microbiology of dental caries

Microbiology of dental caries

Oday altaani

Definition: chronic endogenous infection caused by the normal oral commensal flora.

the initial process of enamel demineralization is usually followed by remineralization

Caries is defined as localized destruction of the tissues of the tooth by bacterial fermentation of dietary carbohydrates.

EpidemiologyDental caries (with periodontal disease) is one

of the most common human diseasesCaries of enamel surfaces is particularly

common up to the age of 20 years, after which it tends to stabilize.

in later life, root surface caries becomes increasingly prevalent, due to gingival recession

Classification

ClassificationDental caries can be classified with respect to the

site of the lesion:

i. pit or fissure caries (seen in molars, premolars and the lingual surface of maxillary incisors)

ii. smooth-surface caries (seen mainly on approximal tooth surfaces just below the contact point)

iii. root surface caries (seen on cementum or dentine when the root is exposed to the oral environment)

iv. recurrent caries (associated with an existing restoration).

Clinical presentation

Clinical presentationThe primary lesion of caries is a well-demarcated,

chalky white lesion in which the surface continuity of enamel has not been breached. This ‘white-spot’ lesion can heal or remineralize (reversible).

However, as the lesion develops, the surface becomes roughened and cavitation occurs.

If the lesion is not treated, the cavitation spreads into dentine and eventually may destroy the dental pulp, finally leading to the development of a periapical abscess and purulent infection

Diagnosis

Diagnosis is usually by a combination of:

i. Direct observation.ii. Probing.iii. Radiographs.iv. Experimental methods. laser fluorescence for

diagnosis of buccal and lingual caries and electrical impedance (resistance) to detect occlusal caries.

v. Microbiological tests

Aetiology

Aetiology

The major factors involved in the aetiology of caries are:

i. host factors (tooth, saliva)ii. diet (mainly the intake of fermentable

carbohydrates)iii. plaque microorganisms (i.e. supragingival plaque).

Host factors

Tooth structure

some areas of the same tooth are much more susceptible to carious attack than others, possibly because of differences in mineral content (especially fluoride).

Host factors

Flow rate and composition of saliva

The mechanical washing action of saliva.high buffering capacity.it is supersaturated with calcium and

phosphorus ions.Delivery vehicle for fluoride.

Dietdirect relationship.The most cariogenic sugar is sucrose Sucrose is highly soluble and diffuses easily into dental plaque, producing extracellular polysaccharides and acids.Cariogenic streptococci produce water-insoluble

glucan from sucrose, which, in addition to facilitating initial adhesion of the organisms to the tooth surface, serve as a nutritional source and a matrix for further plaque development.

Diet

The frequency of sugar intake rather than the total amount of sugar consumed appears to be of decisive importance.

Stickiness and concentration.Period

…Polyol carbohydrates, ‘sugar alcohols’ (e.g. xylitol)

Microbiology

Microorganisms in the form of dental plaque are a prerequisite for the development of dental caries.

mutans streptococci have been recognized as the major group of organisms involved in caries.

Microbiology

Specific plaque hypothesis one or more specific groups of bacteria are principally involved in caries.

Nonspecific plaque hypothesis the disease is caused by a heterogeneous mixture of non-specific bacteria.

…Lactobacillus spp. and Actinomyces spp.

The role of mutans streptococciStreptococcus mutans’ is a loosely applied group

name for a collection of seven different species (S.mutans, S. sobrinus, S. criceti, S. ferus, S. ratti, S. macacae and S. downei) and eight serotypes (a–h).

S. mutans serotypes c, e, f and S. sobrinus serotypes d, g are the species most commonly found in humans, with serotype C strains being the most prevalent, followed by d and e.

The role of mutans streptococciThe evidence for the aetiological role of mutans

streptococci in dental caries includes the following:

correlations of mutans streptococci counts in saliva and plaque with the prevalence and incidence of caries.

mutans streptococci can often be isolated from the tooth surface immediately before the development of caries.

positive correlation between the progression of carious lesions and ‘S. mutans’ counts.

production of extracellular polysaccharides from sucrose.

