Subchondral bone in osteoarthritis: a biologic link with articular cartilage leading to abnormal remodeling

Purpose of review This review deals with new findings highlighting the concept of cross-talk between subchondral bone tissue and articular cartilage that may be crucial for the initiation and/or progression of osteoarthritis. In this review, new factors either produced by subchondral bone tissue or modifying osteoblast metabolism, yet implicated in osteoarthritis, are discussed. Recent findings The development of cartilage degeneration is concomitant with subchondral bone thickness in osteoarthritis, whereas it is related to higher subchondral bone activity and dysregulation in the synthesis of bone proteins. As an immediate consequence, homotrimers of type 1 collagen are formed that could lead to undermineralization of this tissue. This dysregulation also leads to abnormal production of different factors by osteoblasts such as prostaglandins, leukotrienes, and growth factors. Because microcracks or neovascularization provide a link between the subchondral bone tissue and articular cartilage, these factors could contribute to the abnormal remodeling of osteoarthritic cartilage. Summary These findings have an immediate implication for research because new tools need to be developed to study the subchondral bone-cartilage functional unit. Moreover, it could lead to a possible cure for osteoarthritis because this pathology should be considered both a bone and cartilage disease.