Osteopenic effects of high‐fat diet‐induced obesity on mechanically induced alveolar bone remodeling

Luo, Hong; Wu, Hongyan; Tan, Xueying; Ye, Yusi; Huang, Lan; Dai, Hongwei; Li, Mei

doi:10.1111/odi.13651

Cited by 7 publications

(5 citation statements)

References 63 publications

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“…The inconsistencies in research findings may be attributed to the heterogeneity between different studies. Studies have shown that serum concentrations of IL-1β, IL-6, TNF-α, and additional pro-inflammatory cytokines increase in obese mice, along with a significant increase in the ratio of nuclear factor-κB receptor activator ligand/osteoprotegerin in periodontal tissues [ 31 ]. Plasma levels of free fatty acids are often higher in obese patients, and these fatty acids can competitively bind to Toll-like receptor (Toll-like receptor, TLR) 2/4, inhibiting host immune defense against pathogens and leading to immune tolerance and dysbiosis of the periodontal microenvironment [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Association between weight-adjusted-waist index and periodontitis risk: A cross-sectional study

2024

PLoS ONE

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Background There may be an association between obesity and periodontitis, yet no studies have investigated the correlation between the new obesity indicator, the weight-adjusted-waist Index (WWI), and periodontitis. Objective This study aims to investigate the association between the novel obesity index, weight-adjusted-waist index, and periodontitis. Subjects and methods WWI was utilized to assess obesity, through measuring waist circumference (WC) and body weight. We analyzed cross-sectional NHANES data from 2009 to 2014 (1) using multivariate logistic regression to explore WWI’s association with moderate/severe periodontitis; (2) conducting subgroup analyses and interaction tests; and (3) fitting smoothed curves to the age-stratified logistic regression model. Results The study involved 11,256 individuals, with 48.55% having moderate/severe periodontitis. Upon adjusting for all relevant variables, a significant correlation between WWI and moderate/severe periodontitis was observed (OR = 1.08, 95% CI: 1.01–1.17). Compared to the lowest quartile of WWI, there was a significant increase in the likelihood of moderate/severe periodontitis in Quartile 2 (OR = 1.21, 95% CI: 1.06–1.39) and Quartile 3 (OR = 1.23, 95% CI: 1.07–1.42). Subgroup analyses for gender, age, education, smoking, and diabetes highlighted a positive association between WWI and moderate/severe periodontitis in all subgroups, except for the diabetic population and individuals aged 65 years and older. Conclusion The analysis revealed a positive correlation between WWI, a novel obesity index, and moderate/severe periodontitis prevalence through diverse modeling approaches.

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Section: Discussionmentioning

confidence: 99%

Association between weight-adjusted-waist index and periodontitis risk: A cross-sectional study

2024

PLoS ONE

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“…However, in vivo studies showed that locally generated bacterial inflammation inhibited RUNX2 expression and up-regulated c-fos and interleukin (IL)-1 β expression levels in osteoblasts induced by tensile strain, and reduced the osteogenesis of osteoblasts under continuous tensile stress ( Lacey et al, 2009 ; Li et al, 2021 ). Obesity induced by high-fat diet decreases osteoblast activity in alveolar bone of the OTM stretching side ( Luo et al, 2021 ). Therefore, it is necessary to consider several factors to maximize the function of osteoblasts using tensile stress.…”

Section: Mechanical Stimulation With Osteoblastsmentioning

confidence: 99%

Effects of Mechanical Stress Stimulation on Function and Expression Mechanism of Osteoblasts

Liu

Wang

et al. 2022

Front. Bioeng. Biotechnol.

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Osteoclasts and osteoblasts play a major role in bone tissue homeostasis. The homeostasis and integrity of bone tissue are maintained by ensuring a balance between osteoclastic and osteogenic activities. The remodeling of bone tissue is a continuous ongoing process. Osteoclasts mainly play a role in bone resorption, whereas osteoblasts are mainly involved in bone remodeling processes, such as bone cell formation, mineralization, and secretion. These cell types balance and restrict each other to maintain bone tissue metabolism. Bone tissue is very sensitive to mechanical stress stimulation. Unloading and loading of mechanical stress are closely related to the differentiation and formation of osteoclasts and bone resorption function as well as the differentiation and formation of osteoblasts and bone formation function. Consequently, mechanical stress exerts an important influence on the bone microenvironment and bone metabolism. This review focuses on the effects of different forms of mechanical stress stimulation (including gravity, continuously compressive pressure, tensile strain, and fluid shear stress) on osteoclast and osteoblast function and expression mechanism. This article highlights the involvement of osteoclasts and osteoblasts in activating different mechanical transduction pathways and reports changings in their differentiation, formation, and functional mechanism induced by the application of different types of mechanical stress to bone tissue. This review could provide new ideas for further microscopic studies of bone health, disease, and tissue damage reconstruction.

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“…Suppressed osteoblastic marker expression was also observed in NZO osteoblasts including alpha-1 type I collagen, bone gamma-carboxyglutamate protein, and RUNX family transcription factor 2 (Runx2). The HFD-induced model also suggested that obesity downregulated Runx2 in the periodontal area [ 132 ].…”

Section: Mechanisms By Which Obesity Enhances Periodontal Bone Lossmentioning

confidence: 99%

“…Osteoprotegerin (OPG) can block the function of RANKL by competitively binding to RANK. Numerous studies have reported an increased ratio of RANKL/OPG in the periodontal tissue of the obese model, suggesting an activated osteoclast function in the animal [ 132 , 134 ]. The hyperinflammation, increased oxidative stress, and immune cell dysfunction mentioned above can interact with osteoclast formation and function, leading to bone loss.…”

Section: Mechanisms By Which Obesity Enhances Periodontal Bone Lossmentioning

confidence: 99%

Obesity, Bone Loss, and Periodontitis: The Interlink

Zhao

Leung

2022

Biomolecules

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Obesity and periodontitis are both common health concerns that have given rise to considerable economic and societal burden worldwide. There are established negative relationships between bone metabolism and obesity, obesity and diabetes mellitus (DM), and DM and periodontitis, to name a few, with osteoporosis being considered a long-term complication of obesity. In the oral cavity, bone metabolic disorders primarily display as increased risks for periodontitis and alveolar bone loss. Obesity-driven alveolar bone loss and mandibular osteoporosis have been observed in animal models without inoculation of periodontopathogens. Clinical reports have also indicated a possible association between obesity and periodontitis. This review systematically summarizes the clinical periodontium changes, including alveolar bone loss in obese individuals. Relevant laboratory-based reports focusing on biological interlinks in obesity-associated bone remodeling via processes like hyperinflammation, immune dysregulation, and microbial dysbiosis, were reviewed. We also discuss the potential mechanism underlying obesity-enhanced alveolar bone loss from both the systemic and periodontal perspectives, focusing on delineating the practical considerations for managing periodontal disease in obese patients.

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Osteopenic effects of high‐fat diet‐induced obesity on mechanically induced alveolar bone remodeling

Cited by 7 publications

References 63 publications

Association between weight-adjusted-waist index and periodontitis risk: A cross-sectional study

Association between weight-adjusted-waist index and periodontitis risk: A cross-sectional study

Effects of Mechanical Stress Stimulation on Function and Expression Mechanism of Osteoblasts

Obesity, Bone Loss, and Periodontitis: The Interlink

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