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Histopathology of periodontal disease in gnotobiotic rats monoinfected with Eikenella corrodens
Author(s) -
Listgrarten M. A.,
Johnson D.,
Nowotny A.,
Tanner A. C. R.,
Socransky S. S.
Publication year - 1978
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1978.tb00162.x
Subject(s) - eikenella corrodens , connective tissue , junctional epithelium , histopathology , pathology , periodontitis , molar , lesion , biology , anatomy , dentistry , medicine , bacteria , genetics
The histopathology of periodontal disease was studies in gnotobiotic rats monoinfected with Eikenella corrodens , a Gram‐negative rod isolated from a human periodontitis lesion. Animals were sacrificed in pairs from 2–14 weeks after infection and the molar segments scored for severity of periodontal disease by visual inspection. the lesions first appeared in the maxillary molars and were after infection in the maxilla than in the mandible. Specimens taken 2 weeks after infection showed hair impaction in the coronal part of the junctional epithelium and some leukocyte emigration, but no evidence of a cellular infiltrate or vascular anomalies in the connective tissue. Between 3–5 weeks, a crater‐like depression developed interdentally within the connective tissue, the surface of which was Covered by a continous epitheliel lining disrupted by impacted debris. Little mogrationof the epithelial attachment was noted apical to the cemento‐enamel junction. Between 6–8 weeks. The interdental epithelial lining became ulcerated. Impacted hair and other debris were commonly noted within the connective tissue which, however, remained free of plasma cells and only contained isolated lymphocytes. Bone destruction was characterized by marked osteoclastic activity. The tooth Surfaces remained remarkably free of adherent bacteria. In fact, bacteria were only observed in one 13‐week specimen, in association with impacted debris. Contrary to the progress of periodontal breakdown in man and some other species, the most apical extent of the disease process in these animals was located along the central portion of the interdental tissues, rather than along the root surfaces. No correlation or possibly an inverse correlation seemed to exist between the severity of priodontal disease in these animals and their cell‐madiated immune response to the infecting organism.

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