Related Experiment Video
Updated: Nov 3, 2025
Author Spotlight: Comparing Alveolar and Long Bone Remodeling to Explore OTM Model Potential
Published on: July 21, 2023
AT1 and AT2 Receptor Knockout Changed Osteonectin and Bone Density in Mice in Periodontal Inflammation Experimental
Maria Laura de Souza Lima1, Caroline Addison Carvalho Xavier de Medeiros2, Gerlane Coelho Bernardo Guerra3
1Postgraduate Program in Dentistry Sciences, Department of Biophysical and Pharmacology, Federal University of Rio Grande Norte, Natal, RN 59078-900, Brazil.
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.
