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Using an animal model, the UAB researcher’s found that a lack of Sp7, a transcription factor, interupts the maturation of two types of cells ie odontoblasts and amenoblasts, that help create teeth.
The teeth of mammals develop during embryonic growth, though they erupt after birth. Javed, a professor in the UAB, used a mouse model with mutations in both copies of the gene for Sp7.
In Humans, mutations of the Sp7 gene causes osteogenesis imperfecta, a condition that affects the development of bones and craniofacial structures. However, the role of Sp7 in embryonic development was unknown.
Mice lacking Sp7, initial tooth morphogenetic was normal, even though the animals lacked mineralised tooth sockets. The animal failed to produce normal enamel, the super hard matrix layer that cover the tooth. This was due to reduced proliferation, maturation and polarisation of the tooth forming cells called odontoblast and amenoblasts. Odontoblasts form a sheet of columnar cells that deposit dentin. Similarly, amenoblasts form a sheet outside developing tooth to by down enamel.
Without Sp7 , the odontoblasts and amenoblasts were fewer in number and showed disorganised alignment.
The researchers found that Sp7 in normal mice was expressed only in the dental mesenchymal tissue, give rise to odontoblasts; it was not expressed in the oral epithelium that give rise to amenoblasts . 13 different members of the fibroblast growth factor, or fgf, acts as signaling proteins between the two different tissues-dental mesenchyme and oral epithelium.
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