Lipid parameters in obese and normal weight patients with or without chronic periodontitis.

OBJECTIVE: The aim of this study was to evaluate the serum levels of lipids in patients with normal weight (NW) or obesity with or without chronic periodontitis (ChP). MATERIALS AND METHODS: One hundred and sixty non-smoking patients without history of diabetes and/or cardiovascular events were allocated into one of the following groups: NW patients with periodontal health (NWH; n = 40), NW patients with ChP (NWChP; n = 40), obese patients with periodontal health (ObH; n = 40), and obese patients with ChP (ObChP; n = 40). Serum levels of total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides (TRG) were estimated. RESULTS: After adjustments for gender and age, both NW groups presented lower levels of TRG than both obese groups (p < 0.05). The NWH group presented lower levels of LDL than both periodontitis groups (p < 0.05) and the lowest TC/HDL ratio when compared to the other groups (p < 0.05). Females from the NWH group exhibited higher levels of HDL and lower LDL/HDL ratio than females from the ObChP group (p < 0.05). Furthermore, individuals from the ObChP group were more likely to have levels of LDL ≥130 mg/dl and HDL ≤40 mg/dl, compared to those from the NWH group (p < 0.05). CONCLUSIONS: ChP and obesity, jointly or individually, are associated with undesirable pro-atherogenic lipid profiles. CLINICAL RELEVANCE: There is interest in identifying clinical conditions associated with dyslipidemia to improve preventive and treatment strategies. This study demonstrated that ChP, obesity, and the association of both conditions might be related to pro-atherogenic lipid profiles.

Does obesity influence the subgingival microbiota composition in periodontal health and disease?

AIM: To evaluate whether obesity affects the subgingival microbial composition of patients with periodontal health or chronic periodontitis (CP). MATERIALS AND METHODS: Based on periodontal parameters, body mass index and waist-hip ratio, 166 patients were allocated into one of the following groups: Normal weight (NW) patients with periodontal health (n = 44), NW patients with CP (n = 40), obese patients with periodontal health (n = 40) and obese patients with CP (n = 42). Six subgingival biofilm samples per patient were analysed for their content of 40 bacterial species using checkerboard DNA-DNA hybridization. RESULTS: Obese patients with CP harboured higher levels and/or higher proportions of several periodontal pathogens than those with NW and CP, including Aggregatibacter actinomycetemcomitans, Eubacterium nodatum, Fusobacterium nucleatum ss vincentii, Parvimonas micra, Prevotella intermedia, Tannerella forsythia, Prevotella melaninogenica and Treponema socranskii. The proportions of most of these pathogens, as well Campylobacter rectus and Eikenella corrodens, were more increased in the diseased sites of the obese patients than in those with NW. Furthermore, the healthy sites of the obese patients, presenting or not CP, also exhibited higher proportions of some of the pathogens than patients with NW. CONCLUSIONS: Obesity is associated with increased levels and proportions of periodontal pathogens, especially in patients with CP.

Local and serum levels of adipokines in patients with obesity after periodontal therapy: one-year follow-up.

AIM: This study evaluated the effects of scaling and root planing (SRP) on gingival crevicular fluid (GCF) and serum levels of adipokines in patients with chronic periodontitis (CP) with or without obesity. METHODS: Twenty patients with obesity and 20 patients without obesity, all with CP, received SRP. Serum and GCF levels of resistin, adiponectin, leptin, tumour necrosis factor [TNF]-α and interleukin [IL]-6 were evaluated by enzyme-linked immunosorbent assay at baseline, 3, 6 and 12 months post-therapy. RESULTS: SRP reduced the amounts of TNF-α in deep sites and increased the concentration of adiponectin in shallow sites of non-obese patients (p < 0.05). SRP increased the concentrations of TNF-α and leptin in patients with obesity (p < 0.05). GCF levels of TNF-α were higher in patients with obesity than in patients without obesity at all time-points (p < 0.05). There were no changes in serum levels of any adipokines for any group after therapy (p > 0.05). Patients with obesity exhibited higher serum levels of leptin at all time-points and IL-6 at 3 months post-therapy (p < 0.05). CONCLUSIONS: Obesity may modulate systemic and periodontal levels of adipokines in favour of pro-inflammation, independently of periodontal therapy. SRP did not affect the circulating levels of adipokines in patients with or without obesity.

Effects of scaling and root planing on clinical response and serum levels of adipocytokines in patients with obesity and chronic periodontitis.

BACKGROUND: Despite several investigations suggesting that obesity is a risk indicator for periodontitis, little is known about the effect of obesity on periodontal treatment response. The aim of this study is to evaluate the effects of scaling and root planing (SRP) on clinical parameters and circulating levels of leptin and adiponectin in patients with obesity with chronic periodontitis (CP). METHODS: Twenty-four patients with obesity and CP and 24 patients without obesity with CP were submitted to SRP. Clinical parameters were assessed at baseline and 3 and 6 months after therapy. Serum levels of leptin and adiponectin were evaluated at all time points, using enzyme-linked immunosorbent assay. RESULTS: SRP improved the clinical parameters of both groups at 3 and 6 months (P < 0.05). Nonetheless, the patients without obesity presented a lower mean probing depth (PD) at 6 months after therapy and a greater reduction in PD from baseline to 6 months in the full-mouth analysis (primary outcome variable) and in initially deep sites (P < 0.05). Leptin serum levels were higher in patients with obesity than in patients without obesity at all time points (P < 0.05). No changes in the serum levels of leptin and adiponectin were observed in groups with and without obesity after therapy (P > 0.05). CONCLUSIONS: Patients with obesity and CP presented lower reductions in PD than patients without obesity with CP at 6 months after SRP. Furthermore, the treatment did not affect the circulating levels of leptin and adiponectin in any group.

