Caries is an infectious disease

True. But this really does depend on how you define "infectious disease". Caries differs from classical examples of infectious diseases such as cholera, tuberculosis, poliomyelitis, diptheria and smallpox in a number of ways.

For example:

1. the disease is multifactorial
2. there is more than one microbial agent
3. the bacterial agent is a commensal

The development of caries depends on the interaction between the host defences, dental plaque, the diet and a susceptible tooth surface and, of course, time because caries does not happen overnight. Certainly, caries is not viewed as a classical infectious disease by epidemiologists but the argument is by no means straight forward.

For example
No one would argue that HIV is not an infectious disease yet there are parallels with caries since one can be infected with HIV yet not develop symptoms. Furthermore we think that some event triggers the virus resulting in immune suppression and ensuing AIDS. Similarly with Streptococcus mutans which is frequently transmitted to infants where it exists without causing much harm unless it encounters favourable conditions, such as frequent sugar intake, when it will initiate caries.

Caries is a multifactorial disease

There is considerable evidence from animal and human studies showing that caries results from the transmission of Streptococcus mutans so, on balance, it is reasonable to refer to caries as an infectious disease.

Streptococcus mutans can only be isolated from plaque found over white-spot lesions

False. Streptococcus mutans is a commensal and is found in all but edentulous mouths. It is acquired from the individual's mother (carer) during a "window of infectivity" some 12-24 months after the emergence of the first tooth and disappears if all teeth are lost. It's only habitat is, therefore, the tooth.

Sampling any tooth surface or dental plaque will almost inevitably reveal the presence of Streptococcus mutans albeit in relatively low proportions compared with other oral streptococci such as Streptococcus oralis and Streptococcus sanguis.

The proportion of Streptococcus mutans in plaque has, however, been shown to increase in subjects with a high carbohydrate diet and reduce if that diet is replaced with one low in carbohydrates.

The proportion of Streptococcus mutans has also been shown to increase greatly in the dental plaque adjacent to the tooth surface immediately prior to white spot lesion formation at that site. This is interpreted as good evidence for the role of Streptococcus mutans in the initiation of a carious lesion.

Streptococcus sobrinus is more common in human fissure plaque than Streptococcus mutans

False. Although Streptococcus mutans and Streptococcus sobrinus both belong to the "mutans streptococci" they are very different microorganisms. Generally, the prevalence (the percentage of a population carrying the microbe) of Streptococcus mutans is higher than Streptococcus sobrinus but there are wide geographical and age-related variations. Some individuals carry both species at the same time which suggests they occupy different ecological niches.

This is consistent with research on the adhesion capabilities of both species which has shown that Streptococcus sobrinus is better at adhering to smooth surfaces than Streptococcus mutans. Research has also shown that Streptococcus mutans is found more frequently and in higher numbers than Streptococcus sobrinus in fissures.

Lactobacilli are found in high numbers in dental plaque associated with a caries lesion

True. The fact that they can be found in such numbers at the sites of lesions fooled early researchers into thinking that this was because they were the cause of the lesion. Now, of course, we know better.

Plaque at the site of an active lesion will freqently exhibit low pH which greatly favours acidophilic microorganisms such as lactobacilli. These will multiply faster than less acidophilic microbes and soon be present in relatively large numbers.

We now know that Streptococcus mutans is important in initiating a lesion. However, lactobacilli are also fermentative microbes and will contribute organic acids to aid lesion development.

Infants acquire Streptococcus mutans from their mothers within 2 weeks of being born

False. Streptococcus mutans only adhere to teeth and are absent from edentulous mouths. Infants acquire Streptococcus mutans during a "window of infectivity", some 12-24 months after the emergence of the first tooth. The microbe is not necessarily transmitted from their mother although this is the most common source.

It has been suggested that treatment designed to delay the acquisition of Streptococcus mutans in order to allow the rest of the oral flora time to stabilise could delay the onset of caries.

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