RISK FACTORS FOR PERIODONTAL DISEASE.pptx

Risk factors of periodontal disease

1. RISK FACTORS FOR PERIODONTAL DISEASE DR SANUPA DEPT OF PERIODONTICS

2. CONTENTS: INTRODUCTION TERMINOLOGIES RISK FACTORS RISK DETERMINANTS RISK INDICATORS RISK PREDICTORS CATEGORIES OF RISK ELEMEMNTS FOR PERIODONTAL DISEASE RISK FACTORS TOBACCO SMOKING DIABETES PATHOGENIC BACTERIA AND MICROBIAL TOOTH DEPOSITS RISK DETERMINANTS-GENETIC FACTORS AGE GENDER SOCIOECONOMIC STATUS STRESS RISK INDICATORS -HIV/AIDS OSTEOPOROSIS INFREQUENT DENTAL VISIT RISK MARKERS -PREVIOUS HISTORY OF PERIODONTAL DISEASE HIV/AIDS BLEEDING ON PROBING CONCLUSION REFERENCE

3. INTRODUCTION Risk assessment is defined by numerous components . Risk is the probability that an individual will develop a specific disease in a given period . The risk of developing the disease will vary from individual to individual.

4. TERMINOLOGIES; Risk factor :It may be environmental , behavioral , or biologic factors that , when present , increase the likelihood that an individual will develop the disease . To be identified as a risk factor , the exposure must occur before disease onset. Risk determinants/background characteristics: which is sometimes substituted for the term risk factor , should be reserved for those risk factors that can not be modified. Risk indicators :these are probable or putative risk factors that have been identified in cross sectional studies but not confirmed through longitudinal studies. Risk predictors or markers : it is associated with increased risk for disease , do not cause the disease.

5. Categories of Risk Elements for Periodontal Disease RISK FACTORS Tobacco smoking Diabetes Pathogenic bacteria Microbial tooth deposit. RISK DETERMINANTS/BACKGROUND CHARACTERISTICS Genetic factors Age Gender Socioeconomic status Stress RISK INDICATORS HIV/AIDS Osteoporosis Infrequent dental visit RISK MARKERS/PREDICTORS Previous history of periodontal disease Bleeding on probing HIV;AIDS

6. RISK FACTORS 1.TOBACCO SMOKING Tobacco smoking is a well-established risk factor for periodontitis . A direct relationship exist between smoking and prevalence of periodontal disease. The literature consistently indicates a positive association between smoking and chronic periodontitis across the many cross-sectional and longitudinal studies performed over the years( Kinane and chestnut 2000)and the risk attributable to tobacco for chronic periodontitis is between 2.5 and 7. It is not only the risk of developing the disease that is enhanced by smoking , but also the response to periodontal therapy is impaired in smokers . A further feature in smokers is that their signs and symptoms of both gingivitis and chronic periodontitis , mainly gingival redness and bleeding on probing are masked by dampening of inflammation seen for smokers as compared to non-smokers. It affect the progression through effects on :-microbiological profile(increase in anaerobic organism) physiology(decrease in pocket temperature) immune system (decrease chemotaxis )

7. PERIODONTAL CONDITION IN CHRONIC SMOKER

8. EFFECT OF SMOKING ON THE PREVALENCE AND SEVERITY OF PERIODONTAL DISEASE Periodontal Disease Impact of smoking Gingivitis Decrease gingival inflammation and bleeding on probing. Periodontitis Increase prevalence and severity of periodontal destruction. Increase pocket depth , attachment loss and bone loss. Increase rate of periodontal destruction Increase prevalence of severe periodontitis . Increase tooth loss Increase prevalence with increased number of cigarette smoked per day Decrease prevalence and severity with smoking cessation.

9. EFFECTS OF SMOKING ON THE ETIOLOGY AND PATHOGENESIS OF PERIODONTAL DISEASE Etiologic factor Impact of Smoking Microbiology No effect on rate of plaque accumulation Increase colonization of shallow periodontal pockets by periodontal pathogens Increase level of periodontal pathogens in deep periodontal pockets. Immune-inflammatory response Altered neutrophil chemotaxis , phagocytosis , and oxidative burst. Increase TNF and prostaglandin E2 in GCF Increases neutrophil collaginase and elatase in GCF Increase production of prostaglandin E2 by monocyte in response to lipopolysaccharide . Physiology Decrease gingival blood vessels with increase inflammation Decrease GCF flow and bleeding on probing with increase inflammation Decrease sub gingival temperature Increase time needed to recover from local anesthesia.

