Researchers have found a possible mechanism than can prevent and even halt teeth decay due to periodontal diseases.

The scientists from the University of Pennsylvania say that blocking out molecular receptor that the bacteria target during the start of the disease can stop the bacteria from growing in the mouth. Their study on mice has shown that this strategy prevents the disease from progressing and in some cases prevents it.

Periodontal disease is inflammation and infection of gums and bones that support the teeth. In the early stages the disease is called gingivitis. Later, as the disease progresses, the gums become swollen, red and even bleed. In some cases, the gums may come out and the teeth may fall off.

Earlier, researchers had shown that Porphyromonas gingivalis, the bacteria that is associated with many cases of periodontitis, hijacks a receptor called C5aR that is present in white blood cells. The receptor is part of the immune system and can cause serious inflammation if triggered. By blocking this receptor, the bacteria are able to grow and not be affected by the body's immune system. As time passes, the bacteria grow in the mouth and the inflammation becomes more severe.

According to a study published last year, mice that lacked C5aR didn't develop periodontal disease. Also, mice that lacked another set of proteins called toll-like receptors, or TLRs, didn't show bone loss that's associated with periodontitis. These proteins are involved in activation of immune cell response.

Researchers in the current study found that activating both these receptors can trigger off an inflammation while blocking just one receptor - C5aR - with an antagonist C5aRA reduced the inflammation by 80 percent.

When the mice were given C5aRA two weeks after an infection, the strategy still worked. In these mice, the inflammation was reduced by 70 percent.

"Regardless of whether we administered the C5a receptor antagonist before the development of the disease or after it was already in progress, our results showed that we could inhibit the disease either in a preventive or a therapeutic mode," said George Hajishengallis from Penn's School of Dental Medicine and senior author of the paper, according to a statement.

The study is published in the Journal of Immunology.