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Disruption of cholesterol homeostasis triggers periodontal inflammation and alveolar bone loss

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Author(s)
Tran, Thanh-TamLee, GyuseokHuh, Yun HyunChung, Ki-HoLee, Sun YoungPark, Ka HyonKwon, Seung HeeKook, Min-SukChun, Jang-SooKoh, Jeong-TaeRyu, Je-Hwang
Type
Article
Citation
Experimental and Molecular Medicine, v.55, no.12, pp.2553 - 2563
Issued Date
2023-12
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. © 2023, The Author(s).
Publisher
Springer Nature
ISSN
1226-3613
DOI
10.1038/s12276-023-01122-w
URI
https://scholar.gist.ac.kr/handle/local/9852
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