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. 1986 Oct;13(9):850-5.
doi: 10.1111/j.1600-051x.1986.tb02242.x.

Influence of plasma components on luminol-enhanced chemiluminescence from peripheral granulocytes in juvenile periodontitis

Influence of plasma components on luminol-enhanced chemiluminescence from peripheral granulocytes in juvenile periodontitis

B Asman et al. J Clin Periodontol. 1986 Oct.

Abstract

The generation rate of free oxygen radicals as measured by maximal light intensity of luminol-enhanced chemiluminescence from peripheral blood granulocytes (PMN) stimulated with differently opsonized Staphylococcus aureus was studied in 13 patients with juvenile periodontitis (JP) and pair-matched, healthy controls. Plasma proteins related to inflammation were also assayed. When stimulated with bacteria opsonized with autologous serum, the PMN from the JP patients showed a more intensive chemiluminescence than did their pair-matched controls (p less than or equal to 0.0005). The difference was consistent but slightly reduced when using heat-treated serum (p less than or equal to 0.006) or heterologous gammaglobulin (p less than or equal to 0.19) for opsonization. When testing freeze preserved sera from 11 of the compared pairs, the sera from JP patients induced a slightly higher chemiluminescence in PMN from a healthy donor (p less than or equal to 0.031). Protein analysis of the patient sera revealed a slightly higher concentration of complement 4 (p less than or equal to 0.032) and IgM (p less than or equal to 0.030) when compared with their respective pair-matched healthy controls. The influence of other blood components contaminating our assay system was checked on healthy PMN cells. Lymphocytes, platelets, relevant amounts of ADP and serum had no effect on the chemiluminescence. In conclusion, the increased chemiluminescence of peripheral blood granulocytes from patients with juvenile periodontitis seems to be related mainly to the cells. The association with free oxygen radicals and their tissue-damaging potency might be a contributing factor in the pathogenesis of periodontal disease.

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