Dental education guide on tooth eruption problems

INDIAN DENTAL ACADEMY
Leader in continuing dental education
www.indiandentalacademy.com


Contents
Introduction
Mechanisms Of Eruption
Etiology Of Eruption Problems and
Classification
Delayed Tooth Eruption and Classification
Local, Systemic, Genetic
Diagnosis Of Eruption Problems
Treatment Of Eruption Problems
References

Eruption is the developmental process responsible for
moving a tooth from its crypt position through the alveolar
process into the oral cavity to its final position of occlusion
with its antagonist. It is a dynamic process that
encompasses completion of root development,
establishment of the periodontium, and maintenance of a
functional occlusion.
Emergence, on the other hand, should be reserved for
describing the moment of appearance of any part of the
cusp or crown through the gingiva. Emergence is
synonymous with moment of eruption, which is often used
as a clinical marker for eruption.


(Tencate)The

movements teeth make are complex
and may be described in general as:
Preeruptive tooth movement: Made by the
deciduous and permanent tooth germ within tissues
of the jaw before they begin to erupt.
Eruptive tooth movement: Made by tooth to move
from its position within the bone of the jaws to its
functional position in occlusion. It is divided into
intraosseous and extraosseous components.
Posteruptive tooth movement: Maintaining the
position of the erupted tooth in occlusion while the
jaws continue to grow and compensate for occlusal
and proximal tooth wear.

The four possible mechanisms for eruption are
(Tencate,1998)
1. Root Formation 2.Hydrostatic Pressure 3.Bony
Remodelling
4. Periodontal Ligament
Root Formation: Root formation apears to be an obvious
cause of tooth eruption because it undoubtedly causes an
overall increase in the length of the tooth that must be
accommodated by the growth of the root into the bone of
the jaw, by an increase in jaw height, or by the occlusal
movement of the crown.


This situation is however substantiated by the
fact that:
Some teeth erupt a greater distance than the
total length of their roots.
teeth still will erupt after the completion of
root formation.
teeth will still erupt when the Hertwig
epithelial root sheath is removed surgically
rootless teeth erupt.
In conclusion root formation is accomodated
during tooth eruption and is a consequence, not
a cause of the eruption process. However it may
accelerate tooth eruption.

Bone Remodelling: Marks and Cahill(1984)
demonstrated that the dental follicle needs to be
present for tooth eruption.
Bony Remodelling occurs around the erupting
follicle regardless of the presence of a tooth crown or
tooth ,suggesting that remodelling process may be
under the control of the dental follicle.However
experiments do not prove that the dental follicle is
involved in determination of final tooth position.
Hydrostatic Pressure: Van Hassel and McMinn(1972)
hypothesised that the tissue pressure apical to the
erupting tooth was greater than occlusally,thus
theoretically generating an occlusal force.
However no association was demonstrated between
the magnitude of force and the rate of eruption.

Periodontal Ligament: Tencate believed
that the fibroblasts in the periodontal
ligament have a contractile potential and
are responsible for tooth eruption.
Berkovitz1990 also favoured Tencate
and agreed that no one hpothesis can fully
explain the mechanism of tooth eruption
as it is likely to be a multifactorial process.


ETIOLOGY OF ERUPTION PROBLEMS:
Disturbances may occur in any of the phases of eruption.
From an Etiologic point of view three main causes of
eruption disturbances can be distinguished:
1.Ectopic position of the tooth germ,
2.Obstacles in the eruption path
lack of space, follicular collision, presence of compact
bone, supernumerary teeth, odontomas, scar tissue,
non-attached mucosa, giant cell fibromatosis,
odontogenic tumors or cysts.
3.Failures in the eruption mechanisms (i.e. follicle or PDL
defects according to the stage of eruption) due to
trauma, surgery, congenital diseases or other causes.

The first two conditions lead to
impaction and the last according to the
stage in which the eruption disturbance
occurs as primary(before emergence) or
secondary retention(after emergence)
It is therefore necessary to develop a
rational treatment approach in order to
diagnose which of the prerequisites for
eruption have been violated and to what
extent.


