In the August 6, 2010 issue of the Journal of Biological Chemistry (Volume 285, Number 32), a team of National Institute of Dental and Craniofacial Research (NIDCR)-supported scientists and colleagues offer an answer that is rooted in another recent discovery. Two years ago, the group showed for the first time that enamel-forming cells called ameloblasts produce NBCe1, a protein known to transport bicarbonate and thus buffer pH levels in the microenvironment adjacent to the cell. As the authors then explained, pH levels normally vary during enamel formation, suggesting an obvious role and need for NBCe1. But the scientists needed to take the next step and establish that NBCe1 is essential for normal formation of dental enamel. In the current paper, the authors found in mouse studies that their suspicions were correct. Mice bred to produce no NBCe1 developed hypomineralized enamel that was extremely soft and fragile from the ameloblast’s inability to control the acidity levels in its microenvironment.
“The biophysical properties of the enamel are highly perturbed as a direct consequence of abnormal development due to the loss of NBCe1 function,” the authors concluded. “Thus, although it is widely appreciated that the acidity of ingested foods, drinks, or acidic salivary pH can affect enamel once fully formed teeth are exposed to these factors in the oral cavity, the results of this study demonstrate the importance of ‘internal’ acid-base homeostasis in the normal development of enamel in mammals.” Interestingly, the authors noted that this soft-enamel phenotype seems to exist in people born with a rare syndrome called proximal renal tubular acidosis. The condition is caused by alterations in the gene that encodes NBCe1.
(Source: NIDCR, Science News in Brief, September 14, 2010)