INTRODUCTION

As our understanding of periodontal diseases has deepened, it has become clear that certain risk factors are associated with disease development. As dental professionals seek to optimize treatment and improve outcomes for patients, the role of risk assessment and disease management has become increasingly important.

RISK ASSESSMENT..

According to MeSH, risk assessment can be defined as the Qualitative or quantitative estimation of the likelihood of adverse effects that may result from exposure to specified health hazards or from the absence of beneficial influences.
Risk assessment involves dental care providers, identifying patients, and populations at increased risk of developing periodontal disease. The assessment of patients risk to controlsignificant impact on clinical decision making.

 Rather than concentrating on obvious pathology that requires immediate (and typically surgical) intervention, the risk assessment model invites dental care professionals to take a step back and look at the potential development of dental disease over the long term. To improve clinical decision making, risk assessment can reduce the need for complex periodontal therapy, improve patient outcomes and ultimately reduce oral health care costs.

 This presentation reviews the application of risk assessment and disease management to the general population and to groups at risk of developing periodontal disease.

RISK FACTORS
A risk factor can be defined as any environmental, behavioral, or biologic factor that, when present, increases the likelihood that an individual will develop the disease. Risk factorswith a disease but..cause the disease. However, to be identified as a risk factor, the exposure must occur before disease onset.

 Risk factors may be modifiable or non-modifiable.

Modifiable risk factors are usually environmental or behavioral in nature whereas non-modifiable risk factors are usually intrinsic to the individual and therefore not easily changed. Non-modifiable risk factors are also known as determinants.

 Associations identified through longitudinal and interventional studies are termed risk factors whereas associations, based on the observations of cross-sectional and case controlled studies are termed risk indicators.
Thus the term risk factor denotes a greater weight of evidence supporting an association than does the term risk indicator.

CRITERIA FOR CAUSAL RELATION ACCEPTANCE

Causal inference, i.e. the procedure of drawing conclusions related to the cause of disease is a complex issue.
In the 1970s, Hill (1971) formalized the criteria that have to be fulfilled in order to accept a causal relation. These included: Strength of association Dose-response effect Temporal consistency Consistency of the findings Biological plausibility Specificity of the association

1. Strength of association:
- Stronger the association between the potential risk factor and disease, the more likely it is that the anticipated causal relation is valid. 2. Dose-response effect: - An observation that the frequency of the disease increases with the dose or level of exposure to a certain factor supports a causal interpretation.

3. Temporal consistency:
- It is important to establish that the exposure to the anticipated causative factor occurred prior to the onset of the disease. - This may be difficult in case of diseases with long latent periods or factors that change over time. 4. Consistency of the findings:

- If several studies investigating a given relationship generate similar results, the causal interpretation is strengthened.

5. Biological Plausibility:
- It is advantageous if the anticipated relationship makes sense in the context of current biological knowledge. - Less that is known about the etiology of given disease, more difficult it become to satisfy this criterion. 6. Specificity of the association:

- If the disease is found to be associated with only one factor among a multitude of factors tested, the causal relationship is strengthened.

- it is important that the criteria described are meant as guidelines when a causal inference is established.
- None of them, however, is either necessary or sufficient for a causal interpretation. - Strict adherence to any of them without concomitant consideration, may result in incorrect conclusions.

PRINCIPLES OF RISK ASSESSMENT PROCESS

According to BECK (1994): STEPS: Identification of factors to be associated with the disease. In case of multiple factors, Multivariate risk assessment model must be developed that discloses which combination of factors does most effectively discriminate between health and disease. Assessment: new populations are screened for this combination of factors. Targeting: exposure to the identified factors is modified by prevention or intervention and the effectiveness of the approach in suppressing the incidence of the disease is evaluated

 Thus, according to this process, potential or putative risk factors are first identified and thereafter tested until their significance as true risk factor is proven.

PERIODONTAL RISK FACTORS

According to Borrell and Papanou (2005):

- Non amenable to intervention ( non modifiable background factors)

- Modifiable factors (environmental, acquired and behavioral)

NON MODIFIABLE BACKGROUND FACTORS

AGE:
Aging.increased incidence.. - Studies on periodontal disease prevalence, extent, and severity show more disease in older age groups compared with younger groups. - However it has been suggested that the increased level of periodontal destruction observed with aging is the result of cumulative destruction rather than a result of increased rates of destruction, thus aging is not a risk factor per se.

