| First Author | Tran TT | Year | 2023 |
| Journal | Exp Mol Med | Volume | 55 |
| Issue | 12 | Pages | 2553-2563 |
| PubMed ID | 38036731 | Mgi Jnum | J:351106 |
| Mgi Id | MGI:7571672 | Doi | 10.1038/s12276-023-01122-w |
| Citation | Tran TT, et al. (2023) Disruption of cholesterol homeostasis triggers periodontal inflammation and alveolar bone loss. Exp Mol Med 55(12):2553-2563 |
| abstractText | 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 alpha (RORalpha) 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-RORalpha axis is a potential treatment mechanism for PD as a systemic disorder manifestation. |
