Proceedings of the International Conference on Evidence Based Practice in Dentistry pptx

The prevention of oral diseases caused by smoking is empha-sized in a review of the documented harmful effects ofsmoking on oral health; it is proposed that dentists shouldmake time duri

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Proceedings of the International Conference on

Evidence Based Practice

in Dentistry

Kuwait, October 2–4, 2001

Faculty of Dentistry, Health Sciences Centre, Kuwait University

21 figures, 6 in color, 14 tables, 2003

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Medical and Scientific Publishers

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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

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Evidence Based Practice in Dentistry

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

Dentis-try, Kuwait University, October 2–4, 2001 The

confer-ence provided an ideal opportunity to exchange ideas and

discuss new developments in the field of dentistry,

espe-cially the latest trends in the evidence-based approach to

dental care As the former President of Kuwait

Universi-ty, 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

re-evaluation, and the evidence must be weighed according

to the strengths and weaknesses of the scientific methods

applied.’

The evidence-based approach has been widely

dis-cussed in various healthcare fields and has influenced

teaching throughout the world With its emphasis on

pre-vention and its use of previous, analogous evidence to

design treatment plans, the evidence-based approach

dif-fers fundamentally from traditional methods of

interven-tion, which focus on clinical outcomes The stages of the

approach, including the synthesis and assessment of

evi-dence, 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

‘re-peat 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-sized in a review of the documented harmful effects ofsmoking on oral health; it is proposed that dentists shouldmake time during office visits to counsel patients on theseeffects and guide them through smoking cessation pro-grams

As research in the field of dentistry develops andexpands and the evidence-based approach gains wide-spread acceptance, traditional treatments are steadily giv-ing way to new strategies of managing oral health issues Aclear move away from tradition is discussed in an articledevoted to treatment planning for older, partially dentatepatients It is proposed that the usual method of totaltooth replacement is not necessary, and the targeted

‘shortened dental arch’ is more effective and gives a highlevel of patient satisfaction Exciting new research onstem cells and tissue regeneration indicate a distant buthopeful possibility to grow new teeth to solve the ever-present problems of dental caries and periodontal dis-ease

The second theme of the conference was ‘The ment of Dental Education and Oral Health,’ with aregional emphasis The dental curricula of schools in twoGulf countries, Kuwait and Iran, are presented in thissupplement, as is the issue of community health in Africa.The dental curriculum at Kuwait University’s newly es-tablished Faculty of Dentistry aims to promote oral health

Develop-in Kuwait through education, research and communityinvolvement It incorporates recent trends in healthcare,including the evidence-based approach which has become

an important component of comprehensive dental careclinical work In Iran, many new dental schools have beenestablished over the past 20 years, offering both under-

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graduate and postgraduate training programs The

num-ber of dentists and specialists in Iran is steadily

increas-ing, and just recently dental services have been

incorpo-rated into the public healthcare system Efforts are also

underway in Africa to integrate oral health programs into

general health services, through the technical and

finan-cial support of WHO/AFRO It is hoped that such

pre-ventive programs and new intervention strategies will

improve the level of oral health in many African

coun-tries

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

promo-tion 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

professionals and researchers from around the world, and

we look forward to another successful conference in cember, 2003

De-We would like to express the Conference OrganisingCommittee’s gratitude to Kuwait University for its con-tinued support of our conferences, and the AdvancedTechnology Company for the financial support of this

conference We are also indebted to the Medical

Princi-ples and Practice Editor-in-Chief, Professor Farida

Al-Awadi, and Editor, Professor Azu Owunwanne, for theirhelp, strong support and commitment to publish this sup-plement Lastly, we would like to personally thank theauthors for their participation, contributions and cooper-ation

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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

Prof A John Spencer

Key Words

Evidence-basedW PreventionW 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

ap-proach to the prevention of oral disease, to examine the

assessment of clinical trial evidence, to examine

emerg-ing approaches to assessemerg-ing population-wide

interven-tions 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

understand-ing to the burden of oral disease and its determinants,

rather than a consideration of the efficacy or

effective-ness of interventions in clinical dental research A

sys-tematic 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

reassess-ment 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

creates a substantial challenge which can only be met byincreased research activity, improved quality of informa-tion and the appropriate application of the outcomes ofresearch to policy making for the prevention of oral dis-ease

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 itmeans, whether it is feasible, how to conduct it and theoutcome of its use are not well understood The evidence-based approach to the prevention of oral disease relies onknowledge of the effectiveness of identical, similar, oranalogous interventions usually carried out and evaluated

in a different setting at a different time Toward the end ofthe 1990s some journals published systematic reviewsand meta-analyses, or evidence-bases, using quantitativescientific methods and consulting scholars around theworld about specific methods of appraising and quantify-ing the benefits and risks of interventions However, itwas found that outside a few areas of health care, clinicaltrial evidence is scarce, particularly in many areas of den-tistry Many everyday decisions on health care, includingprevention of oral diseases, are based on public healthprograms and policies founded on less scientific evidence

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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

evidence-based approach and a range of old and new methods for

the assessment of evidence seem to be gaining greater

clar-ity This paper provides an overview of the

evidence-based approach to prevention, and points out some of the

limitations to applying evidence to population-wide

inter-ventions 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

moni-tored 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,

as presented in figure 1 Each aspect of this evidence loopfor the prevention of oral diseases is necessary for sounddecisions on either an individual or population level Fol-lowing the various stages ensures that resources are notused to address less important problems or alter less sig-nificant determinants, and that preventive interventionsare not maintained beyond their useful life should theburden of disease alter The loop also recognizes thatsome interventions might work less satisfactorily in dif-ferent contexts

Burden of Oral Disease

In the evidence loop the problem is first identified,defined and prioritized through information on the bur-den of oral disease, which is the assessment of the magni-tude and impact of oral health problems among patients

or populations To design the appropriate intervention,determinants of the disease are delineated and the level ofavoidable disease is assessed – i.e how much of the dis-ease is due to mutable risk factors and what proportion ofthe burden of disease is avoidable

