Dental changes in children with congenital Zika syndrome.

OBJECTIVE: To describe oral alterations in children with congenital Zika syndrome (CZS). METHODS: This was a case series, whose research instrument was a structured questionnaire, associated with the use of medical record data and extra and intraoral clinical examination. RESULTS: Thirty-two children were evaluated, the majority male (18/32%-56.3%), mean age 22 months (SD = 2.71). It was also observed that the majority of the patients (19/32%-59.4%) presented a low family income. All the children had a mean head circumference of 29.43 cm (SD = 1.42). Regarding the alterations, an ogival-shaped palate was observed in 14 children (43.7%), and delayed chronology of eruption was observed in 15 children (46.9%), of whom 7 children (21.9%) did not present eruption of the upper left lateral incisor (p = .0002) and upper right lateral incisor (p = .002) until the moment of analysis. Additionally, 03 children with yellowish dental pigmentation were identified in erupted teeth after the onset of phenobarbital use. Enamel hypoplasia was identified in 9 children (28.1%) and only one child with ankyloglossia. CONCLUSION: CZS may present delayed chronology of eruption, ankyloglossia, ogival-shaped palate, and enamel hypoplasia, requiring dental follow-up aimed at prevention, promotion, and rehabilitation of the health of these children.

Cytomegalovirus induces stage-dependent enamel defects and misexpression of amelogenin, enamelin and dentin sialophosphoprotein in developing mouse molars.

Of the approximately 8,400 children born each year in the US with cytomegalovirus (CMV)-induced birth defects, more than one third exhibit hypoplasia and hypocalcification of tooth enamel. Our prior studies indicated that CMV severely delayed, but did not completely interrupt, early mouse mandibular first molar morphogenesis in vitro. The aim of the present study was to examine the effects of CMV infection on progressive tooth differentiation and amelogenesis. Since initial CMV infection in human fetuses can occur at different developmental times, we varied the stage of initial viral infection (that is, Cap stage, Early Bell stage and Bell stage), as well as the duration of infection. CMV infection of embryonic mouse mandibular first molars in vitro induces tooth dysmorphogenesis and enamel defects in a developmental stage- and duration-dependent manner. Cap stage- and Early Bell stage-infected molars exhibit enamel agenesis and Bell stage-infected molars exhibit enamel hypoplasia. This viral-induced pathology is coincident with stage-dependent changes in Amelx, Enam and Dspp gene expression, distribution of amelogenin, enamelin and DSP proteins, cell proliferation localization and dedifferentiation of secretory ameloblasts. Importantly, our data indicate that specific levels of Amelx and Dspp gene expression define whether mouse CMV induces enamel agenesis or hypoplasia.