Rotten teeth are the signs of a disease which is called dental caries or tooth decay. In medicine and dentistry an individual area of rot in a tooth is called a carious lesion. A rotten tooth is called a carious tooth.

History of the caries epidemic

Caries of root surfaces occurred in a small proportion of adults in ancient societies, just as it does in 'primitive' societies today. The disease can occur after periodontal disease has caused gingival recession, if the diet contains a high level of carbohydrates, such as plant starches. When such caries occurs it usually causes few problems. The lesions tend to increase in size relatively slowly, over many years. The associated progression of periodontal disease usually causes the loosening and then loss of teeth before such caries progresses sufficiently to cause more severe infection. A very different kind of caries developed and became a problem for people in Europe and then in North America in the 1700's.

The manufacture, distribution and marketing of sucrose as a food additive became common through the development of the sugar cane industry in North America, then the sugar beet industry in Europe.

A large proportion of people in the countries where sucrose became widely available developed rapidly-advancing dental caries which began in the tooth enamel. For reasons that we now understand well, these individuals experienced pain, severe localized infection within relatively dense bone and then systemic illness. Suddenly, a disease which could be extremely painful and even deadly became common in children and young adults.

When the epidemic began no-one understood its cause. All that people could do at the time was treat its consequences. Treatment was by surgery, usually by extracting the tooth, and was very difficult for the surgeon (and very painful for the patient). Surgeons were not particularly admired at the time, because their work was crude, painful and often failed. A new type of surgeon, the dental surgeon, was needed. The dental profession began as a group of people who were also not very admired, but were very much needed.

How the disease has been treated in the past

It is useful to consider caries treatment in three historical phases.

Phase 1

When the enamel caries epidemic began, the disease was thought to be gangrene of the teeth. Gangrene is death of part of the body. If left untreated, a gangrenous area increases in size until the afflicted individual became ill and died. Caries was treated as gangrene of other parts of the body was treated at that time, by surgical removal. Extraction was the equivalent of amputation for gangrenous limbs. The surgical specialty of dentistry developed because of the high demand for caries treatment by extraction. Extraction is physically difficult in young people with good periodontal health. However it was effective in eliminating the disease from an individual when all of the teeth had gone.

When debridement by extraction was the principal method of treatment diagnosis was simple. It was appropriate to respond to patients' symptoms of discomfort or pain and to make the diagnosis of disease at that stage. 'Maintaining the vital force' through good nutrition and good general health was the only preventive strategy available. There is no evidence that this approach was effective.

An alternative method of surgical removal, and a simpler one than extraction, was local debridement by cleaning out the decayed area. Many dentists advocated using a small file to abrade away approximal areas of teeth, including the area of the early lesion, to treat the disease. After the file was used the area was left open to saliva. This had some advantages because it was a simple treatment and the decay was slow to recur. But it also had the disadvantages that food tended to lodge between the teeth and the teeth tended to move over time.

Local removal and then filling the resultant cavity was also attempted. The decay was removed with hand scrapers ('excavators) or rotating burs. The early filings sealed badly and tended to fail within months, or a few years at most, because of continuing decay. Despite its low success rate, some dentists used fillings because they were less difficult and, in a time when there was no local anesthesia, less traumatic for the patient.

Early fillings were metal - lead, tin or gold. Each of these metals could be pressed or hammered into the cavity. Pure gold was the most difficult of these metals to handle, but tended to last longer if it was very carefully placed and thoroughly condensed. Small bundles of very thin sheets of pure gold, called gold foil, were added one-by-one with tiny instruments and welded together using small hammers, called mallets. A mixture of silver and mercury, called dental amalgam, was also used to fill cavities. The mixture is initially soft, so it can be packed into the cavity with only moderate pressure, and because of chemical reactions between the silver and mercury new compounds are formed and it becomes hard.

Phase 2

The concept that caries was gangrene continued well into the 20th Century, and many patterns of care which flow from that concept continue up to the present time.

