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Lipopolysaccharide (LPS) was extracted from Porphyromonas gingivalis (W83) by the Westphal procedure, nuclease-digested and ultracentrifuged. Fibroblasts were obtained from human gingival tissue and rat periosteum, grown to confluence then stimulated in serum-free medium with 0.1, 1.0 and 10.0 micrograms/ml LPS. The levels of prostaglandin E2 (PGE2) and interleukin-1 beta (IL-1 beta) released were measured after 2, 4 and 6 d by specific radioimmunoassays. Unstimulated gingival fibroblasts produced low levels of PGE2 (24.5 +/- 1.5 (SD) ng/ml) and IL-1 beta (0.34 +/- 0.29 ng/ml). LPS stimulated statistically significant dose-related increases in PGE2 and IL-1 beta at the concentrations of LPS tested. At 10.0 micrograms/ml, LPS-stimulated fibroblasts produced 363.5 +/- 40.3 ng/ml PGE2 and 1.81 +/- 0.1 ng/ml IL-1 beta in 6 d. These results demonstrate that LPS from P. gingivalis is capable of stimulating PGE2 and IL-1 beta release from fibroblasts. This would appear to be an additional mechanism by which LPS can induce tissue breakdown in periodontal disease.

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Ten examples of oral pyogenic granuloma occurring during pregnancy and oral contraceptive therapy are presented in order to illustrate the effects on oral tissues of altered levels of female sex hormones. The mechanisms of these effects are discussed and it is concluded that pyogenic granulomata represent an exaggerated response to local irritants, especially dental plaque, which can in most cases be controlled by adequate oral hygiene procedures.

The bone resorbing activity of suspensions or supernatants of freeze-dried powdered gingiva was studied by measuring the release of 45Ca from prelabeled fetal rat long bones in organ culture. Two preparations of noninflamed attached gingiva showed no bone resorbing activity, whereas all six preparations of inflamed marginal gingiva tested showed a dose-related stimulation of 45Ca release. Evidence of an osteoclastic mechanism was provided by the inhibition of the bone resorbing activity by calcitonin and cortisol and the minimal activity observed on dead bones. The activity was heat stable and not blocked by human serum. Three different prostaglandin synthetase inhibitors did not inhibit the activity. Immunoassay showed that PGE was present in gingival powder preparations at concentrations in the range 229-2438 pg/mg dry weight. This was insufficient to account for the observed bone resorbing activity by a factor of 50-350. It was concluded that in addition to PGE, inflamed gingiva contains other heat-stable bone resorbing factor(s).

Epithelial proliferation of various regions of macaque gingival epithelium, as measured by uptake of locally injected H«^-thymidine, showed regional differences which could be explained in part by the size and nature of the inflammatory infiltrate invariably found in gingival biopsies. The proliferative activity of oral sulcular epithelium was greater than that of oral epithelium and was negatively correlated with the size of the area of infiltrated connective tissue. On the other hand labelling of oral epithelium was positively correlated with size of infiltrate, the effect decreasing with distance of the epithelium from the infiltrate.

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