Abstract
Background: The aim of this study was to evaluate the role of AT1 and AT2 receptors in a periodontal inflammation experimental model. Methods: Periodontal inflammation was induced by LPS/Porphyromonas gingivalis. Maxillae, femur, and vertebra were scanned using Micro-CT. Maxillae were analyzed histopathologically, immunohistochemically, and by RT-PCR. Results: The vertebra showed decreased BMD in AT1 H compared with WT H (p < 0.05). The femur showed increased Tb.Sp for AT1 H and AT2 H, p < 0.01 and p < 0.05, respectively. The Tb.N was decreased in the vertebra (WT H-AT1 H: p < 0.05; WT H-AT2 H: p < 0.05) and in the femur (WT H-AT1 H: p < 0.01; WT H-AT2 H: p < 0.05). AT1 PD increased linear bone loss (p < 0.05) and decreased osteoblast cells (p < 0.05). RANKL immunostaining was intense for AT1 PD and WT PD (p < 0.001). OPG was intense in the WT H, WT PD, and AT2 PD when compared to AT1 PD (p < 0.001). AT1 PD showed weak immunostaining for osteocalcin compared with WT H, WT PD, and AT2 PD (p < 0.001). AT1 H showed significantly stronger immunostaining for osteonectin in fibroblasts compared to AT2 H (p < 0.01). Conclusion: AT1 receptor knockout changed bone density, the quality and number of bone trabeculae, decreased the number of osteoblast cells, and increased osteonectin in fibroblasts.
Highlights
The renin-angiotensin system (RAS) is an important regulator of blood pressure and water balance in mammals [1,2,3]
The vertebra showed a significant difference between the wild type mice (WT) H and a>]. The type 1 receptor (AT1) H with decreased bone morphometric density (BMD) (p < 0.05)
The amount of linear bone loss was higher for the AT1 receptor knockout periodontal inflammation-disease (AT1 PD) group when compared to its respective control (AT1 H) (Figure 2)
Summary
The renin-angiotensin system (RAS) is an important regulator of blood pressure and water balance in mammals [1,2,3]. When stimulation of this system is excessive, it leads to effects on the sympathetic nervous system mediating vascular hypertrophy and proinflammatory pathways [1]. The type 1 receptor (AT1) is the main target of Ang II, and its function is to regulate blood pressure, vasoconstriction, and oxidative stress [2]. Femur, and vertebra were scanned using Micro-CT. Results: The vertebra showed decreased BMD in AT1 H compared with WT H (p < 0.05).
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