 GENDER:

Periodontal disease.. men at comparable ages.

Diseases related to attachment loss and bone height are more common. - Men exhibit poor oral hygiene and report fewer visits to the dentist, than women. - Female estrogen hormone protect against destructive periodontal bone loss.

 RACE:

Assessment related to race, socio-economic status (SES) and poverty have been unsuccessful in making associations with periodontal disease.
Race/ ethnicity is a social construct that determines an array of opportunities related to access, status and resources. As a result,

- Race and SES are strongly intertwined, suggesting that the racial effect may partially attributed to confounding by SES due to the unequal meaning of SES indicators across racial groups.

 In a study of risk indicators for African Americans and Caucasian Americans, there were more indicators related to socioeconomic status.

- For e.g. Prevotella intermedia was a risk indicator for African Americans but not for Caucasian Americans. But when persons from both races belong to the same socioeconomic group, differences in periodontal disease disappeared.

 GENETIC FACTORS: affect most oral conditions.

a. Genetic aspects of localized Juvenile Periodontal disease: - LJP has a familial aggregation and has been thought to be a genetically determined condition. - According to Long, Beaty, Hart , Saxby; periodontitis is a because of autosomal mode of inheritance (transmission). - According to some studies, genetic abnormalities in neutrophil function may also associatebecause in LJP, the nuetrophil functions are associated with genetic polymorphisms.

 Attempts to associate human leukocyte antigens (HLA) with JP are conflicting.

- Reinholdt and colleagues.LJP patients have higher prevalence of HLA-AG, HLA-A28, HLA-BW15.

b. Genetic aspects of adult periodontitis: Three approaches have been carried out, - Human leukocyte antigen associations

- Twin studies,
- Genetic polymorphisms

i.

Human leukocyte antigen association:

- Early studies negative association of periodontitis with HLA-A2.

- Klouda, Amer and colleagues showed: increase in HLA-Ag in patients with periodontitis, which was related to report presented by Reinholdt for JP.

ii. Twin studies:

- Carried out on 26 sets of twins aged 12-17 years, 7 pairs: monozygotic and 19: dizygotic. - No differences in gingival recession, gingival crevice depth, gingival bleeding, calculus or plaque.
- Michalowicz and colleagues: alveolar bone was significantly affected by genetic factors. - The same group found: genetic influence on gingivitis, probing depth, attachment loss and plaque.

- These studies are provocative, leading to hypothesis relating to genetic factors in periodontal disease.
- However, data must be reviewed cautiously, - Changes in alveolar bone height may be genetic due to anatomic variation and may or may not be related to periodontal disease per se.

iii. Genetic Polymorphisms:

- Are associated with adult periodontitis.

- For e.g. Kornman studied genetic polymorphisms in Proinflammatory Cytokines IL-1. AND TN F-.
- This genotype was only responsible for PD in non smokers and not in smokers.

 Van Schie and colleagues: relation between polymorphism pattern & periodontitis.
Hence, it appears that candidate gene polymorphisms are a useful approach in assessing genetic factors in both JP & AP.

 Pregnancy: Periodontal disease has been shown to be associated with preterm delivery and low birth weight`.

A recent study found a significant association between preterm birth and third-molar periodontal disease in pregnant women.
Analysis of gingival crevicular fluid has demonstrated significantly higher levels of the inflammatory mediator prostaglandin E2 in women who delivered preterm low-birthweight infants.

 However, other research has failed to demonstrate a link between preterm low-birth-weight babies and periodontal disease. Although a causal connection has not been established, it is appropriate to advise expectant mothers about the importance of good oral health, including the use of antimicrobial rinses to mitigate the impact of pathogenic bacteria.

MODIFIABLE [ENVIRONMENTAL, ACQUIRED & BEHAVIORAL]

Periodontal Microflora: - There are over 400 genera and species of micro-organisms.

- Three mainly implicated as etiogenic agents:

i. Porphyromans gingivalis, ii. Tannerella forsythia (Bacteroides forsythus) and

iii. Actinobacillus actinomycetemcomitans.

