Osteoarthritis (OA) is a degenerative joint disorder resulting in destruction of articular cartilage, osteophyte formation, and subchondral bone sclerosis. The S100 family and receptor for advanced glycation end products (RAGE) participate in regulating inflammation, even in the production of matrix metalloproteinases (MMPs). MMP-1 degrades cartilage, which may result in OA development. Moreover, polymorphisms in RAGE, S100A8, and MMP-1 have a marked effect on ligand binding and transcription regulating. In this study, we investigated the potential genetic contribution of the RAGE, S100A8, and MMP-1 genes to OA. We performed a matched case-control association study and genotyped OA patients and healthy controls, who were analysed by polymerase chain reaction-restriction fragment length polymorphism assays. A total of 314 patients were diagnosed with knee OA and underwent total knee replacement. The control group included 268 individuals who had standard X-rays of the knee joints to confirm K/L<2 and were matched by age and gender. Single-nucleotide polymorphisms in RAGE (557G/A), S100A8 (rs3795391A/G), and MMP-1 (-519A/G) were evaluated. S100A8 rs3795391A/G and MMP-1 -519A/G showed no significant difference between OA patients and healthy controls. RAGE 557G/A showed a significant association between OA patients and healthy controls (P<0.05, respectively). Our results suggest that the investigated polymorphism in the RAGE gene play a role in OA in the Taiwanese population.
Disclosure: The authors declared no competing interests.