Mechanical signals modulate the C-type natriuretic peptide receptors via cGMP and PKG dependent pathways

compression) (Figure). Supernatant GAG content, marker of matrix remodeling, appeared unaffected by the treatment. Conclusions: Mechanical stimulation plays a central role in the maintenance of cartilage homeostasis, but is also involved in the pathogenesis of OA. Our data seem to indicate that physiological compression of OA human cartilage tissue could counteract the effect of the inflammatory milieu by modulating cartilage matrix component metabolism. These data stimulate further studies to better elucidate the role of mechantransduction on cartilage behaviour both in normal and pathologic conditions. It is of particular interest the use of healthy human cartilage, where the absence of an altered tissue homeostasis could better highlight the effect of loading.