Evidence Based Practice in Dentistry (Medical Principles and Practice)

Evidence-based medicine
Free download. Book file PDF easily for everyone and every device. You can download and read online Evidence Based Practice in Dentistry (Medical Principles and Practice) file PDF Book only if you are registered here. And also you can download or read online all Book PDF file that related with Evidence Based Practice in Dentistry (Medical Principles and Practice) book. Happy reading Evidence Based Practice in Dentistry (Medical Principles and Practice) Bookeveryone. Download file Free Book PDF Evidence Based Practice in Dentistry (Medical Principles and Practice) at Complete PDF Library. This Book have some digital formats such us :paperbook, ebook, kindle, epub, fb2 and another formats. Here is The CompletePDF Book Library. It's free to register here to get Book file PDF Evidence Based Practice in Dentistry (Medical Principles and Practice) Pocket Guide.

techedbrains.com/assets/500/jeh-hombres-osos.php Regardless of the level of evidence or approaches to its appraisal, the evidence loop is completed by implementation, monitoring and reassessment. Too frequently an intervention for which evidence has been found beneficial is inadequately reassessed over time in target patients or populations, but without reassessment it is difficult to determine the value and necessity of maintaining a given intervention. All of the stages of the evidence-based approach are very important and taken together, they offer a rational way forward to improve oral health and dental care.

Conclusion Although the evidence-based approach is 30 years old, just what it means, whether it is feasible, how to conduct it and the outcome of its use are not well understood. This situation holds in dentistry in general and in areas like the prevention of oral disease in particular. In order to present a comprehensive evidence-based approach to the prevention of oral diseases, an evidence loop has been presented. The evidence for the prevention of oral diseases begins with an understanding of the burden of oral disease at different life stages and the proportion which is avoidable, given associations with mutable determinants of disease.

This provides a broad underpinning health policy and priority setting giving direction to both individual and population-wide preventive interventions. The key questions to be addressed about those interventions focus on the beneficiaries, efficacy, efficiency, public perceptions and side effects. New York, Oxford University Press, Geneva, WHO, Canberra, Australian Institute of Health and Welfare, Validity and responsiveness testing. Community Dent Oral Epidemiol ;— Background Paper.

Melbourne, NPHP, BMJ ;— The Cochrane Collaboration. Oxford, Update Software, JAMA ;— How to get started: The evidence-based medicine working group. New York, Churchill-Livingstone, J Public Health Dent ;— Community Dent Oral Epidemiol ;— J Public Health Dent ;— Melbourne, National Public Health Partnership, Br Med J ;— Resources for Planning. Oral Health. Community Dent Health ;— J Dent Res ;, abstr Clin Oral Invest ;— Rather, restorative treatment has often covered up the disease processes in the short term and created a new problem: that of maintenance and re-restoration of restored teeth.

Thus, standard invasive dental treatments that are commonly provided fail to address the fundamental bacterial nature of the diseases. Indeed, these treatments rather readily generate and perpetuate a totally unacceptable chain of events. This chain embraces many shortcomings, which themselves nurture what may be described as the repeat restorative cycle. The time has come to correct this iniquity. Much more emphasis should be placed upon the assessment of each and every caries or periodontal lesion, with a view to implementing specific preventive measures and allowing the natural arrest of disease processes to occur.

The universal adoption of a preventive evidence-based approach to making dental treatment decisions could be by far the most powerful factor in reducing the restorative burden of dental services. There is a need to move wholeheartedly and contentedly into the preventive era. Karger AG, Basel Introduction Traditional restorative dentistry has had a strong influence on dental education and practice in many parts of the world, and invasive restorative treatment has tended to take precedence over non-invasive preventive measures. Indeed, many dentists seem to believe that traditional dental treatment automatically results in oral health [1].

Dental caries and periodontal diseases, both bacterial in nature, are largely preventable from the start.

Navigation menu

But they are not always prevented; rather, the forces leading to the diseases are allowed to remain out of balance with those that lead to health. The situation prevails today whereby the scientific basis of these diseases has largely been established [2, 3], but the services providing appropriate dental care to manage them remain out of date and fail to be properly evidence-based.

When the diseases occur, there is a need for a real and responsible commitment by the dentist to help the patient revert to a disease- Richard J. Caries Caries is not simply a one-way process. All carious lesions involve both demineralisation and remineralisation phases [4]. A lesion increases in size only when the calcium and phosphate ion exchange between the tooth and the saliva, mediated by bacterial plaque, favours net mineral loss over long time periods. Such lesions may be described as active.

On the other hand, if and when the conditions are such that the calcium and phosphate ion exchange favours mineral gain over time, the lesion may be described as arrested. Causing carious lesions to arrest should be a primary preoccupation of dentists. Caries is very much related to environmental and lifestyle habits such as bacterial plaque, dietary patterns, and fluoride usage, which are themselves very much linked to things like living conditions, economic factors, education levels, school routines, work routines, home and leisure routines, social habits, and personal whims and fancies.

