焦磷酸钙和基础磷酸钙沉积病:年度回顾

Geraldine Mary McCarthy
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引用次数: 0

摘要

含钙晶体沉积疾病是疼痛和残疾的常见原因,但研究相对较少。目前还没有发现药物可以阻止焦磷酸钙(CPP)或碱性磷酸钙(BCP)晶体的沉积或溶解。与痛风和尿酸生物学领域相比,2022年发表的与钙晶体沉积疾病相关的研究数量相对较少。在CPP沉积(CPPD)疾病中,主要在流行病学、影像学、外科治疗和Gitelman综合征方面取得进展。关于BCP晶体,我们在体外研究了其对肌腱细胞的影响,结果表明BCP晶体可能通过与肌腱细胞的相互作用降低肌腱基质的完整性。钙化参与骨关节炎(OA)的进展被很好地证明有助于进一步发现OA进展的过程。2022年发表的钙晶体沉积病的机制和遗传学研究较少,在治疗方面也没有任何突破,这表明未来在这些主题下有丰富的研究空间。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Calcium Pyrophosphate and Basic Calcium Phosphate Deposition Diseases: The Year in Review 2022
Calcium-containing crystal deposition diseases are a common cause of pain and disability but remain relatively under-investigated. No drug has been identified that can prevent deposition or effect dissolution of either calcium pyrophosphate (CPP) or basic calcium phosphate (BCP) crystals. In comparison to the field of gout and urate biology, published research in relation to calcium crystal deposition diseases in 2022 was relatively modest in quantity. In CPP deposition (CPPD) disease, progress was made mainly in epidemiology, imaging, surgical management and Gitelman’s syndrome. In relation to BCP crystals, the effect on tenocytes in vitro was explored and results indicate that BCP crystals likely reduce tendon matrix integrity via their interaction with tenocytes. The involvement of calcification in the progression of osteoarthritis (OA) was elegantly demonstrated contributing to further discovery of the process of OA progression. There was a paucity of mechanistic and genetic studies in calcium crystal deposition diseases published in 2022, nor any breakthrough in therapy, showing that there is abundant scope for investigation under these themes in the future.
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