A single gene caps the tooth

A report in the Proceedings of the National Academy of Sciences, made available online last week, has shed new light on how teeth grow. A gene has been identified as essential for the formation of enamel in the early stages of tooth development. Professors Chrissa Kioussi and Mark Leid and team at Oregon State University, US, are the first to demonstrate such a genetic factor.

Enamel, the strongest substance in our bodies, encapsulates teeth. Its great strength derives from an extremely high content of minerals like calcium phosphate. Once damaged however enamel cannot re-grow, as the producer-cells are shed when the tooth pierces through the gums after birth. Tooth decay is thus irreversible.

Using genetically modified mice, lacking a gene called Ctip2, the researchers were able to show that teeth begin development normally, but stall at the stage when encapsulation normally occurs. Tooth cells called ameloblasts, which normally secrete the proteins required for enamel formation, depend upon Ctip2 to function. By labelling the cells with a fluorescent marker and comparing teeth between normal and mutant mice, Professor Leid and colleagues noticed that the mutant mice had a significant drop in the number of ameloblasts, with nearly no enamel.

Ctip2 is a type of protein called a transcription factor. Its job is to bind to DNA and regulate the 'reading' of nearby genes. In this way a transcription factor indirectly influences the production of other proteins. Without Ctip2, the group showed that a protein called ameloblastin is not produced. Ameloblastin is a key mediator in enamel production.

Paul Sharpe, professor in tooth development at the Dental Institute at King's College London, UK, was positive about the findings. 'If you could find some way of growing ameloblasts that make enamel, you could find a way to repair teeth'. Professor Sharpe is interested in the use of stem cells for tooth regeneration. However, since the revisions to the Human Tissue Act in 2006, it has been difficult to obtain tooth samples to study.

Dr Kioussi said: 'A lot of work would still be needed to bring this to human applications, but it should work. It could be really cool, a whole new approach to dental health'.

Also published last week in the journal Science was the surprising finding that deletion of single gene, Osr2, leads to the appearance of teeth outside of the normal tooth row. The work, led by Rulang Jiang, professor of genetics at the Rochester Medical Centre, US, offers hope for the future treatment of missing teeth or cleft palates.