Evidence-based dentistry

Consider the patient who has an active class II carious lesion that has extended well into the dentine. Most clinicians would agree that when this stage of caries development has been reached, it is necessary to excise the diseased tissue and make good the defect with a restoration [5].

But that is just one phase. It is also necessary to bring about a change in the environment of the tooth and of the rest of the dentition so as to prevent further caries, including the development of new primary carious lesions [6]. Thus, proper caries management is all about identifying the main aetiological factors, and selecting and targeting specific efficacious preventive measures to help overcome specific imbalances.

It is also about causing patients to make relevant adjustments, in a highly focused manner, to their dietary patterns, oral hygiene habits and fluoride and chlorhexidine, xylitol, etc. Fissure sealants may also be necessary. The whole process will need monitoring and perhaps fine-tuning over time [7]. Caries prevention works, so once a preventive philosophy prevails, then the whole attitude to invasive procedures changes. Many carious lesions that would have been restored under the traditional model of dental treatment can be made to arrest, and many existing but morphologically deteriorated restorations can be allowed to continue to function satisfactorily [8].

Where restorations are required, they will necessarily be minimally invasive and of high technical quality [9]. Thus the routine use of rubber dam, magnification, sharp hand instruments, welladapted contoured matrix bands, all used with finesse at every stage, becomes integral with modern preventionbased restorative dentistry. Periodontal Diseases Plaque-induced periodontitis is believed to involve periods dominated by tissue destruction and periods dominated by tissue repair [10]. Between these fluctuations of activity there appear to be periods of quiescence and stability.

Consider the patient who has gingivitis and destructive periodontitis, in whom plaque-induced inflammation has led to apical migration of the gingival epithelial attachment to the root surface of the tooth. The aim of treatment is to arrest attachment loss and cause a reduction in pocket depth; indeed, the aim is normal-looking gingival tissue with pocketing no greater than about 4 mm which does not bleed or discharge pus on probing.

The treatment should take the form of effective daily oral hygiene carried out by the patient, plus professional scaling and removal of noxious elements in the periodontal pockets, including the removal of the complex subgingival mass of bacteria which may be adhering to the root surfaces. Other treatment, such as the reshaping of restorations, may also be necessary. As with caries, the prevention phase is critical. However, whatever the patient does, plaque may return to the deeper parts of the gingival crevice, so ongoing professional care may be needed at specific sites.

Med Princ Pract ;12 suppl 1 —21 13 It is necessary to ask, and where necessary address in depth, some questions regarding the treatment and prevention of destructive periodontal disease. For example: a How well does the patient remove visible plaque on an ongoing basis? 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. Often it does not. Several experts have indicated that proper subgingival scaling and root planing take some 5—7 min per tooth [13], or more [14].

Evidence-based Dentistry: Making Clinical Decisions

Further, ineffective scaling and polishing may actually do more harm than good, in that while failing to achieve its objective, it may cause damage to the attachment and to the hard dental tissues, even to the extent of taking away some of the high-fluoride outer zones of the teeth [15]. By far the most important thing to do is to inform the patient that it is his or her success with daily plaque control that is the vital factor in determining the long-term outcome. And if the patient is a tobacco smoker, then attempting to convince him or her to quit the habit should be seen as an important component of the preventive dental package, since smoking has a markedly adverse effect upon periodontal inflammation and healing [16].

Dental professionals should appreciate that giving preventive advice in the form of oral hygiene instruction is 14 Med Princ Pract ;12 suppl 1 —21 not of itself a preventive measure. The preventive measure succeeds when the patient actually achieves excellent daily oral hygiene; it is this latter which must be the objective. Why the Problem? Why does evidence-based quality general dental care constitute a challenge to the profession?

After all, dentists are professionals, and professionals should, by definition, avow to offer the best for their patients. Ask the World Health Organization or any health minister whether or not it is better to have diseases such as polio, yellow fever, cholera or AIDS in a community or to prevent their occurrence. What has contributed enormously to the present profile of traditional dentistry, including the teaching in dental schools, has been the widespread dissemination of G. The world saw a proliferation of dental schools with vast areas of clinical space devoted to operative dentistry.

The clinics became powerhouses, dominating all other activities and engulfing large portions of curricula. Black, who has been described as the Father of Dentistry, were alive today, he would have been at the forefront of the taming and turning process [18]. A problem here lies in the fact that it is rather easy for both patients and dentists alike to naively believe that operative dental treatment automatically results in oral health. And many dentists have little experience of disease control as distinct from providing operative treatment , even though they should, theoretically at least, have retained the necessary knowledge from their undergraduate training days.

However, the stark facts of the matter are that patients in a low-risk category for caries can inadvertently be shifted towards a significant risk of ongoing replacement restorations once the first set of restorations has been placed in the teeth [19]. Elderton To illustrate this point, it is relevant to consider a prospective study of dental treatment provided to a large random sample of dentate adults in Scotland.

