The association of ADAM12 polymorphism with osteoarthritis susceptibility: a meta-analysis

• Published in: Therapeutics and clinical risk management 2017-01, Vol.13, p.821-830
• Main Authors: Wu, Zhen, Xu, Xin-Wei, Zhang, Xiao-Wen
• Format: Article
• Language: English
• Subjects: ADAM12 polymorphism; Arthritis; Genes; Genetic aspects; Genetic polymorphisms; Health aspects; Males; Meta-analysis; Original Research; Osteoarthritis; Polymorphism; Population; Proteins; Rheumatology; Risk factors
• ISSN: 1176-6336; 1178-203X; 1178-203X
• DOI: 10.2147/TCRM.S134581

The pathology of osteoarthritis (OA) is partly attributed to genetic factors; however, the role of polymorphism is still controversial. It is necessary to perform a meta-analysis to investigate this possible correlation. Case-control studies on the association between OA susceptibility and polymorphism were comprehensively collected by searching PubMed, Embase, and Web of Science. Odds ratios (ORs) and 95% confidence intervals (CIs) were pooled to evaluate OA risk that was possibly conferred by variant. The analyses were performed not only among general population but also in male and female groups. A total of 8 studies with 10 populations were finally included in this meta-analysis. In the general population, 4 comparisons were carried out (C allele vs G allele, CC vs GG, GC + CC vs GG, and CC vs GC + GG) and found that polymorphism was not associated with increased OA vulnerability. On the other hand, the analyses stratified by gender made 5 comparisons (C allele vs G allele, CC vs GG, GC vs GG, GC + CC vs GG, and CC vs GC + GG). It was shown that polymorphism (GC + CC vs GG) was a risk factor for OA among male patients (OR =1.45, 95% CI =1.04-2.01). Sensitivity analysis indicated that it was an unstable outcome. No correlation was identified in women. Neither heterogeneity nor publication bias was detected in the analyses mentioned above. polymorphism is likely to be associated with OA susceptibility among male patients, other than the general population. More studies are needed to confirm this observation. The mechanism by which variant plays a role in OA pathogenesis is also warranted and important for interpreting this possible correlation.