Ea Hang-Korng, Lioté Frédéric
Inserm U606 Fédération de Rhumatologie, Hôpital Lariboisière, 2 rue Ambroise Paré, F75475 Paris Cedex 10, France.
Curr Rheumatol Rep. 2004 Jun;6(3):221-7. doi: 10.1007/s11926-004-0072-6.
Calcium-containing crystals are the most common class for the osteoarthritic joint. They are responsible for acute periarthritis and destructive arthropathies, and for tissue deposits mimicking tumor-like masses. These crystals encompassed mainly calcium pyrophosphate dihydrate and basic calcium phosphate crystals, with the latter being related to hydroxyapatite, carbonate-substituted apatite, and octacalcium phosphate. Calcification deposit mechanisms will be reviewed with respect to extracellular inorganic pyrophosphate dysregulation mainly caused by modulation of specific membrane channel disorders. Genetic defects have been extensively studied and identified mutation of specific genes such as ANKH and COL. Pathogenesis of crystal-induced inflammation is related to synovial tissue and direct cartilage activation. Besides classical knee or wrist pseudogout attacks or Milwaukee shoulder arthropathies, clinicians should be aware of other specific common presentations, such as erosive calcifications, spinal cord compression by intraspinal masses, ligamentum flavum calcification, or atypical calcified tophus. Promising clinical results for preventing calcium crystal deposits and cartilage degradation are lacking. Practical imaging tools are needed to monitor reduction of calcification of fibrocartilage and articular cartilage as markers of drug efficacy.
含钙晶体是骨关节炎关节中最常见的类型。它们可导致急性关节炎和破坏性关节病,以及类似肿瘤样肿块的组织沉积。这些晶体主要包括二水焦磷酸钙和碱性磷酸钙晶体,后者与羟基磷灰石、碳酸取代磷灰石和八钙磷酸钙有关。钙化沉积机制将主要针对由特定膜通道紊乱调节引起的细胞外无机焦磷酸调节异常进行综述。遗传缺陷已得到广泛研究,并鉴定出ANKH和COL等特定基因的突变。晶体诱导炎症的发病机制与滑膜组织和直接软骨激活有关。除了典型的膝关节或腕关节假性痛风发作或密尔沃基肩关节病外,临床医生还应了解其他特定的常见表现,如侵蚀性钙化、脊髓内肿块压迫脊髓、黄韧带钙化或非典型钙化痛风石。目前缺乏预防钙晶体沉积和软骨降解的有前景的临床结果。需要实用的成像工具来监测纤维软骨和关节软骨钙化的减少,以此作为药物疗效的指标。