No abstract

A water-soluble lipopolysaccharide from Salmonella enteritidis and a phenol-soluble lipopolysaccharide from Leptotrichia buccalis were applied topically to the healthy marginal gingivae of beagle dogs. Saline was applied to contralateral areas as an internal control. Increases in vascular permeability were monitored by measurement of gingival fluid, and the collected gingival fluid samples were assayed for kininogenase and kinin activities. Both lipopolysaccharides induced an inflammatory response, as indicated by increased gingival fluid flow. Kininogenase-kinin activities paralleled the increases in gingival fluid flow, with the highest values being associated with peak increases in gingival fluid. The results indicate that both lipopolysaccharides, although different in lipid solubility, penetrate healthy sulcular epithelium and initiate an inflammatory response which is mediated in part by the kallikrein-kinin system. Interrelationships between this system and other inflammatory mediators suggest that kinin generation not only plays a role in the early phases of acute gingival inflammation, but may also contribute to the activation of other mediators appearing later in the response and in chronic inflammatory lesions.

No abstract

Rabbit polymorphonuclear leukocytes were incubated with a sonically treated suspension of pooled dental plaque to determine if the plaque would induce release of lysosomal enzymes from the polymorphonuclear leukocytes. Cells incubated with plaque at 37°C released significantly greater amounts of the lysosomal enzymes, 8-glucuronidase and lysozyme, than did cells incubated with plaque at 00C or without plaque at 37°C. This response was both dose and time dependent. Release of the cytoplasmic enzyme lactate dehydrogenase was minimal, and there were no significant differences in lactate dehydrogenase release between cells at 0 and 37°C, or without plaque. These results indicate that dental plaque can induce the selective release of lysosomal enzymes, which could be involved in the periodontal injury produced by dental plaque.

No abstract