Background: Vital pulp therapy preserves and maintains the integrity and the health of dental pulp tissue that has been injured by trauma, caries or restorative procedures. The enhancement of cells viability and formation of reparative dentine and new blood vessels are vital determinants of the success of direct pulp capping. Therefore, the aims of this study was to evaluate and compare the in vitro osteogenic, odontogenic and angiogenic effects of mineral trioxide aggregate (MTA), calcium hydroxide [Ca(OH) 2 ], Biodentine and Emdogain on dental pulp stem cells (DPSCs) and examine the effects of the tested materials on cell viability. Methods: DPSCs were treated with MTA, Ca(OH) 2 , Biodentine or Emdogain. Untreated cells were used as control. The cell viability was measured by MTT assay on day 3. Real-Time PCR with SYBR green was used to quantify the gene expression levels of osteogenic markers (alkaline phosphatase and osteopontin), odontogenic marker (dentin sialophosphoprotein) and angiogenic factor (vascular endothelial growth factor) on day 7 and day 14. Results: All capping materials showed variable cytotoxicity against DPSCs (77% for Emdogain, 53% for MTA, 26% for Biodentine and 16% for Ca(OH) 2 compared to control (P value < 0.0001). Osteopontin (OPN) and dentin sialophosphoprotein (DSPP) gene expression was increased by all four materials. However, alkaline phosphatase (ALP) was upregulated by all materials except Emdogain. Vascular endothelial growth factor (VEGF) expression was upregulated by all four tested materials except Ca(OH) 2. Conclusions: Our results suggest MTA, Biodentine and Emdogain exhibit similar attributes and may score better than Ca(OH) 2. Emdogain could be a promising alternative to MTA and Biodentine in enhancing pulp repair capacity following dental pulp injury. However, further future research is required to assess the clinical outcomes and compare it with the in vitro findings.
T cells may interact with a number of bacterial surface antigens, an encounter which has the potential to downmodulate host immune responses. Neisseria meningitidis, a human colonizer and an agent of septicemia and meningitis, expresses Opa proteins which interact with the CEACAM1 receptor expressed on activated T cells. Since CEACAM1 can act as an inhibitory receptor and T cells in subepithelial tissues may encounter whole bacteria, which often express Opa proteins in vivo, this study assessed primarily if Opa proteins expressed on meningococci affect T-cell functions. In addition, Opa-containing outer membrane vesicles (OMV) have been used as vaccine antigens, and therefore Opa ؉ and Opa ؊ OMV were also studied. While Opa ؉ bacteria adhered to CEACAM-expressing T cells, both the Opa ؉ and Opa ؊ phenotypes induced no to a small transient depression, followed by a prolonged increase in proliferation as well as cytokine production. Such responses were also observed with heat-killed bacteria or OMV. In addition, while anti-CEACAM antibodies alone inhibited proliferation, on coincubation of T cells with bacteria and the antibodies, bacterial effects predominated and were Opa independent. Thus, while Opa proteins of N. meningitidis can bind to T-cell-expressed CEACAM1, this is not sufficient to overcome the T-cell recognition of bacterial factors, which results in a proliferative and cytokine response, an observation consistent with the ability of the host to establish lasting immunity to Opa-expressing meningococci that it frequently encounters. The data also imply that Opa-proficient vaccine preparations may not necessarily inhibit T-cell functions via CEACAM1 binding.
