The paper shows that osteoporosis (OA) changes the SF content and the lipid profile substantially. To estimate the implication of the lipid environment in case the articular cartilage (AC) changes, we measured friction coefficient normal samples, with early and late stages of (OA). During joint inflammation and osteoarthritis, enzymatically activated β2-Glycoprotein I is transformed into antibody conformation. Our hypothesis about cartilage degradation of PL bilayers by antibodies (β2-Glycoprotein I) is considering antiphospholipid syndrome (APS), which was not discussed in the literature before. Deactivated PL molecule has no ability to form bilayers, lamellar phases, and liposomes. The phospholipid content in synovial fluid (SF) during joint inflammation, osteoarthritis, and rheumatoid arthritis is significantly higher (2-3 times) above the normal concentration of PL, and has a poor boundary-lubricating ability is deactivated.
Keywords: Antiphospholipid syndrome (APS); Articular cartilage degradation; Friction coefficient; Phospholipids deactivation; β(2)-Glycoprotein I, β(2)-GPI as deactivator.
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