Clinical implications of risks factors in daily periodontal practice

Introduction : the concept of conception

Periodontitis progresses in an " infectious cycle " which ultimately leads to destruction of all or part of the periodontium, leading to loss of function (^{Slots and Taubman, 1992}) (^{fig. 1}).

For a periodontal infection to occur, it is first of all necessary to have (amongst other things) a source of one or more infectious agents (bacteria, viruses, parasites) which must then be transmitted to the host. In periodontitis, both the elimination of the source and transmission of the infecting agent from one subject to another are very difficult to achieve (^{Glass and Jensen, 1988} ; ^{Greenstein and Lamster, 1997}).

The pathogenic agents must also be capable of adhering and proliferating on the tissues of the host (^{Gibbons, 1989}). Toothbrushing is capable of detaching and disorganising, at least partially, the biofilm represented by dental plaque. However, in the case of some severe periodontal infections, this strictly mechanical approach is totally or partially ineffective (^{Haffajee et al., 1997}).

The infecting agents must be capable of overcoming the defence mechanisms of the host. For example Actinobacillus actinomycetemcomitans has a cytotoxic effect on polymorphonuclear neutrophils and monocytes (^{Baehni et al., 1979}). Similarly, Porphyromonas gingivalis produces proteases which are capable of degrading immunoglobulins which are produced against them (^{Killian, 1981}). In addition, it has been shown that lipopolysaccharides (LPS) produced especially by Porphyromonas gingivalis modify the immune response in such a way that the defense mechanisms normally directed to protect the periodontal tissues reverse their original role and turn themselves against the host for review, see (^{Page et al., 1997}). In effect, the infected tissues are first invaded then destroyed by enzymes (metaloproteases such as collagenases, elastases, etc.) synthesised, then excreted by certain bacteria and, above all, by some host cells (^{Reynolds et al., 1997}).

For the infectious cycle described above to occur, four conditions must be met simultaneously (^{Sokransky, 1992} ; ^{Charon, Joachim and Sandelé, 1995}) :

1. The presence of pathogenic bacteria

2. The absence of protective organisms

3. The presence of a favourable environment for the pathogenic organisms

4. Innate or acquired deficiency of the immune system

It is apparent that the presence of pathogenic organisms is an essential, but not the only factor needed to initiate periodontal damage.

Protective and pathogenic bacteria

There are about 20 species of pathogenic bacteria amongst the 400 or so which can colonise the oral cavity (^{Mouton and Robert, 1994}). Amongst these Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Campylobacter rectus, Bacteroides forsythus and some of the treponemas are most often associated with active lesions (^{Darveau et al., 1997}) (^{table I}).

The protective organisms (antagonists of the above) are mostly Gram positive, aerobic cocci, fusiform and filamentous organisms (streptococci and actinomyces) (^{Charon et al., 1993}). The use of broad spectrum antibiotics (tetracycline, for example) can modify this protective flora.

The dento-gingival environment

The presence of calculus on the tooth surface can obstruct the entrance to a pocket and create an environment that is favourable for the growth of anaerobic, pathogenic bacteria (if they are present). Also, calculus provides a surface which is favourable for the adhesion of and proliferation of bacteria. It should be noted, however, that " deep " scaling, undertaken without sufficient care for the periodontal tissues, may open a pathway for pathogenic bacteria (^{Charon, 1997}). Lastly, the cervical margins of a denture (whether it is well-fitting or not) can create an environment favourable for the growth of pathogenic bacteria at the heart of the dento-gingival area.

The breakdown of defence mechanisms

It would appear that over 80 % of patients suffering from advanced periodontitis have a genetically determined defect which is expressed in an excessive production of IL-1α, TNF-α , prostaglandin-E2, reduced production of Ig2 and of Fc immunoglobulin receptors on the surface of neutrophils (^{Page et al., 1997}). In addition, Porphyromonas gingivalis is capable of inhibiting the adhesion of leucocytes to endothelial cells, thus blocking the first stages of the protective inflammatory reaction (^{Darveau et al., 1997}). Patients suffering from advanced destructive periodontitis seem to have a genetically determined dysfunction of polymorphonuclear neutrophil chemotactic, phagocytic and oxygen-dependent bactericidal activity (^{Van Dyke et al., 1984} ; ^{Charon et al., 1985}). Host response is also modified by smoking, to an extent which is similar to the genetically determined effects on the immune system (^{Page et al., 1997}).

