title: A longitudinal study of interleukin-1 gene polymorphisms and periodontal disease in a general adult population.
abstract: BACKGROUND
  Cross-sectional studies have demonstrated that a specific polymorphism (allele 2 of both IL-1A +4845 and IL-1B +3954) in the IL-1 gene cluster has been associated with an increased susceptibility to severe periodontal disease and to an increased bleeding tendency during periodontal maintenance. The aim of the present study was to investigate the relationship between IL-1 genotype and periodontitis in a prospective longitudinal study in an adult population of essentially European heritage.
  
  
  METHODS
  From an ongoing study of the Oral Care Research Programme of The University of Queensland, 295 subjects consented to genotyping for IL-1 allele 2 polymorphisms. Probing depths and relative attachment levels were recorded at baseline, 6, 12, 24, 36, 48 and 60 months using the Florida probe. Periodontitis progression at a given site was defined as attachment loss > or =2 mm at any observation period during the 5 years of the study and the extent of disease progression determined by the number of sites showing attachment loss. Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans and Prevotella intermedia were detected using ELISA.
  
  
  RESULTS
  38.9% of the subjects were positive for the composite IL-1 genotype. A relationship between the IL-1 positive genotype and increased mean probing pocket depth in non-smokers greater than 50 years of age was found. Further, IL-1 genotype positive smokers and genotype positive subjects with P. gingivalis in their plaque had an increase in the number of probing depths > or =3.5 mm. There was a consistent trend for IL-1 genotype positive subjects to experience attachment loss when compared with IL-1 genotype negative subjects.
  
  
  CONCLUSIONS
  The results of this study have shown an interaction of the IL-1 positive genotype with age, smoking and P. gingivalis which suggests that IL-1 genotype is a contributory but non-essential risk factor for periodontal disease progression in this population.
authors.affiliation: The University of Queensland School of Dentistry, Oral Care Research Programme, Brisbane, Australia. m.cullinan@mailbox.uq.edu.au
authors.forename: M P
authors.initials: MP
authors.lastname: Cullinan
authors.forename: B
authors.initials: B
authors.lastname: Westerman
authors.forename: S M
authors.initials: SM
authors.lastname: Hamlet
authors.forename: J E
authors.initials: JE
authors.lastname: Palmer
authors.forename: M J
authors.initials: MJ
authors.lastname: Faddy
authors.forename: N P
authors.initials: NP
authors.lastname: Lang
authors.forename: G J
authors.initials: GJ
authors.lastname: Seymour
mesh_terms: D000328:Adult; D000367:Age Factors; D016976:Aggregatibacter actinomycetemcomitans / Q000302:isolation & purification; D001315:Australia; D003773:Dental Plaque / Q000382:microbiology; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D007375:Interleukin-1 / Q000235:genetics*; D016014:Linear Models; D008297:Male; D017622:Periodontal Attachment Loss / Q000235:genetics; D010518:Periodontitis / Q000235:genetics*; D011110:Polymorphism, Genetic; D016966:Porphyromonas gingivalis / Q000302:isolation & purification; D018713:Prevotella intermedia / Q000302:isolation & purification; D011446:Prospective Studies; D012307:Risk Factors; D012907:Smoking
chemical_list: D007375:Interleukin-1