Evidence Based Practice in Dentistry (Medical Principles and Practice)

Proceedings of the International Conference on

Evidence Based Practice in Dentistry Kuwait, October 2–4, 2001 Faculty of Dentistry, Health Sciences Centre, Kuwait University

Guest Editors

J.M. Behbehani, Kuwait E. Honkala, Kuwait

21 figures, 6 in color, 14 tables, 2003

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Vol. 12, Suppl. 1, 2003

Contents

1 Preface Behbehani, J.M.; Honkala, E. 3 An Evidence-Based Approach to the Prevention of Oral Diseases Spencer, A.J. 12 Preventive (Evidence-Based) Approach to Quality General Dental Care Elderton, R.J. 22 Tobacco and Oral Diseases. Update on the Evidence, with

Recommendations Reibel, J. 33 The Evidence for Prosthodontic Treatment Planning for Older, Partially

Dentate Patients Omar, R. 43 Stem Cells and Tissue Engineering: Prospects for Regenerating Tissues in

Dental Practice Thesleff, I.; Tummers, M. 51 Dental Education in Kuwait Behbehani, J.M. 56 Dental Education and Dentistry System in Iran Pakshir, H.R. 61 Development of Oral Health in Africa Thorpe, S.J.

65 Author Index 65 Subject Index

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Evidence Based Practice in Dentistry Kuwait, October 2–4, 2001

Med Princ Pract 2003;12(suppl 1):1–2 DOI: 10.1159/000069848

Preface

This supplement is based on papers presented at the Second International Conference of the Faculty of Dentistry, Kuwait University, October 2–4, 2001. The conference provided an ideal opportunity to exchange ideas and discuss new developments in the field of dentistry, especially the latest trends in the evidence-based approach to dental care. As the former President of Kuwait University, Professor Faiza M. Al-Khorafi, stated in her opening remarks, ‘In science, we need to question continuously, what is the evidence? We look to science for answers, but quite often science can only give us the best estimate for probabilities. Our research results need continuous reevaluation, and the evidence must be weighed according to the strengths and weaknesses of the scientific methods applied.’ The evidence-based approach has been widely discussed in various healthcare fields and has influenced teaching throughout the world. With its emphasis on prevention and its use of previous, analogous evidence to design treatment plans, the evidence-based approach differs fundamentally from traditional methods of intervention, which focus on clinical outcomes. The stages of the approach, including the synthesis and assessment of evidence, the application of that evidence to a particular case, and finally the monitoring and reassessment of the intervention, are presented in detail in this supplement. The preventive aspect of this approach is also addressed in an article that re-evaluates traditional approaches to the restoration of carious teeth, which give rise to the ‘repeat restoration cycle’ and in fact mask the underlying disease process rather than prevent its occurrence. The prevention of oral diseases caused by smoking is empha-

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sized in a review of the documented harmful effects of smoking on oral health; it is proposed that dentists should make time during office visits to counsel patients on these effects and guide them through smoking cessation programs. As research in the field of dentistry develops and expands and the evidence-based approach gains widespread acceptance, traditional treatments are steadily giving way to new strategies of managing oral health issues. A clear move away from tradition is discussed in an article devoted to treatment planning for older, partially dentate patients. It is proposed that the usual method of total tooth replacement is not necessary, and the targeted ‘shortened dental arch’ is more effective and gives a high level of patient satisfaction. Exciting new research on stem cells and tissue regeneration indicate a distant but hopeful possibility to grow new teeth to solve the everpresent problems of dental caries and periodontal disease. The second theme of the conference was ‘The Development of Dental Education and Oral Health,’ with a regional emphasis. The dental curricula of schools in two Gulf countries, Kuwait and Iran, are presented in this supplement, as is the issue of community health in Africa. The dental curriculum at Kuwait University’s newly established Faculty of Dentistry aims to promote oral health in Kuwait through education, research and community involvement. It incorporates recent trends in healthcare, including the evidence-based approach which has become an important component of comprehensive dental care clinical work. In Iran, many new dental schools have been established over the past 20 years, offering both under-

graduate and postgraduate training programs. The number of dentists and specialists in Iran is steadily increasing, and just recently dental services have been incorporated into the public healthcare system. Efforts are also underway in Africa to integrate oral health programs into general health services, through the technical and financial support of WHO/AFRO. It is hoped that such preventive programs and new intervention strategies will improve the level of oral health in many African countries. As reflected in the presentations at this conference, the vibrant research activity in the field of dentistry and the efflorescence in dental education and oral health promotion promise continued improvements in both dental healthcare delivery and patients’ quality of life in the coming years. It was an honor for the Faculty of Dentistry at Kuwait University to host this conference and welcome

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professionals and researchers from around the world, and we look forward to another successful conference in December, 2003. We would like to express the Conference Organising Committee’s gratitude to Kuwait University for its continued support of our conferences, and the Advanced Technology Company for the financial support of this conference. We are also indebted to the Medical Principles and Practice Editor-in-Chief, Professor Farida AlAwadi, and Editor, Professor Azu Owunwanne, for their help, strong support and commitment to publish this supplement. Lastly, we would like to personally thank the authors for their participation, contributions and cooperation. Dr. Jawad M. Behbehani Dr. Eino Honkala Dean Chairman Faculty of Dentistry Organizing Committee

Preface

Evidence Based Practice in Dentistry Kuwait, October 2–4, 2001

Med Princ Pract 2003;12(suppl 1):3–11 DOI: 10.1159/000069846

An Evidence-Based Approach to the Prevention of Oral Diseases A.J. Spencer Social and Preventive Dentistry, The University of Adelaide, Adelaide, S.A., Australia

Key Words Evidence-based W Prevention W Oral diseases

Abstract The evidence-based approach has become the mantra of health care and service delivery. But just what it means, whether it is feasible, how to build it and the outcome of its use are not well understood. The aims of this paper are to provide an overview of an evidence-based approach to the prevention of oral disease, to examine the assessment of clinical trial evidence, to examine emerging approaches to assessing population-wide interventions and oral health promotion, and to illustrate some principles and issues through examples from preventive dentistry. The evidence-based approach to prevention is presented using an evidence loop, which emphasizes that the evidence-base should begin with an understanding to the burden of oral disease and its determinants, rather than a consideration of the efficacy or effectiveness of interventions in clinical dental research. A systematic review of evidence from clinical dental research is compiled and assessed, after which the intervention is decided upon and implemented. The evidence loop is completed by the monitoring of outcomes and reassessment of the intervention process. Attention is also given to steps in assessing non-randomized population-wide interventions and evidence on oral health promotion based on expert opinion. The requirement for evidence

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creates a substantial challenge which can only be met by increased research activity, improved quality of information and the appropriate application of the outcomes of research to policy making for the prevention of oral disease. Copyright © 2003 S. Karger AG, Basel

Introduction

The evidence-based approach has become the mantra of health care and service delivery. It includes all aspects of dentistry, not the least prevention. But just what it means, whether it is feasible, how to conduct it and the outcome of its use are not well understood. The evidencebased approach to the prevention of oral disease relies on knowledge of the effectiveness of identical, similar, or analogous interventions usually carried out and evaluated in a different setting at a different time. Toward the end of the 1990s some journals published systematic reviews and meta-analyses, or evidence-bases, using quantitative scientific methods and consulting scholars around the world about specific methods of appraising and quantifying the benefits and risks of interventions. However, it was found that outside a few areas of health care, clinical trial evidence is scarce, particularly in many areas of dentistry. Many everyday decisions on health care, including prevention of oral diseases, are based on public health programs and policies founded on less scientific evidence

Prof. A. John Spencer Social and Preventive Dentistry The University of Adelaide Adelaide, SA 5005 (Australia) Tel. +61 8 8303 5438, Fax +61 8 8303 4858, E-Mail [email protected]

Fig. 1. An evidence loop for the prevention of oral diseases.

than is required or desired. Not only is more evidence needed, but new ways of examining population-wide interventions and programs for oral health promotion are also needed to assist decision-making. A number of levels of evidence and methods to assess them are being developed. New concepts for an evidencebased approach and a range of old and new methods for the assessment of evidence seem to be gaining greater clarity. This paper provides an overview of the evidencebased approach to prevention, and points out some of the limitations to applying evidence to population-wide interventions and some issues in oral health promotion.

Evidence-Based Approach to Oral Disease Prevention

The evidence-based approach to prevention begins with the identification and definition of an oral health problem for which an objective for oral health gain can be stated. Related evidence on the efficacy of interventions is synthesized and assessed, after which an intervention plan is decided upon and implemented. Finally, the oral health outcomes among patients or populations are monitored and the whole process reassessed over time. These fundamental components might be expanded into a more detailed evidence loop for the prevention of oral diseases,

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as presented in figure 1. Each aspect of this evidence loop for the prevention of oral diseases is necessary for sound decisions on either an individual or population level. Following the various stages ensures that resources are not used to address less important problems or alter less significant determinants, and that preventive interventions are not maintained beyond their useful life should the burden of disease alter. The loop also recognizes that some interventions might work less satisfactorily in different contexts. Burden of Oral Disease In the evidence loop the problem is first identified, defined and prioritized through information on the burden of oral disease, which is the assessment of the magnitude and impact of oral health problems among patients or populations. To design the appropriate intervention, determinants of the disease are delineated and the level of avoidable disease is assessed – i.e. how much of the disease is due to mutable risk factors and what proportion of the burden of disease is avoidable. Numerous ways exist to measure the burden of disease. Summary health measures such as Disability-Adjusted Life Years (DALYs) provide a common metric. The DALY was first used in a comprehensive assessment of the global burden of disease and injury in 1990 by the World Bank [1] and has been adopted by the

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World Health Organization to inform health planning [2]. DALYs provide a way to link the cause and occurrence of a disease to both short- and long-term health outcomes, including impairments, functional limitations (disability) and death. One DALY is a lost year of ‘healthy’ life. DALYs are a combination of years of life lost (YLL) due to premature death and equivalent years of life lived with disability (YLD). Such population-wide ‘summary health measures’ have been emphasized recently in the development of health policies. A report on the burden of disease and injury in Australia [3] identified oral disease as one of the top dozen major disease groups for non-fatal burden of disease. While mental and nervous system disorders were of substantially higher burden than any others, oral disease ranked in a group of diseases/disorders that are considered highly preventable, such as injuries and infectious diseases. The oral diseases included were dental caries, periodontal disease and subsequent edentulism. Years of life lived with disability were predominantly linked to dental caries (56.2%), then to periodontal disease (30.3%) and finally to edentulism (13.5%). Young and middleaged adults experienced more years of life lived with disability from dental caries than did older adults, while the years of life lived with disability from periodontal disease were distributed among middle-aged adult groups. The main challenge of using summary health measures is ensuring that the burden of disease is appropriately estimated, so current estimates of the burden of oral disease in DALYs require further consideration. Estimates of the incidence of new disease from cross-sectional prevalence data are not entirely reliable, because the assumptions made in the translation of prevalence to incidence data do not recognize the recurrence of the most common oral diseases (dental caries and periodontal disease) at previously affected sites. Furthermore, the estimates for the amount of disability associated with each oral disease need scrutiny. The summary health measures cited above apply a system of averaged levels of disability, handicap, mental wellbeing, pain and cognitive impairment using a modified version of the EuroQoL health status instrument; by these measures, the disability weights for gingivitis and dental caries were the lowest of all diseases or disorders [4], indicating that the weights need further investigation. Research using generic quality of life measures among dental patients has shown a low level of impacts; however, this type of research will help assess the relative weightings ascribed to common oral diseases. Orally specific measures of quality of life show a greater sensitivity for oral impacts than do measures for general quality of life

[5], and they have been developed to identify those oral diseases of greater burden that should be considered as targets for prevention [6]. An evidence-based approach to prevention, therefore, requires knowledge of the relative burden of disease associated with particular oral diseases at different stages of life and the proportion of that burden of disease that is avoidable given associations with mutable determinants of disease.

Evidence-Based Approach to Oral Disease Prevention

Med Princ Pract 2003;12(suppl 1):3–11

Determinants of Oral Disease Preventive programs should be based on conceptual and empirical evidence of the determinants of variation in oral disease among patients or population groups in order to identify more points of intervention in the prevention of oral disease. The conceptual model illustrated in figure 2 identifies three discrete yet closely interrelated stages or levels of determinants: upstream, midstream, and downstream [7]. Upstream level factors: The framework identifies social, physical, economic and environmental factors as being the most fundamental determinants of oral health. These include a range of interrelated factors such as education, employment, occupation, working conditions, income, housing, and area of residence. The framework also indicates that these fundamental determinants are themselves influenced by even more upstream factors, namely, government policies, globalisation, and culture. Midstream level factors: Social, physical, economic and environmental contexts throughout life influence health either indirectly via psychosocial processes and dental health behaviours, or more directly, for example via injuries. The dental care system also plays some part in determining oral health within a society. However, it plays only a modest and moderating role. Downstream level factors: Ultimately, oral diseases are a consequence of adverse biological reactions to changes or disruptions in various physiological systems. The poorer health profile of some patients or population subgroups is due in part to longer-term adverse physiological and biological changes that are brought about by poorer psychosocial health and more harmful dental health behaviours. The concept of ‘avoidable oral disease’ is based on an understanding of these wider determinants for most oral diseases and the evidence-base for the effectiveness of possible interventions. Three issues at the centre of new approaches to prevention are multifactorial causes of chronic (including oral) disease, shared risk factors, and life stages. It may be more effective and efficient to build

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Fig. 2. Determinants of oral disease.

preventive efforts around common risk factors than to develop separate preventive programs for each disease. Activities to prevent many of the risk factors may be undertaken in common settings, such as schools or health centres. Current knowledge suggests that oral health outcomes are likely to be best when prevention is promoted throughout life (beginning with the prenatal period and infancy and extending through childhood, adolescence, adulthood and older adulthood), because risks and preventive factors accumulate and interact over a lifetime in a dynamic process. The principles, approaches and messages of health promotion (e.g. empowerment, equity, health literacy, healthy behaviours, supportive environments) and specific preventive interventions are relevant throughout a lifetime, but each life stage also has unique contextual and behavioural aspects, and therefore particular strategies to reduce risk factors and strengthen prevention are needed. Integrated models are emerging that address the continuum of opportunities for prevention, such as the one presented in figure 3, which was developed for Australia’s chronic disease strategy [8]. In such models people are distributed across different target groups: the well population, those at risk, those diagnosed with disease, and those with controlled disease. Interventions are specific to these stages and have different objectives, such as preventing movement into the at-risk group, preventing progression to established disease, or averting recurrence of disease and loss of oral function. In such as approach to pre-

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vention, the evidence-base on different interventions is a key component of the support systems. Synthesis of the Evidence-Base for Preventive Interventions and Decision-Making The evidence-based approach makes use of evaluative research on the effects of an intervention to determine the likely benefits or adverse consequences of intervention for particular individuals or populations. When possible, evidence of beneficial outcomes, rather than biological plausibility or anticipated effects, is used [9]. Evidence of benefits is derived predominantly from epidemiologic research, which provides quantitative estimates of efficacy or effectiveness. Summary estimates of effectiveness are generated by a critical review of research data from two or more studies using systematic review methods [10]. Subgroup analyses may be used to identify characteristics of people for whom an intervention is most or least effective. The starting point for the traditional evidence-based approach, therefore, is the searching for and collation of the scientific evidence on a given intervention. Questions concerning the intervention should be considered carefully and in detail. Narrow rather than broad questions assist the systematic review of evidence, but the question must still be likely to support practical and potentially useful interventions given favourable evidence. Considerable emphasis is placed on the transparency and reproducibility of the literature search. Finding studies relevant to an intervention is not easy; beyond sifting

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Fig. 3. An integrated model for the opportunities for prevention of oral diseases.

through a mass of literature, there are problems of duplicate publications and accessing the ‘grey literature’ such as conference proceedings, reports, theses and unpublished studies, as well as the new web-based literature which is growing exponentially. As an initial step it is helpful to find out if a systematic review has already been done. If not, published original articles need to be found through searches of databases using very explicit criteria for inclusion/exclusion in the review. Bibliographies of identified studies can lead to further relevant studies, and hand searching and writing to experts are also essential. The fate of all identified studies needs to be tracked, whether included or excluded in the review. Relevant studies are then summarized and the research appraised. Numerous guides are available to assist the process of abstracting information from selected studies and putting them in evidence table formats. Many research publications, however, fail to include all the information sought; this could be addressed by adhering to a minimum set of information items that could reasonably be expected in research publications, such as those suggested by the CONSORT statement [11]. Once the review is compiled, evidence is assessed to determine the validity, reliability and precision of the estimates of efficacy of the preventive intervention as well

as the size, importance and relevance of beneficial effects, according to the following criteria: E Strength of evidence: was the research good enough to support a decision on whether or not to implement an intervention? E Size of the effect: what were the research results? E Relevance: do they apply to the potential recipients of the preventive intervention [12]? The level of evidence indicates the validity of evaluative research and takes into account the design of the study, its potential for eliminating bias, and the methods and analysis used [13]. An example of a classification of the level of evidence based on study design is presented in table 1. As an illustration, we will apply the three above-mentioned assessment issues (strength of evidence, size of the effect, and relevance) to the evidence-base for an oral health preventive intervention: fissure sealants performed in a clinic-based dental program for school children. Fissure sealants have been the subject of much clinical trial research. The level of evidence is high because the clinical intervention can be randomly assigned to either children or one of a contralateral pair of teeth, eliminating bias and, with appropriate statistical testing, chance from outcomes.

Evidence-Based Approach to Oral Disease Prevention

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Table 1. Level of evidence and study design

Level of evidence

Study design

I

Evidence obtained from a systematic review of all relevant randomized controlled trials

II

Evidence obtained from at least one properly designed randomized controlled trial

III-1

Evidence obtained from well-designed pseudo-randomized controlled trials (alternate allocation method)

III-2 (observational)

Evidence obtained from comparative studies with concurrent or historical control groups, cohort studies, casecontrol studies or interrupted time-series with a control group

III-3 (comparative)

Evidence obtained from comparative studies with historical control

IV

Evidence obtained from case series

Excluded

Evidence from expert opinion and consensus of an expert committee

Source: [14].

The size of the effect has been expressed variously as rates of retention of sealants over time or statistically significant reductions in dental caries increment. Other research has highlighted the intriguing potential for sealants to prevent caries on adjacent non-sealed surfaces, indicating that the effect may be larger than the prevention of dental caries on sealed pit and fissure surfaces [15]. However, there were more studies on the retention of sealants than on caries increment, raising questions on the appropriateness and relevance of outcomes. Retention is not the same as caries prevention [16]. In this example, it should be pointed out that different studies may have used different measures of effect. Clearly, only studies using the same measures are comparable. It must be decided if studies using different measures will be grouped together or if the type of effect measurement will be a criterion for including the study in the evidencebase or excluding it. Furthermore, the quality of individual studies can vary even within a single level of evidence, according to the study design; to address this potential drawback, a quality score can be given to each study based on methodological features like randomization, blinding, and retention of subjects. Since this is a subjective judg-

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ment, most systematic reviews are based on quality scores given by two or more individuals. The level of agreement among assessors needs to be reported. After the research is appraised, the next stage is the synthesis, or pooling, of the evidence. While this might take a qualitative approach with some overview statement, most often quantitative methods like meta-analysis are used. Meta-analysis relies upon the similarity of studies and increases the power and generalizability of effects. Analyses vary depending on the type of effect measurement used (binary or continuous) and whether it is independent or paired (as in many fissure sealant trials), as well as on the sensitivity of the analysis and the potential for publication bias. Sensitivity can be tested by analysing studies that are rated at different levels of evidence separately and comparing results. Another way to test sensitivity is to categorize by quality score those studies that fall within a single level of evidence; this way, studies in different categories of quality score can be analyzed separately, or studies in lower quality categories sequentially added to the analysis and the results compared. A number of discrete approaches exist to examining publication bias including funnel plots and regression asymmetry. Once the evidence is synthesized, decisions must be made about how to apply the evidence, taking into consideration the transferability of outcomes to patients or population groups and the predicted effects of implementing the intervention. With regard to transferability, both the beneficial and harmful effects of an intervention need to be considered in the collective group of patients and different subgroups among those patients. Baseline risk of disease must also be taken into account. To apply the evidence to individuals, absolute benefits in target populations are predicted, and it is decided whether predicted benefits outweigh any predicted harm. While some guides to synthesis and decision-making end here, the evidence-based approach to the prevention of oral diseases includes a number of other important issues, such as considerations of efficiency, public perceptions and side effects. Efficiency is determined by the relationship between the resources used and the outcome; it includes economic analyses such as cost-effectiveness or cost-benefit analyses. These techniques are also important aspects of the evidence-base for prevention [17]. Perceptions of the public and side effects are covered briefly in later sections. Implementation, Monitoring and Reassessment Once a decision on the appropriate oral health preventive intervention has been made, based either on a sys-

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tematic review of randomized clinical trials or an assessment of observational studies, the intervention is implemented. The last stage of the evidence loop is the monitoring of patients or population groups and the reassessment of the value and necessity of continuing the intervention. While the importance of this final stage is readily acknowledged, all too frequently resources and energy are expended on the intervention and little effort goes into monitoring the outcome. Without this reassessment at the local level, questions on whether a program should continue or be modified will be inadequately addressed. Limitations of the Rules of Evidence Applied to Population-Wide Interventions Recently, a number of limitations to the classic appraisal and application of evidence for preventive interventions have come under scrutiny [18, 19]. Most public health, population-wide preventive interventions are programmatic in nature, covering numbers of people in defined areas. But studies are rarely conducted on such interventions, and when they are, they are observational studies and not randomized. Evidence derived from observational research is considered to be of a lower level because of its potential for bias. However, this devaluation of observational studies emphasises the issue of bias and fails to recognize the importance of transferability. Randomized clinical trials also have drawbacks because they are conducted among unrepresentative samples of the population. In addition, recruitment to a trial is often associated with greater compliance with the intervention than might be reasonably expected in the population, leading to the distinction between a randomized clinical trial and a community trial [20]. Furthermore, a randomized clinical trial takes place over a shorter period, possibly masking either a decrease in efficacy over the longer term or the emergence of side effects. These difficulties with the accepted hierarchy of evidence are illustrated by the issue of water fluoridation. While cluster randomized controlled trials of water fluoridation could be designed in theory, studies of this type are unknown. Instead, evidence on water fluoridation is generally derived from observational studies of discrete geographic areas with and without fluoridation, before and after the water fluoridation was introduced. While these designs may have been the most feasible, acceptable and appropriate [21], they are considered to be at a lower level in the evidence hierarchy [22]. The issue that emerges is how to view a preventive measure where there is a large number of studies which are all individually at a lower level of evidence. A recent report argued that because of

Evidence-Based Approach to Oral Disease Prevention

the number of studies, the level of evidence should be regarded as higher than that indicated by their study design alone [23]. Another interesting evidence issue illustrated by the case of water fluoridation is the public’s perception of the intervention. An intervention will only be implemented if there is general public support for its application. Despite the successful implementation of water fluoridation programs in many countries, the public still does not know much about it and expresses occasional concern about its safety, while a sizeable minority of the population may be undecided or opposed to it [24, 25]. Therefore, public perception may assist or impede the implementation of an evidenced-based preventive intervention, ultimately determining whether the community will benefit from the measure.

