Hwang Kyu Rim, Murrell George A C, Millar Neal L, Bonar Fiona, Lam Patrick, Walton Judie R
Orthopaedic Research Institute, St. George Hospital Campus, University of New South Wales, Sydney, NSW, Australia.
Orthopaedic Research Institute, St. George Hospital Campus, University of New South Wales, Sydney, NSW, Australia.
J Shoulder Elbow Surg. 2016 Jun;25(6):981-8. doi: 10.1016/j.jse.2015.10.015. Epub 2016 Jan 5.
The pathophysiologic mechanisms behind proliferation of fibroblasts and deposition of dense collagen matrix in idiopathic frozen shoulder remain unclear. Accumulation of advanced glycation end products (AGEs) with cross-linking and stabilization of collagen has been hypothesized to contribute to this pathophysiologic process. This study investigated whether the immunoreactivity of AGEs is higher in patients with idiopathic frozen shoulder than in the control groups.
Shoulder capsule samples were collected from 8 patients with idiopathic frozen shoulder, 6 with unstable shoulders (control 1), and 8 with rotator cuff tears (control 2). The samples were hematoxylin and eosin stained and analyzed by immunohistochemistry using antibodies against AGEs. Immunoreactivities were rated in a blinded fashion from none (0) to strong (3). Immunohistochemical distribution within the capsule was noted.
Frozen shoulder patients had greater frequency and severity of self-reported pain (P = .02) than rotator cuff tear patients and more restricted range of motion in all planes (P < .05) than patients of the instability and rotator cuff tear groups. Hematoxylin and eosin-stained capsular tissue from frozen shoulder showed fibroblastic proliferation, increased numbers of adipocytes, and increased subsynovial vascularity. Immunoreactivity of AGEs was stronger in frozen shoulder capsules (2.8) than in instability (0.3; P = .0001) and rotator cuff tear (1.1; P = .016) capsules.
This study highlights a potential role for AGEs in the pathogenesis of frozen shoulder. The overexpression of AGEs may explain the fibroblastic proliferation and deposition of collagen matrix in idiopathic frozen shoulder.
Basic Science Study; Histology.
特发性冻结肩中成纤维细胞增殖和致密胶原基质沉积背后的病理生理机制仍不清楚。有人提出,晚期糖基化终产物(AGEs)的积累以及胶原蛋白的交联和稳定化促成了这一病理生理过程。本研究调查了特发性冻结肩患者中AGEs的免疫反应性是否高于对照组。
从8例特发性冻结肩患者、6例肩部不稳定患者(对照组1)和8例肩袖撕裂患者(对照组2)中采集肩关节囊样本。样本进行苏木精-伊红染色,并使用抗AGEs抗体通过免疫组织化学进行分析。免疫反应性以盲法从无(0)到强(3)进行评分。记录囊内的免疫组织化学分布情况。
与肩袖撕裂患者相比,冻结肩患者自我报告的疼痛频率和严重程度更高(P = 0.02),并且在所有平面上的活动范围比不稳定组和肩袖撕裂组患者更受限(P < 0.05)。冻结肩患者苏木精-伊红染色的囊组织显示有成纤维细胞增殖、脂肪细胞数量增加以及滑膜下血管增多。冻结肩关节囊内AGEs的免疫反应性(2.8)强于不稳定组(0.3;P = 0.0001)和肩袖撕裂组(1.1;P = 0.016)的关节囊。
本研究突出了AGEs在冻结肩发病机制中的潜在作用。AGEs的过度表达可能解释了特发性冻结肩中成纤维细胞增殖和胶原基质沉积的现象。
基础科学研究;组织学。