Epidemiology of periodontal risk factors

It is evident that the possibility of all the four conditions described above occurring simultaneously is minimal. This is why most cases of gingivitis are stable and why a large number of cases of periodontitis progress relatively slowly (as in the case of ordinary chronic adult periodontitis) (^{Charon et al., 1995} ; ^{Charon, 1997}).

In addition, the severity of each of these four conditions can vary and therefore account for the diversity of clinical features (^{fig. 2}). For example, the virulence of pathogenic bacteria and variations in immune response may be significant. For a given severity of disease, the frequency with which these four conditions are met may be increase to a greater or lesser extent. This is the case in early onset periodontitis (rapidly progressive, localised juvenile periodontitis) or where there has been severe, often generalised, loss of attachment at a relatively early age, because of frequent bursts of disease activity following one after the other (^{Page et al., 1997}) (^{fig. 3a}, ^3b, ^3c and ^3d).

All clinicians agree that the severity of periodontal disease is not the same for all subjects. Recent research has confirmed this clinical impression and has shown that some subjects are more at risk of the four conditions for periodontal damage being met simultaneously (^{fig. 3a}, ^3b, ^3c and ^3d).

All clinicians in everyday practice are likely to encounter patients without attachment loss despite being at high risk of developing severe pathology whatever their speciality or wherever they practise.

At the dawn of the 21st Century, it is probable that more and more patients will be less likely to accept a debilitating loss of teeth and will demand that our profession provides a specific and effective preventive strategy, as well as clinical procedures capable of detecting those patients who are at risk at a very early stage, in order to prevent periodontal damage before it has occurred. This is especially important because we have developed complex and expensive treatments (tooth and implant supported dentures, orthodontic and restorative procedures) which are in danger of failure in susceptible patients if the periodontal risk is not 1) detected early, and then 2) minimised or even eliminated (^{Grace and Smales, 1989}). Our profession possesses a large arsenal of therapeutic procedures once periodontal disease is established. In contrast, we have at our disposal relatively few means of determining if an individual is resistant or susceptible to periodontal breakdown.

The management of periodontal risk has become a major problem for dentists. Even if there has been considerable progress on this area, it seems that there are no clearly defined and 100 % reliable techniques which will predict if a subject is at high or low risk in relationship to periodontal diseases (^{Charon, 1992}).

The acclaimed study of ^{Löe et al. (1986}) was one of the first to show that not all cases of gingivitis necessarily progressed to advanced periodontitis which would put the integrity of the dental arch in danger (^{fig. 4}). In effect, a minority (estimated at a few percent) of subjects may have gingival inflammation (due to total or relative lack of toothbrushing) and not suffer particularly severe attachment loss. Therefore, there exists a group of subjects who are " immune " to destructive periodontal diseases.

Beside these resistant subjects, a great majority (about 80 %) of cases of gingivitis will progress relatively slowly to a severity of periodontitis which is not particularly debilitating, suggesting that, in these subjects, the four conditions necessary for periodontal destruction occur together infrequently and/or to an insufficient degree (^{fig. 4}).

Finally, a minority of subjects (5 to 15 %, depending on the study) experience a rapid loss of attachment which will render them partially or totally edentulous by the age of 50 (^{Becker et al., 1979} ; ^{Buckley and Crowley, 1984} ; ^{Baelum et al., 1988} ; ^{Burt, 1988} ; ^{Löe et al., 1986} ; ^{MacFall et al., 1989}).

Characteristics and detection of subjects at risk

The predominant approach to the prevention of periodontal diseases has for a long time been the systematic, complete control of gingivitis by the institution of strict standards of dental hygiene (^{Alcouffe, 1988}). Therefore, all patients have been encouraged to " clean " their teeth very thoroughly three times a day for three minutes and to consult their dentist for scaling, polishing and " prophylaxis " (^{Rateitschak and Wolf, 1986}). For the majority of subjects, this form of prevention is unrealistic both for financial reasons and reasons of human weakness. Also, dental hygiene (to have " clean " teeth) does not prevent periodontitis in some high risk patients (^{Burt, 1991}). Therefore, our object must be to concentrate our efforts and resources to the benefit of those patients who are most at risk of developing severe periodontitis, rather than those who are not, or less so. One can easily understand, therefore, that it is no longer possible (or ethical) to treat all cases of gingivitis (which affect a large number of patients) as if they are all susceptible to progressing to " aggressive " periodontitis (as has been suggested in the 1960s) (^{Orban, 1955}).

