Narrative review synthesizing evidence on how the subchondral bone microenvironment — through aberrant remodeling, angiogenesis, and sensory nerve innervation — drives both cartilage destruction and pain in osteoarthritis, and what therapeutic targets this framework suggests.
When an OA patient reports pain disproportionate to their radiographic cartilage loss, think subchondral bone: aberrant bone remodeling, type H vessel ingrowth, and sensory nerve innervation via netrin-1 can generate neuropathic pain (present in ~23% of OA patients) that won't respond to NSAIDs alone — and explains why bone-targeted therapies like bisphosphonates and anti-NGF antibodies are showing more promise than cartilage-repair strategies.
Narrative review synthesizing evidence on how the subchondral bone microenvironment — through aberrant remodeling, angiogenesis, and sensory nerve innervation — drives both cartilage destruction and pain in osteoarthritis, and what therapeutic targets this framework suggests.
When an OA patient reports pain disproportionate to their radiographic cartilage loss, think subchondral bone: aberrant bone remodeling, type H vessel ingrowth, and sensory nerve innervation via netrin-1 can generate neuropathic pain (present in ~23% of OA patients) that won't respond to NSAIDs alone — and explains why bone-targeted therapies like bisphosphonates and anti-NGF antibodies are showing more promise than cartilage-repair strategies.