Toegel Stefan, Martelanz Luca, Alphonsus Juergen, Hirtler Lena, Gruebl-Barabas Ruth, Cezanne Melanie, Rothbauer Mario, Heuberer Philipp, Windhager Reinhard, Pauzenberger Leo
Department of Orthopedics and Trauma Surgery, Karl Chiari Lab for Orthopaedic Biology, Medical University of Vienna, Vienna, Austria.
Ludwig Boltzmann Institute for Arthritis and Rehabilitation, Vienna, Austria.
Bone Joint Res. 2024 Oct 21;13(10):596-610. doi: 10.1302/2046-3758.1310.BJR-2024-0026.R1.
This study aimed to define the histopathology of degenerated humeral head cartilage and synovial inflammation of the glenohumeral joint in patients with omarthrosis (OmA) and cuff tear arthropathy (CTA). Additionally, the potential of immunohistochemical tissue biomarkers in reflecting the degeneration status of humeral head cartilage was evaluated.
Specimens of the humeral head and synovial tissue from 12 patients with OmA, seven patients with CTA, and four body donors were processed histologically for examination using different histopathological scores. Osteochondral sections were immunohistochemically stained for collagen type I, collagen type II, collagen neoepitope C1,2C, collagen type X, and osteocalcin, prior to semiquantitative analysis. Matrix metalloproteinase (MMP)-1, MMP-3, and MMP-13 levels were analyzed in synovial fluid using enzyme-linked immunosorbent assay (ELISA).
Cartilage degeneration of the humeral head was associated with the histological presentation of: 1) pannus overgrowing the cartilage surface; 2) pores in the subchondral bone plate; and 3) chondrocyte clusters in OmA patients. In contrast, hyperplasia of the synovial lining layer was revealed as a significant indicator of inflammatory processes predominantly in CTA. The abundancy of collagen I, collagen II, and the C1,2C neoepitope correlated significantly with the histopathological degeneration of humeral head cartilage. No evidence for differences in MMP levels between OmA and CTA patients was found.
This study provides a comprehensive histological characterization of humeral cartilage and synovial tissue within the glenohumeral joint, both in normal and diseased states. It highlights synovitis and pannus formation as histopathological hallmarks of OmA and CTA, indicating their roles as drivers of joint inflammation and cartilage degradation, and as targets for therapeutic strategies such as rotator cuff reconstruction and synovectomy.
本研究旨在明确骨关节炎(OmA)和肩袖撕裂性关节病(CTA)患者肱骨头软骨退变及盂肱关节滑膜炎的组织病理学特征。此外,评估免疫组织化学组织生物标志物反映肱骨头软骨退变状态的潜力。
对12例OmA患者、7例CTA患者及4例尸体供者的肱骨头和滑膜组织标本进行组织学处理,采用不同的组织病理学评分进行检查。在进行半定量分析之前,对骨软骨切片进行免疫组织化学染色,检测I型胶原、II型胶原、胶原新表位C1,2C、X型胶原和骨钙素。采用酶联免疫吸附测定(ELISA)法分析滑液中基质金属蛋白酶(MMP)-1、MMP-3和MMP-13的水平。
肱骨头软骨退变与以下组织学表现相关:1)软骨表面有血管翳过度生长;2)软骨下骨板有孔隙;3)OmA患者有软骨细胞簇。相比之下,滑膜衬里层增生是CTA中炎症过程的主要显著指标。I型胶原、II型胶原和C1,2C新表位的丰度与肱骨头软骨的组织病理学退变显著相关。未发现OmA和CTA患者之间MMP水平存在差异。
本研究提供了正常和患病状态下盂肱关节内肱骨头软骨和滑膜组织的全面组织学特征。突出了滑膜炎和血管翳形成作为OmA和CTA的组织病理学标志,表明它们在关节炎症和软骨降解中的驱动作用,以及作为肩袖重建和滑膜切除术等治疗策略的靶点。