AT1 and AT2 Receptor Knockout Changed Osteonectin and Bone Density in Mice in Periodontal Inflammation Experimental Model

The aim of this study was to evaluate the role of AT1 and AT2 receptors in a periodontal inflammation experimental model. Periodontal inflammation was induced by LPS/ . Maxillae, femur, and vertebra were scanned using Micro-CT. Maxillae were analyzed histopathologically, immunohistochemically, and by RT-PCR. The vertebra showed decreased BMD in AT1 H compared with WT H ( < 0.05). The femur showed increased Tb.Sp for AT1 H and AT2 H, < 0.01 and < 0.05, respectively. The Tb.N was decreased in the vertebra (WT H-AT1 H: < 0.05; WT H-AT2 H: < 0.05) and in the femur (WT H-AT1 H: < 0.01; WT H-AT2 H: < 0.05). AT1 PD increased linear bone loss ( < 0.05) and decreased osteoblast cells ( < 0.05). RANKL immunostaining was intense for AT1 PD and WT PD ( < 0.001). OPG was intense in the WT H, WT PD, and AT2 PD when compared to AT1 PD ( < 0.001). AT1 PD showed weak immunostaining for osteocalcin compared with WT H, WT PD, and AT2 PD ( < 0.001). AT1 H showed significantly stronger immunostaining for osteonectin in fibroblasts compared to AT2 H ( < 0.01). AT1 receptor knockout changed bone density, the quality and number of bone trabeculae, decreased the number of osteoblast cells, and increased osteonectin in fibroblasts.