Asporin and the Mineralization Process in Fluoride-Treated Rats

Abstract

Microarray analysis of odontoblastic cells treated with sodium fluoride has identified the asporin gene as a fluoride target. Asporin is a member of the small leucine-rich repeat proteoglycan/protein (SLRP) family that is believed to be important in the mineralization process. In this study, asporin expression and distribution were investigated by systematic analysis of dentin and enamel, with and without fluoride treatment. Specific attention was focused on a major difference between the two mineralized tissues: the presence of a collagenous scaffold in dentin, and its absence in enamel. Normal and fluorotic, continually growing incisors from Wistar rats treated with 2.5 to 7.5 mM sodium fluoride (NaF) were studied by immunochemistry, in situ hybridization, Western blotting, and RT-qPCR. Asporin was continuously expressed in odontoblasts throughout dentin formation as expected. Asporin was also found, for the first time, in dental epithelial cells, particularly in maturation-stage ameloblasts. NaF decreased asporin expression in odontoblasts and enhanced it in ameloblasts, both in vivo and in vitro. The inverse response in the two cell types suggests that the effector, fluoride, is a trigger that elicits a cell-type-specific reaction. Confocal and ultrastructural immunohistochemistry evidenced an association between asporin and type 1 collagen in the pericellular nonmineralized compartments of both bone and dentin. In addition, transmission electron microscopy revealed asporin in the microenvironment of all cells observed. Thus, asporin is produced by collagen-matrix-forming and non-collagen-matrix-forming cells but may have different effects on the mineralization process. A model is proposed that predicts impaired mineral formation associated with the deficiency and excess of asporin.

Chronic Exposure to Bisphenol A Exacerbates Dental Fluorosis in Growing Rats

“…(29) These observations are consistent with the ability of these agents to induce enamel hypomineralization. (6,29) These observations were supported by µCT analysis ( Figure 1D). Comparison of transversal sections at the same anatomical landmark (the zone of incisor eruption from the bone) evidenced a significant lower enamel density in rats exposed to BPA alone or in combination with NaF than in control animals ( Figure 1E).…”

“…(29) These observations are consistent with the ability of these agents to induce enamel hypomineralization. (6,29) These observations were supported by mCT analysis (Fig. 1D).…”

“…(6,29) Typical enamel fluorosis was observed in rats treated by 5 mM NaF with alternative white and orange bands ( Figure 1B, C). A moderate phenotype was observed here at P65 in rats exposed to BPA, with 12.5% of enamel breakdown, in accordance with our previous data (Supplemental Figure 1).…”

“…Rats exposed to BPA or fluoride are good experimental models for MIH and DF, respectively. (6,29) Typical enamel fluorosis was observed in rats treated by 5 mM NaF with alternative white and orange bands (Fig. 1B, C).…”

L’émail

“…Seront altérées les dents en cours de minéralisation au moment de l'exposition. Un exemple classique est la fluorose dentaire résultant de l'ingestion excessive de fluor [25]. Des doses prophylactiques, plus faibles, ont au contraire un effet bénéfique dans la prévention des caries (ce qui explique la diminution significative de leur prévalence au cours de ces dernières décennies) [26].…”