Throughout the late 20th Century, as a result of extensive scientific research, an increasingly detailed concept of the nature of caries has developed. There is now compelling evidence that the disease is not “gangrene”, as suggested by GV Black. There are therefore very strong grounds for changing the ways that the disease is treated.

Much of the information for this website is derived from the text book entitled “Preservation and Restoration of Tooth Structure”, 2nd Edition, by Mount and Hume which is listed in the References. There will be several references back to the book and the student is urged to study the original for information in depth. We are grateful to the co-authors who contributed so much to the success of the book.

First it is necessary to discuss the actual nature of the disease and its progress through tooth structure. One description of a disease is “a disorder with recognizable signs and a known cause” and this is a fair description of caries. However, before the signs can appear there will need to be modification of the oral environment to allow the establishment of the disorder.

   A large body of data show that caries is the progressive loss of tooth mineral, that is demineralisation, as a result of bacterial activity, and once surface cavitation has occurred, it will be followed by bacterial invasion into the demineralised tooth structure beneath. It is necessary in the first place to recognize the structure of the surface enamel on the tooth crown as well as the dentine beneath. Also an essential element in the initiation of the disease is the presence of the biofilm which constantly covers all surfaces of all teeth and, if removed by oral hygiene procedures will instantly reform. 

Caries is a very complex disease that cannot be described in simple terms because there are at least four inter-related factors involved. These can be listed as follows –

• Bacteria
• Dietary Sucrose
• Frequency of Eating
• Saliva

   A discussion of each of these factors is available by clicking on the appropriate word in the list above.

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 the dental biofilm. They adhere well to the tooth surface, produce higher amounts of acid from sugars than most other bacterial types, can survive well 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. It is also important to note that S. mutans can be transmitted from one person to another e.g. mother to child. When the proportion is low (less than 0.1%) the patient is at low risk. However, there are many other species of bacteria in the biofilm and there is no clear indication as to which is the primary cause and which others make a contribution to demineralisation. It is necessary at this point to keep an open mind so the overall bacteriology of the oral environment is discussed further.

Factor 2. Caries is dependent on dietary sucrose

    Dietary sucrose changes both the thickness and the chemical nature of the oral biofilm. Mutans streptococci and some of the 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 biofilm substantially, and also change the chemical nature of its extracellular space from liquid to gel. The gel limits movement of some ions. Thick biofilm allows the development of an acid environment against the tooth surface, protected from salivary buffering. Thicker plaque occurs in pits and fissures (which is why Site 1 lesions begin there), just beneath the contact area between adjacent teeth (Site 2) and in patients with poor oral hygiene, near the gingival margin (Site 3). See further discussion on the significance of biofilm.

Factor 3. Caries is driven by frequency of eating

    Each time plaque bacteria come into contact with food or drink containing simple sugars 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 apatite crystals of the enamel rods in adjacent tooth structure. This is called demineralisation. The pH within the biofilm will fall dramatically within seconds of contact with dietary sugars, and may stay low for up to 2 hours. However, when the pH returns to neutral the apatite crystals can re-grow, using calcium, phosphate and fluoride ions trapped within the biofilm or held in the saliva. This is called remineralisation. There is a continuous cycle of demineralisation followed by  remineralisation within the oral environment leading normally to a stable balanced situation. Caries represents failure of the maintenance of the balance between demineralisation and remineralisation. That is to say, when the attacks of demineralisation occur too frequently for remineralisation to compensate fully the end result is net loss of mineral from selected areas of the tooth surface and caries progresses.

Factor 4. Caries is modified by Saliva

    Saliva is the one significant natural buffer against high acid levels in the oral environment so a high flow rate is required if a balance is to be maintained. The balance between demineralisation and remineralisation can be substantially modified by the salivary flow rate so the following factors must be taken in to account - 

 • Salivary gland pathology may occur in connective tissue disease.

