{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T17:34:00Z","timestamp":1791912840860,"version":"4.3.4"},"reference-count":37,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,6,20]],"date-time":"2005-06-20T00:00:00Z","timestamp":1119225600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2005,8]]},"abstract":"<jats:p><jats:bold>Objective:\u2002<\/jats:bold> The responsiveness of the sympathetic nervous system (SNS) and the hypothalamic\u2013pituitary\u2013adrenal (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\u2010selective neurotoxic drug 6\u2010hydroxydopamine (6\u2010OHDA), which destroys peripheral noradrenaline terminals, would influence immune responses to Gram\u2010negative bacterial lipopolysaccharide (LPS) stimulation, and the progression of ligature\u2010induced periodontal disease in Fischer\u2003344 rats.<\/jats:p><jats:p><jats:bold>Material and methods:\u2002<\/jats:bold> 6\u2010OHDA (40\u201360\u2003\u00b5g\/kg) or vehicle was injected intraperitoneally (i.p.) on days 1, 3 and 5, 10\u2003days before application of the ligatures, and thereafter weekly in doses of 80\u2003\u00b5g\/kg. Periodontal disease was assessed when the ligatures had been in place for 49\u2003days. At 24 and 2\u2003h before decapitation, all rats received LPS (150\u2003\u00b5g\/kg i.p.) to induce a robust immune and HPA axis response.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> The 6\u2010OHDA\u2010treated rats showed significantly reduced bone loss as measured by digital X\u2010rays (<jats:italic>p\u2003&lt;<\/jats:italic>\u20030.01), and enhanced levels of the cytokines transforming growth factor\u2010\u03b2 (<jats:italic>p\u2003=<\/jats:italic>\u20030.05) and interleukin\u20106 (<jats:italic>p\u2003=<\/jats:italic>\u20030.05), as well as the HPA axis derived hormone corticosterone (<jats:italic>p\u2003=<\/jats:italic>\u20030.01), induced by LPS stimulation.<\/jats:p><jats:p><jats:bold>Conclusions:\u2002<\/jats:bold> 6\u2010OHDA\u2010induced chemical sympathectomy inhibits ligature\u2010induced periodontal disease in this model. This effect may be attributable to the well\u2010documented 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\u2010OHDA.<\/jats:p>","DOI":"10.1111\/j.1600-0765.2005.00803.x","type":"journal-article","created":{"date-parts":[[2005,6,20]],"date-time":"2005-06-20T12:58:41Z","timestamp":1119272321000},"page":"325-330","source":"Crossref","is-referenced-by-count":33,"title":["Chemical sympathectomy inhibits periodontal disease in Fischer\u2003344 rats"],"prefix":"10.1111","volume":"40","author":[{"given":"Torbj\u00f8rn","family":"Breivik","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yngvar","family":"Gundersen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Per 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