 P. gingivalis and P. intermedia: PD in older adults.

P. gingivalis and B. forsythus: increased risk for attachment loss and alveolar bone loss. Presence of pathogens to is not sufficient.

 The odds ratio of developing periodontal disease in an individual who harbors one of the putative perio. Pathognes is not high enough to consider them a risk factor.
Presence of A. actinomycetemcomitans confrs no additional risk of developing LAP, despite it is necessary for the disease to develop. It has been shown that P. intermedia, P. gingivalis and Fusobacterium nucleatum may be risk indicators for periodontal disease in a diverse population, though they are not risk factors.

 Socio- economic status (SES):

- Gingivitis and poor oral hygiene can be related to lower SES.

- This can be attributed to decreased dental awareness and decrease frequency of dental visits compared with more educated individuals of higher SES. - Lower SES alone does not result in increased risk for periodontitis has to be adjusted with other risk factors, such as smoking and poor oral hygiene.

 Stress & psychological factors: - The incidence of NUG increases in emotional and physiologic stress. - Emotional stress may interfere with normal immune function and may result in increased levels of circulating hormones which can affect the periodontium. - Association between psychological factors and risk behaviors ( smoking, poor oral hygiene)chronic periodontitis.

 Individuals with stress are more likely to develop clinical attachment loss and loss of alveolar bone.
This may be due to link between stress and increase in production of IL-6 Also the host response to P. gingivalis infection may be compromised in psychologically stressed individuals.

 Despite existing evidence from case control and cross sectional studies, no longitudinal or interventional studies have been published that confirm psychological stress as a risk factor for P.D. Perhaps the relationship is due to the fact that individuals under stress are less likely to perform regular good oral hygiene and prophylaxis.

 Tobacco Smoking:
The history of association investigated in the middle of the last century. Recently, many epidemiological, clinical and in vitro studies have proven that smoking negatively impacts periodontal health. The incidence of CAL and ABL increases with increased smoking - Heat from smoke may enhance attachment loss, and the increased calculus deposits that often result from smoking can enhance plaque retention.

- Nicotine can diminish collagen synthesis, protein secretion and may inhibit bone formation.

 Former smokers (clinically 5 or more years since quitting), experience less AL than current smokers and more than never smokers. The likelihood of developing periodontal disease exhibits dose dependency.
Odds ratio for developing perio. disease: - Current heavy smokers: 7.2 - Current light smokers: 3.2 - Former smokers: 1.6

 Smoking is associated with reduced gingival bleeding. Smokers may experience less gingival bleeding than non smokers. It is suggested that,alterations of the caliber of the blood vessels perfusing the gingival tissues.

These findings suggest.. a reduced reliance on the use of gingival bleeding as an indicator of gingival inflammation when assessing a smokers periodontal health.

 Some in vitro studies have shown altered gingival crevicular fluid, inflammatory cytokine profiles, immune cell function and altered proteolytic regulation in smokers.
Also majority of the periodontal treatments are less successful in smokers.

Nonetheless, the results of these studies are inconsistent and no clear mechanism has emerged to explain how smoking may affect periodontal disease.
Smoking and genetic polymorphisms is the new area of research

 Diabetes Mellitus:
- It is modifiable factorthough it cannot be cured, it can be controlled. - It is clear risk factor for periodontitis. - In general, no difference in impact has been determined between type I & Type II.

 Kinane found that,.direct relationship while, Taylor et al.bidirectional relationship.

A study on Pima Indians showed an odds ratio of 2.8 to 3.4 for developing periodontitis in Type II diabetics to non diabetics.

 Diabetes does not cause gingivitis or periodontitis but..

- It alters the response of the periodontal tissues to local factors, - hastening bone loss and - delaying post surgical healing of periodontal tissues. Frequent perio. abscess is important feature of perio. disease in diabetics. Glucose ^es in blood and gingival fluid > ^es in bact. Activity + polymorphonuclear leukocyte > decrease in collagen synthesis.

 OBESITY: (BMI _> 30)

Involvement of hyper-inflammatory state and aberrant lipid metabolism as well as the pathway of insulin resistance = enhanced breakdown of periodontal tissue support. Number of recent studies point to a positive association. Saito et al.waist to hip ratio, BMI, and body fat .significant risk indicators.