Numerous ways exist to measure the burden of ease Summary health measures such as Disability-Ad-justed Life Years (DALYs) provide a common metric.The DALY was first used in a comprehensive assess-ment of the global burden of disease and injury in 1990

dis-by the World Bank [1] and has been adopted dis-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

dis-ease ranked in a group of disdis-eases/disorders that are

con-sidered 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

middle-aged adults experienced more years of life lived with

dis-ability from dental caries than did older adults, while

the years of life lived with disability from periodontal

dis-ease were distributed among middle-aged adult groups

The main challenge of using summary health measures

is ensuring that the burden of disease is appropriately

esti-mated, 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

dis-eases (dental caries and periodontal disease) at previously

affected sites Furthermore, the estimates for the amount

of disability associated with each oral disease need

scruti-ny The summary health measures cited above apply a

sys-tem of averaged levels of disability, handicap, mental

well-being, 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],

indi-cating 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

weight-ings 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 oraldiseases of greater burden that should be considered astargets for prevention [6]

An evidence-based approach to prevention, therefore,requires knowledge of the relative burden of disease asso-ciated with particular oral diseases at different stages oflife and the proportion of that burden of disease that isavoidable given associations with mutable determinants

of disease

Determinants of Oral Disease

Preventive programs should be based on conceptualand empirical evidence of the determinants of variation

in oral disease among patients or population groups inorder to identify more points of intervention in the pre-vention of oral disease The conceptual model illustrated

in figure 2 identifies three discrete yet closely interrelatedstages or levels of determinants: upstream, midstream,and downstream [7]

Upstream level factors: The framework identifies cial, physical, economic and environmental factors asbeing the most fundamental determinants of oral health.These include a range of interrelated factors such as edu-cation, employment, occupation, working conditions, in-come, housing, and area of residence The framework alsoindicates that these fundamental determinants are them-selves influenced by even more upstream factors, namely,government policies, globalisation, and culture

so-Midstream level factors: Social, physical, economicand environmental contexts throughout life influencehealth either indirectly via psychosocial processes anddental health behaviours, or more directly, for examplevia injuries The dental care system also plays some part

in determining oral health within a society However, itplays 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 Thepoorer health profile of some patients or population sub-groups is due in part to longer-term adverse physiologicaland biological changes that are brought about by poorerpsychosocial health and more harmful dental health be-haviours

The concept of ‘avoidable oral disease’ is based on anunderstanding of these wider determinants for most oraldiseases and the evidence-base for the effectiveness ofpossible interventions Three issues at the centre of newapproaches to prevention are multifactorial causes ofchronic (including oral) disease, shared risk factors, andlife 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

pre-ventive factors accumulate and interact over a lifetime in

a dynamic process The principles, approaches and

mes-sages of health promotion (e.g empowerment, equity,

health literacy, healthy behaviours, supportive

environ-ments) and specific preventive interventions are relevant

throughout a lifetime, but each life stage also has unique

contextual and behavioural aspects, and therefore

partic-ular strategies to reduce risk factors and strengthen

pre-vention are needed

Integrated models are emerging that address the

con-tinuum 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

dis-tributed across different target groups: the well

popula-tion, 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-vention, the evidence-base on different interventions is akey component of the support systems

Synthesis of the Evidence-Base for Preventive Interventions and Decision-Making

The evidence-based approach makes use of evaluativeresearch on the effects of an intervention to determine thelikely benefits or adverse consequences of intervention forparticular individuals or populations When possible, evi-dence of beneficial outcomes, rather than biological plau-sibility or anticipated effects, is used [9] Evidence of ben-efits is derived predominantly from epidemiologic re-search, which provides quantitative estimates of efficacy

or effectiveness Summary estimates of effectiveness aregenerated by a critical review of research data from two ormore studies using systematic review methods [10] Sub-group analyses may be used to identify characteristics ofpeople for whom an intervention is most or least effec-tive

The starting point for the traditional evidence-basedapproach, therefore, is the searching for and collation ofthe scientific evidence on a given intervention Questionsconcerning the intervention should be considered careful-

ly and in detail Narrow rather than broad questions assistthe systematic review of evidence, but the question muststill be likely to support practical and potentially usefulinterventions given favourable evidence

Considerable emphasis is placed on the transparencyand reproducibility of the literature search Finding stud-ies 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

dupli-cate publications and accessing the ‘grey literature’ such

as conference proceedings, reports, theses and

unpub-lished 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

re-search appraised Numerous guides are available to assist

the process of abstracting information from selected

stud-ies 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

reason-ably 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:

support a decision on whether or not to implement anintervention?

the preventive intervention [12]?

The level of evidence indicates the validity of

evalua-tive research and takes into account the design of thestudy, its potential for eliminating bias, and the methodsand analysis used [13] An example of a classification ofthe level of evidence based on study design is presented intable 1

As an illustration, we will apply the three tioned assessment issues (strength of evidence, size of theeffect, and relevance) to the evidence-base for an oralhealth preventive intervention: fissure sealants performed

above-men-in a clabove-men-inic-based dental program for school children sure sealants have been the subject of much clinical trialresearch The level of evidence is high because the clinicalintervention can be randomly assigned to either children

Fis-or one of a contralateral pair of teeth, eliminating biasand, with appropriate statistical testing, chance from out-comes

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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, case- control 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

sig-nificant reductions in dental caries increment Other

research has highlighted the intriguing potential for

seal-ants to prevent caries on adjacent non-sealed surfaces,

indicating that the effect may be larger than the

pre-vention 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

Reten-tion is not the same as caries prevenReten-tion [16]

In this example, it should be pointed out that different

studies may have used different measures of effect

Clear-ly, 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

evidence-base or excluding it Furthermore, the quality of

individu-al 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-ment, most systematic reviews are based on quality scoresgiven by two or more individuals The level of agreementamong assessors needs to be reported

