Fight Aging!

The modern age of antibiotics didn't do a great deal to combat the inexorable processes that contribute to tooth decay and gum disease, as it things turned out. One might have thought so at the outset: bacteria in the mouth are causing issues, we're developing all sorts of enormously improved methods of killing bacteria, ergo tooth decay and commonplace gum disease like gingivitis and should soon be a thing of the past. Alas not so, however - nothing is straightforward in the world of medicine. As one consideration, many of the hundreds of bacterial species in the mouth are actually beneficial.

In recent years, there has been some progress towards more sophisticated solutions. These include methods of sabotaging key mechanisms in problem bacterial species so as to leave other bacteria unharmed, or of targeting bacteria by their surface chemistry or other markers. For example:

• The End of Tooth Decay Looms Large
• The Possibility of Eliminating Tooth Decay
• Progress Towards Cavity Vaccines

I noticed another line of work in this field; here researchers are sabotaging the progression of gum inflammation caused by bacteria:

Penn-Led Research Suggests a New Strategy to Prevent or Halt Periodontal Disease

Porphyromonas gingivalis, the bacterium responsible for many cases of periodontitis, acts to "hijack" a receptor on white blood cells called C5aR. The receptor is part of the complement system, a component of the immune system that helps clear infection but can trigger damaging inflammation if improperly controlled. By hijacking C5aR, P. gingivalis subverts the complement system and handicaps immune cells, rendering them less able to clear infection from the gum tissue. As a result, numbers of P. gingivalis and other microbes rise and create severe inflammation. According to a study published [last year], mice bred to lack C5aR did not develop periodontitis.

[The] researchers synthesized and administered a molecule that blocks the activity of C5aR, to see if it could prevent periodontitis from developing. They gave this receptor "antagonist," known as C5aRA, to mice that were then infected with P. gingivalis. The C5aRA injections were able to stave off inflammation to a large extent, reducing inflammatory molecules by 80 percent compared to a control, and completely stopping bone loss. And when the mice were given the antagonist two weeks after being infected with P. gingivalis, the treatment was still effective, reducing signs of inflammation by 70 percent and inhibiting nearly 70 percent of periodontal bone loss.

I suspect that the next generation will very rarely visit dentists, as much of the need for regular dental services will be removed by products based on this and similar sorts of research.