Comparison of trabecular bone structure in individuals with healthy periodontium and stage III/IV, grade C periodontitis by fractal analysis.

OBJECTIVE: The aim was to perform fractal analysis (FA) to compare differences in trabecular microarchitecture in interdental and antegonial regions on panoramic radiographs in periodontally healthy patients and those with stage III/IV, grade C periodontitis, and to compare the effects of patient age and sex on FA results. STUDY DESIGN: Clinical and radiographic records from 33 periodontally healthy individuals and 28 individuals with aggressive periodontitis were obtained from the faculty archives. Three regions of interest (ROIs) were chosen bilaterally from interdental bone around the mandibular first molar and canine and the antegonial region. The mean fractal dimension (FD) values of the ROIs were calculated. Significance of differences was established at P < .05. RESULTS: FD values of all 3 ROIs in the periodontitis group were significantly lower than values in the control group (P ≤ .004). FD was not affected by patient age (P = .357) or sex (P = .216). There were no significant correlations between FD and age in either group (P ≥ .093). FD values differed significantly between sexes in only one ROI. CONCLUSIONS: FA can effectively detect trabecular microarchitectural differences in patients with aggressive periodontitis compared to periodontally healthy individuals. This technique might be useful in predicting the susceptibility of patients to periodontal disease.

Celastrol restricts experimental periodontitis related alveolar bone loss by suppressing inflammatory cytokine response.

Introduction: Periodontitis is a common chronic inflammatory disease characterized by the destruction of the supporting structures of the teeth. The host defense mechanisms are responsible for inflamatuar and destructive reactions in periodontitis. Celastrol is one of the most promising components of the plant in Eastern and Southern China that has a long history of use in traditional medicine for the treatment of inflammatory conditions. Aim: The aim of this animal study was to inspect the preventive or restrictive effects of celastrol on periodontitis-related inflammatory host response and alveolar bone loss. Methods: 24 male Sprague Dawley rats were randomly assigned into 3 groups: control, experimental periodontitis (Ep), and experimental periodontitis-celastrol (Ep-Cel). Periodontitis was induced by placing ligatures sub-paramarginally around the mandibular first molars of the rats in the Ep and Ep-Cel groups and maintaining the ligatures for 15 days. For 14 days following the ligature placement, celastrol administration (1 mg/kg BW day) for the Ep-Cel group and vehicle injection for the control and Ep groups was carried out. At the end of the experiment, mandibula and gingiva samples were obtained after the euthanasia. Alveolar bone loss was measured on serial histological slices; Tumor Necrosis Factor-α and Interleukin-1ß levels were measured on gingiva samples by ELISA. Results: Systemic celastrol administration significantly restricted the alveolar bone loss that was higher in rats with periodontitis. (p < 0.05) Tumor Necrosis Factor-α and Interleukin-1ß levels that were high in the gingiva of the rats with periodontitis were found significantly lower in rats administered celastrol. (p < 0.05). Conclusion: Celastrol restricted periodontitis-related alveolar bone loss by suppressing the inflammatory response.

Remediation of Pb-diesel fuel co-contaminated soil using nano/bio process: subsequent use of nanoscale zero-valent iron and bioremediation approaches.

The effectiveness of the nano/bio process was investigated as a remediation option for co-contaminated soils. Nano/bio process is a hybrid treatment method that may be defined as the use of nanoscale zero-valent iron (nZVI) and bioremediation approaches subsequently/concurrently. Different bioremediation approaches (bioattenuation, biostimulation, and/or bioaugmentation) were performed together with nZVI application to remediate Pb- and diesel fuel-spiked soils. Nutrient (N and P) and activated sludge amendment were made to realize biostimulation and bioaugmentation, respectively. The nZVI application decreased the total percentage of the most mobile and bioavailable soil Pb fractions (exchangeable and carbonate-bound) from 68.3 to 31.7%. The biodegradation levels of nZVI-applied co-contaminated soils were significantly higher than the soils without nZVI indicating the positive effect of the reduced mobility, bioavailability, and toxicity of Pb content. The use of nano/biostimulation or nano/bioaugmentation treatments resulted in higher than 60% total n-alkane degradation, whereas 89.5% degradation was obtained by using nano/biostimulation + bioaugmentation. Hydrocarbon-degrader strains belonging to phyla Actinobacteria, Proteobacteria, or Firmicutes were identified from samples subjected to nano/bio process and the strains from biostimulation and bioaugmentation treatments were different. These results indicate that the stress on the microbial population caused by the co-contamination might be subsided and the biodegradation of alkanes might be improved by using the nano/bio process.