There are only few cross-sectional studies, so, inferences on temporality or mechanisms are not possible.

 CANCER:

Patients who have cancer and who undergo chemotherapy and radiation therapy may experience significant deleterious oral complications, including oral mucositis, xerostomia, radiationinduced dental caries and even osteoradionecrosis.
Opportunistic infections such as Candida albicans have been shown to increase in frequency with mucositis and immunosuppression. The antibiotics and steroids used to treat these infections can result in secondary infections by the normal oral flora.

 DIETARY FACTORS:
i. CALCIUM: - Nishida & co-workers evaluated the role - The group who ingested lower levels of Ca in diet,. Increased risk.

- Some authors showed that, women (20-30) had lower serum calcium levels showed significantly higher risk (odds: 6.1)

ii. VITAMIN C:
- Maintains health of gingiva.

- Severe vit. C deficiency: SCOBUTIC gingivitis.

- NHANES III (1988-1992): less intake of vit. C = increased risk , specially among current tobacco users. - Actual mechanism is not clear.

 MEDICATIONS:
i. PHENYTOIN: ii. CYCLOSPORIN: iii. DIHYDROPYRIDINES: - Overgrowth of gingiva. - Gross increase in size: dramatic expansion of connective tissue component. - t/t: replacement of a drug & perio theray or surgery.

STRENGTH OF ASSOCIATION OF MODIFIABLE AND NON MODIFIABLE FACTORS WITH DESTRUCTIVE PERIODONTAL DISEASE.

RISK INDICATORS FOR PERIODONTAL DISEASE

HIV/AIDS: It has been hypothesized that, the immune dysfunction associated increases susceptibility. Studies revealed, HIV/AIDS patients had severe necrotizing ulcerative periodontitis. Also higher risk for periodontal pockets and CAL.

 OSTEOPOROSIS:
It is systematic factor..oral bone, (alveolar process with peri. Infection). From the assessment of osteoporosis in the jaws by dual photon absorptiometry, it was found that reduction in total skeletal mass is directly related to reduction in mandibular density. (Chesnut, Henrikson et al)

 INFREQUENT DENTAL VISITS:

Failure to visit the dentist regularly as a risk factor for peridontitis is controversial. One study demonstrated an increased risk for severe periodontitis in patients who had not visited the dentist for 3 or more years. Whereas another demonstrated that there was no more loss of attachment or bone loss in individuals who did not seek dental care over a 6 year period.

RISK MARKERS/ PREDICTORS FOR PERIODONTAL DISEASE

POOR ORAL HYGIENE: Since bacterial plaque is by far the most important etiologic agent for the occurrence of periodontal diseases (for review, see Kornman and Le, 1993), it is evident that the full mouth assessment of the bacterial load must have a pivotal impact in the determination of the risk for disease recurrence. Studies to date have not identified the level of plaque infection compatible with maintenance of periodontal health.

 However, in a clinical set-up, a percentage of tooth surfaces covered by visible plaque of 20-40% might be tolerable in most patients.
It is important to realize that the full mouth plaque score has to be related to the host response of the patient, i.e. compared to inflammatory parameters.

 PREVIOUS HISTORY OF PERIODONTAL DISEASES:

History of previous periodontal disease is a good clinical predictor of risk for future disease. Patients with the most severe existing loss of attachment are at the greatest risk for future loss of attachment.

PART: II

SUBJECTIVE RISK ASSESSMENT

The patient's risk assessment for periodontitis may be evaluated on the basis of a number of clinical conditions whereby no single parameter displays a more paramount role. The entire spectrum of risk factors and risk indicators ought to be evaluated simultaneously. For this purpose, a functional diagram has been constructed including the following aspects:

1. Percentage of bleeding on probing,

2. Prevalence of residual pockets greater than 4 mm (3-5 mm), 3. Loss of teeth from a total of 28 teeth,

4. Loss of periodontal support in relation to the patient's age,

5. Systemic and genetic conditions, and 6. Environmental factors, such as cigarette smoking.

 Each parameter has its own scale for minor, moderate and high-risk profiles. Modifications may be made to the functional diagram if additional factors become important according to new evidence.

1. PERCENTAGE OF SITES WITH BLEEDING ON PROBING (BOP)

Bleeding on gentle probing represents an objective inflammatory parameter which has been incorporated into index systems for the evaluation of periodontal conditions (Le and Silness, 1963; Mhlemann and Son, 1971).

