better than that!
REFERENCES National Osteoporosis Foundation. (2002). America’s bone health: The state of osteoporosis and low bone mass in our nation. Washington, DC: Author.
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Osteoporosis Newman, E. D., Ayoub, W. T., Starkey, R. H., Diehl, J. M., & Wood, G. C. (2003). Osteoporosis disease management in a rural health care population: Hip fracture reduction and reduced costs in postmenopausal women after 5 years. Osteoporosis International, 14,146–151. Newman, E. D., Olenginski, T. P., Perruquet, J. L., Hummel, J., Indeck, C., & Wood. G. C. (2004). Using mobile DXA to improve access to osteoporosis care. Journal of Clinical Densitometry, 7, 71–75. Newman, E. D., Olenginski, T. P., Perruquet, J. L., Hummel, J., & Hummer, M. (2005). At your service—Implementation of a mobile DXA program to improve access to osteoporosis testing. Arthritis and Rheumatology, 52, S408. U.S. Department of Health and Human Services. (2004). Bone health and osteoporosis: A report of the surgeon general. Public Health Service, Office of the Surgeon General, Rockville, MD. Retrieved August 27, 2007 from http://www.surgeongeneral.gov/library/bonehealth/
A Model For Community Outreach: Cooperative Extension Osteoporosis Prevention and Screening Programs
The area of bone health is ideally suited to a public health approach to health promotion. (U.S. Department of Health and Human Services, Bone Health and Osteoporosis: A Report of the Surgeon General )
Introduction
W
13 Marilyn A. Corbin Jane Trainor Chin-Fang Liu Sarah H. Gueldner
ith the application of what we have learned from research findings, prevention of osteoporosis is now an option for most persons. While methods of diagnosing and treating osteoporosis have progressed dramatically in the past decade, the best solution is to prevent osteoporosis from occurring in the first place, or, if that is not possible, to detect and treat it before a fracture occurs. Toward this goal, the incidence and impact of osteoporosis can best be reduced by educating the global populace about lifestyle choices that maximize peak bone mass in children and youth, and minimize bone loss in older age. This chapter features the broad-based Cooperative Extension Program as an effective way to deliver innovative osteoporosis education and screening programs to people who live in outlying areas of Pennsylvania, which has the fifth highest prevalence of osteoporosis in the nation. The first section describes Creating Health: Osteoporosis Prevention Program, a statewide osteoporosis awareness, education, and heel-scan-screening program that is featured as a model that others might use. This multisite program is being instituted by the Pennsylvania State University Cooperative Extension Program, in collaboration with numerous community partners. The program accesses the national Cooperative Extension Program, a network of nonformal public education offered through land-grant universities in every state and created to bring vital education to people in rural
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urban communities to improve their quality of life and well-being. The individual programs often include health-related information and demonstrations. The extension program has been in existence for more than 90 years and has become a trusted and popular source of information for rural communities. While each program is administered by a state university, each county in the state has an extension educator or agent who is responsible for arranging the educational programs in the county. In Pennsylvania, more than a million individuals participate in extension programs each year. Osteoporosis prevention has been adopted as a major educational thrust for many states, and the discussion demonstrates the potential of this tremendous educational network for reducing the incidence and impact of osteoporosis in America.
About Cooperative Extension As a nonformal educational system, the mission of the Cooperative Extension organization is to bring research-based educational programs, information, and knowledge to participants who desire to improve their quality of life. Extension personnel provide an important bridge between the land-grant university researchers and the community by being able, first, to identify community needs, and second, to select, translate, and transmit relevant, research-based information to help address those needs. This is a unique system that draws on collaboration with federal, state, and local partners to provide practical, evidence-based, problem-solving information to people and communities, in response to clear expressions of citizen and community needs. Cooperative Extension is affiliated with the U.S. Department of Agriculture’s Cooperative State Research, Education, and Extension Service (CSREES) agency, and is located within land-grant universities situated in every state in the nation. Extension programs are typically delivered by extension faculty and educators located in state, regional, and county extension offices. The fundamental mission is to enable people to improve their lives and communities through learning partnerships that are grounded in university research and scholarship. Each cooperative extension program sets educational priorities based upon demographics, state and county data, indicators of need, community and audience need, stakeholder input, clear reason and justification, and the gap between the needs and the current situation. Extension educators organize programs based on a program development process targeted to specific audience groups. This process includes program planning, design, implementation, and evaluation. In the program development process, logic modeling helps identify the specific components of a program, starting with the expected impact and continuing with the resources, activities, and target audience participation, in order to determine the likelihood of the program’s achieving its intended impact (Corbin, Kiernan, Koble, Watson, & Jackson, 2005). Extension educators carefully select learning experiences for a program, taking into account the knowledge, learning styles, and skills of their target audience. Through a variety of educational delivery strategies, information is delivered face-to-face through workshops, classes, and demonstrations. Other techniques used to convey educational information include one-on-one consultation and teaching, and dissemination of information on the Internet and through mass media. Key message points are directed
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through repetition of information to people who need and desire to make behavioral changes that prevent or minimize a problem or address an issue. Often a series of nonformal classes is organized, with participants enrolled for a specific number of sessions. Participants benefit from the group interaction as the classes serve as a source of motivation, inspiration, and socialization. Classes with a group of interested participants have proven to be an effective way to communicate the importance of lifestyle changes (Klotzbach-Shimomura, 2001). In health-related prevention programs, the transtheoretical model, also known as the stages of change model (Prochaska, DiClemente, & Norcross, 1992), is often used to frame educational initiatives. The model serves as a guide to shape the key message points, the class sessions, the educational information, and the motivation strategies. Typically, individuals are at different stages of change and readiness to change behavior. The stages of change model shows that, for most persons, a change in behavior occurs gradually, with the individual moving from being uninterested, unaware, or unwilling to make a change (precontemplation), to considering a change (contemplation), to deciding and preparing to make a change. Genuine, determined action is then taken and, over time, attempts to maintain the new behavior occur. Relapses may occur and become part of the process of working toward lifelong change. Extension educators frequently work with their local health care community groups to design interactive, hands-on educational preventative programs using the stages of change model, which brings added value to participants. Extension educators also use indirect contacts (non-face-to-face) to reach target audiences. These contacts are made through the mass media, including articles in newsletters, news releases to newspapers, radio, television programs, and informational Web sites. Many extension educators author newspaper columns in which they feature timely information related to their educational programs and their communities. The mass media create an awareness of problems, issues, or major points, build confidence in local programs, and are adaptable to a wide range of audiences and subject matter information. The media also serve as effective supplements and reinforcements of teaching activities (Seevers, Graham, Gamon, & Conklin, 1997). More and more educators are also participating in coordinated school and community health planning committees in which they focus on specific health issues. Education on health issues such as bone health to prevent osteoporosis is often conducted through research-based community educational programs. The importance of stakeholders working together to address the issue of bone health is supported by the surgeon general (U.S. Department of Health and Human Services [USDHHS], 2004). Extension programs reaching individuals, families, and consumers are targeted to meet specific issues and needs. For example, extension health and wellness programs address the importance of good nutrition across the lifespan, and they are designed to prevent the onset of many of the major chronic diseases affecting Americans. Specific programs may address the needs of certain audiences who are more likely to be at risk for various diseases. Osteoporosis prevention programs focus on why osteoporosis is a health problem, the risks associated with the disease, and how to prevent the disease. Other issues that are addressed by extension educators when conducting osteoporosis programs include how to prevent falls and stop smoking. When addressing audiences prone to osteoporosis, consumption of calcium-rich foods and increased participation in weight-bearing exercise are encouraged. Extension educators, who may also be registered
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dietitians, provide motivation, inspiration, and sound educational advice to encourage individuals to consider (or reconsider) their lifestyle practices and activities.
Creating Health: Osteoporosis My bones were like sponges. (Participant in the Penn State University Creating Health: Osteoporosis Prevention Program)
A specific example of a well-designed extension educational program, involving multiple program delivery approaches, is described below. The Creating Health: Osteoporosis Prevention Program was developed, as part of the Creating Health initiative, for extension educators to use throughout the Pennsylvania Commonwealth to address osteoporosis—a major health issue in Pennsylvania, which has the fifth highest incidence of osteoporosis in the nation (National Osteoporosis Foundation [NOF], 2003). The purpose of the Creating Health initiative, a collaboration between Penn State Cooperative Extension and Penn State Public Broadcasting, is to convey messages that help people build upon their culture of self-reliance to develop preventative behaviors and improve their health. A principal goal is to motivate audiences to engage themselves and their families in healthier lifestyles and behaviors. This initiative responds, in particular, to the needs of many rural citizens in Pennsylvania who are faced with barriers to accessing health services (Office of Rural Health, 2003). Through a network of faculty from the Pennsylvania State University and county extension educators from across the state, an outreach advisory board was established to envision the project, frame the key message points, suggest program design, provide nutrition and medical expertise, develop the curriculum materials, and review and edit the final products. The advisory board met on a quarterly basis to offer additional suggestions to improve the quality of the initiative. The target audience for the program included community audiences of civic and women’s groups, schoolteachers, high school and college students, health coalitions, senior citizens, home health caregivers, human service employees, and the general public. Because people of all ages, including both men and women, can develop osteoporosis, the program was designed with flexibility so that the extension educator could tailor the program to the local audience. The program was conducted with community partners such as offices on aging, senior citizens’ centers, and the Pennsylvania Department of Health. The program, delivered in a variety of formats, concentrated on describing the effects and risk factors associated with osteoporosis, the physical activity and nutritional practices necessary to reduce the risk of osteoporosis, and testing procedures to determine if one has osteoporosis. The curriculum included presentation materials and a documentary on prevention. PowerPoint visual presentations, scripts, and evaluation tools were available, as well as a poster exhibit titled “Osteoporosis: The Silent Disease,” highlighting risk factors, symptoms, and recommended practices to change lifestyle habits in order to reduce risk. A resource notebook for extension educators provided additional information. A 30-minute documentary on osteoporosis prevention, produced by Penn State Public Broadcasting, was accessible to educators. They could tune in during a live
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broadcast or view the documentary on video or DVD at a later time. The documentary featured personal vignettes of people who are working to prevent osteoporosis as well as of those who have the disease. It was designed so that participants could easily relate to the personal stories of people challenged with bone health issues. The documentary guided participants in learning how to incorporate nutrition and physical activity recommendations into their lifestyles. Active learning approaches to topics such as determining calcium-rich foods, stopping bone “robbers,” calcium alternatives, calcium supplements, and physical activity were incorporated into the program to empower participants with realistic and practical strategies to make lifestyle changes. The designers of the Creating Health: Osteoporosis Prevention Program found these topics to be integral in reducing the risk of developing osteoporosis. Group discussion and interaction encouraged participants to share personal experiences. The Creating Health: Osteoporosis Prevention Program reflects the collaboration of different outreach units within the university, including Penn State Cooperative Extension at the state and local level, Penn State Public Broadcasting, and the School of Nursing. The PowerPoint visuals and scripts were written by an extension faculty member from the discipline of food science, and the program evaluation was developed by an evaluation specialist and a continuing education staff member. The content of the exhibit itself was developed by cooperative extension educators; the resource notebook was developed by the faculty member and the cooperative extension state program leader; and the documentary was produced by Penn State Public Broadcasting staff with input from the faculty member and the state program leader. A variety of additional educational materials were made available to ensure up-to-date information. Brochures and publications were made available from the Arthritis Foundation, the National Osteoporosis Foundation, the National Fluid Milk Processor Promotion Board, and the National Dairy Council. Other research-based information was incorporated as new research findings were released or published. At the community level, the typical approach to delivering the 2- to 2.5-hour program by the extension educator included a welcome and warm-up activity, a video presentation with audience discussion, and a presentation of examples of sources of calcium. Additional scheduled classes included a review presentation with PowerPoint visuals. In some cases, a demonstration of calcium-rich food products and a discussion regarding lactose intolerance and calcium supplements were added. Additionally, four learn-at-home lessons were distributed to people interested in learning more: Boosting Calcium Intake With Nonfat Dry Milk, Boosting Calcium Intake With Low-Fat Yogurt, Boosting Calcium Intake With Canned Salmon, and Boosting Calcium Intake With Tofu. A bonus in some communities was the opportunity to offer osteoporosis screenings. The Penn State School of Nursing in the College of Health and Human Development launched Stand Tall Pennsylvania, a statewide osteoporosis risk assessment, screening, and educational program that could be scheduled during public gatherings, church meetings, business or professional meetings, and various informal gatherings. In addition to the distribution of educational materials and individual risk assessments, a portable ultrasound heel scan was offered free of charge to women 40 years of age or older. In some communities, extension educators organized presentations during health fairs, mall-walking programs, food and nutrition demonstrations, and county fairs, and
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some initiated multiple mass media stories. Presentations were made at the request of civic organizations, church groups, adult continuing care communities, senior citizens’ service centers, and health organizations. In summary, the Penn State Cooperative Extension health and nutrition programs provide educational information that allows program participants across the commonwealth to make better, informed choices. Additionally, when participants apply the educational information to their lives, they can increase their sense of well-being, increase their physical stamina, and have a higher quality of life for more years. Extension programs such as the Creating Health: Osteoporosis Prevention Program provide good public value. If health care costs are reduced for doctors, treatment, medicines, inpatient care, nursing home care, and outpatient services, individuals will have more resources to meet other living expenses. Preventing osteoporosis means a reduced burden on the individual and the family from ill health and its consequences, which in turn benefits the community.
Other Program Examples The following programs are examples of successful bone health and osteoporosis prevention programs conducted in several other states and communities, and on the Internet.
A Practical Guide to Bone Health Developed in Michigan by a collaborative team of public health practitioners, A Practical Guide to Bone Health was designed as a 45-minute session presented in either a flip-chart or PowerPoint format. The content emphasizes physical activity, diet quality, and the importance of calcium and vitamin D. Consumers were guided to better food choices with a section on shopping for food. Registered dietitians and staff representing the Michigan State University Extension, the Michigan Nutrition Network, the United Dairy Industry, and the Michigan Department of Community Health developed the educational materials. The program was conducted in urban and rural sites, especially for low-income populations. Pretests and posttests assessed basic knowledge and intent to change behavior. Before the program, 28% reported inadequate calcium intake and 30% reported inadequate physical activity. At posttest, 50% of those with low calcium intake indicated their intent to eat three or more servings of calcium-rich foods per day. Of those with low activity levels, 62% intended to increase their physical activity to at least 30 minutes 3 times a week. An additional 13% indicated their intent to increase activity to 30 minutes 5 times a week (Cyzman, Bour, Mclaury, & Lyles, 2005).
Bone Builders Bone Builders was started by the University of Arizona Cooperative Extension in Maricopa County and the College of Public Health in 1998, with the support of community organizations and a grant from St. Luke’s Health Initiative. Bone Builders teaches women of all ages and older men to reduce their risks for developing osteoporosis by
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improving nutrition and weight-bearing exercise. Through the partnership, more than 100 partners, including county health departments, health providers, and interested citizens, campaign to spread the message of preventing osteoporosis. The Bone Builders train-the-trainer volunteer program teaches women about osteoporosis, distributes materials, and conducts prevention activities in communities, worksites, and churches. In 1997, the program was expanded to seven additional counties through the efforts of the Arizona Osteoporosis Coalition and the Arizona Department of Health Services. In 2003, Bone Builders staff and volunteers taught 447 classes to 12,916 people plus 1,712 individual contacts. Bone Builders’ displays and volunteers at 107 health fairs reached an additional 22,595 people in 10 Arizona counties. Bone Builders’ newest program is Physical Activity for Inactive Seniors. The 10-week series is designed to help improve fitness levels for seniors who are not physically active. Bone Builders and community volunteers work with local senior centers to provide individual fitness assessments and to teach activities to improve balance to prevent falls, increase endurance and strength, and improve flexibility. Each exercise class includes a mini-lesson on reducing the risks for osteoporosis through good nutrition and physical activity (see http://www.bonebuilders.org/).
Bone Estrogen Strength Training (BEST) The Bone Estrogen Strength Training (BEST) study, funded by the National Institute of Health, identified the six BEST exercises that are most effective for preventing osteoporosis and improving bone mineral density in postmenopausal women. The six BEST exercises, training protocols, and specific programming and motivational strategies help women adhere to a lifetime of exercise for bone health. The program is conducted at the University of Arizona through Cooperative Extension (see http://ag.arizona.edu/nsc/ new/nutrition_health/bestbook.htm).
Bones: Don’t Wait Until You Break One to Find Out That You Have Osteoporosis In Nebraska, the Planned Approach to Community Health group sponsored this program due to the test results of health fair participants. The team, consisting of public health employees, registered dietitians, a Nebraska Cooperative Extension specialist, extension educators, and physicians, provided credible expertise in human nutrition, health, exercise, and medicine during the classes. The educational sessions emphasized prevention, risk factors, diagnosis, and treatment of osteoporosis. The participants were able to ask questions directed to the physicians and nutrition professionals (Driskell, Pohlman, & Naslund, 2003).
Calcium, It’s Not Just Milk The Calcium, It’s Not Just Milk program was designed in Nevada to increase the amount of low-fat, calcium-rich foods eaten by 11- to 14-year-old children. Using the Calcium, It’s Not Just Milk curriculum, science teachers lead classroom discussions and direct students in hands-on activities. Students learn how much calcium they need and how important it is for them to get enough calcium every day. Students conduct experiments
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to learn about the relationship between calcium and bone strength. They also use food labels to find foods with calcium and estimate how much of their daily calcium needs a specific food provides. So that the children can taste a variety of foods with calcium, special events are conducted, including free samples of foods such as fortified orange juice, flavored milks, yogurt, string cheese, broccoli, and bean and cheese burritos. Games and contests are used to reinforce important concepts. Outside of school, print and broadcast media channels are used to remind students to choose foods containing calcium. Evaluation of the program has shown that both students and teachers like the program, listing the food-sampling events and classroom lessons as their favorite components. The program has been successful in improving students’ knowledge of their calcium needs and the importance of getting enough calcium at this particular time in their lives. At the end of the program, students are more aware of foods with calcium, better understand the relationship between calcium and healthy bones and teeth, and more often eat calcium-rich foods. In the past 5 years, the program has reached over 6,500 middle school students in low-income communities in northern and southern Nevada. This program is a collaborative effort by the University Cooperative Extension and the Nevada Nutrition Network. Interested individuals and groups should contact Mary Wilson, MS, RD, Extension Nutrition Specialist, University of Nevada Cooperative Extension, 2345 Red Rock St., Ste. 100, Las Vegas, NV 89146 (
[email protected]. edu) (see also http://www.unce.unr.edu/programs/health/index.asp?ID=14).
