Evaluation of adding nanosized natural zeolite to photodynamic therapy against P. gingivalis biofilm on titanium disks.

BACKGROUND: Antibacterial photodynamic therapy (aPDT) can be used as an adjunctive therapy for eliminating bacterial biofilm. The application of nanotechnology in aPDT, which is a growing trend, has improved the delivery of photosensitizers (PSs) into microorganisms. Encapsulation of molecules and ions is considered an outstanding potential feature of zeolites. This study sought to enhance the effect of aPDT using a diode laser (810 nm) with a potential PS, indocyanine green (ICG), combined with nanosized natural zeolite (NZ), against biofilm of P. gingivalis on sandblasted, large-grit, and acid-etched (SLA) implant titanium disks surface. METHODS: A bacterial suspension of standard P. gingivalis (™ATCC® 33277) strains was prepared. To prepare bacterial biofilm, the titanium disks were added to 48 microtubes containing bacterial suspension, and divided into eight groups, i.e., the control groups (positive and negative), and 6 test groups (ICG; NZ; Diod laser; NZ+ICG; aPDT; NZ+aPDT). After the treatments, the total number of colony-forming units per disk was calculated. Finally, the data was analyzed, and the eight groups were compared together. RESULTS: The highest reduction in the number of P. gingivalis was seen in group 8 (NZ+aPDT) with 3.55 log10 CFU/ml and the antibacterial effect of 45.7% compared with the negative control group. Conversley, group 5 (Diode Laser solely) represented the highest mean of colony count with the lowest antibacterial effects per disk (6.42 log10 CFU/ml, 1.8%). CONCLUSIONS: The antibacterial effect of NZ+aPDT against P. gingivalis biofilm was noticeable. Thus, adding NZ to ICG improved the result of aPDT in this study.

Comparison of relative TLR-2 and TLR-4 expression level of disease and healthy gingival tissue of smoking and non-smoking patients and periodontally healthy control patients.

BACKGROUND: Toll-like receptors are a family of sensor proteins that induce the inflammatory diseases in context of microbial infection. The role of these proteins in periodontal disease and their interaction with smoking status are yet to be investigated. The aim of the present study was to evaluate the effect of smoking on gene expression of toll like receptor 2 (TLR-2) and toll-like receptor 4 (TLR-4) in patients with periodontitis. METHODS: RNAs were extracted from gingival biopsies of healthy sites (no bleeding on probing and pocket depth ≤3 mm) as well as diseased sites (with bleeding on probing and pocket depth ≥5 mm) of 20 smoker and 17 non-smoker subjects with chronic periodontitis. Gingival biopsies from eight periodontally healthy, never-smoker subjects served as control. Real-time PCR was carried out to evaluate the relative quantities of TLR-2 and TLR-4 mRNA concentrations. RESULTS: Regardless of smoking status, the relative expression levels of TLR-2 and TLR-4 were significantly greater (about 3 fold) at diseased sites compared to healthy sites of patients with periodontitis and healthy controls (p < 0.05). In sites with periodontitis, smoking caused an increase of about 6.5 fold in mRNA levels of TLR-4 in gingival tissue (p < 0.05). CONCLUSIONS: Although periodontitis might significantly increase TLR-2 and TLR-4 gene expression in gingival tissues, smoking habit in periodontitis subjects could selectively potentiate TLR-4 gene expression.