Osteoarthritis and bone mineral density: are strong bones bad for joints?

Abstract

Osteoarthritis (OA) is a common and disabling joint disorder affecting millions of people worldwide. In OA, pathological changes are seen in all of the joint tissues including bone. Although both cross-sectional and longitudinal epidemiological studies have consistently demonstrated an association between higher bone mineral density (BMD) and OA, suggesting that increased BMD is a risk factor for OA, the mechanisms underlying this observation remain unclear. Recently, novel approaches to examining the BMD-OA relationship have included studying the disease in individuals with extreme high bone mass, and analyses searching for genetic variants associated with both BMD variation and OA, suggesting possible pleiotropic effects on bone mass and OA risk. These studies have yielded valuable insights into potentially relevant pathways that might one day be exploited therapeutically. Although animal models have suggested that drugs reducing bone turnover (antiresorptives) may retard OA progression, it remains to be seen whether this approach will prove to be useful in human OA. Identifying individuals with a phenotype of OA predominantly driven by increased bone formation could help improve the overall response to these treatments. This review aims to summarise current knowledge regarding the complex relationship between BMD and OA.

Blocking PI3K/AKT signaling inhibits bone sclerosis in subchondral bone and attenuates post‐traumatic osteoarthritis

“…In addition, the inhibition of SDF‐1 receptor has been shown to attenuate the angiogenesis and hypertrophy of articular chondrocytes (Murata et al, ; Wang, & Zhou, ; Wei et al, ). Although, these studies illustrate the contribution of the subchondral bone remodeling to articular cartilage degeneration and hypertrophy, and that the subchondral bone changes should be regarded as a new target in OA, the response cell types and potential molecular cross‐talk signals of subchondral bone in OA progression remain unclear (Hardcastle, Dieppe, Gregson, Davey Smith, & Tobias, ; Pelletier et al, ; Zhen et al, ). Here, using a mouse PTOA model and in vitro studies, we distinguished the regulatory role of PI3K/AKT signaling in the subchondral bone changes, in the potential cross‐talk between subchondral osteoblasts and articular chondrocytes, and in cartilage degeneration.…”

Reduced Osteoarthritis Severity in Aged Mice With Deletion of Macrophage Migration Inhibitory Factor

“…Because of conflicting reports of bone density differences in MIF −/− mice compared to wild‐type mice and the possibility that bone density differences could influence the development of OA , we measured trabecular bone parameters by micro‐CT scans of the proximal metaphysis of the tibia from 8‐week‐old and 12‐month‐old male MIF −/− and wild‐type mice. The 8‐week‐old male MIF −/− mice had significantly greater bone volume fraction (Figure A), tissue mineral density (Figure B), and connectivity density (Figure C) than the age‐matched wild‐type mice.…”

Relationships between cartilage thickness and subchondral bone mineral density in non-osteoarthritic and severely osteoarthritic knees: In vivo concomitant 3D analysis using CT arthrography

“…Furthermore, DXA imaging is a two-dimensional modality that does not allow any subregional analysis such as in our study. In fact, the many limitations of DXA have led some authors to suggest that its use in epidemiological research should be restricted 48,49 . The present study also differs from this previous work by analyzing medial-to-lateral ratios in addition to compartmental measures and by testing for correlations between sBMD and CTh data all gathered on the femur.…”