Porphyromonas gingivalis regulates atherosclerosis through an immune pathway.

Atherosclerosis (AS) is a chronic inflammatory disease, involving a pathological process of endothelial dysfunction, lipid deposition, plaque rupture, and arterial occlusion, and is one of the leading causes of death in the world population. The progression of AS is closely associated with several inflammatory diseases, among which periodontitis has been shown to increase the risk of AS. Porphyromonas gingivalis (P. gingivalis), presenting in large numbers in subgingival plaque biofilms, is the "dominant flora" in periodontitis, and its multiple virulence factors are important in stimulating host immunity. Therefore, it is significant to elucidate the potential mechanism and association between P. gingivalis and AS to prevent and treat AS. By summarizing the existing studies, we found that P. gingivalis promotes the progression of AS through multiple immune pathways. P. gingivalis can escape host immune clearance and, in various forms, circulate with blood and lymph and colonize arterial vessel walls, directly inducing local inflammation in blood vessels. It also induces the production of systemic inflammatory mediators and autoimmune antibodies, disrupts the serum lipid profile, and thus promotes the progression of AS. In this paper, we summarize the recent evidence (including clinical studies and animal studies) on the correlation between P. gingivalis and AS, and describe the specific immune mechanisms by which P. gingivalis promotes AS progression from three aspects (immune escape, blood circulation, and lymphatic circulation), providing new insights into the prevention and treatment of AS by suppressing periodontal pathogenic bacteria.

Plaque control alleviated renal damage that was aggravated by experimental periodontitis in obese rats.

OBJECTIVE: This study aimed to evaluate the influence of experimental periodontitis on renal damage in obese rats. MATERIALS AND METHODS: Thirty-two male Sprague Dawley rats were randomly allocated into 4 groups with 8 animals each: obese rats (obese group), obese rats with periodontitis (periodontitis obese group), obese rats with periodontitis that underwent plaque control (plaque-control obese group), and healthy rats (healthy group). Rats were fed a high-fat diet to establish an obesity model. Experimental periodontitis was induced by local ligation with silk around the bilateral maxillary second molars. The plaque control was accomplished by removing ligations and local wiping with an antiseptic rinse. Histology was used to observe the gingival inflammation and clinical attachment level (CAL) to further assess bone loss and to also observe renal structure. Serum creatinine, urea nitrogen, and kidney injury molecule-1 (KIM-1) levels were measured to evaluate renal function. Renal Toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), serum C-reactive protein (CRP), lipopolysaccharides (LPS), and interleukin-1ß (IL-1ß) were measured to evaluate renal and systemic inflammation. RESULTS: Periodontal histology showed that in the periodontitis obese group, the epithelial barrier was considerably eroded by inflammatory cells, which infiltrated into the subepithelial connective tissue and lamina propria. A periodontal pocket was forming accompanied by the loss of attachment. The extent of infiltration of inflammatory cells and the CAL were significantly higher than those of the obese group (p < .001). In the plaque-control obese group, although the inflammatory condition was significantly improved than in the periodontitis obese group, the clinical attachment level with the presence of fiber hyperplasia could not be restored. Renal histology showed that renal tubular structural damage was aggravated in the periodontitis obese group, including vacuolar degeneration, exfoliation of the proximal tubular epithelial cell lining, multifocal loss of the brush border, and movement of several nuclei from the basement membrane to the lumen. These alterations were improved in the plaque-control obese group. Kidney TLR4 and NF-κB mRNA levels increased significantly in the periodontitis obese group compared to the obese group (p = .015 and p = .015, respectively) and decreased significantly in the plaque-control obese group (p = .028 and p = .021, respectively). Kidney TLR4 and NF-κB protein expression in the plaque-control obese group were significantly lower than those in the periodontitis obese group (p < .001 and p = .043, respectively). Serum creatinine and KIM-1 levels significantly decreased in the plaque-control obese group compared to the periodontitis obese group (p = .001 and p = .002, respectively). At 21 weeks (1 week after periodontal ligation), serum CRP levels in the periodontitis obese group were significantly higher than that in the healthy group (p = .017). Other serum inflammatory markers (LPS and IL-1ß) did not change significantly. CONCLUSION: Experimental periodontitis induced dysfunction and structural destruction of the kidney in obese rats. Plaque control relieved renal damage.

Influence of periodontitis and scaling and root planing on insulin resistance and hepatic CD36 in obese rats.