It showed that the amount of operative treatment the patients received over a 5-year period related very much to their dental office attendance patterns and to the number of teeth which already contained restorations [20]. Indeed, it was found that the average number of tooth surfaces restored during any one course of treatment was approximately the same on average, regardless of the frequency of the courses.


Thus the patients who went to the dentist more frequently received more restorations per unit of time almost in direct proportion to the number of courses of treatment received. Further, the proportion of restorations that were replacements increased markedly as the total number of restorations present increased. Somewhat inevitably, therefore, it was found that the more restorations a patient had, the more the patient was likely to receive. And the people who received the most restorations tended to be relatively well educated and conditioned to visiting their dentists regularly.

Certainly it cannot be assumed that dentistry, as widely practised, is necessarily good for the teeth. The corresponding figures for other countries may differ somewhat from those given above, but it is likely that equivalent scenarios are found elsewhere.

  • Evidence-based Dentistry Network?
  • How to apply evidence-based principles in clinical dentistry.
  • Top navigation: Contact, Library account!
  • Navigation menu;
  • What is EBP?.
  • Field-Programmable Gate Arrays;

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].

Caries is not managed as a disease [6, 8]. Thus The use of outdated concepts of cavity design perpetuating Black-type cavities involving excessive cutting of sound tooth substance is commonplace [30, 31] and Dentists fail to appreciate the exacting nature of restorative procedures. Sadly These restorations often contain characteristics consistent with inbuilt obsolescence. In addition Bur damage, for example, is imparted commonly to the adjacent tooth [32] and Non-physiological approximal contours frequently lead to plaque accumulation and periodontal disease.

Thus, for example, Ditched margins are commonly assumed to signal failure of the restoration [5, 30] and Existing restorations are readily deemed to have failed [20, 34], particularly if the patient has just changed from a previous dentist [35]. However The matter of why restorations have failed is not questioned by the dentist or patient. Further, one cannot escape the fact that Bacteriological, mechanical and chemical insult to the pulp is increasingly likely to occur.

However The crown fails to properly fit the margins of the prepared tooth and, if visible, The crown looks artificial. However The periodontal disease is not properly evaluated or documented. Indeed The periodontal disease is not prevented or treated. Instead Further scaling takes place, leading to clean teeth for another day. But inevitably Bacterial plaque returns to continue the disease process and Irreversible alveolar bone loss is liable to take place as periodontitis takes a hold.

At the same time Halitosis becomes a real issue for the patient but The halitosis is not even considered by the dentist. Indeed Dentists tend to forget that patients do not like having restorative treatment [40, 41]. Sadly Burn-out rather readily sets in and the dentist spirals downwards [43].

Some members of the profession have made this break already and are providing excellent evidence-based quality dental care. In addi- tion, they report a marked improvement in the quality of their working lives as a result. Sadly, it has to be noted that many dental school teachers have very definitely not made the break. It is clear that considerable changes are required in dental education [50]. Yet the profession is steeped in the use of the term when often no treatment is in fact provided, just restorations that readily lock the patient into the repeat restoration cycle, each restoration being less prophylactic and more iatrogenic than the one before.

Indeed, it seems that the supply-and-demand forces of the marketplace will reinforce the scientific argument and put increasing pressure upon dentists to adopt a more preventive approach to the management of caries, defective restorations and periodontal diseases. Then the patient who attends regularly will become less ready to accept an apparently unending commitment to restorations and re-restorations, with scales and polishes thrown in from time to time.

As caring professionals, dentists should stop pretending that operative treatment is necessarily rational. Thus, there is a fundamental need for a reappraisal of dental education. Initiative and innovation are now required in order to bring about the necessary changes in dental education to suit it Quality General Dental Care Med Princ Pract ;12 suppl 1 —21 The Repeat Restoration Cycle Research over the last 20 years or so has made it possible to assemble a model of the potential chain of events that embraces many shortcomings of traditional restorative treatment, namely the repeat restoration cycle.

This potential chain of events is given in table 1. The contents of this table form an integral part of the text of this paper and should be read at this stage. The repeat restoration cycle is driven by a culture of drill-related dentistry. Further, there is an apparent disregard for the inevitable weakening of the teeth in the process, especially as the restorations are placed and replaced over the years. After all, by virtue of the repeat restoration cycle, it is inescapable that restorations are often not very durable many surviving only for a few years [44—49].

And, of course, restorations do not cure caries anyway. The characteristics of the repeat restoration cycle are totally unsatisfactory in an age of potential evidencebased dentistry and at a time of increasing accountability. Yet there is a strong implicit message to patients that any operative treatment suggested is both necessary and worthwhile. But the dental school was yesterday. In light of the repeat restoration cycle, is it really surprising that the profession suffers from low morale and stagnant motivation, when mechanistic solutions to biological problems weigh so heavily in many dental practices?

