RESUMO
OBJECTIVES: The purpose of the present study was to discover how hyperbaric oxygen therapy (HBOT) could reduce orthodontic relapse by altering the expressions of hypoxia-inducible factor (HIF)-1 messenger ribonucleic acid (mRNA), type I collagen (Col I), and matrix metalloproteinase-1 (MMP-1) in the gingival supracrestal fibers in rabbits. MATERIALS AND METHODS: This study involved 44 male rabbits (Oryctolagus cuniculus) randomly divided into the normal group (K0), the orthodontic group without HBOT (K1), and the orthodontic group with HBOT (K2). Following orthodontic separation of the two upper central incisors, a retention phase and relapse assessment were performed. The HBOT was performed for a period of 2, 4, 6, 8, and 10 days after retention. HIF-1α transcription was assessed employing real-time polymerase chain reaction, whereas Col I and MMP-1 proteins were examined using immunohistochemistry. The orthodontic relapse was measured clinically using a digital caliper. STATISTICAL ANALYSIS: We used the one-way analysis of variance followed by Tukey's post hoc for multiple comparisons to measure differences between pairs of means; a p-value of 0.05 was considered statistically significant. RESULTS: HBOT significantly increased the HIF-1α mRNA expression (p = 0.0140), increased Col I (p = 0.0043) and MMP-1 (p = 0.0068) on the tensioned and pressured side of the gingival supracrestal fibers, respectively, and clinically decreased the relapse (p = 3.75 × 10-40). CONCLUSION: HBOT minimizes orthodontic relapse by influencing HIF-1α expression, collagen synthesis (Col I), and degradation (MMP-1). This result suggests that HBOT has the potential to be used as an adjunctive method in the orthodontic retention phase.
RESUMO
BACKGROUND: Dental caries is a widespread disease that causes dental tissue destruction and leads to local and general complications. Gram-positive bacteria including Streptococcus mutans, Streptococcus sanguinis, and Enterococcus faecalis take part in dental caries formation. Gram-positive bacteria have cell walls that consistof a thick layer of peptidoglycan which maintains the strength and rigidity of the bacteria, as well as bacteria guard from internal osmotic pressure. The biosynthesis of peptidoglycan involves many enzymes, including the Mur family, penicillin binding protein (PBP), and sortases. PURPOSE: This research has the intention to screen and examine the antibacterial compound of edible plant Kemangi (Ocimum basilicum L.) in terms of how it fights against some oral pathogenic bacteria of E. faecalis ATCC 29212, S. mutans ATCC 25175, and S. sanguinis ATCC 10566. MATERIALS AND METHODS: The O. basilicum L. was macerated by several organic solvents to obtain the extracts, before then being purified using several combinations of chromatography methods and the compound was discovered via spectroscopic methods. For the assay against bacteria, the extracts and compounds were tested using agar well diffusion and microdilution assay. RESULTS: The isolated compound was identified as ß-sitosterol. The compound activity against bacteria was evaluated by in vitro assay against S. sanguinis ATCC 10566 and E. faecalis ATCC 29212 with the MIC and MBC value of 25,000 and 50,000 ppm, respectively. The compound was also tested by in silico study using the molecular docking method. The molecular interaction between ß-sitosterol and the protein target showed a lower binding affinity value than the native ligand and other positive controls for each protein. Based on the amino acid residue bound to the ligands, ß-sitosterol on MurA and SrtA is not competitive to the positive control, showing potential as a natural antibacterial agent. Meanwhile, on the MurB and PBP, ß-sitosterol and positive control do compete with each other. CONCLUSION: The compound, isolated from O. basilicum L. leaf, was determined as ß-sitosterol, which has the molecular formula C29H50O. The antibacterial activity of ß-sitosterol by in vitro assay showed weak antibacterial activity, yet exhibited the potential to inhibit the biosynthesis of peptidoglycan and prevent bacteria cell wall formation by inhibiting MurA and SrtA activity via docking simulation.