Role of bacterial products in periodontitis

Since the two major theories assume that either a hypersensitivity to plaque immunogens or a direct tissue damage caused by plaque constituents plays the dominant role in the etiology of periodontitis, we first investigated the nature of the immune response to and the endotoxin content of human plaque. It was found that pooled human plaque samples contained a very low but significant level of endotoxin, as determined by phenol‐water extraction, by pyrogenicity in New Zealand white rabbits, by local Shwartzman skin test, and by the Limulus lysate assay. A measurable humoral immune response could be elicited by human plaque material if injected into guinea pigs intraperitoneally. Intragingival application of the same material was a less efficient route of immunization. This humoral immune response was measured by passive hemagglutination and immune counterelectrophoresis. Cell‐mediated immune response, as measured by skin sensitivity, lymphoblast transformation and rosette formation assays in guinea pigs, sensitized either intragingivally or intraperitoneally, gave diverse results. No cell‐mediated immune response could be detected by using the lymphoblast transformation assay. A weak but positive reaction could be elicited in one‐third to one‐half of the sensitized animals by injecting them intradermally or by testing rosette formation of their spleen cells with plaque‐coated sheep erythrocytes. The weak and inconsistent results do not rule out the possibility that cell‐mediated immune responses and their mediators cause human periodontitis, but they make us cautious in considering such events as the sole factors in the development of the disease. As of now, we have even less reason to exclude the possibility that certain types of immune responses to plaque protect the patient from periodontitis.