10. EFFECTS OF SMOKING ON RESPONSE TO PERIODONTAL THERAPY Therapy Effects of smoking Non surgical Decrease clinical response to root-surface debridement Decrease reduction in pocket depth Decrease gain in clinical attachment levels Decrease negative impact of smoking with increase level of plaque control Surgery and implants Decrease pocket depth reduction and decrease gain in clinical attachment levels after access flap surgery Increase deterioration of furcations after surgery Decrease gain in clinical attachment levels,decrease bone fill,increase recession,and increase membrane exposure after guided tissue regeneration Increase risk for implant failure and periimplantitis Maintenance care Increase pocket depth and attachment loss during maintenance therapy Increase disease recurrence in smokers Increase need for retreatment in smokers Increase tooth loss in smokers after surgical therapy

11. 2.Diabetes Diabetes is a clear risk factor for periodontitis . Epidermiologic data demonstrate that prevalence and severity of periodontitis are significantly higher in patients with type 1 or type2 DM than those without diabetes and the level of diabetic control is an important variable in this relationship. Several studies suggest a two way relationship between diabetes and periodontitis with more severe periodontal tissue destruction in people with diabetes but also a poorer metabolic control of diabetes in subject with periodontitis . The outcome of periodontal treatment in well controlled diabetes mellitus patient is similar to that of non diabetic subject which poorly controlled diabetes display an inferior outcome.

12. - Periodontal condition in patient with diabetes-

13. Oral manifestations in patients with diabetes; cheilosis ,mucosal drying and cracking , burning mouth and tongue, diminished salivary flow , and alterations in the flora of oral cavity with greater predominance of candida albicans ,hemolytic streptococci ,and staphylococci . an increased rate of dental caries has also been observed . The influence of diabetes on the periodontium ; enlarged gingiva ,sessile or pedunculated gingival polyps,polypoid gingival proliferation , abcess formation , periodontitis,and loosened teeth. Periodontal disease is considered to be the sixth complication of diabetes .

14. Bacterial pathogens : patients with type 1 diabetes mellitus and periodontitis have been reported to have a subgingival flora that composed mainly of capnocytophaga,anaerobic vibrios and actinomyces species.porphyromonas gingivalis , prevotella intermedia and aggregatibacter actinomycetemcomitans,black pigmented species especially p.gingivalis,p.intermedia,and c.rectus -are prominent in severe periodontal lesions on those with type2 diabetes. Polymorphonuclear leukocyte function: the increased susceptibility of patients with diabetes to infection has been hypothesized as bieng caused by PMN deficiencies that results in impaired chemotaxis , defective phagocytosis , or impaired adherence.in patients with poorly controlled diabetes , the function of PMNs , monocytes , and macrophages is impaired.as a result,the primary defense mounted by PMNs against periodontal pathogens is diminished and bacterial proloferation is more likely .

15. Management of diabetic patient in the dental office For a controlled diabetic for a non surgical therapy ,no antibiotic premedication is required.However , before surgical procedures prophylactic antibiotics are recommended. Patient should be asked to bring their glucometer to the dental office at each appoinment . Patient should check their blood glucose before any long procedure to obtain a baseline level. If the procedure lasts several hours,it is often beneficial to check the glucose level during the procedure to ensure that the patient does not become hypoglycemic. After the procedure ,the blood glucose can be checked again to asses fluctuations overtime. If the patient feels symptoms of hypoglycemia during the procedure ,blood glucose level should be checked immediately . This may prevent onset of severe hypoglycemia ,which is a medical emergency.

16. 3.Pathogenic Bacteria and Microbial Tooth Deposits: It is well documented that accumulation of bacterial plaque at the gingival margin results in the development of gingivitis and that the gingivitis can be reversed with the implimentation of oral hygiene measures. Patient with severe loss of attachment have minimal levels of bacterial plaque on the affected teeth,indicating that quantity of plaque is not of major importance of disease process. However , although quantity may not indicate risk, there is evidence that the composition or quality ,of the complex plaque biofilm is of importance. In terms of quality of plaque , three specific bacteria have been identified as etiologic agents for periodontitis :Aggregatibacter actinomycetemcomitans,p.gingivalis,and tennerella forsythia.

17. P.gingivalis and T.forsythia are often found in chronic periodontitis,whereas AAAis often associated with aggressive periodontitis . Additional evidence that these organisms are causal agents include the following: 1.Their elimination or suppression impacts the success of therapy. 2.There is a host response to these pathogens. 3.Virulance factors are associated with these pathogens. 4.Inoculation of these bacteria into animal models induces periodontal disease. Moderate evidence also suggest that campylobacter rectus,Eubacterium nodetum,fusobacterium nucleatum,prevotella intermedia ,and treponema denticola are etiologic factors in periodontitis .

