Association Between Periodontitis and Gestational Diabetes Mellitus: Systematic Review and Meta‐Analysis

Lima, Rafael Paschoal Esteves; Cyrino, Renata Magalhães; Dutra, Bernardo de Carvalho; Silveira, Juliana da; Martins, Carolina Castro; Cota, Luís Otávio Miranda; Costa, Fernando Oliveira

doi:10.1902/jop.2015.150311

Cited by 37 publications

(30 citation statements)

References 40 publications

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“…in 2016 conducted a systematic review and meta‐analysis and concluded that there was substantial clinical, methodologic and statistical heterogeneity among the studies. The scientific evidence cannot affirm a positive association between periodontitis and GDM (Esteves Lima et al., ).…”

Section: Discussionmentioning

confidence: 99%

Association between periodontal disease and gestational diabetes mellitus—A prospective cohort study

Kumar

Sharma

Verma

et al. 2018

J Clinic Periodontology

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Section: Discussionmentioning

confidence: 99%

Association between periodontal disease and gestational diabetes mellitus—A prospective cohort study

Kumar

Sharma

Verma

et al. 2018

J Clinic Periodontology

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“…Porphyromonas gingivalis (P. gingivalis ) is the major periodontal bacteria (Seymour et al, 2007), and its lipopolysaccharide derived from P. gingivalis (PgLPS) induces executive pro-inflammatory responses through various types of cells, including macrophages, leptomeningeal cells, microglia and fibroblasts (Wu et al, 2008; Liu et al, 2013; Wu and Nakanishi, 2015; Li et al, 2016). Recently, substantial clinical evidence has shown that periodontitis causes or hastens not only other systemic diseases, such as atherosclerosis and diabetes (Lalla and Papapanou, 2011; Velsko et al, 2014; Esteves Lima et al, 2016) and rheumatoid arthritis (Leech and Bartold, 2015; Silvestre et al, 2016), but also neurodegenerative diseases, such as Alzheimer’s disease (Noble and Scarmeas, 2009; Poole et al, 2013), through persistent systemic inflammation and neuroinflammation. However, the factors responsible for the maintenance of this whole-body pro-inflammatory condition are poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Cathepsin S Is Involved in Th17 Differentiation Through the Upregulation of IL-6 by Activating PAR-2 after Systemic Exposure to Lipopolysaccharide from Porphyromonas gingivalis

Dekita

et al. 2017

Front. Pharmacol.

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Positive links have been found between periodontitis and numerous diseases in humans via persistent inflammation throughout the body. However, the main factors responsible for maintaining this pro-inflammatory condition are poorly understood. The spleen, the largest secondary immune organ, is a central hub regulating the immune response/inflammation due to the dendritic cell (DC) response to CD4+ T cell subtype differentiation, and lysosomal proteinase cathepsin S (CatS) is known to be involved in DC functions. In the present study, we found that CatS-induced IL-6 production by splenic DCs subsequently promotes Th17 differentiation, in response to systemic exposure to lipopolysaccharide derived from Porphyromonas gingivalis (PgLPS). The population of CD11c+ DCs was significantly increased in the splenic marginal zone (MZ) locally of wild-type (DBA/2) mice with splenomegaly but not in that of CatS deficient (CatS-/-) mice after systemic exposure to PgLPS for 7 consecutive days (5 mg/kg/day, intraperitoneal). Similarly, the population of Th17+CD4+ T cells was also significantly increased in the splenic MZ of wild-type mice but not in that of CatS-/- mice after PgLPS exposure. Furthermore, the increase in the Th17+ CD4+ T cell population paralleled increases in the levels of CatS and IL-6 in CD11c+ cells in the splenic MZ. In isolated primary splenic CD11c+ cells, the mRNA expression and the production of IL-6 was dramatically increased in wild-type mice but not in CatS-/- mice after direct stimulation with PgLPS (1 μg/ml), and this PgLPS-induced increase in the IL-6 expression was completely abolished by pre-treatment with Z-Phe-Leu-COCHO (Z-FL), the specific inhibitor of CatS. The PgLPS activated protease-activated receptor (PAR) 2 in the isolated splenic CD11c+ cells was also significantly inhibited by CatS deficiently. In addition, the PgLPS-induced increase in the IL-6 production by splenic CD11c+ cells was completely abolished by pre-treatment with FSLLRY-NH2, a PAR2 antagonist, as well as Akti, a specific inhibitor of Akt. These findings indicate that CatS plays a critical role in driving splenic DC-dependent Th17 differentiation through the upregulation of IL-6 by activating PAR2 after exposure to components of periodontal bacteria. Therefore, CatS-specific inhibitors may be effective in alleviating periodontitis-related immune/inflammation.

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“…indicated a significant association between periodontitis and GDM in the meta‐analyses of four cross‐sectional studies (OR 1.67, 95% CI 1.20–2.32) and two case–control studies (OR 2.66, 95% CI 1.52–4.65). However, with the inclusion of one case–control study, the significance was null (meta‐analysis of three case–control studies: OR 1.69, 95% CI 0.68–4.21) because the sensitivity tests for these case–control studies showed a lack of consistency …”

Section: Epidemiological Resultsmentioning

confidence: 99%

Periodontal diseases and adverse pregnancy outcomes

Komine‐Aizawa

Aizawa

Hayakawa

2018

J of Obstet and Gynaecol

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From last decade of the 20th century, numerous epidemiological studies and intervention trials have attempted to prove the relationships between maternal periodontal diseases and adverse pregnancy outcomes (APO). Periodontal diseases are considered a risk factor for APO, including preterm birth, fetal growth restriction, low birthweight, pre-eclampsia and gestational diabetes. However, the efficacy of periodontal treatment during pregnancy is controversial. Two pathogenic mechanisms might explain the potential effect of periodontal diseases on pregnancy outcomes. First, periodontal bacteria originating in the gingival biofilm directly affect the feto-placental unit subsequent to bacteremia. Second, inflammatory mediators secreted by the subgingival inflammatory site are carried to the feto-placental unit, where they then cause an inflammatory response. To elucidate these mechanisms, many researchers have been investigating the use of experimental animal models and in vitro models. In the present review, we summarize the current literature on the relationship between periodontal diseases and APO from epidemiological studies, animal models studies and in vitro studies, and speculate on the possible mechanism of periodontal diseases affecting pregnancy outcomes.

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Association Between Periodontitis and Gestational Diabetes Mellitus: Systematic Review and Meta‐Analysis

Cited by 37 publications

References 40 publications

Association between periodontal disease and gestational diabetes mellitus—A prospective cohort study

Association between periodontal disease and gestational diabetes mellitus—A prospective cohort study

Cathepsin S Is Involved in Th17 Differentiation Through the Upregulation of IL-6 by Activating PAR-2 after Systemic Exposure to Lipopolysaccharide from Porphyromonas gingivalis

Periodontal diseases and adverse pregnancy outcomes

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