Jump Start Your Bones© Attaining peak bone mass during adolescence is a key determinant in reducing the risk of osteoporosis in later years. Educating adolescents as to the importance of consuming at least four calcium-rich foods daily and participating in physical activity for at least an hour each day can greatly advance osteoporosis prevention. Rutgers Cooperative Extension responded by developing a school-based curriculum, called Jump Start Your Bones©, targeted to seventh- and eighth-grade youth. The curriculum contains a total of 12 lessons, designed to be used in family and consumer sciences, health, physical education, and life science classrooms, three lessons per discipline. This osteoporosis curriculum uses hands-on activities to increase knowledge and change behavior in youth aimed toward increasing the accumulation of peak bone mass density (see http://www. ces.ncsu.edu/depts/fcs/pub/2001f/shimomura.html).
Project Healthy Bones Project Healthy Bones is a 24-week exercise and osteoporosis education curriculum developed by Rutgers Cooperative Extension, New Jersey, involving peer advocate trainers as role models. Program partners include the New Jersey Department of Health and Senior Service, the Association of Retired and Senior Volunteer Program Directors, Inc. (RSVP), the Saint Barnabas Health Care system, and the Rutgers Cooperative Extension. More than 1,400 older New Jersey citizens have participated in the program. Each session runs for 6 months, meeting 1.5 hours a week. Class size is set at 15. Often there are people on waiting lists for the classes. Participants have become a peer-support network and have bonded to nurture and encourage positive health behaviors in each
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other. Participants tracked weekly exercise progression. Analysis showed substantial progression from the first exercise level to the next level and a statistically significant increase in the amount of weight lifted. Improvements were evident in participants completing between 12 and 23 weeks of the program and those finishing the entire 24week cycle (Klotzbach-Shimomura, 2001; see also http://www.joe.org/joe/2001june/ iw6.html).
Strong Women™ The Strong Women™ program, developed by Dr. Miriam E. Nelson of the School of Nutrition Science and Policy, Tufts University, Boston, Massachusetts, was prompted by her research on female subjects to determine if walking would help their bone density. After she discovered that walking had very little effect on bone density in the hip, a followup study determined that women who strength-trained twice a week for a year actually gained an average of 1% of their bone density (Nelson, 2000). The Strong Women™ book series has created an interest in evidence-based community exercise programs for middleaged and older women. The Strong Women, Strong Bones program combines three key major components: nutrition, physical activity, and medication if necessary. Cooperative extension educators have been conducting Strong Women™ programs across the country for about five years. Because extension educators have an excellent reputation for teaching nutrition education classes in the community, and because extension programs put research into practice, these educators are unusually well received and effective. Applying these strengths, they are able to eliminate the primary barriers to exercise participation by enabling communities to offer the program in such a way that its suggested exercises are easy to learn and can be performed with low-cost equipment in a variety of settings. Valuable components of the program include participant screening, a medical history and current health survey, a physical activity readiness questionnaire (PAR-Q & YOU), and specific subject-matter content such as the importance and sources of calcium and “My Pyramid” information for the participants. Handouts with nutrition education information and demonstrations of the exercises are utilized. The exercise program includes warm-ups and cool-downs, sets and repetitions of exercises, and a focus on technique, progression, and intensity. Breathing and safety are also addressed. Strong Women™ programs are reinforced with a Website, a newsletter, and special events (see www.strongwomen.com).
Stand Tall Pennsylvania Stand Tall Pennsylvania: A Collaborative Screening Initiative to Measure Bone Density in Women Who Live in Rural Pennsylvania is a partnership between the Pennsylvania State University School of Nursing, the Pennsylvania State University Cooperative Extension, and the Pennsylvania Geriatric Education Center, made up of the aging centers at the Pennsylvania State University, the University of Pittsburgh, and Temple University. The way to reach individuals for osteoporosis screening is to find them where they work, visit, and engage in recreation. In order to accomplish this goal, inroads need to be made with groups or organizations that work directly with the targeted population in various settings. Being a land-grant institution, Penn State University has a primary
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mission to meet the needs of the citizenry. To meet those needs, Penn State has always had a large and very active cooperative extension organization. Educational programs range from horticultural (master gardeners), 4-H youth development, and animal sciences, to family needs such as nutrition, life skills, and after-school programs. The first step in implementing the screening program was for members of the screening team to attend several regional meetings and to volunteer as a member on community advisory boards. This led to the opportunity to present a program for an annual arts and crafts workshop, and to offer on-site osteoporosis screening using the Sahara ultrasound heel scanner. The program was so well received by participants that other county extension educators began to contact Penn State to request osteoporosis screenings at their craft fairs, health fairs, and other community activities. In time other organizations, including the Department of Health and several faith-based institutions, heard about the heel screenings and invited the School of Nursing to bring the program to their gatherings as well. So, the Penn State School of Nursing faculty began to actively involve their RN to BS nursing students in the screening and education project. Materials, including dietary information offered free by national and regional osteoporosis organizations, were available to all who stopped by the screening stations at various community functions. When the screening was first started, approximately 25 women took advantage of it. But as the screenings continued to spread in and around the surrounding communities, additional public locations were added, including the State Capitol Rotunda and the annual Pennsylvania Farm Show. During one 2-day workshop/fair, more than 100 participants were screened and given educational materials about osteoporosis. Participating in the osteoporosis screening program has turned out to be an excellent learning opportunity for nursing students in their community nursing courses and provides a valuable health service to pre- and postmenopausal women in the community. The 2-day women’s holiday workshops sponsored by the Cooperative Extension Program were especially fertile events for screening, typically yielding 30–50 heel scans each day, which is impressive, considering that it takes about 5–8 minutes to perform the heel scan and measure the height for each person. The heel-scanning station was set up at one of the exhibit tables located around the sides of the large meeting room, and attendees were encouraged by the moderator to come to the booth for height and bone density measures during breaks. The moderators gave the attendees permission to feel free to go quietly to the scanning station one at a time even during the actual meeting sessions. It was not unusual for two generations of women (i.e., mother and daughter; aunt and niece) to attend the programs together, and often they came together to have their heels scanned during the 2-day events. The women were also invited to fill out the Merck SCORE risk assessment sheet (Figure 13.1), and educational handouts provided by the National Osteoporosis Foundation and other sources were offered without charge. When the scanning was finished, each woman was given a printout of her T-score and was encouraged to take it to her primary care physician when she went for her next appointment. Those who had T-scores of -1.5 or lower were gently told by the nurse screeners that their scores were low and were counseled to make an appointment with their physician as soon as possible to discuss follow-up testing and perhaps treatment measures. Several of the participants have come back to tell us that their physician did in fact order the more reliable full body DXA scan and started them on a medication regime. Unfortunately, we learned that one participant with a T-score of -2.5 sustained
Figure
13.1
The Osteoporosis Evaluation SCORE Sheet for assessing risk for developing osteoporosis. Reprinted with permission from Merck & Co. Copyright © 1996 Merck & Co., Inc. Whitehouse Station, NJ, U.S.A. All rights reserved. No reproduction, modification, republication or any other use of this questionnaire, including the creation of derivative works, is allowed without the prior written permission of Merck & Co., Inc.
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a Colles’ fracture over the weekend, before she could get an appointment to see her physician. More than 1,000 women are scanned each year at events of this type. The ultrasound heel scanner for the project (which costs between $9,000 and $12,000) was purchased through a gift to the Penn State School of Nursing from a private foundation for the Stand Tall Pennsylvania osteoporosis awareness and screening project. Supported by funds from the Binghamton University Foundation and the Crane Fund for Widows and Children, a screening program based on this model is now being offered by the Decker School of Nursing at Binghamton University, in New York State, which has the third highest incidence of osteoporosis in the United States. While the heel-screening program was primarily a health care initiative, it also provided data for a faculty research program profiling the prevalence of low bone mass in rural women and risk the factors associated with it. The application for permission to use the data for research was submitted to and approved by the university’s institutional review board as an ongoing research study. Therefore, while the screenings and educational counseling services were provided without charge to all who came, participants were also invited to participate in the research study and were given an implied consent form detailing the purpose and requirements if they wished to participate. (They were of course told that their heels would be scanned regardless of whether or not they chose to participate in the study.) More than 400 participants chose to participate in the study. The findings revealed that 23.5% of the sample had low bone density, placing them at 1.5 to 2 times greater risk for fracture of the hip or spine. The findings also confirmed the Merck SCORE risk assessment tool to be a reliable indicator ( p = –.001) of low bone density, and showed age at menopause to be positively correlated with T-scores ( p = .032). Comparison of self-reported height to the measured height on the day of data collection found that almost all the participants were significantly shorter than they thought they were ( p = .001). The findings also supported the unique contribution of estrogen to bone strength, which, in light of recent evidence of risks associated with hormone replacement therapy, underscores the need for research to develop equally effective alternative preventative therapies. The success and findings of this bi-state study have been presented at a number of national and regional multidisciplinary meetings and have been published as chapters in the Encyclopedia of Nursing Research (Gueldner, Britton, & Stucke, 2006), and in the Encyclopedia of Gerontology (Gueldner, Grabo, Britton, Pierce, & Lombardi, 2006). In addition, the collaborative initiative inspired the publication of a CD on bone health by the Pennsylvania Geriatric Education Center (available at http://www.temple.edu/ aging/gecpa_prog_priority.htm), and led to the publication of a book, Preventing and Managing Osteoporosis (Gueldner, Burke, & Wright, 2000).
Summary The mission of Cooperative Extension to help people improve their quality of life has proven to be a viable and meaningful university outreach function. With the continuing aging and increased longevity of the population, osteoporosis prevention programs sponsored by Cooperative Extension are of great benefit to individuals, families, and
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society. Not only do individuals benefit and improve their health, but also the community benefits by having a healthier population of citizens who are able to make valuable contributions to work and volunteerism. The beauty of extension programs is that they are based upon the needs of the community and developed by extension educators who provide the intellectual and educational leadership for the programs. As a resource in the community, extension educators are catalysts to stimulate program implementation and collaboration that goes beyond just responding to needs—they make valuable contributions to the knowledge base and the nonformal educational structure in a community. Extension educators are on the front lines, helping to shape and address the public scholarship of the university outreach mission. Citizen and community access through cooperative extension brings a progressive and dynamic program to the local people. Community education programs that prevent and address major health issues, such as osteoporosis, are necessary and important strategies in enabling communities to nurture a healthy and productive citizenry.
REFERENCES Corbin, M., Kiernan, N. E., Koble, M., Watson, J., & Jackson, D. (2005). Using the logic model to plan extension and outreach program development and scholarship. Journal of Higher Education Outreach and Engagement, 10(1), 61–77. Cyzman, D., Bour, N., Mclaury, R., & Lyles, J. (2005). Retooling an osteoporosis prevention program to serve low-income populations: A Practical Guide to Bone Health. Retrieved July 6, 2007, from http://www.cdc.gov/pcd/issues/2005/apr/04_0142s.htm Driskell, J., Pohlman, D., & Naslund, M. (2003). Value of an educational program on osteoporosis. Journal of Extension, 41(5). Retrieved July 6, 2007, from http://www.joe.org/joe/2003october/ rb6.shtml Gueldner, S. H., Britton, G., & Stucke, S. (2006). Osteoporosis. In J. Fitzpatrick and M. Wallace (Eds.), Encyclopedia of nursing research (pp. 430–433). New York: Springer Publishing. Gueldner, S. H., Burke, M. S., & Wright, H. S. (Eds.). (2000). Preventing and managing osteoporosis. New York: Springer Publishing. Gueldner, S. H., Grabo, T. M., Britton, G., Pierce, C., & Lombardi, B. (2006). Osteoporosis and aging related bone disorders. In J. Berrien (Ed.), Encyclopedia of gerontology. London: Elsevier. Klotzbach-Shimomura, K. (2001). Project Healthy Bones: An osteoporosis prevention program for older adults. Journal of Extension, 39(3), pp. 293–303. Retrieved July 6, 2007, from http://www. joe.org/joe/2001june/iw6.html National Osteoporosis Foundation. (2003). Guidelines. Retrieved July 6, 2007, from http://www.nof .org/osteoporosis/bonemass.htm Nelson, Miriam. (2000). Strong women, strong bones. New York: G. P. Putnam’s Sons. Office of Rural Health. (2003). The Pennsylvania Rural Hospital Flexibility Program/Critical Access Hospital Program. Retrieved July 6, 2007, from http://porh.cas.psu.edu/cah Prochaska, J. O., DiClemente, C. C., & Norcross, J. C. (1992). In search of how people change. American Psychology, 47, 1102–1104. Seevers, B., Graham, D., Gamon, J., & Conklin, N. (1997). Education through cooperative extension. Albany, NY: Delmar. U.S. Department of Health and Human Services. (2004). Bone health and osteoporosis: A report of the surgeon general. Public Health Service, Office of the Surgeon General, Rockville, MD. Retrieved August 15, 2007 from http://www.surgeongeneral.gov/library/bonehealth/
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H
ealth policy can be defined as the line of argument or decision that influences a course of action to improve the health of a population (National Osteoporosis Society of the United Kingdom, 2005; Shi & Singh, 2004). “Policy encompasses the choices that a society, segment of society, or organization makes regarding its goals and priorities and the ways it will allocate its resources to attain those goals” (Mason, Leavitt, & Chaffee, 2002, p. 8). While health policy is often thought to be a “collection of authoritative decisions made within government that pertain to health and the pursuit of health” (Longest, 1998, p. xxi), it is considered by some to include policies in the private sector as well (Hanley, 1998, as cited in Harrington & Estes, 2004). International organizations as well as individual national governments, organizations, and agencies play vital roles in policy making regarding bone health and osteoporosis prevention and treatment. Policy formulation in this arena encompasses several major components:
Geraldine R. Avidano Britton Katherine Kaby Anselmi Laura Pascucci
1 . Consensus agreement on the definition of bone health and osteo2. 3.
4. 5.
porosis Research support to build the science base for evidenced-based recommendations Epidemiology of the disease in specific populations, including risk levels, and influence of consumer and clinician behavior on bone health outcomes Primary and secondary prevention, efficacy of population screening Dietary guidelines, food labeling
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6 . Diagnostic techniques and treatment services for bone disease and
fractures 7 . Economic impact (cost-benefit analysis) of prevention and treat-
ment services 8 . Lifestyle choices that improve bone health 9 . Awareness among health care systems, communities, clinicians, and the pub-
lic of the impact of osteoporosis and its prevention and treatment 1 0 . Influence of health insurance coverage and financial incentives
Policy Makers and Stakeholders International On the world stage, the United Nations’ World Health Organization (WHO), the Bone and Joint Decade, and the International Osteoporosis Foundation (IOF) have spearheaded international strategies and policy recommendations to address the global burden of osteoporosis. The WHO, through scientific work groups and expert task forces, develops guidelines, policies, and state-of-the-art consensus reports that offer recommendations for decision makers. For example, in 1994, a WHO expert panel operationalized the definition of osteoporosis and osteopenia on the basis of bone mineral density (BMD): Osteoporosis: T-score < –2.5 (BMD value of more than 2.5 deviations below the mean for young adult women) Osteopenia: T-score < –1 (BMD value between 1 and 2.5 standard deviations below the mean for young adult women) Another international example is a recent report emanating from the WHO Regional Office for Europe’s Health Evidence Network (Johnell & Hertzman, 2006), which highlights the following policy considerations: 1 . Evidence shows that several interventions are effective in the prevention of
osteoporosis: moderate physical activity, adequate intake of calcium and vitamin D, smoking cessation, and drug therapy in high-risk groups. 2 . There needs to be increased awareness of osteoporosis including dissemination of research findings among the general population, health care professionals, and health care systems in order to promote prevention and early detection of risk factors. 3. More research is needed to determine the cost-effectiveness of general screening programs and of treating low-risk populations in reducing the risk of fractures. 4 . Current research findings regarding pharmacological treatments are applicable to certain high-risk groups under controlled conditions but are not always generalizable to the general population.
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The Bone and Joint Decade 2000–2010 is a multidisciplinary campaign developed in partnership with consumer and professional organizations, research bodies, scientific journals, health care providers, governments, and nongovernmental organizations in consultation with global and regional stakeholders (BJDonline, 2006). The goal of the Bone and Joint Decade is to improve the health-related quality of life for those with osteoporosis and other musculoskeletal disorders throughout the world, especially in developing countries. The governments of 60 countries are supporting this campaign. Likewise, the aims of the International Osteoporosis Foundation (2005) are to further policy initiatives that raise
Table
14.1
International Agencies and Organizations: Bone Health Initiatives/Reports Organization
Initiatives/Reports
WHO Study Group
Assessment of fracture risk and its application to screening for postmenopausal osteoporosis. (1994). Report of WHO Study Group. Geneva, Switzerland: World Health Organization (WHO Technical Report Series, No. 843).
WHO/FAO Expert Consultation
Diet, nutrition and the prevention of chronic diseases. (2003b). Report of Joint WHO/FAO Expert Consultation. Geneva, Switzerland: World Health Organization (WHO Technical Report Series, No. 916).
WHO Scientific Group
Prevention and management of osteoporosis. (2003c). Report of WHO Scientific Group. Geneva, Switzerland: World Health Organization (WHO Technical Report Series, No. 921).
WHO Scientific Group
The burden of musculoskeletal conditions at the start of the new millennium. (2003a). Report of WHO Scientific Group. Geneva, Switzerland: World Health Organization (WHO Technical Report Series, No. 919).
WHO Regional Officefor Europe’s Health Evidence Network (HEN)
What evidence is there for the prevention and screening of osteoporosis? (2006). Report of WHO Regional Office for Europe.
International Society for Clinical Densitometry
Position statement: The writing group for the ISCD Position Development Conference. (2004). Journal of Clinical Densitometry, 7(1), 7–12.
