In intrusive luxation the teeth are forcefully intruded
into the bone. Because of the direction of displacement,
a comminuting fracture of the socket also occurs. The
frequency of pulp necrosis is very high. At least 85–95
per cent of mature intruded teeth become necrotic.
Pulp canal calcification and progressive root resorption
are expected to occur in 4 and 48 per cent of cases,
respectively.
Treatment of intruded teeth can be complicated by
the fact that most intruded teeth are also associated
with crown fractures.
Delayed repositioning leaves
roots in intimate contact with bone and this influences
the onset of replacement resorption. Thus, mature teeth
should be repositioned as soon as possible and the
pulps removed immediately or as soon as possible once
the soft tissues have healed sufficiently to do so, in
order to help prevent the onset of inflammatory root
resorption.
Although immediate (i.e., surgical)
repositioning is the treatment of choice for mature teeth
in adults (>17 years of age), orthodontic repositioning
is another option for managing such injuries.
Intruded immature teeth behave somewhat differently
and more treatment options are available. The apex is
open and the bone in children is softer and more
malleable. In these teeth, the extent of the intrusion and
the presence of associated crown fractures are
important prognostic considerations. All intruded teeth
in a paediatric population survived for five years if the
intrusion was less than 3mm, 90 per cent if the
intrusion was between 3mm and 6mm, and only 45 per
cent if the intrusion was greater than 6mm.
Almost all surviving intruded immature teeth undergo pulp canal
calcification. Pulp necrosis is usually diagnosed within
six months but may develop up to two years later in
open-apex teeth.
In open-apex teeth, awaiting
spontaneous eruption has been reported to lead to the
best outcomes.
However, careful monitoring must be
carried out to ensure that resorptive defects are detected
and treated early. Root resorption has been reported to
occur in a large number of cases.
It can be seen from the above that luxation injuries
result in a much higher incidence of pulp necrosis than
do injuries involving fracture of the teeth. As would be
expected, the risk of pulp necrosis increased with the
extent of the injury; concussion and subluxation
represent the least risk, followed in ascending order by
extrusive, lateral and intrusive luxation. Intrusive
luxation appears to be the most serious type of injury
with regard to the development of pulp necrosis and the
development of root resorption. Teeth that have been
luxated should be identified and observed over a long
period. Teeth with completed root formation
demonstrate a greater risk of pulp necrosis than teeth
with incomplete root formation. In particular,
development of pulp necrosis after injury has been
shown to be significantly related to the diameter of the
apical foramen.
For extruded and laterally luxated
teeth, the smaller the diameter, the greater the
probability of pulp necrosis. Intruded teeth with
incomplete root development are associated with a
much higher probability of pulp survival than teeth
with complete root development.
The diagnosis of pulp necrosis following luxation
injury needs careful attention. The initial condition of
the pulp may be one in which only the nerve supply has
been damaged and the potential for revascularization
without concomitant neuron-regeneration cannot be
dismissed. The extent of apical displacement has been
found to be significantly related to the incidence of pulp
necrosis for intrusive luxations but not extrusive and
lateral luxations.
Sensibility tests, though useful,
may be unreliable in luxated teeth. Discolouration and
periapical radiolucent lesions are the most important
diagnostic features to be noted for subluxation,
extrusive luxation and lateral luxation. The presence of
inflammatory root resorption is an important factor in
establishing the diagnosis of pulp necrosis and infection
in replanted and intruded teeth,
and pulp extirpation
must be carried out at the earliest radiographic sign of
this process occurring.
There is one factor that should not be overlooked
when assessing radiographic changes in luxated teeth.
While a rare occurrence, transient apical breakdown is
believed to be a non-infected apical remodeling process,
which can mimic pulp necrosis radiographically and in
clinical tests and observations. Andreason
examined 637 cases of luxated teeth and identified this process in
4.2 per cent of teeth. The majority of these teeth
demonstrated a periapical radiolucency, as well as
colour and/or electrometric sensibility changes. All
teeth showed resorptive widening of the apical
foramen. All signs and symptoms later returned to
normal. Recognition of transient apical breakdown is
important if unnecessary endodontic treatment is to be
prevented. Transient apical breakdown is more
common in mild luxation injuries in fully formed or
almost fully formed teeth. A case can be made for
observing asymptomatic teeth with early signs of pulp
necrosis in selected cases, but only where the clinician
is absolutely confident that the patient is likely to
comply with frequent recall investigations. Continued
root development and calcification within the canal
must be regarded as a positive indication of a vital pulp
even in the absence of a positive response to pulp
sensibility testing. Regular radiographic examination is
necessary. Endodontic therapy must be commenced at
the first radiographic evidence of inflammatory root
resorption.