RESUMEN
Minocycline, the synthetic derivative of the antibiotic tetracycline, has been used for a variety of medical treatments. One such use for minocycline is for acne vulgaris. Although widely used, minocycline has a common side effect of discoloration of tissues, including bone, skin, and mucosa. This case report presents a 19-year-old female patient with a history of long-term minocycline therapy for acne vulgaris who presented for periodontal esthetic crown lengthening. The initial exam revealed a blue-gray discoloration of the mucosa. Upon surgical exploration, it was discovered that the discoloration originated from the underlying alveolar bone with minimal gingival involvement. Surgical removal and recontouring of the bony exostoses revealed that the bone remained deeply stained. Although the discolored bone was not fully removed, the patient was able to obtain an acceptable esthetic result.
RESUMEN
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.
Asunto(s)
Oxidorreductasas de Alcohol/fisiología , Boca/embriología , Hueso Paladar/embriología , Animales , Fisura del Paladar/etiología , Fisura del Paladar/fisiopatología , Modelos Animales de Enfermedad , Ratones , Boca/fisiología , Movimiento , Retinoides/deficienciaRESUMEN
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.