Soluble sonic extracts of several strains of Treponema denticola and Treponema vincentii were examined for their abilities to alter proliferation of both murine and human fibroblasts. We found that sonic extracts of all tested strains of T. denticola caused a dose-dependent inhibition of murine and human fibroblast proliferation when assessed by both DNA synthesis ([3H]thymidine incorporation) and direct cell counts. T. vincentii had only a minimal inhibitory effect at comparable doses. No inhibition was observed when sonic extracts were added simultaneously with [3H]thymidine, indicating that suppression was not due to the presence of excessive amounts of cold thymidine in the extract, nonspecific effects on thymidine utilization by the cells (transport and incorporation), or degradation of label. RNA ([3H]uridine incorporation) and protein ([3H]leucine incorporation) synthesis were similarly altered after exposure to the T. denticola sonic extracts. There was no effect on cell viability as measured by trypan blue exclusion. Inhibition could be reversed by extensive washing of the cells within the first few hours of exposure to sonic extracts. Preliminary characterization and purification indicated that the inhibitory factor(s) is not endotoxin since it is heat labile, and elutes in a single, well-defined peak on a Sephadex G-150 chromatography column corresponding to a molecular weight of approximately 50,000. Since oral spirochetes have been implicated in the pathogenesis of periodontal disorders, it is possible that they contribute to the disease process by inhibition of fibroblast growth and therefore may, at least in part, account for the loss of collagen seen in diseased tissue.

Polymorphonuclear leukocytes (PMNs) encounter spirochetes in the diseased gingival crevice. The purpose of this investigation was to learn more about the nature and potential consequences of in vitro PMN‐spirochete interactions. Isolated spirochetes (various strains of Treponema denticola and T. vincentii) were incubated with human peripheral blood PMNs. PMNs were able to interact with these organisms demonstrating increased oxygen consumption, chemoluminescence, and phagocytosis. Serum was not an absolute prerequisite for phagocytosis, but oxygen consumption and chemoluminescence were generally not observed unless organisms were preopsonized with fresh serum. In spite of the fact that large numbers of spirochetes could be identified within PMN phagosomes, biochemical and ultrastructural evidence indicated limited degranulation on the part of the phagocytic cells. This can be contrasted to other plaque organisms which stimulated dose‐dependent degranulation in association with the phagocytic process. In fact, PMNs pretreated with soluble extracts of spirochetes, but not with non‐spirochetal organisms, were generally less responsive to zymosan‐induced degranulation. The data suggest that spirochetes may limit fusion of lysosomes to phagosomes and thereby influence the course of the inflammatory process in response to these as well as other organisms. These findings may be relevant in explaining the mechanisms of infection associated with the colonization of the gingival crevice by spirochetes.