Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hung Hom, Hong Kong.
Department of Orthopaedics & Traumatology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong.
Prog Biophys Mol Biol. 2019 Nov;148:21-31. doi: 10.1016/j.pbiomolbio.2017.12.004. Epub 2017 Dec 22.
Osteoarthritis (OA) is a whole-joint disorder, and non-cartilage articular pathologies, e.g. subchondral bone disturbance, contribute substantially to the onset and progression of the disease. In the early stage of OA, abnormal mechanical loading leads to micro-cracks or micro-fractures that trigger a reparative process with angiogenesis and inflammatory response. With the progression of disease, cystic lesion, sclerosis and osteophytosis occur at tissue level, and osteoblast dysfunction at cellular level. Osteoblasts derived from OA sclerotic bone produce increased amount of type I collagen with aberrant Col1A1/A2 ratio and poor mineralization capability. The coupling mechanism of bone resorption with formation is also impaired with elevated osteoclastic activities. All these suggest a view that OA subchondral bone presents a defective fracture repair process in a chronic course. It has been found that T and B cells, the major effectors in the adaptive immunity, take part in the hard callus formation at fracture site in addition to the initial phase of haematoma and inflammation. Infiltration of lymphocytes could interplay with osteoclasts and osteoblasts via a direct physical cell-to-cell contact. Several lines of evidence have consistently shown the involvement of T and B cells in osteoclastogenesis and bone erosion in arthritic joints. Yet the biological link between immune cells and osteoblastic function remains ambiguous. This review will discuss the current knowledge regarding the role of immune cells in bone remodelling, and address its implications in emerging basic and clinical investigations into the pathogenesis and management of subchondral bone pathologies in OA.
骨关节炎（OA）是一种全关节疾病，而非软骨关节的病理学改变，如软骨下骨紊乱，对疾病的发生和进展有重要贡献。在 OA 的早期，异常的机械负荷导致微裂纹或微骨折，引发血管生成和炎症反应的修复过程。随着疾病的进展，在组织水平上会出现囊性病变、硬化和骨赘形成，在细胞水平上会出现成骨细胞功能障碍。OA 硬化骨来源的成骨细胞产生大量的 I 型胶原，具有异常的 Col1A1/A2 比值和较差的矿化能力。破骨细胞活性升高，骨吸收与形成的偶联机制也受损。所有这些都表明 OA 软骨下骨在慢性病程中呈现出有缺陷的骨折修复过程。已经发现，T 细胞和 B 细胞作为适应性免疫的主要效应器，除了血肿和炎症的初始阶段外，还参与骨折部位的硬骨痂形成。淋巴细胞的浸润可以通过直接的细胞间物理接触与破骨细胞和成骨细胞相互作用。有几条证据一致表明 T 细胞和 B 细胞参与关节炎关节中的破骨细胞生成和骨侵蚀。然而，免疫细胞和成骨细胞功能之间的生物学联系仍然不清楚。这篇综述将讨论免疫细胞在骨重塑中的作用的现有知识，并探讨其在新兴的基础和临床研究中对 OA 软骨下骨病理学发病机制和治疗的意义。