There is a clear need for all those involved in providing oral health care, especially licensing bodies and those responsible for health care delivery, to widen their perceptions of the issues at stake and thereby enable forward-looking curriculum development. Either the profession stands up and says what good dentistry is, or the public and politicians will force their way, and the profession will then be in a defensive position and less ready to respond in an acceptable manner. Conclusions more emphasis should be placed upon the assessment of each and every carious and periodontal lesion with a view to allowing a possible natural arrest of the processes to occur, aided by specific preventive measures as appropriate.

Existing restorations should not necessarily be replaced just because there is a moderate degree of marginal breakdown. In view of the adverse potential of the repeat restoration cycle, the withholding of restorative treatment when appropriate may itself be considered a prime preventive measure. Indeed, the universal adoption of a preventive, evidence-based approach to treatment decisions could be by far the most powerful factor in reducing the restorative burden of dental practice.

Standard, invasive dental treatments such as restorations and scaling are in general not an effective way to manage dental caries and periodontal diseases. Int Dent J ; — Cambridge, Cambridge University Press, Oxford, Heinemann Medical Books, , chapter 12, pp — Oxford, Heinemann Medical Books, , chapter 13, pp — Br Dent J ;— Int Dent J ; —24, Oxford, Heinemann Medical Books, , chapter 14, pp — Periodontal diagnosis and prognosis.

Oxford, Heinemann Medical Books, , chapter 9, pp — Non-surgical treatment and maintenance. Acta Odontol Scand ;— J Periodontol ;— J Clin Periodontol ;— J Dent Res ; J Dent Res ; — J Am Dent Assoc ;— Dent Update ;— Chicago, Quintessence, , chapter 6, pp — A study comparing clinically undetected lesions in molar teeth of 14—year-old children in and Br Dent J ; — Oxford, Heinemann Medical Books, , chapter 11, pp — Restor Dent ;—8. London, London Hospital Medical College, , monograph 2, pp 45— J Dent Res ;— Br Dent J ;— J Dent Res ; Proc Br Paedod Soc ;— London, Quintessence, London, Department of Health and Social Security, J Dent ;— A systematic review.

Int Dent J ;— J Can Dent Assoc ;— From a qualitative point of view the latter is obviously the most serious tobacco-related effect in the mouth. Quantitatively, however, importance has been attached to periodontitis, which affects a large proportion of the population, and during recent years more attention has been given to implant survival rates.

Since the initial suspicion of the relation between smoking and lung cancer in the s [1], the famous study of British doctors, among many others, established a causal relationship between smoking and death from major diseases, including cancer of the lung and other types of cancer, respiratory diseases such as obstructive pulmonary disease, vascular diseases, and peptic ulcers [2, 3]. As part of the healthcare system dentists have an obvious interest in these diseases, but it could be argued that other members of the health system have more important roles to play as far as these and many other smoking-related diseases are concerned.

However, since there is weighty evidence that smoking has a considerable influence on oral health, it is not unreasonable that dentists should play an important role in preventing the harmful effects of smoking on human tissues in general and oral tissues in particular. The oral effects of smoking range from harmless stains of teeth and dental restorations to serious diseases such as oral cancer table 1. Quantitatively, however, importance has been attached to other diseases or issues related to smoking such as periodontitis, which affects a large proportion of Jesper Reibel School of Dentistry 20, Norre Allee DK— Copenhagen N Denmark Tel.

There are several general reviews and informational booklets for dentists on the effects of smoking in the mouth [5, 6]. Part of this consensus paper has been cited at www. 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 affects mostly middle-aged or elderly people and is more common in men than in women [8]. The incidence varies worldwide table 2 [9]. In this report, oral cancer is used synonymously with squamous cell carcinoma originating from the mucosal surface epithelium. Numerous studies in various populations have shown that smokers have a substantially higher risk of oral cancer than nonsmokers [10—16].

The studies are primarily concerned with the use of cigarettes, but pipe and cigars seem to carry an equal or even higher risk [13, 16]. There is a clear dose-response relationship, with risk decreasing after smoking cessation. In some studies it was shown that 10 years after quitting, former smokers have the same risk of oral cancer as people who never smoked, whereas other studies show that the risk decreases dramatically but remains at a level somewhat higher than that found in people who never smoked [12, 17].

Ethnic differences in the incidence and mortality of oral cancer exist, but the information available is scarce [18, 19]. The relationship between the use of smokeless tobacco and oral cancer has been discussed at length. The apparent discrepancies between different researchers probably derive from the fact that there are great differences in habits and products around the world, which makes a general statement on this subject impossible. Snufff-habits as they appear in Scandinavia carry none or very low risks of oral cancer [20, 21], but the use of other types of smokeless tobacco in other parts of the world seems to pose a substantial cancer risk [22].

Although the underlying mechanisms are not known in detail, it is plausible that smoking could lead to cancer since carcinogens in tobacco smoke can induce changes in DNA. In recent years much attention has been given to smoking-related mutations in a tumor suppressor gene coding for the protein p This protein is important in regulating cell proliferation and has a role in the repair of DNA damage [23].

