Periodontal treatment with topical antibiotics improves glycemic control in association with elevated serum adiponectin in patients with type 2 diabetes mellitus.

OBJECTIVES: Chronic inflammation of periodontitis aggravates glycemic control in type 2 diabetic patients through aggravation of insulin resistance. Increased or decreased release of various inflammatory mediators, such as high sensitivity C-reactive protein (hs-CRP), tumor necrosis factor (TNF)-α, interleukin (IL)-6 and adipokines, such as adiponectin, leptin, and resistin, are presumed to be responsible for developing and progressing insulin resistance. The purpose of this study was to examine the effects of periodontal treatment on glycemic control, serum inflammatory mediators and adipokines in type 2 diabetes patients with periodontitis. METHODS: Twenty-one type 2 diabetic patients with periodontitis received periodontal treatment with topical antibiotics (intervention group) and 8 patients did not receive periodontal treatment (control group). Periodontal examination, including probing pocket depth (PPD) and bleeding on probing (BOP), and blood sampling were performed at baseline, 2 and 6 months after periodontal treatments. Glycated hemoglobin (HbA1c), hs-CRP, TNF-α, IL-6, adiponectin, leptin, and resistin were analyzed. RESULTS: In the intervention group, improvements of PPD and BOP, decrease in HbA1c and elevation of serum adiponectin were observed, while in the control group, all parameters were not changed. Generalized linear model revealed that changes of serum adiponectin and TNF-α and change of BOP correlated significantly with the reduction of HbA1c at 6 months after periodontal treatments. CONCLUSION: The results demonstrated that periodontal treatment improves periodontal status and glycemic control with elevation of serum adiponectin in type 2 diabetic patients. The results suggest that HbA1c is reduced by amelioration of insulin resistance due to elevated serum adiponectin after periodontal treatments.

The anti-phospholipid antibody-dependent and independent effects of periodontopathic bacteria on threatened preterm labor and preterm birth.

PURPOSE: Periodontal disease is considered to be a risk factor for threatened preterm labor (TPL) and preterm birth (PB), but pathogenic mechanisms have not yet been elucidated. We hypothesized that infection with periodontopathic bacteria may enhance thrombosis through molecular mimicry with TLRVYK peptides on beta-2 glycoprotein I, a target molecule in anti-phospholipid syndrome. This study aimed to examine the effects of periodontitis on TPL and PB. METHODS: Ninety-five pregnant women (47 TPL and 48 healthy subjects) participated. Periodontal clinical parameters and periodontopathic bacteria were examined. Molecular mimicry between TLRVYK peptides and homologous peptides on the periodontopathic bacteria was examined by enzyme-linked immunosorbent assay (ELISA) using rabbit polyclonal antibodies specific for the respective peptides (SIRVYK on Aggregatibacter actinomycetemcomitans, TLRIYT on Porphyromonus gingivalis, and TLALYK on Treponema denticola). Serum high-sensitivity C-reactive protein, anti-TLRVYK and anti-SIRVYK IgG antibodies were measured using ELISA. RESULTS: Among the rabbit antibodies specific for the bacterial homologous peptides, only anti-SIRVYK IgG antibody reacted with TLRVYK peptides. Multivariable analysis showed that anti-SIRVYK IgG antibody was significantly associated with diagnosis of TPL. Of 95 births, 14 (14.7 %) delivered preterm. The preterm birth rate was higher in the anti-SIRVYK IgG antibody >median group than in the ≤median group. Of the 47 TPL subjects 13 had PB, and ordinal logistic regression analysis revealed that past smoking, presence of P. gingivalis and anti-SIRVYK IgG antibody were significantly correlated with PB. CONCLUSIONS: Infection with P. gingivalis and the antibody response to SIRVYK might be associated with TPL and PB.

Improvement of glycemic control after periodontal treatment by resolving gingival inflammation in type 2 diabetic patients with periodontal disease.

UNLABELLED: Aims/Introduction: Chronic inflammation aggravates glycemic control in patients with type 2 diabetes mellitus. An increase or decrease in the release and activities of various inflammatory mediators, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and C-reactive protein (CRP), are presumed to be responsible for inducing insulin resistance. The purpose of the present study was to examine the effects of non-surgical periodontal treatment incorporating topical antibiotics on glycemic control and serum inflammatory mediators in patients with type 2 diabetes mellitus with periodontitis. MATERIALS AND METHODS: Periodontal inflammation and periodontal tissue destruction were evaluated by bleeding on probing (BOP) and the probing pocket depth (PPD), respectively. A total of 41 patients with type 2 diabetes and periodontitis received periodontal treatment with the topical application of antibiotics four times within a 2-month period. A periodontal examination, including PPD and BOP, and venous blood sampling were carried out at baseline and at 2 and 6 months after periodontal treatment. Glycated hemoglobin (HbA1c), and serum levels of high-sensitivity (hs)-CRP, TNF-α and IL-6 were analyzed. RESULTS: A generalized linear model showed significant associations between the change in the HbA1c values at 6 months after periodontal treatment, and the change in the BOP, baseline TNF-α levels and the baseline mean PPD. CONCLUSIONS: As BOP is a marker of total gingival inflammation, these results suggest that non-surgical periodontal therapy with topical antibiotics in patients with mild periodontitis might improve glycemic control by resolving periodontal inflammation. Such treatments might be insufficient for the amelioration of insulin resistance in type 2 diabetic patients with severe periodontitis. This trial was registered with the University Hospital Medical Information Network (no. UMIN000006693). (J Diabetes Invest, doi: 10.1111/j.2040-1124.2012.00209.x, 2012).