After the research is appraised, the next stage is thesynthesis, or pooling, of the evidence While this mighttake a qualitative approach with some overview state-ment, most often quantitative methods like meta-analysisare used Meta-analysis relies upon the similarity of stud-ies and increases the power and generalizability of effects.Analyses vary depending on the type of effect measure-ment used (binary or continuous) and whether it is inde-pendent or paired (as in many fissure sealant trials), aswell as on the sensitivity of the analysis and the potentialfor publication bias Sensitivity can be tested by analysingstudies that are rated at different levels of evidence sepa-rately and comparing results Another way to test sensitiv-ity is to categorize by quality score those studies that fallwithin a single level of evidence; this way, studies in dif-ferent categories of quality score can be analyzed sepa-rately, or studies in lower quality categories sequentiallyadded to the analysis and the results compared A number

of discrete approaches exist to examining publication biasincluding funnel plots and regression asymmetry

Once the evidence is synthesized, decisions must bemade about how to apply the evidence, taking into consid-eration the transferability of outcomes to patients or pop-ulation groups and the predicted effects of implementingthe intervention With regard to transferability, both thebeneficial and harmful effects of an intervention need to

be considered in the collective group of patients and ferent subgroups among those patients Baseline risk ofdisease must also be taken into account To apply the evi-dence to individuals, absolute benefits in target popula-tions are predicted, and it is decided whether predictedbenefits outweigh any predicted harm

dif-While some guides to synthesis and decision-makingend here, the evidence-based approach to the prevention

of oral diseases includes a number of other importantissues, such as considerations of efficiency, public percep-tions and side effects Efficiency is determined by the rela-tionship between the resources used and the outcome; itincludes economic analyses such as cost-effectiveness orcost-benefit analyses These techniques are also importantaspects of the evidence-base for prevention [17] Percep-tions of the public and side effects are covered briefly inlater sections

Implementation, Monitoring and Reassessment

Once a decision on the appropriate oral health ventive intervention has been made, based either on a sys-

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pre-tematic review of randomized clinical trials or an

assess-ment of observational studies, the intervention is

imple-mented The last stage of the evidence loop is the

monitor-ing 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

ac-knowledged, 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

contin-ue 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

ap-praisal and application of evidence for preventive

inter-ventions have come under scrutiny [18, 19] Most public

health, population-wide preventive interventions are

pro-grammatic 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

ob-servational research is considered to be of a lower level

because of its potential for bias However, this

devalua-tion of observadevalua-tional 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

random-ized clinical trial takes place over a shorter period,

possi-bly masking either a decrease in efficacy over the longer

term or the emergence of side effects

These difficulties with the accepted hierarchy of

evi-dence are illustrated by the issue of water fluoridation

While cluster randomized controlled trials of water

fluori-dation could be designed in theory, studies of this type are

unknown Instead, evidence on water fluoridation is

gen-erally derived from observational studies of discrete

geo-graphic 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

the number of studies, the level of evidence should beregarded as higher than that indicated by their studydesign alone [23]

Another interesting evidence issue illustrated by thecase of water fluoridation is the public’s perception of theintervention An intervention will only be implemented ifthere is general public support for its application Despitethe successful implementation of water fluoridation pro-grams in many countries, the public still does not knowmuch about it and expresses occasional concern about itssafety, while a sizeable minority of the population may beundecided or opposed to it [24, 25] Therefore, public per-ception may assist or impede the implementation of anevidenced-based preventive intervention, ultimately de-termining whether the community will benefit from themeasure

Evidence Issues in Oral Health Promotion

Health promotion programs which aim to improveoral health often promote a mix of interventions, or a

‘portfolio’ [19] These may be effective, but they do not fitwell the requirements for evidence of effectiveness Alsoimportant is the context or setting of interventions andhow it may shape the outcome

For example, an oral health promotion program might

be built around existing ‘healthy’ baby activities such asantenatal and parent education and well-baby and immu-nization checks [26, 27] There is an emerging interest inthis oral health promotion opportunity, but little researchhas been conducted [28] Interventions may be adoptedthat are a combination of approaches that represent cur-rent ‘best practice’ in health education, behaviouralchange, avoidance of common risk factors, and monitor-ing of health care providers Recent reviews of health pro-motion for oral health have evaluated such oral healthpromotion interventions and adjusted the thresholds forlevels of evidence, specifically including expert opinionand influential reports as a low but acceptable level of evi-dence They also weighed the revised levels of evidenceagainst the potential benefit for oral health [23] Thepotential benefit can be classified as one of the following:

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A practical guide for decision-makers to use in

select-ing a portfolio or mix of interventions for oral health

motion has recently been proposed as part of health

pro-motion planning and practice improvement [19] Unlike

the approaches required for scientific, quantitative

evi-dence, such frameworks hope to ensure that the best

avail-able 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:

interven-tions;

necessary [19]

While such an approach uses the best evidence

avail-able, the disadvantages of these portfolios of

interven-tions are that they can never disentangle their component

effects, or might not be open to falsification

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

dis-eases 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

indi-vidual and population-wide preventive interventions

The key questions to be addressed about those

interven-tions focus on the beneficiaries, efficacy, efficiency, public

perceptions and side effects

A systematic review of the literature is a key nent of the evidence-based approach Guidance is avail-able for the searching, selecting, abstracting and apprais-ing, synthesis and decision-making on clinical trial evi-dence While these guidelines are readily applicable toclinical interventions, difficulties arise in the areas of pop-ulation-wide interventions and oral health promotion, asexemplified by the issue of water fluoridation where ran-domization is not feasible, but lower level evidence isavailable from community trials Further difficulties arise

compo-in the area of oral health promotion where portfolios ofinterventions are common More recently evidence-basedprocesses have emerged that are more appropriate forthese later situations

Regardless of the level of evidence or approaches to itsappraisal, the evidence loop is completed by implementa-tion, monitoring and reassessment Too frequently anintervention for which evidence has been found beneficial

is inadequately reassessed over time in target patients orpopulations, but without reassessment it is difficult todetermine the value and necessity of maintaining a givenintervention All of the stages of the evidence-basedapproach are very important and taken together, theyoffer a rational way forward to improve oral health anddental care

Acknowledgement

This paper is based on a presentation at the 7th World Congress

on Preventive Dentistry April 24–27, 2001, Beijing, China.