BACKGROUND: The aim of the study was to explore the influence of periodontitis and scaling and root planing (SRP) on insulin resistance and hepatic CD36 in obese rats with periodontitis. METHODS: Thirty-two specific pathogen free Sprague-Dawley rats were randomly divided into four groups of eight animals each as follows: healthy rats (healthy group), obese rats (obesity group), obese rats with periodontitis (non-therapy group), and obese rats with periodontitis who underwent periodontal SRP (therapy group). Rats were fed with a high-fat diet for 16 weeks to build an obesity model. Periodontal inflammation was induced by performing periodontal ligation with Porphyromonas gingivalis. The tissue around the maxillary second molars, bilaterally, were collected. The periodontal attachment level (from the cemento-enamel junction to the bottom of the periodontal pocket) of the second molars was measured in all groups. All rats were subjected to fasting blood glucose, insulin, and serum C-reactive protein tests (CRP). Insulin resistance was evaluated by homeostasis model assessment of insulin resistance (HOMA-IR), oral glucose tolerance test (OGTT), and area under the curve (AUC). The liver was excised to detect intrahepatic free fatty acid (FFA) levels and pathologic observation. Real-time quantification PCR, western blot, and immunohistochemistry were applied to detect hepatic CD36 expression. RESULTS: Compared with the obesity group, HOMA-IR, AUC, intrahepatic FFA, and protein expression, and mRNA levels of hepatic CD36 in the non-therapy group were significantly increased (P < 0.05). HOMA-IR, AUC, CRP, protein expression, and mRNA levels of hepatic CD36 were all significantly decreased (P < 0.05) 2-weeks after SRP. CONCLUSIONS: Periodontitis increases insulin resistance while scaling and root planning could improve insulin resistance. Hepatic CD36 regulation may be considered a potential mechanism for this phenomenon.

[Effects of non-surgical periodontal therapy on serum inflammatory markers and metabolic level in obese rats].

OBJECTIVE: To investigate the effects of non-surgical periodontal therapy on serum inflammatory factors and metabolism levels in obese rats with experimental periodontitis. METHODS: Sixteen obese rats with experimental periodontitis were randomly divided into treatment group and control group with non-surgical periodontal therapy and no treatment, respectively. Oral glucose tolerance test was performed before treatment and 2 weeks after the treatment. All the rats were sacrificed 2 weeks after treatment and the orbital vein blood was taken to detect fasting blood glucose, fasting insulin, and serum level of C-reactive protein (CRP). Results Two weeks after periodontal treatment, fasting blood glucose (t=2.445, P=0.034) and beta cell function index (t=-2.543, P=0.027) were significantly lower in the treatment group than in the control group. Compared with those in the control group, CRP level (t=2.388, P=0.028) and the area under the curve in the oral glucose tolerance test (t=12.053, P=0.000) decreased significantly in the treatment group. CONCLUSION: Non-surgical periodontal treatment can reduce serum CRP level and improve glucose metabolism in obese rats.

[Beneficial effect of periodontal therapy on insulin resistance and lipid metabolism in obese rats with periodontitis].

OBJECTIVE: To investigate the effect of periodontal therapy in controlling periodontitis and on insulin resistance and lipid metabolism in obese rats with periodontitis. METHODS: Sprague-Dawley rats were randomized into normal group (group C), obese group (group O), periodontitis combined with obesity group (group P) and periodontal treatment group (group T). The obese rats in groups P and T were subjected to ligation of the maxillary second molar with silk thread to induce experimental periodontitis, and the rats in group T received periodontal therapy after the ligation. All the rats were sacrificed at the age of 24 weeks for measurement of blood lipids, insulin and blood glucose levels, and insulin resistance index (HOMA-IR) was calculated. The expressions of insulin receptor substrate-1 (IRS-1) and IRS-2 in the liver tissues were detected using real-time quantitative polymerase chain reaction (RT-PCR). RESULTS: Compared with the obese rats in group O, the rats in group P showed significantly higher HOMA-IR and LDL-C and lower expressions of IRS-1 and IRS-2 mRNA expression and HDL-C level (P<0.05). Compared with those in group P, the mRNA expressions of IRS-1 and IRS-2 and HDL-C level were significantly increased and LDL-C level, TC level and HOMA-IR were all decreased in group T (P<0.05), but the level of TG was comparable between the two groups. Pathological examination revealed lessened inflammatory cell infiltration and tissue destruction in the upper jaw of the rats in group T; the rats in group P presented with the most obvious upper jaw destruction and steatosis and inflammatory cell infiltration in the liver. CONCLUSION: Periodontal inflammation can downregulate the expression of IRS-1 and IRS-2 and increase insulin resistance and dyslipidemia in obese rats. Periodontal therapy produces a beneficial effect in improving insulin resistance and reducing dyslipidemia in obese rats.

