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RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, BANGALORE KARNATAKA ANNEXURE−II PROFORMA FOR REGISTRATION OF SUBJECTS FOR DISSERTATION 1. NAME OF THE CANDIDATE Dr. DISHA NAGPAL AND ADDRESS (IN BLOCK POST GRADUATE STUDENT, LETTERS) DEPARTMENT OF PERIODONTICS, COLLEGE OF DENTAL SCIENCES, DAVANGERE−577 004 KARNATAKA. 2. NAME OF THE COLLEGE OF DENTAL SCIENCES, INSTITUTION DAVANGERE−577 004 KARNATAKA. 3. COURSE OF STUDY AND MASTER OF DENTAL SURGERY IN PERIODONTICS SUBJECT 4. DATE OF ADMISSION TO 22nd MAY 2012 COURSE 5. TITLE OF THE TOPIC DETECTION AND COMPARISON OF SELENOMONAS SPUTIGENA IN SUBGINGIVAL BIOFILMS IN CHRONIC PERIODONTITIS PATIENTS. AND AGGRESSIVE 6. BRIEF RESUME OF THE INTENDED WORK : 6.1 Need for the study : The role of oral microbiota in etiology of periodontal disease has been well established and specificity may exist among certain bacterial species/groups and the various forms of periodontal disease.1 The complexity and diversity of periodontal microbiota has been confirmed by numerous studies.2 However, only a few species have been recognised as periodontal pathogens, namely Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis and Tannerella forsythia.3 The microbiota of localized and generalised forms of aggressive periodontitis contain higher proportions of Aggregatibacter actinomycetemcomitans compared with that of chronic periodontitis, whereas the proportions of red complex pathogens,4 do not differ between these periodontal conditions, despite their clinical differences.5 These observations suggest that further analyses of the microbiota are necessary in order to explain differences in clinical outcomes.It was observed that Selenomonas species dominated the disease sites of subjects with Generalized Aggressive Periodontitis6 and Chronic Periodontitis.2 Selenomonas sputigena was the most frequently detected bacterial species which was multiflagellated , motile, anaerobic rods and further characterised as etiological agent in periodontal disease.7 However, the detection of this bacteria is needed because its etiological and pathological role in periodontal diseases is still unclear and information on absolute numbers and proportions of organisms in samples is important in distinguishing the species associated with periodontal health/disease and to evaluate the effects of periodontal therapy. Therefore, the purpose of the present study is to detect and compare the levels of Selenomonas sputigena in subgingival biofilms from patients with Aggressive Periodontitis, Chronic Periodontitis and Periodontally healthy control subjects. . 6.2 Review of literature : A study was conducted to detect oral motile bacteria directly from dental plaque, specific PCR primers for Centipeda periodontii and Selenomonas sputigena were designed based on the sequence analysis of their 16S rDNA. The primers were specific and sensitive enough to amplify DNA fragments from the available oral bacteria. The detection limit was fewer than 10 bacterial cells per sample. It was also possible to detect these bacteria in dental plaque. The prevalence of these bacteria varied in each sample. The specific primers designed in this study clarified the epidemiology of periodontal disease.8 A study was conducted to compare the levels of Selenomonas sputigena and uncultivated/unrecognized Selenomonas species in subgingival biofilms from periodontally healthy subjects and from subjects with Generalized Aggressive Periodontitis. The results showed that S. sputigena and Mitsuokella sp. Human Oral Taxon (HOT) 131 may be associated with the pathogenesis of generalized aggressive periodontitis, and their role in the onset and progression of this infection should be investigated further.9 The microbial population in 73 Rapidly Progressive Periodontitis (RPP) lesions in 10 young adults aged 2535 years(5 males,5 females)was studied in relation to the clinical parameters probing depth, bleeding on probing and suppuration, which were recorded at the sampled sites. Significant differences between bleeding index 0, 1, and 2 (P < 0.05) in frequency of detection were found for P. intermedia, Campylobacter concisus, Selenomonas sputigena, and Peptostreptococcus micros at bleeding sites and for Streptococcus sanguis, Actinobacillus actinomycetemcomitans, and B. forsythus (P<0.001) at non-bleeding sites.10 In yet another study, clinical, microbiological and immunological factors were examined using data from a subject with periodontosis. The subject was monitored at bimonthly intervals for 26 months at 6 sites per tooth for redness, plaque, suppuration, bleeding on probing, pocket depth, and attachment level. Subgingival plaque samples were taken from these sites for predominant cultivable and dark field evaluation before, 5 months and 13 months after treatment by Widman flap surgery and systemic tetracycline. The proportions of Actinobacillus actinomycetemcomitans and Selenomonas sputigena were elevated in active sites, while proportions of Bacteroides intermedius were elevated in control sites. 