These all mean the same thing; that certain bacteria have overgrown on certain parts of the tooth surface and have produced so much acid that the tooth mineral has dissolved or decayed, forming a cavity. This is a relatively slow process and does not hurt until the decay has extended near the pulp, at which time the nerves in the pulp are excited or irritated by products produced by the bacteria, and/or by hot or cold temperatures. Your dentist can detect cavities long before this, by either a visual exam, (he or she can see the cavity, or detect it by touch with a dental instrument), or by radiographs which give an estimate of how deep the decay has spread. At this stage the dentist recommends removing the decayed part of the tooth and replacing it with a dental restoration usually called an amalgam, but the restoration could be made of gold, porcelain or polymers. This is a necessary and traditional way to treat dental decay.

But, if you want to prevent the recurrence of decay, one should determine what risk factors are present and then seek to eliminate or to control them. One risk factor is newly erupting teeth, so that infants between 1 to 3, children from 6 to 7, and teenagers from 12 to 14 are most at risk to decay. If these age groups already have decay, then added effort should be made to control for a bacterial infection usually due to a group of germs known as the mutans streptococci and lactobacilli.

The mutans streptococci, in the germ world, are world class athletes when it comes to grabbing any sugar that enters the mouth in the form of candies, gums, or other sweetened snack-type foods. They don’t need much sugar in order to lower the pH (form acid) on the teeth, causing the tooth to dissolve. For example a few grams of sugar a day (only 8 to 10 calories), taken repeatedly between meals can cause decay. This is because the millions upon millions of bacteria that normally live on your teeth are in a feast or famine situation. They normally divide every 2 to 4 hours, so that some bacteria, provided that there were no snacks, would never see sugar during their lifetime. But when a snack comes along containing soluble sugar, these bacteria are ready to gorge themselves. This is what the mutans streptococci are best at, quickly taking into their cells all the sugar that comes their way.

The mutans streptococci convert the sugar to energy which enables them to grow and divide, but also, very cleverly, convert some of the sugar to intracellular polysaccharide storage compounds and extracellular glue like polymers that enable them to better stick to the teeth. Each of these metabolic pathways contributes to the process of decay. When they form energy, they also produce acid as a waste product. This acid lowers the pH at the surface of the tooth. The tooth is designed, like bone, to buffer when there is a pH drop, so that tooth mineral dissolves releasing calcium and phosphate ions, and these ions when supplemented with the buffer systems in the saliva prevent the pH from reaching the low levels where holes or cavities form in the teeth. These normal protective mechanisms of the teeth and saliva were adequate to protect humans from dental decay throughout human history, until the mid to late 19^th century when sugar became readily available. Prior to the wide scale availability of sugar only the affluent, who could afford delicacies containing sugar, were susceptible to dental decay. After sugar became affordable, an epidemic of dental decay swept through populations enjoying the sugar-sweeten goodies.

But many other types of germs that live on the teeth can also form acid from sugar and would contribute to the decay process. This accumulation of bacterial types in the dental plaque was what the early dental researchers saw when they studied dental decay. Their research tools and state of knowledge did not allow them to differentiate between the various types of germs, so they, using the powers of clinical observation, concluded that dental decay occurred in mouths with poor oral hygiene. Their recommendations to combat this problem was to devise means to clean the teeth using brushes, tooth pastes and floss among other devices. This approach was a colossal failure, perhaps due to the fact that sugar was often used to make the toothpastes more palatable. (The Mary Poppins approach). So instead of preventing decay, tooth brushing may well have exaggerated it. Dental decay became almost universal and was among the leading causes for rejection into the military for World Wars I and II and the Korean War. The caries epidemic ended when sugar was removed from toothpastes and fluoride put in, when water was fluoridated, when sugar substitutes, such as xylitol, became available, and dental sealants were placed over susceptible tooth surfaces. The success of these approaches can be measured by the closing of nine dental schools in the US and others in Europe.

But none of these approaches was specifically directed towards combating a mutans streptococci infection on the teeth, so that today dental decay is still a problem, but certainly not the universal scourge that existed up until about 1960. Further reductions in decay require that treatment needs to be focused on individuals infected with the mutans streptococci at the time when they are most at risk to a cariogenic infection. For this we need to know a little bit more as to why the mutans streptococci are so very good at causing decay

The mutans streptococci are very successful in surviving in the acid environment that they create. So are the lactobacilli, another germ that has been linked to human dental decay. Most other oral bacteria cannot live at these low pHs, and their numbers drop off in the plaque. But the mutans streptococci and lactobacilli can continue to grow when the pH  becomes acidic. At about pH 5 some interesting phenomena occurs at the interface between the dental plaque and the tooth. At this pH, known as the critical pH, the salivary buffers are overwhelmed, and the tooth, itself, begins to dissolve releasing phosphate ions to buffer the acids produced by these acid-resisting species (known as aciduric species). If the supply of carbohydrates is high, from snacking,  these aciduric bacteria continue to grow and contribute to the low pH that dissolves the tooth causing decay. If the pH does not increase after the meal or snack is over, allowing the tooth to heal itself via the remineralizing power of the saliva, a cavity results. Do you remember above when I mentioned that the mutans streptococci form intracellular and extracellular polysaccharides from sugar. Well these polysaccharides can be broken down when the dietary sugar is gone, causing the pH at the tooth plaque surface to remain low for long periods of time after a snack is consumed. This would result in continued dissolution of the tooth, resulting in even more decay. If a sugar snack is taken while the pH is low, then the period of tooth dissolution could last for hours. 