18. Anatomical factors such as furcutions , root concavities, developmental grooves , cervical enamel projections ,enamel pearls ,and bifurcation ridges , may predispose the periodontium to disease as a result of their potential to harbor bacterial plaque and present a challenge to the clinician during instrumentation. Similarly , the presence of sub gingival and overhanging margins can result in increased plaque accumulation , increased inflammation , and increased bone loss. The presence of calculus ,which serve as a reservoir for bacterial plaque ,has been suggested as a risk factor for periodontitis .

19. RISK DETERMINANTS 1.GENETIC FACTORS Evidence indicate that genetic differences between individuals may explain why some patients develop periodontal disease and others do not. Studies conducted in twins have shown that genetic factors influence clinical measures of gingivitis , probing pocket depth , attachment loss and inter proximal bone height. The familial aggregation seen in localized and generalized aggressive periodontitis also is indicative of genetic involvement in these disease. Kornman et al demonstrated that alterations in specific genes encoding the inflammatory cytokines interleukin was associated with severe chronic periodontitis in non smoking subject. Overall ,it appears that changes in the IL genes may be only one of several genetic changes involved in the risk for chronic periodontitis . Immunologic alterations such as neutrophil abnormalities , monocytic hyper responsiveness to lypopolysaccharide stimulation in patients with localized aggressive periodontitis and alterations in the monocyte /macrophage receptor for the fc portion of antibody , also appear to be under genetic control. Genetic play a role in regulating the titer of the protective immunoglobulin G2 antibody response to AAA in patients with aggressive periodontitis .

20. 2.Age Both the prevalence and severity of periodontal disease increase with age . It is possible that degenerative changes related to aging may increase susceptibility to periodontitis . It is also possible that the attachment loss and bone loss seen in older individuals are the results of prolonged exposure to other risk factors over a persons life , creating a cumulative effect over time. Periodontal disease is not an inevitable consequence of the aging process and that aging alone does not increase disease susceptibility . However , it remains to be determined whether changes related to the aging process , such as intake of medication , decreased immune function , and altered nutritional status , interact with other well defined risk factors to increase susceptibility to periodontitis .

21. Evidence of loss of attachment may have more consequence in patients. The younger the patient , the longer the patient has for exposure to causative factors. In addition , aggressive periodontitis in young individuals often is associated with an unmodifiable risk factor such as genetic predisposition to disease. Therefore , young individuals with periodontal disease may be at greater risk for continued disease as they age.

22. Effects of aging on the periodontium Gingival epithelium Thinning and decreased keratinization of the gingival epithelium . Increase in epithelial permeability to bacterial antigens , and decreased resistance to functional trauma. Flattening of rete pegs and altered cell density. Gingival connective tissue Increase in age results in coarser and denser gingival connective tissue. Increased rate of conversion of soluble to insoluble collagen , increased mechanical strength , and increased denaturing temperature . Periodontal ligament Decreased number of fibroblast and a more irregular structure . Decreased organic matrix production , epithelial cell rest ,and increased amount of elastic fiber. Width of periodontal ligament space will decrease if the tooth is unopposed or increase with excessive occlusal loading.

23. Cementum Increase in cemental width this increase may be 5-10 times with increasing age. The increase in width is greater apically and lingually . Increase in surface irregularity . Alveolar bone More irregular periodontal surface of bone and the less regular insertion of collagen fibers.

24. Effect of aging on the progression of periodontal diseases A comparison of developing gingivitis between younger and older individuals demonstrated a grester inflammatory response in older subject. In the older age group the findings included a greater amount of infiltrated connective tissue,increased gingival crevicular fluid flow , and increased gingival index. Age is inevitibly associated with an increased loss connective tissue attachment .

25. Aging and the response to treatment of the periodontium The successful treatment of periodontitis requires both meticulous home plaque control by the patient and meticulous supra gingival and sub gingival debridement by the therapist. If plaque control is not ideal , the continued loss of attachment is inevitable . further more , without effective periodontal therapy , the progression of disease may be faster with increasing age.

26. 3.GENDER: Gender plays a role in periodontal disease . Surveys conducted in the united states since 1960 demonstrate that men have more loss of attachment than women. In addition , men have poorer oral hygiene than women , as evidence by higher level of plaque and calculus.