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Preventive (Evidence-Based) Approach

to Quality General Dental Care

Richard J Elderton

University of Bristol, Bristol, UK

Richard J Elderton, BDS, LDS RCS (Eng), PHD (Lond)

Key Words

Dental cariesW Dental practiceW Dental treatmentW

Evidence-based dentistryW Periodontal diseasesW Repeat

dental restorationsW 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

inva-sive dental treatments that are commonly provided fail

to address the fundamental bacterial nature of the

dis-eases Indeed, these treatments rather readily generate

and perpetuate a totally unacceptable chain of events

This chain embraces many shortcomings, which

them-selves nurture what may be described as the repeat

re-storative cycle The time has come to correct this

iniqui-ty Dental caries and periodontal diseases are dynamic

conditions which need ‘managing’ with a focused

cock-tail 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

restora-tive burden of dental services It is clear that dental

edu-cation and practice need to rise proactively to the

chal-lenge, or changes will be forced upon them while theyare in a defensive position There is a need to movewholeheartedly and contentedly into the preventive era

Introduction

Traditional restorative dentistry has had a strong fluence on dental education and practice in many parts ofthe world, and invasive restorative treatment has tended

in-to take precedence over non-invasive preventive sures It appears that many dentists erroneously presumethat dental caries can be ‘treated away’ with restorationsand that periodontal diseases can also be ‘treated away’ byregular scalings Indeed, many dentists seem to believethat traditional dental treatment automatically results inoral health [1]

mea-Dental caries and periodontal diseases, both bacterial

in nature, are largely preventable from the start But theyare not always prevented; rather, the forces leading to thediseases are allowed to remain out of balance with thosethat lead to health The situation prevails today wherebythe scientific basis of these diseases has largely been estab-lished [2, 3], but the services providing appropriate dentalcare to manage them remain out of date and fail to beproperly evidence-based

Thus, much of the profession appears still to be ded to the traditional invasive ‘treatment’ that fails toaddress the causes of the diseases When the diseasesoccur, there is a need for a real and responsible commit-ment by the dentist to help the patient revert to a disease-

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wed-free status by restoring the balance so that the forces

tend-ing to prevent the diseases outweigh the forces

contribut-ing to their progression

Caries

Caries is not simply a one-way process All carious

lesions involve both demineralisation and

remineralisa-tion 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

life-style 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

clini-cians would agree that when this stage of caries

develop-ment has been reached, it is necessary to excise the

dis-eased 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,

includ-ing 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

Fis-sure 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

profes-sion be managing caries?’ the answer has to be by

estab-lishing regimens with patients, such that the diseases are

arrested and prevented from recurring through

environ-mental and lifestyle measures (though backed up by

pro-cedures to restore form and function where appropriate)

It is essential that the regimens advised are tailored to the

individual, and that they are sympathetic to the al’s environmental and lifestyle characteristics

individu-Caries prevention works, so once a preventive phy prevails, then the whole attitude to invasive proce-dures changes Many carious lesions that would have beenrestored under the traditional model of dental treatmentcan be made to arrest, and many existing but morphologi-cally deteriorated restorations can be allowed to continue

philoso-to function satisfacphiloso-torily [8]

Thus, modern quality dentistry requires the dentist tohave the wisdom and courage to ‘go modern’ with restora-tive 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 ber dam, magnification, sharp hand instruments, well-adapted contoured matrix bands, all used with finesse atevery stage, becomes integral with modern prevention-based restorative dentistry

rub-Periodontal Diseases

Plaque-induced periodontitis is believed to involveperiods dominated by tissue destruction and periodsdominated by tissue repair [10] Between these fluctua-tions of activity there appear to be periods of quiescenceand stability Net loss of epithelial attachment and alveo-lar bone destruction occur when the interactions betweenthe bacteria and the patient’s responses are out of equilib-rium such that they favour pathological destruction andloss of structure [11]

Consider the patient who has gingivitis and destructiveperiodontitis, in whom plaque-induced inflammation hasled to apical migration of the gingival epithelial attach-ment to the root surface of the tooth The aim of treat-ment is to arrest attachment loss and cause a reduction inpocket depth; indeed, the aim is normal-looking gingivaltissue with pocketing no greater than about 4 mm whichdoes not bleed or discharge pus on probing The treatmentshould take the form of effective daily oral hygiene carriedout by the patient, plus professional scaling and removal

of noxious elements in the periodontal pockets, includingthe removal of the complex subgingival mass of bacteriawhich may be adhering to the root surfaces Other treat-ment, such as the reshaping of restorations, may also benecessary As with caries, the prevention phase is critical.However, whatever the patient does, plaque may return tothe deeper parts of the gingival crevice, so ongoing profes-sional 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

pre-vention 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’

tech-nique of brushing as opposed to a method involving

clean-ing of the gclean-ingival 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

assum-ing 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

pre-vent further disease [12]?

(g) And, worst of all, is the dentist living under the

illu-sion 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

Sev-eral 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

attach-ment 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

con-trol 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

den-tal package, since smoking has a markedly adverse effect

upon periodontal inflammation and healing [16]

Dental professionals should appreciate that giving

pre-ventive advice in the form of oral hygiene instruction is

not of itself a preventive measure The preventive

mea-sure succeeds when the patient actually achieves excellent

daily oral hygiene; it is this latter which must be the tive

objec-Why the Problem?

