title: Reactive change in proliferative activity of the junctional epithelium after topical application of lipopolysaccharide.
abstract: IT IS WELL ESTABLISHED THAT apical migration of junctional epithelium (JE) along a root surface is an important factor in periodontal pocket formation and deepening. However, the exact mechanism and, more specifically, the role of inflammatory products in influencing the activity of cells within the JE is not known. To address this issue lipopolysaccharide (LPS) was applied topically into rat molar gingival sulcus and then tissues evaluated immunohistochemically for expression of proliferating cell nuclear antigen (PCNA). Tissues were prepared for histological analysis at designated times. Histologically, infiltration of neutrophils with associated edema was noted in JE and gingival connective tissues 6 hours after LPS application and was prominent at 12 hours. These inflammatory changes persisted in the 2- and 3-day specimens, and disappeared at 5 days. In normal gingiva, before the LPS application, the JE showed few PCNA positive cells, while almost all cells in the basal and suprabasal cell layers of the oral gingival epithelium and the oral sulcular epithelium were PCNA positive. No increase in the number of PCNA positive cells in the JE beyond zero time was observed at 6 and 12 hours after LPS application. One day after LPS application, PCNA positive cells appeared in the basal cell layer of the JE, with a continued increase number of PCNA positive cells in the JE continued at 2 and 3 days. By day 5 the number of PCNA positive cells were decreasing with return to a normal range by 7 days. These results showed that 1) under normal physiological conditions, cells within the JE have minimal mitotic activity and 2) the JE cells can enter the proliferating cell cycle when exposed to LPS, and suggest that the enhanced proliferating activity in the JE is an important factor for the deepening of the periodontal pocket, if the connective tissue attachment is broken down.
authors.affiliation: Department of Oral Pathology, Hiroshima University, School of Dentistry, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Takata
authors.forename: M
authors.initials: M
authors.lastname: Miyauchi
authors.forename: I
authors.initials: I
authors.lastname: Ogawa
authors.forename: H
authors.initials: H
authors.lastname: Ito
authors.forename: J
authors.initials: J
authors.lastname: Kobayashi
authors.forename: H
authors.initials: H
authors.lastname: Nikai
mesh_terms: D000818:Animals; D002455:Cell Division; D004846:Epithelial Attachment / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D004926:Escherichia coli; D066298:In Vitro Techniques; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D017622:Periodontal Attachment Loss / Q000209:etiology; D010514:Periodontal Pocket / Q000209:etiology; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar
chemical_list: D008070:Lipopolysaccharides; D018809:Proliferating Cell Nuclear Antigen