The placement of a ligature around the second maxillary molar of the conventional rat caused osteoclastic bone resorption and simultaneously, alveolar bone formation. The number of peripheral mononuclear cells in the blood and lymphoblastic transformation of spleen cells in response to concanavalin A increased. Cyclophosphamide (CY), an immunosuppressive agent, given shortly after placing the ligature suppressed the lymphoid reactions, spleen size, and bone formation and enhanced bone destruction. CY given in higher doses also suppressed the number of PMN cells. Septicemia developed in several of these animals. Pseudomonas aeruginosa, Klebsiella pneumoniae and Escherichia coli were isolated from the blood and/or ligature. Antibiotics prevented bone destruction. Without placing a ligature, the high dose of CY did not result in bone loss. These findings suggest that 1) bone destruction of the ligature‐treated rat is of bacterial origin, 2) CY suppresses proliferation of osteoblasts but does not seem to interfere with the activity of osteoclasts, and 3) suppression of the host defenses greatly facilitates bone destruction.

The morphologic features and pattern of bacterial invasion of the periodontal tissue in ligature‐induced periodontal defects of immunosuppressed rats were studied. Silk ligatures were placed circumferentially on the maxillary left second molar of 24 Sprague‐Dawley rats. The treatment group (14 rats) received Cytoxan (75 mg/kg) the day after ligature placement and at Day 4. The control group (10 rats) received no medication. All animals were sacrificed on Day 8 and the maxillae processed for light and electron microscopy. Only ligated sites in immunosuppressed animals exhibited bacterial invasion. Invading bacteria consisted of microcolonies of Gram‐negative and Gram‐positive coccoid cells and rods located near the tissue surface. Each microcolony consisted of morphologically homogeneous microorganisms. The deeper sites revealed a diffuse invasion of Gram‐negative rods which appeared morphologically similar. Other features associated with invasion were complete destruction of epithelial tissue next to the ligature and the lack of inflammatory cells in the gingival region. These findings, when compared to those of other reports of tissue penetration by bacteria, point to the necessity of differentiating between bacterial invasion of gingival tissues, associated with penetration of tissues by proliferating bacteria, and bacterial translocation, a situation in which bacteria are passively carried into the tissues, for example by mechanical manipulation immediately before or during biopsy taking, or possibly during processing for histology.

The periodontia of immunosuppressed rats were examined by light and electron microscopy. Bacterial invasion was noted in the periodontal tissues of septicemic ligature-treated animals. Invading bacteria consisted of gram-negative rods which were morphologically similar to the Pseudomonas aeruginosa strain isolated from the mouth of one of the septicemic animals.

Patients suffering from periodontitis or periodontosis were selected for the study. Further subdivision of these groups was based on the presence or absence of herpes and/or adenoviruses in their oral lymphocytes and epithelial cells. The phagocytic and bactericidal activities of oral leukocytes isolated from the same individuals were compared with virus carriage. In the periodontitis group, 60.5%, and in the periodontosis group 61.5% of patients carried viruses, while this was established only in 21.1% of control cases. On the other hand, emigration and sulcular gathering of the less viable polymorphonuclear leukocytes was elevated but their phagocytotic activity was decreased among periodontitis patients. Bactericidal capacity was significantly lowered among those subjects who carried viruses in their cells, as compared with virus-free persons, especially in the periodontitis group. The functions of the polymorphonuclear leukocytes accumulated in the sulcus gingivalis may be modified by mediators released from the virus-carrying cells. These mediators could achieve a greater concentration locally, and the damaged leukocytes would not be able to eliminate the microbes continuously so that the accumulation of bacterial products, among them endotoxins, could lead to periodontal inflammation.