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  • Disruption of cholesterol homeostasis triggers periodontal inflammation and alveolar bone loss.

Disruption of cholesterol homeostasis triggers periodontal inflammation and alveolar bone loss.

Experimental & molecular medicine (2023-12-01)
Thanh-Tam Tran, Gyuseok Lee, Yun Hyun Huh, Ki-Ho Chung, Sun Young Lee, Ka Hyon Park, Seung Hee Kwon, Min-Suk Kook, Jang-Soo Chun, Jeong-Tae Koh, Je-Hwang Ryu
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.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Anti-RORA (AB3) antibody produced in rabbit, IgG fraction of antiserum
Sigma-Aldrich
Anti-Rabbit IgG (whole molecule)–Peroxidase antibody produced in goat, affinity isolated antibody, buffered aqueous solution