LAUSR

AIMS To explore the role of C-reactive protein (CRP) in periodontitis and diabetes and its mechanism in alveolar bone homeostasis. MATERIALS AND METHODS In vivo, normal and Crp knockout rats were randomly divided into: control, diabetes, periodontitis, and diabetes and periodontitis (DP) groups respectively. The diabetes model was established using a high-fat diet combined with streptozotocin (STZ) injection. The periodontitis model was established by ligature combined with lipopolysaccharide injection. Alveolar bones were analyzed using microCT, histology, and immunohistochemistry. In vitro, human periodontal ligament cells (hPDLCs) were treated with lipopolysaccharide and high glucose. CRP knockdown lentivirus or CRP overexpression adenovirus combined with a PI3K/AKT signaling inhibitor or agonist were used to explore the regulatory mechanism of CRP in osteogenesis and osteoclastogenesis of hPDLCs, as evidenced by ALP staining, WB and qPCR. RESULTS In periodontitis and diabetes, CRP knockout decreased the alveolar bone loss and the expression levels of osteoclastogenic markers, while increasing the expression levels of osteogenic markers. CRP constrained osteogenesis while promoting the osteoclastogenesis of hPDLCs via PI3K/AKT signaling under high glucose and pro-inflammatory conditions. CONCLUSIONS CRP inhibits osteogenesis and promotes osteoclastogenesis via PI3K/AKT signaling under diabetic and pro-inflammatory conditions, thus perturbing alveolar bone homeostasis. This article is protected by copyright. All rights reserved.