Protein That Prevents Further Cartilage Damage

Source: Lawrence Livermore National Laboratory

Summary: Researchers performed in vivo experiments on animal models of post-traumatic osteoarthritis and found that a protein acts as a protective molecule immediately post joint injury to inhibit cartilage loss and joint calcification.

Patients with anterior cruciate ligament (ACL) ruptures are 2 times more likely to develop post-traumatic osteoarthritis (PTOA). Annually, there are 900,000 knee injuries in the U.S, which account for 12 % of all osteoarthritis (OA) cases. PTOA leads to reduced physical activity, deconditioning of the musculoskeletal system, and in severe cases, requires joint replacement to restore function. There may be a protein in the body that hinders cartilage degradation in patients with a torn ACL. Researchers from the Lawrence Livermore National Laboratory performed in vivo experiments on animal models of post-traumatic osteoarthritis and found that a protein called sclerostin (encoded by Sost gene in humans) acts as a protective molecule immediately post joint injury to inhibit cartilage loss and joint calcification. The study findings were published in the Journal of Bone and Mineral Research.


When joints were injured using a noninvasive technique that tears the anterior cruciate ligament in the knee, a protein, Sclerostin or Sost, which is normally not expressed in the articular cartilage, turned on immediately post-injury (red; anti-Sost sntibody). This protein serves a protective role by slowing down cartilage degradation that normally occurs post-injury. Extracellular matrix of articular cartilage is highlighted in green using a Collagen II antibody, and nuclei are in blue. Credit: Lawrence Livermore National Laboratory

To determine whether elevated levels of sclerostin play a protective role in PTOA, the team examined the progression of OA using a noninvasive tibial compression overload model. Biomechanical disturbances and physical manifestations in the joint contribute to the emergence of intra-articular lesions. Cartilage lesions become further exacerbated through molecular changes in the joint, including the increase in the production of matrix-degrading enzymes, such as aggrecanases and metalloproteinases. Elevated levels of these enzymes enhance the loss of articular cartilage, increase the amount of pain experienced and lead to impaired joint mobility in more than 50% of individuals that sustained an ACL tear. The results suggest that elevated levels of sclerostin, immediately post-injury, can aid the joint in maintaining its articular cartilage integrity in PTOA.

Lead author, Gaby Boots said, “We discovered that administering sclerostin to injured joints would significantly slow down cartilage degradation post-injury. The development of treatments that can be delivered to joints immediately post-injury could provide attractive alternatives to surgery.”

More Information: Jiun C. Chang et al. SOST/Sclerostin Improves Post Traumatic Osteoarthritis and Inhibits MMP2/3 Expression After Injury, Journal of Bone and Mineral Research (2018). DOI: 10.1002/jbmr.3397

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