5 months after treatment, proportions of A. actinomycetemcomitans, S. sputigena and Eikenella corrodens were significantly decreased in the previously active sites and proportions of B. intermedius and E. corrodens were significantly decreased in the control sites.11 A study was conducted to quantitatively compare the bacterial population structure in plaque from the gingival margin of two groups of patients – one with gingivitis and another with necrotizing ulcerative gingivitis nucleatum/Fusobacterium (NUG).The analyses showed that the fusiform taxa (Fusobacterium periodonticum, Leptotrichia buccalis, Tannerella forsythensis, and Capnocytophaga sp.), Campylobacter rectus, Prevotella intermedia, Prevotella nigrescens, Selenomonas sputigena and treponemes were present in both groups with high prevalence. Porphyromonas gingivalis and Actinomyces gerencseriae were much more prevalent in the NUG group.12 6.3 Objectives of the study : 1 )To detect the levels of Selenomonas sputigena in subgingival biofilms from patients with Aggressive Periodontitis,Chronic Periodontitis and Periodontally healthy control subjects. . 2)To compare the levels of Selenomonas sputigena in subgingival biofilms from patients with Aggressive Periodontitis,Chronic Periodontitis and Periodontally healthy control subjects. 7.MATERIALS AND METHODS : 7.1 Source of data : The patients for this study will be selected from the out patient Department of Periodontics, College Of Dental Sciences, Davangere, Karnataka. The subjects between 20-55 years of age will be included in this study. 7.2 Method of Collection of Data (including sampling procedure, if any) : Sample size: 90 patients ( 45 males and 45 females). Study design: A clinical and microbiological study with a total of 90 patients (45 males,45 females) with Chronic Periodontitis, Generalized Aggressive Periodontitis and Periodontally healthy subjects will be included in this study. The patients are divided into 3 groups as follows: Group I (30) - Periodontally healthy subjects Group II (30) - Chronic Periodontitis Subjects Group III (30) - Generalized Aggressive Periodontitis Subjects. Study period : The duration of this clinical study will be one year, from January 2013-January 2014. Clinical parameters : Following clinical parameters will be recorded at baseline visit using a UNC15 probe: 1. Plaque Index (Silness P. and Loe H., 1964) 2. Gingival Index (Loe H. and Silness J, 1963) 3. Gingival bleeding index (Ainamo & Bay, 1975) 4. Probing Pocket Depth 5. Clinical Attachment Level 6. Suppuration[Present(1) or Absent(0)] 7. Radiographic assessment( Orthopantomogram ) SELECTION CRITERIA: 7 S These patients will be selected consecutively during the study period as and when they are present with following inclusion and exclusion criteria from both the sexes. The medical and dental histories will be obtained and a full mouth periodontal examination will be performed. Based on these data, periodontal diagnosis will be made and subjects who will fulfill the inclusion and exclusion criteria will be participating in this study. Inclusion criteria: Subjects had to have at least 20 teeth and needed to meet the following criteria in order to be included in this study: Periodontally healthy9 — 1)20-55 years(15 males and 15 females) 2) Sites with probing depth and clinical attachment level measurements of ≤ 3 mm. 3) ≤ 10% of sites exhibiting bleeding on probing. Generalized Aggressive Periodontitis9 — 1) ≤ 30 years of age (15 males and 15 females) 2) A minimum of six permanent incisors and/or first molars with at least one site each with probing depth and clinical attachment level of ≥ 5 mm with vertical bone loss radiographically. 3) A minimum of six teeth (other than first molars and incisors) with at least one site each with probing depth and clinical attachment level of ≥ 5 mm with vertical bone loss radiographically. 