RESUMO
Background: Polylactic-co-glycolic acid and zinc oxide (PLGA-ZnO) nanocomposite has been investigated for its antibacterial properties, which could be beneficial for adding to wound dressings after periodontal surgery. However, its cytotoxicity against human gingival fibroblasts (HGFs) remains unclear and should be evaluated. Methods: ZnO nanoparticles were synthesized using the hydrothermal method. These metallic nanoparticles were incorporated into the PLGA matrix by the solvent/non-solvent process. The nanomaterial was evaluated by field emission scanning electron microscopy (FESEM), Fourier transform infrared (FTIR), thermogravimetric analysis (TGA), and x-ray diffraction (XRD) analyses. HGF cells were acquired from the National Cell Bank and categorized into four groups: ZnO, PLGA, ZnO-PLGA, and control. The cells were exposed to different ZnO (1, 20, 40, 60, 80, and 100 µg/mL) and PLGA (0.2, 4, 8, 12, 16, and 20 µg/mL) concentrations for 24 and 48 hours. The cytotoxicity was tested using the MTT assay. The data were analyzed using SPSS 25, and P<0.05 was considered statistically significant. Results: ZnO nanoparticles exhibited significant toxicity at≥40 µg/mL concentrations after 24 hours. Cell viability decreased significantly at all the tested concentrations after 48 hours of exposure. PLGA-ZnO cell viability in 24 hours was similar to the control group for all the concentrations up to 80 µg/mL. Conclusion: ZnO nanoparticles could be toxic against HGF in high concentrations and with prolonged exposure. Therefore, incorporating ZnO nanoparticles into a biocompatible polymer such as PLGA could be a beneficial strategy for reducing their toxicity.
RESUMO
Statement of the Problem: Periodontitis is a multifactorial disease caused by periopathogens and its severity is determined by the host immune response. Gingival crevicular fluid (GCF) can be used for non-invasive testing to assess the host response in periodontal treatment. Pentraxins are the classic mediators of inflammation and pentraxin-3 can be used as a marker to assess response to therapy, which was investigated in this study. Purpose: This study aimed to assess the effect of non-surgical periodontal therapy on GCF level of pentraxin-3 in patients with chronic periodontitis. Materials and Method: 25 patients with chronic periodontitis (CP) and 25 periodontally healthy controls were evaluated. Pocket probing depth, clinical attachment loss, plaque index, gingival index, and bleeding on probing were measured in both groups. GCF samples were collected using paper strips to assess the level of pentraxin-3. In the CP group, GCF samples were collected from the highest clinical attachment loss, pocket probing depth, and bone loss at baseline and six weeks after non-surgical therapy. The level of pentraxin-3 in the GCF was quantified by enzyme-linked immunosorbent assay (ELISA). Data were analyzed using SPSS version 23. Results: Pentraxin-3 in GCF of CP patients before treatment (6.72±4.63 ng/mL) was higher than the control group (4.43±2.85 ng/mL). Pentraxin-3 in patients after non-surgical therapy (3.2±2.66 ng/mL) decreased significantly compared to the baseline (p= 0.04) and its level after treatment was not significantly different from the control group (p= 0.14). Conclusion: Pentraxin-3 in GCF of CP patients was higher than healthy controls and decreased in response to non-surgical periodontal therapy. Thus, it can be used as an inflammatory marker for detection of patients at risk of CP. However, further studies with larger samples and longer follow-ups in different populations are required to confirm our findings.
