Comparison of the Proportion of Non‐Classic (CD14+CD16+) Monocytes/Macrophages in Peripheral Blood and Gingiva of Healthy Individuals and Patients With Chronic Periodontitis

Jagannathan, Raghunathan; Lavu, Vamsi; Rao, Suresh Ranga

doi:10.1902/jop.2013.120658

Cited by 33 publications

(27 citation statements)

References 18 publications

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“…Previous studies have reported an increase in the proportion of non-classical monocytes in periodontitis (28,29). We investigated whether peripheral monocytes from periodontitis patients (52.6 ± 5.1 years old; 2 females and 3 males) present differential S100A12 expression and secretion when compared with monocytes from periodontally healthy participants (42.4 ± 15.9 years old; 3 females and 2 males), and whether this difference was related to a particular subset.…”

Section: S100a12 Expression Is Altered In Circulating Monocytes From mentioning

confidence: 96%

S100A12 Expression Is Modulated During Monocyte Differentiation and Reflects Periodontitis Severity

et al. 2020

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Section: S100a12 Expression Is Altered In Circulating Monocytes From mentioning

confidence: 96%

S100A12 Expression Is Modulated During Monocyte Differentiation and Reflects Periodontitis Severity

et al. 2020

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“…In this study, we selected macrophages because macrophagemediated inflammatory response plays a crucial role in development of periodontal disease (Charon et al 1981;Shapira et al 1996;Jagannathan et al 2014). Results showed that LPS induced IL-6 secretion from bone marrow-derived macrophages, while PA had no effect, although it did enhance the stimulatory effect of LPS by 2-fold (Fig.…”

Section: Hfd Enhances Lps-stimulated Cytokine Expressionmentioning

confidence: 99%

Metabolic Syndrome Exacerbates Inflammation and Bone Loss in Periodontitis

Zhang

et al. 2014

J Dent Res

111

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Clinical studies have shown that metabolic syndrome (MetS) is associated with increased risk of developing periodontitis. However, the underlying mechanisms remain largely unknown. Since it is known that lipopolysaccharide (LPS)-activated toll-like receptor 4 signaling pathways play a crucial role in periodontitis, we hypothesized that MetS enhances LPS-induced periodontal inflammation and alveolar bone loss. In this study, we induced MetS in C57BL/6 mice by feeding them high-fat diet (HFD), and we induced periodontitis by periodontal injection of Aggregatibacter actinomycetemcomitans LPS. We found that mice fed a HFD had significantly increased body weight, plasma lipids, insulin, and insulin resistance when compared with mice fed regular chow, indicating that the mice developed MetS. We also found that a HFD markedly increased LPSinduced alveolar bone loss, osteoclastogenesis, and inflammatory infiltration. Analysis of gene expression in periodontal tissue revealed that HFD and LPS injection cooperatively stimulated expression of cytokines that are known to be involved in periodontal tissue inflammation and osteoclastogenesis-such as interleukin 6, monocyte-chemotactic protein 1, receptor activator of nuclear factor kappa-B ligand, and macrophage colony-stimulating factor. To further understand the potential mechanisms involved in MetS-boosted tissue inflammation, our in vitro studies showed that palmitic acid-the most abundant saturated fatty acid (SFA) and the major SFA in the HFD used in our animal study-potently enhanced LPS-induced proinflammatory gene expression in macrophages. In sum, this study demonstrated that MetS was associated with increased periodontal inflammation and alveolar bone loss in an LPS-induced periodontitis animal model. This study also suggests that SFA palmitic acid may play an important role in MetS-associated periodontitis by enhancing LPS-induced expression of inflammatory cytokines in macrophages.

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“…Studies have suggested that monocytes during or after periodontal pathogen challenge could contribute to inflammation in periodontitis-associated systemic disease, such as aortic inflammation [11,12]. One study has shown an increased percentage of CD14 + CD16 + monocytes in the peripheral blood of patients with chronic periodontitis compared to healthy individuals [13] but, overall, data on peripheral blood monocyte populations in periodontitis are scarce.…”

Section: Introductionmentioning

confidence: 99%

Comparative analysis of immune cell subsets in peripheral blood from patients with periodontal disease and healthy controls

Cheng

Saleh

Karim

et al. 2018

Clinical and Experimental Immunology

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Periodontitis is a chronic inflammatory disease caused by the colonization of teeth by the bacterial plaque biofilm and the resultant host immune responses in adjacent periodontal tissues. Disease severity can vary dramatically between patients with periodontitis, with some subjects displaying inflammation without bony destruction (gingivitis), while others experience chronic progressive or rapidly aggressive gingival connective tissue damage and bone loss. To determine whether peripheral immune dysregulation is associated with periodontitis, we performed extensive analysis of immune cell subsets in peripheral blood from patients with chronic or aggressive periodontitis versus periodontally healthy control subjects. Peripheral blood mononuclear cells (PBMC) from patients with chronic periodontitis or aggressive periodontitis and from periodontally healthy controls were analysed by 8-10-colour flow cytometry for the frequencies of various lymphocyte subsets, including interleukin (IL)-17-, interferon (IFN)-γ-, tumour necrosis factor (TNF)-α- and IL-10-producing cells, and the frequencies and phenotype of monocytes. Cytokine levels in serum from the different groups were determined by Luminex assay. We found no significant differences in the frequencies of major immune cell populations [CD4 T cells, CD8 T cells, γδ T cells, CD4 CD45RO CD25 CD127 regulatory T cells (T ), CD19 B cells, CD14 monocytes] or of cytokine-producing T cells, or in the phenotype of CD14 monocytes in peripheral blood from these patient cohorts. Additionally, no significant differences were observed in serum levels of prototypical inflammatory cytokines. These results suggest that the local gingival inflammatory response is not reflected by obvious changes in major blood immune cell subset frequencies.

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Comparison of the Proportion of Non‐Classic (CD14+CD16+) Monocytes/Macrophages in Peripheral Blood and Gingiva of Healthy Individuals and Patients With Chronic Periodontitis

Abstract: This study demonstrates an increased proportion of CD14+CD16+HLA-DR++ monocytes/macrophages in the peripheral blood and gingiva of patients with CP.

Cited by 33 publications

References 18 publications

S100A12 Expression Is Modulated During Monocyte Differentiation and Reflects Periodontitis Severity

S100A12 Expression Is Modulated During Monocyte Differentiation and Reflects Periodontitis Severity

Metabolic Syndrome Exacerbates Inflammation and Bone Loss in Periodontitis

Comparative analysis of immune cell subsets in peripheral blood from patients with periodontal disease and healthy controls

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