Abstract
The pathological changes observed in Osteoarthritis (OA) and Rheumatoid Arthritis (RA) affects the entire joint structure resulting in pain, surface change, molecules modification and dysfunction. In our study, we report molecular deactivation mechanism surface active phospholipids and cartilage matrix in (OA) and (RA). Deactivated PLs can be related to high friction leading to articular cartilage damage. The interaction occurs between antibodies β2-Glycoprotein I (β2-GPI) protonated amino acid functional group (-NH3+) and the phospholipid functional group (-PO4-): (β2-GPI) (-NH3+) + PL(-PO4-) → (-NH3+-PO4-) In a proposed articular cartilage damage of OA and RA, a substantial progress has been made towards understanding the mechanisms of PLs deactivation that lead to the degradation of the cartilage surface.
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