Delayed tooth eruption is the most commonly
encountered deviation from the normal eruption
Conditions reported to be associated with Delayed tooth
eruption are:
Local:
Mucosal Barriers-scar tissue: trauma/surgery
Gingival Fibromatosis/ gingival hyperplasia
Supernumerary teeth
Odontogenic tumours
Non Odontogenic Tumours
Enamel Pearls
Injuries to Primary teeth
Ankylosis of deciduous teeth
Premature loss of primary teeth
Lack of resorption of deciduous tooth

Apical periodontitis of deciduous teeth
Regional Odontodysplasia
Impacted primary teeth
Ectopic eruption
Arch- Length deficiency and skeletal pattern
Radiation damage
Oral Clefts
Segmented odontomaxillary dysplasia


Systemic:
Nutrition
Vitamin D resistant rickets
Endocrine disturbances
Hypothyroidism
Hypoparathyroidism
Hypopituitarism
Pseudohypoparathyroidism
Long term chemotherapy
Hiv Infection
Cerebral Palsy
Dysosteosclerosis
Drugs
Phenytoin

Anemia
Celiac disease
Prematurity/ Low birth weight
Ichthyosis
Genetic disorders
Familial/ Inherited
Tobacco Smoke
Idiopathic


Genetic disorders associated with DTE
Amelogenesis Imperfecta
Apert syndrome
Carpenter syndrome
Cherubism
Chondro ectodermal dysplasia
Cleidocranial dysplasia
Congenital hypertrichosis lanuginosa
Dentin dysplasia
Mucopolysaccharidosis
Down syndrome
Dyskeratosis congenita
Ectodermal dysplasia
Ekman-Westborg-Julin syndrome

Epidermolysis bullosa
GAPO syntlrome (growth retardation, alopecia,
pseudoanodontia.and optic atrophy)
Gaucher disease
Gingival fibromatosis associated syndromes
Gardners syndrome
Gorlins syndrome
Mc-Cune-Albright syndrome(Polyostotic
fibrous dysplasia)
Osteopetrosis (marble syndrome (polyostotic
fibrous dysplasia)
Neurofibromatoses
Oculoauriculo vertebral spectrum (Goldenhar
syndrome/hemifacial microsomia)
Osteoglophonic dyspalsia

Osteogenesis imperfecta
osteopetrosis
Otodental dysplasia
Parry-Romberg syndrome (progressive
hemifacial atrophy)
Progeria (Hutchinson-Gilford syndrome)
Rothmund-Thompson syndrome
Sclerosteosis
Shokier syndrome (hereditary anodontia spuria)
SHORT syndrome
Singleton-Merten syndrome
VonRecklinghausen neurofibromatosis
22q 11 deletion syndrome


Supernumerary teeth: About 28% to
60% of white people in 1984 have
been reported with supernumerary
teeth which can cause crowding,
displacement, rotation, impaction,or
delayed eruption of the associated
teeth.
The most common supernumerary
tooth is the mesiodens followed by a
fourth molar in the maxillary arch.
Different forms of supernumerary
teeth have been associated with
different effects on the dentition:
the tuberculate type is more
common in patients with delayed
tooth eruption the conical form has
been associated with displacement.
Supplemental
Odontome(not accepted universally)

Arathi R, Ashwini R(MCODS, Mangalore )JIPDS,2005
Reported a case with both supplemental and tuberculate
type of supernumerary teeth. The supernumerary teeth was
found in the region of premolar predominantly and lower
incisor region.
The central incisor showed clear signs of tuberculate type
with many cusps and dens invagination.


Regional odontodysplasia, also called "ghost
teeth:' is an unusual dental anomaly that might
result from a somatic mutation or could be due
to a latent virus in the odontogenic epithelium.
Affected teeth exhibit a delay or total failure in
eruption. Their shapes are markedly altered,
generally very irregular, often with evidence of
defective mineralization.
Central incisors, lateral incisors. and canines
are the most frequently affected teeth, in either
the maxillary or mandibular arch, and deciduous
and permanent teeth can be affected.
Abnormality in the tooth structure itself might
be responsible for the eruptive disorders seen in
this condition.

Odontomas: are also associated with
delayed tooth eruption. Actually delayed
tooth eruption is an alerting sign to
diagnose odontomas.
Mucosal Barrier: Any failure of the
follicle of an erupting tooth to unite with
the mucosa will entail in a delay in the
breakdown of the mucosa and constitute
a barrier to emergence.
Gingival hyperplasia resulting from
various causes (hormonal or hereditary
causes, vitamin C defi-ciency, drugs such
as phenytoin) might cause an abundance
of dense connective tissue or acellular
collagen that can be an impediment to
tooth eruption.