Assessment of tissue oxygenation of periodontal inflammation in smokers using optical spectroscopy.

BACKGROUND: We have recently developed a periodontal diagnostic tool that was validated in non-smokers with periodontitis. Tobacco smoking is a recognized risk factor for periodontal diseases that can mask gingival bleeding and lead to a false negative diagnosis. Therefore, the purpose of current study is to further validate this instrument in smokers with periodontal diseases. METHODS: Using a portable optical near-infrared spectrometer, optical spectra were obtained, processed and evaluated from healthy (n = 108), gingivitis (n = 100), and periodontitis (n = 79) sites of 54 systemically healthy smokers. A modified Beer-Lambert unmixing model that incorporates a non-parametric scattering loss function was used to determine the relative contribution of deoxygenated haemoglobin (Hb) and oxygenated haemoglobin (HbO2 ) to the overall spectrum. The balance between tissue oxygen delivery and utilization in periodontal tissues was then assessed. RESULTS: Tissue oxygen saturation was significantly decreased in the gingivitis (p = 0.016) and periodontitis (p = 0.007) sites, compared to the healthy sites. There was a trend towards increased concentration of Hb and decreased concentration of HbO2 from healthy to diseased sites, without statistical significance (p > 0.05). CONCLUSIONS: Optical spectroscopy can determine tissue oxygenation profiles of healthy and diseased sites in smokers. The spectral profile of periodontal sites in smokers generally resembles those from non-smoking patients.

Receptor activator of nuclear factor-kappa B ligand/osteoprotegerin ratio in sites of chronic periodontitis of subjects with poorly and well-controlled type 2 diabetes.

BACKGROUND: The aim of this study is to evaluate the levels of osteoclastogenesis-related factors (soluble receptor activator of nuclear factor-kappa B ligand [sRANKL] and osteoprotegerin [OPG]) in gingival crevicular fluid (GCF) from subjects with poorly and well-controlled type 2 diabetes and chronic periodontitis before and after periodontal therapy. METHODS: Eighteen subjects with well-controlled diabetes (glycated hemoglobin [HbA1c] levels ≤ 8%) and 20 subjects with poorly controlled diabetes (HbA1c levels >8%) were enrolled in this study. All subjects were submitted to non-surgical periodontal therapy. GCF sampling and clinical periodontal parameters were assessed at baseline and 3 and 6 months post-therapy. Total amounts and concentrations of sRANKL and OPG in GCF were analyzed by enzyme-linked immunosorbent assay (ELISA). RESULTS: Total amounts and concentrations of sRANKL and RANKL/OPG ratios were higher in poorly controlled subjects than in well-controlled subjects at baseline and 3 and 6 months post-therapy (P <0.05). In addition, RANKL/OPG ratios decreased in well-controlled subjects (P <0.05) but not in poorly controlled subjects (P >0.05) at 3 months post-therapy. Almost all clinical parameters improved significantly for both groups post-treatment (P <0.05). CONCLUSION: RANKL/OPG ratios in untreated and treated periodontitis sites may be negatively influenced by poor glycemic control in subjects with type 2 diabetes.

Hypertension may affect tooth-supporting alveolar bone quality: a study in rats.

BACKGROUND: This study evaluates the ligature-induced bone loss (BL) and quality of tooth-supporting alveolar bone in spontaneously hypertensive rats (SHRs) by histometric, histochemical, and immunohistochemical analyses and assesses the effects of lercanidipine on these parameters. METHODS: Wistar rats and SHRs were assigned to one of the following groups: normotensive rats (n = 15), untreated SHRs (n = 15), and treated SHRs (n = 15). The latter group was treated daily with lercanidipine for 45 days. Two weeks after the beginning of drug administration, the first right mandibular molar received a cotton ligature, whereas the contralateral tooth was left unligated. The following parameters were analyzed in the furcation area of decalcified histologic sections: BL, bone density (BD), number of positive cells for tartrate-resistant acid phosphatase (TRAP+), and expression of receptor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin (OPG). RESULTS: In ligated teeth, no significant differences among groups were found regarding BL, TRAP+ cells, and the ratio of RANKL/OPG+ cells (P >0.05), although the expression of RANKL was decreased in the treated SHR group (P <0.05). Increased BL and decreased BD were observed around unligated teeth of the untreated and treated SHR groups (P <0.05). In the furcation area of the unligated teeth, the untreated SHR group presented a higher number of TRAP+ cells and higher ratio of RANKL/OPG+ cells compared to the other groups. CONCLUSIONS: SHRs present harmful alterations in the quality of tooth-supporting bone, independently of inflammation. In addition, the administration of lercanidipine for 45 days decreased the expression of bone-resorption markers.