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Abstract
Osteoarthritis, OA, affects a significant portion of the canine population and is a major source of joint pain and decreased quality of life. Given the lack of disease modifying therapies, the search for factors that influence disease severity and progression continues. As obesity is a common co-morbidity in the canine, weight loss is an important management strategy. In humans, obesity leads to progression in hand OA, indicating that biomechanical changes are not the sole factor in disease progression. While there is evidence for a link between adipokines and human OA, there is no evidence regarding the role of adipokines in canine OA. In a first set of experiments leptin was quantified in synovial fluid (SF) from healthy dogs and those with OA and compared to body condition score (BCS), radiographic severity of OA, and Liverpool Osteoarthritis in Dogs (LOAD) score. Synovial fluid was higher in overweight dogs compared to ideal weight dogs and no difference based on the presence of OA was found. No correlation was found between SF leptin and radiographic severity of OA. There was a weak correlation between SF leptin and LOAD. In a second experiment, SF and serum cytokines were quantified in dogs with OA and in healthy control dogs. Concentrations of SF IL-8, MCP-1 and IL-6 were significantly higher in dogs with OA compared to healthy dogs. There was no significant correlation between serum or SF chemokines/cytokines. Additionally, no correlation was found between any SF cytokine/chemokine and SF leptin.The final set of experiments involved quantification of SF resistin in healthy dogs and those with OA. Serum and SF resistin was evaluated for correlation with BCS, radiographic severity of OA, and LOAD. There was no difference in serum or SF resistin based on BCS or OA status. There was no correlation between SF resistin and LOAD, or radiographic score. Given these findings along with evidence that resistin is released from monocyte cell lines in people, release of resistin from canine peripheral blood mononuclear cells and adipocytes was investigated. Results of the cell cultures indicate that resistin is released from T cells but not from adipocytes