Evidence Issues in Oral Health Promotion

Health promotion programs which aim to improve oral health often promote a mix of interventions, or a ‘portfolio’ [19]. These may be effective, but they do not fit well the requirements for evidence of effectiveness. Also important is the context or setting of interventions and how it may shape the outcome. For example, an oral health promotion program might be built around existing ‘healthy’ baby activities such as antenatal and parent education and well-baby and immunization checks [26, 27]. There is an emerging interest in this oral health promotion opportunity, but little research has been conducted [28]. Interventions may be adopted that are a combination of approaches that represent current ‘best practice’ in health education, behavioural change, avoidance of common risk factors, and monitoring of health care providers. Recent reviews of health promotion for oral health have evaluated such oral health promotion interventions and adjusted the thresholds for levels of evidence, specifically including expert opinion and influential reports as a low but acceptable level of evidence. They also weighed the revised levels of evidence against the potential benefit for oral health [23]. The potential benefit can be classified as one of the following: E beneficial; E likely to be beneficial; E trade-off between beneficial and adverse effects; E unknown; E unlikely to be beneficial, and E likely to be ineffective or harmful [23].

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A practical guide for decision-makers to use in selecting a portfolio or mix of interventions for oral health promotion has recently been proposed as part of health promotion planning and practice improvement [19]. Unlike the approaches required for scientific, quantitative evidence, such frameworks hope to ensure that the best available evidence, knowledge and expertise are brought to bear on the problem at hand and that the portfolio ensures a comprehensive approach to addressing the problem. The distinct steps of the portfolio approach are: E convene a decision-making group; E specify the issue to be addressed; E agree to the criteria against which to judge interventions; E weigh the criteria to be used to evaluate options; E brainstorm a long-list of interventions likely to fulfil the criteria; E specify a short-list of interventions for more detailed evaluation; E evaluate the short-listed interventions against the weighted criteria; E score and prioritise the interventions; E reflect on the outcomes of the exercise and refine if necessary [19]. While such an approach uses the best evidence available, the disadvantages of these portfolios of interventions are that they can never disentangle their component effects, or might not be open to falsification.

A systematic review of the literature is a key component of the evidence-based approach. Guidance is available for the searching, selecting, abstracting and appraising, synthesis and decision-making on clinical trial evidence. While these guidelines are readily applicable to clinical interventions, difficulties arise in the areas of population-wide interventions and oral health promotion, as exemplified by the issue of water fluoridation where randomization is not feasible, but lower level evidence is available from community trials. Further difficulties arise in the area of oral health promotion where portfolios of interventions are common. More recently evidence-based processes have emerged that are more appropriate for these later situations. Regardless of the level of evidence or approaches to its appraisal, the evidence loop is completed by implementation, monitoring and reassessment. Too frequently an intervention for which evidence has been found beneficial is inadequately reassessed over time in target patients or populations, but without reassessment it is difficult to determine the value and necessity of maintaining a given intervention. All of the stages of the evidence-based approach are very important and taken together, they offer a rational way forward to improve oral health and dental care.

Acknowledgement This paper is based on a presentation at the 7th World Congress on Preventive Dentistry April 24–27, 2001, Beijing, China.

Conclusion

Although the evidence-based approach is 30 years old, just what it means, whether it is feasible, how to conduct it and the outcome of its use are not well understood. This situation holds in dentistry in general and in areas like the prevention of oral disease in particular. In order to present a comprehensive evidence-based approach to the prevention of oral diseases, an evidence loop has been presented. The evidence for the prevention of oral diseases begins with an understanding of the burden of oral disease at different life stages and the proportion which is avoidable, given associations with mutable determinants of disease. This provides a broad underpinning health policy and priority setting giving direction to both individual and population-wide preventive interventions. The key questions to be addressed about those interventions focus on the beneficiaries, efficacy, efficiency, public perceptions and side effects.

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References 1 World Bank: World Development Report 1993: Investing in Health. New York, Oxford University Press, 1993. 2 World Health Organization: The World Health Report 1999. Geneva, WHO, 1999. 3 Mathers C, Vos T, Stevenson C: The Burden of Disease and Injury in Australia. Canberra, Australian Institute of Health and Welfare, 1999. 4 Stouthard M, Essink-Bot M, Bonsel G, Barendregt J, Kramers P: Disability weights for diseases in the Netherlands. Rotterdam, Department of Public Health, Erasmus University, 1997. 5 Cunningham SJ, Garratt AM, Hunt NP: Development of a condition-specific quality of life measure for patients with dentofacial deformity. II. Validity and responsiveness testing. Community Dent Oral Epidemiol 2002;30:81– 90. 6 Slade GD (ed): Measuring Oral Health and Quality of Life. Chapel Hill, Dental Ecology, University of North Carolina, 1997. 7 Turrell G, Oldenburg B, McGuffog I, Dent R: Socio-Economic Determinants of Health: Towards a National Research Program and a Policy and Intervention Agenda. Brisbane, School of Public Health, Queensland University of Technology, 1999. 8 National Public Health Partnership: Preventing Chronic Disease: A Strategic Framework. Background Paper. Melbourne, NPHP, 2001. 9 Chalmers I: What do I want from health research and researchers when I am a patient? BMJ 1995;310:1315–1318. 10 Mulrow CD, Oxman AD (eds): Cochrane Collaboration Reviewers Handbook; in: The Cochrane Library. The Cochrane Collaboration. Oxford, Update Software, 1999. Accessed online: http://www.update.software.com/ccweb/ cochrane/hbook.htm.

Evidence-Based Approach to Oral Disease Prevention

11 Begg C, Cho M, Eastwood SW, Mo˘her D, Olkin I, Pitkin R, Rennie D, Schulz KF, Simel D, Stroup DF: Improving the quality of reporting of randomized controlled trials: The CONSORT statement. JAMA 1996;276:637–639. 12 Oxman AD, Sackett DL, Guyatt GH: Users guides to the medical literature. 1. How to get started: The evidence-based medicine working group. JAMA 1993;270:2093–2095. 13 Sackett DL, Richardson WS, Rosenberg W, Haynes RB: Evidence-Based Medicine: How to Practice and Teach EBM. New York, Churchill-Livingstone, 1997. 14 National Health and Medical Research Council: A Guide to the Development, Implementation and Evaluation of Clinical Practice Guidelines. Canberra, NHMRC, 1999. 15 Bravo M, Baca P, Llodra JC, Osovio E: A 24month study comparing sealant and fluoride varnish in caries reduction on different permanent first molar surfaces. J Public Health Dent 1997;57:184–186. 16 Deery C, Fyffe HE, Nugent ZJ, Nuttall NN, Pitts NB: A proposed method for assessing the quality of sealants – the CCC Sealant Evaluation System. Community Dent Oral Epidemiol 2001;29:83–91. 17 Niessen LC, Douglass CW: Theoretical considerations in applying benefit-cost and cost-effectiveness analyses to preventive dental programs. J Public Health Dent 1984;44:156– 168. 18 Rychetnik L, Frommer M: A Proposed Schema for Evaluating Evidence on Public Health Interventions. Melbourne, National Public Health Partnership, 2000. 19 National Public Health Partnership: Deciding and Specifying an Intervention Portfolio. Melbourne, NPHP, 2001.

20 O’Mullane DM: Efficiency in clinical trials of caries preventive agents and methods. Community Dent Oral Epidemiol 1976;4:190–194. 21 Black N: Why we need observational studies to evaluate the effectiveness of health care. Br Med J 1995;312:1215–1218. 22 Irwig LM, Cumming C: Study types in population health research; in Leeder S, Wigglesworth E (eds): Research on Health in Human Populations. Melbourne, The Menzies Foundation, 1988, Menzies Technical Reports No 3, pp 39– 54. 23 Wright FAC, Satur J, Morgan MV: EvidenceBased Health Promotion. Resources for Planning. 1. Oral Health. Melbourne, Health Development Section, Public Health Division, Department of Human Services, 2000. 24 Spencer AJ, Slade GD, Davies MJ: Water fluoridation in Australia. Community Dent Health 1996;13:27–37. 25 Spencer AJ, Stewart JF: Support for water fluoridation in Australia. J Dent Res 1997;76:394, abstr 3044. 26 Jones CM, Tinanoff N, Edelstein BL, Schneider DA, DeBerry-Summer B, Kanda MB, Brocato RJ, Blum-Kemelar D, Mitchell P: Creating partnerships for improving oral health of low-income children. J Public Health Dent 2000;60:193–196. 27 Tinanoff N, Palmer CA: Dietary determinants of dental caries and dietary recommendations for pre-school children. J Public Health Dent 2000;60:197–206. 28 Gunoy H, Dmoch-Bockhorn K, Gunay Y, Geurtsen W: Effect on caries experience of a long-term preventive program for mothers and children starting during pregnancy. Clin Oral Invest 1998;2:137–142.

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Evidence Based Practice in Dentistry Kuwait, October 2–4, 2001

Med Princ Pract 2003;12(suppl 1):12–21 DOI: 10.1159/000069841

Preventive (Evidence-Based) Approach to Quality General Dental Care Richard J. Elderton University of Bristol, Bristol, UK

Key Words Dental caries W Dental practice W Dental treatment W Evidence-based dentistry W Periodontal diseases W Repeat dental restorations W Repeat restoration cycle

Abstract Restorative and scaling treatments have not generally provided an effective method for managing dental caries and periodontal diseases. Rather, restorative treatment has often covered up the disease processes in the short term and created a new problem: that of maintenance and re-restoration of restored teeth. Thus, standard invasive dental treatments that are commonly provided fail to address the fundamental bacterial nature of the diseases. Indeed, these treatments rather readily generate and perpetuate a totally unacceptable chain of events. This chain embraces many shortcomings, which themselves nurture what may be described as the repeat restorative cycle. The time has come to correct this iniquity. Dental caries and periodontal diseases are dynamic conditions which need ‘managing’ with a focused cocktail of preventive and refined restoration care. Much more emphasis should be placed upon the assessment of each and every caries or periodontal lesion, with a view to implementing specific preventive measures and allowing the natural arrest of disease processes to occur. The universal adoption of a preventive (evidence-based) approach to making dental treatment decisions could be by far the most powerful factor in reducing the restorative burden of dental services. It is clear that dental education and practice need to rise proactively to the chal-

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lenge, or changes will be forced upon them while they are in a defensive position. There is a need to move wholeheartedly and contentedly into the preventive era. Copyright © 2003 S. Karger AG, Basel

Introduction

Traditional restorative dentistry has had a strong influence on dental education and practice in many parts of the world, and invasive restorative treatment has tended to take precedence over non-invasive preventive measures. It appears that many dentists erroneously presume that dental caries can be ‘treated away’ with restorations and that periodontal diseases can also be ‘treated away’ by regular scalings. Indeed, many dentists seem to believe that traditional dental treatment automatically results in oral health [1]. Dental caries and periodontal diseases, both bacterial in nature, are largely preventable from the start. But they are not always prevented; rather, the forces leading to the diseases are allowed to remain out of balance with those that lead to health. The situation prevails today whereby the scientific basis of these diseases has largely been established [2, 3], but the services providing appropriate dental care to manage them remain out of date and fail to be properly evidence-based. Thus, much of the profession appears still to be wedded to the traditional invasive ‘treatment’ that fails to address the causes of the diseases. When the diseases occur, there is a need for a real and responsible commitment by the dentist to help the patient revert to a disease-

Richard J. Elderton, BDS, LDS RCS (Eng), PHD (Lond) Visiting Professor of Preventive and Restorative Dentistry University of Bristol, 83 Bell Barn Road Stoke Bishop Bristol BS9 2DF (UK) Tel./Fax +44 117 968 6234, E-Mail [email protected]

free status by restoring the balance so that the forces tending to prevent the diseases outweigh the forces contributing to their progression.

Caries

Caries is not simply a one-way process. All carious lesions involve both demineralisation and remineralisation phases [4]. A lesion increases in size only when the calcium and phosphate ion exchange between the tooth and the saliva, mediated by bacterial plaque, favours net mineral loss over long time periods. Such lesions may be described as active. On the other hand, if and when the conditions are such that the calcium and phosphate ion exchange favours mineral gain over time, the lesion may be described as arrested. Causing carious lesions to arrest should be a primary preoccupation of dentists. Caries is very much related to environmental and lifestyle habits such as bacterial plaque, dietary patterns, and fluoride usage, which are themselves very much linked to things like living conditions, economic factors, education levels, school routines, work routines, home and leisure routines, social habits, and personal whims and fancies. Consider the patient who has an active class II carious lesion that has extended well into the dentine. Most clinicians would agree that when this stage of caries development has been reached, it is necessary to excise the diseased tissue and make good the defect with a restoration [5]. But that is just one phase. It is also necessary to bring about a change in the environment of the tooth and of the rest of the dentition so as to prevent further caries, including the development of new primary carious lesions [6]. Thus, proper caries management is all about identifying the main aetiological factors, and selecting and targeting specific efficacious preventive measures to help overcome specific imbalances. It is also about causing patients to make relevant adjustments, in a highly focused manner, to their dietary patterns, oral hygiene habits and fluoride (and chlorhexidine, xylitol, etc.) usage as appropriate. Fissure sealants may also be necessary. The whole process will need monitoring and perhaps fine-tuning over time [7]. So, in addressing the question ‘How should the profession be managing caries?’ the answer has to be by establishing regimens with patients, such that the diseases are arrested and prevented from recurring through environmental and lifestyle measures (though backed up by procedures to restore form and function where appropriate). It is essential that the regimens advised are tailored to the

Quality General Dental Care

individual, and that they are sympathetic to the individual’s environmental and lifestyle characteristics. Caries prevention works, so once a preventive philosophy prevails, then the whole attitude to invasive procedures changes. Many carious lesions that would have been restored under the traditional model of dental treatment can be made to arrest, and many existing but morphologically deteriorated restorations can be allowed to continue to function satisfactorily [8]. Thus, modern quality dentistry requires the dentist to have the wisdom and courage to ‘go modern’ with restorative treatment decision making – substituting preventive care for some invasive procedures. Where restorations are required, they will necessarily be minimally invasive and of high technical quality [9]. Thus the routine use of rubber dam, magnification, sharp hand instruments, welladapted contoured matrix bands, all used with finesse at every stage, becomes integral with modern preventionbased restorative dentistry.

Periodontal Diseases

Plaque-induced periodontitis is believed to involve periods dominated by tissue destruction and periods dominated by tissue repair [10]. Between these fluctuations of activity there appear to be periods of quiescence and stability. Net loss of epithelial attachment and alveolar bone destruction occur when the interactions between the bacteria and the patient’s responses are out of equilibrium such that they favour pathological destruction and loss of structure [11]. Consider the patient who has gingivitis and destructive periodontitis, in whom plaque-induced inflammation has led to apical migration of the gingival epithelial attachment to the root surface of the tooth. The aim of treatment is to arrest attachment loss and cause a reduction in pocket depth; indeed, the aim is normal-looking gingival tissue with pocketing no greater than about 4 mm which does not bleed or discharge pus on probing. The treatment should take the form of effective daily oral hygiene carried out by the patient, plus professional scaling and removal of noxious elements in the periodontal pockets, including the removal of the complex subgingival mass of bacteria which may be adhering to the root surfaces. Other treatment, such as the reshaping of restorations, may also be necessary. As with caries, the prevention phase is critical. However, whatever the patient does, plaque may return to the deeper parts of the gingival crevice, so ongoing professional care may be needed at specific sites.

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It is necessary to ask, and where necessary address in depth, some questions regarding the treatment and prevention of destructive periodontal disease. For example: (a) How well does the patient remove visible plaque on an ongoing basis? (b) Is the patient still using the non-favoured ‘roll’ technique of brushing as opposed to a method involving cleaning of the gingival crevice? (c) Has the dentist or hygienist effectively taught the patient a realistic method of plaque control, tailored to his or her individual needs? (d) Has the dentist unwittingly implied that multiple daily toothbrushings are desirable or indeed a panacea for oral health (which they are not)? Certainly, such multiple daily toothbrushings are irrational with respect to caries as well as periodontal diseases, for it is well known that disease-causing plaque takes longer than 24 h to become established. (e) Has flossing advice been sufficient? (f) Is the patient or the professional incorrectly assuming that antibacterial mouthwashes used in the long term are able to make up for deficiencies in mechanical plaque control and that they can therefore be relied upon to prevent further disease [12]? (g) And, worst of all, is the dentist living under the illusion that a ‘quick scale and polish’ from time to time itself constitutes appropriate care/treatment? Often it does not. It is easy to fail with preventive care and treatment against periodontitis, on the false basis that it can be accomplished by means of a regular ‘scale and polish’, along with a few minutes of instruction about oral hygiene and some general advice given every now and again. Several experts have indicated that proper subgingival scaling and root planing take some 5–7 min per tooth [13], or more [14]. Further, ineffective scaling and polishing may actually do more harm than good, in that while failing to achieve its objective, it may cause damage to the attachment and to the hard dental tissues, even to the extent of taking away some of the high-fluoride outer zones of the teeth [15]. By far the most important thing to do is to inform the patient that it is his or her success with daily plaque control that is the vital factor in determining the long-term outcome. And if the patient is a tobacco smoker, then attempting to convince him or her to quit the habit should be seen as an important component of the preventive dental package, since smoking has a markedly adverse effect upon periodontal inflammation and healing [16]. Dental professionals should appreciate that giving preventive advice in the form of oral hygiene instruction is

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not of itself a preventive measure. The preventive measure succeeds when the patient actually achieves excellent daily oral hygiene; it is this latter which must be the objective.

Why the Problem?

Why does evidence-based quality general dental care constitute a challenge to the profession? Surely it should naturally form the basis of all dentistry, shouldn’t it? After all, dentists are professionals, and professionals should, by definition, avow to offer the best for their patients. The old adage ‘Prevention is better than cure’ is well known, but if dental diseases do occur, it is important to treat them as non-invasively as possible. Ask the World Health Organization or any health minister whether or not it is better to have diseases such as polio, yellow fever, cholera or AIDS in a community or to prevent their occurrence. The answer does not need stating, so why do large segments of the dental profession appear to ‘accept’, as if it were inevitable, the occurrence of avoidable dental diseases such as dental caries and periodontal diseases? What has contributed enormously to the present profile of traditional dentistry, including the teaching in dental schools, has been the widespread dissemination of G.V. Black’s principles of cavity preparation in the early part of the last century, followed by a phenomenal growth in operative dentistry over the years, particularly up to about 1975. The world saw a proliferation of dental schools with vast areas of clinical space devoted to operative dentistry. The clinics became powerhouses, dominating all other activities and engulfing large portions of curricula. Hume [17] has described the phenomenon as a restorative tiger that needs ‘taming and turning’. If G.V. Black, who has been described as the Father of Dentistry, were alive today, he would have been at the forefront of the taming and turning process [18]. A problem here lies in the fact that it is rather easy for both patients and dentists alike to naively believe that operative dental treatment automatically results in oral health. And many dentists have little experience of disease control (as distinct from providing operative treatment), even though they should, theoretically at least, have retained the necessary knowledge from their undergraduate training days. However, the stark facts of the matter are that patients in a low-risk category for caries can inadvertently be shifted towards a significant risk of ongoing replacement restorations once the first set of restorations has been placed in the teeth [19].

Elderton

To illustrate this point, it is relevant to consider a prospective study of dental treatment provided to a large random sample of dentate adults in Scotland. It showed that the amount of operative treatment the patients received over a 5-year period related very much to their dental office attendance patterns and to the number of teeth which already contained restorations [20]. Indeed, it was found that the average number of tooth surfaces restored during any one course of treatment was approximately the same on average, regardless of the frequency of the courses. Thus the patients who went to the dentist more frequently received more restorations per unit of time (almost in direct proportion to the number of courses of treatment received). Further, the proportion of restorations that were replacements increased markedly as the total number of restorations present increased.

Somewhat inevitably, therefore, it was found that the more restorations a patient had, the more the patient was likely to receive. And the people who received the most restorations tended to be relatively well educated and conditioned to visiting their dentists regularly. Overall, it was found that 50% of restorations were placed in the teeth of just 12% of the population. This 12% therefore represents a group at high risk of receiving yet more restorations; after all, they had their restorations examined more frequently than those who attended more rarely, so the chances of a morphologically defective restoration being targeted for replacement were greater in these individuals. Certainly it cannot be assumed that dentistry, as widely practised, is necessarily good for the teeth. The corresponding figures for other countries may differ somewhat from those given above, but it is likely that equivalent scenarios are found elsewhere.

Table 1. The potential chain of events which leads to many shortcomings of traditional restorative dental treatment and nurtures the repeat restoration cycle

The patient visits the dentist but Clinical examination procedures are often rather simplistic and casual and Diagnostic tests (for caries and other lesions) are largely subjective [21–23], so it is not surprising that Caries diagnoses are often inaccurate [23–25]. y At the same time Caries status is not properly taken into account and Caries risk factors are not generally considered [26]. y Even in doubtful situations Undertaking restorations is considered to amount to ‘good dentistry’ [27], so it comes as little surprise that Restorative decisions tend to be idiosyncratic and somewhat aggressive [27–29]. y Thus Caries aetiologic factors are not modified and Preventive backup is inadequate [8], i.e. Caries is not managed as a disease [6, 8]. y Indeed Dentists appear to gain fulfilment by cutting away sound tooth substance (such cutting being a primary function of the high-speed drill). Thus The use of outdated concepts of cavity design (perpetuating Black-type cavities involving excessive cutting of sound tooth substance) is commonplace [30, 31] and Dentists fail to appreciate the exacting nature of restorative procedures. y

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Table 1 (continued)

It is no surprise therefore that Restorations of mediocre quality are readily placed [30, 31]. Sadly These restorations often contain characteristics consistent with inbuilt obsolescence. In addition Bur damage, for example, is imparted commonly to the adjacent tooth [32] and Non-physiological approximal contours frequently lead to plaque accumulation and periodontal disease. y In due course the patient is recalled but Recall assessments of restorations tend to be idiosyncratic [33]. Thus, for example, Ditched margins are commonly assumed to signal failure of the restoration [5, 30] and Existing restorations are readily deemed to have failed [20, 34], particularly if the patient has just changed from a previous dentist [35]. However The matter of why restorations have failed is not questioned by the dentist or patient. y Nevertheless Restorations are readily cut out and replaced in spite of The causes of failure often not being identified correctly [36]. y It is almost ubiquitous that The cavities increase in size when restorations are replaced [30, 37] and consequently that The teeth become weaker [39]. y It is no surprise to find that Errors in the previous restorations are often repeated in the new ones [30] so that The inbuilt obsolescence in the restorations is perpetuated. y Inevitably, as they increase in size The restorations become more complex and difficult to carry out [38, 39] and Correct chemical treatment of the cavity, where necessary, becomes less certain. Further, one cannot escape the fact that Bacteriological, mechanical and chemical insult to the pulp is increasingly likely to occur. y Overall The dentist fails to realise the iatrogenic nature of the ‘treatment’. Indeed The dentist genuinely believes he/she is making the patient more healthy. At the same time The patient is under the illusion that he/she is actually being made more healthy. y But deterioration continues such that, for example, Gross fracture of the tooth may occur and Crowning may be effected as a ‘cure-all’ procedure. However The crown fails to properly fit the margins of the prepared tooth and, if visible, The crown looks artificial. y

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Elderton

Table 1 (continued)

Inevitably Plaque stagnation, halitosis and periodontal disease (and perhaps caries also) increase. y In due course The need or perceived need for endodontic treatment arises. y However Root canal preparation is often inadequate and Root canal obturation is often incomplete, leaving a nidus for continuing bacterial proliferation. y Not surprisingly Periapical seepage of bacterial toxins occurs so The periapical lesion persists. y This may lead to Apicectomy and retrograde root filling taking place, though without first making the root canal filling adequate. y Surprisingly, with this invasive procedure The dentist now feels he/she really is saving the patient’s dentition. y But The tooth fails to settle and symptoms continue so Repeat compromised endodontic or apicectomy treatment takes place and inevitably Pain and sepsis remain ongoing. y At some stage A post is liable to be placed, further weakening the tooth. y Patronisingly The dentist blames the patient for having a weak tooth with unfavourable root canal morphology so The tooth is extracted. y Nevertheless The dentist feels overall that he/she has done a good job in providing ‘quality’ care over the years. y To overcome the missing tooth A bridge is placed but unfortunately The occlusion and aesthetics are altered unfavourably and the patient is dissatisfied. y In due course The bridge gets replaced but There is minimal accompanying anticaries or antiperiodontal disease advice. y Next An abutment tooth fails and is extracted so A larger bridge is made involving more teeth. y

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Table 1 (continued)

Because the bridge morphology is compromised Plaque accumulates and periodontal disease increases. y Indeed, from the very beginning, the following almost ubiquitous and vain scaling scenario is likely: Each scaling results in clean teeth for a day but Bacterial plaque then returns, engendering further periodontal disease. However The periodontal disease is not properly evaluated or documented. Indeed The periodontal disease is not prevented or treated. Instead Further scaling takes place, leading to clean teeth for another day. But inevitably Bacterial plaque returns to continue the disease process and Irreversible alveolar bone loss is liable to take place as periodontitis takes a hold. At the same time Halitosis becomes a real issue for the patient but The halitosis is not even considered by the dentist. Over the years The scaling cycle is repeated many times in the absence of proper periodontal care/treatment so The periodontal disease carries on, largely unabated. y Not surprisingly Further tooth loss occurs. y In an attempt to restore appearance A removable partial denture is made. y But somewhat inevitably The periodontal disease continues to spread. y Whether privately or through third-party funding Costs continue to spiral as the dentition deteriorates. y Looking at the wider scene, it is clear that Dentists fail to appreciate that the public is not very satisfied. Indeed Dentists tend to forget that patients do not like having restorative treatment [40, 41]. y Thus The public is unhappy about dental services [42] and The dentist feels dissatisfied also [43]. Indeed The dentist becomes increasingly disillusioned with dental practice and He/she loses any zest for quality care. Sadly Burn-out rather readily sets in and the dentist spirals downwards [43]. y This inevitably means that Any hope of quality dental care is gone forever.

