Abstract
The initiation or progression of periodontitis might involve a local renin-angiotensin system (RAS) in periodontal tissue. The aim of this study was to further characterize the local RAS in human and rat periodontal tissues between healthy and periodontally-affected tissue. Components of the RAS were investigated using in vitro, ex vivo and in vivo experiments involving both human and Wistar rat periodontium. Although not upregulated when challenged with P. gingivalis-lipopolysaccharide, human gingival and periodontal ligament fibroblasts expressed RAS components. Likewise, healthy and inflamed human gingiva expressed RAS components, some of which were shown to be functional, yet no differences in expression were found between healthy and diseased gingiva. However, in inflamed tissue the immunoreactivity was greater for the AT1R compared to AT2R in fibroblasts. When compared to healthy tissue, ACE activity was increased in human gingiva from volunteers with gingivitis. Human-gingiva homogenates generated Ang II, Ang 1-9 and Ang 1-7 when incubated with precursors. In gingiva homogenates, Ang II formation from Ang I was nearly abolished only when captopril and chymostatin were combined. Ang 1-7 formation was significantly greater when human gingiva homogenates were incubated with chymostatin alone compared to incubation without any inhibitor, only captopril, or captopril and chymostatin. In rat gingiva, RAS components were also found; their expression was not different between healthy and experimentally induced periodontitis (EP) groups. However, renin inhibition (aliskiren) and an AT1R antagonist (losartan) significantly blocked EP-alveolar-bone loss in rats. Collectively, these data are consistent with the hypothesis that a local RAS system is not only present but is also functional in both human and rat periodontal tissue. Furthermore, blocking AT1R and renin can significantly prevent periodontal bone loss induced by EP in rats.
Highlights
The renin-angiotensin system (RAS) regulates or modulates numerous physiological functions including blood pressure, electrolyte balance, inflammation and the release of various peptide hormones
Histological analysis indicated that the number of plasmocytes were significantly increased in the gingiva of donors classified as having gingivitis (60±43) when compared to the number of plasmocytes in the gingiva from healthy donors (7±4, data not shown)
In 2009 Santos et al demonstrated the presence of some local RAS components in the rat gingiva providing a possible connection between periodontal disorders and the RAS [1]
Summary
The renin-angiotensin system (RAS) regulates or modulates numerous physiological functions including blood pressure, electrolyte balance, inflammation and the release of various peptide hormones. Peptides such as vasopressin and angiotensinogen (AGT) are released and transported through the circulatory system as part of the extended RAS modulating inflammation, oxidative stress, fibrosis and cell proliferation. Prorenin is converted to renin; this rate-limited step releases renin into the circulatory system thereby cleaving AGT forming angiotensin I (1–10) (Ang I). ACE can cut Ang 1–9 to form Ang 1–7, and alamandine can be formed by Ang 1–7. Ang II can form angiotensin III (2–8), angiotensin A and angioprotectin
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