Why does evidence-based quality general dental careconstitute a challenge to the profession? Surely it shouldnaturally form the basis of all dentistry, shouldn’t it? Afterall, dentists are professionals, and professionals should,

by definition, avow to offer the best for their patients Theold adage ‘Prevention is better than cure’ is well known,but if dental diseases do occur, it is important to treatthem as non-invasively as possible Ask the World HealthOrganization or any health minister whether or not it isbetter 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 seg-ments of the dental profession appear to ‘accept’, as if itwere inevitable, the occurrence of avoidable dental dis-eases such as dental caries and periodontal diseases?What has contributed enormously to the present pro-file of traditional dentistry, including the teaching in den-tal schools, has been the widespread dissemination ofG.V Black’s principles of cavity preparation in the earlypart of the last century, followed by a phenomenal growth

in operative dentistry over the years, particularly up toabout 1975 The world saw a proliferation of dentalschools with vast areas of clinical space devoted to opera-tive dentistry The clinics became powerhouses, dominat-ing all other activities and engulfing large portions of cur-ricula Hume [17] has described the phenomenon as a re-storative 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 ofthe taming and turning process [18]

A problem here lies in the fact that it is rather easy forboth patients and dentists alike to naively believe thatoperative dental treatment automatically results in oralhealth And many dentists have little experience of dis-ease control (as distinct from providing operative treat-ment), even though they should, theoretically at least,have retained the necessary knowledge from their under-graduate training days However, the stark facts of thematter are that patients in a low-risk category for cariescan inadvertently be shifted towards a significant risk ofongoing replacement restorations once the first set of res-torations has been placed in the teeth [19]

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To illustrate this point, it is relevant to consider a

pro-spective study of dental treatment provided to a large

ran-dom 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

(al-most in direct proportion to the number of courses of

treatment received) Further, the proportion of

restora-tions that were replacements increased markedly as the

total number of restorations present increased

Somewhat inevitably, therefore, it was found that themore restorations a patient had, the more the patient waslikely to receive And the people who received the mostrestorations tended to be relatively well educated and con-ditioned to visiting their dentists regularly Overall, it wasfound that 50% of restorations were placed in the teeth ofjust 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 fre-quently than those who attended more rarely, so thechances of a morphologically defective restoration beingtargeted for replacement were greater in these individuals.Certainly it cannot be assumed that dentistry, as widelypractised, is necessarily good for the teeth The corre-sponding figures for other countries may differ somewhatfrom those given above, but it is likely that equivalentscenarios 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

Dentists appear to gain fulfilment by cutting away sound tooth substance (such cutting being a primary function of the high-speed drill).

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Table 1 (continued)

It is no surprise therefore that

Restorations of mediocre quality are readily placed [30, 31].

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]

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

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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

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.

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

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]

Any hope of quality dental care is gone forever.

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The Repeat Restoration Cycle

Research over the last 20 years or so has made it

possi-ble to assempossi-ble a model of the potential chain of events

that embraces many shortcomings of traditional

restora-tive 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

‘com-fortable’ when they intervene invasively [8, 20, 42]

Fur-ther, there is an apparent disregard for the inevitable

weakening of the teeth in the process, especially as the

res-torations 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

surviv-ing only for a few years) [44–49] And, of course,

restora-tions do not cure caries anyway

The characteristics of the repeat restoration cycle are

totally unsatisfactory in an age of potential

evidence-based 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’

under-taken in dental practice is not at variance with what was

taught in dental school But the dental school was

yester-day Today’s patients require today’s care

In light of the repeat restoration cycle, is it really

sur-prising that the profession suffers from low morale and

stagnant motivation, when mechanistic solutions to

bio-logical problems weigh so heavily in many dental

prac-tices?

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

any-thing the dentist suggests

Moving Forward towards Evidence-Based

Dental Care

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

den-tition in as intact a state as possible Some members of the

profession have made this break already and are

provid-ing excellent evidence-based quality dental care In

addi-tion, they report a marked improvement in the quality oftheir 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 arerequired in dental education [50]

By referring to restorations as ‘treatment’, the sion has drifted hopelessly away from evidence-baseddentistry [6] Yet the profession is steeped in the use of theterm when often no treatment is in fact provided, just res-torations that readily lock the patient into the repeat res-toration cycle, each restoration being less prophylacticand more iatrogenic than the one before Thus, to thepatient who asks ‘Do I need any treatment?’ it is a verynaive dentist who replies, ‘Yes, two fillings.’ A moreappropriate reply might begin along the lines of, ‘Yes, youhave two carious lesions, so we need to set about alteringthe nature of the chemical processes going on in yourmouth in order to cause the lesions to arrest ’

profes-With the public’s increasing awareness of the comings of traditional restorative dentistry and, at thesame time, a heightened understanding of the possibilitiesfor prevention, patients can be expected more and more

short-to demand preventive ‘quality’ dental care Indeed, itseems that the supply-and-demand forces of the market-place will reinforce the scientific argument and put in-creasing pressure upon dentists to adopt a more pre-ventive approach to the management of caries, defectiverestorations and periodontal diseases Then the patientwho attends regularly will become less ready to accept anapparently unending commitment to restorations andre-restorations, with scales and polishes thrown in fromtime to time

As caring professionals, dentists should stop ing that operative treatment is necessarily rational Pre-vention and the promotion of health are becoming in-creasingly necessary in order to satisfy the requirements

pretend-of today’s people, undertaken within a context pretend-of dence-based oral health care The real challenges for thefuture are: (1) for dental education to accept whole-heartedly the changes mentioned in this paper, and to ‘runwith them’; (2) for dental practice to put the changes intoaction out in the field, and (3) for licensing bodies andremuneration systems to develop in sympathy

evi-Thus, there is a fundamental need for a reappraisal ofdental education But questions remain as to how univer-sity teaching staffs can be brought fully up to date so as toassist the change in emphasis towards prevention andthereby help tame Hume’s [17] restorative tiger [18] Ini-tiative and innovation are now required in order to bringabout the necessary changes in dental education to suit it