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Elderton

It is essential that the dental profession breaks away from yesterday’s concepts in favour of dental care aimed at optimising oral health and maintaining the natural dentition in as intact a state as possible. Some members of the profession have made this break already and are providing excellent evidence-based quality dental care. In addi-

tion, they report a marked improvement in the quality of their working lives as a result. Sadly, it has to be noted that many dental school teachers have very definitely not made the break. It is clear that considerable changes are required in dental education [50]. By referring to restorations as ‘treatment’, the profession has drifted hopelessly away from evidence-based dentistry [6]. Yet the profession is steeped in the use of the term when often no treatment is in fact provided, just restorations that readily lock the patient into the repeat restoration cycle, each restoration being less prophylactic and more iatrogenic than the one before. Thus, to the patient who asks ‘Do I need any treatment?’ it is a very naive dentist who replies, ‘Yes, two fillings.’ A more appropriate reply might begin along the lines of, ‘Yes, you have two carious lesions, so we need to set about altering the nature of the chemical processes going on in your mouth in order to cause the lesions to arrest ...’ With the public’s increasing awareness of the shortcomings of traditional restorative dentistry and, at the same time, a heightened understanding of the possibilities for prevention, patients can be expected more and more to demand preventive ‘quality’ dental care. Indeed, it seems that the supply-and-demand forces of the marketplace will reinforce the scientific argument and put increasing pressure upon dentists to adopt a more preventive approach to the management of caries, defective restorations and periodontal diseases. Then the patient who attends regularly will become less ready to accept an apparently unending commitment to restorations and re-restorations, with scales and polishes thrown in from time to time. As caring professionals, dentists should stop pretending that operative treatment is necessarily rational. Prevention and the promotion of health are becoming increasingly necessary in order to satisfy the requirements of today’s people, undertaken within a context of evidence-based oral health care. The real challenges for the future are: (1) for dental education to accept wholeheartedly the changes mentioned in this paper, and to ‘run with them’; (2) for dental practice to put the changes into action out in the field, and (3) for licensing bodies and remuneration systems to develop in sympathy. Thus, there is a fundamental need for a reappraisal of dental education. But questions remain as to how university teaching staffs can be brought fully up to date so as to assist the change in emphasis towards prevention and thereby help tame Hume’s [17] restorative tiger [18]. Initiative and innovation are now required in order to bring about the necessary changes in dental education to suit it

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The Repeat Restoration Cycle

Research over the last 20 years or so has made it possible to assemble a model of the potential chain of events that embraces many shortcomings of traditional restorative treatment, namely the repeat restoration cycle. This potential chain of events is given in table 1. The contents of this table form an integral part of the text of this paper and should be read at this stage. The repeat restoration cycle is driven by a culture of drill-related dentistry. Thus, many dentists have an urge to place and replace restorations, apparently feeling ‘comfortable’ when they intervene invasively [8, 20, 42]. Further, there is an apparent disregard for the inevitable weakening of the teeth in the process, especially as the restorations are placed and replaced over the years. After all, by virtue of the repeat restoration cycle, it is inescapable that restorations are often not very durable (many surviving only for a few years) [44–49]. And, of course, restorations do not cure caries anyway. The characteristics of the repeat restoration cycle are totally unsatisfactory in an age of potential evidencebased dentistry and at a time of increasing accountability. Yet there is a strong implicit message to patients that any operative treatment suggested is both necessary and worthwhile. It is well known that most ‘treatment’ undertaken in dental practice is not at variance with what was taught in dental school. But the dental school was yesterday. Today’s patients require today’s care. In light of the repeat restoration cycle, is it really surprising that the profession suffers from low morale and stagnant motivation, when mechanistic solutions to biological problems weigh so heavily in many dental practices? Patients often do not understand what is going on – they do not understand the repeat restoration cycle – and as ‘consumers’ they have varying levels of faith, ranging from suspicion and distrust to acceptance of virtually anything the dentist suggests.

Moving Forward towards Evidence-Based Dental Care

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to the needs of the changing world. There is a clear need for all those involved in providing oral health care, especially licensing bodies and those responsible for health care delivery, to widen their perceptions of the issues at stake and thereby enable forward-looking curriculum development. Either the profession stands up and says what good dentistry is, or the public and politicians will force their way, and the profession will then be in a defensive position and less ready to respond in an acceptable manner.

Conclusions

more emphasis should be placed upon the assessment of each and every carious and periodontal lesion with a view to allowing a possible natural arrest of the processes to occur, aided by specific preventive measures as appropriate. Existing restorations should not necessarily be replaced just because there is a moderate degree of marginal breakdown. In view of the adverse potential of the repeat restoration cycle, the withholding of restorative treatment when appropriate may itself be considered a prime preventive measure. Indeed, the universal adoption of a preventive, evidence-based approach to treatment decisions could be by far the most powerful factor in reducing the restorative burden of dental practice.

Standard, invasive dental treatments such as restorations and scaling are in general not an effective way to manage dental caries and periodontal diseases. Much

References 1 Elderton RJ, Mjör IA: Changing scene in cariology and operative dentistry. Int Dent J 1992; 42:165–169. 2 Johnson NW (ed): Risk Markers for Oral Diseases: Dental Caries. Cambridge, Cambridge University Press, 1991. 3 Johnson NW (ed): Risk Markers for Oral Diseases: Periodontal Diseases. Cambridge, Cambridge University Press, 1991. 4 Silverstone LM: Dental caries; in Elderton RJ (ed): The Dentition and Dental Care. Oxford, Heinemann Medical Books, 1990, chapter 12, pp 214–236. 5 Elderton RJ: Principles in the management and treatment of dental caries; in Elderton RJ (ed): The Dentition and Dental Care. Oxford, Heinemann Medical Books, 1990, chapter 13, pp 237–262. 6 Elderton RJ: Treating restorative dentistry to health. Br Dent J 1996;181:220–225. 7 Elderton RJ: Principles of decision-making to achieve oral health; in Ulrig U (ed): Professional Prevention in Dentistry. Baltimore, Williams & Wilkins, 1994, chapter 1, pp 1–27. 8 Elderton RJ: Overtreatment with restorative dentistry: When to intervene? Int Dent J 1993; 43:17–24, 98. 9 Elderton RJ: Operative treatment of dental caries; in Elderton RJ (ed): The Dentition and Dental Care. Oxford, Heinemann Medical Books, 1990, chapter 14, pp 263–305. 10 Palmer RM, Floyd PD: Periodontology: A clinical approach. 2. Periodontal diagnosis and prognosis. Br Dent J 1995;178:225–227. 11 Davies R: Periodontal diseases; in Elderton RJ (ed): The Dentition and Dental Care. Oxford, Heinemann Medical Books, 1990, chapter 9, pp 164–176.

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12 Palmer RM, Floyd PD: Periodontology: A clinical approach. 3. Non-surgical treatment and maintenance. Br Dent J 1995;178:263–268. 13 Johansen JR, Gjermo F, Bellini HT: A system to classify the need for periodontal treatment. Acta Odontol Scand 1973;31:297–305. 14 Hill RW, Ramfjord SP, Morrison EC, Appleberry EA, Caffesse RG, Kerry GJ, Nissle RR: Four types of periodontal treatment compared over two years. J Periodontol 1981;52:655– 662. 15 Addy M, Koltai R: Control of supragingival calculus: Scaling and polishing and anticalculus toothpastes – an opinion. J Clin Periodontol 1994;21:342–346. 16 Bergstrom J, Eliasson S: Cigarette smoking and alveolar bone height in subjects with a high standard of oral hygiene. J Clin Periodontol 1987;14:466–469. 17 Hume WR: Research, education, caries and care: taming and turning the restorative tiger. J Dent Res 1992;71:1127. 18 Elderton RJ: The G.V. Black IADR Year of Oral Health Lecture. J Dent Res 1994;73: 1794–1796. 19 Anusavice KJ: Treatment regimens in preventive and restorative dentistry. J Am Dent Assoc 1995;126:727–743. 20 Elderton RJ, Davies JA: Restorative dental treatment in the General Dental Service in Scotland. Br Dent J 1984;157:196–200. 21 Kidd EAM: The diagnosis and management of the early carious lesion in permanent teeth. Dent Update 1994;11:69–81. 22 Kidd EAM: Caries diagnosis within restored teeth; in Anusavice KJ (ed): Quality Evaluation of Dental Restorations. Chicago, Quintessence, 1989, chapter 6, pp 111–123.

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23 Sawle RF, Andlaw RJ: Has occlusal caries become more difficult to diagnose? A study comparing clinically undetected lesions in molar teeth of 14–16-year-old children in 1974 and 1982. Br Dent J 1988;164:209–211. 24 Kidd EAM, Pitts NB: A reappraisal of the value of the bitewing radiograph in the diagnosis of posterior approximal caries. Br Dent J 1990; 169:195–200. 25 Rytomaa I, Jarvinen V, Jarvinen J: Variation in caries recording and restorative treatment plan among university teachers. Community Dent Oral Epidemiol 1979;7:335–339. 26 Elderton RJ: Caries in society and its preventive management; in Bell CJ (ed): Heinemann Dental Handbook. Oxford, Heinemann Medical Books, 1990, chapter 11, pp 128–136. 27 Elderton RJ: Treatment variation in restorative dentistry. Restor Dent 1984;1:3–8. 28 Elderton RJ, Nuttall NM: Variation among dentists in planning treatment. Br Dent J 1983; 154:201–206. 29 Nuttall NM, Elderton RJ: The nature of restorative dental treatment decisions. Br Dent J 1983;154:363–365. 30 Elderton RJ: The quality of amalgam restorations; in Allred H (ed): Assessment of the Quality of Dental Care. London, London Hospital Medical College, 1977, monograph 2, pp 45– 81. 31 Elderton RJ: Cavo-surface angles, amalgam margin angles and occlusal cavity preparations. Br Dent J 1984;156:319–324. 32 Cardwell JE, Roberts BJ: Damage to adjacent teeth during cavity preparation. J Dent Res 1972;51:1269–1270.

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33 Merrett MCW, Elderton RJ: An in vitro study of restorative dental treatment decisions and secondary caries. Br Dent J 1984;157:128– 133. 34 Nuttall NM: Capability of a national epidemiological survey to predict General Dental Service treatment. Community Dent Oral Epidemiol 1983;11:296–301. 35 Davies JA: The relationship between change of dentist and treatment received in the General Dental Service. Br Dent J 1984;157:322–324. 36 Elderton RJ, Merrett MCW: Variation among dentists in identifying reasons for marginal deterioration of restorations. J Dent Res 1987;66: 838. 37 Elderton RJ: A new look at cavity preparation. Proc Br Paedod Soc 1979;9:25–30. 38 Fisher FJ: Toothache and cracked cusps. Br Dent J 1982;153:298–300.

Quality General Dental Care

39 Wise MD: Failure in the Restored Dentition: Management and Treatment. London, Quintessence, 1995. 40 Nuttall NM: Characteristics of dentally successful and dentally unsuccessful adults. Community Dent Oral Epidemiol 1984;12:208– 212. 41 Todd JE, Lader D: Adult Dental Health 1988 United Kingdom. London, Her Majesty’s Stationery Office, 1991, part 4:21, pp 217–234. 42 Schanschieff SG, Shovelton DS, Tulmin JK: Report of the Committee of Enquiry into Unnecessary Dental Treatment. London, Department of Health and Social Security, 1986. 43 Osborne D, Croucher R: Levels of burnout in general dental practitioners in the south-east of England. Br Dent J 1994;177:372–377. 44 Clarkson JE, Worthington HV, Davies RM: Restorative treatment provided over five years for adults regularly attending general dental practice. J Dent 2000;28:233–239.

45 Downer MC, Azli NA, Bedi R, Moles DR, Setchell DJ: How long do routine dental restorations last? A systematic review. Br Dent J 1999; 187:432–439. 46 Elderton RJ: Longitudinal study of dental treatment in the General Dental Service in Scotland. Br Dent J 1983;155:91–96. 47 Gray JC: An Evaluation of the Average Lifespan of Amalgam Restorations; MSc thesis University of London, London, 1976. 48 Mjör IA, Burke FJT, Wilson NHF: The relative cost of different restorations in the UK. Br Dent J 1997;182:286–289. 49 Mjör IA, Jokstad A, Qvist V: Longevity of posterior restorations. Int Dent J 1990;40:11–17. 50 Elderton RJ: Changing the course of dental education to meet future requirements. J Can Dent Assoc 1997;63:633–639.

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Evidence Based Practice in Dentistry Kuwait, October 2–4, 2001

Med Princ Pract 2003;12(suppl 1):22–32 DOI: 10.1159/000069845

Tobacco and Oral Diseases Update on the Evidence, with Recommendations

Jesper Reibel Department of Oral Medicine, Clinical Oral Physiology, Oral Pathology & Medicine, School of Dentistry, University of Copenhagen, Copenhagen, Denmark

Key Words Oral health W Tobacco W Smoking

Introduction

Abstract It is well known that smoking contributes to the development of lung cancer and cardiovascular disease, and there is weighty evidence that it has a considerable influence on oral health. Smoking has many negative effects on the mouth, including staining of teeth and dental restorations, reduction of the ability to smell and taste, and the development of oral diseases such as smoker’s palate, smoker’s melanosis, coated tongue, and, possibly, oral candidosis and dental caries, periodontal disease, implant failure, oral precancer and cancer. From a qualitative point of view the latter is obviously the most serious tobacco-related effect in the mouth. Quantitatively, however, importance has been attached to periodontitis, which affects a large proportion of the population, and during recent years more attention has been given to implant survival rates. Dentists have an important role to play in preventing the harmful effects of smoking in the mouth, and consequently smoking counselling should be as much a part of the dentist’s job as plaque control and dietary advice. Copyright © 2003 S. Karger AG, Basel

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Accessible online at: www.karger.com/mpp

The role of smoking in the development of lung cancer and cardiovascular disease is well known. Since the initial suspicion of the relation between smoking and lung cancer in the 1950s [1], the famous study of British doctors, among many others, established a causal relationship between smoking and death from major diseases, including cancer of the lung and other types of cancer, respiratory diseases such as obstructive pulmonary disease, vascular diseases, and peptic ulcers [2, 3]. As part of the healthcare system dentists have an obvious interest in these diseases, but it could be argued that other members of the health system have more important roles to play as far as these and many other smoking-related diseases are concerned. However, since there is weighty evidence that smoking has a considerable influence on oral health, it is not unreasonable that dentists should play an important role in preventing the harmful effects of smoking on human tissues in general and oral tissues in particular. The oral effects of smoking range from harmless stains of teeth and dental restorations to serious diseases such as oral cancer (table 1). From a qualitative point of view the latter, obviously, is of utmost importance, since the fiveyear relative survival rate for intraoral cancer is about 50% [4]. Quantitatively, however, importance has been attached to other diseases or issues related to smoking such as periodontitis, which affects a large proportion of

Jesper Reibel School of Dentistry 20, Norre Allee DK–2200 Copenhagen N (Denmark) Tel. +45 35326720, Fax +45 35326722, E-Mail [email protected]

Table 1. Effects of smoking on the mouth

Discolorations of teeth and restorations Coated/hairy tongue Reduced ability to taste and smell Smokers’ melanosis Smokers’ palate Dental caries Oral candidosis Increased failure rates for dental implants Periodontal disease Smokers’ white patch/leukoplakia Oral cancer

Oral Cancer

the population, or implant survival, which has come into focus more and more during recent years. There are several general reviews and informational booklets for dentists on the effects of smoking in the mouth [5, 6]. Within the European Union (EU) the Working Group on Tobacco and Oral Health distributed informational material to dentists in EU countries and published a comprehensive review from a consensus meeting organized by the Working Group [7]. Part of this consensus paper has been cited at www.whocollab.od.mah.se/ expl/tobacco.html. The aim of this article is to provide a concise, didactic update on the effects of smoking on oral health, with an emphasis on recent evidence and achievements. When possible, reference is given to detailed and comprehensive reviews of available literature in the field. Also provided are practical and realistic guidelines for dentists to help their patients in their efforts to quit smoking.

The majority of oral cancers, constituting 2–3% of all cancers worldwide [8], are squamous cell carcinomas developing from the mucosal surface epithelium (fig. 1) [4]. Oral cancer affects mostly middle-aged or elderly people and is more common in men than in women [8]. The incidence varies worldwide (table 2) [9]. In this report, oral cancer is used synonymously with squamous cell carcinoma originating from the mucosal surface epithelium. Numerous studies in various populations have shown that smokers have a substantially higher risk of oral cancer than nonsmokers [10–16]. The studies are primarily concerned with the use of cigarettes, but pipe and cigars seem to carry an equal or even higher risk [13, 16]. There is a clear dose-response relationship, with risk decreasing after smoking cessation. In some studies it was shown that 10 years after quitting, former smokers have the same risk of oral cancer as people who never smoked, whereas other studies show that the risk decreases dramatically but remains at a level somewhat higher than that found in people who never smoked [12, 17]. Ethnic differences in the incidence and mortality of oral cancer exist, but the information available is scarce [18, 19]. The relationship between the use of smokeless tobacco and oral cancer has been discussed at length. The apparent discrepancies between different researchers probably derive from the fact that there are great differences in habits and products around the world, which makes a general statement on this subject impossible. Snufff-habits as they appear in Scandinavia carry none or very low risks of oral cancer [20, 21], but the use of other types of smokeless tobacco in other parts of the world seems to pose a substantial cancer risk [22]. Although the underlying mechanisms are not known in detail, it is plausible that smoking could lead to cancer since carcinogens in tobacco smoke can induce changes in DNA. In recent years much attention has been given to smoking-related mutations in a tumor suppressor gene coding for the protein p53. This protein is important in regulating cell proliferation and has a role in the repair of DNA damage [23]. Mutations in the gene may lead to an accumulation of DNA damage in the cells, which may play an important role in the development of cancer. Many studies on the relationship between smoking and oral cancer have been appropriately controlled for various confounders such as diet (low intake of fresh fruit and vegetables increases the risk of developing oral cancer [24, 25]), social status, and, not the least important, alcohol abuse. Smoking and excessive alcohol intake synergisti-

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Table 2. Oral cancer: age-standardized

(world population) incidence rates per 100,000 [9] Population Denmark UK: England and Wales France: Bas-Rhin US: Iowa China: Shanghai Hong Kong Japan: Osaka Thailand: Chang Mai India: Trivandum

Men 6.5 3.2 21.0 8.2 1.8 4.1 3.0 4.7 8.2

Women 2.1 1.3 2.1 2.6 1.3 2.0 1.3 2.5 2.5

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cally increase the risk of developing oral cancer [10, 12, 14]; it has been estimated that between 75 and 90% of all cases are explained by the combined effect of smoking and alcohol use. This could be because alcohol dissolves certain carcinogenic compounds in tobacco smoke and/or alcohol increases the permeability of the oral epithelium [26]. In Greece, where the incidence of oral cancer in general is low, a study showed a similar synergistic effect between tobacco and alcohol [27], and in a study on 300 patients at an addiction unit in Hungary, 8 oral carcinomas were diagnosed (2.7%, mean age 39 years) [28]. All of the 300 patients had a daily smoking and alcohol habit; about half of them smoked more than 20 cigarettes a day and consumed the equivalent of 2–3 liters of wine daily. Thus, screening of risk groups, defined primarily by tobacco and alcohol habits, seems well founded. There is overwhelming and consistent evidence that smoking causes oral cancer. A recent study, however, showed that only one third of patients who had undergone treatment for oral cancer [29]! Thus, the public needs to be informed of the risks, in particular during their visits to the dental office.

Oral Precancer

Oral leukoplakia, the most common premalignant lesion in the mouth, is far more common in smokers than in non-smokers (fig. 2) [30, 31]. A recent study suggests that leukoplakias in the floor of the mouth are associated with smoking habits, whereas leukoplakias at the lateral borders of the tongue are more common among nonsmokers [32]. Smokeless tobacco induces wrinkled changes in the oral mucosa at the site where the quid is placed [20, 33– 36], but at least some of these changes seem to be reversible [36, 37]. Bearing in mind the role of smoking in the development of oral cancer, it is not easy to understand why leukoplakias associated with a smoking habit seem to have a better prognosis in terms of future transformation to cancer than those in non-smokers [38, 39]. In populationbased studies from India it has been shown that cessation of tobacco use substantially decreases the incidence of oral leukoplakias [40], and since it has been shown recently that smoking is positively correlated to the presence of epithelial dysplasia in oral precancerous lesions [41], it is fair to conclude that it is an important and necessary task for the dentist to inform patients of the relationship between smoking and oral leukoplakias.

