Dental Caries
Dental Caries
Dental Caries
Definitions:
Progressive, largely irreversible bacterial damage to teeth exposed to the oral environment.
Decalcification of enamel & dentine with consequent softening and gradual destruction of
the tooth
Etiology:
Many bacteria ferment sugars to produce acid or secrete enzymes that digest proteins.
Plaque (a soft, thin film of food debris, mucin & dead epithelial cells, providing a medium
for bacterial growth) is the chief etiologic factor in caries and periodontal disease.
Viridans streptococci are among the most numerous bacteria that can be isolated from the
mouth.
This group includes Streptococcus mutans, S. salivarius, S. mitior and S. sanguis.
This complex community of bacteria, termed dental plaque, contains Streptococcus
mutans, which is a necessary agent for the production of dental caries.
S. mutans has been shown to be transmissible from parents or caregivers to infants at the
time of tooth eruption.
Other bacteria such as a few strains of lactobacilli, enterococci & actinomyces have been
shown to be capable of causing caries under special conditions, but are less virulent.
Risk factors
Decay is affected by several factors:
1. Bacteria, (Bacterial plaque containing 3. Susceptible tooth surfaces
cariogenic bacteria) 4. Low levels of fluoride
2. High-carbohydrate diet, (Bacterial 5. Time
substrate, especially sugar)
1. Cariogenic bacteria
Essential features of cariogenic bacteria therefore include the following capabilities:
a) To form acid from any appropriate substrates, i.e. to be acidogenic.
-To produce a pH sufficiently low (usually lower than pH 5) to decalcify tooth
substance
b) To survive and continue to produce acid at low levels of pH, i.e. to be aciduric
c) To have attachment mechanisms for firm adhesion to smooth tooth surfaces.
d) To produce abundant polysaccharides for the formation of bacterial plaque matrix.
e) To produce insoluble polysaccharides that resist dissolution by saliva or dietary fluids.
3. Bacterial plaque
Plaque is a tenaciously adherent deposit that forms on tooth surfaces.
It consists of an organic matrix containing a dense concentration of bacteria.
Bacteria exist in the mouth either freely in saliva (the fluid phase) or in an adherent mass on
surfaces such as the teeth (the solid phase, or bacterial plaque).
Bacterial plaque forms thick deposits in stagnation areas where it is undisturbed.
4. Plaque polysaccharides
These substances, synthesised by bacteria, play an essential role in the pathogenesis of
dental caries.
The bacterial polysaccharides are both intracellular and extracellular.
The proportions of the different types of polysaccharide, and the overall amounts formed,
depend both on the kinds of bacteria present and the different dietary sugars available.
On a sucrose-rich diet the main extracellular polysaccharides are glucans.
Fructans formed from fructose are produced in smaller amounts.
SUCROSE is the most important foodstuff serving as bacterial substrate;
1. Because of its metabolism by S. mutans to the glucans necessary for plaque formation
and function.
2. Because it is readily metabolized to form acid.
3. Because it is eaten in greater quantity than any other sugar.
The cariogenicity of sucrose depends on the fact that it is
1. An effective substrate for acidogenic 2. A major substrate for plaque
bacteria formation.
Pathogenesis:
Enamel caries develops in four main phases:
1. The early lesion 3. Bacterial invasion of enamel
2. Phase of enamel destruction 4. Secondary enamel caries.
S. mutans bacteria produce acidic metabolic end products from dietary fermentable
carbohydrates, which demineralize the enamel.
When carbohydrates are left on the teeth after eating or drinking, bacteria metabolize them
and produce acids.
These acids slowly demineralize the enamel protecting the tooth and result in caries.
This demineralization is reversible in the early stages of caries development, but as the
process progresses, cavitation occurs, and bacteria further invade the mineral portion of the
tooth.
Once this occurs, failure to stop the process inevitably leads to loss of the tooth.
The essential components necessary for the development of dental caries are:
1. Acidogenic bacteria 4. Low levels of fluoride
2. Fermentable carbohydrates 5. Time
3. Susceptible host (see below)
Host characteristics that alter the susceptibility to caries include:
1. Salivary 2. Salivary pH 3. Salivary Flow rate
composition (Xerostomia)
4. Immunologic 5. Quality of tooth 6. Tooth morphology
factors maturation
Defects in any of these factors may result in increased risk of dental caries.
The end effect of caries is to break down enamel & dentine & to open a path for bacteria to
reach underlying tissues.
This causes infection and inflammation of the pulp and, later, of the periapical tissues.
Acute pulpitis and periodontitis caused in this way are the most common causes of
toothache.
Infection can spread from the periapical region to the jaw and beyond.