Mutations in the gene may lead to an accumulation of DNA damage in the cells, which may play an important role in the development of cancer. Many studies on the relationship between smoking and oral cancer have been appropriately controlled for various confounders such as diet low intake of fresh fruit and vegetables increases the risk of developing oral cancer [24, 25] , social status, and, not the least important, alcohol abuse. In Greece, where the incidence of oral cancer in general is low, a study showed a similar synergistic effect between tobacco and alcohol [27], and in a study on patients at an addiction unit in Hungary, 8 oral carcinomas were diagnosed 2.

All of the patients had a daily smoking and alcohol habit; about half of them smoked more than 20 cigarettes a day and consumed the equivalent of 2—3 liters of wine daily. Thus, screening of risk groups, defined primarily by tobacco and alcohol habits, seems well founded.

There is overwhelming and consistent evidence that smoking causes oral cancer. A recent study, however, showed that only one third of patients who had undergone treatment for oral cancer [29]! Thus, the public needs to be informed of the risks, in particular during their visits to the dental office. Oral Precancer Oral leukoplakia, the most common premalignant lesion in the mouth, is far more common in smokers than in non-smokers fig.

A recent study suggests that leukoplakias in the floor of the mouth are associated with smoking habits, whereas leukoplakias at the lateral borders of the tongue are more common among nonsmokers [32]. Smokeless tobacco induces wrinkled changes in the oral mucosa at the site where the quid is placed [20, 33— 36], but at least some of these changes seem to be reversible [36, 37]. Bearing in mind the role of smoking in the development of oral cancer, it is not easy to understand why leukoplakias associated with a smoking habit seem to have a better prognosis in terms of future transformation to cancer than those in non-smokers [38, 39].

In populationbased studies from India it has been shown that cessation of tobacco use substantially decreases the incidence of oral leukoplakias [40], and since it has been shown recently that smoking is positively correlated to the presence of epithelial dysplasia in oral precancerous lesions [41], it is fair to conclude that it is an important and necessary task for the dentist to inform patients of the relationship between smoking and oral leukoplakias.

Thus, after smoking cessation a substantial number of smoking-related leukoplakias will disappear [42]. This subgroup of smoking-related leukoplakias may have a low malignant potential. Is it possible, then, to predict if a given white lesion will disappear upon smoking cessation? There is at least one characteristic clinical finding that tells us that the lesion is tobacco-induced: fine white striae that imitate a fingerprint pattern in the mucosa [43].

These lesions are referred to as fingerprint lesions or a pumice stone type of lesion fig. They will invariably disappear upon tobacco cessation fig. If a comparison was made between leukoplakias not associated with a smoking habit and leukoplakias associated with a smoking habit but failing to disappear upon smoking cessation, the malignant potential would presumably be the same.

Periodontal Disease During the last 20 years numerous cross-sectional and longitudinal studies have demonstrated a clear relationship between smoking and periodontal disease [for reviews, see 44, 45]. Periodontitis is more prevalent and more severe in smokers, characterized by deeper periodontal pockets, greater attachment loss and more furcation defects [46—52].

In many studies smoking was suggested to be an independent risk factor for periodontal disease after controlling other factors: oral hygiene, plaque, calculus, and socioeconomics. The relative risk of periodontal disease among smokers has been reported to be between 2. Initially, it was thought that a higher amount of plaque in smokers explained such findings, but the rate of plaque accumulation does not seem to be higher in smokers than in nonsmokers [53, 54].

Recent studies, a few of which are population-based, support earlier findings on periodontal disease in smokers [55—61] and show that cigar and pipe smoking have simi- Reibel Fig. Squamous cell carcinoma in the floor of the mouth in a heavy smoker. Leukoplakia characterized by whitish changes, erythematous areas, and nodules in the right buccal commissure in a heavy smoker. Biopsy revealed slight epithelial dysplasia and candidosis. Some would classify this lesion as a chronic hyperplastic candidosis. White changes in right buccal commissure in a heavy smoker. Note fingerprint-like pattern or pumice stone appearance.

A dose-dependent response has been suggested [48, 56, 62], strengthening the evidence that smoking is a risk factor for periodontal disease. Furthermore, the disease is more severe in current smokers as compared to former smokers [56, 59, 63, 64]. It should be emphasized, however, that studies comparing periodontal disease in current and former smokers were not randomised. The patients who succeed in stopping their smoking habit might be a subgroup of smokers who have an otherwise healthier way of life than those who continue to smoke.

But randomising smoking cessation in a scientific context might not be feasible and would, furthermore, pose ethical problems. The effect of smoking on adult patients with manifest periodontitis could be blurred by general health problems and by the progressive process of periodontal disease itself. A recent study on young healthy people without or with minimal periodontitis, however, reveals a clear negative effect of smoking on the periodontal tissues [65].