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An explanation for the finding that leukoplakias associated with a smoking habit have a better prognosis than those not associated with a smoking habit could be that a proportion of smoking-related leukoplakias may not have reached the point of no return. Thus, after smoking cessation a substantial number of smoking-related leukoplakias will disappear [42]. This subgroup of smoking-related leukoplakias may have a low malignant potential. Is it possible, then, to predict if a given white lesion will disappear upon smoking cessation? There is at least one characteristic clinical finding that tells us that the lesion is tobacco-induced: fine white striae that imitate a fingerprint pattern in the mucosa [43]. These lesions are referred to as fingerprint lesions or a pumice stone type of lesion (fig. 3). They will invariably disappear upon tobacco cessation (fig. 4) and are generally regarded as non-premalignant. If a comparison was made between leukoplakias not associated with a smoking habit and leukoplakias associated with a smoking habit but failing to disappear upon smoking cessation, the malignant potential would presumably be the same. The latter group of leukoplakias would possibly include smoking-induced leukoplakias as well as leukoplakias that developed independently of the patient’s smoking habit. Thus, without knowing the fate of a given leukoplakia upon smoking cessation the wording ‘smoking-induced’ should be avoided in favor of the wording ‘smoking-associated’.

Periodontal Disease

During the last 20 years numerous cross-sectional and longitudinal studies have demonstrated a clear relationship between smoking and periodontal disease [for reviews, see 44, 45]. Periodontitis is more prevalent and more severe in smokers, characterized by deeper periodontal pockets, greater attachment loss and more furcation defects [46–52]. In many studies smoking was suggested to be an independent risk factor for periodontal disease after controlling other factors: oral hygiene, plaque, calculus, and socioeconomics. The relative risk of periodontal disease among smokers has been reported to be between 2.5 and 6 compared to nonsmokers [47, 49]. Initially, it was thought that a higher amount of plaque in smokers explained such findings, but the rate of plaque accumulation does not seem to be higher in smokers than in nonsmokers [53, 54]. Recent studies, a few of which are population-based, support earlier findings on periodontal disease in smokers [55–61] and show that cigar and pipe smoking have simi-

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Fig. 1. Squamous cell carcinoma in the floor of the mouth in a heavy smoker. Fig. 2. Leukoplakia characterized by whitish changes, erythematous areas, and nodules in the right buccal commissure in a heavy smoker. Biopsy revealed slight epithelial dysplasia and candidosis. Some would classify this lesion as a chronic hyperplastic candidosis. Fig. 3. White changes in right buccal commissure in a heavy smoker. Note fingerprint-like pattern or pumice stone appearance. Fig. 4. Same lesion as in figure 3 after 3 months’ of tobacco abstinence. Fig. 5. Smokers’ palate in pipe smoker. Fig. 6. Smokers’ melanosis in the floor of the mouth in a heavy smoker.

lar effects as cigarettes [55]. A dose-dependent response has been suggested [48, 56, 62], strengthening the evidence that smoking is a risk factor for periodontal disease. Furthermore, the disease is more severe in current smokers as compared to former smokers [56, 59, 63, 64]. It should be emphasized, however, that studies comparing periodontal disease in current and former smokers were not randomised. The patients who succeed in stopping their smoking habit might be a subgroup of smokers who have an otherwise healthier way of life than those who continue to smoke. But randomising smoking cessation in a scientific context might not be feasible and would, furthermore, pose ethical problems. The effect of smoking on adult patients with manifest periodontitis could be blurred by general health problems and by the progressive process of periodontal disease itself. A recent study on young healthy people without or with minimal periodontitis, however, reveals a clear negative effect of smoking on the periodontal tissues [65]. The mechanisms underlying the negative effects of smoking on periodontal tissues are largely unknown.

Studies have shown more periopathogens in smokers than in nonsmokers, but other studies have not supported this finding. Divergent results are likewise seen in recent studies [66–68]. Most of these studies were conducted on patients with severe periodontitis, but a recent study on young adults with healthy periodontium showed that typical periopathogens are more frequent in smokers than in nonsmokers after controlling variations in oral hygiene, suggesting that smoking is involved in the early development of the disease. A recent study suggested that the effect of smoking on periodontal disease was a reduction in the regression of the disease rather than an effect on the progression of disease [69]. Since divergent results on the composition of the subgingival microflora have been reported, an explanation of the effect of smoking on periodontal tissues has been sought in smoking-induced alterations in the host response. Based on recent reviews [44, 70], it seems fair to conclude that plausible biological explanations exist. Recent studies support earlier findings of impaired humoral, cellular and innate immune reactions and effects via the

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cytokine and adhesion molecule systems [71–75]. A clinically suppressed hemorrhagic responsiveness of the periodontium has been demonstrated in smokers [76]. This may make it more difficult to detect early stages of diseases in smokers and might interfere with diagnostic tests on disease severity and activity. Treatment failures seem to predominate among smokers, although the effect of smoking on treatment success is variable [for review, see 44]. The results of recent studies are in line with these findings [58, 77]. Former smokers seem to respond to periodontal therapy in a manner similar to nonsmokers, but as mentioned above smokers who decide to stop smoking and succeed in their efforts may differ in other risk characteristics from smokers who do not quit their habit. The use of smokeless tobacco has been associated with local gingival recession at the site of placement, but there is no evidence that it is associated with generalized or severe periodontal disease [78]. In concluding this section it can be stated that there is no doubt that smoking negatively influences periodontal health, although to what degree may be difficult to assess because most studies were done on selected patient groups and the results are difficult to apply directly to the general population. Further evidence is needed to determine the effect of smoking cessation on disease progression and treatment and the basic causal connection between smoking and periodontal disease still needs to be elucidated. A recent study assessing the evidence for a causal association between smoking and adult periodontitis suggests that such an association exists, but randomized controlled human prospective studies or community intervention studies are needed [79]. There is substantial evidence that intervention in the smoking habits of the patients should form an integral part of treatment plans and general preventive measures in the dental setting.

Implant Survival

Several studies have indicated a negative effect of smoking on the survival of dental implants [for review, see 80], and recent studies support this finding [81–84]. In some studies, however, patient characteristics are not reported in detail, confounding factors do not always seem optimally controlled, and multivariate analyses are rarely included. Implant failures believed to be attributable to smoking seem to be more common in the maxilla than in the mandible. Contrary to the general previous belief, it has been recently suggested that the increase in

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the number of implant failures in smokers is not the result of poor healing or ossointegration, but is due to the exposure of peri-implant tissues to tobacco smoke [83], possibly linking the smoking effects on implant survival to the smoking effects on periodontitis. A smoking cessation protocol has been suggested to improve the success rate of Brånemark implants [85]. The protocol involved complete cessation of smoking for 1 week before and 8 weeks after initial implant placement. It was concluded that the protocol demonstrated considerable promise in improving the success rates of implant integration in smokers who complied; however, it was noted that the sample size for smokers was relatively small. Furthermore, as touched upon above and acknowledging the problems attached to this, the study did not include a randomization of patients in terms of those following the protocol and those continuing their smoking habit. There seems to be no doubt that smoking can be associated with higher rates of implant failure and altered periimplant conditions, but as indicated above the magnitude of the problem is difficult to assess from available studies. In general, it seems desirable to improve clinical trials in the field of oral implants [86].

Saliva and Caries

Studies on the effects of smoking on saliva flow rates and composition show varying results and are difficult to compare [for a comprehensive review, see 7]. Tobacco usage immediately stimulates salivary flow, but there is no long term effect on saliva flow rates. The pH of saliva rises during smoking, but over longer time periods most studies indicate that smokers have slightly reduced pH and buffering power compared to nonsmokers. A consistent finding is an increased concentration of thiocyanate in saliva. A component in normal saliva, thiocyanate is also present in tobacco smoke, and its concentration in saliva can be used to monitor tobacco exposure. A recent study showed that smoking is associated with lower salivary cystatin activity and output of cystatin C during gingival inflammation [72]. Cystatins are thought to contribute to maintaining oral health by inhibiting certain proteolytic enzymes. In addition this study confirmed earlier results that showed no significant differences in salivary flow rates between smokers and non-smokers. Rather few studies have shown a relationship between smoking and a higher incidence of dental caries [51, 87, 88]. Recent studies support these findings [89, 90]. There is no evidence of any direct aetiological relationship, but

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the findings of higher counts of lactobacillus and, although various results are reported, Streptococcus mutans in smokers [91] may explain this relationship. It is interesting, although not easy to explain, that maternal smoking is associated with the occurrence of caries in preschool children, even when adjusted for social class, nutritional status, and weekly expenditure on confectioneries [92]. In previous studies there was insufficient evidence to support an association between smokeless tobacco and dental caries [7]. A recent study from the USA, however, indicates an association, in particular in terms of root surface caries. This may be explained by the high proportion of sugar in some types of smokeless tobacco [93]. Thus, there are a few studies suggesting an association between tobacco usage and dental caries, although a direct aetiological relationship is lacking. It seems at least that smoking is a risk indicator of increased caries activity.

Other Effects of Smoking on the Mouth

Aesthetics, Smell and Taste Smoking causes discoloration of teeth, dental restorations, and dentures, affecting the aesthetic appearance of the mouth [94, 95], and it contributes more to discoloration than does the consumption of coffee and tea [96]. Smoking is a common cause of halitosis, and it affects the acuity of smell and taste [97, 98]. Odor identification was affected in a dose-related manner and olfactory function improved upon cessation of smoking [97]. Nonsmokers were able to detect salt (NaCl) concentrations 12–14 times lower than the lowest concentration heavy smokers were able to detect [99]. Smoker’s Palate Smoker’s palate, especially seen in pipe smokers, is an asymptomatic lesion appearing as a white change in the palate often combined with multiple red dots located centrally in small elevated nodules (fig. 5). It is closely related to smoking habits [100, 101], and the prevalence is 1–2% in Scandinavia. Smoker’s palate is not premalignant [102], whereas the palatal keratosis associated with reverse smoking, as seen primarily in Asia, is a premalignant lesion [103].

of about 30%, most prevalent on the anterior attached gingiva, is seen in heavy smokers (smokers melanosis) (fig. 6) [104]. Recently it was shown that smokers in a Turkish population had significantly more pigmented oral surfaces than non-smokers [105]. The changes are symptomless, it is not premalignant, and it seems that the pigmentation is reversible upon smoking cessation [104, 106]. Hairy tongue and coated tongue are other harmless lesions related to smoking, although they can be seen in nonsmokers as well [100, 101, 107]. Oral Candidosis A relationship between oral candidosis and smoking has been suggested for a long time (fig. 2), but the exact pathogenic influence of smoking is not known. The suspicion arises from studies in which patients with oral candidosis turned out to be smokers in all [108, 109] or in the vast majority of cases [110]. Another study of the oral presence of Candida strains in healthy adults and in patients with oral leukoplakia and erythematous candidosis also suggested that smoking is a predisposing factor for candidal infection [111]. After antimycotic therapy smokers had relapses of the candidal infection in all cases [109], and in HIV-infected patients smokers were less likely to respond to systemic antimycotic treatment than nonsmokers [112]. Further studies are indeed needed to establish a firm aetiological relationship between smoking and oral candidosis, but it seems fair to inform smokers about the possible relationship and consequences for treatment.

Tobacco Intervention in Dental Practice

Smoker’s Melanosis and Hairy Tongue In non-Caucasians melanin pigmentation in the oral mucosa is normally seen; however, in North European Caucasians it is far less prevalent (about 10%) and has normally a subtle appearance. A pigmentation prevalence

Are dentists actively engaged in tobacco intervention matters? In several studies it has been shown that the majority of dentists consider encouraging their patients to stop smoking [113–118], but few dentists always or often discuss tobacco habits with their patients [113, 116–120]. It was recorded in a study from Italy that more dentists are engaged in tobacco cessation activities [121]. The main barriers to providing tobacco cessation services to patients are lack of reimbursement, lack of confidence in the effectiveness of advice from the dental profession, and lack of knowledge and material to hand out to patients [116–118, 120]. Although few studies are available, it seems that clinical interventions in dental care are as effective as those in other healthcare settings [122]. In spite of this, policies and practices of European dental schools need considerable improvement [123].

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Fig. 7. The five As.

Tobacco intervention includes tobacco cessation activities, prevention, and public policy development. Preferably, dentists should be competent in all three areas. For the purpose of this review only tobacco counselling in daily practice will be touched upon. The World Dental Federation (FDI) adopted a Position Statement on Tobacco in 1996 [124] in which all oral health professionals are urged to integrate tobacco use prevention and cessation services into their routine and daily practice. Recommendations: How to Help Our Patients? Guidelines for healthcare providers about tobacco cessation activities are similar in Europe and the United States [6, 125]. The 5 major steps (the 5 As) are designed to be brief, requiring 3 minutes or less of direct clinician time (fig. 7) [122, 126] [see also http://www.surgeongeneral.gov/tobacco/(go to ‘Clinician materials’; consumer ma-

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terials are also available)]. The primary goal is to ensure that every patient who uses tobacco is identified and offered at least a brief intervention at each clinical visit. The following is a summary of the suggested guidelines [122], along with some personal opinions. Ask patients about smoking. A system should be implemented that ensures that every patient at every visit is asked about tobacco use, and the answer documented in the patient’s record. Advise all smokers to stop. A prescriptive approach should be avoided. Rather, the healthcare professional or the dentist should provide the patients with information and advice, reinforcing the patients’ own motivation when possible and emphasizing the benefits of stopping. Immediate benefits will often motivate the patients more effectively than long-term benefits. Grisly pictures and morbid statistics often stimulate patient denial. Instead, dentists should demonstrate the oral effects of tobacco if present, or inform patients about the increased risk of poor response or healing after dental procedures relevant to the patient. Assess the patient’s willingness to stop. If the patient is willing to make an attempt to quit, dentists should assist the patient. If a patient is not at all interested in stopping it is, in my view, rarely beneficial to push the patient. Instead, the dentist should accept the patient’s decision and make a note in the record for future reference. Dentists should ensure that the patient is aware of the staff’s willingness to help, for instance by providing the patient with written information or/and asking the patient in a subsequent visit to reconsider his or her decision. Depending on the training and resources of the dentist and staff, the following steps can be taken in the dental office, or the patient can be referred to a tobacco cessation specialist. Assist the patient in stopping. If a patient has a desire to stop, the dentist should help the patient set a realistic quitting date which should be soon but not immediately so that the patient has time to prepare. If consultation time is limited, self-help materials that provide the patient with necessary information about smoking cessation can be provided. Nicotine replacement therapy (nicotine gum, inhaler, nasal spray, or skin patch) can be very helpful [122, 126–129]. Special consideration should be given to selected populations [122, 126]. Whatever the approach, the dentist should see to it that the patient leaves the office with a concrete plan for stopping and information about how to prepare for the quitting date and how to successfully stop, keeping in mind that most smokers relapse three to five times before succeeding in stopping.

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Arrange follow-up contact. Follow-up contacts are very important as the chances of a successful outcome are improved when patients know their progress will be reviewed. The dentist should confirm the quitting date, show continuing support, and follow through if the patient was successful or encourage another try if unsuccessful. Follow-ups may be by telephone call, letter, office visit, or a combination of these, and if possible the dentist should arrange to see the patients within one or two weeks after the quitting date and consider a second follow-up one or two months later. It is important that the entire dental team is aware of the relationship between smoking and oral problems. The clinical staff should be familiar with current facts and encouraged to actively participate in tobacco intervention routines. In particular, dental care workers should encourage tobacco preventive measures among adolescents [130, 131].

Conclusions

The lesions and conditions caused in whole or in part by tobacco use are well known, and there is weighty evidence that smoking has considerable influence on oral health. But tobacco use is a modifiable risk factor for oral and general disease, and an obvious professional interest in tobacco intervention can make a big difference in the health of an individual or the outcome of a given disease. Dentists have probably the greatest access to ‘healthy’ smokers in the healthcare system, and even in the absence of tobacco-related diseases in the mouth, the dentist will easily recognize the patient’s smoking status. These facts place dentists in a favourable position to help prevent tobacco-related diseases, and interested practitioners should pursue more formal training in smoking cessation counselling, which should be as much a part of their job as plaque control and dietary advice.

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Evidence Based Practice in Dentistry Kuwait, October 2–4, 2001

Med Princ Pract 2003;12(suppl 1):33–42 DOI: 10.1159/000069842

The Evidence for Prosthodontic Treatment Planning for Older, Partially Dentate Patients Ridwaan Omar Department of Prosthetic Dental Sciences, College of Dentistry, King Saud University, Riyadh, Saudi Arabia

Key Words Prosthodontics W Prosthetic dentistry W Treatment needs and decisions W Limiting treatment goals W Shortened dental arch W Evidence-based practice

replacement of all lost molars may be inappropriate in older, partially dentate individuals. A more limited yet targeted strategy is both more effective and more efficient, and should not be seen as compromised care. Copyright © 2003 S. Karger AG, Basel

Abstract This paper provides a review of the available evidence for traditional prosthodontic need determination and management strategies for older, partially dentate individuals, and compares it to the documented functional benefits of a more limited yet targeted approach to alleviating morphological shortfalls for this group of people, at the population level. The reasons for which the traditional total replacement strategy is not universally applicable or viable are discussed, and research is presented which tests many of the assertions made for the mandatory replacement of posterior teeth. Evidence is presented of the growing prosthodontic challenge posed by an increasing number of middle-aged and older partially dentate individuals in society: many of their remaining teeth are in poor condition, yet few such patients are willing to accept the prospect of becoming edentulous. The shortened dental arch concept is discussed and proposed as an appropriate strategy when complex intervention is to be avoided, inadvisable, or not possible. At the population level, current evidence suggests that prosthodontic strategies aimed at the restoration and/or

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© 2003 S. Karger AG, Basel 1011–7571/03/0125–0033$19.50/0

Fax + 41 61 306 12 34 E-Mail [email protected] www.karger.com

Accessible online at: www.karger.com/mpp

Introduction

Adult dental health continues to improve in a number of industrially developed countries [1–3]. From a prosthodontic perspective, patterns of tooth loss are changing, with steady reductions in the numbers of edentulous individuals [4, 5], and accompanying increases among older age groups of those who are partially dentate [2, 5]. Since these people would have experienced higher disease levels historically, many of the retained teeth would already have been restored [3]. Against this background of changing dental demographic profiles, there are also changes in population demographics [6], culminating in a larger proportion of ageing, dentate people. But being dentate is an advantage in terms of oral functional benefits only if the inherent risks of a few poorly distributed, perhaps structurally and/or biologically compromised teeth can be minimised [7]. At the same time, fewer of these individuals are willing to accept their partially dentate condition as a natural prelude to edentulism.

Prof. Ridwaan Omar Department of Prosthetic Dental Sciences College of Dentistry, King Saud University PO Box 60169, Riyadh 11545 (Saudi Arabia) Tel./Fax +966 1 488 5241, E-Mail [email protected]

The challenges for prosthodontic treatment planning so posed are further compounded by the differences in dental health that exist both within [8, 9] and between countries [10]. Prosthodontic treatment of depleted, broken-down dentitions varies widely, but the replacement of missing teeth has traditionally been its cornerstone. That the patient benefits from such an approach at an individual level cannot be disputed. Yet at the population level, and especially so amongst the growing numbers of middle-aged and older partially dentate patients, such an approach has limited applicability [11]. Molars are the teeth most affected by disease, with 85% of them either missing, decayed, unsound or restored, according to a survey conducted in the United Kingdom [9]. Restoration and/or replacement of such teeth, often of a repetitive nature, must include a consideration of the high initial cost of treatment, its cost-effectiveness, longevity and repairability. For these reasons, as well as medical and physical constraints, it is necessary that a patient’s functional needs be more realistically and precisely defined. In this way, interventions might be more purposefully designed to achieve more effective and efficient long-term outcomes. In this review, the ways in which the partially dentate patient has been customarily evaluated and managed are described, and evidence is presented relating to the rationale, execution and clinical outcome. Substantive research findings, with special reference to the concept of the shortened dental arch (SDA) [12], are presented which suggest a reassessment of conventional treatment needs and goals. How the evidence might point the way to more appropriate management strategies for the growing number of ageing, partially dentate patients at the population level is considered.

Conventional Prosthodontic Paradigms

The primary aim of oral health care is the maintenance of a healthy, natural, functional dentition for life. The adult dentition is not a morphologically stable entity, being subject to continuous changes arising from physiological as well as pathological processes throughout life. An accumulation of such changes, due to a lack of preventive and restorative intervention, and generally as a function of increasing age, can lead to partial, and in some cases total, loss of teeth. A likely deterioration in oral function follows. Dentistry has sought to reverse any threats to the integrity of the dentition by applying prosthodontic solutions

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in the belief that a loss of arch intactness would result in a reduction in oral health. This traditional therapeutic model gave rise to the ‘28-tooth syndrome’, which dictated the need for complete dental arches, i.e. 28 teeth, 14 in each arch [13]. Such a state of completeness ensured, or at the very least contributed to, optimal health by providing occlusal stability through maximal bilateral intercuspal tooth contacts. In this way, treatment needs were invariably shaped by the imperative for total tooth replacement, failure of which would almost certainly result in occlusal instability (and occlusal discrepancies), risk of temporomandibular disorders (TMD), and reduced chewing ability. Within the mechanical framework described, an idealised morphological template was used to evaluate the acceptability of an existing occlusion. It was also the blueprint upon which the planned future occlusion was designed. Several other mechanical axioms evolved, including the beliefs that any overload of the system has to be avoided [14], and that teeth with increased mobility pose a risk to a positive overall prognosis [15]. Not surprisingly, for many years much of the prosthodontic research focused on how to optimise the technology for fabricating prostheses. In contrast, little attention was given to the actual therapeutic goals that were being sought through the application of the said technology [16].

