We investigated a possible cause-and-effect relationship between sensitization against Actinomyces viscosus Nyl and destructive periodontal disease in RIC-Sprague-Dawley rats. Germfree rats (66) were either immunized with A. viscosus Nyl (day 20) or orally infected with A. viscosus Nyl (days 38 and 39) or both. We measured alveolar bone loss in maxillary and mandibular molars, in vitro Tlymphocyte responsiveness, and serum antibody titers. In immunized and monoassociated rats bone loss in both jaws progressed rapidly between days 37 and 72, whereas the rate of further resorption decreased until day 100. In monoassociated rats, development of bone loss was much slower, and the maxiimum resorption measured was, at best, half of the bone loss compared with the former group. However, no amplification of bone loss by immunization was observed in a second experiment using 63 conventional rats kept in relative gnotobiosis. Antibody titers to A. viscosus Nyl in gnotobiotic monoassociated rats were higher in immunized animals, whereas no difference was found in the respective groups of the relative gnotobiotic experiment. The fact that immunization more than doubled alveolar bone loss in gnotobiotic monoassociated rats confirms the allergic nature of the disease. The lack of such an effect under conventional conditions points to suppressor mechanisms whose decrease might convert stable periodontal lesions into progressive ones.

No abstract

The T‐cell triggered effector systems have been emphasized as the most important agents mediating periodontal disease in recent years. It was therefore tempting to investigate whether T‐cell suppression with cyclosporin A (CS‐A) had an effect on the establishment and progression of the disease in rats monoassociated with Actinomyces viscosus Ny 1. The experiment was carried out with two treatments (16 rats each) in two isolators. In one of the isolators CS‐A was added to the high sucrose diet 2000 aiming at a dosage of 15 mg per day and kg bodyweight. In the second isolator (control) the same diet without CS‐A was fed. At day 25, 38, 52 and 65 four animals from each treatment were removed from the isolators. Dental plaque and alveolar bone loss were evaluated. The cellular composition of blood and histological changes of periodontal lesions on a light and electron microscopic level were monitored. In addition antibody titers and the T‐cell suppressing effect of individual serum samples of all animals were determined. Despite clearcut treatment differences in antibody titers as well as an interference by the sera of CS‐A treated animals with the Con A dependent lymphocyte activation, bone loss was observed in both groups. Haematological and histological investigation revealed only minor differences between the two treatments. It is concluded that periodontal disease in monoinfected rats seems to be the result of a multitude of pathomechanisms and not to be strictly correlated with T‐cell dependent hypersensitivity.

Cell-mediated cytotoxicity against syngeneic fetal rat fibroblasts that require in vitro exposure of effector cells to Actinomyces viscosus Nyl fractions was investigated by measuring the uptake of radioactivity by fibroblasts during a 2-h pulse with [14C]aminoisobutyric acid after 1 to 3 days of coculture with splenic effector cells. By using splenocytes from inbred RIC-Sprague-Dawley rats as effector cells and syngeneic embryonic rat fibroblasts as target cells, strong cellmediated cytotoxicity dependent on the in vitro exposure to an A. viscosus Nyl fraction was observed, but only within a small range of effector-to-target cell ratios (3:1 to 10:1). Concanavalin A and lipopolysaccharide from Escherichia coli induced a comparable cytotoxicity, indicating that the effect might be connected with the mitogenic activity of the A. viscosus Nyl fraction. Splenocytes from rats immunized with A. viscosus Nyl and from control rats induced similar levels of cytotoxicity in 72-h cytotoxicity assays. In shorter assays (24 h), however, splenocytes from immune animals induced low cytotoxicity, which was, however, significantly higher than that induced by splenocytes from control animals. We conclude that both antigen-and mitogen-dependent cell-mediated effector mechanisms are operative in this system and that the two normally overlapping effects can be experimentally separated. This new system describes a fibroblast impairment in the presence of splenocytes and bacterial components and may provide a useful model for studying pathogenic mechanisms operative in periodontal disease.

No abstract