Cartilage allows well known and high biomechanics performances thanks to the complex organization of extracellular matrix which is able to maintain an elevated hydration even under considerable pressures. Matrix macromolecules synthesis and destruction is regulated by chondrocytes which in physiologic conditions are able to assure a turnover, however slow, of the damaged macromolecules. In this homeostasis determinantly take part numerous cytokines which have inflammatory/destructive, inhibiting matrix destruction and growth factor functions. Several situations can interfere with the various phases of the complex cartilage metabolism: genetic factors, biomechanics factors, inflammatory situations. In the last ones there is an abundant production of cytokines which stimulate synthesis of high quantity of metalloproteinases with consequent proteoglycans loss, collagen denaturation and breakage and chondrocyte diffuse necrosis. Even Nitric Oxide seems to have a pro-inflammatory role contributing to cartilage degradation. The cartilage physiologic defense systems are: proteases inhibitors, cytokines inhibitors and chondrogenic growth factors. These mechanisms are however quantitatively inadequate to avoid tissue damage. In osteoarthritis, widespread cartilaginous pathology, often coexist typical lesions and presence of calcium pyrophosphate (CPPD) and hydrossiapatites (HA) crystals. The pathogenetic role of these calcifications in osteoarthritis is still not so clear. Crystals seem to be characteristic of old patients with a more severe disease where cartilage has an abnormal tendency to mineralize. Osteoarthritis and matrix calcification, in some subjects, seem to have converging mechanisms. Nether less this not always happens but, it occurs even without cartilage damage, as in the idiopathic CPPD deposit disease where are more active producing crystals mechanisms. In the last years, thanks to new pathogenetic acquisitions and to informations obtained by arthroscopic procedure, we have considerably increased our knowledge of the cartilage biomechanics properties and of the mechanisms regulating the homeostasis of this tissue. All this opens new and interesting therapeutic perspectives.
|Translated title of the contribution||Articulations and cartilaginous damage|
|Number of pages||6|
|Publication status||Published - Aug 2002|
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