The Evidence for Tooth Replacement Strategies

If there were generally little risk attached to prosthetic tooth replacement, the options for treatment would be largely a matter of personal choice, both for the patient and the provider. Since risks are known to exist, the decision-making process must take into account the effectiveness and efficiency of the available treatment options. This is particularly pertinent for older, partially dentate patients, who are more likely to experience complications arising from a history of repeat restorations [17] as well as various barriers to treatment. Traditionally, clinical decision-making comprised an exchange in which the patient expressed a complaint and the provider gave advice, made a decision, and provided treatment, after considering all the factors and intuitively allowing the process to be influenced by similar past experiences [18]. The process is prone to wide variations, which affects the quality of care [19]. In contrast with the old standard of ‘commonly accepted practice’, the new model for decision-making is based on the concept of evidence-based practice [20]: while still starting with the

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patient’s problem, any uncertainty about its solution is overcome by converting the problem into an answerable question. The best current literature relating to the question is identified and critically appraised for its validity and applicability to the given clinical condition, and a decision reached [18]. While clinical judgement must remain an integral part of fully informed decision-making, it cannot afford to ignore the evidence. The ways in which scientific evidence has influenced the definition of functional needs and the derivation of prosthodontic treatment goals are reviewed in the following subsections. Tooth Loss and Occlusal Instability In 1937, Hirshfeld [21] listed the series of events that could follow the loss of a single lower first molar, which was seen as concrete support for the concept of arch integrity (fig. 1). As a result of tooth movement, there would be loss of stable, supporting tooth contacts, possible loss of occlusal vertical dimension, and functional problems including occlusal interferences, especially of the non-working type. This has been, and to a large extent remains, the prevailing view. Research evidence on the subject has been contradictory, with one study reporting that very few unopposed teeth supraerupted over 5 years [22], and another that all unopposed teeth had supraerupted over periods of up to 15 years [23]. Recently, it was reported that molars which were documented as unopposed for periods longer than 10 years did not all supraerupt: one fourth of the sample supraerupted by more than 2 mm beyond the occlusal plane, and the rest by less than 2 mm or not at all; teeth losing antagonists after 26 years of age had a lower risk of supraeruption (fig. 2) [24]. It follows that the sequelae of tooth loss show wide individual variation, due to local and systemic factors, with potentially positive or negative influences and with known or unknown effects [25]. Loss of all or most of the posterior teeth has traditionally been considered a significant risk for occlusal instability, giving rise to extensive and uncontrolled migration of teeth, and leading to posterior bite collapse, overclosure and further breakdown of the dentition [26]. In follow-up studies over 9 years [27, 28], researchers investigated the stability of the SDA, which consists of 20 teeth (fig. 3) [12]. Based on a number of occlusal indicators, including intercuspal occlusal contact, anterior tooth relationships, interdental spacing, occlusal wear and alveolar bone levels, durable occlusal stability was confirmed, with initial minor changes being characterised as self-limiting and adaptive. No contribution to occlusal stability was gained

Evidence for Prosthodontic Treatment Planning

Fig. 1. Potential instability following loss of a lower first molar:

migration in the form of tipping, rotation and supraeruption; opening of proximal contacts leading to food impaction; uneven marginal ridges; occlusal interferences; alveolar bone loss at the site of the lost tooth [after ref. 21].

Fig. 2. A 59-year-old man who lost his lower right first molar more than 10 years previously; there is little sign of migration or supraeruption of teeth.

from the use of removable partial dentures (RPD), and there was no continuing periodontal breakdown as long as any pre-existing periodontal condition had been treated. In summary: (1) The consequences of posterior tooth loss show wide individual variation and are at least partly predictable, which suggests a management strategy of wait-and-see as opposed to mandatory immediate replacement. (2) The risks of bite collapse, and the consequent need for interceptive prosthodontic therapy to replace molars in SDA patients, are unsupported.

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been observed in SDA patients [41]. Aside from this, the observed correlation between osteoarthrosis of the temporomandibular joints and lack of molar support is confounded by the fact that increasing age is common to both tooth loss and degenerative changes of the temporomandibular joints [42]. Thus, any presumed cause-effect relationship is minimal when adjusted for age [34]. Besides loss of molar support, occlusal discrepancies have also been considered to be of aetiological significance in TMD [43]. Although the evidence for such an association is either weak or non-existent [34], there may be some circumstantial evidence that occlusal discrepancies play a predisposing role.

Fig. 3. SDA, up to and including the second premolars [after ref.

12].

Tooth Loss, Occlusal Instability and Bruxism Occlusal disharmony was believed to precipitate bruxism [29], which, in turn, could be relieved by occlusal modification [30]. Since occlusal instability arising from tooth loss was at one time considered a likely cause of occlusal disharmony [26], missing teeth were replaced in order to treat, or indeed prevent, bruxism. However, nocturnal bruxism is an innate activity of central origin [31], which may be classified as a stress-related sleeping disorder [32, 33]. Although research has failed to show any lasting harmful effects caused by bruxism in healthy individuals [34], excessive occlusal wear can occur in some cases, which may require prosthodontic correction [35]. The management of tooth wear, which usually has a multifactorial aetiology [36], can present a difficult challenge. In summary: (1) Occlusion is not currently considered to be amongst the essential aetiological factors for bruxism, and thus there is no place for occlusal therapy, including prostheses, in its prevention or treatment. (2) In cases of advanced occlusal wear, treatment should be limited to solving specific problems, although this may very well indicate extensive reconstruction in some cases [37].

Tooth Loss and TMD Loss of molar support was believed to be an aetiological factor in TMD, which led to the strategy of replacing molars in order to prevent as well as treat the condition. However, research findings do not support such a notion [38–40]. Neither has an increased risk for TMD, or a tendency for more signs and symptoms to develop with time,

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In summary: (1) Currently, it would appear that the capacity of the masticatory system to adapt to tooth loss is great, and does not warrant replacement on preventive grounds alone. (2) In general terms, given the known potential for prostheses to provoke sudden changes, it would be prudent to exercise caution when considering prosthodontic therapy in a patient, who, at the time of planned intervention, has signs and symptoms of TMD. (3) While prosthodontic treatment might be indicated in patients with loss of teeth together with occlusal discrepancies, it cannot be promoted as a method of preventing or treating TMD, and certainly not as an alternative for failed conventional treatment of TMD.

Tooth Loss and Chewing Ability Objectively assessed chewing efficiency, using test foods for example, decreases almost linearly with the number of remaining occluding teeth [44–46]. Under simulated SDA conditions, chewing efficiency was similarly reduced with decreasing number of post-canine teeth [47]. However, there is no such clear correlation between a reduced posterior occlusion and patient-perceived masticatory ability. Most reports confirm that 20 well-distributed teeth provide adequate chewing function [48–50]. In a group of older adults, eating satisfaction was reported with 21 or more remaining natural teeth, 2 or more contacting pairs of posterior teeth, and no RPD [7]. Furthermore, the risks associated with RPDs, especially distal extension types, in the absence of meticulous oral hygiene measures are well known [51, 52]. This, together with their instability due to alveolar ridge resorption [53] and a feeling of discomfort, which discourages patients from wearing them [54, 55], weigh against their use for the replacement of missing posterior teeth, especially in older patients [7, 56]. In summary: (1) Objective tests show that chewing efficiency decreases in relation to the number of remaining occluding teeth.

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(2) Subjectively, there is no such correlation for reported chewing ability, with chewing satisfaction generally reported with 20 or more remaining teeth. (3) Distal extension RPDs do not contribute to subjective chewing ability.

Further Considerations in the Assessment of Treatment Need

Much of what has been discussed so far has related to so-called objective assessments of patients’ prosthodontic needs, the basis of which is that the reconstitution of missing parts determines clinical success. The importance of this input into the decision-making process should not be devalued, yet there are other aspects that need to be considered. It is increasingly recognised that a successful long-term outcome also depends on fully defining the extent of a patient’s functional impairment, and then identifying an effective and efficient means of addressing the resultant need. Patient’s perceptions of the consequences of their damaged and/or depleted dentitions, the degree of their resulting functional impairment, and the extent to which the treatment addresses their problems are also important. Such subjective assessments are generally substantially lower than those made by professionals [57]. Adaptation Many natural dentitions deviate from the criteria used to define a physiologic occlusion, yet appear to be healthy [58]. The inconsistency is explained on the basis of the adaptive capacity of the individual. Any disruption of morphological integrity is accompanied by either a greater, or lesser, but generally unpredictable, degree of adaptation for the maintenance of satisfactory function, or leads to a non-physiologic state. Prosthodontic therapy seeks to counteract the challenges to the patient’s adaptive ability, as well as to avoid itself becoming an additional challenge to adaptive ability. Adaptive responses take time to manifest. Thus, since the perceived need for tooth replacement is greatest immediately following tooth loss and then subsides [59], and secondary morphological changes following tooth loss are frequently self-limiting [28], it is important to adopt a wait-and-see approach in the process of determining treatment need. In summary: (1) Adaptation influences the degree of functional impairment. (2) Morphological deficits alone are therefore of limited value in determining a patient’s treatment need.

Evidence for Prosthodontic Treatment Planning

Patient-Perceived Needs and Outcomes Patient demand for replacement of missing posterior teeth is relatively weak [60, 61]. A comprehensive review of patients’ satisfaction with their oral status and perceived need for treatment showed that aesthetics play a far stronger role in determining need than does chewing function, and that 20 or more ‘well-distributed’ teeth provided sufficient chewing ability; in people over 45 years of age, such an arrangement satisfied their needs in relation to both appearance and function [62]. This consensus dovetails well with the SDA concept [28]. The primary reason for which patients request crowns is aesthetic improvement [63, 64], and they request fixed partial dentures (FPD) to replace unsatisfactory or failed prostheses [63]. The level of patients’ satisfaction with treatment correlates with the degree to which their demands or expectations are met [65]. Patient-based assessments of treatment outcomes have been advocated as a means to gain more substantive information on the effect of oral disorders on health-related quality of life [66]. Thus, people expect their forthcoming prosthodontic treatment to enhance their sense of wellbeing, which may arise from a perception that oral functional status can be linked to general health [67]. In summary: (1) Patient demand for posterior tooth replacement is relatively weak. (2) Patients’ satisfaction with treatment depends on their expectations being met.

Treatment Efficiency and Longevity Well-controlled clinical studies have shown that patients provided with properly designed RPDs wear their dentures and are satisfied with the results [53]. In population surveys, however, RPDs appear to be a mixed blessing. Although they serve an important function when replacing missing anterior teeth, their impact on eating ability and overall satisfaction when used to replace posterior teeth is generally not positive [7]. Fixed prostheses are accepted more favourably by patients, but also incur a short- and longer-term biological cost, as well as the risk of technical complications. In general practice settings, success rates of 65–68% after 15–20 years have been reported for FPDs [68, 69], compared to 10-year survival rates of 50% for RPDs [55]. Secondary caries and mechanical failures are the most frequent reasons for further treatment, or for frank failure of FPDs [68–70]. FPDs with cantilever extension units have typically shown higher failure rates than conventional end-abutment designs [71, 72], although the difference is negligible in the longer term [69].

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It has also been shown that patients with distal extension cantilever FPDs have better overall outcomes over 5 years compared to patients with distal extension RPDs [73]. Significantly fewer replacements and modifications, lower caries prevalence, better perceived function, and greater cost-effectiveness were observed for cantilever FPDs as compared to RPDs, and could be a preferred prosthodontic option in selected posterior distal extension cases. At the population level, however, such solutions are inapplicable, while the demand for RPDs will be triggered only when a considerable number of posterior teeth have been lost [74]. In general, if an older patient has enough wellpositioned natural teeth to provide adequate eating, anterior aesthetics would be best restored using simple anterior FPDs rather than RPDs, provided that this can meet the patient’s aesthetic needs.

these patients are willing to accept the prospect of edentulism. On the other hand, in the midst of shrinking health care budgets, there are increasing demands from authorities and patients alike for cost-effectiveness and efficiency in the treatments prescribed. Clearly, whenever feasible, the ideal of a complete dentition must remain. Yet such a goal might neither be attainable for general, dental or financial reasons, nor indeed be necessary [11]. When constraints apply, priorities need to be set, and the World Health Organization has adopted as a goal the maintenance of 20 functioning teeth without the need for a prosthesis [78]. While there is much individual variation in the minimum number of teeth required for adequate function, the 20-tooth threshold is valid at the population level [11]. Thus, strategies aimed broadly at meeting such a functional target would seem to be appropriate.

In summary: (1) Properly designed and maintained RPDs provide good patient satisfaction. (2) In population surveys, FPDs are more universally acceptable to patients than RPDs. (3) In older, partially dentate patients who have adequate chewing ability, it is best to treat anterior spaces with simple FPDs.

The SDA Concept Classically, the SDA occlusion consists of 20 teeth (all upper and lower incisors, canines and premolars) (fig. 3). In practice, strict conformity with this arrangement is unlikely due to the obvious variability in patterns of tooth loss. In the foregoing review, much of the research relating to SDA has already been described, and confirms the achievement of occlusal stability and satisfactory levels of oral function without undue effects [11]. The management strategy adopted is one that prioritises treatment goals when there is a need to simplify a complex treatment plan. This is accomplished by directing resources and treatment efforts towards preservation of the functionally strategic and sustainable region of the dentition, namely the anterior and premolar teeth. Molars, which are at a high risk for dental disease and are generally lost earlier than other teeth [9, 79], receive a lower priority for restoration and therefore retention. Thus the quantity, complexity, and expense of treatment in the molar regions can be reduced, along with the associated higher risks of failure [80]. All available maintenance and restorative care can be targeted towards the anterior and premolar region of the dentition. A prerequisite would be that the latter teeth should have a good prognosis, and any major problems, such as caries, periodontal disease, and severe tilting/drifting as a result of discontinuous arches, should be confined mainly to the molar region. Essentially, the SDA strategy seeks to provide a functionally adequate dentition for middle-aged or older adults with a history of compromised oral health. Highrisk younger individuals, who absorb disproportionately large amounts of health care budgets [81], are also potential candidates for such an approach, although an occlu-

Collating the Evidence

The blueprint guiding prosthodontic planning is gradually transforming itself from one in which professionally perceived morphological shortfalls drive prosthodontic treatment, to one in which patient-perceived functional impairment plays a more central role. However, the adoption of evidence-based therapeutic options varies amongst clinicians, which could conceivably give rise to the apparent idiosyncrasies of decision-making. Surveys of dentists’ attitudes towards treatment needs, in the presence of unfolding evidence, have produced interesting results. On the question of the risk of supraeruption of unopposed teeth, a large majority of dentists felt the risk was high, and cited this as a reason for replacing missing teeth; the group was equally divided between immediate replacement and observation [75]. Most of the dentists who were asked about their attitutes towards the SDA concept agreed with it; fewer had managed a small number of patients with the strategy, although some felt that prosthetic extension of the arches was sometimes needed [76, 77]. In many ways, the growing number of older, partially dentate individuals presents a mounting challenge for prosthodontic management. On the one hand, fewer of

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sion up to the first molars, or 8 occlusal units (molars counting as 2 units), is then recommended [25]. In complex treatment plans, the SDA approach offers the alternative of less treatment, which is also less complicated, less time-consuming and less expensive. Whether or not the results are inferior to that of the full-scale reconstructive approach has not been demonstrated. Indeed, as regards accepted prosthodontic reconstructive methods, there is no conclusive evidence on the relative merits of the various methods of occlusal reconstruction, or the superiority of one occlusal scheme over another [82]. Neither is there any evidence on the superiority of technically sophisticated methods over simpler ones. A long-term follow-up of patients treated with cross-arch FPDs showed that various occlusal factors, such as occlusal contact pattern, number and intensity of occlusal contacts, and centric relation-intercuspal position relationship, had no significant influence on subjective function [83]. Similar findings were reported for mandibular implant-supported fixed prostheses opposing maxillary complete dentures [84]. It follows that many of the past rigid formulae for occlusal reconstruction, whose patient benefits were confidently presented as ‘self-evident’, lack scientific evidence, and are in serious need of objective evaluation. Nevertheless, any repositioning of the prosthodontic method as a result of credible new evidence should not imply a compromise of the principles of quality care. The evidently deliberate limiting of treatment goals with an SDA approach prompts the question whether the mere absence of complaint about functional problems can be a justification for not trying to improve function by appropriate restoration [85]. An individualised patient management approach demands that such questions always be posed, as was the case in figure 4. On the other hand, the SDA strategy aims to rationalise the management dilemmas that arise when constraints prevail, as was the case in figure 5. Such issues are particularly pertinent at the population level, but not exclusively so.

Conclusion

Due to changes in patterns of dental disease and tooth loss, an increasing number of older adults have more teeth. However, these teeth have more restorations, which are often large and complex and require time as well as advanced skills to maintain. Traditional prosthodontic strategies for managing such a problem, whilst selectively applicable on an individual basis, may be both inadequate and inappropriate at the population level. The evidence

Evidence for Prosthodontic Treatment Planning

Fig. 4. a, b A 55-year-old woman who was unhappy about her appearance and lack of lower posterior teeth; the upper fixed prosthesis had failed with caries, non-vital teeth and loss of periodontal support at several sites. c Prosthodontic treatment comprised an upper full-arch metal-ceramic splint on 5 abutments with telescopic retainers and a lower distal extension RPD.

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indicating that it is necessary to change the way in which clinicians plan and deliver treatment to reflect the new situation is compelling. Considerations of functional visà-vis morphological impairment should more strongly influence the nature of the treatment, in order to more definitively and accurately target patients’ needs. Research has shown the relevance of the SDA concept for managing the older adult with a reduced, compromised dentition.

Fig. 5a, b. A 72-year-old man who had all his molars extracted 7

years previously at his request: he was worried that the amalgam restorations in his molars were ‘poisoning’ him and he was not content to have the restorations replaced with another material; there is no sign of instability of the resulting shortened dental arches, and neither is there any plan to provide prostheses to improve his chewing ability; the upper left lateral incisor was recently extracted for periodontal reasons and the space temporarily restored with composite resin; the marks on his teeth were made for the purpose of occlusal analysis (courtesy of Dr. Anders Johansson, Örebro, Sweden).

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Evidence for Prosthodontic Treatment Planning

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58 Mohl ND: Diagnostic rationale: An overview; in Mohl ND, Zarb GA, Carlsson GE, Rugh JD (eds): A Textbook of Occlusion. Chicago, Quintessence, 1988, pp 179–184. 59 Bergendal B: The relative importance of tooth loss and denture wearing in Swedish adults. Community Dent Health 1989;6:103–111. 60 Liedberg B, Norlen P, Öwall B: Teeth, tooth spaces, and prosthetic appliances in elderly men in Malmö, Sweden. Community Dent Oral Epidemiol 1991;19:164–168. 61 Tervonen T, Knuuttila M: Prevalence of signs and symptoms of mandibular dysfunction among adults aged 25, 35, 50 and 65 years in Ostrobothnia, Finland. J Oral Rehabil 1988; 15:455–463. 62 Elias AC, Sheiham A: The relationship between satisfaction with mouth and number and position of teeth. J Oral Rehabil 1998;25:649– 661. 63 Walton TR: A ten-year longitudinal study of fixed prosthodontics. 1. Protocol and patient profile. Int J Prosthodont 1997;10:325–331. 64 Oates AJ, Fitzgerald M, Alexander G: Patient decision making in relation to extensive restorative treatment. Part I: Characteristics of patients. Br Dent J 1995;178:449–453. 65 Allen PF, McMillan AS, Locker D: An assessment of sensitivity to change of the oral health impact profile in a clinical trial. Community Dent Oral Epidemiol 2001;29:175–182. 66 Locker D, Slade G: Association between clinical and subjective indicators of oral health status in an older adult population. Gerodontology 1994;11:108–114. 67 Hakestam U, Glantz E, Söderfeldt B, Glantz P-O: What do patients expect from extensive restorative treatment? Eur J Prosthodont Rest Dent 1996;4:53–57. 68 Glantz P-O, Niler K, Jendresen MD, Sundberg H: Quality of fixed prosthodontics after 15 years. Acta Odontol Scand 1993;51:247–252. 69 Lundquist E, Karlsson S: Success rate and failures for fixed partial dentures after 20 years of service. Part I. Int J Prosthodont 1998;11:133– 138. 70 Hämmerle CH, Ungerer MC, Fantoni PC, Brägger U, Bürgin W, Lang NP: Long-term analysis of biologic and technical aspects of fixed partial dentures with cantilevers. Int J Prosthodont 2000;13:409–415. 71 Randow K, Glantz PO, Zöger B: Technical failures and some related clinical complications in extensive fixed prosthodontics: An epidemiological study of long-term clinical quality. Acta Odontol Scand 1986;44:241–255. 72 Karlsson S: Failures and length of service in fixed prosthodontics after long-term function. Swed Dent J 1989;13:185–192. 73 Budtz-Jørgensen E: Prosthodontics for the Elderly: Diagnosis and Treatment. London, Quintessence, 1999, pp 89–92. 74 Basker R, O’Mullane DM: Removable prosthodontic service related to need and demand; in Öwall B, Käyser AF, Carlsson GE (eds): Prosthodontics: Principles and Management Strategies. London, Mosby-Wolfe, 1996, pp 223– 235.

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75 Lyka I, Carlsson GE, Wedel A, Kiliaridis S: Dentists’ perception of risks for molars without antagonists: A questionnaire study of dentists in Sweden. Swed Dent J 2001;25:67–73. 76 Allen PF, Witter DF, Wilson NH, Käyser AF: Shortened dental arch therapy: Views of consultants in restorative dentistry in the United Kingdom. J Oral Rehabil 1996;23:481–485. 77 Allen PF, Witter DJ, Wilson NH: A survey of the attitudes of members of the European Prosthodontic Association towards the shortened dental arch concept. Eur J Prosthodont Rest Dent 1998;6:165–169. 78 WHO Expert Committee: Recent Advances in Oral Health. World Health Organ Tech Rep Ser 826. Geneva, WHO, 1992.

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79 Hujoel PP, Loë H, Anerud A, Boysen H, Leroux BG: Forty-five-year tooth survival probabilities among men in Oslo, Norway. J Dent Res 1998;77:2020–2027. 80 Chace R, Low SB: Survival characteristics of periodontally involved teeth: A 40-year study. J Periodontol 1993;64:701–705. 81 Öwall B, Käyser AF, Carlsson GE: Prosthodontics around the world; in Öwall B, Käyser AF, Carlsson GE (eds): Prothodontics: Principles and Management Strategies. London, MosbyWolfe, 1996, pp 9–19. 82 Thornton LJ: Anterior guidance: Group function/canine guidance – a literature review. J Prosthet Dent 1990;64:479–482.

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83 Yi SW, Carlsson GE, Ericsson I, Wennström JL: Long-term follow-up of cross-arch fixed partial dentures in patients with advanced periodontal destruction: Evaluation of occlusion and subjective function. J Oral Rehabil 1996; 23:186–196. 84 Wennerberg A, Carlsson GE, Jemt T: Influence of occlusal factors on treatment outcome: A study of 109 consecutive patients with mandibular implant-supported foxed prostheses opposing maxillary complete dentures. Int J Prosthodont 2001;14:550–555. 85 Wright PS: The shortened dental arch – to restore or not (editorial). Eur J Prosthodont Rest Dent 1996;4:51.