 Although there is no established acceptable level of prevalence of bleeding on probing in the dentition above which a higher risk for disease recurrence has been established. a BOP prevalence of 25% has been the cut-off point between patients who maintained periodontal stability for 4 years and patients with recurrent disease in the same time frame in a prospective study in a private practice (Joss et al, 1994).

 Further evidence of BOP percentages between 20 and 30% determining a higher risk for disease progression originates from studies of Claffey et al (1990) and Badersten et al (1990). In assessing the patient's risk for disease progression, BOP percentages reflect a summary of the patient's ability to perform proper plaque control, the patient's host response to the bacterial challenge and the patient's compliance, especially when only few residual pockets remain after active periodontal therapy.

 The percentage of BOP, therefore, is used as the first risk factor in the functional diagram of risk assessment (Fig. 1).
The scale runs in a quadratic mode with 4, 9, 16, 25, 36 and > 49% being the critical values on the vector. Individuals with low mean BOP percentages (< 10% of the surfaces) may be regarded as patients with a low risk for recurrent disease (Lang et al, 1990), while patients with mean BOP percentages > 25% should be considered to be at high risk for periodontal breakdown.

2. PREVALENCE OF RESIDUAL POCKETS 5 MM (RESIDUAL POCKET GREATER THAN 4 MM):

The enumeration of the residual pockets with probing depths greater than 4 mm represents(to a certain extent) the degree of success of periodontal treatment rendered. Although this figure per se does not make much sense, when considered as a sole parameter, the evaluation in conjunction with other parameters such as bleeding on probing and/or suppuration will reflect existing ecological niches from and in which reinfection might occur.

 It is, therefore, conceivable that periodontal stability in a dentition would be reflected in a minimal number of residual pockets.
Presence of high frequencies of deep residual pockets and deepening of pockets during supportive periodontal care has, in fact, been associated with high risk for disease rogression (Badersten et al, 1990; Claffey et al, 1990).

 In assessing the patient's risk for disease progression, the number of residual pockets with a probing depth of 5 mm is assessed as the second risk indicator for recurrent disease in the functional diagram of risk assessment (Fig. 1).
The scale runs in a linear mode with 2, 4, 6, 8, 10 and 12% being the critical values on the vector. Individuals with up to 4 residual pockets may be regarded as patients with a relatively low risk, while patients with more than 8 residual pockets as individuals with high risk for recurrent disease.

 3. Loss of teeth from a total of 28 teeth

Although the reason for tooth loss may not be known, the number of remaining teeth in a dentition reflects the functionality of the dentition. Mandibular stability and individual optimal function may be assured even with a shortened dental arch of premolar to premolar occlusion, i.e. 20 teeth.

 The shortened dental arch does not seem to predispose the individual to mandibular dysfunction (Witter et al, 1990, 1994).
However, if more than 8 teeth from a total of 28 teeth are lost, oral function is usually impaired (Kyser, 1981, 1994, 1996). Since tooth loss also represents a true end point outcome variable reflecting the patient's history of oral diseases and trauma, it is logical to incorporate this risk indicator as the third parameter in the functional diagram of risk assessment (Fig. 1).

 The number of teeth lost from the dentition without the third molars (28 teeth) is counted, irrespective of their replacement. The scale runs also in a linear mode with 2, 4, 6, 8, 10 and 12 being the critical values on the vector. Individuals with up to 4 teeth lost may be regarded as patients in a low risk category, while patients with more than 8 teeth lost may be considered as being in a high-risk category. Rationale for this stems from the significance of further tooth loss in terms of preservation of the function of the dentition.

 4. Loss of periodontal support in relation to the patient's age

The extent and prevalence of periodontal attachment loss (i.e. previous disease experience and susceptibility), as evaluated by the height of the alveolar bone on radiographs, may represent the most obvious indicator of subject risk when related to the patient's age.

In light of the present understanding of periodontal disease progression, and the evidence that both onset and rate of progression of periodontitis might vary among individuals and during different time frames (Van der Velden, 1991), it has to be realized that previous attachment loss in relation to the patient's age does not rule out the possibility of rapidly progressing lesions.

