Osteoarthritis (OA) has traditionally been considered as a non-inflammatory disease, because synovial fluid analysed from OA joints presents fewer leukocytes compared with that of rheumatoid arthritis (RA), reactive arthritis and even septic arthritis . However, over the last decades, the gap between inflammatory and degenerative arthritis is becoming less defined.
Among the many different types of arthritis conditions, Osteoarthritis (OA) also known as degenerative arthritis is the most common. Our lack of understanding of the basic mechanisms that initiate and maintain the disease remains a major challenge in the search for an effective and safe cure. Recent studies suggest that TGF-beta/Smad pathway plays a critical role through regulation of articular chondrocyte hypertrophy and maturation during osteoarthritis development. This indicates decreased TGF-beta response might be correlated with increased incidence of OA.
Osteoarthritis is associated with gradually developing loss of cartilage, which in the stationary phase of disease progression leads to the formation of osteophytes and joint space narrowing, and in the last phase results in bone repair and remodeling. Multiple factors contribute to the degradation of cartilage in OA, by either directly or indirectly regulating the anabolic and catabolic pathways of the cartilage matrix. Complement system consists of more than 50 soluble and membrane-bound serum proteins that connects innate and acquired immunity.
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