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The neutral pH inside the cell reverts HF to F−. Excess F− within the cell interferes with ER homoestasis, inducing ER stress and activation of the UPR (Figure 5), resulting in compromised ameloblast function.
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Conclusions: The low pH environment of maturation stage ameloblasts facilitates the uptake of \(F^−\), causing increased cell stress that compromises ameloblast function, resulting in dental fluorosis.
The low pH environment of maturation stage ameloblasts facilitates the uptake of F−, causing increased cell stress that compromises ameloblast function, resulting in dental fluorosis.
We propose therefore that the observed phenotype of the ITGB6 mutation is due to the combined effects of a lack of MMP20 and compromised ameloblast cell cell binding resulting in hypomineralization, structural abnormalities and where ameloblast strain is maximal, pitting due to the integrity of the ameloblast monolayer being compromised.
Enamel structure reflects ameloblast function.
By studying the structure of the superficial enamel, information about ameloblast function toward the end of the secretory stage may be obtained.
Consequently, ameloblast function during enamel development may be impaired, and this may culminate in dental fluorosis.
The defects appear to be related to altered ameloblast function during the transitional and maturation phases.
Our data provide valuable information in respect of maturation stage ameloblast function, the precise details of which remain obscure.
These people have compromised executive function.
Compromised suppressive function of CNS3-deficient Treg cells.
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