Scientific Research

Scientific Research

ClO2 and Mouth Problems

Decay occurs when bacterial plaque attaches to the exposed tooth surface. Living in bacterial plaque, Streptococcus mutans, a species of bacteria, produces acid which attacks the minerals in enamel, cementum, and dentin. This leads to the destruction we know as dental decay or caries. A specially formulated chlorine dioxide (ClO2) toothpaste helps remove plaque and prevent its return.

Starting with a clean tooth, the first step in plaque formation is the attachment to exposed tooth surfaces of carbohydrate-protein molecules that come from saliva. The dental literature calls this pellicle. Chemists call it glycoprotein.

Bacteria stick to the pellicle and add to its volume by converting sugar into complex carbohydrates. Bacteria can live and use the carbohydrates and glycoproteins for nutrients. The ClO2 can chemically destroy these glycoproteins and complex carbohydrates. This leaves an environment that is less conducive to the caries process.

Periodontal diseases, gingivitis, and periodontitis are associated with bacterial plaque, but the process is very different.

All tissues of the mouth are covered with epithelial cells. These cells are a little different from the epithelial cells that make up your skin, but they are of the same family of cells. Both oral epithelium and skin epithelium are constantly being worm away by friction and use, but nature takes care of us by rapidly replacing our epithelial cells. Those cells that attach gingival (gums) to our teeth are, in health, replaced every two to four days. Research has shown that when inflammation is present, the rate of epithelial cell replacement is increased up to as little as six hours.

In a healthy mouth, these dead epithelial cells are shed into saliva, swallowed, and digested fast enough that they don’t putrefy and give the patient bad breath. When, in inflammation, these cells are shed at a faster rate, many remain in the mouth and degrade chemically into what are known as volatile sulphur compounds (VSC). These compounds cause Halitosis. This cellular debris encourages the growth of more bacteria, contributing to more disease. When they die, they degrade into chemicals, which can become VSC. The debris from epithelial cell and bacterial cell death become nutrients for further bacterial growth. It is a vicious cycle, wherein more cell death promotes more bacteria, which promote more cell death.

Chlorine dioxide (ClO2) destroys this organic debris. The most common use of ClO2 is in preparation of drinking water, particularly that which comes out of rivers in cities like St. Louis on the Mississippi River. First, the water is gassed with chlorine to kill the bacteria, but this leaves all the organic debris to make a tumbler of water seem unsafe. To remove these organic solutes, ClO2 is added to make the water clear and appear usable. In the same manner, the ClO2 gets rid of dead bacteria, dead epithelial cells, and food debris from the mouth. As in drinking water, this is also how ClO2 neutralizes the chemicals of bad breath.

Bad breath (malodor or halitosis) is caused by three chemical compounds that are the end degradation products of dead epithelial cells and dead bacteria. These compounds are: hydrogen sulphide (H-S-H) – 30%; methyl mercaptan (CH3-S-H) – 60%; and dimethyl sulphide (CH2-S-CH3) – 10%.

ClO2 produces oxygen, which chemically degrades the VSC by breaking the valence bonds with oxygen (O2) at the sulphur atoms. Thus 2H2S+3O2+2H2O+2SO2. The odor is not masked by a stronger odor. The bad smell is gone.

The VSC play a primary role in the series of events, causing gingivitis and periodontitis. When VSC are absent, the toxins from bacteria do not cross the epithelial barrier. When the VSC are present, they alter the epithelial barrier, allowing the bacterial toxins to penetrate through the epithelium into the deeper tissues. These act as antigens to start the immune response, which starts the inflammatory reaction that cause tissue destruction to form periodontal pockets.

Methyl mercaptan (CH3-S-H) has an adverse effect on collagen, weakening the strength of the collagen strand. When exposed to methyl mercaptan for 24 hours, the process is reversible; when exposed for 48 hours or more, the process is irreversible.

