title: Kinetics of immune cell and bone resorptive responses to endodontic infections.
abstract: Infection of the dental pulp stimulates a host immune response in the periapical region (the periapical "lesion") with the concomitant resorption of bone. The cell composition of human or rat periapical lesions is mixed, consisting of T, B, and "null" lymphocytes, plasma cells, macrophages, polymorphonuclear leukocytes, and mast cells. Cells are thus present which mediate a broad spectrum of immunological phenomena. In order to determine which of these mechanisms contribute to periapical bone resorption, a rat model system has been used in which periapical lesions are induced by pulp exposure and infection from the oral environment. In this model, a rapid period of lesion expansion and bone destruction occurs between days 1 and 15 after exposure (active phase), with a chronic phase characterized by lesion stabilization commencing thereafter. Phenotypic analysis of the cellular infiltrate has shown that T helper cells predominate during the active phase, whereas increased numbers of T suppressor cells are associated with chronicity. Extracts of periapical lesions contain bone-resorbing activity, as determined by the release of 45Ca from prelabeled a rat long bones in organ culture. Higher levels of bone-resorbing activity are present during the active than in the chronic phase. Characterization of bone-resorbing activity indicates the presence of resorptive mediators which are heat labile and protease sensitive and which are distinct from lipopolysaccharide. Preliminary biochemical fractionation indicates that resorptive mediators fractionate in the 15,000- to 60,000-dalton molecular mass range, presumably cytokines such as interleukin 1 and tumor necrosis factor. These studies demonstrate the utility of the rat model for studying mechanisms of periapical lesion pathogenesis and implicate T helper cell-mediated activities, in particular those leading to macrophage activation and cytokine production, in periapical lesion expansion.
authors.affiliation: Department of Immunology, Forsyth Dental Center, Boston, MA 02115, USA.
authors.forename: P
authors.initials: P
authors.lastname: Stashenko
authors.forename: S M
authors.initials: SM
authors.lastname: Yu
authors.forename: C Y
authors.initials: CY
authors.lastname: Wang
mesh_terms: D016301:Alveolar Bone Loss / Q000276:immunology; D000818:Animals; D001424:Bacterial Infections / Q000276:immunology; D003789:Dental Pulp Exposure / Q000150:complications / Q000382:microbiology; D008262:Macrophage Activation; D010485:Periapical Periodontitis / Q000209:etiology / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D006377:T-Lymphocytes, Helper-Inducer / Q000502:physiology; D050378:T-Lymphocytes, Regulatory / Q000502:physiology