Biomolecules· 2026Q1· Review
Lipid Metabolic Reprogramming in Periodontitis-Associated Alveolar Bone Remodeling: Mechanisms, Signaling Pathways, and Therapeutic Implications
- 0citations
- Q1SCImago
- 2026year
Short summary
Periodontitis-associated bone loss is driven by lipid metabolic reprogramming, where physiological lipid metabolism supports bone health, but dyslipidemia and inflammation promote bone loss by increasing harmful lipid metabolites that suppress bone formation and stimulate bone resorption.
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Key points
- Physiological lipid metabolism supports osteoblast function and bone remodeling.
- Dyslipidemia and inflammation in periodontitis increase harmful lipid metabolites (free fatty acids, oxidized lipoproteins, cholesterol derivatives, sphingolipids).
- These metabolites enhance oxidative stress, inflammasome activation, and pro-inflammatory responses, leading to suppressed osteogenesis and stimulated osteoclastogenesis.
- Key regulatory networks involved include PPARγ–Wnt/β-catenin, AMPK–mTOR, NF-κB/NLRP3, and GSK3β–NRF2/ferroptosis signaling.
AI-generated from the title and abstract; the full text is not read.
Abstract
Periodontitis-associated alveolar bone loss reflects not only persistent inflammation but also profound metabolic remodeling within the periodontal microenvironment. This review synthesizes current evidence on how lipid metabolic reprogramming regulates periodontal bone remodeling and its therapeutic significance. Under physiological conditions, fatty acid uptake and β-oxidation, lipid droplet turnover, and lipid-derived signaling support osteoblast bioenergetics, stem-cell osteogenesis, and balanced bone remodeling. In contrast, dyslipidemia and chronic inflammatory stress promote the accumulation of free fatty acids, oxidized lipoproteins, cholesterol derivatives, and sphingolipid metabolites, thereby enhancing reactive oxygen species production, lipid peroxidation, inflammasome activation, and pro-inflammatory immune polarization. These changes suppress osteogenic differentiation, stimulate osteoclastogenesis, and impair periodontal regeneration. We further integrate major regulatory networks, including PPARγ–Wnt/β-catenin, AMPK–mTOR, NF-κB/NLRP3, and GSK3β–NRF2/ferroptosis signaling. Therapeutic strategies targeting these lipid–redox–immune circuits include specialized pro-resolving lipid mediators, n-3 polyunsaturated fatty acids, statins, metabolic modulators, and local biomaterial- or nanocarrier-based delivery systems. Accordingly, lipid metabolic reprogramming may provide a framework for developing metabolism-oriented adjunctive and regenerative strategies for periodontitis.
The authors' abstract, as published at the source. Biomolecules, 2026 · DOI ↗
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Field: Periodontics
PeriodonticsDentistry