The oxygen generated by ClO2 restores the oxygen in saliva and plaque. If oxygen is present, the anaerobic (non-oxygen users) bacteria cannot survive. Since the anaerobic bacteria are associated with periodontitis, reducing their growth potential helps prevent the formation of periodontal pockets and bone loss.


The FDA controls the therapeutic claims that a proprietary company may use in marketing. This does not apply to the relationship between a dentist of hygienist and the patient.
FDA has no jurisdiction over the practice of medicine.

The following explains the effect of Chlorine Dioxide and the therapeutic benefit, as recognized by the patent office.

  • Removal of 90% oral malodor
    Splitting the sulphur bonds in H2S and CH3-S-DH3 neutralizes the odor. Competitive mouth rinses mask existing odor with a stronger odor.

  • Inhibition of pellicle formation
    Dental plaque forms in sequential steps. Deviations are uncommon. These steps are: The Hydroxyapatite crystals of enamel, cementum, and dentin have positive polarity Sulphated glycoproteins from saliva and oral mucous glands have a negative polarity, and thus deposit as film on clen hydroxyapatite of the tooth surface. This is known as pellicle. Sulphated glycoproteins are destroyed by ClO2. The negatively charged pellicle attracts positively charged bacteria, usually S. sanguis, at first, with a secondary population of S. mutans.

  • S sanguis and S. mutans
    These and other organisms have reduced motility and are killed at 99% in-vitro by 0.1% stabilized ClO2.

  • Glycosyltransferases
    Both S. sanguis and S. mutans produce glycosyltransferases, enzymes that convert sucrose into glucose and fructose. These are subsequently converted into long-chain glucans (dextrans) and fructans (levans). Glycosyltransferases, which are glycoproteins, are destroyed by stabilized ClO2, inhibiting dextran formation.

  • Dextran
    The principle component of aging dental plaque is dextran. This acts as a nutrient for bacteria and as a vehicle for most dental pathogens. Dextrans are split at carbon double bonds, reducing nutrient supply and anaerobic environment.

  • O2 Tension: Aerobic Bacteria
    S. sanguis and S. mutans are aerobic bacteria. These, with actinomyces and other aerobic species, use progressive amounts of oxygen derived from salivary fluids. Aerobic organisms in this plaque cause dental decay (S. Mutans) and gingivitis.
    As plaque ages, the numbers of aerobic bacteria increase, reducing the amount of available oxygen. The O2 tension is lowered in the plaque mass and in the saliva (the O2 source). This causes a shift in the bacteria, reducing the number of aerobic organisms and permitting the anaerobic bacteria to invade and multiply. Oxygen tension in plaque mass is raised by O2 available from ClO2 when used as a mouth rinse, causing a reverse bacterial shift from anaerobic to aerobic.

  • Anaerobic Bacteria
    The primary anaerobic bacteria present in plaque are the putative pathogens of periodontitis. Of special consideration are P. intermedius, P. gingivalis, F. nucleatum, and Actinobacillus actino-mycetemcomitans. These pathogens of periodontitis are killed by ClO2 at 0.1% in ten seconds in-vitro.

Mechanism of ClO2 Activity

ClO2 is one of the strongest oxidizing agents known. Its redox capacity is greatest with compounds containing sulphur, and it is highly active with organic nitrogenous compounds and lipids when nitrogen or carbon has double bonds.

ClO2 is a highly effective germicide, viricide, and fungicide. It reduces bacterial motility. As a germicide, it is effective by the release of O2 to react with sulphur or nitrogen or carbon double bonds. It also produces HOCl, hypochlorous acid, a germicide used extensively during World War I and later, until antibiotics became available.

  • Stability
    ClO2 is stable between pH of 6.5 to 8.0 with a shelf life claim at two to three years.

  • Toxicology
    Extensive studies with small animals, primates, and human volunteers reveal ClO2 does not cause skin or eye irritation. It is not a carcinogen. Fifty human volunteers at Ohio State University drank a ClO2 solution for twelve weeks and showed no clinical or laboratory changes of significance.

    Toxicology studies have been submitted to the FDA, which reported no concerns regarding safety.