Trang 24

to the needs of the changing world There is a clear need

for all those involved in providing oral health care,

espe-cially licensing bodies and those responsible for health

care delivery, to widen their perceptions of the issues at

stake and thereby enable forward-looking curriculum

de-velopment 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

man-ner

Conclusions

Standard, invasive dental treatments such as

restora-tions and scaling are in general not an effective way to

manage dental caries and periodontal diseases Much

more emphasis should be placed upon the assessment ofeach and every carious and periodontal lesion with a view

to allowing a possible natural arrest of the processes tooccur, aided by specific preventive measures as appro-priate Existing restorations should not necessarily bereplaced just because there is a moderate degree of mar-ginal breakdown In view of the adverse potential of therepeat restoration cycle, the withholding of restorativetreatment when appropriate may itself be considered aprime preventive measure Indeed, the universal adop-tion of a preventive, evidence-based approach to treat-ment decisions could be by far the most powerful factor inreducing the restorative burden of dental practice

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24 Kidd EAM, Pitts NB: A reappraisal of the

val-ue 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 ventive management; in Bell CJ (ed): Heine- mann Dental Handbook Oxford, Heinemann Medical Books, 1990, chapter 11, pp 128–136.

pre-27 Elderton RJ: Treatment variation in tive dentistry Restor Dent 1984;1:3–8.

restora-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 storative dental treatment decisions Br Dent J 1983;154:363–365.

re-30 Elderton RJ: The quality of amalgam tions; in Allred H (ed): Assessment of the Qual- ity of Dental Care London, London Hospital Medical College, 1977, monograph 2, pp 45– 81.

restora-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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of restorative dental treatment decisions and

secondary caries Br Dent J 1984;157:128–

133.

34 Nuttall NM: Capability of a national

epidemio-logical survey to predict General Dental

Ser-vice treatment Community Dent Oral

Epi-demiol 1983;11:296–301.

35 Davies JA: The relationship between change of

dentist and treatment received in the General

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36 Elderton RJ, Merrett MCW: Variation among

dentists in identifying reasons for marginal

de-terioration 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

suc-212.

41 Todd JE, Lader D: Adult Dental Health 1988 United Kingdom London, Her Majesty’s Sta- tionery Office, 1991, part 4:21, pp 217–234.

42 Schanschieff SG, Shovelton DS, Tulmin JK:

Report of the Committee of Enquiry into necessary Dental Treatment London, Depart- ment of Health and Social Security, 1986.

Un-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.

chell DJ: How long do routine dental tions last? A systematic review Br Dent J 1999; 187:432–439.

restora-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 span of Amalgam Restorations; MSc thesis University of London, London, 1976.

Life-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 terior restorations Int Dent J 1990;40:11–17.

pos-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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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

It is well known that smoking contributes to the

develop-ment 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

den-tal 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,

peri-odontal disease, implant failure, oral precancer and

can-cer From a qualitative point of view the latter is

obvious-ly 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

Introduction

The role of smoking in the development of lung cancerand cardiovascular disease is well known Since the initialsuspicion of the relation between smoking and lung can-cer in the 1950s [1], the famous study of British doctors,among many others, established a causal relationshipbetween smoking and death from major diseases, includ-ing cancer of the lung and other types of cancer, respirato-

ry diseases such as obstructive pulmonary disease, lar diseases, and peptic ulcers [2, 3] As part of the health-care system dentists have an obvious interest in these dis-eases, but it could be argued that other members of thehealth system have more important roles to play as far asthese and many other smoking-related diseases are con-cerned However, since there is weighty evidence thatsmoking has a considerable influence on oral health, it isnot unreasonable that dentists should play an importantrole in preventing the harmful effects of smoking onhuman tissues in general and oral tissues in particular.The oral effects of smoking range from harmless stains

vascu-of teeth and dental restorations to serious diseases such asoral cancer (table 1) From a qualitative point of view thelatter, obviously, is of utmost importance, since the five-year relative survival rate for intraoral cancer is about50% [4] Quantitatively, however, importance has beenattached to other diseases or issues related to smokingsuch as periodontitis, which affects a large proportion of

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Table 1 Effects of smoking on the mouth

Discolorations of teeth and restorations

Table 2 Oral cancer: age-standardized

(world population) incidence rates per

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

Work-ing Group on Tobacco and Oral Health distributed

infor-mational material to dentists in EU countries and

pub-lished a comprehensive review from a consensus meeting

organized by the Working Group [7] Part of this

consen-sus 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

Oral Cancer

The majority of oral cancers, constituting 2–3% of allcancers worldwide [8], are squamous cell carcinomasdeveloping from the mucosal surface epithelium (fig 1)[4] Oral cancer affects mostly middle-aged or elderly peo-ple and is more common in men than in women [8] Theincidence varies worldwide (table 2) [9] In this report,oral cancer is used synonymously with squamous cell car-cinoma originating from the mucosal surface epithelium.Numerous studies in various populations have shownthat smokers have a substantially higher risk of oral can-cer than nonsmokers [10–16] The studies are primarilyconcerned with the use of cigarettes, but pipe and cigarsseem to carry an equal or even higher risk [13, 16] There

is a clear dose-response relationship, with risk decreasingafter 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 otherstudies show that the risk decreases dramatically butremains at a level somewhat higher than that found inpeople who never smoked [12, 17] Ethnic differences inthe incidence and mortality of oral cancer exist, but theinformation available is scarce [18, 19]

The relationship between the use of smokeless tobaccoand oral cancer has been discussed at length The appar-ent discrepancies between different researchers probablyderive from the fact that there are great differences in hab-its and products around the world, which makes a generalstatement on this subject impossible Snufff-habits as theyappear in Scandinavia carry none or very low risks of oralcancer [20, 21], but the use of other types of smokelesstobacco in other parts of the world seems to pose a sub-stantial cancer risk [22]

Although the underlying mechanisms are not known indetail, it is plausible that smoking could lead to cancersince carcinogens in tobacco smoke can induce changes inDNA In recent years much attention has been given tosmoking-related mutations in a tumor suppressor genecoding for the protein p53 This protein is important inregulating cell proliferation and has a role in the repair ofDNA damage [23] Mutations in the gene may lead to anaccumulation of DNA damage in the cells, which mayplay an important role in the development of cancer.Many studies on the relationship between smoking andoral cancer have been appropriately controlled for variousconfounders such as diet (low intake of fresh fruit and veg-etables increases the risk of developing oral cancer [24,25]), social status, and, not the least important, alcoholabuse Smoking and excessive alcohol intake synergisti-

