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导致关节和骨骼破坏的炎症性疾病:类风湿关节炎和血友病性关节病。

Inflammatory diseases causing joint and bone destruction: rheumatoid arthritis and hemophilic arthropathy.

机构信息

Bone and Cartilage Regenerative Medicine, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo-Ku, Tokyo, 113-8655, Japan.

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.

出版信息

J Bone Miner Metab. 2024 Jul;42(4):455-462. doi: 10.1007/s00774-024-01520-8. Epub 2024 Jun 10.

Abstract

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.

摘要

各种疾病和病症都会导致关节紊乱。骨关节炎(OA)的特征是关节软骨退化、滑膜炎和周围骨组织的合成代谢变化。相比之下,类风湿关节炎(RA)和血友病性关节病(HA)则显示出滑膜炎引起的明显骨组织破坏。RA 是一种代表性的自身免疫性疾病。RA 发病的主要组织是滑膜膜,涉及产生分解代谢细胞因子和酶的各种免疫细胞。血友病是一种由凝血因子缺乏引起的遗传性疾病。反复的关节内出血通过过多的铁沉积导致慢性滑膜炎,并导致受影响关节的破坏。尽管这两种关节疾病的诱因完全不同,但在 RA 和 HA 的发病机制中存在许多共同的细胞因子和酶。本综述重点关注 RA 和 HA 中关节和骨破坏的相似性。这些见解可能有助于通过利用 RA 的先进治疗方法为患有关节病和骨质疏松症的血友病患者开发更好的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efb0/11415468/c157fe313bc5/774_2024_1520_Fig1_HTML.jpg

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