The fastidious and systematic refinement of cavity design and filling technologies in the early 1900's, mainly through the work of dentists in North America, changed the nature of caries treatment. Through this work the outcome of the restorative approach was improved until by mid-century it became preferable to extraction. Carefully-placed restorations (which by mid-century included fillings, onlays and crowns) tended to leak less. It became commonplace for restorations to last several years before they failed through continuing decay.

Complete removal of carious enamel and dentin was thought to be an essential part of successful filling design. Restorative materials did not adhere to teeth. In order for them to stay in place decayed areas had to be modified in shape, with hand or rotary cutting instruments, to make retentive cavity forms. Cavity shapes were also modified to increase the strength of the tooth and restoration. Minimal sizes of cavities were also mandated, so that the junction between the filling and tooth was on areas of the tooth where caries did not usually begin, in the hope that this would result in restorations which would last longer before recurrent decay occurred. This was called 'extension for prevention'. The act of making a restoration therefore usually involved the removal of substantial amount of tooth structure, often several times more than was actually decayed.

Preparing large cavities in hard tooth structure with hand cutting instruments (chisels, hatchets and hoes) was very slow and difficult, but it became easier as rotary cutting instruments (rotary burs) were developed and refined. By the 1970's high-speed, air turbine-driven rotary cutting instruments became widely available. It became relatively easy to prepare large cavities using tungsten carbide burs and industrial diamond-impregnated rotary instruments.

Diagnosis in Phase 2

In phase 1 patients' symptoms had been central to diagnosis. Perhaps unfortunately the main symptom of caries, pulpal pain, develops relatively late, when substantial amounts of tooth structure

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have been lost. Waiting for pain to develop was not a good strategy if fillings were to be used as the method of treatment. The most successful way to manage caries using filling technologies involved finding the decay early, whether it was new caries (primary caries, on previously unrestored tooth surfaces) or recurrent caries (adjacent to existing restorations).

Detection became essentially the same as diagnosis. Diagnostic technologies were developed which aided early detection, namely:

• Direct visual inspection
• Indirect vision (using the mouth mirror)
• Auxiliary external illumination
• Transillumination
• The use of sharp explorers (to detect softened enamel, particularly in pits and fissures)
• Radiography
• Separation and the use of floss silk to aid in detection of approximal lesions.

Prevention in phase 2

In the 1950s the concept that caries was caused by acids produced by bacterial action on residual food on and around the teeth became widely accepted. Brushing teeth after meals to remove residual food was widely advocated as a preventive strategy but had little effect on caries rates. Advising patients to change their food choices and to eat less often was a rational approach, but few individuals took that advice.

In the 1970s the concept that caries was caused by dental plaque became widely accepted. Patients were advised to brush and floss teeth to remove plaque. The epidemiological discovery that fluoride in the diet and then the experimental demonstration topical application of fluoride both decreased caries experience led to the dietary fluoride supplements in children, water fluoridation and the use of topical fluorides in dentifrices, rinses and gels. The combination of fastidious plaque removal and fluoride use was shown to be effective in reducing caries in individuals and in whole populations.

The development of polymeric materials which bonded to enamel brought with it the ability to seal fissures. Fissures are areas of high likelihood for caries initiation in individuals who have the disease. Sealed fissures have a greatly reduced incidence of caries initiation. During this phase, when all individuals were considered to be at risk for caries, placement of fissure sealants in all children and young adults was an appropriate preventive strategy.

Standard of care in Phase 2

By mid-century the principal method of treatment of caries had become the restoration. Extraction was reserved for the extensively restored tooth which could no longer retain a restoration or which had fractured, or for patients who could not afford restorative treatment. The accepted standard of care for patients who could afford repeated restoration was to be examined frequently (usually at 6-monthly intervals) using the best aids to detection available. The repeated cycles of tooth restoration resulted in larger and larger restorations. Ideally, this continued until the patient died of old age. Improvements in restorative materials, particularly those which adhere to teeth and therefore tend not to leak(e.g. composite resin in some applications, and glass ionomer cement) and those which release fluoride (e.g. glass ionomer cement) increased the longevity of restorations. Unfortunately, however, extensively restored teeth sometimes fracture and must be extracted. Fixed bridges, removable dentures and implant-supported replacements could be offered to assist patients who had lost teeth because of this style of care. Because virtually the entire population of the industrialized societies with had caries (except those who had no teeth), it was appropriate to apply these preventive technologies to everyone with teeth. 'Prevention' was essentially the same for everyone. 'Cure' was not a concept that was used in dentistry relative to caries in this phase, because the only cure for caries was to extract all of the teeth.

