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Current concepts on pathogenesis of dental caries

Dental caries is an irreversible microbial disease of calcified tissues of the teeth,


characterised by de-mineralisation of inorganic portion and destruction of organic
substance of the tooth, which often lead to cavitation.

Dental caries is caused by acid (Chemical Theory) produces by microorgamism


(parasitic theory) from fermentation of dietary carbohydrate. Miller’s Chemoparasite
theory (Acidogenic Theory) ,which is the most acceptible theory , state that dental decay is a
combination of chemical and septic theories that consist of two stages: Decalcification of soft
tissue due to fermentation of starch and sugar and dissolution of softened residue. It is
proposed that different kind of food, like bread and sugar that incubated with saliva, at
body temperature , 37 ‘C within 48 hours will cause decalcification of crown of tooth and
production of lactic acid that will lead to caries. Miller believed that caries was not caused
by any single organisms but rather a variety of microorganisms. His theory can be
schematically represented as follows:

According to current consepts, susceptible host is required for progression of tooth


caries. Tooth morphology is one of the determinant. Pit and fissure areas in posterior teeth
especially molars are more susceptible to caries. These areas are more readily to trap food,
bacteria, and debris. To elaborate, the surface of tooth that are more prone to caries is
different among the teeth.

Maxillary arch Occlusal > mesial > distal > lingual > buccal

Mandibular arch Occlusal > buccal > mesial > distal > lingual

All teeth Occlusal > mesial > distal > buccal > lingual
Besides, misaligned teeth, teeth that are out of position and are rotated are more prone to
dental caries due to easier stagnation of bacteria.
Different area of tooth have different rate of decay due to its composition. Surface
enamel are more caries resistance than subsurface because it contain higher level of
fluoride, zinc, lead and are more mineralised than the subsurface. It also contain higher
organic matrix but lower in carbon dioxide and less water content .

Diet play important role in dental caries. Fibrous food cleanses teeth and stimulates
saliva while soft and sticky food increase risk of caries. Diet rich in phosphate, molybdenum
and vanasium are good in caries prevention. However, carbohydrate increases risk of caries.
The more frequent the intake of carbohydrates, the more is the likelihood for caries to occur,
as there is a steady supply of substrate to the bacteria to produce acid constantly.Intake of
sucrose between meals, especially sticky food will increase progression to caries. First,
carbohydrate is broken down to produce fructose, sucrose and fructose. These molecules
diffuse rapidly into plaque due to its low molecular weight . These are easily available for
fermentation for plaque bacteria that will then cause acid production and subsequently
demineralisation of enamel. Besides, diet containing adequate vitamin A,D,E,K, B complex
and minerals can reduce dental caries. However, lack of the vitamin can lead to enamel
hypoplasia

Caries cannot occur without microorganism. According to Miller’s Theory, one or


more bacteria are involved in progression of dental caries. Example of microorganisms
include streptococci species like S.Mutans, S,Sanguis and S.Salivarius ; Lactobacillus and
Actinomyces that include A.Naselundi, A.israeli, and A.naselundi. S.Mutans which is
acidogenic synthesis dextrans from sucrose with the help of enzyme glucosyl transferase.
Dextrans adhere plaque more firmly to the tooth which then cause more tooth decay. S.
Mutans usually adhere and grow on hard and smooth surface of teeth and form adhesive
plaque. It synthesis intracellular polysaccharide in form of amylopectin that help acid
production even if sucrose is absent. Lactobacilus , which is gram positive, are not capable
of adhering on smooth surface . Hence, they usually found in deep fissures and act as
secondary invaders . While Actinomyces, gram positive bacteria usually colonies dental
plaques and cause root caries. Veilnella, gram negative cocci is anticariogenic due to lack of
enzyme required for glycolysis.
Distribution of microorganism is different at different area of tooth. For instance,
S.Mutans is highest in pits and fissures and is lesser in smooth surface caries. In root caries,
higher number of Actinomyces and S.Anguis are detectable while in deep dentinal caries,
Lactobacilli and Arachina. These can be illustrated in the table below.
Bacterium Fissure Approximal Gingival Crevice
Streptococcus +++++ +++ +++
Actinomyces +++ ++++ +++

Lactobacillus +/- +/- +/-


Veillonella ++ +++ ++
Fusobacterium - + +
Spirocetes - - +
Gram Negative Anaeorobes + /- + ++

Dental plaque can contribute to dental caries. Plaque is a soft,


tenacious, biofilm on the tooth surfaces and intraoral appliances
exposed to the saliva, harbouring a diverse range of bacteria
embedded in a matrix of glycoproteins of salivary origin. It also holds
the acids on tooth surface for long duration and protects the acids
produced by the bacteria from getting neutralized by the buffering
actions of saliva. These acidogenic microorganism demineralise
cementum and dentin, while proteolytic organisms hydrolyse dentin
collagen matrix. As time progresses,the composition of microflora
changes due to altered environmental conditions (pH and nutritional
sources ). This favours formation or gram negative microorganism
like Provotella and Porphyromonas species which are aciduric that
will ferment carbohydrates and produce acid. They then secrete
extracellular polysaccharides (glucans and fructans) and intracellular
polysaccharides that are glycogen-storage compound used for energy
production. Glucans contribute to plaque matrix whereas fructans are
labile and can be metabolised under carbohydrate-restricted
conditions.

Acids also play important role in dental caries. Acids is produced


due to fermentation of carbohydrates and this results in drop in saliva
pH at plaque tooth interface. When PH dropped to PH5.5 (critical PH), saliva ceases
to be saturated with calcium and phosphate and demineralization of tooth surface starts .
When PH drop to PH5.0, subsurface demineralisation occurred. when PH further drop to
PH3.0 - 4.0, enamel will start to etch and resorb. Such repeated attacks of acid
results in cavitations of tooth .
In this case , saliva act as buffer that neutralise acid by demineralisation and
remineralisation of teeth, hence changing the pH. Example of buffer substance include
bicarbonate, which increases with salivary flow. Urea, phosphates, ammonia, nitrites are
other buffering agents in saliva. These changes can be illustrtated by Stephen’s Curve as the
diagram below.
Saliva also act as antibacterial agent. Saliva contain lactoferrin , which is iron-binding
protein that bind to iron to prevent iron from being used by bacteria and lysozyme that is
antimicrobial and can alter the intermediary glucose metabolism. Saliva also contain organic
substacnce that can prevent caries like peroxidase, ammonia ,urea, amylase, statherin ,
mucin, and salivary IgA that can inhibit bacterial adherence to tooth surface by binding to
surface adhesins of bacteria and then neutralise the negative charge on bacterial surface.
However, decreased rate of salivary flow will increase rate of dental caries. People suffering
from decreased salivary secretion is known as xerostomia and it is often associated with
Sjogren’s Syndrome. Viscosity of saliva is also affect rate of caries; too thick saliva increase
plaque accumulation while too thin saliva contains less minerals and bicarbonate that will
the increase the risk of caries.

All of these factors lead to demineralisation of dentin, and later dental caries time
progresses.