Patterns of caries formation
Dental caries disease is usually classified by four different factors:
1. According to anatomic site of the lesion,
2. According to the severity or rate of progession of the lesion,
3. According to age patterns at which lesions predominate, and
4. According to therapies that can induce decay.
Complications
A carious tooth is tender, and mastication is painful.
All carious lesions must be eradicated by some means.
Failure to do so leads to invasion of the pulp chamber (PULPITIS) with inflammation,
pain, swelling & exudation.
Since the tooth pulp is encased in a rigid structure (dentin), necrosis of the tissue within the
pulp chamber occurs due to increased pressure (from inflammatory edema), which
prevents blood flow (=Compartment syndrome).
An ensuing buildup of toxic products in this space will force extension of the process into
the tissue surrounding the root apices, forming a PERIAPICAL/DENTOALVEOLAR
ABSCESS.
CELLULITIS with acute pain ensues, with swelling of soft tissues as the products drain to
the outside.
If the body defenses respond adequately, the infection may transiently resolve, but acute
recurrence is common.
Treatment
Interruption of the caries process is the aim of any treatment with subsequent rebuilding of
lost tooth structure utilizing choices from an array of methods.
Depending on the extent to which the damage has progressed, this may involve entering the
pulp chamber, cleansing and sterilizing the internal space within the crown and root, and
obturating that space.
A final resort is EXTRACTION of the tooth with subsequent REPLACEMENT also by a
variety of means.
Restorative care and simple extractions in children over three years of age are readily
provided using local anesthesia
In the early stages of decay, the tooth may be sensitive to temperature changes or, especially,
to sweets.
At this point, the tooth can be repaired by removing the caries and filling the defect.
As the decay progresses, more pain may be involved and root canal therapy is usually
necessary.
Once an abscess has formed, with or without swelling, a choice must be made between root
canal therapy and removal of the tooth.
In the presence of cellulitis or facial space abscess, extraction is usually the treatment of
choice.
The pathological principles underlying conservative treatment of the teeth are to stop
existing disease, to prevent its recurrence and to preserve a healthy pulp: “DUPWO”
1. Removal of Decayed enamel and dentine
2. Removal of Unsupported enamel
3. Protection of the Pulp
4. The placing of a Watertight restoration
5. Restoration of the Original form of the tooth.
Dental restorations:
Incipient lesions should be remineralized , if possible, by cleaning followed by repeated
fluoride applications.
Fillings are inserted after removal of caries.
o Temporary fillings:
A temporary filling may be left in place for 6 to 10 wk in the hope that a tooth will retain its
vitality and deposit secondary dentin to seal the pulp exposure.
Dycal ivory (Calcium hydroxide) - stimulates dentin formation.
Calcinol (may also be used as Lining (insulator) over amalgam which is
thermo-conductive).
Glass Ionomar Cement (GIC) (may be used as permanent for anterior teeth).
o Permanent fillings:
(a)The most common is silver amalgam (Mercury+ Tin+ Copper+Silver, & occasionally
zinc, palladium, or indium).
Amalgam is a relatively long-lasting, inexpensive product, used for > 150 yr; amalgam
fillings last an average of 14 yr, but with good oral hygiene, many last > 40 yr.
If a tooth has extensive decay, simply removing decay may undermine its structure.
In such a case, a dentist removes the decay, fills the sites with cement, and grinds the outer
tooth surfaces, so that an artificial crown, usually of gold, may be placed
(b) Porcelain fused to a metal crown or a porcelain jacket crown is used for anterior teeth
because porcelain resembles enamel.
(c) Glass Ionomar Cement (GIC) used for anterior teeth & lateral aspects of teeth
Dental appliances:
Missing teeth should be replaced by fixed bridges, osseointegrated implants, or partial or
complete dentures to prevent movement of remaining natural teeth, which causes cosmetic
and occlusion problems.
A bridge is composed of false teeth soldered to each other &, at each end, to a crown that is
cemented to abutment teeth.
An implant is typically a root form, often titanium. One or more are placed into the bone
where they ankylose.
After a period of healing, artificial teeth are attached to the implants. Implants are not readily
removable.
A partial denture, typically an appliance with clasps that snap over abutment teeth, may be
removed for cleaning.
Part of the occlusal stress is borne by the soft tissues under the denture, often on both sides
of the jaw.
Complete dentures are removable appliances used when no teeth remain.
They help a patient chew and improve speech and appearance, but they do not provide the
efficiency or tactile sensations of good natural dentition.
Dental sealants
Dental sealants are plastic resins that can be painted on the teeth most prone to decay
(molars & premolars) and serve as a barrier against acid-induced decay.