The mechanisms underlying the negative effects of smoking on periodontal tissues are largely unknown. Studies have shown more periopathogens in smokers than in nonsmokers, but other studies have not supported this finding. Divergent results are likewise seen in recent studies [66—68]. Most of these studies were conducted on patients with severe periodontitis, but a recent study on young adults with healthy periodontium showed that typical periopathogens are more frequent in smokers than in nonsmokers after controlling variations in oral hygiene, suggesting that smoking is involved in the early development of the disease.

A recent study suggested that the effect of smoking on periodontal disease was a reduction in the regression of the disease rather than an effect on the progression of disease [69]. Since divergent results on the composition of the subgingival microflora have been reported, an explanation of the effect of smoking on periodontal tissues has been sought in smoking-induced alterations in the host response. Based on recent reviews [44, 70], it seems fair to conclude that plausible biological explanations exist.

Recent studies support earlier findings of impaired humoral, cellular and innate immune reactions and effects via the Tobacco and Oral Diseases Med Princ Pract ;12 suppl 1 —32 25 cytokine and adhesion molecule systems [71—75]. A clinically suppressed hemorrhagic responsiveness of the periodontium has been demonstrated in smokers [76].

Evidence-based Dentistry Network

This may make it more difficult to detect early stages of diseases in smokers and might interfere with diagnostic tests on disease severity and activity. Treatment failures seem to predominate among smokers, although the effect of smoking on treatment success is variable [for review, see 44]. The results of recent studies are in line with these findings [58, 77]. Former smokers seem to respond to periodontal therapy in a manner similar to nonsmokers, but as mentioned above smokers who decide to stop smoking and succeed in their efforts may differ in other risk characteristics from smokers who do not quit their habit.

Evidence-Based Dentistry

The use of smokeless tobacco has been associated with local gingival recession at the site of placement, but there is no evidence that it is associated with generalized or severe periodontal disease [78]. In concluding this section it can be stated that there is no doubt that smoking negatively influences periodontal health, although to what degree may be difficult to assess because most studies were done on selected patient groups and the results are difficult to apply directly to the general population.

Further evidence is needed to determine the effect of smoking cessation on disease progression and treatment and the basic causal connection between smoking and periodontal disease still needs to be elucidated. A recent study assessing the evidence for a causal association between smoking and adult periodontitis suggests that such an association exists, but randomized controlled human prospective studies or community intervention studies are needed [79].

There is substantial evidence that intervention in the smoking habits of the patients should form an integral part of treatment plans and general preventive measures in the dental setting. Implant Survival Several studies have indicated a negative effect of smoking on the survival of dental implants [for review, see 80], and recent studies support this finding [81—84]. In some studies, however, patient characteristics are not reported in detail, confounding factors do not always seem optimally controlled, and multivariate analyses are rarely included.

Implant failures believed to be attributable to smoking seem to be more common in the maxilla than in the mandible. Contrary to the general previous belief, it has been recently suggested that the increase in 26 Med Princ Pract ;12 suppl 1 —32 the number of implant failures in smokers is not the result of poor healing or ossointegration, but is due to the exposure of peri-implant tissues to tobacco smoke [83], possibly linking the smoking effects on implant survival to the smoking effects on periodontitis.

The protocol involved complete cessation of smoking for 1 week before and 8 weeks after initial implant placement. It was concluded that the protocol demonstrated considerable promise in improving the success rates of implant integration in smokers who complied; however, it was noted that the sample size for smokers was relatively small. Furthermore, as touched upon above and acknowledging the problems attached to this, the study did not include a randomization of patients in terms of those following the protocol and those continuing their smoking habit.

There seems to be no doubt that smoking can be associated with higher rates of implant failure and altered periimplant conditions, but as indicated above the magnitude of the problem is difficult to assess from available studies. In general, it seems desirable to improve clinical trials in the field of oral implants [86]. Saliva and Caries Studies on the effects of smoking on saliva flow rates and composition show varying results and are difficult to compare [for a comprehensive review, see 7].

Tobacco usage immediately stimulates salivary flow, but there is no long term effect on saliva flow rates. The pH of saliva rises during smoking, but over longer time periods most studies indicate that smokers have slightly reduced pH and buffering power compared to nonsmokers. A consistent finding is an increased concentration of thiocyanate in saliva. A component in normal saliva, thiocyanate is also present in tobacco smoke, and its concentration in saliva can be used to monitor tobacco exposure.

A recent study showed that smoking is associated with lower salivary cystatin activity and output of cystatin C during gingival inflammation [72]. Cystatins are thought to contribute to maintaining oral health by inhibiting certain proteolytic enzymes. In addition this study confirmed earlier results that showed no significant differences in salivary flow rates between smokers and non-smokers.

Rather few studies have shown a relationship between smoking and a higher incidence of dental caries [51, 87, 88].

Data, Research Interpretation, and Evidence-Based Dentistry

clinical decisions is well established in health care, including. dentistry. Defence of .. are based on evidence-based practice or principles. • The Centre for. Proceedings of the International Conference onEvidence Based Practice in Dentistry Kuwait, October 2–4, Faculty.