Injuries to deciduous teeth have also been implicated
as a cause of DTE of the permanent teeth.
Traumatic injuries can lead to ectopic eruption or
some disruption in normal odontogenesis in the form of
dilacerations or physical displacement of the
permanent germ.
Cystic transformation of a nonvital deciduous incisor
might also cause delay in the eruption of the
permanent successor.
The eruption of the succedaneous teeth is often
delayed after the premature loss of deciduous teeth
before the beginning of their root resorption. This can
be explained by the abnormal changes that might
occur in the connective tissue overlying the permanent
tooth and the formation of thick, fibrous gingiva.

Ankylosis, resulting from the fusion of the cementum or
dentin with the alveolar bone, is the most common local
cause of delayed deciduous tooth exfoliation. Ankylosis
occurs commonly in the deciduous dentition, usually
affecting the molars, and has been reported in all 4
quadrants, although the mandible is more commonly
affected than the maxilla. Ankylosed teeth will remain
stationary while adjacent teeth continue to erupt through
continued deposition of alveolar bone, giving the clinical
impression of infraocclusion.


Arch-length deficiency is often mentioned as an etiologic
factor for crowding and impactions. In a recent study of the
relationship between formation and eruption of the maxillary
teeth and the skeletal pattern of the maxilla, a shortened
palatal length was found to delay the eruption of the maxillary
second molar, although no delay in tooth formation was
observed.
Arch-length deficiency might lead to DTE, although more
frequently the tooth erupts ectopicaliy
X-radiation has also been shown to impair tooth eruption.
Ankylosis of bone to tooth was the most relevant finding in
irradiated animals. Root formation impairment, periodontal
cell damage, and insufficient mandibular growth also seem to
be linked to tooth eruption disturbances due to x-radiation.

Alveolar Clefts:
Failure of union of
the embryonic facial
processes leads to
discontinuity and
disorientation of cells of
the primodial dental
lamina.
Alveolar cleft occurs in the
region of Maxillary lateral
incisor.
This leads to variation in
number, morphology and
enamel formation of teeth
in the cleft area.

Canine Impaction was seen in 36% of the cases when
lateral incisors where missing.
Supernumerary teeth is also found associated with this
condition and it decreases with the increase in clefting.


Systemic factors:
Nutrition: The influence of nutrition on
calcification and eruption is less significant
compared with other factors.Nevertheless,
delayed eruption is often reported in patients who
are deficient in some essential nutrients.
(1966,1988)
Disturbance of the endocrine glands
usually has a profound effect on the entire body,
including the dentition. Hypothyroidism,
hypopituitarism, hypoparathyroidism, and
pseudohypoparathyroidism are the most common
endocrine disorders associated with DTE.

In hypothyroidism, failure of thyrotropic
function on the part of the pituitary gland or an
atrophy or destruction of the thyroid gland per
se leads to cretinism (congenital
hypothyroidism) in a growing person. The
dentofacial changes in cretinism are related to
the degree of thyroid dcficiency.
In hypopituitarism or pituitary dwarfism, the
eruption and shedding of the teeth are delayed,
as is the growth of the body in general. The
dental arch has been reported to be smaller than
normal; thus it cannot accommodate all the
teeth, so a malocclusion develops. The roots of
the teeth are shorter than normal in dwarfism,
and the supporting structures are retarded in
growth.

Weinberg and Berkowitz 2001 studied the dental
manifestations in 70 children perinatally infected with HIV
and indicated that delayed dental eruption was directly
associated with clinical symptoms. DTE did not seem to
correlate with CD4 positive T-lymphocyte depletion. The
investigators concluded that HIV infection itself is not
associated with DTE, but, rather, the onset of the clinical
symptoms is.
Pope and Curzon1991 found that unerupted deciduous and
permanent teeth were more common in individuals with
cerebral palsy compared with the controls. The first
permanent molar erupted significantly later. However no
etiology or implicated mechanisms were elaborated.

