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Osteoarthritis is slowly progressive disease characterized by destruction of articular cartilage , subchondral bone sclerosis , and chronic inflammation of the synovium . Symptoms usually manifest as pain, stiffness, swelling and crepitus. Currently, analgesic treatments for osteoarthritis have limited efficacy and accompanied by gastrointestinal and cardiovascular side effects. Cannabinoids are a group of compounds structurally related to Δ9-tetrahydrocannabinol (Δ9-THC), a substance found in the Cannabis sativa plant which has been used for centuries for its psychoactive and medicinal effects. Considering the physiological role of cannabinoid receptors (CB1 And CB2) in controlling multiple responses including pain and inflammation, cannabinoids exert analgesic effects in rodent models of osteoarthritis. However, previous studies have shown that cannabinoids and cannabinoid like-compounds could produce analgesia in a CB1/CB2 independent fashion by interaction with other receptors such as The transient receptor potential vanilloid (TRPV1) and peroxisome proliferator-activated receptors (PPARs). PPARs are nuclear receptors activated by fatty acids, eicosanoids and synthetic agonists. Three PPAR isoforms have been identified—α, β/δ, and γ. PPARs are involved in controlling lipid metabolism, inflammatory and immune responses. Several studies have confirmed the ability of PPAR ligands to inhibit the signaling pathways of joint inflammation and reduce the formation of cartilage catabolic factors. Yet, the analgesic properties of PPAR ligands in osteoarthritis are less clear. My research interest is using rat models of osteoarthritis and molecular biology techniques to investigate the possible role of PPAR receptors in mediating the analgesic effects of different cannabinoids such as WIN-55,212-2, HU210 and cannabinoid-like compounds such as Palmitoylethanolamide (PEA).