Phase 3 - the present

Our Present Understanding of the Disease

Throughout the late 20th Century an increasingly detailed concept of the nature of caries developed, because of scientific research. There is now very strong evidence that the disease is not gangrene. There are therefore strong grounds to change the ways that the disease is treated.

A large body of data show that caries is the progressive loss of tooth mineral, followed by bacterial invasion into the demineralized tooth. It is a relatively complex disease. The nature of caries can be described in terms of five interrelated factors. In addition to helping explain the nature of the disease, each factors gives guidance to how to prevent it and to how it can be cured.

Factor 1. Caries is a bacterial disease

There is abundant evidence that the initiation of caries requires a relatively high proportion of mutans streptococci within dental plaque. These bacteria adhere well to the tooth surface, produce higher amounts of acid from sugars than other bacterial types, can survive better than other bacteria in an acid environment, and produce extracellular polysaccharides from sucrose. When the proportion of s. mutans in plaque is high (in the range 2-10%) a patient is at high risk for caries. When the proportion is low (less than 0.1%) the patient is at low risk. Infection with s mutans usually happens early in childhood by transmission from the mouths of parents or playmates. Because they are more acid tolerant than other bacteria, acid condition within plaque favor the survival and reproduction of mutans streptococci. Two other types of bacteria are also associated with the progression of caries through dentin. These are several species of lactobacillus, and actinomyces viscosus. These bacteria are also highly acidogenic and survive well in acid conditions.

Factor 2. Caries is dependent on dietary sucrose

Dietary sucrose changes both the thickness and the chemical nature of plaque. Mutans streptococci and some other plaque bacteria use the monosaccharide components (glucose and fructose) and the energy of the disaccharide bond of sucrose to assemble extracellular polysaccharides. These increase the thickness of plaque substantially, and also change the chemical nature of its extracellular space from liquid to gel. The gel limits movement of some ions. Thick gel-plaque allows the development of an acid environment against the tooth surface, protected from salivary buffering. Plaque which has not had contact with sucrose is both thinner and better buffered. A diet with a high proportion of sucrose therefore increases caries risk. Thicker plaque occurs in pits and fissures (which is why Site 1 lesions begin there), just beneath the contact area (Site 2) and, in patients with poor oral hygiene, near the gingival margin (Site 3).

Factor 3. Caries is driven by frequency of eating

Each time that plaque bacteria come into contact with food or drink containing simple sugars (monosaccharides such as glucose and fructose, and disaccharides such as sucrose, lactose and maltose) they use them for their metabolic needs, making organic acids as a metabolic by-product. If these acids are not buffered by saliva they dissolve the surface of the apatite crystals of adjacent tooth structure. This is called demineralization. In thick gel-plaque the pH falls within seconds of contact with dietary sugars, and it can stay low for up to 2 hours. When the pH is neutral the same crystals can re-grow, using calcium, phosphate and fluoride from saliva. This is called remineralization. Caries begins and progresses when demineralization outweighs remineralization. Caries therefore depends on the balance between demineralization and remineralization, i.e. on the frequency of eating (and on the microbial composition of the plaque and its chemical nature and thickness, on the local fluoride concentration and on the buffering capacity of saliva). A frequent pattern of eating therefore increases caries risk.