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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

gen-eral 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

carcino-mas 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

le-sion 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

bor-ders 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

revers-ible [36, 37]

Bearing in mind the role of smoking in the

develop-ment of oral cancer, it is not easy to understand why

leu-koplakias associated with a smoking habit seem to have a

better prognosis in terms of future transformation to

can-cer than those in non-smokers [38, 39] In

population-based 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

recent-ly that smoking is positiverecent-ly 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

An explanation for the finding that leukoplakias ciated with a smoking habit have a better prognosis thanthose not associated with a smoking habit could be that aproportion of smoking-related leukoplakias may not havereached the point of no return Thus, after smoking cessa-tion a substantial number of smoking-related leukopla-kias will disappear [42] This subgroup of smoking-relatedleukoplakias may have a low malignant potential Is itpossible, then, to predict if a given white lesion will disap-pear upon smoking cessation? There is at least one charac-teristic clinical finding that tells us that the lesion is tobac-co-induced: fine white striae that imitate a fingerprintpattern in the mucosa [43] These lesions are referred to asfingerprint 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

asso-a compasso-arison wasso-as masso-ade between leukoplasso-akiasso-as not asso-ated with a smoking habit and leukoplakias associatedwith a smoking habit but failing to disappear upon smok-ing cessation, the malignant potential would presumably

associ-be the same The latter group of leukoplakias would bly include smoking-induced leukoplakias as well as leu-koplakias that developed independently of the patient’ssmoking habit Thus, without knowing the fate of a givenleukoplakia upon smoking cessation the wording ‘smok-ing-induced’ should be avoided in favor of the wording

possi-‘smoking-associated’

Periodontal Disease

During the last 20 years numerous cross-sectional andlongitudinal studies have demonstrated a clear relation-ship between smoking and periodontal disease [for re-views, see 44, 45] Periodontitis is more prevalent andmore severe in smokers, characterized by deeper peri-odontal pockets, greater attachment loss and more furca-tion defects [46–52] In many studies smoking was sug-gested to be an independent risk factor for periodontaldisease after controlling other factors: oral hygiene,plaque, calculus, and socioeconomics The relative risk ofperiodontal 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 insmokers explained such findings, but the rate of plaqueaccumulation 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

whit-ish changes, erythematous areas, and

nod-ules in the right buccal commissure in a

heavy smoker Biopsy revealed slight

epithe-lial dysplasia and candidosis Some would

classify this lesion as a chronic hyperplastic

candidosis.

Fig 3 White changes in right buccal

com-missure in a heavy smoker Note

finger-print-like pattern or pumice stone

appear-ance.

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

evi-dence that smoking is a risk factor for periodontal disease

Furthermore, the disease is more severe in current

smok-ers as compared to former smoksmok-ers [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,

fur-thermore, 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

nega-tive 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 thisfinding Divergent results are likewise seen in recent stud-ies [66–68] Most of these studies were conducted onpatients with severe periodontitis, but a recent study onyoung adults with healthy periodontium showed that typi-cal periopathogens are more frequent in smokers than innonsmokers after controlling variations in oral hygiene,suggesting that smoking is involved in the early develop-ment of the disease A recent study suggested that theeffect of smoking on periodontal disease was a reduction

in the regression of the disease rather than an effect on theprogression of disease [69]

Since divergent results on the composition of the gingival microflora have been reported, an explanation ofthe effect of smoking on periodontal tissues has beensought in smoking-induced alterations in the host re-sponse Based on recent reviews [44, 70], it seems fair toconclude that plausible biological explanations exist Re-cent studies support earlier findings of impaired humoral,cellular and innate immune reactions and effects via the

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sub-cytokine and adhesion molecule systems [71–75] A

clini-cally suppressed hemorrhagic responsiveness of the

perio-dontium has been demonstrated in smokers [76] This

may make it more difficult to detect early stages of

dis-eases in smokers and might interfere with diagnostic tests

on disease severity and activity

Treatment failures seem to predominate among

smok-ers, 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

simi-lar 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

smok-ing and periodontal disease still needs to be elucidated A

recent study assessing the evidence for a causal

associa-tion 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

pre-ventive 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

attribut-able 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

the number of implant failures in smokers is not the result

of poor healing or ossointegration, but is due to the sure of peri-implant tissues to tobacco smoke [83], possi-bly linking the smoking effects on implant survival to thesmoking effects on periodontitis

expo-A smoking cessation protocol has been suggested toimprove the success rate of Brånemark implants [85] Theprotocol involved complete cessation of smoking for 1week before and 8 weeks after initial implant placement Itwas concluded that the protocol demonstrated consider-able promise in improving the success rates of implantintegration in smokers who complied; however, it wasnoted that the sample size for smokers was relatively small.Furthermore, as touched upon above and acknowledgingthe problems attached to this, the study did not include arandomization of patients in terms of those following theprotocol and those continuing their smoking habit.There seems to be no doubt that smoking can be associ-ated with higher rates of implant failure and altered peri-implant 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 inthe field of oral implants [86]

Saliva and Caries

Studies on the effects of smoking on saliva flow ratesand composition show varying results and are difficult tocompare [for a comprehensive review, see 7] Tobaccousage immediately stimulates salivary flow, but there is

no long term effect on saliva flow rates The pH of salivarises during smoking, but over longer time periods moststudies indicate that smokers have slightly reduced pHand buffering power compared to nonsmokers A consis-tent finding is an increased concentration of thiocyanate

in saliva A component in normal saliva, thiocyanate isalso present in tobacco smoke, and its concentration insaliva can be used to monitor tobacco exposure A recentstudy showed that smoking is associated with lower sali-vary cystatin activity and output of cystatin C during gin-gival inflammation [72] Cystatins are thought to contrib-ute to maintaining oral health by inhibiting certain pro-teolytic enzymes In addition this study confirmed earlierresults that showed no significant differences in salivaryflow rates between smokers and non-smokers