 Therefore, the actual risk for further disease progression in a given individual may occasionally be underestimated.
Hopefully, the rate of progression of disease has been positively affected by the treatment rendered and, hence, previous attachment loss in relation to patient's age may be a more accurate indicator during SPT than before active periodontal treatment.

 Given the hypothesis that a dentition may be functional for the most likely life expectancy of the subject in the presence of a reduced height of periodontal support (i.e. 25-50% of the root length), the risk assessment in treated periodontal patients may represent a reliable prognostic indicator for the stability of the overall treatment goal of keeping a functional dentition for a lifetime (Papapanou et al, 1988).

 The estimation of the loss of alveolar bone is performed in the posterior region on either peri-apical radiographs, in which the worst site affected is grossly estimated in per cent of the root length or on bitewing radiographs in which the worst site affected is estimated in millimeter.
On bitewing radiographs, one millimeter is considered to be equal to 10% bone loss. The percentage is then divided by the patient's age.

 This results in a factor.

As an example, a 40-year-old patient with 20% of bone loss at the worst affected posterior site would score BL/Age = 0.5. Another 40-year-old patient with 50% bone loss at the worst affected posterior site would score BL/Age = 1.25.

 In assessing the patient's risk for disease progression, the extent of alveolar bone loss in relation to the patient's age is estimated as the fourth risk indicator for recurrent disease in the functional diagram of risk assessment (Fig. 1). The scale runs in increments of 0.25 of the factor BL/Age, with 0.5 being the critical value to discriminate between low and moderate risk and 1.0 being the value for moderate and high risk.

 This, in turn, means that a patient who has lost a higher percentage of posterior alveolar bone than his/her own age is at high risk regarding this vector in a multi-factorial assessment of risk.

 It may be argued that the incorporation of only the worst site with bone loss in the posterior segment may overestimate an individual's rate of periodontal destruction when only an isolated advanced bony lesion is present due to local etiologic factors, while an underestimation of the rate of destruction may exist in a case of generalized advanced disease.
Nevertheless, in patients successfully treated for periodontitis it has recently been demonstrated that the worst site with bone loss in the posterior segment may, indeed, represent the past history of destruction of the entire dentition (Persson et al, 2003).

 5. SYSTEMIC AND GENETIC ASPECTS:

In assessing the patient's risk for disease progression, systemic factors, if known, are only considered as the fifth risk indicator for recurrent disease in the functional diagram of risk assessment (Fig. 1). In this case, the area of high risk is marked for this vector. If not known or absent, systemic factors are not taken into account for the overall evaluation of risk.

 Research on the association and/or modifying influence in susceptibility and progression of periodontitis of physical or psychological stress is sparse (Cohen-Cole et al, 1981; Green et al, 1986; Freeman and Goss, 1993).
The hormonal changes associated with this condition, however, are well documented (Selye, 1950).

 6. CIGARETTE SMOKING:
In assessing the patient's risk for disease progression, environmental factors such as smoking must be considered as the sixth risk factor for recurrent disease in the functional diagram of risk assessment (Fig. 1). While non-smokers (NS) and former smokers (FS; more than 5 years since cessation) have a relatively low risk for recurrence of periodontitis, the heavy smokers (HS; as defined by smoking more than one pack per day) are definitely at high risk.

 Occasional smokers (OS; < 10 cigarettes a day) and moderate smokers (MS; 10-19 cigarettes a day) may be considered at moderate risk for disease progression.

CALCULATING THE PATIENT'S INDIVIDUAL PERIODONTAL RISK ASSESSMENT (PRA) Based on the six parameters specified above, a multi-functional diagram is constructed for the PRA. In this diagram, the vectors have been formed on the basis of the scientific evidence available. It is obvious that ongoing validation may result in slight modifications.

A low PRA patient has all parameters within the low-risk categories or - at the most - one parameter in the moderate-risk category (Fig. 2).

 A high PRA patient has at least two parameters in high risk category.

 In a high-risk patient who yields high BOP percentages and high numbers of residual pockets (Fig. 5), the patient's risk for disease progression may be reduced into the moderate category if further periodontal therapy is provided. These two parameters (BOP and residual pockets) are easily affected by therapy, while other parameters, such as numbers of missing teeth or systemic and genetic factors are either irreversible and cannot be reduced or may only be affected with great additional efforts (smoking cessation).