Factor 4. Caries is modified by fluoride

The mineral of enamel, cementum and dentin is a highly-substituted calcium phosphate salt called apatite. The apatite of newly-formed teeth is rich in carbonate, has relatively little fluoride and is relatively soluble. Cycles of partial demineralization and then remineralization in a fluoride-rich environment creates apatite which has less carbonate, more fluoride and is less soluble. Fluoride-rich, low carbonate apatite can be up to ten times less soluble than apatite low in fluoride and high in carbonate. Topical fluoride also inhibits acid production by plaque bacteria. Fluoride in food and drinks, fluoride in dentifrices and oral rinses and gels, and fluoride in filling materials can therefore all reduce the solubility of teeth, helping to reduce caries risk. These effects are very beneficial, but the amounts of fluoride which can be added to the diet or used topically are limited by safety considerations. High levels of dietary fluoride can cause mottling of tooth enamel during tooth formation, while swallowing even higher levels can cause symptoms of poisoning.

Factor 5. Caries is modified by saliva

High flow-rate saliva is a very effective buffer. The balance between demineralization and remineralization can therefore be altered substantially by the rate of salivary flow. Flow is decreased by salivary gland pathology (as occurs in several connective tissue disease and which can follow radiotherapy and cancer chemotherapy), by many mood-altering drugs and some drugs used in other medical treatment, in dehydration and during sleep. Flow increases naturally during vigorous chewing. A maximum salivary flow rate (which can be tested by collecting all saliva which chewing wax or gum) of less than 0.7 mL/min. is associated with high caries risk.

How the disease is treated today

Given this concept of the nature of the disease, the logical and ethical standards of care for both caries diagnosis and caries management (prevention, cure and repair) are now very different than they were during the time when caries was thought to be gangrene.

The present, molecular concept of the nature of caries leads us to very different concepts of management of the disease. This, coupled with the widespread use of fluoride and the development of restorative materials which adhere to tooth structure and which (in some cases) do not leak, has revolutionized the prevention and cure of caries, as well as the repair of carious defects in teeth. The key features of the new care paradigms are summarized below.

Diagnosis - since we understand caries to be a dynamic process which occurs at the molecular level we can diagnose the disease before irreversible loss of tooth structure occurs. It is now reasonable to state, on the basis of diagnosis, that some people do have the disease, while others do not. Detection of lesions at the macroscopic level can no longer be considered to be diagnosis, for two reasons - (1) the disease is present before lesions can be detected macroscopically and (2) large lesions remain after the disease is cured. Determination of risk state is a reasonable diagnostic goal, as is activity state.

Management

Treatment and cure

The goal of treatment is now to change the local biochemistry so that the patient is no longer losing tooth mineral so that the disease is then cured and the patient healed. This is logical, ethical, appropriate and achievable.

Caries can be treated by one or more of the following:

• Changing the microflora, using agents such as topical chlorhexidine and topical fluoride
• Reducing the amount of dietary sucrose, by dietary choice
• Decreasing the frequency of eating, by dietary choice
• Adding fluoride, particularly through daily application during tooth brushing
• Increasing salivary flow, using mechanical stimulation during vigorous chewing to enhance flow, by changing drugs which reduce flow, or by using drugs to enhance flow

Cure is achieved when diagnostic tests show that the disease is no longer active and the risk is low.

Repair

Restoration of defects, which was previously thought of as treatment of the disease, is now more reasonably considered to be repair. It will be desirable to stop using the term 'treatment' for such repair, because the standard of care for caries treatment is now behavioral and biochemical, not mechanical. If the disease is cured, restorations should no longer fail because of caries. Limitations on restoration longevity should be related only to failure by wear and fatigue under cyclic load.

Prevention

Non-specific preventive strategies, such as education about the risks of high eating frequency, use of fluoride in the diet and in dentifrices, education about the benefits of fastidious daily tooth cleaning, are still appropriate. Fissure sealants are now best reserved for patients who are known (through accurate diagnosis) to be at high risk. Sealants need not be used in individuals who are known not to have the disease.

Some predictions on treatment in the near future

It is very likely that we will develop more exact diagnostic tools for risk and activity assessment - bacterial diagnostics, mineral balance monitoring. The availability of these tools will mean that dentists will work to actively diagnose the disease at the molecular level before irreversible damage occurs, then treat the disease if it is present so that it will be cured, again before damage (i.e., 'cavities') occurs.

It is also very likely that we will develop new tools to cure the disease, such as S. mutans adherence inhibiting antibodies, better remineralizing solutions and improved ways of local delivery of fluoride.