The expression levels of chemotaxis-related molecules CXC chemokine receptor 1, interleukin-8, and pro-platelet basic protein in gingival tissues.

Background/purpose: Excessive host immune response is thought to be an important cause of periodontal tissue damage during periodontitis. The potent chemotaxis produced by locally released chemokines is the key signal to trigger this response. Here, we aimed to investigate the expression of CXC chemokine receptor 1 (CXCR1), and chemokines interleukin-8 (IL-8) and pro-platelet basic protein (PPBP) in human inflammatory gingival tissues compared with healthy tissues. Materials and methods: A total of 54 human gingival tissues, 27 healthy and 27 inflammatory samples, were collected. Fifteen specimens of each group were employed for quantitative reverse transcription polymerase chain reaction to determine the mRNA levels of CXCR1, IL-8, and PPBP. Six samples of each group were used for Western blotting to investigate the protein expression of CXCR1 and for enzyme-linked immunosorbent assay to evaluate the protein levels of IL-8 and PPBP, respectively. Results: The mRNA levels of chemokine receptor CXCR1, chemokine IL-8, and PPBP in inflammatory gingival tissues were significantly higher than those in healthy controls (P < 0.05). The protein levels of CXCR1, IL-8, and PPBP in inflammatory gingival tissues were also significantly higher than those in healthy gingival tissues (P < 0.05). Conclusion: When compared to healthy gingival tissues, the expression of CXCR1, IL-8, and PPBP in inflammatory gingival tissues is higher.

Subgingival Microbial Profiles of Young Chinese Adults with Stage I/II Periodontitis, Gingivitis and Periodontal Health Status.

OBJECTIVE: To analyse the subgingival microbiota of Stage I/II periodontitis, gingivitis with different degrees of severity, and periodontal health in subjects in a Chinese young adult population. METHODS: Subgingival plaque samples were collected from 15 Stage I/II periodontitis patients, 38 gingivitis patients and 15 periodontally healthy individuals, all aged from 18 to 21 years. Gingivitis patients were divided into two subgroups according to the Bleeding Index (BI) of their sampled teeth: gingivitis with above median BI (G-HBI) and below median BI (G-LBI). The subgingival plaque samples were collected from teeth 16, 26, 36, 46, 11 and 31 according to FDI notation. The V3-V4 region of the 16S rRNA gene of all the samples was sequenced and analysed. RESULTS: The Stage I/II periodontitis, gingivitis and periodontal health groups showed distinct subgingival microbiota profiles. When the gingivitis patients were stratified into two subgroups, the community structure of G-HBI showed no significant difference from early-stage periodontitis, but differed from G-LBI and the healthy group. Most periodontitis-related taxa were most abundant in Stage I/II periodontitis, followed by G-HBI, G-LBI and the periodontally healthy group. Porphyromonas gingivalis, Filifactor alocis, Tannerella forsythia, Saccharibacteria TM7 G-5 356, Lachnospiraceae G-8 500, Peptostreptococcaceae spp. and Syntrophomonadaceae VIIIG-1 435 were associated with Stage I/II periodontitis. Porphyromonas 275, Leptotrichia 417 and Saccharibacteria TM7 G-2 350 were associated with gingivitis. Porphyromonas gingivalis was significantly more abundant in G-HBI than in G-LBI. CONCLUSION: Within the limitations of this preliminary study, gingivitis and early-stage periodontitis were associated with an increased degree of dysbiosis in the subgingival microbiota in a Chinese young adult population.

[Effect of peroxisome proliferator-activated receptor-γ on endothelial cells oxidative stress induced by Porphyromonas gingivalis].

OBJECTIVE: To detect the degree of oxidative stress in the process when Porphyromonas gingivalis (P. gingivalis) stimulates human vascular endothelium, And to investigate the effect of peroxisome proliferator-activated receptor(PPAR)γ on oxidative stress during this process. METHODS: Human vascular endothelial cells (HVECs) line EA.hy926 (American Type Culture Collection ,United States) was cultured in high glucose Dulbecco's modified eagle medium (DMEM). Four groups were designed: control group, P. gingivalis infected group, PPARγ activated group and PPARγ blocked group. In control group HVECs were cultured with only DMEM. In P. gingivalis infected group, HVECs were time-dependently stimulated by P. gingivalis W83 from 0 to 12 h. In PPARγ activated group or PPARγ blocked group, PPARγ was pre-activated or blocked by a representative PPARγ agonist(15d-PGJ2 10 µmol/L) or antagonist (GW966210 µmol/L) 30 minutes before the cells were stimulated by P. gingivalis. At 0, 0.5, 1, 1.5, 2, 4, 8, and 12 h, the culture medium was collected individually and centrifuged, and the supernatant was stored for assay. Glutathione peroxidase (GSH-PX) and malondialdehyde (MDA) were analysed by enzyme-linked immunosorbent assay. Cellular reactive oxygen species (ROS) were detected through 2',7'-dichlorofluorescin diacetate (DCFA-DA) fluorescent probe at various time points of the different groups. RESULTS: In P. gingivalis infected group, the levels of GSH-PX [(5.56±0.97) µmol/L] and MDA [(0.84±0.18) nmol/L] were significantly higher than those in control group [GSH-PX(4.71±0.64) µmol/L, MDA (0.59±0.18) nmol/L)]. The levels of GSH-PX and MDA in PPARγ activated group [GSH-PX (5.38±0.84) µmol/L, MDA (0.84±0.22) nmol/L] and in PPARγ blocked group [GSH-PX (5.37±0.76) µmol/L, MDA (0.85±0.14) nmol/L] were significantly higher than those in control group (P<0.05). In the PPARγ activated group, the levels of GSH-PX at 0.5 and 8 h were significantly higher than those from 1.5 h to 4 h (P<0.05), while no difference was observed on the MDA levels at different time points. There was no significant difference at various time points for the levels of GSH-PX and MDA in PPARγ blocked group. The level of cellular ROS detected by DCFH-DA in P. gingivalis infected group was significantly higher than that in control group (10 108.65 ± 1 805.18 vs. 6 049.06 ± 1 199.19,P<0.05). No difference was observed between PPARγ activated group (7 120.94±1 447.30) or PPARγ blocked group (6 727.35±1 483.68) and control group. CONCLUSION: Oxidative stress happens when P. gingivalis stimulates human vascular endothelium. PPARγ may involve in modulating oxidative stress during this process.