Assessment of Microbial Contamination of a Toothbrush Head with and without a Protective Cover: An Ex Vivo Study.

Introduction: The oral cavity is colonized by various groups of microorganisms. Toothbrushing is a common method of maintaining oral hygiene and, upon regular use, can become heavily contaminated with microorganisms. To avoid contamination of the toothbrush with microorganisms from the external environment, toothbrushes can be protected by a protective cap, the significance of which is unknown. Objectives: To assess the microbial contamination of the toothbrush with and without a protective cap and to find the significance of the same against microbial contamination. Materials and methods: An ex vivo study was conducted in the Faculty of Dental Sciences, Sri Ramachandra University. A total of 40 toothbrushes were distributed among dental students aged 18-25 years; 20 were protected by a cap, 20 were unprotected, and instructions were given to recap the toothbrush after brushing. After 1 month of regular usage, toothbrushes were collected, and organisms were identified based on Gram's reaction followed by a biochemical test. Results: From the study conducted, it is evident that the microbial contamination of the unprotected toothbrush is higher than that of the toothbrushes that were protected with a cover. How to cite this article: Manohar R, Venkatesan K, Raja S, et al. Assessment of Microbial Contamination of a Toothbrush Head with and without a Protective Cover: An Ex Vivo Study. Int J Clin Pediatr Dent 2022;15(4):455-457.

RDH10 function is necessary for spontaneous fetal mouth movement that facilitates palate shelf elevation.

Cleft palate is a common birth defect, occurring in approximately 1 in 1000 live births worldwide. Known etiological mechanisms of cleft palate include defects within developing palate shelf tissues, defects in mandibular growth and defects in spontaneous fetal mouth movement. Until now, experimental studies directly documenting fetal mouth immobility as an underlying cause of cleft palate have been limited to models lacking neurotransmission. This study extends the range of anomalies directly demonstrated to have fetal mouth movement defects correlated with cleft palate. Here, we show that mouse embryos deficient in retinoic acid (RA) have mispatterned pharyngeal nerves and skeletal elements that block spontaneous fetal mouth movement in utero Using X-ray microtomography, in utero ultrasound video, ex vivo culture and tissue staining, we demonstrate that proper retinoid signaling and pharyngeal patterning are crucial for the fetal mouth movement needed for palate formation. Embryos with deficient retinoid signaling were generated by stage-specific inactivation of retinol dehydrogenase 10 (Rdh10), a gene crucial for the production of RA during embryogenesis. The finding that cleft palate in retinoid deficiency results from a lack of fetal mouth movement might help elucidate cleft palate etiology and improve early diagnosis in human disorders involving defects of pharyngeal development.

RDH10-mediated retinol metabolism and RARα-mediated retinoic acid signaling are required for submandibular salivary gland initiation.

In mammals, the epithelial tissues of major salivary glands generate saliva and drain it into the oral cavity. For submandibular salivary glands (SMGs), the epithelial tissues arise during embryogenesis from naïve oral ectoderm adjacent to the base of the tongue, which begins to thicken, express SOX9 and invaginate into underlying mesenchyme. The developmental mechanisms initiating salivary gland development remain unexplored. In this study, we show that retinoic acid (RA) signaling activity at the site of gland initiation is colocalized with expression of retinol metabolic genes Rdh10 and Aldh1a2 in the underlying SMG mesenchyme. Utilizing a novel ex vivo assay for SMG initiation developed for this study, we show that RDH10 and RA are required for salivary gland initiation. Moreover, we show that the requirement for RA in gland initiation involves canonical signaling through retinoic acid receptors (RAR). Finally, we show that RA signaling essential for gland initiation is transduced specifically through RARα, with no contribution from other RAR isoforms. This is the first study to identify a molecular signal regulating mammalian salivary gland initiation.