The priority must be for the efforts of qualified periodontists (researchers and/or clinicians) to be concentrated on the detection, treatment and prevention of those cases of gingivitis which are at risk of developing into rapidly progressing periodontitis.

How can we predict which subjects are susceptible to developing severe periodontal diseases ?

In the discussion which is to follow, we present several characteristics of those patients who are " at risk " according to the following proposed definition : An individual at risk is one who, in the absence of effective preventive measures, suffers a debilitating total or partial loss of teeth before the age of 50.

Those subjects at highest risk of developing advanced periodontitis, present with one or more of the following five major clinical features which are consistent with both the existing concept of the pathogenesis and aetiology of periodontal diseases as well as the basic idea of the infectious model (^{Charon et al., 1990b} ; ^{Johnson, 1992} ; ^{Salvi et al., 1997}).

1. Family history of advanced periodontitis

2. Unfavourable response to psychological stress

3. Susceptibility to primary or secondary infections

4. Reduced susceptibility to dental caries

5. History of acute necrotising ulcerative gingivitis

We will see that most of this information can be collected relatively easily and quickly during the course of normal maintenance treatment, in surroundings conducive to mutual confidence (^{Charon and Joachim, 1996}). Furthermore, one must understand that this detection of individuals at risk is carried out on subjects who have not lost attachment but who are at risk of doing so. Therefore, this periodontal risk assessment must be repeated every year.

Equally, it should be understood that the characteristics of subjects at risk of developing severe periodontitis are the same as those who relapse after treatment. As a consequence, if the five characteristics are rediscovered in a patient who has already suffered from periodontitis, rigorous treatment and maintenance must be re-instituted (^{Charon, 1997} ; ^{Axtelius et al., 1997}).

Family history

Researchers have asked the question whether there is a genetic origin for periodontal diseases. For a long time, a search has been made for a correlation between certain genetic markers and periodontal disease, but has been difficult to find. However, in the case of identical twins, it has been shown that individual susceptibility to periodontal problems can be partially attributed to genetic factors (^{Michalowicz et al., 1991} ; ^{Corey et al., 1993}) (^{fig. 5a}, ^5b, ^5c and ^5d ).

Certain families are genetically predisposed to developing severe forms of periodontitis (pre-pubertal, juvenile, post-juvenile and rapidly progressive) (^{Boughman and Neiders, 1986} ; ^{Boughman et al., 1988}). We have already referred to the nature of the genetic defects and their effects on the periodontal tissues. Simply add to that the protection afforded to the periodontal tissues by the production of certain cytokines (IL-10) (^{Kornman et al., 1997}).

A retrospective study we have undertaken, has demonstrated that all patients who presented with rapidly progressive periodontitis (generalised loss of attachment of 60 % or more by the age of 35) gave a family history of advanced periodontitis. Groups of those at " average or low risk " (patients with localised loss of attachment not exceeding 25 % by 60 years) have a much lower percentage of antecedents with severe periodontitis (^{Charon, 1992}) (^{table II}).

This hypothesis of a genetic predisposition to periodontal diseases has now been confirmed (^{Hart, 1996} ; ^{Hart and Kornman, 1997}). The implicated chromosomes are as follows : chromosome 6 (for genes coding for IgG 2, TNF-α, FcγII) ; chromosome 2 (for genes coding for IL-1β) ; chromosome 9 (for genes coding for PGE-2) (^{Hart and Kornman, 1997}). Therefore, we have at our disposal a simple, rapid and relatively inexpensive means of detecting individuals and families with increased risk of developing periodontal diseases. In effect, the great majority of patients with one or more close relatives (father, mother) suffering from periodontitis having led to tooth loss, are well aware of this and will spontaneously refer to it at the first consultation (^{Charon et al., 1995}). In case of doubt, it will soon be possible to take a drop of blood from the finger and see whether the genetic markers for susceptibility are present or absent (PST Test, Medical Science System Inc., USA).

A patient suffering from periodontitis could then be informed of the strong probability that other members of the family could also develop periodontitis. A detailed record, including history, clinical examination and special tests (radiological and microbiological) must, however be fairly systematic in order to confirm the presence or absence of existing loss of attachment.

