Bacterial invasion of periodontal tissues after experimental immunosuppression in rats.
A moderate gingivitis was produced in 3 groups of 10 adult Wistar rats with diet 2000 of Keyes and Jordan (1964) delivered for 30 days with a controlled feeding unit. The first group served as untreated control. The second group received 5 intraperitoneal injections of cyclosporine A (15 mg/kg body weight) from day 20 to 30 to interfere with the activation of T lymphocytes and interleukin synthesis. The third group received 2 intraperitoneal injections of cyclophosphamide (100 mg/kg on day 20 and 25) which induced a severe neutropenia. The gingival areas between the upper molar regions were prepared for light and transmission electron microscopy. In the untreated control group, a layer of polymorphonuclear neutrophils (PMN) was observed between the dental plaque and the junctional epithelium with a round cell infiltration in the superficial connective tissue. No bacterial invasion was observed. In the cyclosporine group, despite the action on T lymphocytes, no bacterial invasion occurred, but a differentiated PMN layer was present between the apical dental plaque and the junctional epithelium. In the cyclophosphamide group an important bacterial invasion was observed in the interdental epithelium as well as in the underlying connective tissue. In the local absence of PMNs, a mixed flora of Gram positive and negative bacteria of various shapes invaded epithelial as well as connective tissue cells and came in contact with the alveolar crestal bone. Resorption of the alveolar crestal bone scored according to the Keyes and Gold method (1955) was significantly more important in the cyclosporine and the cyclophosphamide group when compared to the controls (p less than 0.05). No statistical difference in bone resorption was noted between the cyclosporine and the cyclophosphamide groups. It can be concluded that the PMN layer constitutes the first line of defense opposed to bacterial invasion of the periodontal tissues.
Hemmerle
J
J
Unité INSERM U 157, Faculté de Chirurgie Dentaire, Université Louis Pasteur, Strasbourg, France.
Frank
R M
RM
D016301:Alveolar Bone Loss / Q000382:microbiology / Q000473:pathology; D000818:Animals; D018407:Bacterial Physiological Phenomena; D003238:Connective Tissue / Q000382:microbiology / Q000473:pathology; D003520:Cyclophosphamide / Q000494:pharmacology*; D016572:Cyclosporine / Q000494:pharmacology*; D003773:Dental Plaque / Q000473:pathology; D004848:Epithelium / Q000382:microbiology / Q000473:pathology; D005110:Extracellular Space / Q000382:microbiology; D005881:Gingiva / Q000382:microbiology; D007958:Leukocyte Count; D007962:Leukocytes / Q000187:drug effects / Q000502:physiology*; D009503:Neutropenia / Q000097:blood; D009504:Neutrophils / Q000473:pathology; D010513:Periodontal Ligament / Q000382:microbiology; D010519:Periodontium / Q000382:microbiology* / Q000473:pathology; D051381:Rats; D011919:Rats, Inbred Strains
D016572:Cyclosporine; D003520:Cyclophosphamide