Bernabei Ilaria, So Alexander, Busso Nathalie, Nasi Sonia
Service of Rheumatology, Department of Musculoskeletal Medicine, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Nat Rev Rheumatol. 2023 Jan;19(1):10-27. doi: 10.1038/s41584-022-00875-4. Epub 2022 Dec 12.
Pathological calcification of cartilage is a hallmark of osteoarthritis (OA). Calcification can be observed both at the cartilage surface and in its deeper layers. The formation of calcium-containing crystals, typically basic calcium phosphate (BCP) and calcium pyrophosphate dihydrate (CPP) crystals, is an active, highly regulated and complex biological process that is initiated by chondrocytes and modified by genetic factors, dysregulated mitophagy or apoptosis, inflammation and the activation of specific cellular-signalling pathways. The links between OA and BCP deposition are stronger than those observed between OA and CPP deposition. Here, we review the molecular processes involved in cartilage calcification in OA and summarize the effects of calcium crystals on chondrocytes, synovial fibroblasts, macrophages and bone cells. Finally, we highlight therapeutic pathways leading to decreased joint calcification and potential new drugs that could treat not only OA but also other diseases associated with pathological calcification.
软骨的病理性钙化是骨关节炎(OA)的一个标志。钙化在软骨表面及其深层均可观察到。含钙晶体的形成,通常是碱性磷酸钙(BCP)和二水焦磷酸钙(CPP)晶体,是一个由软骨细胞启动,并受遗传因素、自噬或凋亡失调、炎症以及特定细胞信号通路激活影响而发生改变的活跃、高度调控且复杂的生物学过程。OA与BCP沉积之间的联系比OA与CPP沉积之间的联系更强。在此,我们综述了OA中软骨钙化所涉及的分子过程,并总结了钙晶体对软骨细胞、滑膜成纤维细胞、巨噬细胞和骨细胞的影响。最后,我们强调了可减少关节钙化的治疗途径以及可能不仅治疗OA,还能治疗其他与病理性钙化相关疾病的潜在新药。