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Chemical sympathectomy inhibits periodontal disease in Fischer 344 rats
Author(s) -
Breivik Torbjørn,
Gundersen Yngvar,
Opstad Per Kristian,
Fonnum Frode
Publication year - 2005
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.1600-0765.2005.00803.x
Subject(s) - sympathectomy , medicine , endocrinology , immune system , lipopolysaccharide , corticosterone , stimulation , neurotransmitter , ligature , hormone , central nervous system , immunology
Objective: The responsiveness of the sympathetic nervous system (SNS) and the hypothalamic–pituitary–adrenal (HPA) axis plays a major role in immune regulation and for the outcome of infections and inflammatory disorders. This study was designed to investigate whether chemical SNS denervation with the noradrenaline‐selective neurotoxic drug 6‐hydroxydopamine (6‐OHDA), which destroys peripheral noradrenaline terminals, would influence immune responses to Gram‐negative bacterial lipopolysaccharide (LPS) stimulation, and the progression of ligature‐induced periodontal disease in Fischer 344 rats. Material and methods: 6‐OHDA (40–60 µg/kg) or vehicle was injected intraperitoneally (i.p.) on days 1, 3 and 5, 10 days before application of the ligatures, and thereafter weekly in doses of 80 µg/kg. Periodontal disease was assessed when the ligatures had been in place for 49 days. At 24 and 2 h before decapitation, all rats received LPS (150 µg/kg i.p.) to induce a robust immune and HPA axis response. Results: The 6‐OHDA‐treated rats showed significantly reduced bone loss as measured by digital X‐rays ( p < 0.01), and enhanced levels of the cytokines transforming growth factor‐β ( p = 0.05) and interleukin‐6 ( p = 0.05), as well as the HPA axis derived hormone corticosterone ( p = 0.01), induced by LPS stimulation. Conclusions: 6‐OHDA‐induced chemical sympathectomy inhibits ligature‐induced periodontal disease in this model. This effect may be attributable to the well‐documented ability of the SNS to regulate immune system function primarily via the adrenergic neurotransmitter noradrenaline released at sympathetic nerve terminals. The enhanced HPA axis activation may be a compensatory response that reduces the T helper (Th)2 to Th1 skewing effect of treatment with 6‐OHDA.