Peran Gen TNFRSF11B sebagai Pemicu Osteoporosis Sekunder pada Pasien Artritis Reumatoid

Nur A. Ali; Dika P. Destiani; Riezki Amalia

doi:10.15416/ijcp.2021.10.3.234

Peran Gen TNFRSF11B sebagai Pemicu Osteoporosis Sekunder pada Pasien Artritis Reumatoid

Nur A. Ali, Dika P. Destiani, Riezki Amalia

Abstract

Artritis reumatoid (AR) adalah kelainan autoimun sistemik yang menyebabkan peradangan luas dan persisten pada lapisan sendi sinovial. Pasien dengan AR memiliki risiko lebih besar terkena osteoporosis sekunder. Osteoporosis (OP) sekunder adalah komplikasi umum dari radang sendi seperti AR. Prevalensi OP sekunder pada pasien AR di berbagai belahan dunia dilaporkan antara 22% hingga 36%. Beberapa polimorfisme genetik dapat memengaruhi timbulnya penyakit osteoporosis. Proses remodeling tulang erat kaitannya dengan receptor activator nuclear factor-κB ligand (RANKL)/RANK dan osteoprotegerin (OPG). RANK/ RANKL/OPG adalah memiliki peran penting dalam osteoklastogenesis, karena OPG mampu menghambat diferensiasi dan aktivasi osteoklas. Kajian pustaka ini membahas mengenai hubungan polimorfisme gen TNFRSF11B yang mengkode protein OPG dengan risiko osteoporosis sekunder pada penderita AR. Metode yang digunakan pada kajian pustaka ini adalah dengan penelusuran artikel penelitian dan artikel review dari Pubmed, Cochrane Library, dan Medline dengan kata kunci “TNFRSF11B polymorphism”, “osteoprotegerin polymorphism”, “rheumatoid arthritis”, dan “secondary osteoporosis”. Sebagai hasil kajian pustaka, didapatkan beberapa simpulan berbeda dari studi pengaruh polimorfisme gen TNFRSF11B terhadap OP sekunder pada AR. Gen TNFRSF11B memiliki beberapa polimorfisme yang erat kaitannya dengan remodeling tulang, di antaranya adalah C950T, G1181C, A163G, T245G dan rs4876869.

Kata kunci: Artritis reumatoid, osteoporosis sekunder, polimorfisme, TNFRSF11B

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.

Keywords: Polymorphism, rheumatoid arthritis, secondary osteoporosis, TNFRSF11B

Keywords

Artritis reumatoid, osteoporosis sekunder, polimorfisme, TNFRSF11B

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