Giglio and Sanz 1987,1990,1994 found that other systemic
conditions like anemia (hypoxic hypoxia, histotoxic hypoxia,
and anemic hypoxia) and renal failure, have also been
correlated with DTE and other abnormalities in dentofacial
development.
A Nagpal, Gsharma. A Sarkar and KM Pai 2005 reported a
rare case of multiple unerupted permanent teeth without any
known cause


Diagnosis of Eruption Disturbances:
Accurate diagnosis of eruption problems is an important
but complicated process. When teeth do not erupt at the
expected age, a careful evaluation should be performed to
establish the etiology and the treatment plan accordingly
Diagnosis encompasses a history and clinical
examination, as well as a detailed radiographic examination
allowing a three-dimensional concept of the region
involved. The radiographic technique differs according to
the specific type of teeth involved.
For localization of impacted canine ,3D C.T.
utilizing shade surface display method has been found to
be a very useful & accurate method compared to
conventional techniques.( V.Ravinder,Nikhar Verma,
Ashima Valiathan , JIOS 2002)

Use of 3D C.T. is recommended in cases with
complex anatomical situations after a careful
risk/benefit analysis


Familial information and information from affected
patients about unusual variations in eruption patterns
should be investigated. Clinical examination should be
done methodically and must begin with the overall
physical evaluation of the patient. Although the presence
of syndromes is usually obvious in the mild forms. Only a
careful examination will reveal the abnormalities
Intraoral examination should include inspection.
palpation, percussion, and radiographic examination.
When the cause of the eruption disturbance has
been identified, the problem of how to remedy it arises.
Presently, there exists a series of treatment approaches
aimed at assisting specific parts of the eruption process.
Most of these treatments have the purpose of activating
or establishing an eruption pathway.

Treatment of Eruption Disturbances:
One established principle in the treatment of
eruption disturbances is that an erupting tooth usually
takes the path of least resistance,
Likewise, an ectopically erupting permanent canine
can be guided into a correct eruption path by removing
either adjacent bone or a primary predecessor.
Some of the treatment modalities are:
1. Ectopic Position of the tooth germ
Observation: In some cases spontaneous
uprighting of ectopically positioned permanent teeth may
take place. However, this up righting is unpredictable.

Extraction of primary predecessors has been
found to induce eruption and sometimes even up
righting of ectopically positioned teeth such as
canines and premolars. Removal of a primary
tooth can both accelerate and retard eruption of
the permanent successor
Eruption spurt was found to be especially
prominent in cases of periapical breakdown of
bone due to pulpal complications in the primary
molar.


However, if the extraction was performed very early, for
instance at 4 years of age, the eruption spurt stopped and
the permanent successor erupted later .This delayed effect
has been suggested to be due to the formation of marginal
dense bone or fibrous scar tissue.
Surgical Exposure
i)Surgical exposure usually involves removal of mucosa,
bone and sometimes part of the follicle covering the
permanent tooth so as to establish an eruption pathway.
ii) a. In case of deep impaction, when the surgically
created tract cannot be kept open postoperatively, the
follicle should be left intact so that the eruption process can
be completed.(without exposure of enamel)

b) If the follicle is
damaged, or is in a
superficial position, then
an orthodontic bracket
should be bonded to the
crown so that an orthodontic
extrusion force can take over
the role of the follicle in the
eruption process. (with
exposure of enamel)
The flap is apically
repositioned in order to
prevent labial retraction of
the gingiva. The flap is then
replaced and sutured.

FOLLOW-UP
Surgical exposure usually induces partial eruption
over 2-4 month (range 1 month to 2 years) and the
speed is apparently not age dependent. Full eruption
to the occlusal level usually takes about a year .
The limitation of this procedure appears to
be when ectopic teeth deviate more than 90° from
the normal eruptive path
Surgical Repositioning
Autotransplantation of ectopic tooth germs has
recently been shown to be an effective treatment,
especially for displaced canines and premolars

Drawback: Injury to the periodontal ligament
 root resorption damage to the pulp may
cause unsuccess,ful revascularization 
leading to pulp necrosis.Finally, injury to
Hertwig's root sheath may result in partial or
total arrest of further root development .
This procedure should, therefore, only
be used when other treatment alternatives
are not indicated or are not available


2.Obstruction of the Eruption Pathway
This condition can be divided into the following three
categories:
1. Lack of eruption space (crowding)
2. Follicular collision
3. Obstruction of the eruption pathway by compact bone,
scar tissue, fibromatosis, unattached mucosa, giant cell
fibroma-tosis, odontogenic keratocysts or odon-togenic
tumors
When the etiology has been established, the treatment
principle is to determine the type of obstruction and then
make it possible for the tooth to erupt by eliminating the
cause

Lack of Eruption Space ( Crowding)
Orthodontic evaluation should
reveal whether expansion can
increase the reduced eruption space or
if extraction of the impacted tooth or
adjacent teeth is the treatment of
choice.
Follicle collision
a) seen in the maxillary anterior
region,
b) between the second and the
third molar tooth germs.