The presence or absence of antecedents with severe periodontitis can easily be ascertained during the first interview.

The adverse effects of psychological stress

There are many papers which indicate that a link exists between psychological stress and reduced resistance to certain diseases (^{Cousins, 1988} ; ^{Meyer and Haggerty, 1962}). Studies have shown a direct link between mood, a positive attitude, meditation and an increased immuno-competence (^{Dillon and Totten, 1989} ; ^{Ratliff-Crain et al., 1989} ; ^{Stone et al., 1987}). The effects of repeated episodes of psycho-social stress on the immune system have been described in both man and animals. In general, stress reduces immune response, whereas psychological stimuli, in the absence of anxiety, enhance immune reactions (^{Ballieux, 1991}).

The relationship between stress and certain pathologies of the oral mucosa, such as aphthous ulceration, has been fully documented (^{Peresen, 1989}). However, the influence of stress on the periodontal tissues is only partially understood (^{Green et al., 1986}). A correlation between stress and acute necrotising ulcerative gingivitis is the only one that has been established for reviews see (^{Johnson and Engel, 1986} ; ^{Da Silva et al., 1995}). Patients suffering from acute necrotising ulcerative gingivitis present with a diminution of lymphocytic function and reduced chemotactic and phagocytic capability of neutrophils. ^{Ballieux (1991}) suggests that there is a relationship between certain infections of the oral cavity and immuno-suppression, linked to stress. ^Wilton ) as well as ^Axtelius ) propose that stress is a risk factor for periodontal diseases.

Even if the relationship between stress and periodontal destruction has been suggested since the 1960s, the objective measurement of stress is complicated and the relationship between stress and periodontal diseases remains difficult to prove (^{Baker et al., 1961} ; ^{Davis and Jenkins, 1962} ; ^{Barry and Dutkovic, 1963}).

As clinicians, can we ignore the importance of psychological stress in our patients ?

We believe that certain signs and symptoms, revealed in the medical and personal history of patients, may uncover the existence of stress which may lead to periodontal problems caused by decreased immune response (^{table III} ; ^{fig. 6a} à ^6f ). This view is supported by the fact that the majority of patients with increased risk show subjective signs of stress, contrary to patients at low risk (^{Charon et al., 1992}).

It can be seen that it is of fundamental importance to watch out for signs of psychological stress during the first interview.

Equally, it should be understood that certain attitudes exhibited by the practitioner, whether positive (empathy, competency) or negative (arrogance, harbouring feelings of blame, expressing poor prognosis with inadequate preliminary explanations), can reduce or increase the amount of stress to which the patient is subject. In view of the fact that we have not been trained in this area, it may be appropriate to refer the patient to a psychologist for part of the treatment. However, care is necessary because mismanagement in this domain can lead to devastating results.

Susceptibility to infection

Some individuals will present with systemic conditions or disorders which can increase their individual susceptibility to infection, leading to more severe or more frequent attacks of disease, including periodontal diseases (^{Sandelé et al., 1992}). These systemic disorders are now considered to be secondary factors which enhance attachment loss as much as the primary aetiologic factors do (^{Genco and Löe, 1993}).

An extreme example of a systemic disorder which exposes the individual to infection and which is vitally important for the assessment of prognosis is AIDS (Acquired Immune Deficiency Syndrome caused by one or more of the HIV retroviruses). Some of these patients develop very aggressive periodontal diseases accompanied by ulcerous and/or necrotic lesions which denude the underlying alveolar processes (^{fig. 7}) (^{Sandelé et al., 1992}).

Also, the uncontrolled insulin-dependant diabetic carries the risk of developing severe periodontal disease (^{Cianciola et al., 1982}). It should also be noted that the opposite is also true (the presence of active periodontal disease can present difficulties for the control of diabetes) (^{Salvi et al., 1997}).

In all situations where the number or function of leucocytes are affected, as in neutropenia (^{Cohen and Morris, 1961}), agranulocytosis (^{Bauer, 1946}), defects in neutrophil adhesion, chronic granulomatoses disease of childhood, Papillon-Lefèvre syndrome (^{Van Dyke et al., 1984}), neutropenia caused by chemotherapy for malignant disease, cyclosporin therapy etc., are all risk factors and must therefore be diagnosed and treated (often with the assistance of a competent physician) (^{Tollefsen et al., 1978} ; ^{Robertson et al., 1980}).

