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Osteoarthritis (OA) is a common cause of lameness, pain, and dysfunction in dogs and is estimated to affect > 20% of all dogs over 1year of age (2). Cartilage breakdown products, resulting from mechanical or enzymatic destruction, induce the release of inflammatory cytokines (e.g., interleukin (IL-1, IL-6) or tumor necrosis factor (TNF-α)) by macrophages and chondrocytes, leading to the upregulation of matrix metalloproteinases (MMPs), nitric oxide (NO), and other proteolytic enzymes. Synovial macrophages play a role in triggering inflammatory and destructive conditions through the production of IL-1β and TNF-α, which stimulate chondrocytes to produce inflammatory mediators. IL-1β and TNF-α are the main inflammatory factors involved in OA, with IL-1β driving tissue destruction and TNF-α being associated with inflammation (1, 3). In addition, other cytokines have also been implicated, including IL-6, IL-15, IL-17, IL-18, IL-21, leukemia inhibitory factor, and IL-8 (a chemokine) (1, 4). Platelet-rich plasma (PRP) is a concentrated source of autologous platelets, which contains several different growth factors (platelet-derived growth factor (PDGF), transforming growth factor-beta (TGF-β1), epidermal growth factor (EGF), and vascular endothelial growth factor (VEGF)) and other cytokines that can stimulate the healing of soft tissue (8, 10). Intra-articular injection of autologous platelets has great promise as a potential treatment for OA in dogs (9). When used in the treatment of OA, PRP is thought to reduce inflammation, slow or reverse cartilage degradation, improve blood supply, improve comfort, as well as decrease cartilage damage, synovial membrane hyperplasia, and hemorrhage 1) This work was supported by The Scientific and Technological Research Council of Turkey (TÜBİTAK, Project no. 213O175). Effect of inflammatory marker activity after intra-articular injection of autologous platelet-rich plasma in dogs with osteoarthritis1)