The term minimal intervention (MI) is relatively new in dentistry and has been introduced to suggest that the profession should move away from its current approach to the treatment of dental caries.
It is now widely accepted that caries is a bacterial infection and cannot be treated by surgical means alone. The modern approach to the management of the disease of dental caries relies on dentists taking the role of physicians first and surgeons second.
A logical starting point in any discussion about caries is its definition. To the layperson caries is a cavity, or putting it simply, a ‘hole in the tooth’. Some dentists also hold this view. To both groups the cavity matters because it requires ‘treatment’, which implies a filling (or in severe cases extraction of the tooth). This belief leads to a profession and a public that consider filling teeth the only way to treat caries. The remuneration system is also largely based upon this belief, with dentists expected only to bill for the time the drill is ‘spinning’. The mentality of ‘drill, fill and bill’ is indeed very much alive today. Conversely, little if any remuneration is generated under current fee scales for dental procedures that address detection and prevention of the causes of the caries process in patients.
Scientifically, the above argument makes little sense. Nikiforuk, in a classic textbook of cariology published in 1983, stated: ‘A carious lesion is the result of the action of bacterial metabolic end products localised to the enamel surface by a dental plaque’. Thylstrup and Fejerskov, in another cariology textbook published in 1996, defined caries as ‘a dynamic process, taking place in the microbial deposits (dental plaque) that results in a disturbance of the equilibrium between tooth substrate and the surrounding plaque fluid’.
The above definitions were written 13 years apart but they both support the well-established fact that it is the biofilm on the tooth surface and its inhabitants that are the driving forces for the carious process. The hole in the tooth is nothing more than the outcome of the bacterial infection.
If you accept the argument put forward so far, then it becomes obvious that the role of operative dentistry (to re-establish form and maintain physical integrity of a tooth) should not be the prime driver in the management of the disease. It is only aimed at treating the outcome, not the cause, of the disease.
There has been a large amount of material written of late discussing MI and why we should practise dentistry in this fashion. The World Dental Federation (FDI) recently commissioned a paper on minimal intervention and the authors suggested that the following four principles must be applied to fulfil the description of minimal intervention dentistry:
1. Control the disease through reduction of the cariogenic flora
2. Remineralise early lesions
3. Perform minimal intervention surgical procedures, as required
4. Repair, rather than replace, defective restorations.
In the context of MI, a ‘new age’ dentist needs to assess the patient’s caries risk and activity (or lifestyle) profiles before the first requirement can be fulfilled. The essential aspects of diagnosis involve assessing the underlying caries risk factors, which cannot be detected during a routine examination using ‘mirror and probe’ or even radiographs. Examining the following factors instead can detect disease risk factors:
• Minor salivary gland activity
• Resting pH
• Stimulated salivary flow
• Buffering capacity
• Composition, e.g. Streptococcus mutans count
• Activity, e.g. lactic acid production
• Past exposure
• Current exposure
• Frequency of sugar hits
• Frequency of acid hits
5. History/lifestyle assessment
Factors belonging to the first four categories affect the metabolism of plaque in a direct manner. Those found in the last one only make an indirect contribution. For example, patients from a low socio-economic background tend to have a cariogenic diet because of poor income and a low level of awareness and oral health education.
The importance of lifestyle assessment should not be overlooked. The case report shown here demonstrates how rapidly caries can progress when the oral environment changes. The patient was a healthy 35-year-old physiotherapist who regularly attended for check-ups and had a history of low caries activity (Figure 1).
In 2001 he presented with an extensive carious lesion with suspected pulpal involvement in his lower right second molar (Figure 2). A radiograph taken 12 months previously (Figure 3) showed evidence of early demineralisation, but in view of the perceived low risk profile the decision was made to monitor the lesion. What happened to cause such a dramatic change in his disease activity?
The patient had undergone a lifestyle change. He had decided to improve his fitness and had begun competing in triathlons. The change intended to improve his health and fitness produced significant changes in his mouth. Endurance sports such as triathlons typically lead to dehydration, and consequently reduced saliva production. In an attempt to replace lost body fluids athletes often use sports drinks.
Almost all sports drinks are acidic with a pH well below the critical pH at which enamel begins to demineralise. They also have high sugar content. The plaque bacteria therefore have increased supplies of sugar with which to produce acid. The protection normally provided by the tooth’s natural defence mechanism, saliva, has been severely reduced and the result is rapid progressing of the lesion.
What we learn from this case is that a change in risk factors can produce rapid changes in a patient’s disease activity, and therefore risk status. A history of low disease activity does not mean a person will stay in a low risk category. If dentists understand the disease process and are prepared to monitor their patients regularly for changes in risk profile, then the disease can be treated and the effects reversed before cavitation occurs.