The influence of diabetes on the periodontal tissues

Ryan, Maria Emanuel; Carnu, Oana; Kamer, Angela R.

doi:10.14219/jada.archive.2003.0370

Cited by 147 publications

(156 citation statements)

References 70 publications

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“…A number of systemic diseases that possess a hyperinflammatory component, such as IBD, diabetes, and obesity/metabolic syndrome, are associated with periodontal diseases (14,16,(32)(33)(34)(35)(36). IBD and periodontitis are both chronic inflammatory diseases of the alimentary canal, that appear to involve dysregulation of host cytokine expression induced by the resident microbiota.…”

Section: Discussionmentioning

confidence: 99%

T Cell Response Mediated by Myeloid Cell-Derived IL-12 Is Responsible for Porphyromonas gingivalis-Induced Periodontitis in IL-10-Deficient Mice

Sasaki¹,

Suzuki

Kent

et al. 2008

The Journal of Immunology

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Periodontal disease is a chronic inflammatory disease in the oral cavity, which culminates in alveolar bone loss. Porphyromonas gingivalis is a consensus periodontal pathogen that has been implicated in adult forms of periodontitis. We previously demonstrated that IL-10-deficient mice exhibit a hyperinflammatory phenotype and are highly susceptible to P. gingivalis-induced periodontitis, indicating an important anti-inflammatory effect of IL-10 in suppressing bone loss. In this study, we analyzed the pathway(s) by which IL-10 deficiency leads to severe P. gingivalis-induced periodontitis. Because Stat3 is essential in IL-10 signaling, immune cell-specific Stat3-deficient mice were subjected to P. gingivalis infection to identify the key IL-10-responsive cells in preventing periodontitis. Myeloid cell-specific Stat3-deficient mice exhibited increased periodontal bone loss (p < 0.001), whereas T cell- and B cell-specific Stat3 mice were resistant, suggesting that macrophages (MP) and/or polymorphonuclear leukocytes are the key target cells normally suppressed by IL-10. Myeloid cell-specific Stat3-deficient mice exhibited elevated gingival CD40L gene expression in vivo compared with wild-type controls (p < 0.01), and Stat3-deficient MPs exhibited vigorous P. gingivalis-stimulated IL-12 production in vitro and induced elevated Ag-specific T cell proliferation compared with wild-type MPs (p < 0.01). Of importance, both IL-12p40/IL-10 and T cell/IL-10 double-deficient mice were resistant to P. gingivalis-induced periodontitis, demonstrating roles for both IL-12p40 and T cells in pathogenesis in a hyperinflammatory model of disease. These data demonstrate that P. gingivalis-induced periodontitis in IL-10-deficient mice is dependent upon IL-12p40-mediated proinflammatory T cell responses.

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Section: Discussionmentioning

confidence: 99%

T Cell Response Mediated by Myeloid Cell-Derived IL-12 Is Responsible for Porphyromonas gingivalis-Induced Periodontitis in IL-10-Deficient Mice

Sasaki¹,

Suzuki

Kent

et al. 2008

The Journal of Immunology

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“…There is considerable evidence that the clinical impact of periodontal disease extends beyond the oral cavity (2). Strong associations have been found between periodontitis and a number of systemic conditions, including cardiovascular disease (3,4), preterm delivery and low-birth-weight babies (5), diabetes mellitus (6)(7)(8), and rheumatoid arthritis (9)(10)(11).…”

mentioning

confidence: 99%

Dysbiosis and Alterations in Predicted Functions of the Subgingival Microbiome in Chronic Periodontitis

