Journal of Periodontal Research · 1980 · 88 citations · 54 references
DentistryMicrobiologyPeriodontologyMedical MicrobiologyOral ImmunologyOral MicrobiologyDental PlaqueOral Bacterial InfectionsOral Microbial PathogenesisOral Microbial VirulencePeriodontal InflammationPeriodontal MicrobiologyBactericidal AgentsGrowth Inhibition AssaysHost-microbe Interactions In GingivaMicrobial PlaqueOral Microbial Virulence FactorsOral Pathogenic MicroorganismsPlaque-induced Gingival InflammationPlaque-induced Inflammation
Polymorphonuclear leukocytes (PMNs) come in contact with plaque microorganisms in the gingival sulcus. However, little is known about the ability of PMNs to kill or inhibit the growth of plaque microorganisms. In this study, the bactericidal effects of human PMNs and serum against S. mutans 6715, S. sanguis M5, and A. viscosus T14 virulent and avirulent were examined. Plaque microorganisms grown to stationary phase were incubated with human PMNs and/or serum for 90 minutes at 37°C. The killing and growth inhibition of bacteria were determined by measurement of percent reduction in colony forming units and percent inhibition of 3 H‐uridine uptake by the microorganisms. A. viscosus T14 virulent was the only microorganism significantly killed by human PMNs in the absence of serum. In the presence of fresh but not heat‐inactivated (56°C, 30 minutes) human serum, human PMNs had a significant bactericidal effect against all of the microorganisms tested. Exposure of S. mutans 6715, but not S. sanguis M5, to sucrose inhibited the bactericidal effect of human PMNs in the presence of fresh human serum but not in the presence of rabbit anti‐ S. mutans immunoglobulin. Cytochalasin B markedly inhibited phagocytosis of S. mutans 6715 by human PMNs in the presence of serum. However, cytochalasin B‐treated PMNs still were significantly bactericidal for S. mutans 6715 in the presence of serum. The data suggests that human PMNs may kill or inhibit the growth of certain plaque microorganisms in the gingival crevice. The microbial killing may be influenced by bacterial extracellular polysaccharides and the presence of serum antibodies and complement, both resulting in phagocytosis and extracellular lysosomal release from PMNs.
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