Active inflammatory processes were found to be ongoing in the subchondral bone (the bone underneath the collagen) of those with osteoarthritis.
The suggestion is offered that this ‘deeper’ inflammation may be responsible for some substantial portion of cartilage damage witnessed in osteoarthritis.
Enhanced expression of interleukin-6, matrix metalloproteinase-13, and receptor activator of NF-kappaB ligand in cells derived from osteoarthritic subchondral bone.
Summary of the abstract
BACKGROUND: The aim of this study was to clarify the significance of subchondral bone in the pathology of osteoarthritis (OA) by investigating the expression of inflammatory cytokines, proteases, and receptor activator of NF-kappaB ligand (RANKL)/receptor activator of NF-kappaB (RANK)/osteoprotegerin (OPG) involved in cartilage degeneration.
RESULTS: Higher levels of interleukin-6 (IL-6), matrix metalloproteinase-13 (MMP-13), and RANKL were found in OA SBOs compared to SBOs without OA. The expressions of these genes was greater in patients with severe cartilage damage than in those with mild cartilage damage.
CONCLUSION: The increases in IL-6, MMP-13, and RANKL expression in OA SBOs suggest that in subchondral bone OA progression involves abnormal osseous tissue remodeling, which induces mechanical property changes. Cartilage degeneration in OA may also be due, at least in part, to IL-6 and MMP-13 produced by SBOs. Comprehensive research on these pathological features may lead to the development of more effective therapies for OA by administration of molecules that affect bone remodeling and metabolism.