The role of mutans streptococci ability to initiate and maintain microbial growth and to

continue acid production at low pH values. rapid metabolism of sugars to lactic and other organic acids. ability to attain the critical pH for enamel demineralization

more rapidly than other common plaque bacteria. ability to produce intracellular polysaccharides (IPSs) as

glycogen, which may act as a food store for use when dietary carbohydrates are low.

immunization of animals with specific S. mutans serotypes significantly reduces the incidence of caries.

The role of mutans streptococci

Note: Caries may therefore be an infectious disease in a minority, with a highly pathogenic strain being transmitted from one individual to another.

The role of lactobacilliThey were considered to be candidate organisms for

caries because of:their high numbers in most carious lesions affecting

enamel.the positive correlation between their numbers in

plaque and saliva and caries activity.their ability to grow in low-pH environments (below

pH 5) and to produce lactic acid.their ability to synthesize both extracellular and IPSs

from sucrose.

The role of lactobacilli lactobacilli are rarely isolated from plaque before

the development of caries, and they are often absent from incipient lesions.

it is believed that:• they are involved more in the progression of the

deep enamel lesion (rather than the initiation)• they are the pioneer organisms in the advancing

front of the carious process, especially in dentine.

The role of Actinomyces spp.

Actinomyces spp. are associated with the development of root surface caries (softened without obvious cavitation).

Actinomyces spp. (especially A. viscosus) predominate in the majority of plaque samples taken from root surface lesions

The role of Veillonella

Veillonella is a Gram-negative anaerobic coccus that is present in significant numbers in most supragingival plaque samples.

require lactate for growth.Unable to metabolize normal dietary

carbohydrates.Beneficial effect on dental caries.

Plaque metabolism and dental caries

The main source of nutrition for oral bacteria is saliva.

Oral bacteria have developed a number of regulatory mechanisms, which act at three levels:

i. transport of sugar into the organisms.ii. the glycolytic pathway.iii. conversion of pyruvate into metabolic end

products.


dietary sucrose is broken down by bacterial extracellular enzymes such as glucosyl and fructosyl transferases, with the release of glucose and fructose.

Glucans are mostly used as a major bacterial food source.

the insoluble fructans contribute to the plaque matrix while facilitating the adhesion and aggregation of plaque bacteria and serving as a ready, extracellular food source.


During glycolysis, glucose is degraded immediately by bacteria via the Embden–Meyerhof pathway, with the production of two pyruvate molecules:

Under low sugar conditions, pyruvate is converted into ethanol, acetate and formate (mainly by mutans streptococci).

In sugar excess, pyruvate is converted into lactate molecules.


The mutans group streptococci, being the most acidogenic and aciduric (acid-tolerant), are the worst offenders and reduce the plaque pH to low levels, creating hostile conditions for other plaque bacteria.

Ecological plaque hypothesis

Management of dental caries

The modern philosophy in caries management highlights:

i. early detection.ii. the importance of accurate diagnosis.iii. minimal cavity preparation techniques.iv. active prevention.

Patient evaluation In patients with a low incidence of caries, a case history and

clinical and radiographic examination are probably adequate for treatment planning.

for patients with rampant or recurrent caries, or where expensive crown and bridge work is planned, additional investigations are necessary. These include:

assessment of dietary habits. determination of salivary flow rate and buffering capacity. microbiological analysis.

Microbiological tests in caries assessment

Saliva samples can be used to establish the numbers of S.mutans and Lactobacillus spp. in the oral cavity, as follows:

i. A paraffin wax-stimulated sample of mixed saliva is collected.

ii. In the laboratory, the saliva is appropriately diluted and cultured on selective media.

mitis salivarius bacitracin agar for S. Mutans.Rogosa SL agar for Lactobacillus spp.

high caries activity: >106/ml S. mutans and/or >100 000/ml Lactobacillus spp.

low caries activity: <100 000/ml S. mutans and <10 000/ml Lactobacillus spp.

Microbiological tests in caries assessment

The disease of multifactorial aetiology. Other factors, such as diet, buffering capacity, fluoride content of enamel and degree of oral hygiene, should also be considered.

The main uses of microbiology tests in caries assessment are:

to identify patients who have unusually high numbers of potential pathogens.

to monitor the efficacy of caries prevention techniques, such as dietary and oral hygiene advice and the use of antimicrobial agents such as chlorhexidine.

