The Roles of TNFRSF11B Genes as a Trigger for Secondary Osteoporosis in Rheumatoid Arthritis Cases

Abstract

Rheumatoid arthritis (RA) is an autoimmune disorder responsible for widespread and persistent inflammation of the synovial joint lining. Hence, victims are prone to greater risk of developing secondary osteoporosis (OP), a common complication of arthritis. The global prevalence of secondary OP among RA patients is estimated between 22-36%, although certain genetic polymorphisms pose a possible influence. Also, bone remodeling is closely related to the receptor activator nuclear factor-κB ligand (RANKL)/RANK and osteoprotegerin (OPG). The variables play a significant role in osteoclastogenesis, due to the ability of OPG to inhibit osteoclast differentiation and activation. This literature review discusses the relationship of TNFRSF11B gene polymorphisms that encode OPG protein with the risk of developing secondary osteoporosis in RA patients. The research method encompassed exploring similar articles from Pubmed, Cochrane Library, and Medline, using particular keywords, such as “TNFRSF11B polymorphism”, “osteoprotegerin polymorphism”, “rheumatoid arthritis” and “secondary osteoporosis”. Several distinct conclusions were obtained after analyzing the effects of TNFRSF11B gene polymorphisms on secondary OP in RA cases. Furthermore, the TNFRSF11B gene showed various polymorphisms closely related to bone remodeling, including C950T, G1181C, A163G, T245G and rs4876869.