International Osteoporosis Foundation
Ongoing publication of the journal Osteoporosis International. Sponsorship of IOR Women Leaders’ Roundtable (2002, 2006). Dissemination of national and regional evidenced-based guidelines for health professionals (2006). See http://www.osteofound. org/health_professional/guidelines-list.html
The Bone and Joint Decade
Bone and Joint Network Conferences: (Oman, 2000; Brazil, 2002; Germany, 2003; China, 2004; Canada, 2005). Collaboration on U.S. surgeon general’s report on bone health and osteoporosis (U.S. Department of Health and Human Services, 2004).
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the priority of osteoporosis within health care systems and that encourage national governments and health insurers to support early detection and provide reimbursement for treatment. Other examples of collaborative partners include the International Society for Clinical Densitometry, the International Council of Nurses, the International Society of Orthopedic Surgery and Traumatology, and the European Advisory Council for Women’s Health. Table 14.1 lists some of these agencies and their respective initiatives. The International Society for Clinical Densitometry (Writing Group, 2004) reached agreement on a series of positions that subsequently became the official policy of this organization. These positions include several categories: acceptance of the WHO classification for the diagnosis of osteoporosis in postmenopausal women; the diagnosis of osteoporosis in men, premenopausal women, and children; technical standards for examination of skeletal regions of interest by DXA measurements and for the performance for precision assessment at bone density testing centers; quality assurance; new technologies such as vertebral fracture assessment; indications for bone density testing; and appropriate information for a bone density report, including the proper nomenclature and decimal places. Of interest is the policy that the “WHO classification should not be applied in its entirety to men” (p. 8) and not at all to premenopausal women and children. The policy states that Z-scores, rather than T-scores, should be used for premenopausal women and children.
National: The United States In the United States, many evidenced-based guidelines for bone health have been developed by myriad agencies, governmental bodies, and private organizations. Table 14.2 provides examples of these agencies and their respective initiatives. It should be noted that some agencies have multiple subagencies. For example, the National Institutes of Health (NIH) 2000 consensus statement, Osteoporosis Prevention, Diagnosis and Therapy, had many sponsors: “The primary sponsors of this meeting were the National Institute of Arthritis and Musculoskeletal and Skin Diseases and the NIH Office of Medical Applications of Research. The conference was cosponsored by the National Institute on Aging; National Institute of Diabetes and Digestive and Kidney Diseases; National Institute of Dental and Craniofacial Research; National Institute of Child Health and Human Development; National Institute of Nursing Research; National Institute of Environmental Health Sciences; National Heart, Lung, and Blood Institute; NIH Office of Research on Women’s Health; and Agency for Healthcare Research and Quality” (National Institutes of Health, 2000, p. 3). The U.S. Department of Health and Human Services (USDHHS) coordinates many efforts by the federal government to address the increasing problem of osteoporosis among Americans. Healthy People 2010, one of its major public health initiatives, has two overarching goals that are relevant to bone health: increased quality and years of healthy life, and the elimination of health disparities across different segments of the population. Among this document’s 467 objectives are targets to reduce the prevalence of osteoporosis and the number of hip fractures, as well as dietary and physical activity recommendations (U.S. Department of Health and Human Services [USDHHS], 2000). The U.S. surgeon general’s report, Bone Health and Osteoporosis (USDHHS, 2004), is a more specific effort by the USDHHS, the Office of the Surgeon General, and the Public Health Service to “highlight the importance of the musculoskeletal system to the
Table
U.S. Bone Health Initiatives
14.2
Initiative
Agency
Recommendations
– USDHHS Healthy People 2010, U.S. Depart- – Agency for Healthcare Research and Quality ment of Health and – Centers for Disease Human Services Control and Prevention (USDHHS), 2000 – Food and Drug Administration – Health Resources and Services Administration – National Institutes of Health (NIH) – Office of Disease Prevention and Health Promotion – President’s Council on Physical Fitness and Sports
Objective 2.9: Reduce cases of osteoporosis from 10% of adults aged 50 years and older to 8%. Objective 2.10: Reduce hospitalizations for vertebral fracture from 17.5/10,000 adults aged 65 years and older to 14.0/10,000. Objective 15.28: Reduce hip fractures for females aged 65 and older from 1,055.8/100,000 to 416/100,000, and for males aged 65 and older from 592.7/100,000 to 474/100,000. Objective 19.11: Increase calcium intake from 46% of persons aged 2 years and older to 75%. Objective 22.1–22.15: Increase physical activity.
Bone health and – USDHHS osteoporosis: A report – Public Health Service of the surgeon general – Office of the Surgeon (USDHHS, 2004) General
1. Develop a coordinated public health approach of public, private, nonprofit, academic, and scientific stakeholders to prevent osteoporosis and fractures. 2. Develop a national action plan to improve bone health. 3. Translate the best scientific information for public dissemination.
Screening for osteo- – U.S. Preventive Services Task Force porosis in postmenopausal women: recommendations and rationale (U.S. Preventive Services Task Force (2002))
1. Women aged 65 and older should be screened routinely for osteoporosis, and women at increased risk for osteoporotic fractures should be screened at age 60. 2. Not for or against routine screening in postmenopausal women who are younger than 60 or in women aged 60–64 who are not at increased risk for osteoporotic fractures (p. 527).
Osteoporosis prevention, diagnosis, and therapy: NIH Consensus Development Conference statement (NIH, 2000)
– National Institutes of Health
1. Identify and treat disorders that impede the achievement of peak bone mass in children. 2. Improve diagnosis and treatment of secondary causes of osteoporosis. 3. Collect data to establish testing guidelines for osteoporosis. 4. Develop quality of life measurement tools that incorporate gender, age, race/ethnicity. (Continued)
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Table
(continued)
14.2
Initiative
Agency
Recommendations 5. Conduct randomized clinical trials of combination therapies to prevent or treat osteoporosis. 6. Develop a paradigm for the management of fractures. See NIH News Release, March 29, 2000.
Osteoporosis: Physician Performance Measurement Set, 2006
– American Medical Association and National Committee for Quality Assurance Osteoporosis Work Group – American Academy of Family Physicians – American Academy of Orthopedic Surgeons – American Association of Clinical Endocrinologists – American College of Rheumatology – The Endocrine Society – National Osteoporosis Foundation – Joint Commission on Accreditation of Healthcare Organizations
Accountability Measures: 1. Communication with the physician managing ongoing care postfracture. 2. General population: screening or therapy for women aged 65 years and older. 3. Treatment following fracture. 4. Osteoporosis: pharmacologic therapy. 5. Osteoporosis: counseling for vitamin D and calcium intake. Quality improvement Measure: 6. Glucocorticosteroids and other secondary causes.
health status of Americans and to provide individuals, clinicians, public health officials, policymakers, and other stakeholders with the information and tools they need to improve bone health” (USDHHS, 2004, p. 5). Policy making is implicit in the systemsbased approach to bone health that is advocated in the report. Key stakeholders at different organizational levels, such as government and public health departments, voluntary health organizations and professional associations, academic institutions, health plans, insurers, industries, hospitals, and medical groups, can design and implement formal policies and processes to ensure that individual health care consumers and whole populations are provided with appropriate and timely measures. Specific policies delineated in the surgeon general’s report (USDHHS, 2004) include the following: Financial incentives, such as tax credits to fitness centers and to seniors at risk for falling, to encourage their participation in exercise classes Regulations that require the installation of grab bars in the showers of retirement communities Development of public spaces that provide safe outdoor exercise areas that minimize the risk for falling
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Quality control standards for BMD testing, certification of densitometer operators, and identification of deficiencies in care (Health Plan Employer Data and Information Set [HEDIS] and Assessing Care of Vulnerable Elders [ACOVE] performance measures) See Exhibit 14.1. Ongoing support of monitoring and surveillance of disease prevalence Curricular changes in health professions’ education to include cross-disciplinary, evidence- and systems-based approaches Systems changes (e.g., computerized reminders, algorithms, registries, standing orders, disease management groups, specialized clinics) for small group offices, medical groups, hospitals, and rehabilitation facilities Medicare and private sector coverage of screening, and of pharmacologic and nonpharmacologic treatments.
Exhibit
14.1
HEDIS Performance Measure for Osteoporosis: Health Plan Employer Data and Information Set This is a quality reporting system produced by the National Committee for Quality Assurance (NCQA) that has standard measure and uniform data reporting systems. The measure is defined as “The percentage of women age 67 or older who suffer a fracture who receive a BMD test or prescription treatment for osteoporosis within 6 months of the date of fracture.” www.ncqa.org
ACOVE Quality Indicators for Management of Osteoporosis in Vulnerable Elders (aged 65 and older who are at risk for losing their independence) Prevention/Screening 1. Calcium/vitamin D with corticosteroid use: If a vulnerable elder is taking corticosteroids for > 1 month, then patient should be offered calcium and vitamin D. 2. Pharmacologic preventive therapy: All female vulnerable elders should be counseled about osteoporosis risk and pharmacologic prevention at least once. 3. Prevention: All female vulnerable elders should be counseled at least once regarding intake of dietary calcium. All female vulnerable elders should be counseled at least once regarding weight-bearing exercises. 4. Smoking cessation: All female vulnerable elders who smoke should be counseled annually about smoking cessation.
Treatment 1. Calcium/vitamin D for osteoporosis: If a vulnerable elder has osteoporosis, then calcium and vitamin D supplements should be offered at least once. 2. Other treatments for osteoporosis: If a vulnerable elder is newly diagnosed with osteoporosis, then the patient should be offered treatment with hormone replacement therapy*, SERMS, bisphosphonates, or calcitonin within 3 months of diagnosis. Rand/Pfizer, 2005; www.acove.com
HEDIS Performance Measures and ACOVE Quality Indicators for Management of Osteoporosis * The Women’s Health Initiative findings regarding hormone replacement therapy and the risk of cardiovascular disease indicate this is not currently the therapy of choice.
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Osteoporosis
The National Osteoporosis Foundation (NOF) is a voluntary health organization whose mission is “to prevent osteoporosis, to promote lifelong bone health, to help improve the lives of those affected by osteoporosis and related fractures, and to find a cure” through awareness, education and training, advocacy and research (National Osteoporosis Foundation, 2007). Key priorities include the implementation of the aforementioned surgeon general’s report and the creation of a federally supported national action plan; advocacy for comprehensive private, federal, and state insurance coverage and funding for prevention and education programs on bone health as well as for screening and treatment for patients with osteoporosis; and increased funding for the NIH and other institutes that sponsor osteoporosis and bone research.
Reimbursement: Federal The NOF (2006) is currently advocating for the passage of the following federal legislative bills that are described on its Web site (see www.nof.org): 1 . House Bill 2257—The Medicare Osteoporosis Measurement Act of 2005
Under current guidelines, Medicare covers bone density tests only for estrogen-deficient women at clinical risk for osteoporosis and individuals with a limited range of medical conditions that put them at risk for osteoporosis. This bill would expand Medicare coverage of bone density tests to all individuals at clinical risk for osteoporosis. 2 . House Bill 1081—The Osteoporosis Education and Prevention Act of 2005
This bill would provide information and outreach for the prevention of osteoporosis. The secretary of Health and Human Services would be required to carry out a national campaign to increase awareness about osteoporosis. The assistant secretary of Health and Human Services would be required to carry out an osteoporosis prevention demonstration program by making grants to public and private nonprofit agencies, organizations, and institutions to determine the most effective practices for providing osteoporosis information and outreach services. 3 . House Bill 2946—The Osteoporosis Early Detection and Prevention Act of
2005 This bill would require individual and group insurance plans to provide bone density testing coverage for qualified individuals at clinical risk for osteoporosis. 4 . House Bill 3086—WISEWOMAN Expansion Act of 2005
This bill would allow the Centers for Disease Control and Prevention (CDC) to expand the WISEWOMAN (Well-Integrated Screening and Evaluation for Women Across the Nation) program to provide additional preventive health services, for chronic diseases such as osteoporosis, to certain low-income, uninsured women ages 40–64 (National Osteoporosis Foundation, 2007)
Health Policy and Insurance Reimbursement
209
Exhibit Bone Densitometry Coverage for Medicare Beneficiaries
14.2
Bone Densitometry 1. Covered once every two years for a qualified patient* (23 months must have passed since the month of the last bone mass measurement) 2. If medically necessary, more frequent bone mass measurements may be covered: (not an all-inclusive list) a. Monitoring patients on long-term glucocorticoid (steroid) therapy of more than 3 months. b. Allowing for a confirmatory baseline bone mass measurement (either central or peripheral) to permit monitoring of patients in the future, if the initial test was performed with a technique that is different from the proposed monitoring method.
*Qualified Patient (must meet at least 1 of the following 5 categories) 1. A woman who has been determined by the physician, or a qualified nonphysician practitioner treating her, to be estrogen-deficient and at clinical risk for osteoporosis, based on her medical history and other findings. 2. An individual with vertebral abnormalities as demonstrated by an X-ray to be indicative of osteoporosis, osteopenia (low bone mass), or vertebral fracture. 3. An individual receiving (or expecting to receive) glucocorticoid therapy equivalent to 7.5 mg of prednisone or greater, per day, for more than 3 months. 4. An individual with primary hyperparathyroidism. 5. An individual being monitored to assess the response to or efficacy of an FDA-approved osteoporosis drug therapy. A comprehensive list of specific diagnoses covered for bone density measurement is provided in Appendix B, as retrieved from http://www.umd.nycpic.com/cgi-bin/bookmgr/bookmgr.exe/BOOKS/RD014E01/ FRONT
Medicare is the only federal insurer that mandates coverage of BMD testing (see Exhibit 14.2). Medicare covers these tests for beneficiaries who have indications such as estrogen deficiency, spinal abnormalities, hyperparathyroidism, long-term steroid use, and/or use of osteoporosis pharmaceuticals (see http://www.healthvermont. gov/research/chronic/osteoporosis). The Bone Mass Measurement Act, a Health Care Financing Administration (HCFA) regulation, became effective on July 1, 1998, and implements Provision 186 1 (s)(15)(5) to Section 4106(a)(1) of the Balanced Budget Act (BBA) to Provide for Uniform Coverage of Bone Mass Measurements.
Policy and Reimbursement: Individual States in the United States Only 14 states have mandated osteoporosis-related diagnostic and treatment insurance coverage, meaning that 36 states have not. Education, public awareness, and prevention programs relating to osteoporosis have been legislatively enacted in 34 states, meaning 16
14.3
Table
Yes No
Yes Yes Yes
Yes Yes
Yes Yes Yes
No No Yes
Alaska
Arizona
Arkansas
California
Colorado
Connecticut
Delaware
Florida
Georgia
Hawaii Idaho Illinois
Policy/ legislation
Alabama
State
No No Yes
Yes
Yes
No
No
Yes
Yes
No
Yes
No
No
Coverage of screening Web site
www.ilga.gov/legislation/ BillStatus.
www.doh.state.fl.us/ family/osteo/ www.legisl.state.ga.us/ legis/1995
www.dhss.delaware.gov/
www.dph.state.ct.us/
www.cdphe.state.co.us/
www.dhs.ca.gov/
www.healthyarkansas.com/
www.azleg.state.az.us/
www.legislature.state.al.us/ CodeofAlabama www.hss.state.ak.us
Bone Health Policy by Individual States
Illinois Senate Bill 973; 2744
Conn. House Bill 6970; Conn. Acts, P.A. 99-9; 96245 Del. Code Ann. Tit. 16 § 30-3001 Fla. Stat. § 381.87 & 627.6409 Ga. Code Ann. § 31-15A-1 et seq.; 31-42.1 et seq.
Cal. Acts, Chap. No. 39, 73; Cal Health & Safety Code § 1257 et seq.; § 1367.67 none
Arizona Senate Bills 1248 & 1365 Ark. Stat. Ann. §
AS Code Title 18
Ala. Code § 22-13A-1 et seq.
Statute
(Continued)
Drug coverage for osteoporosis; bone mass measurement & treatment
Education, awareness; diagnostic screening Bone Mass Measurement Coverage Act; education, awareness
2003 initiative & advisory committee Numerous initiatives including drug therapy management pilot Education & awareness
Prevention & treatment education Numerous osteo initiatives
Public health education on bone health of Native American women Numerous osteo initiatives
Comments
No
No Yes
Yes Yes
Yes Yes
Yes
Yes
Yes
Yes Yes
Indiana
Iowa Kansas
Kentucky
Louisiana
Maine
Maryland
Massachusetts
Michigan
Minnesota
Mississippi
Missouri
Yes
Yes
No
Yes
Yes
Yes
No
Yes
Yes
No Yes
No
www.dhss.mol.gov/osteo/ laws
www.msdh.state.ms.us/
www.mphi.org/projectsby funder www.michigan.gov/mdch www.nof.org
www.mass.gov/dph/bfch
www.strongerbones.org www.dhmh.state.md.us
www.maine.gov/dhhs
www.legis.state.law.us
www.chfs.ky.gov/
www.idph.state.ia.us www.kslegislature.org/
www.indystar.com
Miss. Code Ann. § 41-93-1 et seq. Mo. Rev. § 376.1199; 192.640 et seq.
(Continued)
Radiography statute; Department of Health reporting of osteo needs Prevention, treatment, & education program Arthritis & osteo program; prevention, OB/GYN benefits to include osteo also
Education; prevention & treatment program Mich. House Bill 4831; 5723; Mich. Pub. Acts, Act 336, 94 Minn. Stat. § 327.20; Minn. Laws, Chap. 207
Md. Acts, Chap. No. 444; Md. Insurance Code Ann. § 15-823 Mass. Sen. Bill 2282; 689; 4850.
Maine House Bill 924
Prevention & education; bone density testing Insurers to include coverage for bone mass measurement Drug benefits for osteoporosis Education; insurance coverage for bone mass measurement Prevention & education; insurance coverage; education for prevention & treatment
Bone mass measurement, treatment, & management
State ends 6-year program after study finds heel scan unreliable
Ky. House Bill 380; Ky. Rev. Stat. § 17-3163, 22:215.16 La. Rev. Stat. Ann. § 22:215.16
Kan. Stat. Ann. § 40-4601
Ind. Code § 16-41-39.6 et seq.
