Publication:

Mechanisms of action of native collagen type II and Aflapin® on the pathophysiology of osteoarthritis and their evidences

Osteoarthritis (OA) is a degenerative and chronic inflammatory disease that affects the entire joint tissue such as articular cartilage, synovial membrane, subchondral bone, and ligaments. Imbalance between anabolism and catabolism lead to degradation of articular cartilage which may further initiate inflammatory cascades. There is an interplay of mechanical and immune-mediated injuries that lead to cartilage destruction and inflammation in OA. The mainstay of OA treatment involves drugs like paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs) which provide symptomatic relief in many cases; but are unable to inhibit disease progression. Also, long-term use of these drugs, is associated with major safety concerns. Native collagen type II (NC-II) and Aflapin, especially when used in combination, can slow down the disease progression in OA and serve as a safer and effective treatment option for OA. NC-II is non-hydrolyzed collagen having intact triple helix structure with active epitopes and antigenicity. Aflapin is a novel synergistic composition of Boswellia serrata gum resin having higher composition of 3-O-acetyl-11-keto-betaboswellic acid (AKBA). Various experimental studies have demonstrated the mechanisms by which both these agents exert their benefit in OA. Further, multiple clinical studies have demonstrated the efficacy and safety of NC-II and Aflapin, when used individually or as a combination. This is a narrative review of the pathophysiology of OA, current treatment modalities, and non-clinical and clinical evidence of the beneficial effects of NC-II and Aflapin in the management of OA.