Aberrant Periodontal and Systemic Immune Response of Overweight Rodents to Periodontal Infection

Abstract

This study aimed to explore periodontal and systemic immune response of overweight hosts to periodontitis. Forty C57 BL/6J male mice were divided into high (HF) or low fat (LF) diet groups and fed with the two diets, respectively, for 8 weeks. Each diet group was then divided into periodontitis (P) or control (C) groups (n = 10 per group) for 10-day ligation or sham-ligation. Overweight-related parameters including body weight were measured. Alveolar bone loss (ABL) was morphometrically analyzed and periodontal osteoclasts were stained. Periodontal immune response including leukocyte and macrophage number and inflammatory cytokines were analyzed by histology and quantitative PCR. Serum cytokine and lipid levels were quantified using electrochemiluminescence immunoassays, enzyme-linked immunosorbent assays, and biochemistry. It was found that HF group had 14.4% body weight gain compared with LF group (P < 0.01). ABL and periodontal osteoclast, leukocyte, and macrophage number were higher in P group than C group regardless of diet (P < 0.05). ABL and periodontal osteoclast number were not affected by diet regardless of ligation or sham-ligation. Leukocyte and macrophage number and protein level of tumor necrosis factor α (TNF-α) in periodontium and serum interleukin-6 level were downregulated by HF diet in periodontitis mice (P < 0.05). Periodontal protein level of TNF-α was highly correlated with serum interleukin-6 and low-density lipoprotein cholesterol levels (P < 0.01). These findings indicated that impaired immune response occurs both periodontally and systemically in preobesity overweight individuals. Given a well-reported exacerbating effect of obesity on periodontitis, overweight, if let uncontrolled, might place the individuals at potential risk for future periodontal tissue damage.

Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease

“…Although ABL and periodontal osteoclast numbers were not affected by diet regardless of ligation or sham-ligation, leukocyte and macrophage numbers and protein levels of tumor necrosis factor α (TNF-α) in the periodontium and serum interleukin (IL)-6 levels were downregulated in periodontitis mice fed a high-fat diet. These findings indicated that an impaired immune response occurred both periodically and systemically in pre-obesity overweight mice [87]. They also evaluated the effects of obesity on macrophage infiltration and activation in periodontal tissue with periodontitis.…”

Association between obesity and adipokines levels in saliva and gingival crevicular fluid: A systematic review and meta‐analysis

“…TNF‐α can positively self‐regulate its synthesis in adipose tissue and other tissues/fluids . Moreover, a continuous increase of TNF‐α in oral fluids, triggered by obesity, would contribute to the development or worsening of inflammatory conditions such as periodontal disease, a hypothesis supported by experimental and clinical studies . TNF‐α acts through the activation of nuclear factor‐kB (NF‐kB), a transcription factor responsible for the regulation of genes associated with inflammation .…”

“…66 Moreover, a continuous increase of TNF-in oral fluids, triggered by obesity, would contribute to the development or worsening of inflammatory conditions such as periodontal disease, a hypothesis supported by experimental and clinical studies. 19,67 TNF-acts through the activation of nuclear factor-kB (NF-kB), a transcription factor responsible for the regulation of genes associated with inflammation. 9 The production or activity of TNF-is associated with some adipokines, such as leptin, adiponectin, vaspin, and omentin, which may regulate TNF-production through NF-kB activation.…”

Conditions of the Oral Cavity Status in Youth With Alimentary-Constitutional Form of Obesity

“…The most relevant linker is systemic inflammation and impaired immune response by which obesity might trigger aberrant periodontal inflammation and exacerbated alveolar bone loss [8]. Through test carried out on laboratory mice with induced obesity researchers explore significant decrease of alveolar bone level and increase of periodontal osteoclast, leukocyte, and macrophage number in obese mice with periodontitis compared with normal weight mice with induced periodontitis [16]. In periodontal tissues of monosodium glutamate-induced obesity rats activation of oxidative stress and nitrosative stress alteration and depolymerization of main connective tissues biopolymers were detected compared with rats without obesity [1].…”