4)Familial aggregation (at least one other member of the family presenting, or with a history of periodontal disease) Chronic Periodontitis13 – 1)Age>35 years(15 males and 15 females) 2) >30% of the sites involved with periodontal destruction. 3) ≥5mm of Clinical Attachment Loss and Probing Pocket Depth with vertical/horizontal bone loss radiographically. Exclusion criteria: 1) Pregnant or lactating females. 2) Subjects who are smokers. 3) No systemic condition that might influence periodontal status. ( e.g. diabetes, immunological disorders etc.) 4) Patients on antibiotics, steroids, contraceptive drugs/periodontal therapy in preceding 6 months/during the study. Microbiological Examination: Sample collection—The microbial plaque samples were taken prior to the clinical measurements after removing the supragingival plaque at baseline visit, from each selected patient the pooled plaque samples were collected with paper points from 3 interproximal sites with >5mm of clinical attachment loss by using Modified Slot Technique10 for 30 seconds. The collected samples will be subjected for microbiological analysis i.e. detection and comparison of Selenomonas sputigena by using 16S rDNA based PCR assay. Statistical Analysis : Results obtained will be subjected for appropriate statistical analysis. Test for proportions (Z test) will be used to compare between groups. Categorical data will be analyzed by Chi square test. 7.3 Does the study require any investigations or interventions to be conducted on patients or other humans or animals? If so, please describe briefly. Yes, this study involves the collection of the subgingival plaque samples from the Aggressive Periodontitis, Chronic Periodontitis and Periodontally healthy subjects. 7.4 Has ethical clearance been obtained from your institution in case of 7.3? Yes 8. REFERENCES: 1. Albandar JM, Brown LJ, Löe H. Putative periodontal pathogens in subgingival plaque of young adults with and without early-onset periodontitis. J Periodontol 1997;68(10):973–81. 2. Paster BJ, Boches SK, Galvin JL et al. Bacterial diversity in human subgingival plaque. J Bacteriol 2001;183(12):3770–83. 3. American Academy of Periodontology. Consensus report. Periodontal diseases: pathogenesis and microbial factors. Ann Periodontol 1996;1:926–32. 4. Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent RL Jr. Microbial complexes in subgingival plaque. J Clin Periodontol 1998;25(2):134–44. 5. Faveri M et al Microbiological profile of untreated subjects with localized aggressive periodontitis. J Clin Periodontol 2009;36(9):739–49. 6. Faveri M et al Microbiological diversity of generalized aggressive periodontitis by 16S rRNA clonal analysis. Oral Microbiol Immunol 2008;23(2):112–8. 7. Kokeguchi S, Tsutsui O, Kato K, Matsumura T. Isolation and characterization of lipopolysaccharide from Centipeda periodontii ATCC 35019. Oral Microbiol Immunol 1990;5(2):108-12. 8. Sawada S, Kokeguchi S, Takashiba S, Murayama Y. Development of 16S rDNA-based PCR assay for detecting Centipeda periodontii and Selenomonas sputigena. Lett Appl Microbiol 2000;30(6):423-6. 9. Gonçalves LF et al Levels of Selenomonas species in generalized aggressive periodonitis. J Periodont Res 2012; 47(6): 711–8. 10. Kamma JJ, Nakou M, Manti FA. Microbiota of rapidly progressive periodontitis lesions in association with clinical parameters. J Periodontol 1994;65(11):1073-8. 11. Haffajee AD, Socransky SS, Ebersole JL, Smith DJ. Clinical, microbiological and immunological features associated with the treatment of active periodontosis lesions. J Clin Periodontol 1984;11(9):600-18 12. Gmür R, Wyss C, Xue Y, Thurnheer T, Guggenheim B. Gingival crevice microbiota from Chinese patients with gingivitis or necrotizing ulcerative gingivitis. Eur J Oral Sci 2004;112(1): 33–41. 13. Newman MG,Takei HH,Klokkevold PR,Carranza FA. Carranza’s Clinical Periodontology. 10th edn.Noida,India.2009. p.106. 9. SIGNATURE OF CANDIDATE 10. REMARKS OF THE GUIDE 11. NAME & DESIGNATION OF Dr. SHOBHA PRAKASH M.D.S. (IN BLOCK LETTERS) PROFESSOR AND HEAD, 11.1 GUIDE DEPARTMENT OF PERIODONTICS, COLLEGE OF DENTAL SCIENCES, DAVANGERE-577 OO4. 11.2 SIGNATURE 11.3 CO-GUIDE (IF ANY) − 11.4 SIGNATURE − 11.5 HEAD OF THE DEPARTMENT Dr. SHOBHA PRAKASH M.D.S. PROFESSOR AND HEAD, DEPARTMENT OF PERIODONTICS, COLLEGE OF DENTAL SCIENCES, DAVANGERE-577 OO4. 11.6 SIGNATURE 12. 12.1 REMARKS OF THE CHAIRMAN PRINCIPAL & Dr. V. V. SUBBA REDDY M.D.S. PRINCIPAL, COLLEGE OF DENTAL SCIENCES, DAVANGERE-577 004. 12.2 SIGNATURE