14.3
Table
No Pending
Yes No No
Yes Yes Yes Yes Yes
Yes No Yes Yes
No Yes
Nevada
New Hampshire New Jersey
New Mexico
New York
North Carolina North Dakota Ohio
Oklahoma
Oregon Pennsylvania
No No
Yes
Yes
No
No
No
No
Nebraska
Coverage of screening No
Policy/ legislation No
State Montana
(continued)
www.oregon.gov/DHS/ph www.dsf.health.state.pa.us/ health www.strongbonespa.com
www.hhs.state.ne.us/ womenshealth www.leg.state.nev.us/ www.hr.state.nv.us www.dhhs.nh.gov/DHHS/ NHP/ www.state.nj.us/health/ senior/osteo www.cdc.gov/arthritis/ state_programs/ www.health.state.ny.us/ disease/conditions/osteoporosis/ www.communityhealth.dhhs. state.nc.us/oldadult/ www.health.state.nd.us/ DoH www.odh.ohio.gov/odhpr ograms www.health.state.ok.us/ program/cds/arthritis
Web site www.dphhs.mt.gov/
Pa. House Bill 815, 2499; Pa. C. S. 71 § 531-A
Ohio Rev. Code Annotated § 3/17, 3.24, 9.06, 101.23. Okla. Stat. Title 63, § 1-260.3, 36, § 6060.1
N.Y. House Bill 9554, 4755; Senate bill 6454; N.Y.> Acts, Chap. No. 554 N.C. Gen. Stat. § 58-3-174 & Sess. Laws, Chap. 443
N.H. Rev. Stat. § 126:I:1 et. seq. N.J. Stat. § 26:2R-1 et seq.; N.J. Senate Bill 1055, 1053 N.M. Laws, Chap. 116
Nev. Rev. Stat. § 236.065
Statute
(Continued)
Prevention, treatment education program; required insurance coverage for high risk osteo
Awareness programs
Prevention awareness; insured screening Prevention & treatment education Prevention, education; bone mineral density tests, medications Diagnostic tests; prevention & education
Prevention education & awareness Prevention & education
Comments
Yes
No Yes
Yes
No No
Yes Yes Yes
Yes No
South Dakota Tennessee
Texas
Utah Vermont
Virginia Washington
West Virginia
Wisconsin
Wyoming
No
Yes
Yes
No No
No No
Yes
No
Yes
South Carolina
No
Yes
Rhode Island
www.wdh.state.wy.us/
www.dhfs.wisconsin.gov/
www.wvdhhr.org/bph/ oehp/hp/osteo
www.health.utah.gov/ www.healthvermont.gov/ research/chronic/osteo porosis www.vdh.state.va.us www.doh.wa.gov
www.dshs.state.tx.us/osteo
www.state.tn.us/comaging/ www.State.tn.us/health/
www.health.state.ri.us/ disease/osteo/coalition www.scstatehouse.net/ CODE/titl44 www.scdhec.gov/ www.state.sd.us/DOH/
Wis. Stat. § 534, 592, & 3482
Va. Code § 32.1-11.3 Wash. Rev. Code § 28B.20.462 W. Va. Code §§ 16-5M-1, 3316-18. W. Va Senate Bill 125
Tex. Health & Safety Code Ann. § 90.001. Tex Insur. Code Ann. § 21.53C
Tenn. Code Ann. §§68-11501, 56-7-2506, 4-29-228. Tenn. Pub. Acts, H. Jt. Res. 431, 101, 433, 1071
R.I. Gen. Laws § 23-70-1, 42-66.2-3 S.C. Code Annotated § 44125-10
Prevention, education, & screening
Prevention, education, & screening
Early detection, prevention, bone mass measurement coverage
Prevention, treatment, & education programs; Bone Mass Measurement Coverage Act; Council on Osteoporosis
Prevention, treatment options; drug assistance Prevention, treatment, & education program
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Osteoporosis
states have not enacted laws relating to osteoporosis (Weidenbener, 2006). Many states’ departments of health have osteoporosis programs, policy, and legislation under the rubric of women’s health or chronic disease/arthritis. Considering the morbidity and mortality of advanced osteoporosis and the health and economic sequelae of bone deterioration, it is surprising that legislators have not responded more aggressively to this disease. However, because of the variability of reliability of the BMD testing technology, Indiana, in June 2006, ended its 6-year diagnostic screening program (Weidenbener, 2006). For bone health by individual U.S. state, see Table 14.3.
Policy Development: Case Studies Anderson’s original sequential model (Anderson, Brady. Bullock, & Stewart, 1984) identifies six stages in the policy process: (1) problem identification, (2) agenda setting, (3) policy formulation, (4) policy adoption, (5) policy implementation, and (6) policy evaluation. The National Osteoporosis Society of the United Kingdom (2005) exemplifies the application of this model in its adoption of a policy framework easily accessed on its Web site (www.nos.org.uk/nos-policy-positions.htm). Formulated to develop policy papers and position statements on issues related to osteoporosis, it is depicted in the algorithm shown in Figure 14.1.
Public Funding for Osteoporosis Medications: Israel Many countries are utilizing the consensus conference as a tool to develop public policy on a national level. Originally developed by Perry (Perry, 1987; Perry & Kalbret, 1980) to discuss major health issues at the U.S. NIH, this type of conference has been adapted to the needs of different world regions. Shemer (2000) describes the use of the consensus conference by the National Health Services Basket in Israel to formulate a national policy on osteoporosis. This initiative was spurred by research findings related to new-generation medications for osteoporosis, and by pressure from physicians and patients. Coverage of medications by the government required accurate utilization prediction, a needs assessment of the population, information on pharmaco-epidemiology, and compliance and consensus on good medical practice (Shemer, 2000, p. 375). The conference brought together leading experts in the field and resulted in the “adoption of new drugs through public funding, and the acceptance of all the other recommendations for the prevention, detection and treatment of the disease” (Shemer, 2000, p. 376).
Calcium and Vitamin D: United States, Canada Calcium and vitamin D are essential nutrients for bone health, and intake recommendations have evolved over the years. Looker (2003) makes the case that calcium can serve as an exemplar of the interrelationships among research, consumer practices, and public policy. The same case can also be made for vitamin D (Calvo & Whiting, 2006). Data linking calcium to bone health have provided the scientific rationale for the calcium intake recommendations published by the U.S. Food and Nutrition Board of the
Figure
14.1
Practice policy formulation process of the National Osteoporosis Society, United Kingdom. Reprinted with permission from the Policy Framework Summary of the National Osteoporosis Society of the United Kingdom.
216
Osteoporosis
National Academy of Sciences dating back to the early 1940s. Increasingly, the evidence from randomized control trials, particularly calcium’s and vitamin D’s positive effect on the bone density of postmenopausal women and the reduction of fracture risk in women over 60, has supported higher intake allowances (Jackson et al., 2006). One exception has been the evidence that calcium intake during lactation does not influence bone status (Prentice, 2000). In addition, data on consumer consumption of the nutrients in question impact policy development and implementation. The National Health and Nutrition Examination (NHANES) III survey in the United States on calcium intake in the general population indicates that after childhood, female intake, even with supplementation, was below the recommended levels. NHANES III survey data also found little change in vitamin D intake over the last decade, with “few age, race and gender groups meeting dietary intake guidelines” (Calvo & Whiting, 2006, p. 1136). Likewise, studies in Canada found that even in young White women, vitamin D intake at the level of the dietary guidelines did not result in circulating 25-hydroxy vitamin D levels of 80 nmol. These studies did not only fuel changes in dietary recommendations but also in permitted health claims on food and supplement labels; they also led to the inclusion of objectives related to calcium in Healthy People 2010 and to promotional campaigns to increase calcium and vitamin D intake in the United States. The campaigns encouraged increased consumption of natural food sources, fortified foods, and dietary supplements. However, policies are fluid and ever subject to revisions. As new research into the calcium–vitamin D–bone health relationship is reported, policies are periodically reviewed and revised as warranted (Looker, 2003). Because of the lack of strong data regarding younger individuals, the sustained effects after discontinuance of supplementation, and other complexities in the calcium-bone connection, questions have been raised and changes regarding intake recommendations have been made. Examples of such policy changes include revisions with regard to dietary calcium intake during lactation. Emerging issues that may impact policy development include the relationship to bone health of exercise, vitamin D receptor genotype, and mandatory fortification of cereal grain products with vitamin D (Calvo & Whiting, 2006; Looker, 2003).
Summary Health policy that affects bone health is developed by international organizations, individual countries, and, in the United States, by individual states. In order to reduce the prevalence of osteoporosis and the number of fractures worldwide, several initiatives have been undertaken. These decisions made by governments and by private agencies influence the promotion of bone health in several diverse areas: how osteoporosis is defined, how whole populations are screened, and what preventive and treatment measures are the most cost-effective, to name a few. The United Nations’ WHO, the Bone and Joint Decade, and the IOF have spearheaded these efforts. In the United States, Healthy People 2010 and the surgeon general’s report, Bone Health and Osteoporosis (USDHSS, 2004), call for a national action plan to implement systems changes including dietary,
Health Policy and Insurance Reimbursement
217
physical activity, and financing recommendations. Such a plan, however, needs to recognize that policy development is a fluid process and involves a complex interrelationship with research, science, and public health awareness that demands a framework to address the ever-changing data.
REFERENCES Anderson, J. E., Brady, D. W., Bullock, C. S., & Stewart, J. (1984). Public policy and politics in America (2nd ed.). Monterey, CA: Brooks/Cole. BJDonline: Bone and Joint Decade’s Musculoskeletal Portal. (2006). The initiative; the structure; the supporting governments. Retrieved August 9, 2006, from http://www.boneandjointdecade.org Calvo, M. S., & Whiting, S. J. (2006). Public health strategies to overcome barriers to optimal vitamin D status in populations with special needs. Journal of Nutrition, 136, 1135–1139. Harrington, C., & Estes, C. (2004). Health policy: Crisis and reform in the US health care delivery system (4th ed.). Boston: Jones and Bartlett. International Osteoporosis Foundation. (2005). Advocacy and policy. Retrieved August 9, 2006, from http:///www.osteopfound.org/advocacy_policy/index.html Jackson, R. D., LaCroix, A. Z., Gass, M., Wallace, R. B., Robbins, J. C., Lewis, C. R. et al. (2006). Calcium plus vitamin D supplementation and the risk of fractures. New England Journal of Medicine, 354(7), 669–683. Johnell, O., & Hertzman, P. (2006). What evidence is there for the prevention and screening of osteoporosis? WHO Regional Office for Europe, Copenhagen. Retrieved May 18, 2006, from http://wwwleuro .who.int/document/e88668.pdf Longest, B. B. (1998). Health policy making in the United States (2nd ed.). Chicago: Health Administration Press. Looker, A. C. (2003). Interaction of science, consumer practices and policy: Calcium and bone health as a case study. Journal of Nutrition, 133, 1988S–1991S. Mason, D., Leavitt, J., & Chaffee, M. (2002). Policy and politics in nursing and health care (4th ed.). St. Louis: Saunders. National Institutes of Health. (2000). Osteoporosis prevention, diagnosis, and therapy. NIH Consensus Development Conference Statement Online, March 27–29, 2000 (pp. 1–36). Retrieved November 16, 2003 from http://consensus.nih.gov/cons/111/111–statement.htm. National Osteoporosis Foundation. National Osteoporosis Society of the United Kingdom. (2005, August). Policy framework summary. Retrieved August 23, 2006, from www.nos.org.uk/policy/nos-policy-positions.html National Osteoporosis Foundation. (2006). Summary of Osteoporosis Laws & Legislation in the United States. Retrieved July 23, 2006 from http://www.nof.org/advocacy/updates/ stateleg.htm National Osteoporosis Foundation (2007). About NOF: Mission and goals. Retrieved August 25, 2007 from http://www.nof.org/aboutnof/. NIH News Release (2000, March 29). NIH consensus panel addresses osteoporosis prevention, diagnosis, and therapy. Retrieved on August 27, 2006 from http://www.nih.gov/new/pr/mar2000/ od-29.htm. Perry, S. (1987). The NIH consensus development program and the assessment of health-care technologies. New England Journal of Medicine, 317(8), 485–488. Perry, S., & Kalbret, J. T. (1980). The NIH consensus development program and the assessment of health-care technologies. New England Journal of Medicine, 303(3), 169–172. Prentice, A. (2000). Maternal calcium metabolism and bone mineral status. American Journal of Clinical Nutrition, 71(Suppl.), 1312S–1316S. Shemer, J. (2000). Consensus conference as a tool for national health services policy: The case for osteoporosis. Israeli Medical Association Journal, 2, 375–376. Shi, L., & Singh, D. (2004). Delivering health care in America: A systems approach (3rd ed.). Gaithersburg, MD: Aspen. U.S. Department of Health and Human Services. (2000). Healthy People 2010. Washington, DC: Author.
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Osteoporosis U.S. Department of Health and Human Services. (2004). Bone health and osteoporosis: A report of the surgeon general. Public Health Service, Office of the Surgeon General, Rockville, MD. Retrieved June 6, 2006 from http://www.surgeongeneral.gov/library/bonehealth/ U.S. Preventive Services Task Force (2002). Screening for osteoporosis in postmenopausal women: Recommendations and rationale. Annals of Internal Medicine, 137 (6), 526–528. Weidenbener, L. S. (2006, July 6). State dropping osteoporosis test: Questions raised about screenings. Courier-Journal.com. Retrieved July 24, 2006 from http://www.courier-journal.com/apps/pbcs. dll/article?AID=/20060706/NEWS02/6070604. World Health Organization. (1994). Assessment of fracture risk and its application to screening for postmenopausal osteoporosis: Report of WHO Study Group (WHO Technical Report Series, No. 843). Geneva, Switzerland: Author. World Health Organization. (2003a).The burden of musculoskeletal conditions at the start of the new millennium: Report of a WHO Scientific Group (WHO Technical Report Series, No. 919). Geneva, Switzerland: Author. World Health Organization. (2003b). Diet, nutrition and the prevention of chronic diseases: Report of a Joint WHO/FAO Expert Consultation (WHO Technical Report Series, No. 916). Geneva, Switzerland: Author. World Health Organization. (2003c). Prevention and management of osteoporosis: Report of a WHO Scientific Group (WHO Technical Report Series, No. 921). Geneva, Switzerland: Author. Writing Group for International Society for Clinical Densitometry Position Development Conference. (2004). Position Statement of 2003 Conference. Journal of Clinical Densitometry, 7(1), 7–12.
Emerging Approaches in the Prevention of Osteoporosis
Interstitial fluid flow is essential for maintaining bone integrity. Simple, non-invasive approaches which enhance skeletal muscle pumping and thereby ensure sustained interstitial flow through bone have the potential to prevent and treat osteoporosis. (K. J. McLeod)
Introduction
O
15 Carolyn S. Pierce Guruprasad Madhavan Kenneth J. McLeod
steoporosis is characterized by long-term loss of bone tissue. While the bone tissue that remains is normal and fully capable of repairing itself, the effective strength of the skeleton is reduced by the loss, leading to increased risk of fracture following even minor trauma. The most common sites of osteoporotic fractures are those composed principally of trabecular bone, namely, the distal radius, spine, and femoral neck. Osteoporosis is a common occurrence in the aged, usually resulting from slow progressive bone loss, but rapid bone loss can occur during menopause, extended bed rest, cast immobilization, or extended exposure to microgravity. While inhibitors of bone resorption are commercially available, as well as at least one anabolic agent, a pharmacologic approach is neither an appropriate nor a costeffective approach for young and otherwise healthy men and women, who are looking for an osteoporosis prevention strategy that can be utilized over extended time periods. Indeed, recent reports suggest that the extended use of bisphosphonates to prevent bone resorption may lead to serious long-term complications (Bamias et al., 2005; Migliorati et al., 2005; Woo, Hellstein, & Kalmar, 2006). In order to understand the new directions being pursued in the development of preventative strategies for osteoporosis, it is necessary to understand the driving forces behind bone adaptation. It has long been observed that larger animals have larger bones,
220
Osteoporosis
and so it was only natural to hypothesize that adaptation processes are directed toward placing bone mass appropriately within the skeleton to the mechanical loading forces placed on the skeleton during day-to-day activities (Wolff, 1892/1986). In this context, osteoporosis is primarily viewed as a physiologic adaptation to an altered environment, that is, an adaptation by changes in the pattern of mechanical loading of the bone tissue. Indeed, numerous animal studies, in which bone tissue can be loaded in a controlled manner, have shown that mechanical loading of the skeleton can lead to new bone formation. However, investigations specifically addressing the link between mechanical loading and bone mass have shown that there is actually little correlation between mechanical load distributions in bone tissue and bone mass distributions. These results indicate that the bone adaptation is probably not due to the direct influence of mechanical loading but to some phenomenon coupled to the mechanical loading process. Understanding this underlying process is critical, as increased mechanical loading of the skeleton in humans has very little effect on bone adaptation processes. Numerous clinical studies have shown that while high levels of physical activity may be capable of significantly affecting bone mass in the skeleton of children, exercise regimens can produce, at best, only modest increases in bone mass, either in young adults ( Jones, Priest, Hayes, Tichenor, & Nagel, 1977; Snow-Harter, Bouxsein, Lewis, Carter, & Marcus, 1992) or in the elderly (Hoshino et al., 1996; Smith, Gilligan, McAdam, Ensign, & Smith, 1989).
