pH changes observed in the inflamed gingival crevice modulate human polymorphonuclear leukocyte activation in vitro.

Previous studies have noted a positive correlation between gingival inflammation and crevicular pH, which reportedly varies from 6.5 to 8.5. In the present study, we characterized the manner in which deviation from the "physiological" pH of blood (7.2) influences activation of chemotaxis, phagocytosis, superoxide generation, and degranulation by human polymorphonuclear leukocytes (PMNs). Purified PMNs were suspended in HEPES-buffered balanced salts solutions adjusted to pH 6.7, 7.2, 7.7, or 8.2. In a modified Boyden chamber, the chemotactic response to fMet-Leu-Phe was maximal at pH 7.2. In comparison, chemotaxis was significantly depressed at pH 7.7 and pH 8.2 (P < 0.05), but was not significantly different at pH 6.7. Activation of the respiratory burst by fMet-Leu-Phe was optimal at pH 7.2, but was significantly depressed at pH 6.7 and 8.2 (P < 0.05). pH had little effect on N-acetyl-beta-glucosaminidase release from primary granules. However, lactoferrin release from the secondary granules of fMet-Leu-Phe-activated PMNs was significantly lower at pH 7.2 than at pH 6.7 or 8.2 (P < 0.05). Moreover, phagocytosis of opsonized bacteria was significantly lower at pH 7.2 than at pH 7.7. In addition to these effects on functional activation, extracellular pH influenced the magnitude of intracellular Ca2+ mobilization. Peak fMet-Leu-Phe-induced Ca2+ levels were significantly higher at pH 8.2 than at pH 7.2 (P < 0.01). These findings suggest that the pH of the periodontal environment can selectively influence PMN activation, thereby altering the balance between bacteria and the host response.