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. 2013 Oct 1;4(4):286-294.
doi: 10.1177/1947603513495889.

The Roles of Mechanical Stresses in the Pathogenesis of Osteoarthritis: Implications for Treatment of Joint Injuries

Joseph A Buckwalter  1 , Donald D Anderson  2 , Thomas D Brown  2 , Yuki Tochigi  2 , James A Martin  2
Affiliations

The Roles of Mechanical Stresses in the Pathogenesis of Osteoarthritis: Implications for Treatment of Joint Injuries

Joseph A Buckwalter et al. Cartilage. .

Abstract

Excessive joint surface loadings, either single (acute impact event) or repetitive (cumulative contact stress), can cause the clinical syndrome of osteoarthritis (OA). Despite advances in treatment of injured joints, the risk of OA following joint injuries has not decreased in the last 50 years. Cumulative excessive articular surface contact stress that leads to OA results from post-traumatic joint incongruity and instability, and joint dysplasia, but also may cause OA in patients without known joint abnormalities. In vitro investigations show that excessive articular cartilage loading triggers release of reactive oxygen species (ROS) from mitochondria, and that these ROS cause chondrocyte death and matrix degradation. Preventing release of ROS or inhibiting their effects preserves chondrocytes and their matrix. Fibronectin fragments released from articular cartilage subjected to excessive loads also stimulate matrix degradation; inhibition of molecular pathways initiated by these fragments prevents this effect. Additionally, injured chondrocytes release alarmins that activate chondroprogentior cells in vitro that propogate and migrate to regions of damaged cartilage. These cells also release chemokines and cytokines that may contribute to inflammation that causes progressive cartilage loss. Distraction and motion of osteoarthritic human ankles can promote joint remodeling, decrease pain and improve joint function in patients with end-stage post-traumatic OA. These advances in understanding of how altering mechanical stresses can lead to remodeling of osteoarthritic joints and how excessive stress causes loss of articular cartilage, including identification of mechanically induced mediators of cartilage loss, provide the basis for new biologic and mechanical approaches to the prevention and treatment of OA.

Keywords: alarmins; joint injury; joint instability; mechanical loading of joints; post-traumatic osteoarthritis.

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Conflict of interest statement

Declaration of Conflicting Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

References

    1. Marsh JL, McKinley T, Dirschl D, Pick A, Haft G, Anderson DD, et al. The sequential recovery of health status after tibial plafond fractures. J Orthop Trauma. 2010;24(8):499-504. - PMC - PubMed
    1. Praemer AP, Furner S, Rice DP. Musculoskeletal conditions in the United States. Rosemont, IL: American Academy of Orthopaedic Surgeons; 1999.
    1. Felson DT. The epidemiology of osteoarthritis: prevalence and risk factors. In: Kuettner KF, Goldberg VM. editors. Osteoarthritis disorders. Rosemont, IL: American Academy of Orthopaedic Surgeons; 1994. P. 13-24.
    1. Buckwalter JA, Mankin HJ. Articular cartilage II. Degeneration and osteoarthrosis, repair, regeneration and transplantation.J Bone Joint Surg Am. 1997;79(4):612-32.
    1. Buckwalter JA, Martin J, Mankin HJ. Synovial joint degeneration and the syndrome of osteoarthritis. Instr Course Lect. 2000;49:481-9. - PubMed