Role and Mechanism of Mechanical Load in the Homeostasis of the Subchondral Bone in Knee Osteoarthritis: A Comprehensive Review

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Osteoarthritis (OA) is one of the most prevalent degenerative joint diseases, and the knee joint is particularly susceptible to it. It typically affects the entire joint and is marked by the erosion of cartilage integrity, chondrocytopenia, subchondral bone sclerosis and the mild synovial inflammation. Pathological changes in the subchondral bone often serve as initiating factors for joint degeneration. Various predisposing factors, including metabolic disorders, oxidative stress, and abnormal mechanical loading, regulate OA pathogenesis. Of them, mechanical loading is closely associated with the maintenance of the subchondral bone. Disrupted mechanical loading, leading to subchondral bone remodeling, can potentially trigger OA, whereas appropriate loading might ameliorate its progression. Therefore, this narrative review aimed to discuss existing knowledge and explore how mechanical loading mediates changes in the subchondral bone, influencing the development of knee osteoarthritis. Special emphasis is placed on its role and underlying mechanisms in maintaining joint homeostasis.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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