Trefoil factors in saliva and gingival tissues of patients with chronic periodontitis

Background: Trefoil factors (TFFs) are secreted molecules that are involved in cytoprotection against tissue damage and the immune response. TFFs have been detected in saliva and oral tissues, but their clinical significance has never been investigated in patients with chronic periodontitis. The objective of this study is to determine whether TFF expression in saliva and gingival tissues is associated with periodontal pathology. Methods: Saliva and gingival tissue samples were collected from 25 non‐periodontitis individuals and 25 patients with chronic periodontitis (CP). Enzyme‐linked immunosorbent assay and immunohistochemical methods were used to evaluate the expression of TFFs (TFF1, TFF2, and TFF3) in saliva and gingival tissues, respectively. Periodontopathic bacteria were quantified by real‐time polymerase chain reaction. Results: Reduced salivary TFF1 and TFF3 concentrations were observed in patients with CP (P = 0.003 and P <0.001, respectively). Decreased TFF3 expression in gingival tissues of patients with CP was demonstrated (P = 0.041). Levels of salivary TFF3 concentrations were negatively correlated with periodontal pathology and number of Porphyromonas gingivalis and Tannerella forsythia (formerly known as Bacteroides forsythus). Conclusions: Altered expression of TFFs in saliva and gingival tissues was detected in patients with CP. The results suggest that TFF3 may be involved in the pathogenesis of periodontal disease.     

Transforming growth factor-beta stimulates interleukin-11 production by human periodontal ligament and gingival fibroblasts

BACKGROUND: Transforming growth factor (TGF)-beta is a potent multifunctional polypeptide, abundant in the bone matrix. Interleukin (IL)-11 is a pleiotropic cytokine with effects on multiple cell types. The present study was performed to evaluate the regulatory effects of TGF-beta on IL-11 production by human periodontal ligament cells (PDL) and human gingival fibroblasts (HGF). MATERIAL AND METHODS: The expression of TGF-beta receptor in PDL and HGF were observed using flow cytometry. PDL and HGF were stimulated with TGF-beta with or without protein kinase C (PKC) inhibitors and activator. IL-11, bone morphogenetic protein-2 (BMP-2) and TGF-beta mRNA expression was quantified by real-time polymerase chain reaction (PCR). IL-11 production was measured using enzyme-linked immunosorbent assay. RESULTS: PDL and HGF expressed both TGF-beta receptor I and TGF-beta receptor II on the cell surfaces. IL-11 mRNA expression and IL-11 production were augmented by TGF-beta in both PDL and HGF, with higher values in PDL. PKC inhibitors partially suppressed TGF-beta-induced IL-11 production in PDL and HGF, whereas activator enhanced it. TGF-beta mRNA and BMP-2 mRNA expression were up-regulated by TGF-beta in PDL. CONCLUSION: These results suggest that PDL produce IL-11 in response to TGF-beta.     

Internal prostaglandin synthesis augments osteoprotegerin production in human gingival fibroblasts stimulated by lipopolysaccharide

Periodontitis is an inflammatory bone disease caused by Gram-negative anaerobic bacteria. Osteoclast differentiation is regulated by the balance between receptor activator of nuclear factor kappa B ligand (RANKL) and osteoprotegerin (OPG). The purpose of this study was to examine the mechanism of OPG production in human gingival fibroblasts (HGF) stimulated by lipopolysaccharide (LPS) from periodontopathic bacteria. The expressions of Toll-like receptor 2 (TLR-2) and TLR-4 in HGF were examined using flow-cytometry. HGF were stimulated with whole cell extracts or LPS from Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis with or without polymyxin B, a LPS inhibitor. In addition, HGF were stimulated with LPS, prostaglandin E(2) (PGE(2)), various agonists of PGE receptors (EP1, EP2, EP3 and EP4 agonists) with or without indomethacin (IND), a prostaglandin synthesis inhibitor. OPG and PGE(2) production was measured using an enzyme-linked immunosorbent assay (ELISA). HGF expressed both TLR-2 and TLR-4. Both A. actinomycetemcomitans and P. gingivalis LPS augmented OPG expression in HGF. Whole cell extracts from A. actinomycetemcomitans and P. gingivalis augmented OPG production by HGF; the augmentation was suppressed by polymyxin B. IND suppressed OPG production in LPS-stimulated HGF. PGE(2) stimulated HGF to produce OPG. EP1 and EP2 agonists, but not EP3 and EP4 agonists, increased OPG production by HGF. These results suggest that LPS-induced OPG production by HGF is regulated via EP1 and/or EP2 receptors by endogenously generated PGE(2).     

Periodontitis and Gestational Diabetes Mellitus in Non‐Smoking Females

Background: Chronic inflammation has been implicated in the pathogenesis of gestational diabetes mellitus (GDM). Periodontal disease is associated with increased levels of inflammatory mediators and may be a risk factor for GDM. The authors aimed to examine the association between periodontitis and GDM among non‐smoking pregnant females. Methods: This case‐control study included 50 females who were diagnosed with GDM and 50 age‐ and hospital‐matched females without diabetes in Khon Kaen, Thailand. Full‐mouth periodontal examinations were performed during pregnancy by two calibrated dentists who were unaware of the case‐control status. Periodontitis was defined as ≥1 site with probing depth (PD) ≥5 mm and clinical attachment level (CAL) ≥2 mm at the same site. Serum samples were collected to measure C‐reactive protein (CRP), tumor necrosis factor‐α, and interleukin‐6 levels. Analyses were performed using conditional logistic regression. Results: Fifty percent of the case females had periodontitis compared to 26% of the controls. Females with GDM had significantly higher mean PD and CAL, more sites with bleeding on probing, and increased levels of CRP compared to the controls. Periodontitis was significantly associated with GDM (odds ratio = 3.00, 95% confidence interval = 1.19 to 7.56). The association remained significant with additional adjustment for family history of diabetes, prepregnancy body mass index, and weight gain during pregnancy. Conclusions: The results suggest that periodontitis is associated with GDM. Therefore, clinicians should assess periodontal conditions of pregnant females.