Antimicrobial Efficacy of Blended Essential Oil and Chlorhexidine against Periodontal Pathogen (P.gingivalis)-An In Vitro Study.

Background: Essential oils (EOs) have a considerable amount of therapeutic and preventive effect in treating dental diseases due to their wider potential as antibacterial and anti-inflammatory agents. EOs like virgin coconut oil, eucalyptus oil, peppermint oil thyme oil, and clove oil, when used in combination, may further have enhanced antimicrobial effects. However, limited information exists on the synergistic effect of these oils when used in combination, especially on the primary periodontal pathogen Porphyromonas gingivalis. Aim: The current study aims to compare the antimicrobial efficacy of commercially available EO on the periodontal pathogen, P. gingivalis, in comparison to chlorhexidine (CHX). Materials and Methods: Antimicrobial efficacy of EO and CHX was assessed at various concentrations against the periodontal pathogen P. gingivalis, by evaluating the minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC). Results: P. gingivalis was seen to be sensitive at a MIC of 100 µg/ml and 50 µg/ml concentration of the EO, which is regarded as the MIC of EO against P. gingivalis and CHX effectively inhibited microbial growth at 0.4 µg/ml. Conclusion: A combination of EOs possesses a potent antibacterial activity against P. gingivalis, and the antibacterial efficacy increases with increasing concentration of EOs.

Neuroprotective role of luteolin against lead acetate-induced cortical damage in rats.

Luteolin (LUT) is a glycosylated flavonoid compound that has multiple beneficial pharmacological and biological impacts. The current investigation was undertaken to evaluate the putative neuroprotective potency of LUT against neuronal damage induced by lead acetate (PbAc). Twenty-eight rats were placed into four equal groups. Group 1: served as the control group, group 2: rats were supplemented orally with LUT (50 mg kg-1), group 3: rats were intraperitoneally injected with PbAc (20 mg kg-1), and group 4: rats were pretreated with LUT before PbAc injection with the same doses. All animals were treated for 7 days. The exposure to PbAc increased the concentration of lead in the cortical tissue, neuronal lipid peroxidation, and nitric oxide (NO) production and decreased the antioxidant enzymes. Additionally, PbAc enhanced a neuroinflammatory response in the cortical tissue through increasing the pro-inflammatory cytokines secretion and inducible NO synthase expression. Moreover, cortical cell death was recorded following PbAc intoxication as evidenced by the enhancement of the proapoptotic and inhibiting the antiapoptotic markers. Interestingly, LUT supplementation reversed the cortical adverse reactions induced by PbAc. Taken together, these findings may suggest that LUT may be useful for attenuating neuronal damage induced by PbAc through inhibiting the oxidative damage, neuroinflammation, and the cortical cell death.