Toma Takashi, Suenaga Naoki, Taniguchi Noboru, Oizumi Naomi, Yamaguchi Hiroshi, Tome Yasunori, Kanaya Fuminori
1 Department of Orthopedic Surgery, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan.
2 Department of Orthopedic Surgery, Kaisei Hospital, Obihiro, Japan.
J Orthop Surg (Hong Kong). 2019 Jan-Apr;27(1):2309499018816428. doi: 10.1177/2309499018816428.
The aim of this study was to investigate the histopathological changes in the humeral head in cuff tear arthropathy (CTA) compared with those in glenohumeral osteoarthritis (OA) and humeral neck fracture, which served as non-cuff tear controls.
Twenty-three humeral heads extracted at the time of shoulder prosthesis arthroplasty between June 2014 and July 2015 were evaluated in the present study. The diagnoses included four-part humeral neck fracture ( n = 4; average age, 85.0 years), glenohumeral OA ( n = 4; average age, 71.0 years), and CTA ( n = 15; average age, 73.0 years). The humeral heads were evaluated pathologically by hematoxylin and eosin and Safranin-O staining, and the thickness of the articular cartilage was measured.
Fibrillation, thinning, and tearing of the cartilage were observed in the superior area of the humeral heads in CTA and glenohumeral OA. In CTA cases, clusters of chondrocytes in the cartilage were observed. Moreover, the thickness of the cartilage layer in the middle of the humeral head was 1.54 ± 0.07, 0.32 ± 0.46, and 2.19 ± 0.50 mm in humeral neck fracture, glenohumeral OA, and CTA, respectively. The cartilage layer in CTA was thicker than that in glenohumeral OA (CTA vs. OA: p < 0.05).
OA changes in the superior area of the humeral heads and thickening of the cartilage layer from the middle to the inferior of the humeral heads were confirmed histopathologically, suggesting that simultaneous mechanical and nutritional factors might be contributing to CTA pathogenesis. The current study provided the better understanding of cartilage damage and thickening in CTA. This will help guide treatment options in the setting of CTA.
本研究旨在调查与作为非肩袖撕裂对照的盂肱骨关节炎（OA）和肱骨干骨折相比，肩袖撕裂关节病（CTA）肱骨头的组织病理学变化。
本研究评估了2014年6月至2015年7月期间在肩关节假体置换术时取出的23个肱骨头。诊断包括四部分肱骨干骨折（n = 4；平均年龄85.0岁）、盂肱骨关节炎（n = 4；平均年龄71.0岁）和CTA（n = 15；平均年龄73.0岁）。通过苏木精和伊红以及番红O染色对肱骨头进行病理评估，并测量关节软骨的厚度。
在CTA和盂肱骨关节炎的肱骨头上方区域观察到软骨的纤维化、变薄和撕裂。在CTA病例中，观察到软骨中软骨细胞簇。此外，肱骨干骨折、盂肱骨关节炎和CTA中肱骨头中部软骨层的厚度分别为1.54±0.07、0.32±0.46和2.19±0.50mm。CTA中的软骨层比盂肱骨关节炎中的厚（CTA与OA相比：p < 0.05）。
组织病理学证实了肱骨头上方区域的OA变化以及肱骨头中部至下部软骨层的增厚，表明机械和营养因素可能同时导致CTA的发病机制。本研究更好地理解了CTA中的软骨损伤和增厚。这将有助于指导CTA情况下的治疗选择。