Bone Adaptation and Fluid Flow Though mechanical loading, per se, does not appear to significantly affect skeletal adaptation, the nutritional and hormonal support that is tenuously associated with mechanical loading does have a profound influence on the maintenance of bone tissue. While oxygen and low-mass nutrients can diffuse from the capillaries directly to the cell population of even sparsely vascularized tissues such as bone, large proteins are diffusion limited and so are reliant on fluid flow in the tissue for transport to the cells (Montgomery, Sutker, Bronk, Smith, & Kelly, 1988). These large proteins are being continuously extravasated from the capillaries along with interstitial fluid. The flow of this interstitial fluid through the bone tissue is therefore critical to the integrity of bone cells, and, correspondingly, to the maintenance of bone mass. The extravasation of interstitial fluid is primarily dependent on transmural pressures (i.e., the difference between capillary and tissue pressures), but it can also be influenced by pressure gradients developed by the mechanical deformation of bone tissue during exercise. It is this process that provides the link between mechanical loading and bone adaptation. However, as intensive exercise generally represents a small fraction of the daily activity of most individuals (Fritton, McLeod, & Rubin, 2000), the contributions of capillary pressures and tissue pressures can be expected to dominate interstitial fluid flow in bone. Studies performed over the last 4 decades have clearly demonstrated the importance of interstitial fluid flow in the formation and maintenance of bone mass. In the mid-1960s, Keck and Kelly (1965) first demonstrated that increased bone growth was associated with increased venous pressure. These observations led to investigations of interstitial flow in bone, and the demonstration of lymphatic vessels in bone directed
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from the marrow to the periosteal surfaces (Seliger, 1970). Subsequently, it was shown that high venous pressures encouraged bone formation in the absence of any change in blood flow (Kruse & Kelly, 1974), and also that high venous pressure was associated with increased venous filtration (Li, Bronk, An, & Kelly, 1987). The influence of increased venous pressure and increased filtration has been confirmed more recently using the rat hindlimb suspension model of microgravity (Bergula, Huang, & Frangos, 1999). Numerous additional studies have lent support to the theory that blood flow and interstitial fluid flow are critical to the maintenance of bone mass. Colleran and associates (Colleran et al., 2000) showed that decreased blood flow to the limbs results in decreased cancellous bone formation as well as reduced periosteal bone. McDonald and Pitt Ford (1993) demonstrated that an important effect of mechanical loading was the significant alteration of blood flow in bone. Perhaps one of the most important clinical observations regarding the role of venous pressure and filtration was made by Issekutz and colleagues (Issekutz, Blizzard, Birkhead, & Rodahl, 1966), who demonstrated in a population of young men that bed rest resulted in substantially elevated urinary calcium secretion and that no form of supine exercise regimen was capable of inhibiting this calcium loss. However, just six periods of quiet standing for 30 minutes per day returned urinary calcium to normal levels. These study results are consistent with the premise that the influence of gravity (hydrostatic pressure effects) on the fluid within bone is sufficient to increase capillary filtration and interstitial flow, allowing bone mass to be maintained. The proposition that interstitial flow may be a critical factor in the maintenance of bone mass is also consistent with the distribution of bone loss in disuse, whether due to aging, bed rest, or passive inactivity. Bone loss does not occur to any degree in the thorax or cranial regions of the skeleton, where blood pressure and/or gravity can sustain a normal filtration rate, and skeletal muscle pump activity combined with gravity can maintain interstitial fluid return via the lymphatic system. However, at sites where interstitial flow is limited, due to either a lack of adequate filtration or inadequate return, loss of bone mass is commonly observed. Maintenance of bone mass, in summary, requires adequate filtration and transport of nutrients and growth factors through the bone tissue. Adequate filtration, correspondingly, requires high capillary pressures, which are normally produced by the influence of gravity during upright stance. In addition, sustained fluid transport through bone requires effective venous and lymphatic return, which serves to maintain low tissue pressures. Venous and lymphatic return, at least in the periphery of the body, is mediated primarily by skeletal muscle pumping, an often ignored physiologic function. Developing strategies to prevent bone loss, therefore, requires an understanding of how gravity influences fluid flow in the human, and how effective circulation is maintained through skeletal muscle pump activity.
Fluid Flow in Humans Gravitational Effects on Circulation The pumping action of the heart is sufficient to sustain blood circulation for individuals in the supine (or prone) position, but it is not sufficient when an individual is upright.
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When humans are in a supine posture, the peak blood pressure generated by the heart is approximately 100 mmHg throughout the large arteries. Conversely, venous pressures in the supine position range from slightly negative at the right atrium to no more than 15 to 20 mmHg in the peripheral veins. Therefore, the driving pressure from the lower limb vessels back to the heart is only about 20 to 25 mmHg. A pressure of 25 mmHg is equivalent to approximately 25 cm (10 inches) of water, meaning that venous pressure in the supine position is sufficient to raise blood about 25 cm above the lowest point in the body. For most individuals, this pressure is adequate to return blood to the heart when an individual is lying down. However, when humans assume an upright posture, the pressures in the circulatory system change dramatically. For example, when standing, the heart is about 1200 to 1500 cm above the feet. Venous pressures of 25 mmHg are clearly incapable of returning blood to the heart during standing; and indeed, even upright sitting would experience diminished venous return in the absence of a supplemental pump that is capable of significantly increasing venous pressures.
Role of Skeletal Muscle Pumping in Maintaining Fluid Flows Venous return from the extremities during upright posture is accomplished in humans by skeletal muscle activity. In the legs, this “muscle pumping” is predominantly the result of calf muscle contraction synergistically assisted by competent venous valves (Figure 15.1). The role the calf muscles play in driving blood back to the heart against the force of gravity has given rise to the term “second heart.” In returning this venous blood, the calf muscle pump (in particular, the soleus muscle) also serves to maintain arterial blood pressure during upright posture. In the absence of adequate calf muscle pump activity, blood sequestration into the lower extremities can be substantial. Even in healthy individuals, a shift to upright posture typically leads to a 10% blood volume shift of 7 ml/kg, or 300–600 ml, into the lower extremities (Sheperd, 1966). This “loss” of blood volume results in inadequate cardiac refilling and therefore decreased cardiac output per the Frank-Starling mechanism (Rowell, 1993). Additionally, skeletal muscle pumping is essential for lymphatic return from the lower limbs. Upper body lymphatics can drain back to the subclavian vein by gravitydriven flow, and the thoracic region drains during respiratory motion. But the lower limbs lack any explicit lymphatic pump, and so lymphatic fluid return is completely dependent on skeletal muscle activity. While it is widely believed that interstitial fluid extravasated from capillaries is reabsorbed at the venous end of the capillaries, it has been well established that, under normal conditions, capillary flow is unidirectional—from vessel lumen to interstitium—with lymphatic drainage removing filtered interstitial fluid (Zweifach & Intaglietta, 1966). This is not an insubstantial amount of fluid, as has been shown through studies of serum volume changes during a shift in posture. Lymphatic return amounts to approximately 3 liters per day when an individual is supine, or roughly an amount equal to the entire serum plasma volume in an adult. However, the volume of this flow is greatly influenced by the increased hydrostatic forces created by gravity when an individual is upright. For example, up to 20% of serum fluid leaves the vascular system through extravasation within 30 minutes of attaining an upright stance (Hagan, Diaz, & Harvath, 1978). This fluid largely pools in the interstitial
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Figure
15.1
Soleus muscle in synergy with unidirectional valves promotes venous and lymphatic fluid return. In the absence of soleus muscle contraction, blood tends to pool in the legs, resulting in increased venous pressure, while diminished lymphatic return results in peripheral edema and swelling. (Image developed from Gray, 2004.)
spaces of the lower limbs unless it is taken up by the lymphatic system. Inadequate lymphatic return, therefore, results in substantially increased interstitial fluid pressures. These high tissue pressures serve to inhibit extravasation from the vascular supply with a corresponding loss of nutrient delivery to the dependent tissues.
Role of Skeletal Muscle Activity in Maintaining Bone Mass From the above discussion, it should be evident that the maintenance of adequate interstitial fluid flow across the bone tissue is essential for preventing the loss of bone mass that leads to osteoporosis. In order to sustain this interstitial flow, two conditions must be met: 1 . An individual must spend a significant portion of the day upright, so as to
maximize the hydrostatic pressure on the circulatory system. The gravitational
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force operating on the circulatory system ensures high capillary pressures, which lead to high levels of fluid extravasation from the blood supply, thereby providing the nutritional support necessary to maintain bone mass. 2 . The extravasated fluid must be cleared from the tissue surrounding the bone and returned to the circulatory system. If this fluid is not removed, increased tissue pressure (edema) will preclude further interstitial flow, resulting in loss of nutritional support to the tissue and in bone atrophy. For young, healthy individuals, maintaining an upright posture for a significant fraction of the day is not usually an issue, though this factor can be an insurmountable hurdle in the prevention of osteoporosis in the elderly or in bed rest patients. However, ensuring that an individual has sufficient calf muscle pump activity to maintain low tissue pressure and thereby permit sustained interstitial fluid flow through the bone tissue can be more problematic. Even for an individual in good health, age-related changes in the musculature can result in the conversion of the critical Type IIA (fast twitch oxidative) muscle fibers in the soleus into Type IIB (fast twitch glycolytic) muscle fibers, which are unable to sustain continual contraction. Osteoporosis preventative therapy, therefore, becomes a matter of training up the soleus to improve calf muscle pump function. Numerous approaches are currently being pursued for achieving effective calf muscle pump stimulation. These include training based on physical activity regimens, functional electrical stimulation, and reflex-mediated micro-mechanical stimulation of the calf muscles.
Skeletal Muscle Pump Stimulation and Bone Health Physical Activity Physical activity is widely accepted as a successful preventative strategy for a wide variety of conditions. Perhaps best documented are the beneficial influences of exercise on the cardiovascular system, and the ability of exercise to assist type II diabetics in regulating serum glucose levels. Both of these outcomes can be achieved by increasing the activity of any of the voluntary muscles, and so strenuous exercise of many forms has been found to be beneficial for these conditions. However, developing a physical activity regimen capable of enhancing calf muscle pump activity presents a somewhat greater challenge, in that the dominant muscle of the calf muscle pump, the soleus, is largely an involuntary muscle. While the soleus can be voluntarily contracted, this muscle typically fires autonomically when the individual is either sitting or standing in order to maintain balance and posture. Correspondingly, exercises focused on balance and postural control, such as T’ai Chi Chuan, have recently emerged as potential exercise modalities capable of inhibiting bone loss. T’ai Chi Chuan is a unique form of physical activity, characterized by a high demand for neuromuscular coordination, low velocity of muscle contraction, low impact, and minimal weight bearing (Figure 15.2). In a case-controlled study in postmenopausal women (n = 17), T’ai Chi exercise was found to significantly reduce the rate of trabecular bone loss in the tibia (Qin et al., 2002). More recently, the effectiveness of T’ai Chi Chuan in slowing
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Figure
15.2 An illustration of postural movements in T’ai Chi Chuan. T’ai Chi Chuan is an ancient Chinese martial art technique that involves deep diaphragmatic breathing and relaxation, with many fundamental postures that flow imperceptibly and smoothly from one to the other through slow, gentle, and graceful movements. The benefits of T’ai Chi Chuan are improved muscle strength, flexibility, postural balance, and neuromuscular coordination, reduced fall risks, and improved bone density.
bone loss has been demonstrated in a larger prospective study (Chan et al., 2004). In this controlled study of 132 women (mean age: 54±3.5 years), regular practitioners of T’ai Chi Chuan saw a three- to four-fold reduction in their rate of bone loss. In addition to preventing bone loss, T’ai Chi Chuan has the benefit of improving muscle strength, flexibility, and neuromuscular coordination, and thus of reducing fall-related fracture risks in the elderly population (Lane & Nydick, 1999). T’ai Chi Chuan is easily learned and can be practiced throughout one’s lifetime. However, like all exercise programs, it requires that an individual set aside significant time each day to perform the exercises. In Asian societies where T’ai Chi Chuan is linked to other cultural values and activities, high levels of compliance are observed, but it is unclear to what extent T’ai Chi Chuan could become broadly practiced by populations in Western cultures.
Functional Electrical Stimulation Electrical stimulation of muscle (Figure 15.3) is a widely used technique directed to both enhancing intrinsic muscle function and training up muscle so that it can function normally in the absence of external stimulation (Langzam, Nemirovsky, Isakov, & Mizrahi, 2006; Paillard, Noe, Passelergue, & Dupui, 2005). Common application areas include stroke rehabilitation, bladder stimulation, phrenic nerve pacing, and neuroprosthetics (Peckham & Knutson, 2005). In addition, a major focus of electrical muscle stimulation is in the treatment of patients with spinal cord injury (SCI), who commonly experience extensive muscle as well as bone atrophy below the site of injury. One objective of these studies has been to determine whether electrical muscle stimulation can assist in preventing further bone loss in these patients or even serve to augment bone mass. There is compelling physiologic evidence to suggest that direct electrical muscle stimulation should be effective in influencing bone mass. One complication of lower limb muscle atrophy is severe orthostatic hypotension, as the loss of lower limb muscle activity also eliminates any muscle-pumping activity (Claydon, Steeves, & Krassioukov, 2006). In a study of six chronic and acute SCI patients, electrical stimulation of muscles in the lower limbs was found to significantly improve diastolic and systolic pressure, indicative of the ability of such stimuli to activate the muscle pump (Sampson, Burnham, & Andrews, 2000). Consistent with this observation, several studies have demonstrated that electrical stimulation can prevent bone loss and even increase bone mass in the lower limbs in SCI patients. Belanger
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Figure
15.3
Functional electrical stimulation of muscles employed to enhance and train intrinsic muscle function. Evidence supports the concept that electrical stimulation can be effective in maintaining bone mass, but this approach suffers from the discomfort and inconvenience of use. (Image used with permission from the Johns Hopkins University Arthritis Unit.)
and colleagues (Belanger, Stein, Wheeler, Gordon, & Leduc, 2000) reported that stimulation of the quadriceps muscle for 1 hour a day, 5 days a week, over 24 weeks, significantly increased bone mass in the proximal tibia and distal femur. Eser and colleagues (Eser et al., 2003) showed that electrical muscle stimulation for 30 minutes a day, starting immediately after the onset of muscle paralysis, slowed the rate of bone loss in the tibia by 50%. Similarly, in a crossover trial, electrically stimulated cycling activity was able to reverse bone loss in the distal femur and proximal tibia, demonstrating that sustained stimulation was necessary to maintain the bone mass (Chen et al., 2005). However, a more recent study indicates that these effects may be limited to the more distal aspects of the limbs. Clark and colleagues (Clark et al., 2006) addressed the effect of lower limb muscle stimulation on bone mass in the proximal femur and lumbar spine, and while they were able to show a beneficial effect of the stimulation on tibial bone mineral density, no effect was observed at the proximal femur or lumbar spine, where osteoporotic fractures most frequently occur. Clinical results for SCI patients suggest that, at least conceptually, direct electrical stimulation of the musculature may have potential as a means to prevent bone loss. However, electrical stimulation is not conveniently applied, can be painful, and often leads to rapid muscle fatigue, factors that may significantly limit its applicability as a long-term prevention strategy for osteoporosis.
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Mechanical Stimulation As a means of bypassing the complications of direct electrical stimulation of muscle contraction, investigators have recently begun pursuing the concept of using reflexmediated pathways to trigger muscle activity indirectly. Stimulation of a muscle such as the soleus can be readily achieved through such an approach, as it is fundamentally a postural muscle and hence receptive to a wide variety of somatosensory inputs. For example, mechanoreceptors on the plantar surface, such as the Meissner’s Corpuscles, provide feedback on body position when standing, and correspondingly, are linked to the soleus muscle through short-loop reflex arcs. Micromechanical stimulation of the plantar surface stimulates the cutaneous mechanoreceptors, which subsequently initiate calf muscle contraction. Stimulus amplitudes of no more than 20–30 microns are sufficient to stimulate the cutaneous receptors in young adults when applied in the optimal frequency range for these receptors (40–60 Hz), though receptor sensitivity does decrease with increasing age (Inglis, Kennedy, Wells, & Chua, 2002). This strategy has been implemented in a device that can be placed in front of a chair, or under a desk, so that the user can readily obtain calf muscle pump stimulation essentially continuously, in either the home or the workplace (Figure 15.4).
Figure
15.4
Reflex-mediated, calf muscle pump activation can be achieved through plantar stimulation in either the seated or standing position. A small electromagnetic actuator is sufficient to provide a 20-30 micrometer displacement to the plantar surface, which stimulates cutaneous mechanoreceptors and subsequently initiates calf muscle contraction. The lack of any direct attachment to the subject allows convenient use and therefore increases potential as a long-term bone loss preventative strategy.
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Studies utilizing this technology have shown that calf muscle pump activation can be readily enhanced. Stewart, Karman, Montgomery, and McLeod (2004), using plethysmographic techniques, have shown that plantar stimulation can increase lower limb blood flow by close to 50% during upright tilt, while increasing pelvic flow by 35% and even thoracic flow by 20%. In addition, plantar stimulation was shown to almost double lymphatic return pressure. Using cardiovascular monitoring techniques, plantar stimulation has also been shown to significantly enhance venous return from the lower limbs, resulting in reversal of orthostatic hypotension and orthostatic tachycardia (Madhavan, Stewart, & McLeod, 2005). Consistent with these observed effects on lower limb muscle pump activity, sustained plantar stimulation has been shown to significantly increase lower limb muscle strength in postmenopausal women (Russo et al., 2003). Torvinen and colleagues (Torvinen et al., 2003) have shown a similar result for lower leg strength in an 8-month study of 56 young adult men and women in the 19–38 age group. Correspondingly, these effects on the musculature have been observed to affect bone density over the long term. In children, effects of plantar stimulation have been reported as early as 6 months after the start of use (Ward et al., 2004). In adults, a longer duration use appears to be necessary to observe a substantial effect on bone density. In a 1-year-long, randomized, controlled study of postmenopausal women, daily use of plantar stimulation was effective in preventing bone loss in a dose-dependent manner (Rubin et al., 2004). Women who utilized plantar stimulation for 18 minutes a day or more experienced no loss of bone density in the femoral neck, as compared to a 2.1% loss in the control group. Similarly, in the lumbar spine, highly compliant subjects experienced only a 0.1% loss of bone density over the year, versus a 1.6% loss in the control group. These preliminary results, combined with the ease of use of this technology, suggest that this technology may, in the near future, form the basis of a convenient, noninvasive, nonpharmacologic means to prevent or reduce age-related bone loss and osteoporosis.
Concluding Remarks Over the past several decades, physiologic studies have identified interstitial fluid flow as being a dominant factor in the regulation of bone mass. Ensuring adequate interstitial flow through bone tissue must be an essential goal in any long-term strategy for preventing osteoporosis. Sustaining high levels of interstitial fluid flow requires extended periods of upright posture in combination with effective skeletal muscle pumping activity. Because age-related changes in the postural musculature of people commonly result in degradation of skeletal muscle pumping activity, explicit techniques need to be developed to regain this lost function. Here, we have reviewed three techniques currently under development. Balanceoriented exercise programs, such as T’ai Chi Chuan, appear to be capable of preventing bone loss, but they require a commitment level from the individual that may be very difficult to achieve. Sustained electrical stimulation of the musculature has been shown to reverse bone loss, but it can be painful and may not find wide acceptance beyond subpopulations with a very high fracture risk. An alternative approach that has more recently been proposed is reflex-mediated muscle stimulation.
