Subchondral bone microenvironment in osteoarthritis and pain

Area of Science:

• Orthopedics and Rheumatology
• Biomedical Engineering
• Cell Biology

Background:

• Osteoarthritis (OA) is a degenerative joint disease causing pain and disability, with rising global incidence linked to aging and obesity.
• Despite extensive research, the precise role of subchondral bone in OA initiation and progression remains incompletely understood.
• Subchondral bone lesions, such as bone marrow edema and angiogenesis, appear to precede articular cartilage degeneration.

Purpose of the Study:

• To review the current understanding of bone-cartilage crosstalk in osteoarthritis (OA).
• To elucidate the critical role of the subchondral microenvironment in OA pathogenesis.
• To provide an update on OA pathogenesis, interventions, and future research directions focusing on subchondral bone.

Main Methods:

• Literature review of basic and clinical research on osteoarthritis.
• Analysis of evidence regarding subchondral bone changes and their relationship to cartilage degeneration.
• Synthesis of information on therapeutic interventions targeting cartilage versus subchondral bone.

Main Results:

• Subchondral bone abnormalities, including remodeling, angiogenesis, and nerve ingrowth, are implicated in OA progression and pain.
• Evidence suggests subchondral bone lesions develop earlier than cartilage degeneration.
• Interventions targeting subchondral bone show therapeutic promise, contrasting with less successful cartilage-targeted approaches.

Conclusions:

• Subchondral bone plays a critical role in osteoarthritis pathogenesis and progression through complex bone-cartilage crosstalk.
• Abnormalities in the subchondral bone microenvironment significantly contribute to cartilage destruction and pain.
• Future OA research and therapeutic strategies should increasingly focus on targeting subchondral bone.