PurposeThe aim of this study was to evaluate CXCL10 as a biomarker for periodontitis by determining the CXCL10 levels in saliva, serum, and gingival crevicular fluid (GCF) samples from periodontally healthy control subjects and adult subjects with chronic periodontitis.Patients and methodsAdult patients seeking dental treatment at Umm Al-Qura University dental clinic underwent a complete periodontal examination, and saliva, serum, and GCF samples were collected. Subjects were classified as chronic periodontitis patients (n=31) if they have a periodontal probing depth (PD) of ≥4 mm and/or clinical attachment level (CAL) of ≥3 mm in >30% of the teeth. The control group (n=25) had PD ≤3 mm and/or CAL ≤2 mm. ELISA was performed to determine the concentration of CXCL10 in saliva, serum, and GCF samples. Student’s t-test was carried out to evaluate the significant difference between different groups. Spearman’s correlation test was used to analyze the relationship between the levels of CXCL10 and the clinical periodontal parameters. P-value of ≤0.05 was considered significant.ResultsSignificantly higher concentrations of CXCL10 were found in saliva and serum in chronic periodontitis patients as compared with the controls (272±60.4 pg/mL and 72±13.4 pg/mL vs 130±22.2 pg/mL and 44.08±4.5 pg/mL, P≤0.05). The CXCL10 levels in GCF were higher in the periodontitis group as compared with the control group (66.36±32.0 pg/mL and 44.56±17.5 pg/mL, respectively); the difference did not reach statistical significance (P≥0.05). Moreover, serum CXCL10 level was significantly higher in periodontitis patients with moderate to severe bone loss as compared with those with mild bone loss (71.05±4.7 pg/mL vs 54.8±7.7 pg/mL, P≤0.05). The serum CXCL10 levels were found to be related to CAL measurements (r=0.3, P=0.026), while the saliva CXCL10 levels were related to PD measurements (r=0.8, P=0.0007).ConclusionCXCL10 is significantly increased in periodontitis subjects as compared with controls and could be used as a marker for periodontal disease.
Objective The main purpose of this article was to evaluate the effect of probiotics used as an adjunctive to scaling and root planing (SRP) on the periodontal parameters and matrix metalloproteinase-8 (MMP-8) levels in gingival crevicular fluid (GCF) of chronic periodontitis patients. Materials and Methods A total of 25 chronic periodontitis patients who completed the treatment course of 40 subjects, aged 25 to 58 years, participated in this study. They were categorized into two groups: the first group was treated by SRP while the second group was treated by SRP and probiotic lozenges twice a day for 30 days. All patients were evaluated clinically by measuring the plaque index, bleeding index (BI), pocket depth, clinical attachment loss, and immunologically by assaying GCF/MMP-8 at baseline and 30 days after periodontal management. Results There was a significant improvement in periodontal parameters after SRP treatment with and without probiotic lozenges in both groups. However, there was a significant decrease in the BI (p = 0.05) in SRP and probiotic lozenges group after 30 days compared with SRP alone. In addition, there was a significant decrease in GCF/MMP-8 levels after 30 days in patients managed by SRP only (p = 0.017) compared with the baseline in both groups, whereas a highly significant decrease in patients treated by SRP and probiotics (p = 0.001). Conclusion The current study suggested that the probiotics might have a beneficial effect on clinical and immunological outcomes in the management of chronic periodontitis patients. Further research is needed on a large-scale population and for a long recall time to confirm the response to probiotics as an adjunctive to SRP.
SummaryNew Zealand Black (NZB) mice spontaneously develop autoimmune haemolytic anaemia (AIHA). Here the effect of injecting NZB mice with plasmids encoding IL-4 (pIL-4) or IL-10 (pIL-10) on NZB disease was tested. Both constructs delayed the development of anaemia as judged by increased haematocrit values as compared with controls, but neither altered the IgG1 to IgG2 red blood cell (RBC) bound autoantibody levels. The increased haematocrit value was associated temporally with increased RBC bound IgG in NZB mice treated with pIL-10, but not pIL-4. By contrast, up-regulation of splenic macrophage Fcg g g g RIIb2 mRNA was associated temporally with increased haematocrit values in NZB mice given pIL-4. However, no such increase occurred in NZB mice that inhaled a peptide containing a dominant T-cell epitope, although this treatment is known to bias the autoimmune response towards Th2 and to reduce the severity of anaemia. It is considered that IL-4 treatment, in part, ameliorates NZB anaemia by increasing the expression of the inhibitory Fcg g g g RIIb2 and thereby reducing the capacity of splenic macrophages to phagocytose autoantibody coated RBC, but that this mechanism does not explain the beneficial effects of the inhaled peptide.
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