 The factor determining the percentage of experienced alveolar bone loss in relation to the patient's age may be reduced only during a time period of several years.

BIOMARKERS FOR ASSESSMENT OF PERIODONTAL DISEASE (NEED)

Traditional clinical measurements used for periodontal diagnosis are indicators of previous periodontal disease rather than present disease activity. So need for development of new diagnostic tests that can detect the presence of active disease, predict future disease progression and evaluate the response to periodontal therapy.

 Advances in oral and periodontal disease diagnostic research are moving toward methods whereby periodontal risk can be identified and quantified by objective measures such as biomarkers.

 Biomarkers may be defined as a substance that is measured objectively and evaluated as an indicator of normal biologic processes, pathogenic processes , and pharmacologic responses to a therapeutic intervention. Biomarkers, whether produced by normal healthy individuals or by individuals affected by specific systemic diseases, are tell-tale molecules that could be used to monitor health status, disease onset, treatment response and outcome. Informative biomarkers can further serve as early sentinels of disease.

BIOMARKERS IN GINGIVAL CREVICULAR FLUID (GCF) AND SALIVA

According to Armitage (2004), more than 65 GCF constituents have been evaluated as potential diagnostic markers of periodontal disease progression. These markers can be divided into three groups: host-derived enzymes and their inhibitors, inflammatory mediators and hostresponse modifiers, and byproducts of tissue breakdown.

BIOMARKERS IN GINGIVAL CREVICULAR FLUID (GCF) AND SALIVA

CURRENT METHODS FOR PERIODONTAL RISK ASSESSMENT :

In Periodontology, current methods to assess periodontal risk factors include:

- Periodontal Risk Calculator (PRC),

- hexagonal risk diagram for Periodontal Risk Assessment (PRA), - PreViser Risk CalculatorTM, the periodontal risk assessment model developed by Chandra, and - simplified method (UniFe) (Union of European Railway Industries) for periodontal risk assessment.

 The Periodontal Risk Calculator (PRC) and the Periodontal Assessment Tool (PAT): Page et al. developed a computer-based risk assessment tool, the PRC, for objective, quantitative assessment of risk. The calculation of risk using this model is based on mathematically derived algorithms that assign relative weights to nine factors including patient age, smoking history, diagnosis of diabetes, history of periodontal surgery, pocket depth, furcation involvements, restorations or calculus below the gingival margin, radiographic bone height and vertical bone lesions.

 The PRC assigns the individual a level of risk on a scale from 1 (lowest risk) to 5 (highest risk). The Periodontal Assessment Tool (PAT) is an integral part of the Oral Health Information Suite (OHIS)TM (PreViser, Inc., Mount Vernon, WA; www.previser.com) and is considered as a modification of the PRC method.

 Following the input of only twenty-three items taken from a routine periodontal examination, the system generates linguistic and numeric periodontal diagnoses and a risk score for future disease, and prepares a report in two versions; one for the dentists clinical documentation and another for the patient. The traditional documentation of six pocket depth measurements per tooth has been reduced to the deepest pocket for each sextant. PAT also requires the greatest distance of the bone crest to the cemento-enamel junction determined from radiographs, again using one measurement for each sextant and three categories: <2 mm, 2-4 mm, and >4 mm.

 The hexagonal risk diagram for Periodontal Risk Assessment (PRA) Lang and Tonetti28 described a functional diagram based on six parameters for use in estimating an individuals risk for progression of periodontitis. The authors provided evidence supporting the inclusion of each parameter within the diagram. The combined assessment of each parameter allows the assessment of the risk level for disease progression on an individual basis.

Minor modifications of the PRA model described by Lang and Tonetti have been published later.

 The periodontal risk assessment model developed by Chandra In 2007, Chandra31 evaluated a novel periodontal risk assessment model in patients presenting for dental care.

This new model based on the periodontal risk assessment model by Lang and Tonetti where the following parameters are recorded:
- percentage of sites with bleeding on probing, - number of sites with pocket depths 5mm,

- number of teeth lost, bone loss/age ratio,

- Attachment loss/age ratio, - diabetic and smoking status, dental status, other systemic factors and risk determinants.

