April 9, 2009
The dental press seems to run more stories than ever on the future of dentistry in the 21st century. If you’ve read one lately, you’ve probably noticed the term biology-based dentistry. And with good reason. A major research investment is under way to begin to leverage the latest biological discoveries into everyday dental care. How would it work? As envisioned, biology-based dentistry will transform the most fundamental principle of the profession: restoration of form and function. No longer will dentists rely as readily on black-and-white X-rays, mechanical instruments, and ceramo-metallic materials to visualize and repair damaged tissue. They will regenerate form and function (a) using the precision of molecular information – that is, the underlying cause of the actual disease – as their operational guide and (b) employing the body’s own cells and biochemistry as their engineering materials. Dentists also will be equipped to scan the information written into our genes to look for typos that are associated with risk for an oral disease.
Each week, scientific journals present new discoveries and potential pieces of this biology-based future. An interesting example can be found in the March issue of the Journal of Periodontology. A team of NIDCR researchers reports that in African Americans, a relatively common - and clinically detectable- change in a single unit, or nucleotide, of DNA may be associated with aggressive periodontitis. The change, called simply 348T, occurs in the gene that encodes the neutrophil formylpeptide receptor 1, or FPR1. The membrane-bound FPR1 protein plays an important role in allowing white blood cells called neutrophils to recognize invading bacteria and mount the needed infection-fighting response. In the current study, the scientists obtained DNA samples from 63 African Americans (30 diagnosed with AP, 33 healthy volunteers). Interestingly, the volunteers were of a relatively homogenous West African genetic ancestry to help unify the analysis. The researchers detected five previously identified single-nucleotide changes, or SNPs, in the FPR1 gene. Among them was the 348T variant, which substitutes a thymine for the usual cytosine. The researchers found that seven African Americans with AP had the 348T variant in both copies of the FPRI gene, while the SNP was absent in the healthy volunteers. This suggests that, with further research, the variant might be predictive of African Americans who are most at risk for the condition. The authors noted, however, that the biological reasons for the higher frequency of the 348T gene change in those with AP remained unclear. They speculated that the change may alter the structure of the messenger RNA produced from the FPR1 gene and its subsequent translation into protein.