title: Influence of interleukin-1 gene polymorphism on the outcome of supportive periodontal therapy explored by a multi-factorial periodontal risk assessment model (PRA).
abstract: BACKGROUND
  Multi-factorial risk models have been proposed to enhance the ability to predict risk for the progression of treated chronic periodontitis.
  
  
  OBJECTIVE
  to study if the outcomes of supportive periodontal therapy (SPT) based on a multi-factorial periodontal risk assessment are influenced by IL-1 gene polymorphism (IP) status.
  
  
  METHODS
  Information about the IP and smoking status, clinical periodontal conditions and age related bone level measurements were used to calculate a peridontal risk assessment model (PRA). The surface area of this diagram was calculated for 224 subjects who had participated in an SPT program over four years. Baseline and 4-year follow-up data were studied in relation to the IP status.
  
  
  RESULTS
  Positive IP tests were obtained for 80/224 (35.7%) of the subjects. At baseline the mean PRA for the IP positive group was 79.9 units, which at year four had increased to 81.3 units (mean diff: 1.4 units, S.D.+/-16.5, p<0.45, 95% CI: 2.3 to 5.1). At baseline and year four the mean PRA for the IP negative group was 44.2 and 38.6 units, respectively. This difference was statistically significant (mean diff: 5.6, S.D.+/-16.1, p<0.001, 95% CI: 3.0 to 8.3). Independent t-tests confirmed that the IP status was significantly associated with a less favorable change in PRA over the four-year period (PRA difference: 7.04, t=3.01, p<0.003, 95% CI: 2.4 to 11.65). Bleeding on probing, and probing depth values alone did not differ between positive and negative IP status. Regression analysis demonstrated that the best-fit model for change in PRA included bleeding on probing at baseline, IP status, proportional alveolar bone loss in relation to the age, and gender.
  
  
  CONCLUSIONS
  The PRA allowed the assessment of the outcomes of SPT therapy. Subjects with positive IP did not respond to individualized SPT as favorably as did IP negative subjects.
authors.affiliation: School of Dental Medicine, University of Berne, Switzerland.
authors.forename: G Rutger
authors.initials: GR
authors.lastname: Persson
authors.forename: Giedré
authors.initials: G
authors.lastname: Matuliené
authors.forename: Christoph A
authors.initials: CA
authors.lastname: Ramseier
authors.forename: Rigmor E
authors.initials: RE
authors.lastname: Persson
authors.forename: Maurizio S
authors.initials: MS
authors.lastname: Tonetti
authors.forename: Niklaus P
authors.initials: NP
authors.lastname: Lang
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D016301:Alveolar Bone Loss / Q000145:classification; D015331:Cohort Studies; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005884:Gingival Hemorrhage / Q000145:classification; D006801:Humans; D007375:Interleukin-1 / Q000235:genetics*; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D010514:Periodontal Pocket / Q000145:classification; D010518:Periodontitis / Q000209:etiology / Q000628:therapy*; D011110:Polymorphism, Genetic / Q000235:genetics*; D012189:Retrospective Studies; D018570:Risk Assessment; D012737:Sex Factors; D012907:Smoking; D016388:Tooth Loss / Q000145:classification; D016896:Treatment Outcome
chemical_list: D007375:Interleukin-1