[Cytotoxicity evaluation of three kinds of perforation repair materials on human periodontal ligament fibroblasts in vitro].

OBJECTIVE: To select three kinds of perforation repair materials, mineral trioxide aggregate (MTA), Z350, amalgam. And to evaluate the cytotoxicity of three kinds of perforation repair materials on human periodontal ligament fibroblasts (HPDLF) in vitro. METHODS: The proliferation of HPDLF to three perforation repair materials were examined by methyl thiazolyl tetrazolium (MTT) assay at 1, 3 and 5 days. The mRNA expression levels of bone-associated alkaline phosphatase (ALP) and osteocalcin (OC) were determined using a real-time quantitative polymerase chain reaction (PCR). RESULTS: MTA shew almost no inhibition to HPDLF, the expression of ALP mRNA and OC mRNA in the HPDLF cultured on MTA were higher. Z350 induced a slight inhibition to HPDLF, and the expression of ALP mRNA but there was no difference in the expression of OC mRNA. Cell proliferation was significantly impaired by amalgam with grade 3, and the expression of ALP mRNA and OC mRNA were significantly reduced. CONCLUSION: MTA have minimum cytotoxicity on HPDLF and can promote cell differentiation and regenerate of periodontal tissue. Z350 have lower cytotoxicity on HPDLF. Amalgam show highest cytotoxicity on HPDLF in the three materials and inhibit cells differentiation.

[Morphology and microleakage study of repairing subpulpal wall perforation with resinous inlay].

OBJECTIVE: The purpose of this study is to study the sealing ability and the furcal appearance of repairing subpulpal wall perforation with resinous inlay. METHODS: Fifty newly extracted human molars were randomly divided into three experiment groups (group A, group B, group C, 15 teeth each) and one control group (5 teeth). In experiment groups, perforations were made perpendicularly to the center of the pulp chamber floor. Perforations of group A and B were repaired with resinous inlay and sealed by AH Plus sealer and luting glass-ionomer, respectively. Perforations of group C were directly repaired using light-cure composite resin. Perforations were not made in five teeth of control group. The furcal appearances were evaluated under stereomicroscope after repairing. Microleakage was measured by glucose oxidase detection. RESULTS: The fineness rate of furcal appearances with resinous inlay repairing were 83.3%, while the fineness rate of furcal appearances with light-cure composite resin directly repairing were 46.7%. There were statistics difference between resinous inlay repairing and light-cure composite resin directly repairing (P<0.05). There were statistics difference among the daily microleakage of three experiment groups, group A

[Study of apical diffusion of three different kinds of calcium hydroxide preparations in vitro].

PURPOSE: To investigate the diffusion effect of calcium hydroxide in periapical simulation of the diffusion model. METHODS: Pipetman pipette tips, plastic syringes and BHI agar were prepared to be periapical simulation of the diffusion model. 120 simulation models were divided into three groups. Group 1: 100 microl 20% calcium hydroxide suspension were sealed in pipette tips; group 2: 100 microl 90% calcium hydroxide cataplasm were sealed in; group 3: 100 microl calcium hydroxide points were sealed in. By different apical aperture (15#,25#,40#,80#), each group was divided into four subgroups (each subgroup contained 10). Preparation of 12 other simulation models sealed with distilled water were as a control. pH values and Ca(2+) concentration were measured by PH analyzer and calcium analyzer respectively. The data was collected to establish a database, using SPSS13.0 software package, randomized block design ANOVA was performed. RESULTS: The average pH value (8.26, S=0.86) of group 1 was significantly higher than that in group 2 (7.96, S=0.702) and Group 3 (7.83, S=0.59) (P<0.05), but no significant difference was found between group 2 and group 3. The average calcium concentration of group 1 (29.87 ppm. S=10.76) was significantly higher than that in group 2 (24.62 ppm. S=10.40) and group 3(16.42 ppm, S=5.70). There were significant differences among the three groups (P<0.05). The results also showed that the average pH value and the average calcium concentration were increased with apical aperture. There were significant differences between each group (P<0.05). CONCLUSION: The diffusion effect of calcium hydroxide suspension in periapical simulation of the diffusion model is better than calcium hydroxide cataplasm and calcium hydroxide points; the diffusion effect is also proportional to the apical aperture. Supported by Key Research Project of Science and Technology Bureau of Sichuan Province (Grant No.05SG022-007).