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Micromechanical stimulation of the plantar surface has been shown to significantly enhance calf muscle pump activity by activating mechanoreceptors on the surface of the foot, which trigger soleus (calf ) muscle contractions through a reflex arc. This technology has been shown to significantly increase venous and lymphatic return from the lower limbs, enhance blood flow to the lower limbs, and prevent bone loss in postmenopausal women. Convenience of use may lead to wide acceptance of this technology. More importantly, however, the success of this technology has served to refocus attention on the importance of maintaining skeletal muscle pump activity in the goal of preventing bone loss and osteoporosis.
Acknowledgments This work was supported in part by a grant from the New York State Office of Science, Technology, and Academic Research, Albany, New York.
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Ward, K., Alsop, C., Caulton, J., Rubin, C., Adams, J., & Mughal, Z. (2004). Low magnitude mechanical loading is osteogenic in children with disabling conditions. Journal of Bone and Mineral Research, 19, 360–369. Wolff, J. (1892). Das Gesetz der Transformation der Knochen (The law of bone remodeling). Originally published Berlin: Verlag von August Hirshwald; English translation by P. Maquet & R. Furlong, Berlin: Springer Verlag, 1986. Woo, S. B., Hellstein, J. W., & Kalmar, J. R. (2006). Systematic review: Bisphosphonates and osteonecrosis of the jaws. Annals of Internal Medicine, 144, 753–761. Zweifach, B. W., & Intaglietta, M. (1966). Fluid exchange across the blood capillary interface. Federation Proceedings, 25, 1784–1788.
Appendixes
Appendix A Resources and Related Links
This section provides the names of resources and links in government and the private sector related to bone health. Links to nonfederal organizations do not constitute an endorsement of any organization by the federal government, and none should be inferred.
Federal Government Agency for Healthcare Research and Quality (AHRQ) Osteoporosis publications and electronic information http://www.ahrq.gov/news/pubsix.htm
Centers for Disease Control and Prevention (CDC) Growing Stronger: Strength Training for Older Adults http://www.cdc.gov/nccdphp/dnpa/physical/growing_stronger PATCH—CDC’s Planned Approach to Community Health http://www.cdc.gov/nccdphp/patch/index.htm Physical Activity and Health: A Report of the Surgeon General http://www.cdc.gov/nccdphp/sgr/sgr.htm Powerful Bones, Powerful Girls Web Site http://www.cdc.gov/powerfulbones/ http://www.cdc.gov/powerfulbones/parents Powerful Girls Calendar http://www.cdc.gov/powerfulbones/games_fun/calendar_2004.pdf Promoting Better Health for Young People Through Physical Activity and Sports http://www.cdc.gov/nccdphp/dash/presphysactrpt/index.htm VERBTM. It’s What You Do. Youth Media Campaign http://www.cdc.gov/youthcampaign/ WISEWOMAN: Well-Integrated Screening and Evaluation for Women Across the Nation http://www.cdc.gov/wisewoman
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Centers for Medicare and Medicaid Services (CMS) Bone Mass Measurement Health Promotion Initiative http://www.cms.hhs.gov/partnerships/tools/outreach/initiatives/default. asp#bonemass
National Heart, Lung, and Blood Institute (NHLBI) DASH (Dietary Approaches to Stop Hypertension) Eating Plan http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/ Hearts N’ Parks http://www.nhlbi.nih.gov/health/prof/heart/obesity/hrt_n_pk/index.htm National Cholesterol Education Program http://www.nhlbi.nih.gov/about/ncep/
National Institute on Aging (NIA) Exercise: A Guide From the National Institute on Aging http://www.niapublications.org/exercisebook/index.asp Exercise: A Video From the National Institute on Aging http://www.niapublications.org/exercisevideo/index.asp
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) Information Package—Ordering Information http://www.niams.nih.gov/hi/index.htm#ip Osteoporosis Prevention, Diagnosis, and Therapy http://www.odp.od.nih.gov/consensus/cons/111/111_intro.htm Osteoporosis: Progress and Promise http://www.niams.nih.gov/hi/topics/osteoporosis/opbkgr.htm
National Institute of Child Health and Human Development (NICHD) Milk Matters Educational Campaign http://www.156.40.88.3/milk/milk.cfm
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Sisters Together: Move More, Eat Better http://www.win.niddk.nih.gov/sisters/index.htm
National Institutes of Health (NIH) Clinical Trials http://www.ClinicalTrials.gov NIH Osteoporosis and Related Bone Disease—National Resource Center http://www.osteo.org/default.asp
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President’s Council on Physical Fitness and Sports The President’s Challenge http://www.fitness.gov http://www.presidentschallenge.org U.S. Administration on Aging Aging Internet Information Notes: Osteoporosis http://www.aoa.gov/prof/notes/docs/osteoporosis.doc
U.S. Department of Agriculture (USDA) Dietary Guidelines for Americans http://www.usda.gov/cnpp/ School Meals http://www.fns.usda.gov/cnd USDA Food and Nutrition Service http://www.fns.usda.gov United States National Agricultural Library http://www.nal.usda.gov
U.S. Department of Education (USDOE) National Institute on Disability and Rehabilitation Research (NIDRR) http://www.ed.gov/about/offices/list/osers/nidrr/index.html?src =mr
U.S. Department of Health and Human Services (HHS) Dietary Guidelines for Americans http://www.health.gov/dietaryguidelines HealthierUS Initiative http://www.healthierus.gov Healthfinder® Gateway to Reliable Consumer Health Information on the Internet http://www.healthfinder.gov Healthy People in Healthy Communities: A Community Planning Guide Using Healthy People 2010 http://www.healthypeople.gov/publications/HealthyCommunities2001 Healthy People 2010 Toolkit http://www.healthypeople.gov/state/toolkit National Women’s Health Information Center http://www.4woman.gov STEPS to a HealthierUS Initiative http://www.healthierus.gov/steps/index.html
U.S. Food and Drug Administration (FDA) Guidance on How to Understand and Use the Nutrition Facts Panel on Food Labels http://www.cfsan.fda.gov/~dms/foodlab.html U.S. Food and Drug Administration—FDA Consumer Magazine (10/02) http://www.fda.gov/fdac/features/2002/502_men.html
238
Appendix A
State Government Association of State and Territorial Chronic Disease Program Directors Osteoporosis Council http://www.chronicdisease.org/Osteo_Council/osteo_about.htm Osteoporosis Council: Contact Information for State Osteoporosis Directors/ Coordinators http://www.chronicdisease.org/Osteo_Council/osteo_membership.htm Osteoporosis State Program Practices That Work http://www.chronicdisease.org/whc/Practices_that_Work.pdf Osteoporosis 2000: A Resource Guide for State Programs http://www.chronicdisease.org/Osteo_Council/publications/Resource_Guide.pdf
State Osteoporosis Web Sites Alabama Department of Public Health http://www.adph.org/NUTRITION/default.asp?DeptId=115&TemplateId=2022& TemplateNbr=0 Arizona Osteoporosis Coalition http://www.azoc.org http://www.fitbones.org California Department of Health Services, Arthritis and Osteoporosis Unit http://www.dhs.ca.gov/osteoporosis Colorado Department of Public Health and Environment: Osteoporosis Web Site http://www.cdphe.state.co.us/pp/Osteoporosis/osteohom.html Florida Osteoporosis Prevention and Education Program http://www.doh.state.fl.us/family/osteo/default.html Georgia Osteoporosis Initiative http://www.gabones.com Indiana Osteoporosis Prevention Initiative http://www.in.gov/isdh/programs/osteo Kentucky Office of Women’s Physical and Mental Health: Osteoporosis http://chs.ky.gov/womenshealth/resourcecenter/Resources/osteoporosis.htm Maryland Department of Health and Mental Hygiene http://www.strongerbones.org Michigan Department of Community Health http://www.michigan.gov/mdch/0,1607,7–132–2940_2955—-,00.html Mississippi State Department of Health http://www.msdh.state.ms.us/msdhsite/index.cfm/13,0,225,html Missouri Department of Health and Senior Services http://www.dhss.state.mo.us/maop New Jersey Department of Health and Senior Services http://www.state.nj.us/health/senior/osteo New York State Department of Health http://www.health.state.ny.us/nysdoh/osteo/index.htm
239
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Ohio Department of Health http://www.odh.ohio.gov/resources/publications/osteo_guide.pdf Rhode Island Department of Health http://www.health.ri.gov/disease/osteo/index.php Tennessee Department of Health http://www2.state.tn.us/health/healthpromotion/osteoporosis.html Texas Department of Health: Osteoporosis Awareness and Education Program http://www.tdh.state.tx.us/osteo Virginia Department of Health http://www.vahealth.org/nutrition/bones.htm West Virginia Department of Health and Human Resources http://www.wvdhhr.org/bph/oehp/hp/osteo/default.htm
Nongovernment American Academy of Orthopaedic Surgeons (AAOS) http://www.aaos.org
American Academy of Pediatrics (AAP) Policy Statement on Calcium Requirements of Infants, Children, and Adolescents http://aappolicy.aappublications.org/policy_statement/index.dtl#C
American Council on Exercise http://www.acefitness.org
American College of Sports Medicine http://www.acsm.org
American Dietetic Association (ADA) http://www.eatright.org
American Society for Bone and Mineral Research (ASBMR) http://www.asbmr.org
ASBMR Bone Curriculum Web Site http://depts.washington.edu/bonebio/ASBMRed/ASBMRed.html
Bone Builders http://www.bonebuilders.org/
BoneKEy-Osteovision® http://`www.bonekey-ibms.org
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Foundation for Osteoporosis Research and Education (FORE) http://www.fore.org/
Growing Stronger: Strength Training for Older Adults http://nutrition.tufts.edu/research/growingstronger
International Bone and Mineral Society (IBMS) http://www.ibmsonline.org/
International Osteoporosis Foundation (IOF) http://www.osteofound.org/
International Society for Clinical Densitometry (ISCD) http://www.iscd.org/visitors/osteoflash/index.cfm
National Dairy Council (NDC) http://www.nationaldairycouncil.org
National Osteoporosis Foundation (NOF) http://www.nof.org
National Strength and Conditioning Association http://www.nsca-lift.org
Osteoporosis and Bone Physiology, University of Washington http://courses.washington.edu/bonephys
Osteoporosis Education, University of Washington http://www.osteoed.org/faq/index.html#male http://www.osteoed.org
Osteogenesis Imperfecta Foundation (OIF) http://www.oif.org
The Paget Foundation (TPF) http://www.paget.org
Shape Up America! http://www.shapeup.org
U.S. Bone and Joint Decade http://www.usbjd.org
Appendix B Diagnoses That Support Medical Necessity for Bone Densitometry for Reimbursement
ICD-9 Code Hyperparathyroidism, unspecified Primary hyperparathyroidism Secondary hyperparathyroidism, nonrenal Other hyperparathyroidism Cushing’s syndrome (includes latrogenic cortisol excess) Ovarian dysfunction; postablative ovarian failure Ovarian dysfunction; other ovarian failure, premature menopause Ovarian dysfunction; other ovarian failure, other Other endocrine disorders; ectopic hormone secretion, not elsewhere classified Other endocrine disorders; ectopic hormone secretion, unspecified Disorders of menstruation and other abnormal bleeding from female genital tract; absence of menstruation Menopausal and postmenopausal disorders; postmenopausal bleeding Menopausal and postmenopausal disorders; symptomatic menopausal or female climacteric state Menopausal and postmenopausal disorders; postmenopausal atrophic vaginitis Menopausal and postmenopausal disorders; symptomatic states associated with artificial menopause Menopausal and postmenopausal disorders; other specified menopausal and postmenopausal disorders Menopausal and postmenopausal disorders; unspecified menopausal and postmenopausal disorders Other disorders of bone and cartilage; osteoporosis, unspecified Other disorders of bone and cartilage; osteoporosis, senile Other disorders of bone and cartilage; osteoporosis, idiopathic Other disorders of bone and cartilage; osteoporosis, disuse Other disorders of bone and cartilage; osteoporosis, other Other disorders of bone and cartilage; pathologic fracture, fracture of humerus Other disorders of bone and cartilage; pathologic fracture, distal radius and ulna Other disorders of bone and cartilage; pathologic fracture, fracture of vertebrae Other disorders of bone and cartilage; pathologic fracture, fracture of neck of femur Other disorders of bone and cartilage; pathologic fracture, fracture of tibia or fibula Pathologic fracture of other specified site
252.00 252.01 252.02 252.08 255.0 256.2 256.31 256.39 259.3 259.9 626.0 627.1 627.2 627.3 627.4 627.8 627.9 733.00 733.01 733.02 733.03 733.09 733.11 733.12 733.13 733.14 733.16 733.19
242
Appendix B
ICD-9 Code Other disorders of bone and cartilage; other and unspecified Other congenital musculoskeletal anomalies; osteodystrophies, osteogenesis imperfecta Other congenital musculoskeletal anomalies; other specified anomalies of muscle, tendon, fascia, and connective tissue, Ehler-Danlos syndrome Chromosomal anomalies; gonadal dysgenesis Nonspecific abnormal findings on radiological and other examination of body structure, musculoskeletal system Fracture of vertebral column without mention of spinal cord injury; cervical, closed, unspecified level Fracture of vertebral column without mention of spinal cord injury; cervical, closed, first vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, closed, second vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, closed, third vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, closed, fourth vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, closed, fifth vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, closed, sixth vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, closed, seventh vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, closed, multiple vertebrae Fracture of vertebral column without mention of spinal cord injury; cervical open, unspecified level Fracture of vertebral column without mention of spinal cord injury; cervical, open, first vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, open, second vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, open, third vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, open, fourth vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, open, fifth vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, open, sixth vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, open, seventh vertebra Fracture of vertebral column without mention of spinal cord injury; cervical, open, multiple vertebrae Fracture of vertebral column without mention of spinal cord injury; dorsal (thoracic), closed Fracture of vertebral column without mention of spinal cord injury; dorsal (thoracic), open
733.90 756.51 756.83 758.6 793.7 805.00 805.01 805.02 805.03 805.04 805.05 805.06 805.07 805.08 805.10 805.11 805.12 805.13 805.14 805.15 805.16 805.17 805.18 805.2 805.3
243
Appendix B
ICD-9 Code Fracture of vertebral column without mention of spinal cord injury; lumbar, closed Fracture of vertebral column without mention of spinal cord injury; lumbar, open Fracture of vertebral column without mention of spinal cord injury; sacrum and coccyx, closed Fracture of vertebral column without mention of spinal cord injury; sacrum and coccyx, open Fracture of vertebral column without mention of spinal cord injury; unspecified, closed Fracture of vertebral column without mention of spinal cord injury; unspecified, open Fracture of vertebral column with spinal cord injury; cervical, closed, C1–C4 level with unspecified spinal cord injury Fracture of vertebral column with spinal cord injury; cervical, closed, C1–C4 level with complete lesion of cord Fracture of vertebral column with spinal cord injury; cervical, closed, C1–C4 level with anterior cord syndrome Fracture of vertebral column with spinal cord injury; cervical, closed, C1–C4 level with central cord syndrome Fracture of vertebral column with spinal cord injury; cervical, closed, C1–C4 level with other specified spinal cord injury Fracture of vertebral column with spinal cord injury; cervical, closed, C5–C7 level with unspecified spinal cord injury Fracture of vertebral column with spinal cord injury; cervical, closed, C5–C7 level with complete lesion of cord Fracture of vertebral column with spinal cord injury; cervical, closed, C5–C7 level with anterior cord syndrome Fracture of vertebral column with spinal cord injury; cervical, closed, C5–C7 level with central cord syndrome Fracture of vertebral column with spinal cord injury; cervical, closed, C5–C7 level with other specified spinal cord injury Fracture of vertebral column with spinal cord injury; cervical, open, C1–C4 level with unspecified spinal cord injury Fracture of vertebral column with spinal cord injury; cervical, open, C1–C4 level with complete lesion of cord Fracture of vertebral column with spinal cord injury; cervical, open, C1–C4 level with anterior cord syndrome Fracture of vertebral column with spinal cord injury; cervical, open, C1–C4 level with central cord syndrome Fracture of vertebral column with spinal cord injury; cervical, open, C1-C4 level with other specified spinal cord injury Fracture of vertebral column with spinal cord injury; cervical, open, C5–C7 level with unspecified cord injury Fracture of vertebral column with spinal cord injury; cervical, open, C5–C7 level with complete lesion of cord Fracture of vertebral column with spinal cord injury; cervical, open, C5–C7 level with anterior cord syndrome
