Articular cartilage and subchondral bone in the pathogenesis of osteoarthritis

Abstract

The articular surface plays an essential role in load transfer across the joint, and conditions that produce increased load transfer or altered patterns of load distribution accelerate the development of osteoarthritis (OA). Current knowledge segregates the risk factors into two fundamental mechanisms related to the adverse effects of "abnormal" loading on normal cartilage or "normal" loading on abnormal cartilage. Although chondrocytes can modulate their functional state in response to loading, their capacity to repair and modify the surrounding extracellular matrix is limited in comparison to skeletal cells in bone. This differential adaptive capacity underlies the more rapid appearance of detectable skeletal changes, especially after acute injuries that alter joint mechanics. The imbalance in the adaptation of the cartilage and bone disrupts the physiological relationship between these tissues and further contributes to OA pathology. This review focuses on the specific articular cartilage and skeletal features of OA and the putative mechanisms involved in their pathogenesis.

Mesenchymal Stem Cell Alterations in Bone Marrow Lesions in Patients With Hip Osteoarthritis

“…Other selected genes included those previously described as being associated with OA 3, 22 (see also Supplementary Table 4, available on the Arthritis & Rheumatology web site at http://onlinelibrary.wiley.com/doi/10.1002/art.39622/abstract). MSCs derived from trabecular bone from age‐matched controls as well as MSCs derived from the femoral heads of patients with OP were included as controls.…”

Efficacy of zoledronic acid in treatment of teoarthritis is dependent on the disease progression stage in rat medial meniscal tear model

“…We found that immediate ZOL administration significantly, Because of the intimate biological and mechanical relationship of articular cartilage and subchondral bone [10,13,22] , the abnormal remodeling of subchondral bone would aggravate the degeneration of overlying articular cartilage; thus, retarded bone remodeling would slow the degeneration of overlying articular cartilage [9,11,12] . However, because subchondral bone properties are dynamic during disease progression, the abnormal subchondral bone cannot always be modified.…”

“…Meanwhile, the biochemical composition and biomechanical properties of the subchondral bone are altered [9,10] . Therefore, because of an intimate biological and mechanical relationship with articular cartilage, the presence of abnormal subchondral bone influences the integrity of the overlying cartilage [11][12][13] . In addition, abnormalities in subchondral bone, such as exposure of the subchondral bone plate, bone attrition, and bone marrow lesions, have been associated with knee pain [14][15][16][17] .…”

Emerging Ideas: Instability-induced Periprosthetic Osteolysis Is Not Dependent on the Fibrous Tissue Interface

“…This fibrous layer may serve different roles in the periprosthetic zone: one mechanical, leading to component subsidence, and the other biologic, in which osteoclastogenic cytokines are expressed. At the time of revision surgery, the fibrous tissue has been shown in several studies to have the capacity to produce multiple proinflammatory cytokines such as prostaglandin E2, collagenase [8][9][10], and receptor activator of nuclear factor kappaB ligand (RANKL) [18]. This fibrous tissue was found to be heavily infiltrated with particulate cement and polyethylene debris [9], leading to the hypothesis that fibroblasts in the interface membrane respond to particulate wear debris, stimulating the release of osteoclastogenic cytokines [13].…”