Abstract

A large number of experimental studies has demonstrated that angiotensin II (Ang II) is involved in key events of the inflammatory process. This study aimed to evaluate the role of Ang II type 1 (AT1) and Ang II type 2 (AT2) receptors on periodontitis. Methods: Experimental periodontitis was induced by placing a 5.0 nylon thread ligature around the second upper left molar of AT1 mice, no-ligature or ligature (AT1-NL and AT1-L), AT2 (AT2-NL or AT2-L) and wild type (WT-NL or L). Alveolar bone loss was scanned using Micro-CT. Cytokines, peptides and enzymes were analyzed from gingival tissues by Elisa and RT-PCR. Results: The blockade of AT1 receptor resulted in bone loss, even in healthy animals. Ang II receptor blockades did not prevent linear bone loss. Ang II and Ang 1-7 levels were significantly increased in the AT2-L (p < 0.01) group compared to AT2-NL and AT1-L. The genic expression of the Mas receptor was significantly increased in WT-L and AT2-L compared to (WT-NL and AT2-NL, respectively) and in AT1-L. Conclusions: Our data suggest that the receptor AT1 appears to be important for the maintenance of bone mass. AT2 receptor molecular function in periodontitis appears to be regulated by AT1.

Highlights

  • Periodontitis is a chronic inflammatory, multicausal disease [1] and a leading cause of tooth loss in adults [2].The association between periodontitis and cardiovascular disease is proven, and this relationship appears to be independent of other classical risk factors [3]

  • The ratio of bone volume (BV) to total volume (TV) (BV/TV%) showed that bone loss was significantly higher in wild type animals (WT-L) and Ang II type 2 (AT2)-L groups when compared to their respective controls, WT-NL and AT2-NL (p < 0.001)

  • A smaller bone volume was found in the Ang II type 1 (AT1)-NL group when compared to AT2-NL (p < 0.05), suggesting that AT1 receptors appear to be important for the maintenance of bone mass

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Summary

Introduction

The association between periodontitis and cardiovascular disease is proven, and this relationship appears to be independent of other classical risk factors [3]. The control of electrolyte homeostasis and blood pressure in the body is performed by the renin-angiotensin system (RAS). In addition to this vital function, it is responsible for modulating some biological functions such as oxidative stress, inflammation, and hormone peptide release [4,5,6]. RAS components have been proven to be present in various tissues, such as the kidneys, ovaries, liver, brain, adipose tissue, in addition to its presence in oral tissues [8,9,10]

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