The analysis of C-reactive concentration in patients with maxillofacial fractures

The C-reactive protein (CRP) is a constant component of the organism, it is present in blood serum in trace amounts of both healthy people and animals in physiological conditions (1, 2). Macrophage stimulation caused by tissue damage is a necessary condition for CRP synthesis (3, 4, 5). These cells produce pro-inflammatory cytokines which induce the expression of the APR gene. Interleukin 6 (IL-6) is the most important factor that stimulates CRP synthesis as well as all other acute phase proteins (5, 6). Interleukin 1 (IL-1) and tumor necrosis factor (TNF-a) stimulate macrophages, monocytes, fibroblasts, endothelium cells and others to produce IL-6 (6, 7, 8). CRP in the organism performs a defensive and reparative role (2, 3, 9, 10). This protein acts like an opsonin by joining with antigens and pathogen structure ligands and hastening their phagocytosis. CRP attaches to Fey receptors of human monocytes, neutrophils and other leucocytic system cells activating them. Cell stimulation results in a varied effector response, e.g. in the cytotoxic effect, phagocytosis, oxygen explosion or in the release of inflammatory mediators. C-reactive protein complexes with corresponding ligands activate the complement cascade mainly on the classical pathway (similarly to the antigen-antibody complexes). As a result of the