Omar

Evidence Based Practice in Dentistry Kuwait, October 2–4, 2001

Med Princ Pract 2003;12(suppl 1):43–50 DOI: 10.1159/000069840

Stem Cells and Tissue Engineering: Prospects for Regenerating Tissues in Dental Practice Irma Thesleff Mark Tummers Developmental Biology Research Program, Institute of Biotechnology, Viikki Biocenter, University of Helsinki, Helsinki, Finland

Key Words Stem cells W Bioengineering W Tooth W Bone W Periodontal ligament W Dentin W Enamel

Abstract In general, human tissues have a very limited potential to regenerate. However, recent progress in stem cell research and in tissue engineering promises novel prospects for tissue regeneration in dental practice in the future. Stem cells have been discovered in many adult tissues, including teeth, and stem cells from embryos have the potential to form all adult tissues. Embryonic stem cells can now be cultured and even produced from adult cells by the nuclear transfer method. Due to the rapid progress of research in molecular biology, particularly in the field of developmental biology, we are now starting to understand at the level of genes and molecules how the development of dental tissues is regulated. For instance, specific signal molecules have been identified which regulate the development of teeth and bones from progenitor cells. This information is already being used for the generation of dentoalveolar tissues in vitro and in vivo. Could we perhaps grow new enamel, dentine, periodontal ligament, bone, or even whole new teeth for our patients in the future? Copyright © 2003 S. Karger AG, Basel

ABC

© 2003 S. Karger AG, Basel 1011–7571/03/0125–0043$19.50/0

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Accessible online at: www.karger.com/mpp

Introduction

The possibilities to grow new tissue for patients are presently being actively discussed in professional medical and biological journals as well as in the media. Many scientific breakthroughs during recent years have raised expectations that adult tissues could be replaced by biological means (‘regenerative medicine’) rather than by using artificial spare parts and prostheses. It is hoped that it will be possible to regenerate tissues destroyed by diseases such as cancer, diabetes or periodontal disease, and that tissues or perhaps even whole organs that are congenitally missing could be regenerated. In dentistry the hopes are to regenerate dentoalveolar tissues including alveolar bone, periodontal ligament, dentin and enamel, and perhaps even to grow whole new teeth. Like all new therapies, the practice of tissue engineering is based on previous fundamental research dating back decades. Knowledge of the molecular mechanisms of normal embryonic development is essential when tissues and organs are to be regenerated in patients and derives from a long research tradition in the field of developmental biology. For example, the concept that cell differentiation in all multicellular organisms is regulated by signals transmitted between embryonic cells was already introduced in the beginning of the 20th century. The molecular identities of these signals, so-called growth and

Irma Thesleff Institute of Biotechnology University of Helsinki, PO Box 56 FIN–00014 Helsinki (Finland) Tel. +358 9 19159401, Fax +358 9 19159366, E-Mail [email protected]

differentiation factors, have been revealed only during the last two decades. The present immense interest in the prospects of tissue engineering is, however, due to very recent advances in the field of stem cell biology. In this review, we shall first focus on the most important recent discoveries in this field, and then discuss the possibilities to regenerate dental tissues by stimulating the differentiation of stem cells by bioactive signal molecules, the growth and differentiation factors.

What Are Stem Cells?

Stem cells are defined as cells that have the capacity to self-renew as well as to give rise to differentiated progeny. In early embryos all cells are totipotent stem cells, as they have the ability to form all tissues of the organism. There are also stem cells in adult tissues that contribute to the renewal and regeneration of specific tissues. In humans, stem cells are definitely present in all continuously renewing tissues, such as hematopoietic tissue, skin, bone and intestinal epithelium. In addition, stem cells must be present in tissues which regenerate after injury such as liver and muscle. Interestingly, recent evidence indicates that stem cells are much more widely distributed than previously believed. In particular, the identification of stem cells in the adult brain has led to dramatically increased research activity in the field of neuroscience, and to hopes that stem cell therapies may be used to cure brain damage, for instance in Alzheimer’s and Parkinson’s diseases. In the tooth, stem cells were recently identified in adult dental pulp [1]. The researchers transplanted clones of cultured dental pulp cells to muscle and showed that they differentiated into odontoblasts, forming dentine matrix. In similar earlier experiments, it was shown that bone marrow contains stromal stem cells that differentiate into osteoblasts and give rise to bone after transplantation [2]. Stem cells for ameloblasts have been identified in the cervical loop epithelium of rodent incisors [3].

The Stem Cell Niche

For most stem cells there are no known markers which could be used for the localization of stem cells in tissues. However, evidence from a variety of studies indicates that the cells reside in specific locations called stem cell niches [4, 5]. The microenvironment in these niches supports the

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maintenance of stem cell characteristics as well as their self-renewal. The differentiation of the cells first to transit amplifying cells and then to terminally differentiated cell types is stimulated by specific signal molecules, called growth and differentiation factors. Usually the stem cells in different tissues give rise to one or a few cell types. For example, stem cells in the hair follicles give rise to hair matrix cells, sebaceous gland cells and epidermal cells of the skin [6]. Recently, however, evidence has accumulated that stem cells in adult tissues may have the potential to give rise to a variety of different cell types, as was shown when labelled stem cells were transplanted to different locations. It appears that when stem cells are removed from their original niche and encounter a new environment they can be reprogrammed and cross lineage boundaries. For instance, brain stem cells may give rise to haematopoietic cells, and bone marrow cells to epithelium [7, 8]. Hence, there seems to be much more plasticity in the reprogrammable capacity of the stem cell than previously thought.

Embryonic Stem Cells

At present there are no methods available for the isolation of stem cells from their niches in adult tissues, and hence it is not possible to collect them for tissue engineering purposes. Stem cells from human embryos have recently become an alternative source for the regeneration of human tissues. It has been known for more than a century that the cells in the early embryo are totipotent, i.e. they have the capacity to form all tissues. For example, one isolated cell of an 8-cell embryo can give rise to a whole organism. In the blastocyst stage embryo, the cells of the inner cell mass contribute to all tissues of the adult [9]. Within the last 20 years, it has been possible to culture inner cell mass cells as continuous growing stem cell lines. In fact the mouse embryonic stem cell lines form the basis for the production of transgenic mice, in which specific genes are targeted and modified. For instance, the technique of gene targeting in embryonic stem cells is used to produce so-called knockout mice, in which the function of a specific gene is deleted. When the modified cells are mixed with cells from the inner cell mass of a wild-type mouse embryo, they contribute to the newly formed embryo and can differentiate to all embryonic tissues. Some of these cells end up in the germ line and then the genetic modification can be passed on to the offspring. Successful culture of stem cells from human embryos was reported for the first time in 1988 [10], and since then

Thesleff/Tummers

Fig. 1. Schematic depiction of stem cell culture. Fertilized oocytes are cultured until the blastocyst stage. The inner cell mass, which will give rise to the embryo, is collected and cultured. By adding specific growth and differentiation factors to the culture medium the stem cells are forced to differentiate into certain specialized cell types.

the technical and ethical aspects of their use in tissue engineering have been actively discussed in professional journals as well as in the media. For the first time it is possible to analyse the differentiation of human embryonic cells experimentally. Although the mechanisms of embryonic development are astonishingly similar in all mammals, including mice and human beings, there are nevertheless differences; it is very important to learn these differences for the development of stem cell technologies, because small regulatory differences during development can ultimately lead to hugely different results. Therefore, the first application for human embryonic stem cell lines and the first order of business is the fundamental study of human development and cellular differentiation [11], which is essential for gaining knowledge on how to differentiate tissues and maybe even create organs from human cells in the future. It is apparent that this will be a long endeavour and much effort will be required before there is sufficient

knowledge of the molecular mechanisms of human cell differentiation. As a second and more practical application in the future, human embryonic stem cells could provide a source of cells for tissue regeneration. Stem cells could be exposed to specific combinations of growth and differentiation factors in vitro, which would induce their differentiation in desired directions (fig. 1). Different types of tissues could then be grown in culture and afterwards transplanted to the patients. Another possibility is that the totipotent embryonic stem cells could be directly implanted into the patient’s tissues, where they would then differentiate into specific cell types after encountering the appropriate niche. There is, in fact, some evidence that damaged tissues may exert chemotactic influences on stem cells and, thereby, stem cells might be specifically guided to sites where they are needed for tissue regeneration.

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Fig. 2. The technique of therapeutic cloning. The nucleus is removed from a donor oocyte, leaving it without DNA. This empty cell is subsequently fused with a cell from the patient and therefore also with the DNA of the patient. In the environment of the oocyte this DNA is reprogrammed and can regulate embryonic development. The embryo can now be grown until the blastocyst stage, after which the inner cell mass can be collected and used for creating stem cell lines by culturing them. The tissues created with these cell lines will be immunologically identical to that of the patient.

Therapeutic Cloning

One problem of using embryonic stem cell lines for tissue engineering is the potential rejection of these cells by the patient. It could be possible to overcome this problem by producing embryonic stem cells from the patient’s own cells by so-called therapeutic cloning (fig. 2), based on a nuclear transfer technique similar to the one developed for cloning the sheep Dolly. The nucleus of a somatic cell of the patient is transferred to an enucleated oocyte and cultured in vitro until the blastocyst stage, from which a stem cell line is derived. Since the nucleus contains the genetic information of the patient, any tissue produced by this method will be immunologically identical to and not rejected by the patient. The technology behind the method is obviously demanding and at present only partially exists; hence therapeutic cloning is not yet feasible in practice. In addition, it requires donated oocytes and raises a number of ethical issues that are currently being actively discussed.

Future Vision of Stem Cell Therapy

The optimal way to produce stem cells would be to generate undifferentiated cells from a patient’s own differentiated tissue, thereby avoiding the use of donated human oocytes and human embryonic stem cells. The cloning of

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Dolly showed that the cytoplasm of the oocyte provides an environment which can turn back the developmental clock of a transplanted adult nucleus so that it ‘forgets’ its previous state and history and becomes totipotent. If we could learn enough about the factors that turn back the cellular clock, it may be possible in the future to experimentally dedifferentiate adult cells, for example by treating them with a set of specific factors. In fact, the recent findings that suggest a previously unanticipated level of plasticity in some adult cells and their capacity to differentiate in multiple directions (see above) give some indication that this could be possible in the future. This would bring us closer to a scenario as simple as, for instance, taking a skin biopsy of the patient, dedifferentiating the cells, and then inducing their differentiation into desired cell types, such as heart muscle cells, bone cells or brain cells.

Growth and Differentiation Factors

The ability to induce the differentiation of stem cells in desired directions is still a major challenge in stem cell research. Whether the stem cells are derived from embryos or from adult tissues, the molecular mechanisms that guide the differentiation of various types of cells must be understood before specific tissues can be regenerated. The mechanisms that regulate morphogenesis and cell dif-

Thesleff/Tummers

Table 1. Most commonly studied growth

and differentiation factors Growth and differentiation factor families Transforming growth factor-ß (TGF-ß) Bone morphogenetic protein (BMP) Activin Wnt (Wingless) Retinoic acid (RA) Fibroblast growth factor (FGF) Platelet-derived growth factor (PDGF) Hedgehog

ferentiation in the developing embryo have been a subject of intensive research for many decades. One of the pioneers in this field was Hans Spemann, who won the Nobel Prize in 1935 for studies that he performed in the early 1900s on amphibian embryos. He showed that inductive signals generated in one embryonic tissue could regulate the differentiation of neighbouring tissues [9]. These findings initiated a long search for the identity of the actual inductive signals, but it was only after the technological advances in molecular biology that the molecular nature of the signals was discovered. The last 15 years have been an era of intense activity in the field of developmental biology, and a number of scientific breakthroughs have contributed to the current understanding of the molecular signals that regulate cell differentiation. It is now evident that most signals are small secreted molecules called growth factors or differentiation factors. They are hormone-like molecules which are produced in one cell, released outside this cell and then act on other cells; through binding to specific receptors they regulate gene expression, which subsequently affects cellular differentiation (fig. 3). The most commonly studied growth and differentiation factor families are listed in table 1. Growth and differentiation factors have a variety of effects on cells and, typically, the same molecules affect the differentiation of many cell types and organs. The understanding of how growth and differentiation factors regulate cell differentiation has increased rapidly during recent years. There are even some examples of successful use of growth and differentiation factors in the stimulation of mouse embryonic stem cell differentiation. However, we are still far from a situation where we could apply specific cocktails of factors to undifferentiated cells and stimulate their differentiation into specific pathways, thereby producing the desired replacement tissues for patients, or even for experimental animals.

Tooth Replacement by Bioengineering

Fig. 3. Signalling molecules outside the cell transduce their signal

through specific transmembrane receptors into the cell. The signal is then forwarded to the nucleus where it activates the transcription of specific genes. The mRNAs of these genes are translated into functional proteins such as receptors, signalling molecules, or transcription factors. The transcription factors will modulate the expression of certain genes in the same cell. The receptors will move to the cell membrane and are then capable of receiving a signal from outside the cell, and the signalling molecules will be transported out of the cell and hence can communicate with other cells.

Regeneration of Bone, Dentin and Periodontal Ligament by Bone Morphogenetic Proteins

Bone is a very special type of tissue. It undergoes constant turnover, resulting from apposition by osteoblasts and resorption by osteoclasts, and it also has a fantastic ability to regenerate after injury. It has been known for a long time that bone matrix is rich in growth and differentiation factors, and today the molecular nature of the most important of these factors is known. It has been shown that they can stimulate the differentiation of stem cells into bone-forming osteoblasts. The ability of bone matrix to stimulate the formation of new bone was experimentally proven several decades ago by transplanting demineralized bone matrix into muscle [12]. After many decades of intense biochemical research the active sub-

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Fig. 4. The differentiation of stem cell prog-

eny. During stem cell divisions new stem cells are created and cells that will continue to differentiate. In this particular case BMPs are capable of inducing the differentiation of stem cells into preostoblasts and preodontoblasts, which will then continue differentiating into osteoblasts and odontoblasts, respectively.

stance, called bone morphogenetic protein (BMP), was finally isolated and cloned [13]. There are more than 30 BMPs known at present, and many of them induce bone and cartilage formation in vivo when transplanted with carrier substances to soft tissues such as muscle. They also induce the differentiation of osteoblasts and chondrocytes in a variety of cultured cells in vitro. Animal experiments over many years have shown that BMPs have the capacity to stimulate bone formation in different bones, including jawbones. Thus, BMPs stimulate alveolar bone formation around teeth and induce the regeneration of periodontal attachment. They apparently have stimulatory effects on cementoblast differentiation [14, 15]. Clinical trials in humans are presently ongoing in which the effects of BMPs are tested on bone formation in various orthopaedic applications as well as for periodontal regeneration. Although the morphology of dentin matrix differs from that of bone, their biochemical compositions are very similar. Hence, dentin matrix also contains BMPs, and demineralized dentin matrix can stimulate bone formation in muscle. Interestingly, both bone and dentin matrices stimulate dentin formation when implanted into the dental pulp, and this effect can be mimicked by recombinant BMP [16]. Dentin does not normally undergo turnover like bone, but it has the well-known ability to regenerate after pulpal injury. As described above, osteoblastic stem cells have been localized in bone marrow, whereas odontoblast stem cells were recently discovered in the dental pulp. It appears, therefore, that BMPs are growth and differentiation factors which can stimulate the differentiation of pulpal stem cells into odontoblasts and bone marrow stem cells into osteoblasts (fig. 4).

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Could Enamel Be Regenerated?

The regeneration of enamel is clearly more problematic than that of dentin and bone. The enamel organ epithelium, including the ameloblasts, remains as a protective layer on the tooth crown only until eruption, at which point it is lost. Therefore, in contrast to dentin, enamel does not regenerate after traumatic injury. There are conceivably no stem cells for the enamel-producing ameloblasts in adult tissue. It is not impossible, however, that some oral epithelial cells could have the ability to transdifferentiate into ameloblasts under favourable circumstances. Work in our laboratory has led to the identification of epithelial stem cells in the cervical loop of mouse incisors [3]. These teeth erupt continuously, and enamel production continues throughout the life of the animals. Thus, by definition there have to be stem cells for ameloblasts present. Stem cells for ameloblasts apparently reside in the germinative end of the incisors among the stellate reticulum cells located in the centre of the cervical loop epithelium. We have suggested that the maintenance and/or differentiation of these stem cells is stimulated by fibroblast growth factors (FGFs), which are a family of well-known growth and differentiation factors required for the development of a variety of organs, including teeth [17]. We also suggested that FGFs regulate the Notch pathway, which is a molecular signalling pathway involved in stem cell development in other animals and organs [18]. The understanding of the molecular pathways that regulate the differentiation of dental epithelial stem cells into ameloblasts in vivo may lead to the generation of tools whereby oral epithelial cells or other epithelial stem cells could be induced to form enamel.

Thesleff/Tummers

Fig. 5. Signalling between mesenchyme and epithelium plays an important role in the development of epithelial-

mesenchymal organs like the tooth. The same growth and differentiation factors regulate different stages of development. The top panels are epithelial signals and the bottom panels mesenchymal signals. In the boxes are transcription factors regulated by the signals.

The regeneration of whole organs like teeth is certainly much more demanding than the regeneration of individual tissues like bone or dentin. However, this goal may not be as distant as it appeared to be a few years ago. This is due to the rapid progress in the understanding of the molecular mechanisms that regulate the development of embryonic organs in general and of teeth in particular. Teeth develop from oral ectoderm and the underlying mesenchymal cells, and at the time of tooth initiation the epithelial and mesenchymal cells are undifferentiated. Dental epithelium consists of cuboidal cells that form the thickened dental lamina, and the dental mesenchymal cells underneath are morphologically similar to the rest of the jaw mesenchyme. A chain of signaling events, taking place mainly between the epithelium and mesenchyme of the tooth germ, guides morphogenesis through several stages of increasing complexity, accompanied by the progressive differentiation of cells [19]. Numerous molecules that are involved in the complex process of tooth morphogenesis have been identified during the last 20 years. Many growth and differentiation factors have been shown to act as signals mediating the morphogenetic cell-cell interactions during tooth develop-

ment. For instance, our laboratory has discovered signaling centres in the tooth germ epithelium, called enamel knots. Composed of small aggregates of epithelial cells which simultaneously produce more than 10 growth and differentiation factors [20], the enamel knots regulate the formation of tooth cusps and are therefore important organizing centres of tooth development. The targets of the signals regulating tooth development have been identified in some cases, and hence we are beginning to understand the molecular and genetic networks that regulat odontogenesis. Figure 5 shows a schematic illustration of the molecules regulating early tooth morphogenesis. Our laboratory has created a database on the expression patterns of genes associated with tooth morphogenesis (http://bite-it.helsinki.fi). As of July, 2001, patterns of 230 genes are shown in this database. It is conceivable that the completion of the genome project will result in a rapid increase in the number of these genes. Molecular genetic studies of human syndromes have revealed novel genes regulating tooth development. In addition, the genetic analysis of mouse development, in particular the production of transgenic mice, will certainly result in the discovery of more genes that are required for normal tooth development. This accumulation of molecular information will contribute to a more complete understand-

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Prospects to Grow New Teeth?

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ing of the mechanisms that regulate tooth morphogenesis and the roles that growth and differentiation factors play in these processes. Despite the accumulation of molecular information and our understanding of the regulation of tooth development, it is not clear how teeth could be grown in practice. Perhaps one day we will be able to isolate cells that have the capacity to form teeth, and then tooth development could be initiated in vitro. Such multipotential stem cells could be obtained by some of the methods described above. After initiation, the tooth germ could either be transplanted into the mouth or it could be cultured in vitro. This approach would be the most difficult since it would require a thorough knowledge of all processes that govern the formation of the proper three-dimensional structure of the tooth. Alternatively, it is possible that tooth development could be initiated in vivo by applying specific growth and differentiation factors. Some years ago we developed a technique whereby growth factors were introduced locally to embryonic tissue in vitro by small agarose beads that released the factors to surrounding cells [21]. Could it be possible to induce the formation of new teeth in vivo by such beads? It is intriguing that FGF-releasing beads induced extra limbs in chicken embryos when they were implanted in the flank between the

wings and legs [22]. The potential feasibility of tooth regeneration gains additional credibility from the fact that teeth are continuously being replaced in some animals such as fish or amphibians. Furthermore, teeth are often found in human teratomas. These tumours consist of a variety of differentiated tissues, and it is noteworthy that the teeth found in these tumours have quite normal shapes and structures, thus indicating that the program for development is conceivably present very early in the tooth-forming tissue and is therefore not influenced by the surrounding tissues to a significant extent. Therefore, with this approach we would ideally require only to introduce the signal that starts tooth formation and then let nature run its course, without having to worry about the complex processes that occur during tooth development.

Conclusions

Despite the rapid advances in the fields of developmental biology and regenerative medicine, much research is still required before tooth regeneration in dental practice is a reality. In particular, we need a more thorough understanding of the mechanisms of tooth initiation and the characteristics of dental stem cells.

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10 Thomson JA, Itskovitz-Eldor J, Shapiro SS, Waknitz MA, Swiergiel JJ, Marshall VS, Jones JM: Embryonic stem cell lines derived from human blastocysts. Science 1998;282:1145– 1147. 11 Donovan PJ, Gearhart J: The end of the beginning for pluripotent stem cells. Nature 2001; 414:92–97. 12 Urist MR: Bone: Formation by autoinduction. Science 1965;150:893–899. 13 Wozney JM, Rosen V, Celeste AJ, Mitsock LM, Whitters MJ, Kriz RW, Hewick RM, Wang EA: Novel regulators of bone formation: Molecular clones and activities. Science 1988; 242:1528–1534. 14 Talwar R, Di Silvio L, Hughes FJ, King GN: Effects of carrier release kinetics on bone morphogenetic protein-2-induced periodontal regeneration in vivo. J Clin Periodontol 2001;28: 340–347. 15 Ripamonti U, Heliotis M, Rueger DC, Sampath TK: Induction of cementogenesis by recombinant human osteogenic protein-1 (hOP1/BMP-7) in the baboon (Papio ursinus). Arch Oral Biol 1996;41:121–126. 16 Rutherford RB, Wahle J, Tucker M, Rueger D, Charette M: Induction of reparative dentine formation in monkeys by recombinant human

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osteogenic protein-1. Arch Oral Biol 1993;38: 571–576. De Moerlooze L, Spencer-Dene B, Revest J, Hajihosseini M, Rosewell I, Dickson C: An important role for the IIIb isoform of fibroblast growth factor receptor 2 (FGFR2) in mesenchymal-epithelial signaling during mouse organogenesis. Development 2000;127:483–492. Artavanis-Tsakonas S, Rand MD, Lake RJ: Notch signaling: Cell fate control and signal integration in development. Science 1999;284: 770–776. Thesleff I, Nieminen P: Tooth morphogenesis and cell differentiation. Curr Opin Cell Biol 1996;8:844–850. Jernvall J, Thesleff I: Reiterative signaling and patterning during mammalian tooth morphogenesis. Mech Dev 2000;92:19–29. Vainio S, Karavanova I, Jowett A, Thesleff I: Identification of BMP-4 as a signal mediating secondary induction between epithelial and mesenchymal tissues during early tooth development. Cell 1993;75:45–58. Cohn MJ, Izpisua-Belmonte JC, Abud H, Heath JK, Tickel C: Fibroblast growth factors induce additional limb development from the flank of chick embryos. Cell 1995;80:739–746.

Thesleff/Tummers

Evidence Based Practice in Dentistry Kuwait, October 2–4, 2001

Med Princ Pract 2003;12(suppl 1):51–55 DOI: 10.1159/000069843

Dental Education in Kuwait J.M. Behbehani Faculty of Dentistry, Health Sciences Center, Kuwait University, Kuwait

Key Words Dental education W Curriculum W Evidence-based approach W Community-based learning W Comprehensive dental care

Abstract For a long time there has been a need to establish a dental school in Kuwait, due to the fact that the majority of dentists working in Kuwait are expatriates from various countries. An Amiri decree in 1996 made it possible, and the first dental students were admitted to the Kuwait University Faculty of Dentistry in 1998. The mission of the Faculty of Dentistry is ‘to promote oral health in Kuwait through education, research and cooperation with other professional health care institutions as well as the community at large’. A 6.5-year dental curriculum was completed after 2 years of committee work and was accepted by the University Council in 2001. This curriculum incorporates current trends in medical and dental education, such as the evidence-based and community-based approaches, problem-solving methodology for outcomebased learning, and competency achieved through comprehensive patient care. Copyright © 2003 S. Karger AG, Basel

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Introduction

Dental care in Kuwait is delivered by expatriates as well as Kuwaiti dentists who received their training abroad, mainly in Egypt, the United States, the United Kingdom, and the Republic of Ireland. While the Faculty of Medicine was established at Kuwait University in 1973, plans for establishing a Faculty of Dentistry did not start until the early 1980s. The Gulf War delayed these plans until May 26th, 1996, when an Amiri decree was issued for the establishment of the Faculty of Dentistry. The first class of 26 students was admitted to the dental program in September 1998, and they will graduate in January 2005. Once the Faculty of Dentistry was established, a curriculum committee was set up to plan, evaluate and revise the program. The dental curriculum is presently a 6.5year, 13-semester program, including 1.5 years or 3 semesters of preprofessional studies in the Faculty of Science, 2.5 years or 5 semesters of preclinical courses in the Faculty of Medicine, and finally 2.5 years or 5 semesters of clinical training in the Faculty of Dentistry. Dental subjects were incorporated into both the preprofessional and preclinical programs in order to expose the students to clinical experiences early in their training, and medical courses which were less relevant to dentistry were replaced by dental courses (fig. 1). For instance, the Introduction to the Dental Profession course was incorporated into the preprofessional program in the 2nd year, and

Dr. Jawad M. Behbehani Faculty of Dentistry, Health Sciences Center, Kuwait University PO Box 24923 Safat 13110 (Kuwait) Tel. +965 2664502, ext. 7101, Fax +965 2634247, E-Mail [email protected]

Table 1. Major sheet: course titles, numbers and credit hours by

years 1–7 a Preprofessional program Depart- Course ment1 No.

