Dental Carie1

DENTAL CARIES
The carious process in enamel

The earliest clinically visible evidence of enamel caries is the white spot lesion, for
example at the cervical margin of the tooth. This may also be seen on extracted
teeth as a small opaque white area just cervical to where the approximal contact
area was. The colour of the lesion distinguishes it from the adjacent sound enamel,
but at this stage there is no cavity and the enamel overlying the white spot is hard.
In the active lesion it may have a matt surface because there has been direct
dissolution of the outer enamel surface. Sometimes the lesion is shiny and this
would indicate that good plaque control has been re-established and the outer
demineralized enamel has been worn away. This lesion is arrested and sometimes
it may appear brown due to exogenous stains absorbed by this porous region. Both
white and brown spot lesions may have been present in the mouth for some years,
as it is not inevitable for a carious lesion to progress.
Fissures and pits are obvious stagnation areas where plaque can form and mature.
The lesion forms at the entrance to the fissure and the erupting tooth is particularly
susceptible to plaque stagnation.
There are two reasons for this. The first is that children, especially young children,
are not adept at removing plaque.
Secondly the erupting tooth is below the line of the arch and tooth-brushing misses
it unless the brush is brought in at right angles to clean the surface specifically.
The carious process in dentine
Histologically, the carious process may be in dentine before an enamel cavity
forms. On an occlusal surface the lesion widens as it approaches the enamel–
dentine junction, guided by prism direction. Eventually a cavity forms and now the
hole is filled with plaque and the biofilm sits directly on the exposed dentine. At
this stage demineralization spreads laterally along the enamel -dentine junction,
undermining the enamel.
Undermined enamel is brittle and will in due course fracture if subjected to
occlusal forces, producing a large cavity. Undermined enamel is of particular
relevance in cavity preparation because superficially sound but undermined enamel
must often be removed to gain access to demineralized dentine beneath it.
In addition, it is probably unwise to leave undermined enamel occlusally unless it
is supported by an adhesive restorative material.
Pulp–dentine defence reactions
Dentine is a vital tissue containing the cytoplasmic extensions of the odontoblasts
and must be considered together with the pulp since the two tissues are so
intimately connected. The pulp–dentine complex, like any other vital tissue in the
body, is capable of defending itself. The state of the tissue at any time will depend
on the balance between the attacking forces and the defence reactions. The
important defence reactions are tubular sclerosis within the dentine, reactionary
dentine at the interface between dentine and pulp, and inflammation of the pulp.
Tubular sclerosis occurs through precipitation of minerals in the tubular space and
is protective in that it reduces the permeability of the dentine, inhibiting the
penetration of acids and bacterial toxins. Reactionary dentine is formed by the
odontoblasts beneath the carious stimulus. A slowly progressing lesion may give
time for a considerable reparative dentine response, whereas with more acute
larger lesions the response may be disorganized or even non-existent. Regular
removal of the biofilm from the surface of any lesion encourages lesion arrest and
these defense reactions then predominate. This retreat of the pulp from injury has
important implications in the operative management of caries.
Inflammation is the fundamental response of all vascular connective tissues to
injury. Inflammation of the pulp (pulpitis) may, as in any other tissue, be acute or
chronic. In a slowly progressing carious lesion, toxins reaching the pulp may
provoke chronic inflammation. However, once the organisms actually reach the
pulp (a carious exposure), acute inflammation may supervene. Inflammatory
reactions have vascular and cellular components. In chronic inflammation the
cellular components predominate and there may be increased collagen production,
leading to fibrosis but without immediately endangering the vitality of the tooth.
However, in acute inflammation the vascular changes predominate.
Infection is the most common cause of pulpal inflammation and caries is the most
common microbial source. Caries of peripheral dentine will result in pulpal
inflammation and chronic inflammatory cells (macrophages, lymphocytes, and
plasma cells) will infiltrate the pulp near the odontoblast layer. Indeed, this
infiltration may even be seen in initial enamel caries. This chronic inflammatory
reaction is mainly due to the movement of bacterial toxins through the dentinal
tubules. With increasing carious involvement of enamel and dentine, the area of
chronic inflammation increases in size but it is believed to remain localized until
pulp exposure after exposure, bacteria may enter the pulp. Polymorphonuclear
leucocytes may now predominate, and acute inflammation can supervene and
spread throughout the pulp, resulting in pulpal necrosis.
Degenerative or destructive changes in dentine
These include demineralization of dentine, destruction of the organic matrix, and
damage and death of odontoblasts. Since carious enamel is porous, acids, enzymes,
and other chemical stimuli from the tooth surface will reach the outer dentine,
evoking a response in the pulp–dentine complex. Thus, both reparative and
degenerative changes begin before cavitation of the enamel occurs and while the
microorganisms are still confined to the tooth surface. With cavitation of enamel,
bacteria have direct access to dentine and the tissue becomes infected.
