title: Gene polymorphism and protein of human pro- and anti-inflammatory cytokines in Chinese healthy subjects and chronic periodontitis patients.
abstract: BACKGROUND
  Periodontal disease is thought to arise from the interaction of various factors, including the susceptibility of the host, the presence of pathogenic organisms, and the absence of beneficial species. The genetic factors may play a significant role in the risk of periodontal diseases. Cytokines initiate, mediate and control immune and inflammatory responses. The aim of this study is to compare genotypes and soluble protein of pro and anti-inflammatory cytokines (IL-1α, IL-1β, IL-6, IFN-γ, IL-10, TNF-α and IL-4) in subjects with or free of chronic periodontitis.
  
  
  METHODS
  A total of 1,290 Chinese subjects were recruited to this clinical trial: 850 periodontally healthy controls and 440 periodontal patients. All subjects were free of systemic diseases. Oral examinations were performed, and the following parameters were recorded for each subject: supragingival/subgingival calculus, gingival recession, bleeding on probing (BOP), probing depth (PD), clinical attachment loss (CAL), gingival recession and tooth mobility. The peripheral blood samples were collected for genetic and enzyme linked immunosorbent assay (ELISA) analysis. Restriction enzymes were used for digestion of amplified fragments of IL-1α, IL-1β, IL-6, IFN-γ, IL-10, TNF-α and IL-4.
  
  
  RESULTS
  The protein expressions of patient and control samples for IL-1α, IL-1β, IL-6, TNF-α, IFN-γ, IL-10, and IL-4 measured by ELISA confirmed a statistically significant difference (p < 0.001). The digestion of fragments of various genes showed that the pro-inflammatory cytokines IL-1α and TNF-α, and the anti-inflammatory cytokines IL-4 and IL-10 demonstrated a correlation with chronic inflammation in patients (X2: p < 0.001). The remaining genes investigated in patients and healthy subjects (IL-1β, IL-6, IFN-γ and IL-10) did not show any significant difference.
  
  
  CONCLUSIONS
  The cytokine gene polymorphisms may be used as a marker for periodontitis susceptibility, clinical behaviour and severity. This detection offers early diagnosis and induction of prophylaxis to other family members against disease progression.
authors.affiliation: UNIMED Medical Institute, Hong Kong SAR.
authors.forename: Wings T Y
authors.initials: WT
authors.lastname: Loo
authors.forename: Chang-bin
authors.initials: CB
authors.lastname: Fan
authors.forename: Lan-jun
authors.initials: LJ
authors.lastname: Bai
authors.forename: Yuan
authors.initials: Y
authors.lastname: Yue
authors.forename: Yi-ding
authors.initials: YD
authors.lastname: Dou
authors.forename: Min
authors.initials: M
authors.lastname: Wang
authors.forename: Hao
authors.initials: H
authors.lastname: Liang
authors.forename: Mary N B
authors.initials: MN
authors.lastname: Cheung
authors.forename: Louis W C
authors.initials: LW
authors.lastname: Chow
authors.forename: Jin-le
authors.initials: JL
authors.lastname: Li
authors.forename: Ye
authors.initials: Y
authors.lastname: Tian
authors.forename: Liu
authors.initials: L
authors.lastname: Qing
mesh_terms: D000328:Adult; D000368:Aged; D000893:Anti-Inflammatory Agents / Q000378:metabolism*; D044466:Asian People / Q000235:genetics*; D016022:Case-Control Studies; D002681:China; D055113:Chronic Periodontitis / Q000235:genetics*; D016207:Cytokines / Q000235:genetics*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005787:Gene Frequency / Q000235:genetics; D020022:Genetic Predisposition to Disease; D006262:Health; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D018836:Inflammation Mediators