Periodontitis at its worst is affecting 8.5 percent of American adults. But with a new study from the University of Pennsylvania periodontitis may be a worry of the past. Using a mouse model and sophisticated molecular blocking techniques, researcher Dr. Toshiharu Abe and his team have been successful in preventing periodontitis from developing and slowing the progression of the already occurring disease. The study expands on previous research from Drs. John D Lambris and George Hajishengallis, who showed that Porphyromonas gingivalis, the bacteria that is responsible for periodontitis, hijacks a receptor on white blood cells known as 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. Hijacking of the C5aR, P. gingivalis bypasses this complement system and partially disables immune cells. The result is a weakened immune system severely crippled in its ability to prevent infections of the gums.
So what do mice have to do with this? Drs. Hajishengallis and Lambris discovered in the initial study that mice bread without C5aR did not develop periodontitis. Dr. Abe and his colleagues pulled from previous studies that proved mice lacking Toll like receptors, known as TLR2s, also seem to reject periodontitis. Using this study as a base-point the researchers were able to determine if the synergism between the complement system and TLRs was also at play in inflammatory gum disease.
The researchers synthesized a molecule that blocks the C5aR activity. This molecule, known as C5aRA, was given to mice that were then infected with P. gingivalis. The injections of C5aRA were able to stave off inflammation, reducing inflammatory molecules by 80 percent and completely stopping bone loss. Mice given the C5aRA two weeks after infection were still shown to have 70 percent reduced inflammation and nearly 70 percent inhibition of periodontal bone loss. The latter results are important for future human treatment as most people likely to receive the therapy would already be suffering from gum disease.
These results are highly encouraging, leading the team to replicate their success in new mice subjects as well as other animal models. "Our ultimate goal is to bring complement therapeutics to the clinic to treat periodontal diseases," Dr. Lambris told the ADA. "The complement inhibitors, some of which are in clinical trials, developed by my group are now tested in various periodontal disease animal models and we hope soon to initiate clinical trials in human patients."
Is this the beginning of the end of gum disease? Only time will tell, but we are well on our way to a significant advancement of dental treatments for millions.