Rather few studies have shown a relationship betweensmoking 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,

al-though various results are reported, Streptococcus mutans

in smokers [91] may explain this relationship It is

inter-esting, although not easy to explain, that maternal

smok-ing 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

sur-face 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

restora-tions, and dentures, affecting the aesthetic appearance of

the mouth [94, 95], and it contributes more to

discolora-tion than does the consumpdiscolora-tion 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

cen-trally 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

re-verse smoking, as seen primarily in Asia, is a

premalig-nant lesion [103]

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

of about 30%, most prevalent on the anterior attachedgingiva, is seen in heavy smokers (smokers melanosis)(fig 6) [104] Recently it was shown that smokers in aTurkish population had significantly more pigmentedoral surfaces than non-smokers [105] The changes aresymptomless, it is not premalignant, and it seems that thepigmentation is reversible upon smoking cessation [104,106] Hairy tongue and coated tongue are other harmlesslesions related to smoking, although they can be seen innonsmokers as well [100, 101, 107]

Oral Candidosis

A relationship between oral candidosis and smokinghas been suggested for a long time (fig 2), but the exactpathogenic influence of smoking is not known The suspi-cion arises from studies in which patients with oral candi-dosis turned out to be smokers in all [108, 109] or in thevast majority of cases [110] Another study of the oralpresence of Candida strains in healthy adults and inpatients with oral leukoplakia and erythematous candido-sis also suggested that smoking is a predisposing factor forcandidal infection [111] After antimycotic therapy smok-ers had relapses of the candidal infection in all cases [109],and in HIV-infected patients smokers were less likely torespond to systemic antimycotic treatment than non-smokers [112]

Further studies are indeed needed to establish a firmaetiological relationship between smoking and oral candi-dosis, but it seems fair to inform smokers about the possi-ble relationship and consequences for treatment

Tobacco Intervention in Dental Practice

Are dentists actively engaged in tobacco interventionmatters? In several studies it has been shown that themajority of dentists consider encouraging their patients tostop smoking [113–118], but few dentists always or oftendiscuss tobacco habits with their patients [113, 116–120]

It was recorded in a study from Italy that more dentistsare engaged in tobacco cessation activities [121] Themain barriers to providing tobacco cessation services topatients are lack of reimbursement, lack of confidence inthe effectiveness of advice from the dental profession, andlack of knowledge and material to hand out to patients[116–118, 120] Although few studies are available, itseems that clinical interventions in dental care are aseffective as those in other healthcare settings [122] Inspite of this, policies and practices of European dentalschools need considerable improvement [123]

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Fig 7 The five As.

Tobacco intervention includes tobacco cessation

activ-ities, prevention, and public policy development

Prefera-bly, dentists should be competent in all three areas For

the purpose of this review only tobacco counselling in

dai-ly practice will be touched upon The World Dental

Fed-eration (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

ces-sation 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.surgeongener-al.gov/tobacco/(go to ‘Clinician materials’; consumer

ma-terials are also available)] The primary goal is to ensurethat every patient who uses tobacco is identified andoffered 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

imple-mented that ensures that every patient at every visit isasked about tobacco use, and the answer documented inthe patient’s record

Advise all smokers to stop A prescriptive approach

should be avoided Rather, the healthcare professional orthe dentist should provide the patients with informationand advice, reinforcing the patients’ own motivationwhen possible and emphasizing the benefits of stopping.Immediate benefits will often motivate the patients moreeffectively than long-term benefits Grisly pictures andmorbid statistics often stimulate patient denial Instead,dentists should demonstrate the oral effects of tobacco ifpresent, or inform patients about the increased risk ofpoor 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 assistthe 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 decisionand make a note in the record for future reference Den-tists should ensure that the patient is aware of the staff’swillingness to help, for instance by providing the patientwith written information or/and asking the patient in asubsequent visit to reconsider his or her decision De-pending on the training and resources of the dentist andstaff, the following steps can be taken in the dental office,

or the patient can be referred to a tobacco cessation cialist

spe-Assist the patient in stopping If a patient has a desire

to stop, the dentist should help the patient set a realisticquitting date which should be soon but not immediately

so that the patient has time to prepare If consultationtime is limited, self-help materials that provide the pa-tient with necessary information about smoking cessationcan be provided Nicotine replacement therapy (nicotinegum, inhaler, nasal spray, or skin patch) can be very help-ful [122, 126–129] Special consideration should be given

to selected populations [122, 126] Whatever the proach, the dentist should see to it that the patient leavesthe office with a concrete plan for stopping and informa-tion about how to prepare for the quitting date and how tosuccessfully stop, keeping in mind that most smokersrelapse three to five times before succeeding in stopping

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ap-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

pa-tient was successful or encourage another try if

unsuccess-ful Follow-ups may be by telephone call, letter, office

vis-it, 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

encour-age 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 dence that smoking has considerable influence on oralhealth But tobacco use is a modifiable risk factor for oraland general disease, and an obvious professional interest

evi-in tobacco evi-intervention can make a big difference evi-in thehealth 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 willeasily recognize the patient’s smoking status These factsplace dentists in a favourable position to help preventtobacco-related diseases, and interested practitionersshould pursue more formal training in smoking cessationcounselling, which should be as much a part of their job asplaque control and dietary advice

References

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national statistics with two case-control

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Tiêu đề	Proceedings of the International Conference on Evidence Based Practice in Dentistry
Tác giả	J.M. Behbehani, E. Honkala
Trường học	Faculty of Dentistry, Kuwait University
Chuyên ngành	Dentistry
Thể loại	Proceedings
Năm xuất bản	2003
Thành phố	Kuwait

Định dạng
Số trang	69
Dung lượng	2,02 MB