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Composition of mineralizing incisor enamel in cystic fibrosis transmembrane conductance regulator‐deficient mice
Author(s) -
Bronckers Antonius L.J.J.,
Lyaruu Don M.,
Guo Jing,
Bijvelds Marcel J.C.,
Bervoets Theodore J.M.,
ZandiehDoulabi Behrouz,
Medina Juan F.,
Li Zhu,
Zhang Yan,
DenBesten Pamela K.
Publication year - 2015
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/eos.12163
Subject(s) - enamel paint , ameloblast , chemistry , fluoride , calcium , amelogenesis , enamel organ , calcein , biophysics , chloride , medicine , biochemistry , dentistry , inorganic chemistry , biology , membrane , organic chemistry
Formation of crystals in the enamel space releases protons that need to be buffered to sustain mineral accretion. We hypothesized that apical cystic fibrosis transmembrane conductance regulator (CFTR) in maturation ameloblasts transduces chloride into forming enamel as a critical step to secrete bicarbonates. We tested this by determining the calcium, chloride, and fluoride levels in developing enamel of Cftr‐ null mice by quantitative electron probe microanalysis. Maturation‐stage enamel from Cftr‐ null mice contained less chloride and calcium than did wild‐type enamel, was more acidic when stained with pH dyes ex vivo, and formed no fluorescent modulation bands after in vivo injection of the mice with calcein. To acidify the enamel further we exposed Cftr ‐null mice to fluoride in drinking water to stimulate proton release during formation of hypermineralized lines. In Cftr ‐deficient mice, fluoride further lowered enamel calcium without further reducing chloride levels. The data support the view that apical CFTR in maturation ameloblasts tranduces chloride into developing enamel as part of the machinery to buffer protons released during mineral accretion.