Potential association between Fusobacterium nucleatum enrichment on oral mucosal surface and oral lichen planus.

OBJECTIVE: We determined the bacterial community structure of the buccal mucosa in patients with oral lichen planus (OLP) and evaluated the potential association of Fusobacterium nucleatum with OLP. SUBJECTS AND METHODS: We collected buccal mucosal swab samples of patients with OLP (n = 20) and healthy controls (n = 10) and performed 16S rRNA gene sequencing and real-time PCR to determine potentially different bacteria. Damaged and adjacent non-damaged mucosal swab samples of 25 OLP patients were used to detect the amount of F. nucleatum by real-time PCR. RESULTS: Compared with healthy controls, enrichment of Fusobacterium and Granulicatella was more abundant in patients with OLP (p = .0146 and 0.0034). The abundance of Fusobacterium and F. nucleatum was significantly enriched on buccal mucosa of patients with OLP compared with healthy controls (p = .0043 and 0.0235). Compared with adjacent non-damaged buccal mucosa of OLP patients, the amount of F. nucleatum in the damaged mucosa was significantly increased (p = .001). We examined third-level KEGG pathways for bacteria on mucosal surface and found that genes controlling sporulation and ether lipid metabolism were enriched in patients with OLP. CONCLUSIONS: A high amount of F. nucleatum may be associated with OLP. Further studies are required to investigate the precise association of F. nucleatum with OLP.

Scattering center models of backscattering waves by dielectric spheroid objects.

Scattering center models provide a simple and effective way of describing the complex electromagnetic scattering phenomena of targets and have been successfully applied in radar applications. However, the existing models are limited to conducting objects. Numerical results show that scattering centers of dielectric objects are far more complex than conducting objects and most of them are distributed beyond the object. For the lossless and low-loss media, the major scattering contributions to total fields are surface waves and multiple internal reflections rather than the direct reflection. Concise scattering center models for backscattering from dielectric spheroid objects are proposed in this work, which can characterize the backscattered waves by scattering centers with sparse and physical parameters. Good agreement has been demonstrated between the high resolution range profiles simulated by this model with those obtained by Mie series and the full wave numerical method.

MicroRNA-146a regulates the production of cytokines in lymphocytes stimulated by Porphyromonas gingivalis lipopolysaccharide.

OBJECTIVES: This study aimed to investigate the effects of microRNA-146a (miR-146a) on the production of cytokines in lymphocytes stimulated by Porphyromonas gingivalis (P.gingivalis) lipopolysaccharide (LPS). METHODS: Lymphocytes were harvested from mouse spleen and cultured in vitro. The cells were treated with P. gingivalis LPS, miR-146a mimic, or miR-146a inhibitor. Scramble RNA served as the negative control of mimic and inhibitor. The production of inflammatory cytokines was detected by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay. RESULTS: Compared with non-LPS-stimulated group, P. gingivalis LPS could increase the levels of interleukin (IL)-1ß, IL-6, receptor activator NF-κB ligand (RANKL), and IL-10 (P<0.05) and decrease the mRNA level of osteoprotectin (OPG) (P<0.05). However, it did not significantly change the secretion of OPG. Compared with the negative control group, miR-146a mimic upregulated the levels of IL-10 and OPG (P<0.05), downregulated IL-1ß, IL-6, and RANKL (P<0.05). Meanwhile, miR-146a inhibitor had a reverse effect on these cytokines (P<0.05) in P.gingivalis LPS-treated-lymphocytes. CONCLUSIONS: MiR-146a can provide a suitable microenvironment for bone formation by preventing the inflammatory effects of P.gingivalis LPS through the inhibition of IL-1ß, IL-6, and RNAKL, thereby enhancing IL-10 and OPG.

[The effect of B lymphocytes on immune response of periodontal bacteria and osteoclast differentiated reactor-RANKL expression].

PURPOSE: To study whether B lymphocytes involve in bone resorption in periodontal disease by evaluating RANKL expression of B lymphocytes in immune response to aggregatibacter actinomycetemcomitans (Aa). METHODS: The expression of mRNA transcripts involved in day 1 and day 7 responses of cytokines in cultured rat splenocytes was determined by RT-PCR; The percentage of RANKL-expressing IgG positive cells by B cells in cultured rat splenocytes was measured by flow cytometry; and B lymphocytes capacity for induction of osteoclast differentiation was evaluated by TRAP staining. SPSS 10.0 software package was used for statistical analysis. RESULTS: The expression of IL-4 and IL-10 in cultured cells was not changed in the presence of Aa on day 1, after culture for 7 days; The percentage of B lymphocytes, all RANKL mRNA transcripts and percentage of RANKL-expressing IgG positive cells were significantly increased in the presence, compared to the absence of Aa. These increases were considerably greater in cells isolated from immunized than non-immunized rats. B cells from Aa immunized rats significantly increased induction of osteoclast differentiation (P<0.01), and addition of human OPG-Fc into the culture significantly inhibited its induction (P<0.05), and was RANKL-independent. CONCLUSION: B lymphocytes contribute to bone resorption in periodontal disease through involving in the immune response to Aa, up-regulation of RANKL expression and increasing induction of osteoclast differentiation.

[In vitro study on the amelioration of T cell-mediated osteoclastogenesis by anti-RANKL-polyclonal antibody].

PURPOSE: To characterize the effect of receptor activator of NF-kB ligand (RANKL) polyclonal antibody on T cell-mediated osteoclasogenesis. METHODS: Rabbit anti-rat RANKL polyclonal IgG antibody was performed, performing recombinated mouse RANKL-induced osteoclastogenesis in different antibody doses (1microg/mL,5microg/mL and 10microg/mL), the number of TRAP positive multinuclear cells (cells/well) was calculated under microscopy. The cervical lymph nodes in rats were enriched T-cells for in vitro experiments. The T cell-mediated osteoclastogenesis was tested by co-culture assay of RAW 264.7 cells with formalin-fixed T cell or T cell supernatant, the number of TRAP positive multinuclear cells (cells/well) was calculated under microscopy. In some experiments, the concentration of sRANKL (soluble RANKL) was measured in supernatant by ELISA (pg/mL). SPSS 11.5 software package was used for statistical analysis. RESULTS: Rabbit anti-rat RANKL antibody inhibited osteoclastogenesis by recombined mouse RANKL-induced, and dose-dependent; Anti-RANKL antibody inhibited T cell and culture supernatant induced osteoclastogensis, significantly different from that in the group without antibody(P<0.05), and dose-dependent; Anti-RANKL specific antibody also markedly reduced sRANKL concentration in supernatant, significantly different from that in the control group without antibody(P<0.05). CONCLUSIONS: Anti-RANKL specific antibody blocks direct effect of RANKL and interferes with immune T cell-mediated bone resorption by reduction of sRANKL level.