Periodontitis exacerbates the renal degenerative effects of obesity in rats.

BACKGROUND/OBJECTIVES: Obesity and periodontitis are systemic subclinical inflammatory diseases with established negative renal effects. The aim of this animal study was to thoroughly investigate the possible effects of these two diseases on renal structure and function. METHODS: Thirty-two male Sprague Dawley rats were divided into four groups: control (C), obesity (Ob), experimental periodontitis (Ep), and Ob + Ep. The first 16 weeks of the experiment were aimed for the induction of obesity and the last 5 weeks for the induction of periodontitis. Throughout the experimental period, the C and Ep groups were fed standard rat chow, while the Ob groups (Ob and Ob + Ep) were fed high-fat rat chow. Right after the establishment of obesity, periodontal tissue destruction was achieved by placing 3.0 silk sutures in sub-paramarginal position around the cervices of mandibular right-left first molar teeth and preserving them for 5 weeks. On the last day of the 22nd week, following blood collection, all rats were euthanized, and kidneys and mandibles were collected. Alveolar bone loss was measured on microcomputed tomographic slices. Histopathological evaluations (light microscopy, semi-quantitative analysis of renal corpuscle area, and immunohistochemical analysis of caspase-3 activity) were done on right kidneys and biochemical evaluations (malonyl-aldehyde [MDA], glutathione [GSH], total oxidant status [TOS], total antioxidant status [TAS], oxidative stress [OSI], tumor necrosis factor-α [TNF-α], interleukin-1ß [IL-1ß], matrix metalloproteinase [MMP]-8, MMP-9, and cathepsin D [CtD] levels) were done on left kidneys. Renal functional status was evaluated with levels of serum creatinine, urea, and cystatin C. RESULTS: Periodontal bone loss was significantly higher in the Ep and Ob + Ep groups, compared with the C and Ob groups (p < .05). All parameters except TAS and GSH were highest in the Ob + Ep group, and the differences were statistically significant compared with the control group (p < .05). Although the mean TAS and GSH levels were lower in the Ob + Ep group than the other groups, the differences were not statistically significant (p > .05). While the atypical glomeruli score was significantly higher in the Ob + Ep group than in all other groups (p < .05), the acute tubular necrosis and histopathological scores were significantly different only compared with the control group (p < .05). CONCLUSION: This experimental study showed that the negative effects of the co-existence of periodontitis and obesity on inflammatory stress and apoptotic changes in the kidneys together with the functional parameters were significantly more severe, compared with the presence of one of these diseases alone. TNF-α could have a central role in the periodontitis and obesity-related structural and functional renal changes.

Melatonin improves periodontitis-induced kidney damage by decreasing inflammatory stress and apoptosis in rats.

BACKGROUND: Two main aims of this animal study were to inspect the possible effects of periodontitis on the structure and functions of the kidneys and the therapeutic effectiveness of melatonin. METHODS: Twenty-four male Sprague-Dawley rats were randomly divided into three groups: control, experimental periodontitis (Ep), and Ep-melatonin (Ep-Mel). Periodontitis was induced by placing 3.0-silk sutures sub-paramarginally around the cervix of right-left mandibular first molars and maintaining the sutures for 5 weeks. Then melatonin (10 mg/kg body weight/day, 14 days), and the vehicle was administered intraperitonally. Mandibular and kidney tissue samples were obtained following the euthanasia. Periodontal bone loss was measured via histological and microcomputed tomographic slices. On right kidney histopathological and immunohistochemical, and on the left kidney biochemical (malonyl-aldehyde [MDA], glutathione, oxidative stress [OSI], tumor necrosis factor [TNF]-α, interleukin [IL]-1ß, matrix metalloproteinase [MMP]-8, MMP-9, and cathepsin D levels) evaluations were performed. Renal functional status was analyzed by levels of serum creatinine, urea, cystatin-C, and urea creatinine. RESULTS: Melatonin significantly restricted ligature-induced periodontal bone loss (P <0 .01) and suppressed the levels of proinflammatory cytokines (TNF-α and IL-1ß), oxidative stress (MDA and OSI), and proteases (MMP-8, MMP-9, and CtD) that was significantly higher in the kidneys of the rats with periodontitis (P <0.05). In addition, periodontitis-related histological damages and apoptotic activity were also significantly lower in the Ep-Mel group (P <0.05). However, the markers of renal function of the Ep group were detected slightly impaired in comparison with the control group (P >0.05); and the therapeutic activity of melatonin was limited (P >0.05). CONCLUSION: Melatonin restricts the periodontitis-induced inflammatory stress, apoptosis, and structural but not functional impairments.