Recent studies support these findings [89, 90]. There is no evidence of any direct aetiological relationship, but Reibel the findings of higher counts of lactobacillus and, although various results are reported, Streptococcus mutans in smokers [91] may explain this relationship.

It is interesting, although not easy to explain, that maternal smoking is associated with the occurrence of caries in preschool children, even when adjusted for social class, nutritional status, and weekly expenditure on confectioneries [92]. In previous studies there was insufficient evidence to support an association between smokeless tobacco and dental caries [7].

A recent study from the USA, however, indicates an association, in particular in terms of root surface caries. This may be explained by the high proportion of sugar in some types of smokeless tobacco [93]. Thus, there are a few studies suggesting an association between tobacco usage and dental caries, although a direct aetiological relationship is lacking.

It seems at least that smoking is a risk indicator of increased caries activity. Other Effects of Smoking on the Mouth Aesthetics, Smell and Taste Smoking causes discoloration of teeth, dental restorations, and dentures, affecting the aesthetic appearance of the mouth [94, 95], and it contributes more to discoloration than does the consumption of coffee and tea [96]. Smoking is a common cause of halitosis, and it affects the acuity of smell and taste [97, 98].

Odor identification was affected in a dose-related manner and olfactory function improved upon cessation of smoking [97]. Nonsmokers were able to detect salt NaCl concentrations 12—14 times lower than the lowest concentration heavy smokers were able to detect [99]. Recently it was shown that smokers in a Turkish population had significantly more pigmented oral surfaces than non-smokers []. The changes are symptomless, it is not premalignant, and it seems that the pigmentation is reversible upon smoking cessation [, ].

Hairy tongue and coated tongue are other harmless lesions related to smoking, although they can be seen in nonsmokers as well [, , ]. Oral Candidosis A relationship between oral candidosis and smoking has been suggested for a long time fig. The suspicion arises from studies in which patients with oral candidosis turned out to be smokers in all [, ] or in the vast majority of cases []. Another study of the oral presence of Candida strains in healthy adults and in patients with oral leukoplakia and erythematous candidosis also suggested that smoking is a predisposing factor for candidal infection [].

After antimycotic therapy smokers had relapses of the candidal infection in all cases [], and in HIV-infected patients smokers were less likely to respond to systemic antimycotic treatment than nonsmokers []. Further studies are indeed needed to establish a firm aetiological relationship between smoking and oral candidosis, but it seems fair to inform smokers about the possible relationship and consequences for treatment. A pigmentation prevalence Are dentists actively engaged in tobacco intervention matters? In several studies it has been shown that the majority of dentists consider encouraging their patients to stop smoking [—], but few dentists always or often discuss tobacco habits with their patients [, —].

It was recorded in a study from Italy that more dentists are engaged in tobacco cessation activities []. The main barriers to providing tobacco cessation services to patients are lack of reimbursement, lack of confidence in the effectiveness of advice from the dental profession, and lack of knowledge and material to hand out to patients [—, ]. Although few studies are available, it seems that clinical interventions in dental care are as effective as those in other healthcare settings [].

In spite of this, policies and practices of European dental schools need considerable improvement []. The five As. Tobacco intervention includes tobacco cessation activities, prevention, and public policy development. Preferably, dentists should be competent in all three areas. For the purpose of this review only tobacco counselling in daily practice will be touched upon.

The World Dental Federation FDI adopted a Position Statement on Tobacco in [] in which all oral health professionals are urged to integrate tobacco use prevention and cessation services into their routine and daily practice. Recommendations: How to Help Our Patients? Guidelines for healthcare providers about tobacco cessation activities are similar in Europe and the United States [6, ]. The 5 major steps the 5 As are designed to be brief, requiring 3 minutes or less of direct clinician time fig.

The primary goal is to ensure that every patient who uses tobacco is identified and offered at least a brief intervention at each clinical visit. The following is a summary of the suggested guidelines [], along with some personal opinions. Ask patients about smoking. Advise all smokers to stop. A prescriptive approach should be avoided. Immediate benefits will often motivate the patients more effectively than long-term benefits.

Grisly pictures and morbid statistics often stimulate patient denial.

  • Evidence Based Dentistry;
  • Evidence-based practice.
  • Evolution of Networks - From Biological Nets to the Internet and WWW.
  • Outline of Stratificational Grammar.
  • How to apply evidence-based principles in clinical dentistry.

Instead, dentists should demonstrate the oral effects of tobacco if present, or inform patients about the increased risk of poor response or healing after dental procedures relevant to the patient. If the patient is willing to make an attempt to quit, dentists should assist the patient. If a patient is not at all interested in stopping it is, in my view, rarely beneficial to push the patient. Depending on the training and resources of the dentist and staff, the following steps can be taken in the dental office, or the patient can be referred to a tobacco cessation specialist.

Assist the patient in stopping.

