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.
Keywords: B cell; Osteoarthritis; Osteoblast; Osteoimmunology; Subchondral bone; T cell.
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