It is necessary to include in the « high risk » group those patients who are suffering (or have suffered) from post-operative or recurrent infections following routine procedures (for example a history of peritonitis following appendicectomy, or a post-extraction infection). On the basis of our clinical experience and studies undertaken in our practice (^{Charon, 1992}), we would consider that all those who suffer recurrent infections, especially of the upper respiratory tract, are at periodontal risk.

Nowadays, we have sufficient grounds to believe that excessive tobacco use has a major effect on reducing host defences and is often associated with advanced periodontitis (^{Brochut and Cimasoni, 1997a} and ^{Brochut and Cimasoni, 1997b})

Much information can be gained from a patient's medical and dental history during the course of the first interview .

Susceptibility to dental caries

A considerable proportion of high risk patients have had few or no carious lesions. In one study, ^{Sewon et al. (1988}) verified what had, for a long time, only been a clinical impression.

The bacterial flora of the plaque biofilm is a complex ecosystem where certain bacteria enhance or inhibit the growth of others. There is an antagonistic action between Streptococcus sanguis (S. sanguis) and Actinobacillus actinomycetemcomitans (Aa). S. sanguis produces hydrogen peroxide which either by direct action or by enhancing host enzyme activity, kills Aa (^{Myazaki et al., 1984}). Also, the presence of large numbers of Aa can reduce the numbers of streptococci and hence reduce the risk of inducing dental caries (or conversely, an increased number of S. sanguis brings with it a reduction in the number of periodontal pathogens such as Aa.

The bacteria implicated in the causation of periodontal diseases are essentially proteolytic and assaccharolytic, in contrast to those associated with caries which are saccharolytic (^{Loesche, 1968}). This bacterial antagonism explains the reason why there is often very little caries in some patients suffering from advanced periodontitis (^{fig. 8a} and ^8b).

The susceptibility to caries can be determined by simple clinical examination, assessment of panoramic radiograph or (better) by long cone intra-oral radiographs. Information on the susceptibility to caries can therefore be obtained during the first interview.

History of acute necrotising ulcerative gingivitis

Acute necrotising ulcerative gingivitis (ANUG) is characterised by the sudden onset of painful, necrotic, haemorrhagic lesions affecting predominantly the interdental papillae (^{Williams et al., 1992} ; ^{Charon et al., 1995}).

Patients who suffer one or more episodes of ANUG have a greater risk of developing rapidly progressive periodontitis later in life (^{Charon et al., 1990b}). A history of one or more attacks of ANUG in a patient can, therefore, be an additional indication to the practitioner that he is dealing with a high risk patient. Given the characteristic clinical symptoms associated with ANUG, it is unusual for a patient not to mention it in his history. In addition, the clinician can sometimes see the results of the disease in the patient's mouth (loss of papillae). We are beginning to think that ANUG may be the very first stage of rapidly progressive periodontitis, prior to the appearance of clinical signs.

Once again, the first interview and case records are of great help in the detection of high risk subjects.

Clinical implications for healthy subjects with risk factors

One can see the importance of the interview following a detailed clinical examination, for the detection of one or more risk factors. This need not take more than 15 minutes (^{Charon & Joachim, 1996}). It must be followed by clear and adequate explanations to enable the patient to understand the importance of the detection of risk factors.

Clinical and microbiological examination and recall

Once the clinical examination have been completed, we then have a patient who has not lost periodontal attachment but who possesses one or several risk factors. We can find ourselves faced with two extreme situations ; the subject is diagnosed as either 1) high, or 2) low periodontal risk (^{fig. 9}). Evidently, after we have evaluated the significance of each of the factors, it is possible that we may find that the patient is between the two extremes (^{fig. 9}). For the purposes of this paper we will assume that we are faced with either a high risk or low risk patient.

We recommend that in the first instance, samples of subgingival plaque be taken from one or more sites and examined by phase contrast microscopy to determine the motility of plaque organisms, the presence or absence of spirochaetes, motile bacilli or other filaments or cocci. If in doubt, one can resort to microbial culture (Laboral) or to DNA probes (Parogene, Strasbourg ; DMX Pathotek, Zurich), although the results will not be available until one or several weeks later (^{Charon et al., 1993}).

We propose that in order to evaluate the periodontal risk, an examination should be undertaken to determine the presence or absence of putative periodontal pathogens.

