7-days of FREE Audio papers, translation & more with Prime
7-days of FREE Prime access
7-days of FREE Audio papers, translation & more with Prime
7-days of FREE Prime access
https://doi.org/10.1111/jcpe.14112
Journal: Journal of clinical periodontology | Publication Date: Jan 21, 2025 |
To investigate the involvement of low-density lipoprotein receptor-related protein 5 (LRP5) in inflammation and alveolar bone loss in periodontitis. Gingival tissues were obtained from 10 periodontitis patients and 10 healthy individuals. Wild-type (WT) and osteoblast-specific Lrp5 conditional knock-out C57BL/6 (LRP5fl/fl;Oc-Cre) mice were used to establish a ligature-induced mouse model of periodontitis. Human periodontal ligament stem cells (hPDLSCs) were isolated and used to further verify the mechanism through which LRP5 mediates periodontitis invitro. Micro-computed tomography, haematoxylin and eosin staining, immunohistochemistry, quantitative reverse-transcription PCR, western blotting, enzyme-linked immunosorbent assay and RNA sequencing were performed to explore the role of LRP5 in periodontitis and the underlying mechanism. LRP5 expression was down-regulated in human/mouse periodontal tissues compared to that in healthy controls. Compared to those in wild-type mice, the periodontal tissues of LRP5fl/fl;Oc-Cre mice had increased alveolar bone loss, higher proinflammatory cytokine levels, and lower osteogenesis-related factor expression. LRP5 expression was down-regulated in hPDLSCs after lipopolysaccharide treatment invitro. LRP5 knockdown increased proinflammatory cytokine production and inhibited osteoblastogenesis by inhibiting PI3K/c-FOS signalling. LRP5 down-regulation exacerbates inflammation and alveolar bone loss in periodontitis by inhibiting PI3K/c-FOS signalling, suggesting LRP5 as a potential therapeutic target for periodontitis.
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.