Floss, brush and rinse to protect your winning smile — it's advice that shouldn't be ignored. But a new study suggests that gum disease may result from reduced levels of a key enzyme in cells, as well as indifferent dental hygiene.

The enzyme, known as cathepsin C, appears to trigger a complex web of immunological reactions that destroy diseased cells and eliminate infections in the mouth, a notoriously filthy place.

How dirty? Scientists estimate that 6 billion microbes representing 500 different species of bacteria constantly are trying to breach your gums and attack the attachments of your teeth.

The new research suggests that even slightly reduced levels of cathepsin C as a result of a genetic mutation may reduce a person's ability to ward off periodontitis, or deep pockets of infection below the gum line.

Nearly one in every three people suffer from inflammations that cause bleeding and receding gums and chronic dental problems. Recent studies have shown that oral bacteria contribute to ailments ranging from heart disease to premature births.

Restoring the enzyme to normal levels could be a new approach to preventing and treating gum disease and protecting a person's overall health, scientists said. The study is published in the December issue of the journal Nature Genetics.

"We're were suggesting there is a genetic component in the normal population for periodontal disease," said Glenn Nuckolls of the Craniofacial Development Section of the National Institutes of Health, who was not involved in the study.

"If you have this mutation, but you do a really good job of dental hygiene, you might push the onset of the disease to later in life," he said.

A team of oral biologists and geneticists from the University of Manchester in England and other institutions examined patients from eight families with a history of Papillion-Lefevre syndrome, a rare disorder marked by severe gum disease and tooth loss in adolescence.

All of the patients had mutations in the CTSC gene on chromosome 11 and all had nearly complete deficits of cathepsin C. Researchers concluded that the genetic flaws caused the enzyme deficits.

Without the enzyme, the patients' immune systems could not mount an adequate defense against bacteria in dental plaque and infections quickly destroyed membranes and ligaments securing their teeth.

The study's findings are the first explanation for PLS, said Jan Carlsson, an oral biologist at Umea University in Sweden who was not involved in the study.

He and other scientists suggest that less-drastic cathepsin C deficiencies might explain the stubborn recurrence of gum disease in the general population, as well as how infections persist in the body's tissues.

That could be especially true in older patients who suffer from gum diseases; they might gradually lose the capacity to produce sufficient levels of cathepsin C.

Scientists said common gum disease is so widespread that flaws in several genes probably are involved, as well as environmental factors such as bacteria, smoking and a person's dental habits.

One thing is certain, they said: Keep flossing. A genetic cure isn't around the corner.