Clinical performance of light-cured orthodontic adhesives for bonding brackets – an in-vitro study. [version 1; peer review: 1 approved, 2 approved with reservations]

Background The dental profession is seeing a constant influx of new adhesive systems from manufacturers, each claiming to be more dependable than the last. This study assessed the bond strength and adhesive remnants of different light-cured adhesives used for bonding metal brackets to teeth. Methods 80 extracted maxillary premolars with the sound crown structure were acid etched and bonded with brackets on their buccal surfaces utilizing primer and light-cured adhesives into four equal groups, which are Transbond XT, Heliosit, Enlight, and Bracepaste. Shear bond strength (SBS) for de-bonding the brackets were evaluated with Instron- testing machine after 48 hours. The de-bonded samples’ adhesive remnant index (ARI) scores were also measured. Results The maximum mean SBS was found for Transbond XT (12.91 ± 2.0 MPa), followed by Bracepaste (12.87 ± 1.59 MPa), Enlight (11.77 ± 1.87 MPa), and lowest for Heliosit (10.93 ± 1.71 MPa). According to the four point scale, adhesive remnant index (ARI), Transbond XT has the least adhesive residue left on the tooth, followed by Heliosit. Enlight and Bracepaste have a similar distribution of adhesive, with both having a maximum amount left. Conclusion It can be inferred that all groups involved demonstrated a satisfactory level of bond strength from a clinical perspective. Transbond XT is the preferred orthodontic adhesive over the other three adhesives due to its superior SBS and ARI properties

Deposition of 5-Methylcytosine on Enhancer RNAs Enables the Coactivator Function of PGC-1α

The Peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) is a transcriptional co-activator that plays a central role in adapted metabolic responses. PGC-1α is dynamically methylated and unmethylated at the residue K779 by the methyltransferase SET7/9 and the Lysine Specific Demethylase 1A (LSD1), respectively. Interactions of methylated PGC-1α[K779me] with the Spt-Ada-Gcn5-acetyltransferase (SAGA) complex, the Mediator members MED1 and MED17, and the NOP2/Sun RNA methytransferase 7 (NSUN7) reinforce transcription, and are concomitant with the m5C mark on enhancer RNAs (eRNAs). Consistently, loss of Set7/9 and NSun7 in liver cell model systems resulted in depletion of the PGC-1α target genes Pfkl, Sirt5, Idh3b, and Hmox2, which was accompanied by a decrease in the eRNAs levels associated with these loci. Enrichment of m5C within eRNA species coincides with metabolic stress of fasting in vivo. Collectively, these findings illustrate the complex epigenetic circuitry imposed by PGC-1α at the eRNA level to fine-tune energy metabolism