Potential of alveolar bone damage in periodontitis patients with dyslipidemia
1 Department of Oral Biology, Faculty of Dental Medicine, Universitas Airlangga, Jalan Prof Dr Moestopo No 47 Surabaya 60132 Indonesia
2 Department of Physiology, Faculty of Medicine, Universiti Malaya, Lembah Pantai, 50603 Kuala Lumpur, Malaysia.
Review Article
World Journal of Advanced Research and Reviews, 2023, 19(02), 152–161
Publication history:
Received on 17 June 2023; revised on 29 July 2023; accepted on 31 July 2023
Abstract:
Background: Severe periodontitis is the sixth most prevalent disease across the globe. Periodontitis is highly associated with decreased HDL, increased LDL concentrations, and triglycerides. The increase of serum lipid levels beyond the physiological range will change immune cell function by increasing the production of pro-inflammatory cytokines which will interfere with tissue response and affect wound healing thereby increasing susceptibility to periodontitis.
Purpose: To explain the mechanism of increased alveolar bone destruction in patients with periodontitis accompanied by dyslipidemia.
Methods: This study uses a narrative review
Results: Several mechanisms of alveolar bone destruction in periodontitis accompanied by dyslipidemia are through the severity of the metabolic syndrome, serum Lp-PLA2, CRP, chemerin, plasma secretion of TNF-α, IL1β, IL-6, PGE2, IL-2, interferon gamma, matrix metalloproteinases, systemic inflammatory burden, serum triglyceride levels, increased HDL and LDL levels, and decreased serum cholesterol.
Conclusions: Alveolar bone damage in periodontitis accompanied by dyslipidemia can occur through several mechanisms. This study complies with and supports the Sustainable Development Goal No. 3, to ensure healthy lives and promote well-being for all at all ages.
Keywords:
Alveolar Bone Damage; Periodontitis; Dyslipidemia; Public Health; Triglyceride; Inflammation
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Copyright © 2023 Author(s) retain the copyright of this article. This article is published under the terms of the Creative Commons Attribution Liscense 4.0