CH2

Course

Year 1, semester 1 181 English 115 Finite Mathematics 110/111 Chemistry and Chemistry Laboratory or 121/125 Physics and Physics Laboratory Elective Course

Fig. 1. The integration of dental subjects into the preprofessional and preclinical programs of the B Med Sc. a = Introduction to the dental profession; b = oral anatomy; c = oral microbiology; d = oral and systemic pathology; e = oral neuroscience; f = dental biomaterials; g = preclinical oral and maxillofacial radiology; i = preclinical operative dentistry and cariology; j = preclinical removable prosthodontics.

Year 1, semester 2 182 English 110/111 Chemistry and Chemistry Laboratory or 121/125 Physics and Physics Laboratory 101 Biology Introduction to Health Professions/Elective Course Year 2, semester 1 00 201 183 122 127 114 103

Introduction to the Dental Profession3 English Physics Physics Laboratory Chemistry and Chemistry Laboratory Biology

Total CH

dental courses (those with course numbers ending in ‘D’) were introduced into the preclinical program in the 3rd and 4th years of the curriculum (table 1). Simultaneously with curriculum development, the departmental structure of the faculty was determined (table 2).

The Development of the Dental Curriculum

The mission of the Faculty of Dentistry is ‘to promote oral health in Kuwait through education, research and cooperation with other professional health care institutions as well as the community at large’. A communitybased dental curriculum that focuses on the community and empowers local residents is recommended by the World Health Organization (WHO) [1]. In such a program, close cooperation between the community and the educational institution is necessary, creating a new role for dental schools and a new kind of responsibility in teaching [2]. Social sensitivity is therefore considered an important criterion in the recruitment of students, who rotate in different community clinics and extramural programs. No existing curriculum was accepted as a model for the dental program, so the experienced members of the multinational academic staff of the new Faculty of Dentistry were consulted to establish a modern and realistic dental

52

Med Princ Pract 2003;12(suppl 1):51–55

5 3 4 3 5 4

3 3 2 5 3 1 4 3 48

1

Departments refer to the Faculty of Dentistry only; see separate list below. One credit hour (CH) equals 1 h of theoretical studies or at least 2 h of practicals per week for 1 semester. 3 Coordinated by the Vice-Dean for Academic Affairs. 2

curriculum suitable for the needs of Kuwait. The curriculum was completed in 2 years (1999–2000) and accepted by the University Council in 2001. It incorporates current trends in medical and dental education, which are summarized by Harden [3] as follows: (a) education for capability; (b) community orientation; (c) self-directed learning; (d) integration and multiprofessional education; (e) outcome-based education; (f) adaptive curriculum, and (g) assessment-led innovation. These trends reflect the shift that is taking place in the dental profession, from diagnosis and treatment to disease prevention, health maintenance, and health promotion [4]. Several of these trends appear among the nine basic principles that form the philosophy of education at the Faculty of Dentistry (table 3). The principles apply mostly to the clinical program and to those clinical courses that have been incorporated into the preclinical program (courses with numbers that end in ‘D’). Both didactic and clinical dental education was integrated into medicine, since the Faculty of Medicine makes

Behbehani

Table 1 (continued)

Table 1 (continued)

b Preclinical program

c Dental clinical educational program

Depart- Course Course ment No. Year 2, semester 2 302 Anatomy 302 Behavioral Science 302 Biochemistry 302 Physiology

CH

6 2 4 4 16

Year 3, semester 1 303 Anatomy 303 Behavioral Science 303 Biochemistry 303 Physiology

6 2 4 4 16

Year 3, semester 2 304D Anatomy 304 Behavioral Science 304 Biochemistry 304 Physiology

6 2 4 4 16

Year 4, semester 1 400 Pathology 400D Microbiology/Oral Microbiology 400 Pharmacology 400D Neuroscience/Oral Neuroscience

4 4 3 3 14

Year 4, semester 2 401D Oral and Systemic Pathology 401 Pharmacology 401D Neuroscience/Oral Neuroscience 10 411 Dental Biomaterials 30 431 Preclinical Oral and Maxillofacial Radiology 40 441 Dental Anatomy and Function 40 442 Preclinical Operative Dentistry and Cariology 40 443 Preclinical Removable Prosthodontics

4 3 3 2 2 2 4 2

Depart- Course Course ment No. Year 5, semester 1 20 521 Pediatric Dentistry I 20 522 Orthodontics I 30 531 Oral and Maxillofacial Radiology I 30 532 Principles in Medicine I 40 541 Prosthodontics I (Fixed) 40 542 Prosthodontics II (Removable) 40 543 Endodontics I 50 551 Periodontology I 50 552 Oral and Maxillofacial Surgery I 00 501 Comprehensive Dental Care I1

84

The grand total credit hours for the Bachelor of Medical Sciences (BMedSc) degree in the dental program is 132, comprising 48 CH in the preprofessional program and 84 CH in the preclinical program.

The grand total credit hours for the Bachelor of Dental Medicine (BDM) degree is 236 CH comprising 48 CH in the preprofessional program, 84 CH in the preclinical program and 104 CH in the dental clinical educational program. Departments in the Faculty of Dentistry (Faculty No. 12) as referred to in this Major Sheet: Department of Bioclinical Sciences (BCS) = No. 10, Department of Developmental and Preventive Sciences (DPS) = No. 20, Department of Diagnostic Sciences (DS) = No. 30, Department of Restorative Sciences (RS) = No. 40, Department of Surgical Sciences (SS) = No. 50, Nondepartmental activities coordinated by the Vice-Deans = No. 00. 1 Coordinated by the Vice-Dean for Academic Affairs. 2 Coordinated by the Vice-Dean for Research. 3 Coordinated by the Vice-Dean for Research.

Dental Education in Kuwait

2 2 2 4 2 2 2 2 2 3 23

Year 5, semester 2 20 523 Dental Public Health I (Preventive Dentistry) 20 524 Pediatric Dentistry II 20 525 Orthodontics II 30 533 Principles in Medicine II 40 544 Prosthodontics III (Fixed) 40 545 Operative Dentistry 40 546 Endodontics II 50 553 Periodontology II 00 502 Comprehensive Dental Care II1

2 2 2 4 2 3 2 2 3 22

Year 6, semester 1 20 621 Pediatric Dentistry III 20 622 Dental Public Health II (Preventive Dentistry) 20 623 Dental Public Health III (Oral Epidemiology) 20 624 Orthodontics III 30 631 Principles in Medicine III 30 632 Oral Medicine and Clinical Oral Pathology I 40 641 Prosthodontics IV 50 651 Periodontology III 50 652 Oral and Maxillofacial Surgery II 00 601 Comprehensive Dental Care III1 00 602 Community Rotation I2

2 2 2 2 2 2 2 2 2 4 2 24

22 Total CH

CH

Year 6, semester 2 20 625 Dental Public Health IV 20 626 Pediatric Dentistry IV 30 633 Oral and Maxillofacial Radiology II 30 635 Oral Medicine and Clinical Oral Pathology II 40 642 Prosthodontics V 50 653 Oral and Maxillofacial Surgery III 00 603 Comprehensive Dental Care IV1 00 604 Community Rotation II2

2 2 2 2 3 2 7 2 22

Year 7, semester 1 00 701 Comprehensive Dental Care V1 00 702 Community Rotation III2 00 703 Elective Project Study3

8 3 2 13

Total CH

Med Princ Pract 2003;12(suppl 1):51–55

104

53

Table 2. The departmental structure of the Kuwait University

Faculty of Dentistry 1 The Department of Bioclinical Sciences Oral Biology Oral Neurosciences Oral Microbiology Biomaterial Science 2 The Department of Developmental and Preventive Sciences Dental Public Health Orthodontics Pediatric Dentistry 3 The Department of Diagnostic Sciences Oral Pathology/Medicine Oral and Maxillofacial Radiology General Medicine Temporomandibular Disorders 4 The Department of Restorative Sciences Dental Anatomy and Function Fixed/Removable Prosthodontics Operative Dentistry Endodontics Dental Materials 5 The Department of Surgical Sciences Periodontics Oral and Maxillofacial Surgery

Table 3. Basic principles of dental education

1 2 3 4 5 6

Didactic and clinical education integrated with medicine Competency-based curriculum Comprehensive patient care clinical education Emphasis on preventive dentistry and oral health promotion Evidence-based approach, outcome-based education Problem-solving methodology for treatment planning or case management 7 Promotion of ethical behavior and professionalism 8 Community-based learning 9 Lifelong learning

many pedagogical decisions for the core courses in the four faculties (Medicine, Dentistry, Pharmacy, and Allied Health Sciences and Nursing) of the Kuwait University Health Sciences Center (HSC). Dental students take the same preprofessional courses as other HSC students, plus the Introduction to the Dental Profession course in the 2nd year and an elaborate course in Principles in Medicine that is spread over the clinical years.

54

Med Princ Pract 2003;12(suppl 1):51–55

The community-based approach is introduced during the Introduction to the Dental Profession course and is emphasized in the Dental Public Health courses (II and III) during the first semester of the 6th year. Also in the 6th year, community rotations are arranged in cooperation with the Ministry of Health. As a future employer of our graduating dentists, the Ministry of Health plays an important role in the execution of the dental curriculum; several senior staff members of the Ministry of Health give lectures and supervise dental students in their community rotations and other extramural courses, while faculty members work 2 days a week in the Ministry of Health clinics. The community-based approach is also an integral part of some elective studies that require data collection from society and therefore rely on cooperation with community institutions. Comprehensive dental care education involves adult dental care. Contrary to the department-/discipline-based model where a patient consults various specialists, each of whom treat the specific problems that fall into his or her field of expertise, one ‘mentor’ supervises all the treatment procedures across discipline borders. Students learn to treat the whole patient rather than see the patient as separate disease states. Courses on comprehensive dental care start in the first semester of the 5th year and continue until the end of the program. In addition, treatment planning seminars that comprehensively integrate various aspects of different disciplines are conducted in the clinics during the clinical years. A competency-based curriculum lists the competencies to be achieved by the students by the end of the courses and uses an assessment system based on competency rather than clinical requirements for different treatment procedures. The courses in the clinical program are competency-based, and students must acquire competency in one area before moving on to the next. Preventive dentistry and oral health promotion are emphasized in many classes throughout the dental program, and treated in detail in two separate courses on Dental Public Health (I and II) during the 5th and 6th years. The evidence-based approach is used in several seminars that are part of traditional lecture courses as well as in comprehensive dental care clinical work. Students, patients, and colleagues can question the evidence presented, contrary to the traditional approach whereby no one questioned the experts. For an elective study project, students concentrate on the evidence-based approach and compile a comprehensive literature review. Students choose their topics, and advisors are nominated from the specific departments that specialize in those topics.

Behbehani

The problem-solving methodology for treatment planning is introduced during the students’ early exposure to patient clinics before the didactic clinical courses, as well as in the seminars about comprehensive dental treatment planning. Some studies have shown that problem-based learning is superior to traditional education [5, 6], but attempts to implement it in the dental program involved changing the teaching philosophy of the Faculty of Medicine. Therefore, the problem-based method is still not used very much, and lectures cover the bulk of didactic teaching. The importance of ethics and professionalism is promoted in the course on Dental Public Health (IV) and by mentors who act as role models in comprehensive dental care clinics. Finally, lifelong learning goals are adopted along with required computer literacy skills. Gathering information from the Internet is a major feature of all the courses, while elective studies concentrate on obtaining information from original publications rather than textbooks and reviews. The first Medline-based seminar is a part of the Introduction to the Dental Profession course. The dental curriculum at Kuwait University is unique in that the students are exposed at an early stage to the healthcare system in Kuwait, when they go on their first field visits during the Introduction to the Dental Profession course in the 2nd year. In fact, many practical training sessions take place in the national healthcare system, especially in the Kuwait School Health Programs where students implement preventive programs such as sealant and fluoride applications. Dentists from the Ministry of Health supervise students at the Ministry of Health dental

clinics in the three community rotation courses during the last 2 years of the program, and they also give lectures at the university. In addition, subjects such as Oral Health in Kuwait, Healthcare Policy in Kuwait, School Oral Health Programs in Kuwait, and Legal Issues of Dentistry in Kuwait are covered in the Dental Public Health course (IV). Such integration with the national healthcare system has been strongly recommended by the WHO, but few colleges in the world have been able to accomplish it.

Conclusions

By incorporating the latest trends in the dental and healthcare professions, the new 6.5-year dental curriculum at Kuwait University’s recently established Faculty of Dentistry aims to promote oral health in Kuwait through education and research as well as cooperation with healthcare institutions and the community. The program’s emphasis on community involvement early in the program and the Faculty’s close cooperation with the Ministry of Health make it unique to Kuwait. The curriculum was accepted in 2001 by the University Council, and it will be continuously scrutinized and revised as students proceed through the program in the coming years.

Acknowledgments I am grateful to all of my colleagues in the Faculty of Dentistry, who contributed so much to creating the dental curriculum for the Faculty of Dentistry, Kuwait University.

References 1 Hausen H: Oral Health Sciences Education: Relevance to the Community. Geneva, World Consultation on Oral Sciences Education, WHO Workshop, 1994. 2 Formicola AJ, McIntosh J, Marshall S, Albert D, Mitchell-Lewis D, Zabos GP, Garfield R: Population-based primary care and dental education: A new role for dental schools. J Dent Educ 1999;63:331–338.

Dental Education in Kuwait

3 Harden RM: Curriculum change and the assessment of clinical competence. Proc First GCC Conf Faculties of Medicine, Medical Education in the GCC Countries. Kuwait, Faculty of Medicine, Kuwait University, Health Sciences Centre, 1999, pp 169–178. 4 Slavkin HC: The future of clinical dentistry. J Dent Educ 1998;62:751–755.

5 Norman GR, Schmidt HG: The psychological basis of problem-based learning: A review of the evidence. Acad Med 1992;67:557–565. 6 Albanese MA, Mitchell S: Problem-based learning: A review of literature on its outcomes and implementation issues. Acad Med 1993; 68:52–81.

Med Princ Pract 2003;12(suppl 1):51–55

55

Evidence Based Practice in Dentistry Kuwait, October 2–4, 2001

Med Princ Pract 2003;12(suppl 1):56–60 DOI: 10.1159/000069844

Dental Education and Dentistry System in Iran Hamid Reza Pakshir School of Dental Medicine, Shiraz University of Medical Sciences, Shiraz, Iran

Key Words Dental education W Dentistry system W Iran

Abstract Before 1979, there were only 5 undergraduate dental schools in Iran with a total admission of 200 students per year, and only 2,000 dentists and about 50 specialists practicing in the country. Currently, there are 18 dental schools with a total admission of 750 undergraduate students, 5 postgraduate programs in 10 disciplines with a total of 100 students, more than 11,000 dentists (1 dentist per 5,500 population) and nearly 1,000 specialists in the country. Two new schools have recently begun offering specialty training courses in 2 disciplines. The length of the dentistry curriculum is 6 years. Students take general and basic science courses during the first 2 years, then continue on the predental and dental courses for the remaining 4 years. The curriculum has been revised over the past 20 years to establish intership and specialty programs and introduce courses reflecting current trends in the dental profession. Dental services in Iran are provided by both public and private sectors. Oral health care was integrated into the Public Health Care network by 1997, and 4 levels of a Dental Health Care Delivery System were established. The first level is concerned with primary prevention at ‘health houses’, where auxiliary health workers called ‘behvarzes’ provide periodic examinations, referrals, and oral health education. At the next level, oral hygienists and dentists in ‘health centers’ per-

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Fax + 41 61 306 12 34 E-Mail [email protected] www.karger.com

Accessible online at: www.karger.com/mpp

form basic oral health care services such as fillings, scaling, and extraction. At the third level, dentists manage and treat oral diseases in ‘urban health centers’, while the last level is for advanced treatment by specialists in university health centers in the cities. Copyright © 2003 S. Karger AG, Basel

Profile of the Country

The Islamic Republic of Iran, with an area of over 1,648,000 km2, is a vast region in southwest Asia and ranks 16th in the world in surface area. The country is divided into 28 provinces, 285 districts and over 66,000 villages. Based on the latest census, the population of Iran is estimated to be 60,550,000 with a density of 36.44/km2. The percentage of the total population residing in cities is 61.3%, while 38.44% live in rural areas. The annual growth rate in 2000 was 1.47%, with about 46% of the population under 14 years of age, 51.38% under 20, and 4.32% aged 65 years and older. Thus the population of Iran is regarded as one of the youngest in the world (table 1) [1, 2].

National Education System

Article 30 of the Constitution of the Islamic Republic of Iran states, ‘The government is duty-bound to prepare free education facilities for all people upon graduation

Hamid Reza Pakshir Orthodontic Department, School of Dental Medicine Shiraz University of Medical Sciences Shiraz (Iran) Tel. +98 711 6280456, Fax +98 711 6270325, E-Mail [email protected]

from high school. Higher education should be available to all aspirants as the self-sufficiency of the country prescribes’ [2]. The educational system of Iran consists of 1 year of preschool (5 years old), 5 years of primary school (6–11 years old), 3 years of guidance school (12–14 years old), 3 years of high school (15–17 years old), and 1 year of preuniversity programs (18 years old). To enter dental school, a student must have a secondary education diploma or a preuniversity certificate for higher education as well as a passing grade on the National University Entrance Examination. Of the nearly 500,000 preuniversity students in the experimental sciences who apply for higher education in medical universities each year, only about 700 enter dental schools [1, 2]. Another route to dental schools is available to oral hygienists who are selected from the local communities and trained for 3 years in special dental schools, during which they learn skills such as simple fillings, scaling and extraction. After 6 years of service in local rural communities and after passing the entrance examination at the end of their service, they may continue their education to obtain the degree of Doctor of Dental Surgery [1].

Profile of Dental Schools

As shown in table 2, before 1979 only 5 dental schools in 4 cities (2 in Tehran, and the other 3 in Shiraz, Isfahan and Mashad) offered undergraduate dental education to a total of 200 students each year, and only 2 schools offered postgraduate training in 5 disciplines. Currently there are 18 dental schools in Iran, with an annual total admission of 750 undergraduate and 100 postgraduate students. Four of the undergraduate schools offer training programs for dental assistants, with an annual total admission of 100 students, while 3 schools have training programs for dental technicians with the same number of admissions. In 1975, there were only 250 academic staff members working in 5 dental schools. By 1990, there were 400, and currently there are around 800 academic staff members working in different departments in all the schools (table 3). Approximately 700 new dentists graduate each year [3]. In addition to undergraduate programs, the 5 older dental schools, known as ‘mother schools’, now offer postgraduate programs in 10 disciplines. Recently, 2 new dental schools have also started postgraduate programs in 2 disciplines. Following the increase in the number of schools and academic staff, the annual number of post-

Dental Education in Iran

Table 1. Country profile of the Islamic Republic of Iran

Official name Official language Land area, km2 Number of provinces Number of districts Number of villages Population Density of population Annual population growth rate, % Population under 20 years, % Population 65 years and over, % Population/physician Population/dentist Population residing in cities, % Population residing in rural areas, %

The Islamic Republic of Iran Persian (Farsi), Turkish, other 1,648,000 28 285 over 66,000 60,550,000 36.44/km2 1.47 51.38 4.32 2,821 5,500 61 39

Table 2. Profile of Iranian dental schools

Dental schools Dental students (undergraduate) Dental students (postgraduate) Total admissions/year (undergraduate and postgraduate) Graduates/year Postgraduate programs Postgraduate disciplines Academic staff Schools for hygienists Schools for laboratory technicians

1979

2000

5 1,000 20

18 5,000 400

200 150 2 5 150 3 (1990) 2 (1990)

850 700 5–7 10–11 800 3 3

Table 3. Number of academic staff members in various departments of Iranian dental schools

Oral and maxillofacial surgery Oral and maxillofacial pathology Oral and maxillofacial radiology Oral medicine and diagnosis Pediatric dentistry Restorative and aesthetic dentistry Periodontics Prosthodontics (removable) Prosthodontics (fixed) Orthodontics Endodontics Total academic staff members in dental schools

Med Princ Pract 2003;12(suppl 1):56–60

88 27 32 48 71 96 99 63 87 92 90 793

57

Table 4. Dental school curriculum in the Islamic Republic of Iran

Stage 1 Year 1 Year 2 Stage 2 Year 3

Year 4 Years 5 and 6

General courses and a few basic sciences Advanced basic sciences Comprehensive examination Related medical courses such as Otolaryngology and Internal Medicine, and preclinical technique courses Completion of preclinical courses and start of clinical courses Pure clinical courses, community-based dentistry

Degrees offered: DMD, DDS.

graduate students admitted to the programs has increased from 30 to 100 students, and at the present time, around 400 postgraduate students are actively involved in the programs (table 2) [4].