Microbiology of root surface caries

The soft cemental surfaces thus exposed are highly susceptible to microbial colonization by virtue of their irregular and rough surfaces.

high prevalence of Actinomyces naeslundii, Actinomyces odontolyticus and Rothia dentocariosa from human root surface caries.

Lactobacilli, S. mutans together with pleomorphic Gram-positive rods, are also frequent in the deeper dentinal parts of the lesion.

…polymicrobial aetiology for caries initiation and progression on root surfaces.

Prevention of dental cariesThe major approaches to prevention of caries are:i. sugar substitutes.ii. Fluorides.iii. Sealants.iv. reducing cariogenic flora.v. Probiotics: replacement of cariogenic bacteria

by organisms with low or no cariogenic potential.

Sugar substitutesArtificial sweeteners cannot be absorbed and

metabolized to produce acids by the vast majority of plaque bacteria.

Two types of sugar substitute are available:I. nutritive sweeteners with a calorific value, e.g. the

sugar alcohols, sorbitol and xylitol, and lycasin.II. non-nutritive sweeteners, e.g. saccharin and

aspartame.

Fluoridation

Can administered systemically during childhood.

it is incorporated during amelogenesis.The best delivery vehicle is the domestic

water supply (at a concentration of 1 ppm).tablets, topical applications of fluoridated gel

or fluoridated toothpaste may be used.

Fluoridation Fluoride ions exert their anticariogenic effect by:

I. substitution of the hydroxyl groups in hydroxyapatite and formation of fluoroapatite, which is less soluble in acid during amelogenesis.

II. promotion of remineralization of early carious lesions in enamel and dentine.

III. modulation of plaque metabolism by: interference with bacterial membrane permeability. reduced glycolysis. inactivation of key metabolic enzymes by acidifying the cell interior. inhibition of the synthesis of IPSs, especially glycogen.

Fissure sealants

Sealants prevent caries in pits and fissures by eliminating stagnation areas and blocking potential routes of infection.

Early lesions.

Control of cariogenic plaque flora

Control may be achieved by mechanical cleansing, antimicrobial therapy, immunization and replacement therapy.

Mechanical cleansing techniques…it is unlikely that mechanical cleansing even

with flossing, interdental brushes and wood sticks will affect pit and fissure caries.

Control of cariogenic plaque flora Antimicrobial agents:• Chlorhexidine as a 0.2% mouthwash is by far the most effective

antimicrobial in plaque control: Chlorhexidine disrupts the cell membrane and the cell wall

permeability of many Gram-positive and Gram negative bacteria.

It is able to bind tenaciously to oral surfaces and is slowly released into the saliva.

It interferes with the adherence of plaque-forming bacteria, thus reducing the rate of plaque accumulation.

mutans streptococci are exquisitely sensitive to chlorhexidine and are therefore preferentially destroyed.

tooth staining and unpleasant taste…short-term therapy.

Active immunization against dental cariescell wall-associated antigens (antigen I/II) or glucosyl

transferases (extracellular enzymes) from mutans streptococci.

The vaccine may produce its protective effect by: inhibition of the microbial colonization of enamel by

secretory immunoglobulin A (IgA). interference with bacterial metabolism.enhancement of phagocytic activity in the gingival

crevice area due to the opsonization of mutans streptococci with IgA or IgG antibodies.

The antibodies that develop after immunization with most antigens of S. mutans tend to cross-react with heart tissue, and the possibility that heart damage could result has made human vaccine trials very difficult.

Passive immunization when the natural levels of oral mutans streptococci

are suppressed by chlorhexidine, topical application of monoclonal antibodies against antigen I/II of mutans streptococci prevents recolonization by the organisms.

Transgenic plants could be used to produce dimeric antibodies with specificity to antigen I/II of streptococci that are stable in the mouth and persist for longer periods.

Replacement therapy The term probiotic therapy or probiotics is now used for

approaches where the offending pathogen is replaced artificially by innocuous commensals that are allowed to obtain a permanent foothold in the locale.

genetically engineered, low-virulence mutants of mutans streptococci that are deficient in glucosyl transferase or deficient in lactate dehydrogenase activity can be ‘seeded’ into the oral environment.

…These organisms can replace their more virulent counterparts and prevent their re-emergence.

microbiology of dental caries

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