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Trauma, rapidly progressing caries or overzealous removal of caries can
result in exposure of the dental pulp. In these situations a direct pulp
capping technique can be considered in an attempt to preserve the vitality of
the pulp and to stimulate it to produce a calcific barrier to wall off the
exposure.
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However, the health of the pulp and its healing capacity will depend on
a number of factors, including the precipitating event leading to the exposure.
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Following trauma, when a previously sound, asymptomatic tooth suffers a
coronal fracture involving the pulp, it is widely accepted that the direct pulp
cap is the treatment of choice, providing the exposure is small and is treated within 24
hours.In this situation the depth of damage to the pulp tissue is small and the
relatively healthy pulp tissue has considerable reparative potential,
particularly in young teeth with immature apices and a good blood supply.
Dental caries and the pulp dentine
complex reactions
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Dental caries in enamel is a subsurface demineralisation caused by acids produced by
bacteria in the surface
plaque. These acids diffuse into the tooth structure causing demineralisation.
It is only when the relatively more mineralised surface zone breaks down that
bacteria colonize the enamel lesion.
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At the advancing front of a dentine lesion, demineralisation also
precedes bacterial invasion.
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Fuzayama investigated the relationship between dentine softening, discolouration and bacterial
infection and found that
softening preceded discolouration which in turn preceded bacterial invasion.
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Thus bacterial acids and products, such as proteases, diffuse ahead of
the bacteria towards the pulp and a number of factors influence the rate at
which this occurs.These are namely the concentration of bacterial by-products, the permeability
of the dentine and the pulpal fluid pressure.
·
The frequency of sugar consumption and hence acid provoking attacks will
affect the concentration of acid produced in the dental plaque. This in turn
will be moderated to some extent by saliva or whether the lesion is open (frank
cavitation) or closed, but in general the more acid produced the greater the
concentration gradient toward the pulp.
·
The permeability of the
dentine, which resists
this inward diffusion of acid, changes with age. Newly erupted
teeth are more permeable and less mineralised allowing the rapid diffusion of
acids. As such they may
be more susceptible to rapidly progressing caries.
·
Pulp dentine complex reactions to this stimulus are aimed at reducing
the permeability of the dentine. The most common reaction depends upon a vital
odontoblast process and is the deposition of apatite and whitlockite crystals
within the dentinal tubules leading to dentine tubule sclerosis.In addition to this, tertiary dentine may also be laid down by the odontoblast within the pulp chamber.
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If the carious process proceeds unchecked, degenerative changes within
the odontoblasts take place before inflammatory changes within the pulp
occur.This can lead to complete cell death and replacement by odontoprogenitor cells from the subjacent (situated underneath)
cell rich layer. Differentiation of these mesenchymal cells into odontoblast-like
cells, can lead to the production of reparative dentine which, depending on the severity of the carious lesion,
can be irregular with cellular inclusions or if less aggressive resemble normal
tubular dentine.
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Thus there is a fine balance between the speed of the advancing front of
the dentine lesion and the rate at which pulp-dentine defenses can be laid
down.These pulp-dentine reactions require a healthy pulp, however if the carious process continues unchecked
pulpal inflammation will ensue.
·
In an attempt to evaluate the relationship between lesion depth and
pulpal inflammation, Reeves and Stanley (1966) showed that if the advancing
front of the lesion was about 1 mm from the pulp then no significant disturbance occurred. However, once within 0.5 mm of
the pulp more pathological changes occur, but it was only when the reactionary
dentine itself was involved that ‘pathosis of real consequence was seen.
Shovelton also showed that it was only when the lesion was within 0.25 mm–0.3
mm of the pulp that hyperaemia and pulpitis occurred.
·
Thus in final excavation of soft pulpal caries, if direct perforation
of the pulp occurs the relative rate of progression of the lesion has been
faster than the rate of pulp-dentine reactions. At this stage the pulp is likely
to be inflamed and the decision of whether to place a direct pulp cap has to be made.
The direct pulp cap.
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A direct pulp cap usually involves the placement of a calcium hydroxide
preparation directly in contact with an exposed pulp.
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For a direct pulp cap to be successful a number of factors have to be
met .
·
Lin and Langland (1981) have shown that teeth with a history of pain will have an area of
necrosis within the pulp chamber and for many this will extend into the root canal.Bacterial invasion of pulp tissue is
closely related to this necrosis and as such these teeth should be endodontically treated.
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Teeth exposed during
caries removal will inevitably have some degree of inflammation although the histological extent of this
cannot be accurately predicted from a clinical examination.
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It was once thought that only pinpoint exposures could be pulp capped,
however more recent research would suggest that the size of exposure has no
bearing on clinical outcome. Whilst these studies pertain to traumatically
exposed pulps, Mejare and Cvek (1993) have suggested that deep carious exposures be opened up so
that 1 mm–3 mm of exposed pulp can be removed.It is important to draw attention to the
fact that this study was on young posterior teeth and cannot be regarded as a true direct pulp cap, but rather a partial
pulpotomy. This procedure has a number of advantages; it reduces the potential
for introduction of dentine chips into the pulp tissue and it enables good
contact between pulp and capping agent.It also removes superficially
contaminated pulpal tissue.
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It has been shown that dentine chips inadvertently pushed into the pulp tissue cause severe
inflammatory reaction, which can lead
to pulp necrosis.
