Disruption of cholesterol homeostasis triggers periodontal inflammation and alveolar bone loss

2Citations
Citations of this article
13Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Oral diseases exhibit a significant association with metabolic syndrome, including dyslipidemia. However, direct evidence supporting this relationship is lacking, and the involvement of cholesterol metabolism in the pathogenesis of periodontitis (PD) has yet to be determined. In this study, we showed that high cholesterol caused periodontal inflammation in mice. Cholesterol homeostasis in human gingival fibroblasts was disrupted by enhanced uptake through C-X-C motif chemokine ligand 16 (CXCL16), upregulation of cholesterol hydroxylase (CH25H), and the production of 25-hydroxycholesterol (an oxysterol metabolite of CH25H). Retinoid-related orphan receptor α (RORα) mediated the transcriptional upregulation of inflammatory mediators; consequently, PD pathogenesis mechanisms, including alveolar bone loss, were stimulated. Our collective data provided direct evidence that hyperlipidemia is a risk factor for PD and supported that inhibition of the CXCL16-CH25H-RORα axis is a potential treatment mechanism for PD as a systemic disorder manifestation.

Cite

CITATION STYLE

APA

Tran, T. T., Lee, G., Huh, Y. H., Chung, K. H., Lee, S. Y., Park, K. H., … Ryu, J. H. (2023). Disruption of cholesterol homeostasis triggers periodontal inflammation and alveolar bone loss. Experimental and Molecular Medicine, 55(12), 2553–2563. https://doi.org/10.1038/s12276-023-01122-w

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free