Full Retarded Eruption of Permanent Dentition: Report of a Rare Case (8
Permanent tooth eruption occasionally fails due to local, systemic or idiopathic
reasons. Full retardation of eruption is a very rare clinical finding and is
challenging in terms of aetiology. This case report describes the clinical condition
of a 13-year-old boy, where primary teeth were still present in the oral cavity.
Surgical exposure was performed and the patient was followed up for 8 years,
showing partial eruption of some teeth at a slow rate. The working diagnosis
based on clinical and radiographical criteria is idiopathic
loss of eruption potential.
Treatment plan is also discussed in this report.
Received: November 04, 2011;
Accepted: March 16, 2012;
Published: June 30, 2012
Permanent tooth eruption is connected with the exfoliation of the deciduous
predecessors and is defined as the movement of the tooth from the area of development
within the alveolar process to its functional position in the oral cavity (Steedle
and Proffit, 1984). A tooth can be characterized as impacted when it has
not erupted one year after normal eruption time and is impossible to erupt according
to clinical and radiological criteria (Thilander and Jacobsson,
1968) due to systemic or local findings. Idiopathic failure of eruption
owes to lack of eruptive force or defects in the eruption mechanism, leading
to primary or secondary retardation and is challenging in terms of etiology
(Sivakumar et al., 2007). This case refers to
a unique clinical situation where primary teeth in all quadrants were still
present in the mouth of a 13-year old boy, failing to exfoliate despite the
presence of their successors, which were located radiographically. Overall aim
was to study this unique case and treat the patient appropriately according
to his needs.
MATERIALS AND METHODS
Patient was examined. Skeletal development is characterized normal, medical
history is clean and no systemic or genetic anomalies were detected after genetic
evaluation (karyotyping). The patient grew normally, both physically and mentally,
throughout childhood and adolescence and was a product of full-term pregnancy
and uncomplicated delivery. No complication can be attributed to breast feeding
practices (Matthew et al., 2009), as it took
place only for a few days. No allergies, hospitalizations or severe illnesses
and infections were noted while evaluation of thyroid function, calcium, phosphorus,
alkaline phosphatase (Asma et al., 2008) and vitamin
D levels revealed no endocrine or metabolic contribution to craniofacial growth.
Check for cleidocranial dysplasia, which is connected to eruption failure, as
well as hereditary oro-facial digital syndrome (Xavier et
al., 2011), or Crouzon syndrome (Pournima et al.,
2011), were negative. His three siblings had no similar problem but it was
mentioned that a distant relative of the patient had small teeth,
probably referring to preserved deciduous teeth that had not exfoliated, but,
this could not be confirmed. It was also mentioned that primary teeth eruption
Teeth 71 and 81 had been extracted before the first visit in our clinic, when
the patient was 11 years old, but after almost 2 years there was no sign of
permanent teeth eruption. Teeth 31 and 41 were surgically exposed in the oral
cavity during the first visit in our clinic, under local anesthesia. The basic
goal was to promote tooth eruption by removing the physical barrier of soft
tissues and bone but at the same time maintaining the vertical dimensions of
occlusion by teeth contacts. The bone removal was not aggressive in an attempt
to preserve mandibular bone. After the surgical operation it was evident that
these teeth were placed labially compared to their predecessors
position. Orthodontic-assisted eruption was not possible due to lack of teeth
for anchorage, as only primary teeth were present. Moreover anchorage could
not be supported by mini-implants as there was no ideal location for placement,
because of possibility of hurting permanent tooth buds during insertion and
due to lack of sufficient bone.
After 2 months teeth 31 and 41 had partially erupted into the oral cavity and
teeth 16 and 26 erupted at the age of 14 years old, as seen at the cast (Fig.
1a). An image of slow or no eruption of any other teeth was noted still,
after 4 years from the first visit.
|| Short clinical presentation of the case, (a) Eruption of
teeth 16, 26 and 31, 41 as seen in casts and clinical photo respectively
and (b) Clinical and radiographical examination after 8 years
After 8 years few teeth were extracted or had deep carious lesions and tooth
36 had partially erupted. Teeth 31 and 41 had still not reached the occlusal
plane (Fig. 1b). Teeth apices were fully formed and rest of
the teeth remain impacted, as seen at the radiograph. At the area of tooth 54
an image of bone loss was noted, but there is still a bony bridge approximately
3 mm between 54 and his successor. The inclined position of 38 and 48 seems
to act as an additional mechanical obstacle in the eruption process of teeth
37 and 47, respectively (Fig. 1b).
Very few similar cases are presented in the literature. Nodine
(1935) and Quinn (1956) were the first authors to
present such cases, but still no full retardation was noted until 1999 when
OConnell and Torske (1999) described a full retarded
eruption of both deciduous and permanent dentitions.
When generation of eruptive force and pathway clearance fail to couple, teeth
movement cannot keep pace with bone resorption indicating an idiopathic problem
in the eruption mechanism (Steedle and Proffit, 1984;
Ahmad et al., 2006). Since each tooth has a window
of opportunity for successful eruption, disregulations of the mechanisms
during that period, could result in defective tooth eruption. In our case, this
critical period does not seem to have passed, since permanent teeth have erupted
after surgical intervention, at a slow rate. The working diagnosis, based on
clinical and radiographical criteria is idiopathic loss of eruption potential
which led to extreme retardation and eventually failure of eruption, demonstrating
different rates of eruption between maxilla and mandible. A definitive diagnosis
of primary failure of eruption could only be made retrospectively, following
the possible failure of orthodontic movement (Frazier-Bowers
et al., 2010), which was impossible to our case as mentioned above.
Molars also acted secondarily as mechanical obstacles. No real tendency for
generalized ankylosis is noted, as concluded from the radiographic image, the
spontaneous eruption of upper first molars and the eruption of teeth 31 and
41 after the surgical exposure. It is also remarkable that failure of eruption
was not only present in the areas where primary dentition was succeeded by permanent
teeth, but also in the areas of permanent molars, even though the phenomenon
had subclinical appearance, as some of the molars were semi-erupted. Cases with
no obvious etiology for retarded eruption, could be supported by research on
the genetic level (Wise et al., 2002). Specifically,
mutations in parathyroid hormone receptor 1 (PTH1R) genes, which regulate calcium
metabolism during early bone growth, explain several familial non syndromic
cases of primary failure of eruption (Frazier-Bowers et
After the experience of the successful surgical intervention in the area of
teeth 31 and 41, a reasonable treatment plan is the removal of all deciduous
teeth and the underlying bone in order to expose the retained permanent dentition.
There lies however the question of the appropriate sequence of the extractions,
the choice of one time operation or of separate extractions in a longer period
and patient cooperation, as it was difficult to keep up with re-examinations.
Until now, the patient is not complaining for functional or aesthetic disturbances.
He is using his primary teeth as permanent to masticate and showed no signs
of weight loss or other problems relevant to this handicap. He refuses to continue
treatment despite the fact that he was informed about the consequences of long-standing
impaction due to no therapy.
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2: Asma, A.A.A., M.A.W. Rohaya and Z.A. Shahrul Hisham, 2008. Crevicular alkaline phosphatase activity during orthodontic tooth movement: Canine retraction stage. J. Med. Sci., 8: 228-233.
CrossRef | Direct Link |
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CrossRef | Direct Link |
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13: Xavier, A.M., K. Rai, A.M. Hedge and S. Joshi, 2011. Hereditary oro-facial digital syndrome type 1: Diagnosis and management: Case report. Eur. J. Dent. Med.,