Mechanisms of microcrystalline inflammation
Guerne, P.A.
La Revue du Praticien 44(2): 161-166
1994
ISSN/ISBN: 0035-2640 PMID: 8178068 Document Number: 427962
The inflammatory mechanisms which take place in microcrystalline arthropathies can be divided into several stages, each of them being characterized by the activation of a set of mediators. The process begins with activation by crystals of resident cells in the synovial fluid which release various pro-inflammatory factors including several cytokines. Among these, interleukin 1 (IL-1) and tumor-necrosis factor alpha (TNF-alpha) have multiple effects and play a predominant role in the starting of inflammation. With the contribution of humoral factors, also activated by the crystals, IL-1 and TNF-alpha activate notably the endothelial cells to allow leucocyte extravasation. The attraction and massive activation of polymorphonuclear neutrophils (PMNs) which then occurs and characterizes acute microcrystalline arthropathies mainly depend on IL-8, another cytokine secreted by synoviocytes. At the same time, an acute phase systemic reaction principally induced by IL-6 develops. When inflammation is prolonged mechanisms of tissue destruction begin to act, notably by releasing proteases induced by IL-1 and TNF-alpha. These mechanisms are counterbalanced by release of antiproteases, notably those induced by the transforming growth factor beta (TGF-beta) and by IL-6. Finally, these inflammatory processes may limit themselves or even stop spontaneously, due to a series of control mechanisms including cytokines with anti-inflammatory effects, ACTH release and physico-chemical changes in crystals.