Uchihashi Kazuyoshi, Tsuruta Toshiyuki, Mine Hiroko, Aoki Shigehisa, Nishijima-Matsunobu Aki, Yamamoto Mihoko, Kuraoka Akio, Toda Shuji
Department of Pathology and Microbiology, Faculty of Medicine, Saga University, Saga, Japan.
Pathol Int. 2014 Jun;64(6):276-82. doi: 10.1111/pin.12168.
Stenosing flexor tenosynovitis, trigger finger, is a common clinical disorder causing painful locking or contracture of the involved digits, and most instances are idiopathic. This problem is generally caused by a size mismatch between the swollen flexor tendon and the thickened first annular pulley. Although hypertrophic pulleys have been histologically and ultrasonographically detected, little is known about the histopathology of the tenosynovium covering the tendons of trigger fingers. We identified chondrocytoid cells that produced hyaluronic acid in 23 (61%) fingers and hypocellular collagen matrix in 32 (84%) fingers around the tenosynovium among 38 specimens of tenosynovium from patients with trigger fingers. These chondrocytoid cells expressed the synovial B cell marker CD44, but not the chondrocyte marker S-100 protein. The incidence of these findings was much higher than that of conventional findings of synovitis, such as inflammatory infiltrate (37%), increased vascularity (37%), hyperplasia of synovial lining cells (21%), or fibrin exudation (5%). We discovered the following distinctive histopathological features of trigger finger: hyaluronic acid-producing chondrocytoid cells originated from fibroblastic synovial B cells, and a hypocellular collagen matrix surrounding the tenosynovium. Thus, an edematous extracellular matrix with active hyaluronic acid synthesis might increase pressure under the pulley and contribute to the progression of stenosis.
狭窄性屈指肌腱腱鞘炎,即扳机指,是一种常见的临床病症,可导致受累手指出现疼痛性卡顿或挛缩,且大多数病例为特发性。该问题通常由肿胀的屈肌腱与增厚的第一环状滑车尺寸不匹配所致。尽管已通过组织学和超声检查检测到肥厚的滑车,但对于覆盖扳机指肌腱的腱鞘的组织病理学却知之甚少。在38例扳机指患者的腱鞘标本中,我们在23根(61%)手指的腱鞘周围发现了产生透明质酸的软骨样细胞,在32根(84%)手指的腱鞘周围发现了细胞减少的胶原基质。这些软骨样细胞表达滑膜B细胞标志物CD44,但不表达软骨细胞标志物S-100蛋白。这些发现的发生率远高于滑膜炎的传统表现,如炎症浸润(37%)、血管增多(37%)、滑膜衬里细胞增生(21%)或纤维蛋白渗出(5%)。我们发现扳机指具有以下独特的组织病理学特征:产生透明质酸的软骨样细胞起源于成纤维细胞性滑膜B细胞,以及腱鞘周围细胞减少的胶原基质。因此,具有活跃透明质酸合成的水肿细胞外基质可能会增加滑车下方的压力,并促使狭窄进展。