title: Kinetics of Th17-related cytokine expression in experimentally induced rat periapical lesions.
abstract: Th17-related cytokines are essential factors in various pathological states, including inflammatory bone destruction. This study investigated the contribution of Th17-related cytokines to the progress of experimentally induced rat periapical lesions. Periapical pathoses were induced by unsealed exposure of the pulp chamber of the lower first molars. A variety of immunocompetent cells, including CD68(+) macrophages, Ia antigen(+) cells and TCRαβ(+) T cells, were observed in the lesions. The expression levels of Th17-related cytokines, IL-17 and IL-23, and of pro-inflammatory cytokines, IL-1β and IL-6, were significantly increased at 14 days (expansion stage) compared with normal periapical tissues. The expression levels of Foxp3, a regulatory T cell (Treg)-related gene, and of IL-10, an anti-inflammatory cytokine, were higher at 28 days (chronic stage) than at 14 days. These findings suggest that Th17-related cytokines may be primary contributors to the initiation of periapical bone destruction, and that lesion expansion may be regulated by anti-inflammatory mediators.
authors.affiliation: Department of Endodontics, School of Stomatology, Capital Medical University, Beijing, China.
authors.forename: Shusheng
authors.initials: S
authors.lastname: Wei
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Kawashima
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Suzuki
authors.forename: Jing
authors.initials: J
authors.lastname: Xu
authors.forename: Satomi
authors.initials: S
authors.lastname: Takahashi
authors.forename: Mengyu
authors.initials: M
authors.lastname: Zhou
authors.forename: Yu
authors.initials: Y
authors.lastname: Koizumi
authors.forename: Hideaki
authors.initials: H
authors.lastname: Suda
mesh_terms: D016301:Alveolar Bone Loss / Q000276:immunology; D000818:Animals; D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D003789:Dental Pulp Exposure / Q000276:immunology; D018450:Disease Progression; D051858:Forkhead Transcription Factors / Q000032:analysis; D000949:Histocompatibility Antigens Class II / Q000032:analysis; D018836:Inflammation Mediators / Q000032:analysis; D016753:Interleukin-10 / Q000032:analysis; D020381:Interleukin-17 / Q000032:analysis*; D053583:Interleukin-1beta / Q000032:analysis; D053759:Interleukin-23 / Q000032:analysis*; D015850:Interleukin-6 / Q000032:analysis; D008264:Macrophages / Q000276:immunology; D008297:Male; D010483:Periapical Diseases / Q000276:immunology*; D010486:Periapical Tissue / Q000276:immunology; D051381:Rats; D017208:Rats, Wistar; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D058504:Th17 Cells / Q000276:immunology*; D013997:Time Factors; D055114:X-Ray Microtomography / Q000379:methods; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D051858:Forkhead Transcription Factors; D000949:Histocompatibility Antigens Class II; D018836:Inflammation Mediators; D016753:Interleukin-10; D020381:Interleukin-17; D053583:Interleukin-1beta; D053759:Interleukin-23; D015850:Interleukin-6; D016693:Receptors, Antigen, T-Cell, alpha-beta; C539355:CD68 protein, rat; D000097382:CD68 Molecule; C500522:Foxp3 protein, rat
keywords: anti-inflammatory cytokines; chemical mediators; interleukin-17-related cytokines; periapical bone destruction; periapical lesions