The objective of this study was to evaluate the effect of strict supragingival biofilm control on serum inflammatory markers and on periodontal clinical parameters in type 2 diabetes mellitus (T2DM) patients with chronic severe periodontitis. Twenty-four individuals with T2DM and periodontitis were randomly allocated to two treatment groups. The supragingival therapy group (ST, n = 12) received supragingival scaling, whereas the intensive therapy group (IT, n = 12) underwent supra- and subgingival scaling, as well as root planing. Patients from both groups received professional oral hygiene instructions every month. Data regarding visible plaque index (VPI), gingival bleeding index (GBI), bleeding on probing (BOP), probing pocket depth (PPD), clinical attachment level (CAL), serum levels of interleukin (IL)-6, IL-17A, IL-8, tumor necrosis factor α (TNF-α), monocyte chemoattractant protein (MCP)-1 enzyme-linked immunosorbent assay (ELISA), and glycated hemoglobin (HbA1c) levels were obtained at baseline and at 6 months post-therapy. Both therapies resulted in the improvement of almost all clinical periodontal parameters (p < 0.05). There were no differences in TNF-α, IL-8, IL-17A and HbA1c levels in either group (p >0.05), between the two periods. However, MCP-1 levels were significantly reduced in both the ST (p = 0.034) and the IT (p = 0.016) groups, whereas the serum IL-6 levels were significantly reduced only in the IT group (p = 0.001). Strict control of supragingival biofilm has a limited effect on systemic inflammatory markers, and a moderate effect on periodontal clinical parameters.

Diabetes has been associated with periodontitis, but the mechanisms through which periodontal diseases affect the metabolic control remain unclear. Objective: This study aimed to evaluate serum leveis of inflammatory markers, IL-8, IL-6 and monocyte chemoattractant protein 1 (MCP-1), in type 2 diabetic patients in the presence of chronic periodontitis. Material and Methods: Forty two individuals were enrolled in this study and assigned to one of five groups: diabetes mellitus with inadequate glycemic control and periodontitis (DMI+P, n = 10), diabetes mellitus with adequate glycemic control and periodontitis (DMA+P, n = 10), diabetes mellitus without periodontitis (DM, n = 10), periodontitis without diabetes (P, n=6), and neither diabetes nor periodontitis (H, n = 6). Periodontal clinical examination included visible plaque index (PL), gingival bleeding index (GB), probing depth (PD), attachment level (AL) and bleeding on probing (BP). Glycemic control was evaluated by serum concentration of glycated hemoglobin (HbAlc). Inflammatory serum markers IL-8, IL-6 and (MCP-1) were measured by ELISA. Results: DMI+P and DMA+P groups presented higher PD (p=0.025) and AL (p=0.003) values when compared to the P group. There were no significant differences among groups for IL-6, IL-8 and MCP-1 serum levels. Conclusions: Although periodontitis was more severe in diabetic patients, the serum levels of the investigated inflammatory markers did not differ among the groups.

This study investigated the effect of non-surgical periodontal therapy on the composition of subgingival microbiota of patients with chronic kidney disease (CKD). Sixteen CKD pre-dialysis individuals (CKD) and 14 individuals without clinical evidence of kidney disease (C) presenting chronic periodontitis were treated by scaling and root planing. Subgingival samples were collected from each patient and analyzed for their composition by checkerboard at baseline and 3 months post-therapy. Significant differences between groups at baseline were sought by the Mann-Whitney and χ² tests. Changes over time were examined by the Wilcoxon test. At baseline, the CKD group had significantly lower counts of E. faecalis compared to the C group (p < 0.05). After treatment, the levels of a greater number of species were reduced in the C group. Higher levels of A. israelii, C. rectus, F. periodonticum, P. micra, P. nigrescens, T. forsythia, N. mucosa, and S. anginosus (p < 0.05) were found in the CKD group compared to the C group. Also, non-responsive sites in CKD individuals harbored significantly higher levels of pathogenic species (T. forsythia, P. gingivalis, T. denticola, Fusobacterium spp., D. pneumosintes, E. faecalis and S. aureus; p < 0.05) than sites that responded to therapy, as well as non-responsive sites in the C group. The periodontitis-associated subgingival microbiota of CKD and systemically healthy individuals was similar in composition. However, high levels of pathogenic species persisted in the subgingival microbiota of patients with CKD after treatment.

Chronic kidney disease (CKD) is a debilitating systemic condition. Our working hypothesis is that CKD predialysis patients with periodontitis would respond poorly to periodontal treatment owing to immunologic compromise. Twenty-one predialysis patients (group 1) and 19 individuals without clinical evidence of kidney disease (group 2) with chronic periodontitis were subjected to non-surgical periodontal treatment with no antibiotics. Clinical periodontal and systemic parameters were evaluated at baseline and 3 months after treatment. Both groups showed significant and similar post-treatment improvements in all periodontal parameters examined. Most interestingly, periodontal treatment had a statistically significant positive effect on the glomerular filtration rate of each individual (group 1, p = 0.04; group 2, p = 0.002). Our results indicate that chronic periodontitis in predialysis kidney disease patients improved similarly in patients with chronic periodontitis and no history of CKD after receiving non-surgical periodontal therapy. This study demonstrates that CKD predialysis patients show a good response to non-surgical periodontal treatment.