 There is a famous study conducted in Sweden in the early 50’s in which frequent eating of candies lead to a rampant carious situation in young institutionalized adults. This could be associated with the presence of sugar in the saliva for most of the waking day. Frequent eating of sugar snacks will cause the levels of mutans streptococci in the saliva to increase. This increase can be detected by bacteriological tests which look at the saliva, or at the plaque itself. These bacteriological tests were not available when the Swedish studies were conducted, but they are commercially available today from the following suppliers: CRT Bacteria TM (CRTms; Invoclar Vivadent),
Cariocheck Plus TM (CCms; Hain Diagnostika),
Dentocult SM TM (D; Orion Diagnostica),
Mucount TM (M; Showa Yakuhin Kako).

If an individual has more than two decayed teeth ( this number is chosen, so that one wouldn’t be using the test every time that a single tooth is decayed, unless this person has other risk factors, such as newly erupting teeth), then it makes sense to determine how many mutans streptococci this individual has in his or her saliva. Also at the same time one could look for the lactobacilli, the other group of bacteria implicated in dental decay. If both these germs are present in high numbers in the saliva, using tests that are commercially available, then one has identified the bacterial risk factors responsible for the development of decay.

What can you do when there are bacterial risk factors? First the dentist can  check for frequent between meal eating of soluble sucrose (sugar) containing products. If they are being used then, the dentist can  suggest that the subject switch to products containing xylitol as a sweetening agent. Xylitol is an amazing sucrose substitute in that it tastes as good as sucrose. Several studies have shown that it is anticariogenic, i.e., it prevents decay, rather than non-cariogenic like sorbitol, the sucrose substitute usually found in sugarless gums. The mutans streptococci can not use xylitol, and all the enzymes that these germs have to use sucrose become excess baggage, when they are exposed to  xylitol between meals. In a crowded and competitive environment such as the dental plaque, any enzymes that are not useful will make a germ noncompetitive. As a result the levels of the mutans streptococci decrease in the plaque. Xylitol is hard to find in the supermarkets, but should be for sale in most health food stores. The price will be higher, because it is more expensive than sugar to produce, but given its anti-cariogenic activity it is well worth the added cost.

Another treatment, that makes sense in children, especially if they have several decayed baby or primary teeth, is the placing of sealants on the tops of newly erupting premolars and molar teeth. Thus for children aged 6 to 7, the first molars could be sealed, and for teenagers, the second molars, and possibly the premolars could be sealed. This would not be done on everybody, but certainly would be recommended in someone who has prior caries activity.

There is of course fluoride treatments of the type given by the dentist that should be applied after all the dental restorations or fillings are placed.  Everyone should be using a fluoridated toothpaste, as this is essential for caries control. Fluoride does so many good things for the tooth, like helping the saliva to restore, or re-mineralize the beginning carious lesion, known as a white spot. And fluoride is most active as an antibacterial agent at the low pHs that are often found in the plaque after eating. So fluoride can protect against decay by promoting remineralization and by inhibiting the mutans streptococci. A recommended fluoride  mouthrinse would be Act®, (McNeil-PPC Inc), a pleasant tasting sodium fluoride mouthrinse, that has proven anticaries activity.

Another treatment that is available is the use of an antimicrobial agent named chlorhexidine. Chlorhexidine has been used as a skin disinfectant for almost 40 years, but about 20 years ago a prescription mouthrinse has been approved for gum disease. This mouthrinse has not been approved for the treatment of dental decay, but studies performed in Europe, mostly in Sweden, have shown that chlorhexidine, delivered in gels or mouthrinses, is very effective against the mutans streptococci. The chlorhexidine is taken for short periods of time. But chlorhexidine has a bitter taste that may discourage some people, especially children, from using it. But for the adult with recurrent decay, it may be an excellent way to control a mutans streptococci infection. Several groups are making a varnish that releases chlorhexidine slowly from the teeth after the varnish is applied Only a few applications of the varnish are needed per year. A Canadian company (CHX Technologies) will begin selling in 2005 a chlorhexidine varnish  for the reduction of root surface decay in adults. Adults who have a low salivary flow because of various medications, and/or who have exposed root surfaces because of periodontal disease would be at risk for root surface decay. This treatment should be reserved for individuals with one or more risk factors for dental decay.

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