Constitutionally Hyperreactive Neutrophils in Periodontitis

• Autores: Dr. Margareta I. Fredriksson, Anders K. Gustafsson, Kurt G. Bergström, Björn E. Åsman
• Localización: Journal of periodontology, ISSN 0022-3492, Vol. 74, Nº. 2, 2003, págs. 219-224
• Idioma: inglés
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• Resumen

  • Background: Neutrophils constitute the first line of host defense, but their extracellular release of oxygen radicals and proteases may cause tissue destruction. Conflicting results have been reported on the neutrophilic production of oxygen radicals in periodontal patients. These may vary with different forms of periodontitis, the pathway of neutrophil activation studied, and the influence of smoking.

    Methods: Venous blood was taken from 15 patients with severe chronic periodontitis, treated with scaling, with or without surgery. They were matched by age and gender to periodontally healthy controls; all participants were non-smokers. Peripheral neutrophils from the participants were activated with IgGopsonized bacteria, complement-opsonized zymosan, or phorbol myristate acetate (PMA). The total release of oxygen radicals was measured with luminol-enhanced chemiluminescence (CL) and the extracellular release of oxygen radicals with isoluminol- enhanced CL. Antibodies to endotoxin and the concentrations of interleukin (IL)-8 and acute phase proteins in plasma were analyzed to see if these parameters were related to hyperreactivity of the neutrophils.

    Results: Neutrophils from periodontal patients had significantly higher CL when activated via the FcγR pathway, measured as both total generation of oxygen radicals and extracellular generation. The neutrophil generation of oxygen radicals was also higher in patients when complement-opsonized zymosan or PMA was used, but these differences were less pronounced. No significant differences in plasma proteins were found.

    Conclusion: Our findings suggest that the increased CL from peripheral neutrophils in periodontitis may be related to a constitutionally greater responsiveness of the Fcγ-receptor. J Periodontol 2003;74:219-224.