805.4 805.5 805.6 805.7 805.8 805.9 806.00 806.01 806.02 806.03 806.04 806.05 806.06 806.07 806.08 806.09 806.10 806.11 806.12 806.13 806.14 806.15 806.16 806.17
244
Appendix B
ICD-9 Code Fracture of vertebral column with spinal cord injury; cervical, open, C5–C7 level with central cord syndrome Fracture of vertebral column with spinal cord injury; cervical, open, C5–C7 level with other specified spinal cord injury Fracture of vertebral column with spinal cord injury; dorsal, closed, T1–T6 level with unspecified spinal cord injury Fracture of vertebral column with spinal cord injury; dorsal, closed, T1–T6 level with complete lesion of cord Fracture of vertebral column with spinal cord injury; dorsal, closed, T1–T6 level with anterior syndrome Fracture of vertebral column with spinal cord injury; dorsal, closed, T1–T6 level with central cord syndrome Fracture of vertebral column with spinal cord injury; dorsal, closed,T1–T6 level with other specified spinal cord injury Fracture of vertebral column with spinal cord injury; dorsal, closed, T7–T12 level with unspecified spinal cord injury Fracture of vertebral column with spinal cord injury; dorsal, closed, T7–T12 level with complete lesion of cord Fracture of vertebral column with spinal cord injury; dorsal, closed,T7–T12 level with anterior cord syndrome Fracture of vertebral column with spinal cord injury; dorsal, closed, T7–T12 level with central cord syndrome Fracture of vertebral column with spinal cord injury; dorsal, closed, T7–T12 level with other specified spinal cord injury Fracture of vertebral column with spinal cord injury; dorsal, open, T7–T12 level with unspecified spinal cord injury Fracture of vertebral column with spinal cord injury; dorsal, open, T1–T6 level with complete lesion of cord Fracture of vertebral column with spinal cord injury; dorsal, open, T1–T6 level with anterior cord syndrome Fracture of vertebral column with spinal cord injury; dorsal, open, T1–T6 level with central cord syndrome Fracture of vertebral column with spinal cord injury; dorsal, open, T1–T6 level with other specified cord injury Fracture of vertebral column with spinal cord injury; dorsal, open, T7–T12 level with unspecified cord injury Fracture of vertebral column with spinal cord injury; dorsal, open, T7–T12 level with complete lesion of cord Fracture of vertebral column with spinal cord injury; dorsal, open, T7–T12 level with anterior cord syndrome Fracture of vertebral column with spinal cord injury; dorsal, open, T7–T12 level with central cord syndrome Fracture of vertebral column with spinal cord injury; dorsal, open, T7–T12 level with other specified spinal cord injury Fracture of vertebral column with spinal cord injury; lumbar, closed Fracture of vertebral column with spinal cord injury; lumbar, open Fracture of vertebral column with spinal cord injury; sacrum and coccyx, closed, with unspecified spinal cord injury
806.18 806.19 806.20 806.21 806.22 806.23 806.24 806.25 806.26 806.27 806.28 806.29 806.30 806.31 806.32 806.33 806.34 806.35 806.36 806.37 806.38 806.39 806.4 806.5 806.60
245
Appendix B
ICD-9 Code Fracture of vertebral column with spinal cord injury; sacrum and coccyx, closed, with complete cauda equina lesion Fracture of vertebral column with spinal cord injury; sacrum and coccyx, closed, with other cauda equina injury Fracture of vertebral column with spinal cord injury; sacrum and coccyx, closed, with other spinal cord injury Fracture of vertebral column with spinal cord injury; sacrum and coccyx, open, with unspecified spinal cord injury Fracture of vertebral column with spinal cord injury; sacrum and coccyx, open, with complete cauda equina lesion Fracture of vertebral column with spinal cord injury; sacrum and coccyx, open, with other cauda equina injury Fracture of vertebral column with spinal cord injury; sacrum and coccyx, open, with other spinal cord injury Fracture of vertebral column with spinal cord injury; unspecified, closed Fracture of vertebral column with spinal cord injury; unspecified, open Acquired absence of genital organs Other conditions influencing health status; asymptomatic postmenopausal status (age-related) (natural) Encounter for other and unspecified procedures and aftercare; long-term (current) use of steroids Follow-up examination; following completed treatment with high-risk medications, not elsewhere classified
806.61 806.62 806.69 806.70 806.71 806.72 806.79 806.8 806.9 V45.77 V49.81 V58.65 V67.51
Index
Abdominal fullness, 14 Absolute risk (AR) of fracture, 37 Access to care, 181–186 Acetaminophen, 74, 76 ACOVE Quality Indicators for Management of Osteoporosis in Vulnerable Elders, 207 Active range of motion (AROM), 156 Activities of daily living (ADLs) after hip fractures, 84 client-centered approach, 154 –155 common problems, 160 fear of falling and, 142 functional ability, 144 –145 post-fracture functioning, 13 –14 Activities-Specific Balance Confidence Scale, 144 Activity Index and Meaningfulness Scale, 154 –155 Actonel®. See Risedronate Adaptation. See Bone remodeling Adolescents calcium intake, 172 calcium supplementation in, 170 maximizing bone mass, 169 –179 soda consumption, 171–172 vitamin D intake, 172 –173 Aerobic exercise, 121 African American women, 10 Age/aging bone density and, 84 bone mass decrease and, 120 bone mineral density testing and, 38 fracture sites and, 11 of global populations, 16 Alcohol intake, 42, 111 Alendronate (Fosamax®), 48 administration, 51–52 adverse events, 51–52 characterization, 62 efficacy, 49 –50 Alkaline phosphatase, 39, 40 Amenorrhea, 174, 176 American College of Rheumatology, 37
American College of Sports Medicine (ACSM), 121 Ampicillin, drug interactions, 61 Analgesics, 74, 76 Anderson’s sequential model, 214, 215 Androgens, decrease in, 23 Annulus fibrosis, 88 Anorexia nervosa, 176 Antiandrogen therapy, 39 Anticoagulation therapy, 87 Anticonvulsants, 42, 174 –175 Antiepileptics, 174 –175 Aquatic exercise, restorative, 130 Arixtra, 87 Arizona Department of Health Services, 193 Arizona Osteoporosis Coalition, 193 Arthritis Foundation, 191 Arthropathies, low bone density and, 42 Aspirin, 87 Association of Retired and Senior Volunteer Program Directors, Inc. (RSVP), 194 Asthma, corticosteroid therapy, 174 Balance, measures of, 156 –157 Balance assessments, 144 –145, 149 Balance exercise, restorative, 129 Balance screening, 143 –145 Bazedoxifene, 59 Beck Depression Inventory, 159 Bed rest for hip fractures, 86 urinary calcium levels and, 221 Berg Balance Test, 145 Biestrogen (Biest), 58 Binghampton University Foundation, 198 Bioidentical hormone therapy (BHRT), 57–59, 72 Bisphosphonate therapy administration, 51–52 adverse events, 51–52, 219 description, 48 efficacy, 49 –51
247
248 mechanism of action, 48 – 49 pharmacokinetics, 48 – 49 Blood flow, 220 – 222 Bone causes of low density in, 40 – 43 cellular components, 20 – 21 diet and, 103 –115 formation of, 26, 118 loss, 27, 120 – 212 maintenance of, 221 maximization of mass, 169 –179 mechanical stimulation of, 227– 228 physiology of, 20 – 28 skeletal muscle and, 223 – 224 types of, 20 Bone and Joint Decade, 202 – 203 Bone Builders, 192 –193 Bone Estrogen Strength Training (BEST), 193 Bone Health and Osteoporosis (Surgeon General’s report), 5, 204, 205, 206 – 207 The Bone Mass Measurement Act, 209 Bone metastases, 65 Bone mineral content (BMC), 118 Bone mineral density (BMD) calculation of, 9 classification based on, 9 clinical utility of, 38 –39 electrical stimulation of muscle and, 225 – 226 exercise and, 117 femoral, 10 lifestyle issues, 99 Medicare coverage for, 209 osteopenia and, 9 osteoporosis and, 9 reference population for, 9 –10 serial testing, 36 testing of, 33 –35 Bone morphogenic proteins (BMPs), 26 Bone remodeling cycle of, 120 –121 description of, 20, 21– 24 fluid flow and, 220 – 221 phases of, 22 – 23 steps in, 21 Bone resorption calcium from, 23 description, 20 – 21 initiation of, 39 nutrition and, 24 osteoclasts and, 39 phosphorus from, 23 Bone-specific alkaline phosphatase (BSAP), 39 Bone strength, exercise and, 117
Index Bone turnover, markers of, 39 – 40 Bones: Don’t Wait Until You Break One to Find Out That You Have Osteoporosis, 193 Boniva®. See Ibandronate Bonmax, 58 Broadband ultrasound attenuation (BUA), 35 C-telopeptide (CTX), 40 Caffeine intake, 111 Calciferol. See Vitamin D (calcitriol) Calcitonin bone formation and, 26 bone health and, 25 characterization, 63 production of, 25 Calcitonin (salmon) therapy administation, 66 adverse events, 66 analgesic effects of, 66 efficacy, 65 – 66 mechanism of action, 65 pharmacokinetics, 65 Calcitriol (1,25-dihydroxy vitamin D3). See Vitamin D (calcitriol) Calcium, 67– 69. See also Calcium intake absorption of, 67, 71 adverse effects, 68 bone content of, 104 bone health and, 170 –172 from bone resorption, 23 drug interactions, 68 efficacy of therapy with, 71–72 excretion of, 221 food sources of, 106 –107 mechanism of action, 70 mobilization of, 71 peak bone mass and, 104 Calcium, Its Not Just Milk Program, 193 –194 Calcium carbonate (Caltrate) administration, 72 adverse events, 68 cost of, 113 drug interactions, 68 Calcium citrate (Citrical) administration, 72 adverse events, 68 drug interactions, 68 tolerability, 113 Calcium intake during childhood, 170 –172 excessive, 109 –110 formulations, 69 health policy and, 214, 216
249
Index increasing, 172 interfering foods, 106 nephrolithiasis and, 71 osteoporosis paradox, 106 recommendations, 67– 69, 105 –106, 171 risk reduction and, 47 supplementation in children, 170 supplements, 112 –113 Calf muscle activation, 227– 229 Caltrate. See Calcium carbonate Canada, policy development, 214 – 215 Canadian Occupational Performance Measure (COPM), 155 Cancellous bone estrogens and loss of, 24 sites of, 20 structure of, 20 Cancer, 65, 175, 176 Carbamazine, 174 Cefazolin, 87 Celiac disease, 175 Celvista, countries where approved, 58 Cerebral palsy, 175 Chartered Society of Physiotherapy (CSP), 128 Cheese, 112 Children calcium intake, 172 calcium supplementation in, 170 dietary calcium in, 104 exercises for, 121, 122 fractures in, 175 maximizing bone mass, 169 –179 osteoporosis prevention programs, 2 –3, 177 soda consumption, 171–172 vitamin D intake, 172 –173 Cholecalciferol. See Vitamin D Cholesterol, raloxifene and, 60 Cholestyramine (Questran®), 61 Chondrodysplasia, 175 Chronic illness depression and, 158 –159 impact on families, 15 quality of life and, 153 Chronic obstructive pulmonary disease (COPD), 91–92 Circulatory system gravity and, 221– 222 posture and, 223 – 224 Citrical. See Calcium citrate Clindamycin, 87 Collagen, digestion of, 39 Collagen cross-linking, 40 College of Public Health, University of Arizona, 192
Colles’ fractures, 15, 97, 98 Combination antiresorptive therapy, 66 – 67 Community health planning committees, 189 Community outreach programs, 187–199 Compensation strategies, 162 –163 Compression fractures, 88 –97, 90. See also Crush fractures; Spinal fractures; Vertebral fractures diagnosis of, 92 –94 treatment options, 94 –95 Computed tomography (CT), 92 –94 Connective tissue disease, 42 Cooperative Extension Programs, 187, 188 –190 Cooperative State Research, Education and Extension Service (CSREES) agency, 188 Coping skills, 158 Cortical bone estrogens and loss of, 24 sites of, 20 structure of, 20 Corticosteroid therapy, 38 –39, 174 –175 Cost utility analysis, of therapy, 37 Costs, of osteoporotic fractures, 15 –16 Coumadin, 87 Coumestans, 73 Coumestrol, 72, 73 County extension educators, 190 Crane Fund for Widows and Children, 198 Creating Health Initiative, 190 –192 Crosslaps immunoassay, 40 Crush fractures, 14. See also Compression fractures Cutaneous mechanoreceptors, 227 Cystic fibrosis, 175 Cytokine regulation, 25 – 27 Daidzein, 72, 73 Dairy products, 106, 112. See also Nutrition Dancers, bone mineral density, 173 Decker School of Nursing at Binghamton University, 198 Deep vein thrombosis (DVT), 59, 87 Dehydroepiandrosterone (DHEA), 58 Delayed puberty, 176 Demographics global changes, 16 for osteoporosis, 9 –18 Deoxypyridinoline (DPD), 39, 40 Depression, 158 –159 Diet. See Nutrition Dietary Reference Intake (DRI) values, 171 1,25 Dihydroxyvitamin D. See Vitamin D Dioxins (TCDDs), 27 Diphenylhydantoin, 174 Disordered eating, 176
250 Dual energy X-ray absorptiometry (DXA), 34 –35, 117 demographics for screening, 38 efficacy, 182 future directions, 185 mobile equipment, 183 –185 profitability, 185 Early supported discharge programs (ESDPs), 127 Eating disorders, 42 Elderly persons exercise programs for, 122 fall-related mortality, 141 Physical Activity for Inactive Seniors series, 193 Electronic medical records (EMR), 184 Emergency room visits, 15 Encyclopedia of Gerontology, 198 Encyclopedia of Nursing Research, 198 Energy conservation of, 163 diet and, 110 Enterodiol, 72 Enterolactone, 72 Environmental toxins, 27– 28 Erlangen Fitness Osteoporosis Prevention Study (EFOPS), 133 Established Populations for Epidemiologic Studies of the Elderly (EPESE), 13, 144 Estrace®. See Estradiol Estraderm®. See Estradiol Estradiol (Estrace®, Estraderm®, Estrace®, Estring®, Femring®, Vagifem®), 5, 54. See also Bioidentical hormone therapy (BHRT); Estrogen therapy; Estrogens; Hormone replacement therapy; Hormone therapy (HT) Estring®. See Estradiol Estriol, 54 Estriol®, 54 Estrogen receptors, 24 – 25 Estrogen therapy, 53 –57 administration, 57 adverse events, 57 description, 53 –54 efficacy, 56 –57 mechanism of action, 54 –55 pharmacokinetics, 54 –55 Estrogens. See also specific estrogens bone formation and, 26 calcium supplementation and, 105 characterization, 62 cytokine regulation by, 25 – 27 deficiency in, 175 effects on bone, 24 FDA-approved, 54
Index Estrone, 54 Europe, fracture incidence in, 11 Evista®. See Raloxifene Exercise. See also Physical activity amenorrhea and, 174 for children, 121 classes of, 121 fall prevention, 149 importance of, 117–139 lifespan and, 119 –120 long-term effects, 119 –120 Physical Activity for Inactive Seniors series, 193 preventative, 118 –126 program planning, 120 recommendations, 121–122, 127–128 restorative, 127–131 safety issues, 131–132 Exercise programs adherence to, 132 –133 description, 123 –126 efficacy, 123 –126 high-intensity, 132 home-based, 129 External fixation, of fractures, 98 Facet joints, 88, 89 Fall prevention environmental modifications, 146 exercise and, 122 follow-up, 146, 148, 149 –150 osteoporosis and, 141–151 program components, 143 –148 program development, 142 –143 resource identification, 146 strategies, 161–162 Falls causes of, 142 environmental factors in, 142 fear of falling index, 143 –144 getting up after, 146, 147 history of, 143 risk assessment, 148 Falls Efficacy Scale, 144 Family roles, 15 Fear of falling index, 143 –144, 148 Female athlete triad, 176 Femoral neck fractures, 84, 86. See also Hip fractures Femring®. See Estradiol Femur, bone mineral density, 10 Fentanyl, dosing regimens, 74 Fibrous dysplasia, 175 Fluid flow bone adaptation and, 220 – 221
Index in humans, 221– 224 skeletal muscle and, 222 – 223 Forearm fractures, 142 Forteo (teriparatide), 52, 63 Forward Reach test, 144 Fosamax®. See Alendronate Fosamax International Study Trial Group (FOSIT), 50 Fracture Intervention Trials (FITs), 49, 50 Fracture risk, expression of, 37 Fractures. See also specific fractures in childhood, 175 lifetime risks, 11–12 micro “cracks,” 21 monetary costs of, 15 –16 osteoporosis-related, 11 preventative exercise, 118 –126 risk in men, 12 risk of, 34 risk reduction, 118 –119 surgical management of, 83 –100 Fragility fractures, 83 Frank-Starling mechanism, 222 Fruit intake, 112 Furniture selection, 162 Gait Stability Ratio, 145 Geisinger Health System Mobile DXA Program, 181–186 Gender, hip fracture and, 83 Genistein, 72, 73 Geriatric Depression Scale, 159 Geriatric hip fracture programs (GHFPs), 127 Geriatric orthopaedic units (GORUs), 127 Girls, bone mineral density, 173 –174. See also Children Glucocorticoid therapy, 38, 42 Gonadotropin-releasing hormone (GnRH), 54 Goniometry, 156 Granulocyte macrophage colony-stimulating factor (GM-CSF), 26 Gravity, impact of, 221– 222 Ground reaction forces, 119 Growth factors, bone formation and, 26 Gymnasts, bone mineral density, 173 Health Belief Model, 132 Health Care Financing Administration (HCFA), 209 Health People 2010, 204 Health policy Anderson’s sequential model, 214, 215 case studies, 214 – 216 formulation of, 201– 202 international, 202 – 204 national, 204 – 205
