Crystal deposition disease of the shoulder (including calcific tendonitis and milwaukee shoulder syndrome).
Crystal deposition disease of the shoulder (including calcific tendonitis and milwaukee shoulder syndrome).
复制标题
DOI：
10.1007/s11926-003-0074-9
复制
发表时间：
2003-06-01
影响因子：
5
通讯作者：
Halverson, Paul B
中科院分区：
文献类型：
--
作者：
Halverson, Paul B
钙化性肩腱炎是一个动态的过程。骨桥蛋白存在于肌腱钙化周围的细胞中。吸收可能是由含组织蛋白酶K的多核巨细胞介导的。肩袖撕裂与基于白细胞介素-1和增生性滑膜炎的炎症反应有关。金属蛋白酶存在于肩袖撕裂患者的滑液中。一些肩袖大撕裂的患者发展为严重的破坏性关节病，其特征为大量关节积液，这些积液是非炎症性的，但含有碱性磷酸钙晶体。这些晶体在体外刺激金属蛋白酶的产生，也抑制金属蛋白酶抑制剂的产生。ank基因突变导致小鼠进行性关节强直细胞外无机焦磷酸盐减少，而在某些家族性软骨钙质沉着症病例中细胞外无机焦磷酸盐增加。
Calcific tendinitis of the shoulder is a dynamic process. Osteopontin is present in cells surrounding tendon calcifications. Resorption is probably mediated by cathepsin K-containing multinucleated giant cells. Rotator cuff tears are associated with an inflammatory response based on the presence of interleukin-1 and a proliferative synovitis. Metalloproteinases are found in the synovial fluids of patients with rotator cuff tears. Some patients with large rotator cuff tears progress to a severe destructive arthropathy characterized by large joint effusions, which are noninflammatory but contain basic calcium phosphate crystals. These crystals stimulate metalloproteinase production in vitro and also suppress metalloproteinase inhibitor production. Mutations in the ank gene result in decreased extracellular inorganic pyrophosphate in murine progressive ankylosis, and increased extracellular inorganic pyrophosphate in some cases of familial chondrocalcinosis.