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It is important to emphasize that whilst the size of traumatic exposures
is not so important, carious exposures should be small even if they are opened
up further at operation. It is generally agreed that larger carious exposures have a
poor prognosis due to a more severely inflammed pulp, risk of necrosis and bacterial contamination.
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The issue of age is also difficult, as there is no clear cut-off when a
direct pulp cap should no longer be considered. The ageing process is gradual
and with increased
age the pulp tissue becomes more fibrous with a reduction in pulp volume as a result of physiological secondary
dentine formation and reactionary dentine due to external stimuli such as
trauma, caries and tooth wear. The blood supply to the dental pulp is critical to its health and
regenerative capacity, and as this decreases with age so does its capacity to respond to a direct pulp cap.
Hence rather than a chronological age as a cut-off, the biological age of an
individual tooth should be assessed and a previous restorative history is taken
into consideration.
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Finally the location of the exposure is important as there should be no
pulp tissue coronal to the exposure. Exposure in a cervical cavity would lead to reactionary
dentine formation which would restrict the blood supply to the tissue more
coronal to it, leading to necrosis and failure. These teeth should therefore be
root treated.
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Calcium hydroxide to date remains the material of choice for a direct pulp capping
technique in general practice. However, a relatively new material, mineral trioxide aggregate (MTA) has been investigated. It consists of
fine hydrophilic particles, which when mixed with sterile water results in a colloidal
gel of pH 12.5. This gel solidifies to a hard structure within approximately 4 hours. Once set, it has a high compressive strength
comparable to IRM or Super EBA. Pitt-Ford et al., showed that direct pulpal
exposures treated with MTA demonstrated more predictable dentine bridge
formation than calcium hydroxide.However, problems associated with the
material’s difficult handling
properties and prolonged setting time may preclude its widespread acceptance despite its
superior therapeutic properties.
What is the success rate of the pulp cap
technique?
·
Whilst the prognosis of teeth that have received direct pulp caps as a result of trauma
would appear good those with a carious exposure fare less well.
·
In a retro-spective study of 123 direct pulp caps on carious exposures only 37% were clearly successful after 5
years and after 10 years 80% had failed.
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Loss of pulp vitality in these teeth poses a problem as a significant amount of physiological secondary and reactionary
dentine would have developed which has the potential to complicate subsequent
root canal treatment. In addition the root canal system may have become infected and prognosis for root
treatment is less favorable than if vital pulp tissue were removed.These results question the
success of the direct pulp cap for carious exposures.
The indirect pulp cap.
·
When caries is thought to extend close to, or into the pulp, excavation of the pulpal caries can be
stopped at stained but firm dentine.Calcium hydroxide lining is applied over the pulpal
dentine prior to placement of the definitive restoration.This is classically
referred to as the indirect pulp cap.
·
The difficulty with
this technique is knowing how rapid the carious process has been, how much
tertiary dentine has been formed and knowing exactly when to stop excavating to
avoid pulp exposure.
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Using a stepwise approach to caries removal these parameters can be regulated
with a more predictable outcome.
Stepwise excavation.
·
It could be argued that in the absence of any signs and symptoms of
pulpitis, it is over-judicious removal of caries that leads to a pulpal
exposure.
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Bjørndal et al. (1997) investigated 31 teeth with gross caries, which
from a clinical and radiographic examination were thought to have carious
pulpal exposures. In these teeth caries removal was staged over two separate appointments
6–12 months apart.
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At the first appointment, access to the caries was gained and the
periphery of the cavity made completely caries free. Soft, wet and pale
coloured dentine was left pulpally, which has previously been shown to be
heavily infected.The cavity was lined with calcium hydroxide and restored with
glass ionomer and left for 6–12 months.
·
After this period, cavities were re-entered and the dentine in all
teeth was found to be darker in colour, harder and drier in consistency. Microbiological analysis also showed a significant
reduction in cultivable micro-organisms over the period in which the
provisional restorations were in place.
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These findings would imply that by removing some of the carious biomass
and sealing the remaining caries from extrinsic substrate and oral bacteria, the caries left behind after the first
excavation had become less active. This allows time for pulp-dentine complex reactions to take place so that at
the second excavation visit, there is less likelihood of pulpal exposure.
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It has also been suggested that by changing the cavity environment from
an active lesion into the condition of a more slowly progressing lesion, this
will be accompanied by more regular tubular tertiary dentine formation.
Why re-enter?
·
The success of this
technique is dependent upon the integrity of the restoration and its seal.
Regular recall would be essential. In the unlikely event that the restoration
should fail and not be detected, the potentially re-activated lesion would
already be in an advance stage.
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Following sealing caries into the tooth, the carious dentine becomes
dry, harder and darker in colour.As a result there is shrinkage of the tissue
leaving a void beneath the restoration. These two factors support the second stage of
the stepwise excavation.
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However, the work by Mertz-Fairhurst et al.(1998) would suggest that the
interval between first and second excavation is
not critical and could be left for considerably longer than 6–12 months.
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Thus use of a more conservative technique for removing caries in a young
patient with very deep lesions could eliminate the need for the conventional
direct pulp cap technique.
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In those rare instances when this is still required, adoption of the stepwise excavation
technique should result in a minimally inflamed pulp, superior tertiary dentine
formation, less bacterial load and a more predictable pulp cap. Where this is required the use of
calcium hydroxide, whilst acceptable at present, may become replaced by a mineral trioxide aggregate material.
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