251 policy makers, 202 – 208 stakeholders, 202 – 208 United States initiatives, 204 – 208 Health status, self-report of, 144 Healthy People 2010 initiatives, 205 Heat therapy, 130 HEDIS Performance Measure for Osteoporosis: Health Plan Employer Data and Information Set, 207 Heel ultrasound (HUS), 182 Height, loss of, 14. See also Compression fractures Hemiarthroplasty, 86 Heparin therpy, 87 HEROS© Fall Prevention Program for Community Dwelling Older Adults, 143, 144, 148 –150 Hip osteopenia of, 10 osteoporosis of, 10 Hip fractures. See also Femoral neck fractures age and, 11 bone loss and, 105 cost of, 141–142 global rates of, 12 –13 hospitalizations for, 84 incidence of, 118 intertrochanteric, 87 lifetime risk of, 11 medical costs of, 15 –16 morbidity rate, 83 mortality rate, 12, 83 nonsurgical treatment, 86 occult, 85 osteoporosis-related, 11 perioperative complications, 87 predictors of, 15 rehabilitation, 87– 89 restorative exercise, 127–128, 130 signs and symptoms of, 84 treatment of, 85 – 87 types of, 84 – 85 vertebral fracture risk and, 39 Hip hemiarthroplasty, 86 HIP Intervention Program (HIP) trial, 50 –51 Hispanic women, 10 Hologic Discovery—C Bone Densitometer, 183 –185 Home environment assessment, 159 Hormone replacement therapy (HRT), 105, 121 Hormone therapy (HT) alternatives to, 72 combination, 67 efficacy of, 54 –57 Hormones. See also specific hormones bone formation and, 26 in osteoclast formation, 22
252 Hospital admissions for hip fractures, 84, 142 osteoporosis-related, 15 Hydrocodone/APAP, 74 Hydrocodone/ibuprofen, 74 Hydroxyapatite, 67 Hydroxyproline (OHP), 40 Hypercalcaemia, 69 Hyperparathyroidism, 70 Hypocalcaemia, 69 Hypogonadism, 39, 42 Iasofoxifen, function of, 59 Ibandronate (Boniva®), 48, 49 –50, 62 Ibuprofen, dosing regimens, 74 Idiopathic juvenile osteoporosis, 175 Immunoassays, 39, 40 Immunosuppressive therapy, 174 –175 Incentive spirometry, 87 Independence common problems, 159 –161 loss of, 15 maintenance of, 153 –165 self-care and, 155 Indomethacin, 74 Inflammatory bowel disease, 175 Inflammatory diseases, 174 Instrumental activities of daily living (IADLs), 154, 160, 164 Interleukin 1 (IL-1), 22, 26, 27 Interleukin 3 (IL-3), 26 Interleukin 6 (IL-6), 26, 27 Interleukin 11 (IL-11), 26 International Osteoporosis Foundation (IOF), 202, 203 International Society for Clinical Densitometry (ISCD), 35 –39, 184, 203, 204 Internet, use of, 192 Interstitial fluid extravasation, 220, 222, 224 Interstitial fluid flow, 220 – 221 Intertrochanteric fractures, 84 Ipriflavone, 73 Isoflavones, 73, 111 Israel, public policy development, 214 Japanese women, osteoporosis in, 11 Joint protection techniques, 163 Jump Start Your Bones©, 194 Kidney stones. See Nephrolithiasis Klinefelter’s syndrome, 175 Knowles pinning, 86 Kyphex inflatable balloons, 95, 96
Index Kyphoplasty, 76, 95 –97 Kyphosis, 14, 142. See also Compression fractures Laboratory studies, 42 Lactation, bone loss in, 24 Lactose intolerance, 112 Least significant change (LSC), 36 Leisure interests, 160 Leukemic inhibitory factor, 26 Life expectancy, bone loss and, 120 Life roles, quality of life and, 154 Lifespan, exercise and, 119 –120 Lifestyles client-centered approach to, 154 –155 compensation strategies, 162 –163 fall prevention and, 146 fracture prevention and, 99 goals for redesign, 155 prevention strategies, 161–162 prognosis and, 164 redesign outcomes, 164 remediation strategies, 161 Lignans, 72, 73 Loading blood flow and, 221 bone loss and, 120 –121 Long-term care, 14, 84 Lovenox, 87 Loxar, countries where approved, 58 Loxifen, countries where approved, 58 Lung disease, 14, 91–92 Lymphatic drainage, 222, 223 Macrophage colony-stimulating factor (M-CSF), 22, 27 Magnetic resonance imaging (MRI), 92 Malabsorption syndromes, 42 Manual Muscle Test (MMT), 156 Mechanoreceptors, 227 Media, target audiences for, 189 Medical histories, fall prevention and, 144 Medicare coverage, 209 The Medicare Osteoporosis Measurement Act of 2005 (House Bill 2257), 208 Medications, effect on bone health, 174 –175. See also Pharmacotherapy Meissner’s corpuscles, 227 Men discharges to nursing homes, 14 DXA screening guidelines, 39 effect of exercise, 120 fracture risk, 12 mortality rates after hip fractures, 84 prognosis after fractures, 13
253
Index timing of bone loss in, 23 vertebral fractures in, 14 –15 Menarche, late, 176 Menopause, bone loss and, 23, 25 – 26, 104, 120 Merck SCORE risk assessment sheet, 196, 197 Methotrexate, 175 Miacalcin®, 63, 64 – 66 Michigan Department of Community Health, 192 Michigan Nutrition Network, 192 Michigan State University Extension, 192 Micro “cracks,” 21 Microgravity models, 221 Milk. See also Lactation allergies, 172 calcium from, 171 human, 173 per capita consumption, 112 vitamin D fortified, 106 Morbidity, postfracture, 13 –15, 83 Morphine, dosing regimens, 74 Mortality rates, 13 Motor control changes, 157 Multi-Directional Reach Test (MDRT), 144 Muscle mass, exercise and, 120 Muscle pumping, 222 – 223 Muscle spasms, 130 Muscle strength bone health and, 121 measures of, 156 N-telopeptide (NTX) cross-linking, 39, 40 Naproxen, dosing regimens, 74 National Dairy Council, 191 National Fluid Milk Processor Promotion Board, 191 National Institute of Health, 193 National Osteoporosis Foundation (NOF), 181, 191 initiatives, 208 reimbursement initiatives, 208 – 209 survey, 15 treatment recommendations, 37 National Osteoporosis Risk Assessment (NORA) study, 37 National Osteoporosis Society, U.K., 214 Native American women, 11 Natural hormone therapy (NHRT), 57–59 Nelson, Mirian E., 195 Nephrolithiasis, 71, 110 Nevada Nutrition Network, 194 New Jersey Department of Health and Senior Service, 194 Nonsteroidal anti-inflammatory drugs (NSAIDs), 76 Nonvertebral fractures bisophosphonate efficacy in, 50 –51
calcitonin efficacy in, 65 – 66 efficacy of hormonal therapy, 56 parathyroid hormone therapy in, 52 –53 raloxifene efficacy, 61 Norway, fracture incidence in, 10, 11 Nucleus pulposus, 88 Nursing homes after osteoporetic fractures, 14 fear of, 15 osteoporosis-related admissions, 15 vitamin D deficiency in residents of, 69 Nutrition bone health and, 103 –115, 170 –173 bone resorption and, 24 calcium content of foods, 107 calcium-fortified foods, 106 components of, 110 –111 dietary deficiencies, 23 – 24 health policy and, 214, 216 osteoporosis prevention and, 103 recommendations, 112 –113 vitamin D from, 108 Obesity, vitamin D deficiency and, 107–108 Ogen®. See Estrone Oligomenorrhea, 176 Open reduction internal fixation (ORIF), 87, 98 Opioids, pain management, 74, 76 Orchiectomy, 39 Osteoblasts bone formation and, 39 in bone remodeling, 21 celllular interactions, 22 derivation of, 20, 22 effect of estrogens on, 24 location of, 20 measures of function of, 40 parathyroid hormone receptors, 52 Osteocalcin (OC), 39 – 40, 40 Osteochemonecrosis, 51 Osteoclasts action of bisphosphonates, 48 – 49 bone resorption and, 39 cellular interactions, 22 effect of estrogens on, 24 function of, 20 – 21 measures of function of, 40 Osteocytes in bone remodeling, 21 cellular interactions, 20 derivation of, 20, 23 location of, 20 Osteogenesis imperfecta, 175
254 Osteomalacia, 70. See also Rickets Osteomark® immunoassay, 39 Osteopenia, 176 definition, 36, 202 in estrogen deficiency, 25 of hip, 10 Osteoporosis bone micrograph, 23 calcium paradox, 106 complications of, 83 – 84 consequences of, 13 –16 definition of, 33, 36, 202 demographics, 9 –18 incidence of fractures, 1 laboratory testing in, 42 pathogenesis of, 19 – 29 pharmacological management of, 47– 82 prevalence, 9 –10 secondary causes of, 40 – 43 testing, 181–182 top ten states, 12 Osteoporosis: Physical Performance Measurement, 206 The Osteoporosis Early Detection and Prevention Act of 2005 (House Bill 2946), 208 The Osteoporosis Education and Prevention Act of 2005 (House Bill 1081), 208 Osteoporosis Prevention, Diagnosis and Therapy, 204 Osteoporosis prevention programs, 177 Osteoprotegrerin (OPG), 22 Oswestry Disability Questionnaire (ODQ), 118 Oxycodone, dosing regimens, 74 Oxycodone/APAP, dosing regimens, 74 Paget’s disease, 65 Pain control, exercise and, 128 –129 Pain management, 73 –74, 76, 128 –129 Parathyroid hormone (PTH) bone formation and, 26 bone health and, 25 characterization, 63 low bone density and, 42 in osteoclast formation, 22 Parathyroid hormone (PTH) therapy, 52 –53 administration, 53 adverse events, 53 efficacy, 52 –53 mechanism of action, 52 overview, 52 pharmacokinetics, 52 Passive range of motion (PROM), 156 Patient education community-based programs, 190 –192 Cooperative Extension Programs, 188 –189
Index curriculum, 190 exercise adherence and, 132 –133 fall prevention, 146, 149 fracture prevention and, 99 getting up from falls, 147 learn-at-home lessons, 191 media formats, 190 Pennsylvania Geriatric Education Center, 195 Pennsylvania State University Cooperative Extension Programs, 187–192, 195, 196 Pennsylvania State University Public Broadcasting, 190 Pennsylvania State University School of Nursing, 195, 196 Percutaneous pinning, 86, 98 Performance Activities of Daily Living (PADL) battery, 144 Performance Oriented Mobility Assessment (POMA), 145 Pharmacotherapy drug characteristics, 62 – 63 low bone density and, 42 Phenobarbital, 174 Phosphorus, from bone resorption, 23 Photon absorptiometry techniques, 34 Physical activity. See also Exercise bone mass and, 27, 173 –174 electrical stimulation of muscle, 225 – 226 mechanical stimulation of bone, 227– 228 skeletal muscle pump and, 224 – 225 Physical Activity for Inactive Seniors, 193 Physical Disability Index, 144 Physical inactivity, 173 –174 Physical Performance and Mobility Examination, 144 Physical performance measures, 144 –145 Physical Performance Test, 144 Physical therapists, role of, 118 Physician office visits, osteoporosis-related, 15 Phytic acid, 106 Phytoestrogens, 72 –73, 111 Planned Approach to Community Health group, 193 Plantar stimulation, 227– 228 Policy-making, model of, 214, 215 Polychlorobiphenyls (PCBs), 27– 28 Polymethylmethacrylate (PMMA), 86, 95 Postfracture morbidity, 13 –15, 83 Postural control, measures of, 156 –157 Posture, circulatory system and, 223 – 224 A Practical Guide to Bone Health, 192 Pregnancy, bone loss in, 24 Premarin®, 54, 59 Prematurity, 175 Prempro®, 56 Preventing and Managing Osteoporosis, 198
255
Index Prevention programs for children, 177 community outreach and, 187–199 trends in, 219 – 231 Primary care physicians, 184 –185 Prioritization, 163 Productivity, measures of, 155 Progesterone, micronized (Prometrium®), 58 Progesterone, secretion of, 54 Project Healthy Bones, 194 –195 Prometrium®. See Progesterone PROOF study, 65 Prostaglandins, 22, 26 Protein intake, bone health and, 110 –111 Psychological well-being, 15 Psychosocial assessment, 157 Psychosocial problems, 153 Puberty, delayed, 176 Public health priorities, 169 –179 Quadriceps muscle, 226 Quality of life common problems, 159 –161 exercise and, 118 independence and, 153 –165 life roles and, 154 postfracture morbidity and, 13 –15, 83 productivity measures, 155 self-care and, 155 Quantitative computed tomography (QCT), 35 Quantitative ultrasonography (QUS), 35 Quantitative ultrasound index (QUI), 35 Questran® (cholestyramine), 61 Race osteoporosis and, 10 prognosis after fractures, 13 Raloxifene (Evista®), 59 – 64 administration, 61, 64 adverse events, 61, 64 characterization, 63 contraindications, 61 countries where approved, 58 drug interactions, 61 efficacy, 60 – 61 international names for, 59 mechanism of action, 60 pharmacokinetics, 60 Range of motion (ROM) exercise and, 118 measures of, 156 restorative exercises, 129 Raxeto, countries where approved, 58
Readiness for change, 158 Receptor activator of nuclear factor kappa B ligand (RANKL), 22 Receptor activator of nuclear factor kappa B (RANK), 22 Recommended Daily Allowance (RDA), 171 Reference population, 9 –10 Rehabilitation. See also Exercise; Physical activity; Physical therapists, role of after hip fractures, 87– 89 after wrist fractures, 99 costs of, 15 inpatient, 128 Reimbursement, 208 – 209, 214 – 216 Relative risk (RR) of fracture, 37 Relaxation techniques, 130, 163 Remediation strategies, 161 Research, advances in, 2 Resistance training, 120, 121, 129 Rickets, 70, 173 Risedronate (Actonel®), 48 characterization, 62 combination therapy, 66 efficacy, 49 –50 Rutgers Cooperative Extension, 194 Saint Barnabas Health Care System, 194 Scandinavia, hip fracture rates, 12 School health programs, 177, 189 School of Nutrition Science and Policy, Tufts University, Boston, 195 SCORE risk assessment sheet, 196, 197 Scottish Intercollegiate Guidelines Network (SIGN), 130 Screening programs, 38, 176, 195 –196 Selective estrogen reuptake modulators (SERMs), 50, 59 – 64 Self-care, measures of, 155 Self-concept, assessment of, 157–158 Self-help devices, 162, 163 Sequential compression devices (SCDs), 87 SERM 3339, 59 Singh index, 34 Skeletal loading, 120 – 212, 221 Skeletal muscle bone mass and, 223 – 224 electrical stimulation of, 225 – 226 fluid flow and, 222 – 223 Skeletal muscle pump, 224 – 228 Skeleton, human as calcium reserve, 67 calcium storage in, 104 function of, 19
256 number of bones in, 19 osteoporetic changes, 157 Smith’s fractures, 97, 98 Smoking, low bone density and, 42 Social Cognitive Theory, 132 Soda consumption, 171–172 Soleus muscle, function, 223 Southeast Asia, fracture incidence in, 11 Soybean protein, 73 Soy isoflavones, 111 Speed of sound (SOS), 35 Spinal column anatomy of, 88 –92 load distribution, 90, 91 mechanical stability, 88 – 89 Spinal cord injury, 225 – 226 Spinal fractures costs of, 16 functional decline and, 127 lifetime risk of, 11 mortality rates after, 12 osteoporosis-related, 11 rates of, 12 restorative exercise, 128 –131 Spine morphometry, qualitative, 34 Spinous processes, 88, 89 Squash players, 174 St. Luke’s Health Initiative, 192 –193 Stages of Change theory, 132, 189 Stand Tall Pennsylvania, 191, 195 –198 Strength, exercise and, 120 Strong Women,™ Strong Bones program, 195 Study of Orthoporotic Fractures (SOF), 14, 37 Sunlight, 108, 172 Sweden, fracture rates, 12 Swedish women, osteoporosis in, 10 T-scores calculation of, 34 guidelines for treatment, 37 heel ultrasound, 182 interpretation of, 35 –36 reference database, 35 screening programs and, 196 T’ai Chi, 122, 146, 224 – 225 Tamoxifen, use of, 59 Temple University, 195 Tennis players, 174 Teriparatide (Forteo®), 52 –53, 63 Testosterone, 24, 26, 175. See also Hormone therapy (HT) Third National Health and Nutritional Examination Survey (NHANES III), 10
Index Timed Up and Go (TUG) times, 144 Trabecular bone. See Cancellous bone Traction, for hip fractures, 86 TRANCE/RANK/OPGL, 25, 27 Transcutaneous electrical nerve stimulation (TENS), 130 Transforming growth factor β (TGF-β), 26 Transtheoretical model (TTM), 158, 189 Triest (Triestrogen), 58 Triestrogen (Triest), 58 TSE-424, 59 Tumor necrosis factor-α (TNF-α), 26 Turner's syndrome, 175 United Dairy Industry, 192 United Kingdom, osteoporosis in, 10 United States coverage by state, 210 – 213 fracture incidence in, 11 policies by state, 210 – 213 policy development, 214 – 215 University Cooperative Extension, Nevada, 194 University of Arizona Cooperative Extension, 192 –193, 193 University of Pittsburgh, 195 U.S. Department of Health and Human Services (DHHS), 204 Vagifem®. See Estradiol Valproate, 174 Vegan diets, 172 Vegetable intake, bone health and, 112 Vertebrae, load distribution, 90 Vertebral bodies composition of, 89, 91 shape of, 91, 92 Vertebral deformities, 14 –15 Vertebral Efficacy with Risdronate Therapy (VERT), 49 Vertebral fracture assessment (VFA), 35, 184 –185 Vertebral fractures. See also Compression fractures bisphosphonate therapy, 49 –50 calcitonin efficacy in, 65 efficacy of hormonal therapy, 56 hip fractures and risk of, 39 morbidity after, 14 –15 parathyroid hormone therapy in, 52 raloxifene efficacy, 60 – 61 rate of, 83 Vertebroplasty, 76, 95 –97 Vitamin D (calcitriol) bone formation and, 26, 27 bone health and, 25, 107–108 calcium and, 67– 69
257
Index deficiency, 12, 42, 70 efficacy of therapy using, 71–72 function of, 25 mechanism of action, 70 –71 pharmacokinetics, 70 –71 sources of, 108 synthesis of, 69 therapy using, 69 –72 Vitamin D intake calcium metabolism and, 172 –173 excessive, 109 –110 health policy and, 214, 216 recommendations, 67– 68, 70, 105 –106, 109, 171 risk reduction and, 47 sources of, 69 supplements, 105, 109, 112 –113 Walking, bone health and, 121, 133 Weight-bearing exercise, 121, 122 Weight lifting, 119 Weight loss, kyphosis and, 14 White women, 10, 11 WISEWOMAN Expansion Act of 2005 (House Bill 3086), 208 Women. See also Girls; Menopause; specific issues lifetime risk of hip fracture, 83 vertebral fractures in, 14 –15
Women’s Health Initiative (WHI), 54, 56, 105 Work problems, 160 –161 World Health Organization (WHO) classification of osteoporosis, 9 cost utility analysis, 37 global osteoporosis mandates, 3 initiatives and reports, 203 osteopenia definition, 36 osteoporosis definition, 36 policy making, 202 reports of hip fractures, 12 Wrist fractures description, 97 hip fractures following, 15 lifetime risk of, 11 morbidity following, 15 osteoporosis-related, 11 rehabilitation after, 99 restorative, 129 –130 restorative exercise, 131 treatment of, 97–99 X-ray evaluation, 92 Yogurt, 112 Z-scores, 34, 36
