Osteoarthritis (OA) is a chronic, non-infectious, progressive disorder of any synovial joint. OA is characterized by deterioration of the articular cartilage, synovitis, with secondary bony changes. Osteoarthritis is classified as being primary or secondary in nature. Articular cartilage is a very complex and dynamic structure. The cartilage matrix is composed of proteoglycan macromolecules (hyaluronic acid and GAGs), type 1 collagen, and 80% water. The matrix is synthesized and maintained primarily by the chondrocytes.

Secondary osteoarthritis is a more common cause of clinical lameness in the younger dog. It is the consequence of some external event, angular force adversely affecting the healthy articular cartilage, i.e.; abnormal forces impacting normal cartilage. Examples of secondary OA would include overt trauma, joint incongruity (rupture ACL), and joint misalignment (hip dysplasia). Many feline cases are of secondary origin usually with some historical event that can be attributed to have initiated the process. In order to prevent, halt or minimize the degeneration cascade, the underlying joint incongruity must be corrected when possible.

Conversely, Primary arthritis (age-related) results from abnormalities within the cartilage homeostasis and is considered an intrinsic age–related cartilage homeostasis problem. Unfortunately the affected cartilage has limited ability to regenerate and maintain itself in the face of the cumulative effects of ongoing trauma and/or inflammation. Primary osteoarthritis has a slow progressive course, generally involves one or more joints, and is most common in senior patients. The pathophysiology of primary arthritis involves a series of Pathophysiologic steps that eventually becomes a progressive self-perpetuating process. The mediators of the inflammation, pain, and joint destruction include prostaglandins, cytokines, leukotriens, and kinnins. The variation in clinical response of the each of the various pharmacological agent used in treating OA reflects the specific action of each drug / compound on specific inflammatory mediators and or inflammatory pathway. In primary OA, normal joint forces impact abnormal cartilage resulting in chondrocyte damage, release of inflammatory mediators, synovitis and eventual degeneration of the cartilage and boney structures. Unfortunately the affected cartilage has limited ability to regenerate and maintain itself in the face of the cumulative effects of ongoing trauma and/or inflammation. Primary osteoarthritis has a slow progressive self-perpetuating course, generally involves one or more joints, and is most common type in senior pets. In primary arthritis, there is a shift in the cartilage homeostasis towards the catabolic phase. Initially there is decreased production of proteoglycan by the chondrocytes, a loss of chondroitin sulfates and water from the matrix. The resultant articular cartilage is less elastic with less shock absorption. Any minor trauma produces cartilage fissures and chondrocytes damage. Surface cracks produce "flaking" exposing the collagen fibers to wear and tear. Some cracks extend into the deeper layers and bone produce fibrillation. Degrading enzymes are released which further break down cartilage matrix and collagen. These enzymes include serines, collagenase, cathepsins, metalloproteinase's, hyaluronidases, stromelysins, plus the cartilage breakdown products, initiate a mild synovitis The resulting inflamed synovial membrane releases primary inflammatory mediators IL 1, IL6, tissue necrosis factor, proteases, and prostaglandins that further increasing cartilage destruction and inhibiting new matrix production. The further decreased resiliency of the cartilage results in sclerosis of the subchondral bone and osteophyte development in the periarticular margins in advanced cases.