Demineralization of dentine precedes bacterial penetration, and this is of
importance in operative dentistry since an objective is to remove the infected and
necrotic dentine, although uninfected but demineralized dentine may be left.
Plaque retention and susceptible sites
Any site on the tooth surface that favours plaque retention and stagnation is prone
to decay.
The following sites particularly favour plaque retention:
• enamel pits and fissures on occlusal surfaces of molar and premolar teeth buccal
pits of molars and palatal pits of maxillary incisors
• approximal enamel smooth surfaces just cervical to the contact area.
• The enamel at the cervical margin of the tooth at the gingival margin recession,
the area of plaque stagnation is on the exposed root surface.
• The margins of restorations, particularly where there is a wide gap between the
restoration and the tooth or those where the restoration overhangs the margin of the
cavity.
CLASSFICATION OF DENTAL CARIES
Depending on the surface
 Smooth surface
 Root caries
 Pit and fissure
 Recurrent caries
Rampant caries
Rampant caries is the term used to describe a sudden rapid destruction of many
teeth, frequently involving surfaces of teeth that are ordinarily relatively caries-
free.
Rampant caries is most commonly observed in the primary dentition of infants
who continually suck a bottle or comforter containing, or dipped into, a sugar
solution.
Rampant caries may also be seen in the permanent dentition of teenagers and is
usually due to frequent cariogenic snacks and sweet drinks between meals.
It is also seen in mouths where there is a sudden marked reduction in salivary flow
(xerostomia). Radiation in the region of the salivary glands, used in the treatment
of a malignant growth, and Sjögren’s syndrome, an autoimmune condition which
involve the salivary glands, are the most common causes of severe xerostomia. In
addition, a large number of therapeutic drugs, such as antidepressants,
tranquillizers, antihypertensives, and diuretics, retard salivary flow.
The management of rampant caries is more difficult than the management of caries
which has progressed at a slower pace because of the extent of the caries and the
rate at which it progresses. However, the treatment is the same in principle. The
disease is managed by preventing further disease progression and stabilizing
existing lesions before restoring teeth permanently. If caries is not managed by
preventive, non-operative treatment the restorative treatment will be doomed to a
cycle of disease, repair, new disease and further repair, and, before too long,
extraction.
Arrested caries
Arrested caries is in distinct contrast to rampant caries, and the term describes
carious lesions which do not progress. It is seen when the oral environment has
changed from conditions predisposing to caries to conditions that tend to slow the
lesion down. The lesion probably stopped after extraction of the first molar. The
environment changed, becoming less plaque retentive, easier to clean, and more
accessible to saliva. Operative treatment is clearly not necessary.
Root caries
Dentine caries beneath enamel has been considered in the preceding section.
However, root surfaces become exposed in many mouths and these surfaces are
susceptible to root caries and also appear more vulnerable than enamel to
mechanical wear and chemical damage which is usually associated with
periodontal disease and so root caries is more commonly seen in older people. Not
all patients with exposed root surfaces will automatically develop root caries
especially if the biofilm is regularly disturbed with a toothbrush and a fluoride
containing toothpaste.
Secondary or recurrent caries
Placing a restoration does not confer immunity on the tooth, and secondary or
recurrent caries may occur in the tooth tissue adjacent to the filling material.
Secondary caries is the same as primary caries except that it is located at the
margin of a restoration. Like primary caries, it is caused by the metabolic activity
in the biofilm at the tooth or cavity surface. Thus it is most often localized
gingivally where plaque is most likely to stagnate. It can be arrested by regular
disturbance of the biofilm with a fluoride-containing dentifrice.
This emphasizes the point that the best way of managing caries is by preventing
lesion progression and not by filling holes in teeth.
SYMPTOMS OF CARIES
Thus far the signs of caries – that is, what the clinician can detect – have been
considered. However, patients often seek treatment for the symptoms of caries.
What are these symptoms?
Unfortunately, caries presents symptomatically at a relatively late stage. The
patient may feel a ‘hole in a tooth’ with the tongue, brown or black discoloration or
cavities may be seen, or frank pain may be suffered.
Caries, even in dentine, is not painful per se, but cavitation may occasionally
present as mild pain with sweet things or with heat or cold. Normally, the enamel
and the necrotic dentine insulate the sensitive dentine and pulp from these stimuli.
However, a much more common cause of pain, which may be intense, is pulpitis
(the commonest ‘toothache’) which occurs late in the development of a carious
lesion when the caries is very close to the pulp or actually exposing it.
A chronically inflamed pulp may be symptomless or produce only mild symptoms.
In contrast, acute pulpitis is very painful, with the pain often being initiated by hot
and cold stimuli. Unfortunately, the pain is not well localized to the offending
tooth, and the patient may only be able to indicate which quadrant, or even which
side, of the mouth is involved.

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DENTAL CARIES

The carious process in enamel

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