Low periodontal risk

These are patients who present with no, or few of the periodontal risk factors (^{fig. 10}).

In this case, if periodontal pathogens are discovered , it is sufficient to prescribe the traditional hygiene methods. The type of toothpaste to be used is unimportant. However, it may be wise to recommend a toothpaste containing sanguinarine or chlorhexidine (Veadent PerioGard^®, Colgate ; Paroex^®, Pharmadent), in case of exposure to periodontal pathogens.

High periodontal risk

These are the patients who present with one or more risk factors. In these cases two approaches are possible according to whether the flora is 1) compatible with health, or 2) contains putative periodontal pathogens (^{fig. 10}).

If the flora is compatible with periodontal health

It is necessary to put in place a method of plaque control which will ensure that the flora remains compatible with periodontal health. Sanguinarine (Veadent PerioGard^®, Colgate) in both mouthwash and toothpaste appears to be the best recommendation. This agent can control a moderate number of pathogenic bacteria to which the patient may be exposed (^{Charon et al., 1990a}).

Equally, a chlorhexidine-based toothpaste or gel (Paroex^®, Pharmadent) may be used. A 0.12 % aqueous solution chlorhexidine mouthwash (Parodex^®, Pharmadent) may be prescribed but beware that a greater or lesser amount of tooth staining will be inevitable.

If putative periodontal pathogens are present

In cases where there is a combination of periodontal risk factors and pathogenic bacteria, even the most rigorous oral hygiene, when performed with normal commercial toothpastes, is not adequate. If an adequate preventive antimicrobial treatment is not instituted, there is a risk that sooner or later there will be loss of attachment which may be severe.

The use of antiseptics such as hydrogen peroxide (5 to 10 volumes), bicarbonate sodium, 0.2 % chlorhexidine (Corsodyl^®, SmithKline Beecham) or 0.12 % (Parodex, Pharmadent) is especially indicated until the flora becomes compatible with health at which time the patient comes into the high risk/compatible flora group, described above.

In those patients who are severely medically compromised (uncontrolled diabetics, those with haematological disorders, receiving chemotherapy for malignant disease, etc.) antibiotics may need to be prescribed (^{Charon et al., 1995}). The antibiotic regime to be used will depend upon the nature of the flora. It may be metronidazole, either alone or with a macrolide (Flagyl^®, Rodogyl^®), amoxycillin either alone or with clavulanic acid (Clamoxyl^®, Augmentin^®) (^{Van Winkelhoff et al., 1996}).

One can see that, over a period of years, high risk patients may alternate between a compatible and pathogenic flora, depending on how careful they are with their home care measures and/or whether they have contact with persons who may be healthy but who may be carrying a pathogenic flora. In the latter instance the possibility of bacterial transmission exists.

Every patient must be re-evaluated for risk factors every year.

Conclusions

One sees, therefore, that periodontal risk has moved away from the status of occlusion, the width of attached gingiva, the bony architecture and the cleanliness of the teeth (^{Johnson, 1992}).

To detect and deal with periodontal risk, the practitioner must exercise a strictly medical approach in order to achieve significant beneficial outcomes for both the patient and the practitioner. This cannot be done instantaneously with a quick check on the oral hygiene. It must be carefully and thoroughly planned.

We are convinced that our approach to periodontal risk will have to be modified again in years to come, to take into account the considerable progress which has been (and will be) made in genetic and molecular biology. Perhaps with genetic therapy it will even be possible, one day, to prevent the onset of debilitating periodontal disease in many patients (^{Gemmel et al., 1997}).

The authors wish to thank faithfully Charles Crasquin for his help in reviewing this article.

1. It is evident that the clinical appearances of periodontal diseases vary from one person to another and from one disease to another (age of onset, distribution of attachment loss in the mouth, response to treatment rate of progress of disease, etc.).

2. Not only by a simple questionnaire completed by the patient in the waiting room.

3. In the study room, which is better than in the dental chair.

4. The delicate question of fees for the detection of risk factors remains to be resolved because, in France, at least, the health and social insurance system will not pay for prevention.

5. These have long considered to be the only risk factors in periodontology.

6. It will be difficult, given the corporate nature of our profession, to accept this idea.

Demande de tirés à part

Jacques CHARON, 27, quai du Wault, 59800 LILLE - FRANCE. E-mail : jcharon@nordnet.fr.

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