Kirst

Alfant

et al. 2015

Appl Environ Microbiol

185

188

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Chronic periodontitis is an inflammatory disease of the periodontium affecting nearly 65 million adults in the United States. Changes in subgingival microbiota have long been associated with chronic periodontitis. Recent culture-independent molecular studies have revealed the immense richness and complexity of oral microbial communities. However, data sets across studies have not been directly compared, and whether the observed microbial variations are consistent across different studies is not known. Here, we used 16S rRNA sequencing to survey the subgingival microbiota in 25 subjects with chronic periodontal disease and 25 healthy controls and compared our data sets with those of three previously reported microbiome studies. Consistent with data from previous studies, our results demonstrate a significantly altered microbial community structure with decreased heterogeneity in periodontal disease. Comparison with data from three previously reported studies revealed that subgingival microbiota clustered by study. However, differences between periodontal health and disease were larger than the technical variations across studies. Using a prediction score and applying five different distance metrics, we observed two predominant clusters. One cluster was driven by Fusobacterium and Porphyromonas and was associated with clinically apparent periodontitis, and the second cluster was dominated by Rothia and Streptococcus in the majority of healthy sites. The predicted functional capabilities of the periodontitis microbiome were significantly altered. Genes involved in bacterial motility, energy metabolism, and lipopolysaccharide biosynthesis were overrepresented in periodontal disease, whereas genes associated with transporters, the phosphotransferase system, transcription factors, amino acid biosynthesis, and glycolysis/gluconeogenesis were enriched in healthy controls. These results demonstrate significant alterations in microbial composition and function in periodontitis and suggest genes and metabolic pathways associated with periodontal disease. P eriodontal disease is a common disease affecting many adults in the United States. If left untreated, chronic periodontitis (CP) can lead to serious problems such as tooth loss. Indeed, periodontal disease is the number one cause of tooth loss in the United States, accounting for half of all tooth loss in U.S. adults (1). There is considerable evidence that the clinical impact of periodontal disease extends beyond the oral cavity (2). Strong associations have been found between periodontitis and a number of systemic conditions, including cardiovascular disease (3, 4), preterm delivery and low-birth-weight babies (5), diabetes mellitus (6-8), and rheumatoid arthritis (9-11).The activity of periodontal disease is determined by a complex interplay between the immune system and periodontal pathogens (12, 13). Alterations in subgingival microbiota have long been associated with the development and progression of periodontitis (14). In susceptible individuals, perturbations in...

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“…15 The existence of vascular changes in the form of capillary basal membrane thickening due hyperglicemic conditions, also causes disruption of the nutrients and the migration of immune cells into the periodontal tissue. 12 Calprotectin (MRP8 /MRP14) is cytosolic protein that has important functions as chemotactic factor associated with the activation of monocytes and neutrophils, and accumulation of cells of innate immunity in areas of inflammation as well as an antibacterial protein. It also has adhesion, regulation, migration activities of monocytes and neutrophils, and is recently known to have important role in body immunity an a natural immune system of periodontal tissues.…”

Section: Discussionmentioning

confidence: 99%

Expression of MRP8/MRP14 mRNA in Monocytes of Periodontitis: Comparison between Diabetic and Non Diabetic Patients

Syaify

Barunawati

Suryono

et al. 2010

The Indonesian J Dent Res

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The severity of periodontitis on patients with type 2 Diabetes Mellitus patients was strongly thought caused by decreasing of leukocytes function such as monoctyes and neutrophils. In our previous research it was found that calprotectin (MRP8/MRP14) level in leukocytes of periodontitis patients with type 2 DM was higher than periodontitis in non DM. The aim of this study was to determine calprotectin (MRP8/MRP14) mRNA expression in human monocytes of periodontitis patients with type 2 DM and without DM. Monocytes were isolated from the peripheral blood of periodontitis patients with uncontrolled type 2 DM, controlled type 2 DM, and non DM. The expression of total RNA calprotectin (MRP8 and MRP14) were detected by RT-PCR using GAPDH as the innate control. It was observed that the value of MRP8/MRP14 mRNA expression DM patients were higher than non DM, and the highly significant increase expression (p<0.05) was on the uncontrolled type 2 DM. The basal level of MRP8/MRP14 expression increased in monocyte of periodontitis and type 2 DM patients compared with non diabetes subjects. It was suggested that high basal level MRP8/ MRP14 has role in the regulation of severity periodontitis with diabetes mellitus.

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The influence of diabetes on the periodontal tissues

Cited by 147 publications

References 70 publications

T Cell Response Mediated by Myeloid Cell-Derived IL-12 Is Responsible for Porphyromonas gingivalis-Induced Periodontitis in IL-10-Deficient Mice

T Cell Response Mediated by Myeloid Cell-Derived IL-12 Is Responsible for Porphyromonas gingivalis-Induced Periodontitis in IL-10-Deficient Mice

Dysbiosis and Alterations in Predicted Functions of the Subgingival Microbiome in Chronic Periodontitis

Expression of MRP8/MRP14 mRNA in Monocytes of Periodontitis: Comparison between Diabetic and Non Diabetic Patients

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