If a patient has a desire to stop, the dentist should help the patient set a realistic quitting date which should be soon but not immediately so that the patient has time to prepare. If consultation time is limited, self-help materials that provide the patient with necessary information about smoking cessation can be provided.

Nicotine replacement therapy nicotine gum, inhaler, nasal spray, or skin patch can be very helpful [, —]. Special consideration should be given to selected populations [, ]. Whatever the approach, the dentist should see to it that the patient leaves the office with a concrete plan for stopping and information about how to prepare for the quitting date and how to successfully stop, keeping in mind that most smokers relapse three to five times before succeeding in stopping.

Reibel Arrange follow-up contact. Follow-up contacts are very important as the chances of a successful outcome are improved when patients know their progress will be reviewed. The dentist should confirm the quitting date, show continuing support, and follow through if the patient was successful or encourage another try if unsuccessful. Follow-ups may be by telephone call, letter, office visit, or a combination of these, and if possible the dentist should arrange to see the patients within one or two weeks after the quitting date and consider a second follow-up one or two months later.

It is important that the entire dental team is aware of the relationship between smoking and oral problems. The clinical staff should be familiar with current facts and encouraged to actively participate in tobacco intervention routines. In particular, dental care workers should encourage tobacco preventive measures among adolescents [, ]. Conclusions The lesions and conditions caused in whole or in part by tobacco use are well known, and there is weighty evidence that smoking has considerable influence on oral health.

But tobacco use is a modifiable risk factor for oral and general disease, and an obvious professional interest in tobacco intervention can make a big difference in the health of an individual or the outcome of a given disease. These facts place dentists in a favourable position to help prevent tobacco-related diseases, and interested practitioners should pursue more formal training in smoking cessation counselling, which should be as much a part of their job as plaque control and dietary advice. Br Med J ; — Head Neck ;— Indianapolis, Indiana University School of Dentistry, Oral Dis ;— Int J Cancer ;— Prev Med ;— Lyon, IARC, Cancer Res ; — Cancer Res ;— Int J Cancer ;—4.

Eur J Cancer ;— Br J Cancer ;— Alcohol, tobacco, diet and the risk of oral cancer: A pooled analysis of three case-control studies. Eur J Cancer [B] ;31B— Lancet Oncol ;i— Oral Oncol ;— Eur J Cancer [B] ;29B— Cancer ;— J Oral Pathol Med ;— Eur J Cancer [B] ;29B— Oral Oncol ; — Mund Kiefer Gesichtschir ;3: — Br J Oral Maxillofac Surg ;— J Dent Educ ; — Clinical findings.

Swed Dent J Suppl ; — Cancer ; — Acta Derm Vener ;— Crit Rev Oral Biol Med ; — Swed Dent J Suppl ;— J Periodontol ;65 suppl — Risk indicators for attachment loss. J Periodontol ;— Risk indicators for alveolar bone loss. A longitudinal study. Evidence-based dentistry EBD is an approach to oral health care that requires the judicious integration of systematic assessments of clinically relevant scientific evidence, relating to the patient's oral and medical condition and history, with the dentist's clinical expertise and the patient's treatment needs and preferences.

The American Dental Education Association ADEA has incorporated the definition of evidence-based dentistry into core competencies required by dental education programs. These competencies focus on graduates to become lifelong learners and consumers of current research findings and require students to develop skills that are reflective of evidence-based dentistry. A dentist's learning curve for using the evidence-based process can be steep, but there are continuing education courses, workbooks and tools available to simplify the integration of current research into practice.

Much less attention is paid to both the other two spheres of Evidence Based Dentistry; clinical expertise and patient values. Clinical expertise plays a part in the successful outcomes of treatment with diagnostic skills preventing over and under-treatments, technical dental skills maximiing the longevity of surgical and restorative procedures and communication skills being core to patient management and perceived success. Not all patients have the same priorities for their care.

Understanding patient's individual needs, wants and circumstances gives the clinician a place from which to discuss treatment options available with the patient. But this becomes out of date as new information and technology appear. Hence it is important, especially with regards to patient safety, for dentists to be able to keep up to date with developments. Having an understanding of how to interpret research results, and some practice in reading the literature in a structured way, can turn the dental literature into a useful and comprehensible practice tool. For this to happen, EBD learning absolutely needs to be at the heart of dental education.

They also acquire ability to interpret, assess, integrate, and apply data and information in the process of clinical problem solving, reasoning, and decision making. EBD is a life long learning process and help to develop ability to learn independently. Evidence-based dental journals have been developed as resources for busy clinicians to aid in the integration of current research into practice. These journals publish concise summaries of original studies as well as review articles. These critical summaries, consist of an appraisal of original research, with discussion of the relevant, practical information of the research study.

Systematic reviews are also helpful for the busy practitioner because they combine the results of multiple studies that have investigated the same specific phenomenon or question. From Wikipedia, the free encyclopedia. Not to be confused with the Nature journal Evidence-Based Dentistry. This article needs additional citations for verification.

Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. British Dental Journal.