 • Radiotherapy and chemotherapy may alter saliva flow

 • Mood altering drugs, therapeutic and recreational, will modify flow

 • A wide range of drugs used in medical treatment may be involved in flow    modification.

 • Excessive dehydration following strenuous exercise can be implicated

 • Saliva flow almost ceases during sleep

 • Saliva flow will be stimulated best by vigorous chewing but alternate therapies    are available.

      Saliva should be tested for flow rate, bacteriology and buffering capacity for all    patients with a high caries susceptibility.

       It must be noted at this point that there may be other sources of acids which may be involved in both caries and non-caries tooth loss and these can under some circumstances be very significant. Endogenous acids can also be significant because the S. mutans itself will flourish in highly acid conditions.

Factor 5. Caries susceptibility 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 demineralisation followed by remineralisation in a fluoride-rich environment leads to the creation of apatite which has less carbonate and more fluoride and is therefore less soluble. Fluoride-rich, low carbonate apatite can be up to ten times less soluble than apatite that is 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 restorative materials can therefore all reduce the demineralisation of the tooth surface, thus helping to reduce caries risk. The prescription of fluoride for caries control is discussed further.

There is a large number of therapeutic mouth rinses designed to reduce oral bacterial populations and the most effective of these contain chlorhexidine gluconate. Chlorhexidene with a water base or contained in a gel are recommended because those containing alcohol are dehydrating particularly for patients with poor saliva flow. It will ionically adhere to the teeth and oral mucosal surface in high concentrations for many hours offering a prolonged high level of anti-bacterial action. Note that chlorhexidene should not be applied until half an hour after cleaning the teeth with a traditional dentifrice as the sodium laurel sulphate saponification component in dentifrice can notably reduce chlorhexidine activity.

Click here for prescription of chlorhexidene

Factor 7. Caries susceptibility  can be modified by CCP-ACP

    A new remineralisation technology has been developed based upon phosphopeptides from milk casein. These casein phosphopeptides contain multiphosphoseryl sequences that have the ability to stabilize calcium phosphate in nano-complexes in solution as amorphous calcium phosphate. Through their multiple phosphoseryl sequences the CPP bind to the ACP in metastable solution thus preventing its growth to the critical size required for nucleation and phase trans-formation to an insoluble crystalline calcium phosphate. The casein phosphopeptide-amorphous calcium phosphate  nano-complexes (CPP-ACP) have been shown to localize at the tooth surface  and prevent demineralisation. They also react with fluoride ions to produce an amorphous calcium fluoride phosphate which will provide soluble calcium, phosphate and fluoride ions at the tooth surface and these will allow remineralisation at depth within the early caries lesion. This has significant implications because fluoride alone tends to lead to remineralisation of the surface enamel crystals only thus limiting the penetration of further ions in to the lesion. Click here for prescription of CPP- ACP

It is important in this context to be able to differentiate between caries and non-caries tooth loss. In fact the cause of both problems is essentially the same because both are the result of demineralisation.

Depending on the strength of the acid present, the frequency and duration of production and the remineralisation potential in each particular situation, any one of the following sequelae can occur:

1. the enamel may continue to mature becoming more acid resistant

2. chronic caries may develop i.e. slow demin with active remin (subsurface lesion)

3. rapid (rampant) caries may arise i.e. rapid demin with inadequate remin

4. erosion may occur i.e. very rapid demin with no remin at all

It has been shown in vitro that the chemical nature of the acid attack on the tooth surface can be rapidly modified from one causing erosion to one causing caries, and back again, by minor changes to the saturation level of acid ions with calcium and phosphate ions. It is important for the clinician to be able to distinguish erosion from caries lesions. Erosion lesions are usually “cupped” in shape with a smooth firm base and form at the cervical margin or sometimes on the occlusal surfaces.  In contrast, an active caries lesion shows in the enamel as a “white spot” lesion and then enters dentine with a soft irregular base of demineralised collagen. Differentiation is important because erosion is far more difficult to control than caries.