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Titolo:
Hypothalamic-pituitary-adrenal axis activation by experimental periodontaldisease in rats
Autore:
Breivik, T; Thrane, PS; Gjermo, P; Opstad, PK; Pabst, R; von Horsten, S;
Indirizzi:
Univ Oslo, Fac Dent, Dept Periodontol, N-0317 Oslo, Norway Univ Oslo Oslo Norway N-0317 Dent, Dept Periodontol, N-0317 Oslo, Norway Univ Oslo, Fac Dent, Dept Pathol & Forens Odontol, N-0317 Oslo, Norway Univ Oslo Oslo Norway N-0317 athol & Forens Odontol, N-0317 Oslo, Norway Norwegian Def Res Estab, Div Environm Toxicol, N-2007 Kjeller, Norway Norwegian Def Res Estab Kjeller Norway N-2007 ol, N-2007 Kjeller, Norway Hannover Med Sch, Dept Funct & Appl Anat, D-3000 Hannover, Germany Hannover Med Sch Hannover Germany D-3000 Anat, D-3000 Hannover, Germany
Titolo Testata:
JOURNAL OF PERIODONTAL RESEARCH
fascicolo: 5, volume: 36, anno: 2001,
pagine: 295 - 300
SICI:
0022-3484(200110)36:5<295:HAABEP>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; INFLAMMATORY DISEASE; IMMUNE-RESPONSE; STRESS RESPONSE; WISTAR RATS; T-CELLS; SUSCEPTIBILITY; GLUCOCORTICOIDS; CYTOKINES; REACTIVITY;
Keywords:
periodontitis; rats; hypothalamic-pituitary-adrenal axis; glucocorticoids;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
26
Recensione:
Indirizzi per estratti:
Indirizzo: Breivik, T Univ Oslo, Fac Dent, Dept Periodontol, POB 1109,Blindern, N-0317 Oslo, Norway Univ Oslo POB 1109,Blindern Oslo Norway N-0317 17 Oslo, Norway
Citazione:
T. Breivik et al., "Hypothalamic-pituitary-adrenal axis activation by experimental periodontaldisease in rats", J PERIOD RE, 36(5), 2001, pp. 295-300

Abstract

Organisms respond to inflammatory conditions by mounting a co-ordinated complex series of adaptive responses involving the immune, nervous and endocrine systems that are aimed at restoring the homeostatic balance. We have recently shown in a rat model that inappropriate hypothalamic-pituitary-adrenal (HPA) axis regulation and a subsequent inability to mount a suitable glucocorticoid response to gingival inflammation may influence susceptibility to periodontal disease. This study was designed to investigate whether ligature- and bacterial lipopolysaccharide (LPS)-induced inflammation in the gingival connective tissues may activate this physiological axis, and to further explore the significance of HPA regulation in periodontal disease. Experimental periodontal disease was induced in major histocompability complex (MHC)-identical but HPA low (LEW) and high (F344) responding rat strains. We tested (1) whether ongoing periodontal disease activates the HPA axis as measured by corticosterone levels, and (2) whether genetic differences in HPA regulation modulate periodontal disease progression. In the F344 strain,the periodontal tissue destruction was more severe. This observation was associated with a significant increase of corticosterone levels in F344 ratsonly. Addition of LPS at the gingival inflammatory site led to a further increase of corticosterone levels and disease severity in F344 rats. These findings illustrate a positive feedback loop between the HPA axis and periodontal disease: the disease activates the HPA axis, and a genetically determined high HPA responsitivity further increases disease susceptibility.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 01:04:27