27. 4.Socioeconomic status: Gingivitis and poor oral hygiene can be related to lower socioeconomic status. This can most likely be attributed to decreased dental awareness and decreased frequency of dental visit compared with more educated individuals with higher SES. After adjusting for other risk factors , such as smoking and poor oral hygiene , lower SES alone does not result in increased risk for periodontitis .

28. 5.Stress: The incidence of necrotizing ulcerative gingivitis increases during periods of emotional and physiologic stress , suggesting a link between the two. Emotional stress may interfere with normal immune function and may result in increased levels of circulating hormones , which can the periodontium . Adult patients with periodontitis who are resistant to therapy are more stressed than those who respond to therapy. Individuals with financial strain , distress , depression , or inadequate coping mechanism have more severe loss of attachment . Although epidemiologic data on the relationship between stress and periodontal disease are limited , stress may be a putative risk factor for periodontitis .

29. RISK INDICATORS 1. HIV/AIDS: It has been hypothesized that the immune dysfunction associated with HIV infection and AIDS increases susceptibility to periodontal disease. Some studies support that as the degree of immuno suppression increase in adult with AIDS , periodntal pocket formation and loss of clinical attachment also increase. Evidence also suggest that AIDS affected individuals who practice good preventive oral health measures , including effective home care and seeking appropriate professional therapy , can maintain periodontal health.

30. 2.osteoporosis: Osteoporosis has been suggested as another risk factor for periodontitis . Reduced bone mass seen in osteoporosis may aggrevate periodontal disease progression. In a study of 12 women with osteoporosis and 14 healthy women , von Wowern et al reported that the women with osteoporosis had greater loss of attachment than the control subject. In contrast , Kribbs examined pocket depth , bleeding on probing , and gingival recession in women with and without osteoporosis .Although the two groups had significant differences in bone mass , no differences in periodontal status were noted. However , it appears that a link may exist between osteoporosis and periodontitis , and additional studies may need to be conducted to determine whether osteoporosis is a true risk factor for periodontal disease.

31. 3.Infrequent Dental Visit: Identifying failure to visit the dentist regularly as a risk factor for periodontitis 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 dental care compared with those who did over a 6 year of period. Additional longitudinal and intervention studies are necessary to determine whether infrequency of dental visit is a risk factor for periodontal disease.

32. RISK MARKERS 1 . Previous history of periodontal disease: A history of the previos periodontal disease is a good clinical predictor of risk for future disease. Patients with the most sever existing loss attachment are at the greater risk for future loss of attachment. Conversely , patients currently free of periodontitis have a decreased risk for developing loss of attachment compared with those who currently have periodontitis

33. 2.Bleeding on probing: Bleeding on probing is the best clinical indicator of gingival inflammation. Although this indicator alone does not serve as a predictor for loss of attachment ,bleeding on probing coupled with increasing pocket depth may serve as an excellent predictor for future loss of attachment . Lack of bleeding on probing does appear to serve as an excellent indicator of periodontal health.

34. CLINICAL RISK ASSESSMENT FOR PERIODONTAL DISEASE Information concerning individual risk for developing the periodontal disease is obtained through careful evaluation of the patients demographic data , medical history , dental history, and clinical examination. The elements that contribute to increased risk can be identified through the collection of demographic data , including the patients age gender and SES . The medical history may reveal element such as a history of diabetes , smoking , HIV/AIDS , or osteoporosis as well as the perceived level of stress . The dental history can reveal a family history of early tooth loss (suggestive of a genetic predisposition for aggressive periodontitis ) , a previous history of periodontal disease , and information concerning the frequency of oral health care in the past.

35. Clinical risk assessment for periodontal disease DEMOGRAPHIC DATA Age Duration of exposure to risk elements Postmenopausal women Evidence of aggressive disease Male gender Preventive practices Frequency of care SES Dental awareness Frequency of care MEDICAL HISTORY Diabetes Tobacco smoking HIV/AIDS Osteoporosis Stress Dental history Family history of early tooth loss Genetic predisposition to aggressive disease Previous history of periodontal disease Frequency of dental care Clinical examination Plaque accumulation Microbial sampling for putative periodontal pathogen Calculus Bleeding on probing Extent of loss of attachment Aggressive forms of disease Tooth examination Plaque retentive areas Anatomic factors Restorative factors HIV/AIDS.

36. conclusion It is important to understand the etiologic factors and the pathogenesis of periodontal disease to recognize and appreciate the associated risk factors . As a periodontal disease is multifactorial , effective disease management requires a clear understanding of all the associated risk factors.

37. REFERENCE Carranzas clinical periodontology -second south Asia edition

38. THANK YOU