Dental Education Program

The dental curriculum consists of 56 main subjects to be taken over 6 years, or 12 semesters. As shown in table 4, these courses are presented in two stages. In the first stage, which lasts 2 years, students complete a total of 68 credits: 24 credits for general courses and 44 credits for biomedical (basic) sciences. The general courses include: The Islamic Revolution and Its Origin (2), Computers (2), English language (9), Persian Language (3), Family Planning and Population Control (2), Physical Education (2), and History of Islam (4). The basic sciences include: General Pathology (6), Anatomy (6), Immunology (3), Human Histology (3), Biochemistry (5), Embryology (1), Physiology (6), Microbiology (4), Parasitology and Virology (2), Biophysics (2), Public Health (2), Genetics (2) and Psychology (2) [4]. The first stage includes a total of 925 contact hours, of which 568 h are lectures and 357 h are practical training (demonstration and laboratory work). At the end of the first 2 years, students take a comprehensive examination in the basic sciences. After successfully passing the courses in the first stage and the comprehensive examination, students take the predental (preclinical) and dental (clinical) courses in the second stage, which lasts for the remaining 4 years, or 8 semesters. The preclinical section in the second stage requires a total of 35 credits in the following courses: Oral

58

Med Princ Pract 2003;12(suppl 1):56–60

and Maxillofacial Pathology (6), Dental Anatomy (4), Internal Medicine (3), Psychiatry (1), Oral Biology (1), Oral and Dental Histology (3), Ear, Nose and Throat (1), Infection Control in Dentistry (1), Dental Emergency (1), Dental Materials (2), Pharmacology (2), Medical and Dental Terminology (4), Methodology in Medical Sciences (2), Nutrition and Oral Health (1), Medical Ethics (1), Medical Law (1) and Dental Instruments and Equipment (1). This part has a total of 680 contact hours, including 476 h for lectures and 204 h for practical training [4]. In the clinical part of the second stage, which is devoted purely to the dental sciences, students take a total of 115 theoretical and practical credits, including 661 h of lectures (approximately 40 credits) and 2,550 h (approximately 75 credits) for practical courses. The courses are: Orthodontics (7), Endodontics (10), Oral Diagnosis (8), Periodontology (7), Removable Partial Prosthodontics (8), Removable Full Denture (9), Fixed Prosthodontics (11), Oral and Maxillofacial Surgery (11), Restorative and Aesthetic Dentistry (9), Pedodontics (8), Oral Radiology (6), Community Dentistry (6), Comprehensive Dental Treatment (7) and the thesis (8) [4]. In summary, students should successfully pass a total of 218 credits in their 6-year training program as follows: (a) general courses, 24 credits; (b) basic sciences, 44 credits; (c) predental courses, 35 credits, and (d) dental courses, 115 credits. Finally, students submit a thesis to obtain the degree of Doctor of Dental Surgery. But before newly graduated dentists can practice, they must first fulfill certain commitments, such as 2 years of military service or service in deprived areas of the country, after which a license from the concerned ministry can be obtained [2]. The dental curriculum has been revised three times since 1982. The main objective of the first revision was to reduce the dental credits from 220 to 213 by omitting some general courses. In the second revision in 1988, small changes were made in the number of credits, but two major quality changes were also applied: the comprehensive examination was established at the end of the first stage, and an internship program was instituted in the last semester. Finally, the curriculum was changed dramatically in 1999 with the introduction of courses in Community-Based Education, Primary Dental Health Care, Hospital Dental Strategies and Assessment of Medical Emergencies [4]. The postgraduate dental program was also revised in 1999 to update specialty and subspecialty programs such as Maxillofacial Prosthesis, Laser Surgery, Orthognathic Surgery and Implants in Dentistry [3].

Pakshir

Oral and Dental Services

Background Dental services are provided by both public and private sectors. In cities, where 60% of the population resides, about 80% of dental services are provided by private practices, while in rural areas 70% of oral health services are delivered by the governmental sector [1]. After 1979, the Ministry of Health and Medical Education designed the health system based on the Primary Health Care (PHC) network. The Oral Health Department of the PHC network implemented a pilot project in 1995 and 1996 to integrate oral health care into public domains in 4 districts, and the Dental Health Care Delivery System (DHDS) was established. By 1997, the project had expanded all over the country and embraced the following objectives: (a) promotion of public awareness and improvement of community behavior in oral health, and (b) quantitative and qualitative improvements in delivering oral health care services [1]. Before discussing the levels of oral health care and the DHDS, it is worthwhile giving a brief description of the health network system. Health Care Delivery System In 1972, Iran collaborated with the World Health Organisation (WHO) to streamline health care delivery into 4 levels: health houses, health centers, urban centers, and district centers. A health house is the most basic rural facility, covering one or several villages and around 1,500 people. Each health house is staffed by a male and female auxiliary health worker, or ‘behvarz’, who offer PHC services to the population in the area. ‘Behvarzes’ are selected from among young and interested residents and are trained for 2 years at ‘behvarz’ training centers. At the present time, there are nearly 15,000 health houses and 30,000 ‘behvarzes’ in the villages, covering 85% of the rural population [1]. A rural health center is a village-based facility covering 1–5 health houses and approximately 2,500 people. It is staffed by a physician, several health technicians and administrative personnel. An urban health center has the same personnel as a rural health center and provides services to approximately 12,000 people. A district health center is a managerial planning and supervising entity, which supports the preventive and ambulatory health care systems in the district. The district hospital accepts referral cases from both the rural and urban health centers [1].

Dental Education in Iran

Table 5. The Dental Health Delivery System (DHDS)

Level

Trained professionals

Treatment

1

‘Behvarzes’

2

Oral hygienists

3

Dentists and dental nurses and technicians Specialists

Primary Health Care (PHC, primary prevention) health and treatment (secondary prevention) management and treatment (tertiary prevention) research and evaluation, implants, laser, maxillofacial prosthetics

4

Dental Health Delivery System The integration of oral health care into the PHC network was completed by 1997 and aimed to improve community behavior in oral health care. Four levels of the DHDS were established (table 5) [5]. The first level of the DHDS is concerned with primary prevention and designed to remove risk factors. ‘Behvarzes’ at the health houses are responsible for oral health education, periodic examination of teeth, and referrals to higher levels (rural and urban health centers). They also supervise sodium fluoride mouth rinsing in rural areas. In addition to ‘behvarzes’, school health workers and oral hygienists are also involved at this level [1, 5]. At the second level, which covers the early diagnosis and primary treatment of simple dental problems, oral hygienists and dentists in health centers supervise the ‘behvarzes’ in the health houses in their area. They also deliver primary oral health care services such as fillings, pulpotomies, extraction of infected roots, fluoride therapy and scaling [1, 5]. At the third level, or tertiary prevention level, dentists together with dental nurses and technicians are responsible for the management and treatment of dental and oral diseases in urban health centers and clinics. Finally, at the fourth level, advanced treatment is offered by specialists in different disciplines at university health centers in the cities. This specialized treatment will be transferred to district health centers when the required facilities and manpower are available [1, 5].

Oral Health Manpower

The number of dentists in Iran was estimated to be 2,000 before 1979. There are now more than 11,000 (66% men and 34% women), with 1 dentist for every 5,000–

Med Princ Pract 2003;12(suppl 1):56–60

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Table 6. Dental and oral health manpower in Iran

1990 Dentists 3,500 Population/dentist 15,000 Male dentists, % – Female dentists, % – Employed in public sector, % – Employed in private practices, % – Employed in universities, % – Employed in other selected occupations, % – Specialists 100 Hygienists 200 Laboratory technicians 170

2000 11,000 5,500 66 34 10 79 7.3 3.7 1,000 640 570

6,000 citizens, and the number is growing steadily as 700 new dentists graduate each year from dental schools [6]. Only 10% of dentists work in public services, 7.3% at universities and 3.7% in other selected occupations including the armed forces and industries, while the remaining 79% have private practices. Around 1,000 specialists work either in the universities or in private practices. During the past 10 years the number of oral hygienists and laboratory technicians has increased from 200 to around 650

and from 170 to 570, respectively. Finally, more than 30,000 ‘behvarzes’ offer PHC services, including oral health care, to the population in their areas (table 6) [7].

Conclusions

Both dental education and the dental profession in Iran have expanded considerably since 1979. The number of undergraduate schools increased from 5 to 18, and the number of postgraduate programs increased from 2 to 7, with a corresponding increase in enrollment from 200 to 850 students annually (750 undergraduate and 100 postgraduate students). In addition, 3 dental schools now offer programs to train dental nurses, oral hygienists and dental technicians. The dental curriculum has been revised 3 times since 1982 and was recently launched in all dental schools. The number of dentists has increased from 2,000 in 1979 to more than 11,000 in 2000, while the number of specialists has increased from around 50 practicing in the capital to nearly 1,000 all over the country. Oral health has been integrated into public health domains through the DHDS, which consists of 4 levels, from primary prevention through oral health education in the rural areas at the first level up to special types of treatment by specialists in the cities at the fourth level.

References 1 Country Report on Oral Health in the Islamic Republic of Iran. Ministry of Health and Medical Education, Undersecretary for Public Health, Oral Health Department, 2000. 2 Asia-Pacific Centre of Educational Innovation for Development. United Nations Educational, Scientific and Cultural Organization website. Available at: http://www.unescobkk.org/education/acid/higher-edu/Handbook/HB_Iran. htm.

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3 Revised Postgraduate Education Program. Ministry of Health and Medical Education, Curriculum-Planning Committee, 2001. 4 Dental Education Program in Dental Schools of the Islamic Republic of Iran. Ministry of Health and Medical Education, Council for Dental and Subdental Education. 1st ed., 2000.

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5 Sadr SJ: Dental education in Iran: A retrospective review for two decades (1978–1998). Beheshti Univ Dent J 2001;18:1–2. 6 WHO Oral Health Country/Area profile program. WHO collaborating centre website. Available at: http://www.whocollab.od.mah.se/ emro/iran/data/iranmanpow.html/. 7 Iran, General Information, Dental Workforce, Dental Education, FDI World Dental Federation website. Available at: http://www. fdi.org.uk/assets/pdf/informations/Iran.pdf.

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Evidence Based Practice in Dentistry Kuwait, October 2–4, 2001

Med Princ Pract 2003;12(suppl 1):61–64 DOI: 10.1159/000069847

Development of Oral Health in Africa Samuel J. Thorpe World Health Organization Regional Office for Africa, Harare, Zimbabwe

Key Words Poverty W Oral disease W Determinants W Strategy W Africa

Abstract Around 80% of African communities can be considered to be materially deprived. The presence of widespread poverty and underdevelopment in Africa means that communities are increasingly exposed to all of the major environmental determinants of oral disease. Previous approaches to oral health in Africa have failed to recognize the epidemiological priorities of the region or identify reliable and appropriate strategies to address them. Efforts have consisted of providing unplanned, ad hoc and spasmodic curative oral health services, which in most cases are poorly distributed and only reach affluent or urban communities. Realizing the limited impact of existing strategies, the World Health Organization Regional Office for Africa (WHO/AFRO) developed a regional oral health strategy to assist African countries and their partners in identifying priorities and planning preventive-oriented programmes, particularly at the district level. The long-term objective is to provide equitable and universal access to cost-effective quality oral healthcare and thereby significantly reduce the incidence of oral diseases in Africa. Copyright © 2003 S. Karger AG, Basel

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Introduction

According to the United Nations, 32 African countries are among the world’s 48 least developed nations, and 80% of the people in the region fall into the low socioeconomic category [1]. Where affluence does occur, it is limited to a small urban elite whose lifestyles are similar to those in industrialized countries. The severe lack of financial and technical resources has had a direct impact on the health of the population, and while progress is being made on a number of health-related issues in Africa, the health situation in the region gives cause for concern. The main causes of illness and death of children who survive the neonatal period include diarrhoea, acute respiratory infections, malaria, measles alone and in combination, and malnutrition. For women, the main causes of illness and death include complications associated with childbirth. For men and women, they include communicable diseases such as malaria, tuberculosis, and human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS). All of these diseases are often aggravated by emergencies and disasters such as armed conflicts, drought and famine, as well as inadequate access to safe water, sanitation, nutritious foods, essential drugs, primary and secondary education, and family planning. In addition, noncommunicable diseases are emerging in Africa, especially diabetes and hypertension, due to an increase in their associated risk factors (cigarette smoking, use of alcohol, obesity and sedentary lifestyles). The presence of widespread poverty and underdevelopment in Africa means that communities are also exposed to all of the major environmental determinants of oral disease.

Dr. Samuel J. Thorpe Regional Advisor Oral Health, WHO Regional Office for Africa PO Box BE 773, Belvedere, Harare (Zimbabwe) Tel. +263 4 706951/705043, ext. 9366, or +1 321 7339366, Fax +1 321 7339009 E-Mail [email protected]

Current Oral Health Situation in Africa

Dental caries and periodontal diseases are generally considered to be major oral health problems around the world. In African countries, however, they appear to be neither as common nor as severe as in the developed world. The profile of oral disease is not homogenous across Africa, with health indicators varying among countries and across groups within countries. Therefore each community needs to be individually assessed in terms of the basic epidemiological criteria of prevalence, severity (morbidity and mortality), and age-adjusted distribution in the population. Based on this form of analysis, the most severe oral health problems in Africa amongst low socioeconomic communities include cancrum oris (NOMA), acute necrotising gingivitis (ANUG), oral cancer, oral manifestations of HIV/AIDS, facial trauma, and lastly dental caries. NOMA and the associated ANUG are still common among children in Africa. The most recent figure for the annual incidence of NOMA is 20 cases per 100,000 children aged 3–6 years. There are about 140,000 cases of NOMA each year, and tragically about 90% of these children die without receiving any care. NOMA flourishes where poverty is greatest, nutrition is poorest, and general and oral hygiene are neglected. As poverty increases and many children remain malnourished or undernourished with compromised immune systems, the prevalence of conditions such as NOMA is likely to increase [2, 3–6]. The prevalence of oral cancer is also on the increase in Africa. In developing countries, the incidence of oral and pharyngeal cancer is estimated to be 25 cases per 100,000 inhabitants. Rapid urbanization and the increasing use of tobacco and alcohol are considered to greatly increase the incidence of oral precancer [7, 8]. Africa has the highest prevalence of HIV and AIDS infections in the world. Studies have shown that oral manifestations of HIV/AIDS are very widespread, and most commonly include fungal infections such as those caused by candida, necrotizing gingivitis or oral hairy leukoplakia. In a study conducted in South Africa in 1995, 74.4% of HIV-infected patients presented with one or more oral mucosal lesions [8–10]. Maxillo-facial trauma has increased in many countries as a result of interpersonal violence, motor vehicle accidents, and war. Chronic destructive periodontal disease is known to occur in a small proportion of most populations, regardless of location or socioeconomic status [11]. Harmful practices, such as the removal of tooth germs of deciduous canines, extraction of upper and lower anterior

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teeth, and the trimming or sharpening of upper anterior teeth, still prevail in Africa [5]. Fluorosis, which is more likely to occur in malnourished children, is very common in certain parts of Africa such as the Rift Valley area of East Africa [12]. Edentulism, congenital malformations and benign tumors occur, but little prevalence data is available. According to national surveys and smaller studies the prevalence of dental caries is quite low in Africa, but there are substantial regional variations. Data on dental caries prevalence (DMFT) in children aged 12 years, available in AFRO from 39 sub-Saharan countries, show that 13 countries (33%) have a very low DMFT (0.0–1.1), 19 countries (44%) have a low DMFT (1.2–2.6), and 7 (23%) have a moderate DMFT (2.7–4.4). About 90% of these cases represent untreated caries and the inadequacy of current oral health systems to address the problem. The situation is completely different, for example, in some Latin American countries where the DMFT among 12year-olds ranges from high to very high (5–8) [8, 12–14].

Determinants of Oral Health Problems in Africa

Poverty is arguably the most important determinant of health and ill-health. The presence of widespread poverty and underdevelopment in Africa exposes communities to all of the major environmental determinants of oral disease. In a continent where the majority of the population is desperately poor, preventable oral diseases such as NOMA and oral cancer are rife. In addition, increasing urbanization has been shown to lead to observable increases in the prevalence of oral disease, and high levels of bottle feeding in cities have been associated with high rates of baby bottle tooth decay. Greater access to alcohol is associated with higher levels of interpersonal trauma and oral cancer. The African region also faces an acute lack of recent, reliable and comparable data, as well as processes for converting data into information for planning.

Previous Approaches and the Response of the World Health Organization

Previous approaches to improving oral health in Africa have been modelled on those of affluent countries and have therefore failed to recognize the epidemiological priorities of the region and identify reliable and appropriate strategies to address them. Efforts have consisted of

Thorpe

providing unplanned, ad hoc and spasmodic curative oral health services, which in most cases are poorly distributed and reach only affluent or urban communities [5, 8, 15]. The main problems can be traced to the following: E lack of national oral health policies and plans, E inappropriately trained dentists, E services that benefit only affluent and urban communities, E services that are almost entirely curative, E lack of equipment and materials, supplies, and maintenance [16]. A successful approach to oral health in the region needs to take these circumstances into account in order to effectively address the real determinants of oral disease. Prevention-oriented services need to be properly planned, administered, and evaluated, especially those that relate to participatory health education and oral health promotion. The community should be involved in identifying oral health problems, needs and interventions, and the proper balance between personnel types and population needs should be maintained. At its 48th session in September 1998, the World Health Organization/Regional Office for Africa (WHO/ AFRO) adopted an oral health strategy for Africa for the period 1999–2008 that would assist countries in identifying priorities and planning viable programmes. The long-term vision is that all people of the region should enjoy improved levels of oral health through the realization of the following objectives: E a significant reduction of all oral diseases in the region, E equitable access to cost-effective quality oral healthcare, E the adoption of healthy lifestyles [16]. To guide and sustain the effective implementation of this strategy, the following principles were adopted: E The promotion of oral health and the prevention of oral diseases should be given high priority. E Oral health interventions should be focused on the district and its communities. E Interventions which have proven efficacy should be used. E Oral health should be integrated into all public healthcare programmes. E Communities should participate in oral health activities. To focus the limited resources more effectively on these various priorities, the following five strategic orientations have been identified:

1 Advocacy and social mobilization: using social marketing and participatory methods to mobilise support for oral health. 2 Capacity building: developing human resources through appropriate training and retraining programmes. 3 Information, education and communication: providing appropriate information to individuals, families and communities for healthy oral health lifestyles. 4 Equitable access to quality oral health services: achieving greater equity in oral health services, particularly for rural, peri-urban and underserved communities. 5 Promotion of operational research: developing a research culture in order to encourage essential research on oral health problems and needs [16].

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Partnership and Coordination

The district health management team has the primary responsibility for implementing these programmes, strategies and interventions. In order to facilitate the implementation of oral health activities and mobilise resources, partners are being identified and a wide network of interested parties is being established. Partnerships between community interest groups and health and development workers are instrumental for the successful operation of district oral health plans. At the national level, partners include professionals in commerce, industry, dentistry, medicine and allied fields, as well as professional associations, NGOs, aid agencies, WHO and other UN agencies. At the regional level, countries exchange information about their experiences in implementing oral health programmes, in the spirit of Technical Cooperation among Developing Countries (TCDC). In addition, WHO collaborating centres for oral health in the region provide expertise and resources, particularly in the areas of capacity building and research promotion [16]. Coordination among partners is crucial for the implementation of oral health programmes and extends well beyond the mere sharing of information. Where a provincial organizational level exists in a country, it has the responsibility to support district health activities and coordinate programmes that cross district boundaries, providing the link between district and national levels of activity. The provincial level helps districts with the coordination of tender processes, data collection and analysis, planning processes and resource allocation. The national level is responsible for overall coordination, as opposed to programme or service delivery, and must be properly

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equipped for this role. At the regional level, coordination is carried out by the Division of Noncommunicable Diseases, in collaboration with existing WHO structures and governing bodies [16].

Conclusion

A new way of interpreting and responding to oral health problems in Africa is long overdue. It should begin with a systematic interpretation of oral health information through the application of basic epidemiological principles at the most local level possible. Taking the unique context of each community into consideration, strategies must be built that address the social, economic

and environmental circumstances that put communities at risk of ill-health, in order to limit or eradicate known determinants of oral ill-health and disease. To this end, WHO/AFRO has designed preventive programmes and new intervention strategies that aim to provide equitable and universal access to quality oral health services through the district health system. It is quite clear that the successful delivery of interventions that are affordable and effective in improving community oral health depends on the degree to which they can be integrated with general health services, and the extent to which the political, economic and professional powers that govern decision-making in health and development sectors are involved.

References 1 World Bank: World Development Report 1994. World Bank. 2 Contreras A, Falkler AW Jr Enwonwu CO, Idigbe EO, Savage KO, Afolabi MB, Onwujekwe D, Rams TE, Slots J: Human Herpesviridae in acute necrotizing ulcerative gingivitis in children in Nigeria. Oral Micrbiol Immunol 1997;12:259–265. 3 Enwonwu CO: Review of oral diseases in Africa and the influence of socioeconomic factors. Int Dent J 1981;31:29–38. 4 Enwonwu CO: Infectious oral necrosis (cancrum oris) in Nigerian children: A review. Community Dent Oral Epidemiol 1985;13: 190–194. 5 Enwonwu CO: Societal expectations of oral health: Response of the dental care system in Africa. J Publ Hlth Dent 1988;80:84–93. 6 Enwonwu CO: Noma: A neglected scourge of children in sub-Saharan Africa. Bull Wld Hlth Org 1995;73:541–545.

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7 Hille JJ, Shear M, Sitas F: Age standardized incidence rates of oral cancer in South Africa, 1988–1991. J Dent Assoc S Afr 1996;51:771– 776. 8 Hobdell MH, Thorpe SJ: Oral health in Africa: where are we now and why is there inequity? Proceedings of the joint CDA/WHO workshop; in Myburgh NG (ed): Promoting Equity in Oral Health. Cape Town, Faculty of Dentistry and WHO Collaborating Centre, University of the Western Cape, 1996. 9 Arendorf T, Sauer G, Bredenkamp B, Cloete C: Guidelines for the Diagnosis and Management of Oral Manifestations of HIV Infection and AIDS. Cape Town, Faculty of Dentistry and WHO Collaborating Centre, University of the Western Cape, 1997. 10 Tukutuku K, Muyembe-Tamfum L, Kayembe K, Kandi K, Ntumba M: Oral manifestations of AIDS in a heterosexual population in a Zaire hospital. J Oral Pathol Med 1990;19:232–234.

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11 Cuttress TW: Periodontal health and periodontal disease in young people: Global epidemiology. Int Dent J 1986;36:146–152. 12 Manji F, Mosha H, Frencken J: Tooth and surface patterns of dental caries in 12-year-old children in East Africa. Community Dent Oral Epidemiol 1986;14:99–103. 13 Manji F, Baelum V, Fejerskov O: Dental fluorosis in an area of Kenya with 2 ppm fluoride in drinking water. J Dent Res 1986;65:659–662. 14 Fejerskov O, Manji F, Baelum V: The nature and mechanisms of dental flurosis in man. J Dent Res 1990;69:692–700. 15 Thorpe SJ: A Regional Overview of Oral Health Services in Africa. Proceedings of the Medic Africa 1995 workshop on oral health policy; in Myburgh NG (ed): Future Directions for Oral Health in South Africa. Cape Town, Faculty of Dentistry and WHO Collaborating Centre, University of the Western Cape, 1995. 16 World Health Organization, Regional Office for Africa: Oral Health in the African Region: A Region Strategy (1999–2008), 1998.

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Author Index

Behbehani, J.M 1, 51 Elderton, R.J. 12 Honkala, E. 1 Omar, R. 33 Pakshir, H.R. 56

Reibel, J. 22 Spencer, A.J. 3 Thesleff, I. 43 Thorpe, S.J. 61 Tummers, M. 43

Subject Index

Africa 61 Bioengineering 43 Community-based learning 51 Comprehensive dental care 51 Dental caries 12 – curriculum 51 – education 51, 56 – practice 12 – treatment 12 Dentin 43 Dentistry system 56 Determinants, oral disease 61 Enamel 43 Evidence-based approach, dental education 51 – oral disease prevention 3 – dentistry 12 – practice 33

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Iran 56 Limiting treatment goals 33 Oral disease(s) 3, 61 – health 22 Periodontal diseases 12 – ligament 43 Poverty 61 Progenitor cells, bone/tooth development 43 Prosthetic dentistry 33 Repeat dental restorations 12 – restoration cycle 12 Shortened dental arch 33 Smoking 22 Stem cells 43 Strategy, oral health 61 Tobacco 22