Pathological mechanism of joint destruction in haemophilic arthropathy.

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Abstract

[Indexed for MEDLINE] 12. J Bone Miner Metab. 2024 Jul;42(4):455-462. doi: 10.1007/s00774-024-01520-8. Epub 2024 Jun 10. Inflammatory diseases causing joint and bone destruction: rheumatoid arthritis and hemophilic arthropathy. Terashima A(1), Ono K(2)(3), Omata Y(1)(3), Tanaka S(3), Saito T(4). Author information: (1)Bone and Cartilage Regenerative Medicine, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-Ku, Tokyo, 113-8655, Japan. (2)Department of Joint Surgery, Research Hospital, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-Ku, Tokyo, 108-8639, Japan. (3)Orthopaedic Surgery, Sensory and Motor System Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-Ku, Tokyo, 113-8655, Japan. (4)Orthopaedic Surgery, Sensory and Motor System Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-Ku, Tokyo, 113-8655, Japan. tasaitou-tky@umin.ac.jp. Various diseases and conditions cause joint disorders. Osteoarthritis (OA) is characterized by the degeneration of articular cartilage, synovitis, and anabolic changes in surrounding bone tissues. In contrast, rheumatoid arthritis (RA) and hemophilic arthropathy (HA) display marked destruction of bone tissues caused by synovitis. RA is a representative autoimmune disease. The primary tissue of RA pathogenesis is the synovial membrane and involves various immune cells that produce catabolic cytokines and enzymes. Hemophilia is a genetic disorder caused by a deficiency in blood clotting factors. Recurrent intra-articular bleeding leads to chronic synovitis through excessive iron deposition and results in the destruction of affected joints. Although the triggers for these two joint diseases are completely different, many cytokines and enzymes are common in the pathogenesis of both RA and HA. This review focuses on the similarities between joint and bone destruction in RA and HA. The insights may be useful in developing better treatments for hemophilia patients with arthropathy and osteoporosis by leveraging advanced therapeutics for RA. © 2024. The Author(s). DOI: 10.1007/s00774-024-01520-8 PMCID: PMC11415468