Efficacy of Dentaq® Oral and ENT Health Probiotic Complex on Clinical Parameters of Gingivitis in Patients Undergoing Fixed Orthodontic Treatment: A Pilot Study.

OBJECTIVES: Probiotics act as a unique approach to maintaining oral health by supplementing the endogenous oral bacteria with additional naturally occurring beneficial microbes to provide defense against pathogens harmful to teeth and gingiva. The aim of this pilot study was to clinically evaluate the effects of probiotics on plaque accumulation and gingival inflammation in subjects with fixed orthodontics. METHODS: The pilot study was comprised of 15 healthy patients, aged 11 to 18 years, undergoing fixed orthodontic treatment. Patients used an all-natural, dissolving lozenge containing six proprietary probiotic strains (Dentaq® Oral and ENT Health Probiotic Complex)for 28 days. Gingival Index (GI) according to Löe-Silness and Plaque Index (PI) according to Quigley-Hein for all teeth were measured at baseline (Day Zero) and at the end of the probiotic regimen (Day 28). RESULTS: The mean baseline GI and PI scores within each patient decreased by 28.4% and 35.8%, respectively, by Day 28. Patients reported decreased tooth and gingival pain, decreased oral bleeding, and increased motivation to maintain proper oral hygiene over the course of the study. CONCLUSIONS: This pilot study provided preliminary support for the use of Dentaq Oral and ENT Health Probiotic Complex as a safe and effective natural health product for the reduction of plaque accumulation and gingival inflammation. The results demonstrate its potential therapeutic value and open the door for larger scale placebo-controlled clinical studies to verify these findings.

Adenovirus E1A targets the DREF nuclear factor to regulate virus gene expression, DNA replication, and growth.

UNLABELLED: The adenovirus E1A gene is the first gene expressed upon viral infection. E1A remodels the cellular environment to maximize permissivity for viral replication. E1A is also the major transactivator of viral early gene expression and a coregulator of a large number of cellular genes. E1A carries out its functions predominantly by binding to cellular regulatory proteins and altering their activities. The unstructured nature of E1A enables it to bind to a large variety of cellular proteins and form new molecular complexes with novel functions. The C terminus of E1A is the least-characterized region of the protein, with few known binding partners. Here we report the identification of cellular factor DREF (ZBED1) as a novel and direct binding partner of E1A. Our studies identify a dual role for DREF in the viral life cycle. DREF contributes to activation of gene expression from all viral promoters early in infection. Unexpectedly, it also functions as a growth restriction factor for adenovirus as knockdown of DREF enhances virus growth and increases viral genome copy number late in the infection. We also identify DREF as a component of viral replication centers. E1A affects the subcellular distribution of DREF within PML bodies and enhances DREF SUMOylation. Our findings identify DREF as a novel E1A C terminus binding partner and provide evidence supporting a role for DREF in viral replication. IMPORTANCE: This work identifies the putative transcription factor DREF as a new target of the E1A oncoproteins of human adenovirus. DREF was found to primarily localize with PML nuclear bodies in uninfected cells and to relocalize into virus replication centers during infection. DREF was also found to be SUMOylated, and this was enhanced in the presence of E1A. Knockdown of DREF reduced the levels of viral transcripts detected at 20 h, but not at 40 h, postinfection, increased overall virus yield, and enhanced viral DNA replication. DREF was also found to localize to viral promoters during infection together with E1A. These results suggest that DREF contributes to activation of viral gene expression. However, like several other PML-associated proteins, DREF also appears to function as a growth restriction factor for adenovirus infection.