oral health

Oral hygiene and fluoride

Considering the vulnerability of enamel to demineralization and the daily menace of sugar ingestion, prevention of tooth decay is the best way to maintain the health of teeth. Most countries have wide use of toothbrushes, which can reduce the number of bacteria and food particles on enamel. Some isolated societies do not have access to toothbrushes, but it is common for those people to use other objects, such as sticks, to clean their teeth. In between two adjacent teeth, floss is used to wipe the enamel surfaces free of plaque and food particles to discourage bacterial growth. Although neither floss nor toothbrushes can penetrate the deep grooves and pits of enamel, good general oral health habits can usually prevent enough bacterial growth to keep tooth decay from starting.
Common dentistry trays filled with fluoride foam

These methods of oral hygiene have been helped greatly by the use of fluoride. Fluoride can be found in many locations naturally, such as the ocean and other water sources. Naturally occurring calcium fluoride is not the same as sodium fluoride, a byproduct of the fertilizer industry and the fluoride that is added to drinking water. The recommended dosage of fluoride in drinking water depends on air temperature; in the U.S. it ranges from 0.7 to 1.2 mg/L (milligrams per liter). Fluoride catalyzes the diffusion of calcium and phosphate into the tooth surface, which in turn remineralizes the crystalline structures in a dental cavity. The remineralized tooth surfaces contain fluoridated hydroxyapatite and fluorapatite, which resist acid attack much better than the original tooth did. Fluoride therapy is used to help prevent dental decay.

Many groups of people have spoken out against fluoridated drinking water. One example used by these advocates is the damage fluoride can do as fluorosis. Fluorosis is a condition resulting from the overexposure to fluoride, especially between the ages of 6 months to 5 years, and appears as mottled enamel. Consequently the teeth look unsightly, although the incidence of dental decay in those teeth is very small. It is important, however, to note that all substances, even beneficial ones, are detrimental when taken in extreme doses. Where fluoride is found naturally in high concentrations, filters are often used to decrease the amount of fluoride in water. For this reason, codes have been developed by dental professionals to limit the amount of fluoride a person should take. These codes are supported by the American Dental Association and the American Academy of Pediatric Dentistry. The acute toxic dose of fluoride is ~5 mg/kg of body weight. Furthermore, whereas topical fluoride, found in toothpaste and mouthwashes, does not cause fluorosis, its effects are also less pervasive and not as long-lasting as those of systemic fluoride, such as when drinking fluorinated water.[37] For instance, all of a tooth's enamel gains the benefits of fluoride when it is ingested systemically, through fluoridated water or salt fluoridation (a common alternative in Europe). Only some of the outer surfaces of enamel can be reached by topical fluoride. Thus, despite fluoridation's detractors, most dental health care professionals and organizations agree that the inclusion of fluoride in public water has been one of the most effective methods of decreasing the prevalence of tooth decay.

How to Dental Medicine

PITTSBURGH, April 15 – Certain genetic variations may be linked to higher rates of tooth decay and aggressive periodontitis, according to two recently published papers by researchers at the University of Pittsburgh School of Dental Medicine and their collaborators.

Alexandre R. Vieira, D.D. S., Ph.D., senior author of both papers and an assistant professor of oral biology, and his colleagues at the School of Dental Medicine found that the rate of dental caries was influenced by individual variations, or polymorphisms, in a gene called beta defensin 1(DEFB1), which plays a key role in the first-line immune response against invading germs. The findings are available online in the Journal of Dental Research.

"We were able to use data gathered from our Dental Registry and DNA Repository, the only one of its kind in the world, to see if certain polymorphisms were associated with the development of caries," Dr. Vieira said. "This could help us find new ways to treat people who are particularly susceptible to tooth decay, a problem that afflicts millions of Americans."

For the study, the researchers analyzed nearly 300 anonymous dental records and accompanying saliva samples from the registry, assigning each case a DMFT score based on the presence of decayed teeth, missing teeth due to caries, and tooth fillings, as well as a DMFS score, based on decayed teeth, missing teeth, and filled surface of a tooth. In general, individuals with fewer caries have lower DMFT and DMFS scores.

Saliva samples contained one of three variants, dubbed G-20A, G-52A and C-44G, of the DEFB1 gene. Individuals who carried a G-20A copy had DMFT and DMFS scores that were five-times higher than for people who had other variants. The G-52A polymorphism was associated with lower DMFT scores.

"It's possible that these variations lead to differences in beta defensin's ability to inhibit bacterial colonization," Dr. Vieira said. "In the future, we might be able to test for these polymorphisms as clinical markers for caries risk."

In a second paper, published last week in PLoS One, Dr. Vieira, colleagues at Pitt and collaborators in Brazil studied saliva samples of 389 people in 55 families to look for genetic links to aggressive periodontitis, which is rapid and severe destruction of the gums and bone that starts at a young age and is thought to be more common in Africans and those of African descent. Brazil's population is composed primarily of Caucasians of Portuguese ancestry, Africans and native Indians.

They found hints of an association between the disease and the FAM5C gene. While further testing did not find any mutations or polymorphisms that bore out a relationship, other experiments showed elevated levels of FAM5C expression, or activation, in areas of diseased periodontal tissue compared to healthy tissue.

"The FAM5C gene recently was implicated in cardiovascular disease, in which inflammation plays a role, just as in periodontitis," Dr. Vieira said. "More research is needed to see if variation in the gene is associated with different activity profiles."