 The simplified method (UniFe) for periodontal risk assessment

In 2009, Trombelli and co-workers proposed a new objective method (UniFe) (Union of European Railway Industries) in order to simplify the risk assessment procedures. Risk assessment according to UniFe method is based on five parameters, derived from the patient medical history and clinical recordings. parameters are as follows: smoking status, diabetic status (both type 1 and type 2), number of sites with probing depth 5mm, bleeding on probing score, and bone loss/age records.

THE CURRENT METHODS FOR PERIODONTAL RISK ASSESSMENT; ARE WE ON THE RIGHT TRACK? Regarding the literature, confusing trials for setting risk elements for periodontal disease could be found. For instance, as reviewed by Borrel and Papapanou, a distinction was made between putative factors (non-modifiable background factors) and modifiable factors (environmental, acquired, and behavioral).

 Accordingly, age, gender, and gene polymorphisms were considered as non-modifiable background factors, whereas microbiota, smoking, diabetes mellitus, osteoporosis, HIV infection, and psychosocial factors were considered as modifiable background factors.

 On the other side, some authors tended to consider smoking, diabetes, pathogenic bacteria, and microbial tooth deposits as risk factors for periodontitis, whereas age, gender, socioeconomic status, stress, and genetic factors were considered as risk determinants, and HIV infection, osteoporosis, and infrequent dental visits were considered as risk indicators for periodontitis.
However, it seems to be that there is a recent agreement to accept specific bacteria, cigarette smoking, and diabetes mellitus as the major established risk factors for periodontitis. The rest of risk elements for periodontitis still need to be confirmed in future.

 Regarding the current methods for periodontal risk assessment, it seems to be that the use of risk calculators holds much promise in the clinical practice. However, the lack of such evidence still exists.
Chandra and Trombelli et al. tried to modify the hexagonal risk diagram for periodontal risk assessment of Lang and Tonetti, and found acceptable results at detecting potential risk groups.

 Although the validation and accuracy of the PreViser Risk CalculatorTM and the information required for its use have been reported, the whole software seems to more powerful in demonstrating a detailed description of the patients current situation (i.e. Diagnosis), and to give several treatment options related to every individual case.
In other words, this method is more likely to present a comprehensive and systematic approach to clinical decision-making for periodontists. Therefore, it is a little bit far away from being a tool that concentrates on important and the most strong risk elements for periodontitis.

 However, as is the case with the Lang/Tonetti tool, the functional diagram of Chandra and of Trombelli et al. should be only used during SPT to evaluate possible progression of the periodontal disease and not for patients who visit the dental clinic for the first time.
That would be more plausible.

SUMMARY
The role of risk factors and risk assessment in the prediction of clinical periodontal outcomes has been a subject of much interest.
To date, it is accepted that specific pathogenic bacteria (Porphyromonas gingivalis, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans), cigarette smoking, and diabetes mellitus are the major established risk factors for periodontitis.

 Although several approaches have been developed to assess the factors which may interfere with periodontal diseases onset and/or progression, some contradictions regarding the classification, the definition, and the assumed implemented factors do exist among all these methods.

REFERENCES
Chester W. Douglass. Risk assessment and management of periodontal disease. JADA, Vol. 137 http://jada.ada.org November 2006.
Aous Dannan. Periodontal Risk Assessment; Are We On The Right Track. AOSR 2011;1(3):162-167. Lei Zhang, Bradley S. Henson, Paulo M. Camargo & David T. Wong. The Clinical Value Of Salivary Biomarkers For Periodontal Disease. Periodontology 2000, Vol. 51, 2009, 25 37. Gun-Bak Rheu, Suk Ji, Jae-Jun Ryu. Risk assessment for clinical attachment loss of periodontal tissue in Korean adults. J Adv Prosthodont 2011;3:25-32.

REFERENCES
Raul I. Garcia, Martha E. Nunn & Thomas Dietrich. Risk calculation and periodontal outcomes. Periodontology 2000, Vol. 50, 2009, 6577.

A. Kazemnejad, F. Zayeri, A.R. Rokn, and M.J. Kharazifard. Prevalence and risk indicators of periodontal disease among highschool students in Tehran. Eastern Mediterranean Health Journal, Vol. 14, No. 1, 2008 119.

THANK YOU