UC Merced

Post traumatic osteoarthritis or PTOA is characterized as a painful and debilitating joint disease. The physiological effects that occur during progression and chronic disease are severe joint pain, inhibition of movement, and degradation of the cartilage and underlying bone. PTOA is rampant worldwide, affecting millions of individuals. In the United States alone, PTOA is the 5th leading cause of physical disability and carries the 8th highest financial burden on the healthcare system . The articular knee joint is supported by cartilage on both the tibia and femur and a soft membrane capsule known as the synovial lining which contains fluid essential in joint lubrication. The synovial fluid is crucial for maintaining joint movement and restraining compressive stress induced by daily activities. For many individuals, these tissues will sustain their functionality into old age. Within the next two decades the Center for Disease Control has projected a rise in osteoarthritis that correlates to the aging population in the United States. Additionally, nearly 12% of all cases of OA are induced by trauma. Currently, there are no effective preventatives, limited treatments, and poor biochemical prognosis for detecting OA and PTOA progression. Nearly 50% of individuals who encounter a traumatic knee injury and do not proceed with reconstructive surgery are diagnosed with PTOA. Interestingly, the remaining individuals spontaneously resolve this disease, continuing daily activities without pain, disability, and knee joint degradation. These individuals are thought to have a regenerative mechanism associated with their injury response. Due to the complex nature PTOA, researchers use mouse strains with differing susceptibilities to PTOA to elucidate regenerative mechanisms associated trauma. This study identifies the MRL/MpJ mouse as a PTOA-resistant model in studying the PTOA onset after tibial compression injury. By induction of an ACL rupture, several changes are seen in chondrocyte subpopulations and joint stromal cells that attenuate severe degradation of cartilage and bone through interaction with myeloid populations in the immune system. In short, this research identifies potential cellular and molecular targets for drug delivery and pharmacological intervention that may hinder the severe joint degradation seen in patients around the globe.