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Dental plaque and caries

Topic Progress:

Dental Plaque and Caries

Author: Sanketh DS, MDS

Dental caries is a microbial disease of the calcified tissues of the tooth, characterised by demineralization of the inorganic portion and dissolution of the organic portion of the tooth. It is a dynamic process where the balance between mineralization and demineralization tilts in favour of demineralization. This balance depends on several factors like structure of tooth, dental plaque, saliva, micro-organisms, diet consumed and frequency of food consumption. A significant factor influencing the formation of dental caries is “dental plaque”.


Formation of Dental Plaque

Dental plaque is a yellowish-white deposit/biofilm that forms on teeth and other hard structures in the oral cavity. It comprises predominantly of bacterial communities in a matrix of exfoliated epithelial cells, bacterial and salivary proteins. In addition to proteins the matrix may also harbour carbohydrates like glucans, fructans and other polysaccharides synthesized by bacteria, lipid material and inorganic constituents like calcium and phosphate. The dental plaque biofilm cannot be removed by physiologic tongue movements, salivary flow or when flushed with water. However it could be removed on tooth brushing.

Dental plaque formation starts with the acquired pellicle formation. Acquired pellicle is a coating made of salivary glycoproteins, on the surface of the tooth which immediately forms in a matter of seconds after tooth brushing. This coating of salivary pellicle helps in adherence of bacteria to the tooth via receptors that are recognised by bacterial molecules called adhesins. These are primary colonizers in the dental plaque. Extracellular polysaccharides secreted by bacteria help in adhesion of more bacteria on the existing bacteria in the plaque. Secondary colonizers kick in afterwards and bacteria continue to grow and adhere to each other. Bacteria along with their metabolites, cellular debris and salivary proteins accumulate and together form the plaque mass which continues to grow and mature.

Proposed theories of disease

There were two schools of thought with regards to plaque causing dental caries. One was “Non-Specific plaque hypothesis” and the other “Specific Plaque hypothesis”. Non-Specific plaque hypothesis stated that the entire microflora in plaque were collectively pathogenic and were responsible for the disease. Specific plaque hypothesis on the other hand stated that only particular bacterial species in plaque were pathogenic.

However, Marsh had proposed another theory called the “Ecological Plaque hypothesis”, where he considered disease to result due to an ecological imbalance in the plaque microfloral community. Once plaque is formed, the bacterial composition of the plaque is diverse and varies at different sites. There is microbial homeostasis or balance maintained between the different species of microbial community in the plaque, in spite of subtle changes in different environmental factors like salivary flow, diet and host defence mechanisms.  Plaque could also harbour pathogenic caries causing bacteria but they are present in very small proportions and are not enough to cause disease. However, a major environmental change or ecological shift could lead to an imbalance in the bacterial community, favouring excess growth and survival of pathogenic species leading to disease like dental caries.  

Mechanism of caries formation

As far as caries is concerned, a major shift in homeostasis could occur as a result of excess intake of sugar in the form of fermentable carbohydrates especially sucrose. Now, Streptococcus mutans and lactobacilli species have been implicated in causing dental caries. S.mutans metabolizes most of sucrose to meet its energy needs and produces lactic acid. Some of sucrose is also used to form extra-cellular polysaccharides like glucans and fructans. S.mutans possesses an enzyme called invertase which can cleave sucrose to glucose and fructose. Using another set of enzymes called glucosyl transferase and fructosyl transferase, S.mutans further converts glucose and fructose to extra-cellular polysaccharides called glucans and fructans respectively. Fructans are easily soluble and are used as a reservoir for further energy needs. However, glucans are insoluble and help in further adherence and accumulation of more caries causing streptococci. S.mutans contains glucans binding proteins which help in adhesion. Glucans also increase the bulk of plaque, cause further diffusion of sucrose and block the outward diffusion of acid.

This increase in lactic acid could decrease the pH of the local environment making it very acidic. Caries causing bacteria like S.mutans and lactobacilli species can thrive (aciduric) and proliferate in such environments and start to increase in population. Besides thriving, they produce more acid (acidogenic) and this ecologic shift to an acidic environment increases cariogenic bacterial population and decreases the non-cariogenic bacterial population altering the balance or homeostasis of the bacterial community.

Now, an increase in acidic environment locally is usually buffered and neutralized within 30-60 minutes by calcium and phosphate ions in the saliva. The problem arises when the pH falls to 5.5 (“critical pH”) or below. In order to buffer the acidic environment, minerals from the saliva keep moving to the tooth-plaque interface. However, the saliva starts to get under-saturated, with minerals. To meet the mineral demand in the saliva, hydroxy-apatite (HA) crystals from the tooth start to disintegrate and move to the saliva. On removal of the acidic environment, the saliva, now super-saturated with minerals, precipitates minerals back to the tooth, re-mineralizing it. If the acidic environment persists, HA crystals would continue to disintegrate forming a cavitation on the tooth surface.


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