Evaluation of recurrence of periodontal disease after treatment in obese and normal weight patients: Two-year follow-up.

BACKGROUND: Obesity may represent a chronic low-grade inflammation, but there is a lack of long-term longitudinal studies. The aim of this longitudinal study was to evaluate the recurrence of periodontal disease in obese and normal weight patients submitted to scaling and root planing. METHODS: The study included 22 patients who had received periodontal treatment 2 years previously, 13 obese and nine non-obese. The patients were evaluated for anthropometric measurements of body mass index, waist circumference, waist-to-hip ratio, and fat percentage through bioimpedance. The following periodontal parameters were recorded: visible plaque index (VPI), gingival bleeding index (GBI), probing depth (PD), clinical attachment level (CAL), and bleeding on probing (BOP). The immunological evaluation analyzed the proinflammatory cytokines interleukin-1 beta (IL-1ß), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) in the gingival crevicular fluid (GCF). RESULTS: Obese and normal weight patients did not differ in relation to the periodontal parameters of VPI, GBI, PD, CAL, or BOP 2 years after completion of the periodontal therapy. Sites with periodontitis in obese individuals showed higher levels of IL-6 and TNF-α in the gingival fluid (P <0.05). CONCLUSION: Obese and normal weight individuals had similar periodontal behaviors, with low recurrence of the periodontal disease; however, obesity was related to increased inflammatory activity in gingival fluid, which may become a risk indicator for future greater recurrence of the disease in the presence of inadequate plaque control.

Expression of interferon-γ, interferon-α and related genes in individuals with Down syndrome and periodontitis.

BACKGROUND: Recently, attenuation of anti-inflammatory and increase of pro-inflammatory mediators was demonstrated in individuals with Down syndrome (DS) in comparison with euploid patients during periodontal disease (PD), suggesting a shift to a more aggressive inflammation in DS. AIM: To determine the influence of DS in the modulation of interferons (IFNs) signaling pathway in PD. MATERIALS AND METHODS: Clinical periodontal assessment was performed and gingival tissue samples obtained from a total of 51 subjects, including 19 DS individuals with PD, 20 euploid individuals with PD and 12 euploid individuals without PD. Expression levels of interferon-gamma (IFNG) and interferon-alpha (IFNA), and their receptors IFNGR1, IFNGR2, IFNAR1 and IFNAR2, the signaling intermediates Janus kinase 1 (JAK1), signal transducer and activator of transcription 1 (STAT1) and interferon regulatory factor 1 (IRF1) were determined using real time quantitative polymerase chain reaction (qPCR). RESULTS: Clinical signs of periodontal disease were markedly more severe in DS and euploid patients with PD in comparison to euploid and periodontally healthy patients. There was no difference on mRNA levels of IFNA, IFNG, INFGR2, IFNAR1 and IFNAR2 between DS and euploid individuals, even though some of these genes are located on chromosome 21. STAT1 and IRF1 mRNA levels were significantly lower in DS patients in comparison with euploid individuals with PD. In euploid individuals, PD was associated with an increased expression of IFNGR1, IFNGR2, IFNAR1, STAT1 and IRF1. CONCLUSIONS: Reduced expression of STAT1 and IRF1 genes indicate an impaired activation of IFNs signaling in individuals with DS and PD. Expression of IFNA, IFNG and IFN receptors was not altered in DS patients, indicating that indirect mechanisms are involved in the reduced activation of IFN signaling.

The role of obesity as a modifying factor in patients undergoing non-surgical periodontal therapy.

BACKGROUND: Earlier studies have shown an association between obesity and periodontitis, which is mediated by cytokine production. The aim of this study is to assess the role of obesity as a modifying factor on periodontal clinical parameters and on circulating proinflammatory cytokine levels in subjects undergoing non-surgical periodontal treatment. METHODS: Twenty-seven obese subjects and 25 normal-weight subjects were enrolled in this study. Subjects in both groups had generalized chronic periodontitis. The periodontal parameters measured before and 3 months after non-surgical periodontal therapy were: visible plaque index, bleeding gingival index, bleeding on probing, probing depth, and clinical attachment level. In addition, subjects underwent anthropometric measurements and serum analyses of fasting glucose, glycated hemoglobin, interleukin-1ß, interleukin-6, tumor necrosis factor-α, and interferon-γ. RESULTS: Periodontal therapy significantly decreased visible plaque index, bleeding gingival index, bleeding on probing, probing depth of 4 to 6 mm, probing depth ≥7 mm, clinical attachment level of 4 to 6 mm, and clinical attachment level ≥7 mm in both groups (P ≤0.05). Circulating proinflammatory cytokines significantly decreased in obese and normal-weight subjects after periodontal treatment (P ≤0.05). However, interleukin-6 and tumor necrosis factor-α levels remained higher in obese subjects 3 months after treatment (P ≤0.05). CONCLUSION: Obesity does not seem to play a negative role by interfering in the improvement of the periodontal clinical response or decreasing circulating proinflammatory cytokine levels after periodontal treatment.

Myeloperoxidase as inflammatory marker of periodontal disease: experimental study in rats.

RATIONALE: Previous studies have used myeloperoxidase (MPO) as an inflammatory marker to estimate the accumulation of neutrophils in inflamed regions. OBJECTIVE: The aim of this experimental study was to quantify the levels of MPO related to experimental periodontal disease in rats. METHODS: Periodontal disease was induced in a group of rats using placement of a ligature around molar teeth. A group of rats without ligature placement served as a control. Measurements were made on the 3(rd), 7(th), 15(th) and 30(th) day from baseline. Gingival tissues were taken for quantification of MPO levels by ELISA. RESULTS: The rats with induced periodontal disease showed statistically higher MPO levels (p < 0.05) when compared to control rats. A significant increase in the levels of MPO released on days 7 and 30 was observed, with higher levels in the group with induced periodontitis. CONCLUSION: The levels of MPO were found to be higher in rats with induced periodontal disease, confirming the hypothesis that MPO may serve as an inflammatory marker for periodontitis.