Physiopathology of intratendinous calcific deposition.
Physiopathology of intratendinous calcific deposition.
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DOI：
10.1186/1741-7015-10-95
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发表时间：
2012-08-23
期刊：
影响因子：
9.3
通讯作者：
Maffulli N
中科院分区：
文献类型：
--
作者：
Oliva F;Via AG;Maffulli N
在钙化性肌腱病（CT）中，钙沉积在肌腱的物质中，伴有慢性活动相关疼痛、压痛、局部水肿和不同程度的活动范围减少。CT在肩袖、冈上肌、跟腱和髌腱中特别常见。钙化沉积物的存在可能会恶化肌腱病的临床表现，增加断裂率，恢复时间较慢，术后并发症的发生率较高。CT的发病机制仍有争议，但似乎是一个积极的细胞介导的过程和肌腱的局部尝试，以补偿原来的刚度下降的结果。肌腱愈合包括许多连续的过程，并且在愈合的不同阶段的干扰可能导致组织病理学变化的不同组合，将正常愈合过程转移到异常途径。本文就CT背后的发病机制理论作一综述。更好地了解其发病机制对于开发有效的治疗模式和改善临床结果至关重要。
In calcific tendinopathy (CT), calcium deposits in the substance of the tendon, with chronic activity-related pain, tenderness, localized edema and various degrees of decreased range of motion. CT is particularly common in the rotator cuff, and supraspinatus, Achilles and patellar tendons. The presence of calcific deposits may worsen the clinical manifestations of tendinopathy with an increase in rupture rate, slower recovery times and a higher frequency of post-operative complications. The aetiopathogenesis of CT is still controversial, but seems to be the result of an active cell-mediated process and a localized attempt of the tendon to compensate the original decreased stiffness. Tendon healing includes many sequential processes, and disturbances at different stages of healing may lead to different combinations of histopathological changes, diverting the normal healing processes to an abnormal pathway. In this review, we discuss the theories of pathogenesis behind CT. Better understanding of the pathogenesis is essential for development of effective treatment modalities and for improvement of clinical outcomes.
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影响因子：
--
作者：
CANNON, RB;SCHMID, FR
通讯作者：
SCHMID, FR
影响因子：
82.9
作者：
Bi, Yanming;Ehirchiou, Driss;Young, Marian F.
通讯作者：
Young, Marian F.
DOI：
10.1001/jama.1941.02820220019004
发表时间：
1941-04-01
影响因子：
--
作者：
Bosworth, BM
通讯作者：
Bosworth, BM
影响因子：
5.5
作者：
Choi, S. T.;Kim, J. H.;Lee, S. -K.
通讯作者：
Lee, S. -K.
影响因子：
5
作者：
Halverson, Paul B
通讯作者：
Halverson, Paul B