The reason for the impaction effect of colliding
follicles is probably neither the follicles can resorb the
other, and therefore the eruption of both teeth becomes
impossible.
The treatment of choice in these cases is to remove
one of the colliding tooth germs. In the case of
supernumerary teeth, this decision is easy, whereas in the
second and third molar region it is more complicated
(depending on which one is in a clinically more
favourable position)


Obstruction of Eruption Pathway by
Hard or Soft tissue
ERUPTION CYST
The eruption cyst is a rare
phenomenon, which appears as a
bluish, translucent, elevated domeshaped lesion of the alveolar mucosa
overlying the erupting tooth.
It is not a true cyst, but rather
results from hemorrhage into the dental
follicle. It may occur during the eruption
of both primary and permanent teeth.
The most common treatment is
removal of a portion of the gingiva
overlying the crown of the tooth to
facilitate eruption

ERUPTION SEQUESTRUM
Tiny fragment of non vital hard tissue overlying an
erupting permanent molar that consists of bone or
cementum particles induced by the follicle. The
condition is of little clinical significance because it
generally does not seem to interfere with normal
eruption.(No Treatment).
Compact Bone
a)In the case of premature extraction of primary
molars,.
b)After transplantation of an iliac graft to a cleft
palate site, (it may present as an obstacle to an erupting canine)
The treatment of choice in both cases is a surgical
uncovering procedure, with or without enamel exposure
depending on the depth of the tooth germ

ODONTOMAS
Odontomas occur in the
maxilla more often than in the
mandible and in almost half of the
cases are known are combined
with impacted teeth.They also lead
to impaction of the involved tooth.
The treatment of choice is removal
of the odontoma. Thus, three out of
four impacted teeth can be
expected to erupt subsequent to
removal of odontomas.


The surgical procedure for removing an odontoma
firstly consists of a flap procedure whereby full access
to the odontoma is created. Bone covering the
odontoma is excised and it is removed.
Deep position - The follicle around the impacted tooth
is left intact
Superficial position - Exposure to the enamel is
carried out


Scar Tissue:
• Normally seen after cleft palate surgery
and after trauma .
• Apparently obstructs the collagenolytic
capacity of the follicle.
• There is also the possibility that a defect
has occurred in the follicle.
• Irrespective of etiology, the treatment of
choice is an uncovering procedure, including
enamel exposure.


ODONTOGENIC GIANT CELL
FIBROMATOSIS
It is a pathologic condition with
development of a fibrous tissue layer
dominated by giant cells.
They prevent normal eruption.
This condition has been recorded
in the first and second molar region,
with a strong preference for the
mandible.
The treatment of choice is surgical
exposure, which routinely leads to
successful eruption

ADENOMATOID ODONTOGENIC
TUMOR
Occurs in the second decade of life.
Radiographically :usually has a
pericoronal location and the radiographic
appearance of a follicular cyst extends
below the cervical region of the tooth.
Histologically: very similar to
ameloblasts .
Treatment - Curettage has been found
sufficient, without evidence of
recurrence , and normal tooth eruption
has been reported following conservative
excision or even incomplete removal of
the tumor

ODONTOGENIC KERATOCYST
The lesions represent cystic
changes in remnants of the dental
lamina (Serres pearls). During ex
pansion of these cysts, adjacent
unerupted teeth may be secondarily
involved, resulting in the radiographic
appearance of a follicular cyst.
Usually occurs in the second and
third decade of life,
The third molar and canine regions
are most frequently involved.

Radiographically, small keratocysts have
a unilocular appearance, whereas larger
cysts have a multilocular appearance.
Treatment: Cystectomy, and to prevent
recurrence, a part of the alveolar
mucosa covering the alveolar process is
resected as it contains large number of
epithelial remnants.


3.Defects in the Follicle or PD L
Found to occur subsequent to traumatic dental
injuries and cleft-lip-palate surgery , in relation to
congenital disorders such as amelogenesis
imperfecta and cleidocranial dysplasia , and
associated with hyperplastic follicles, central
odontogenic fibromas, and follicular cysts . All of
these events may lead to primary or secondary
retention
Diagnosis of a folliclerelated defect relies primarily on
a radiographic examination.


Ankylosis in the Follicle or the PD L
Recent studies have shown that 20%
of eruption disturbances affecting the first
and second molars are caused by an
ankylosis of the tooth
The etiology of this ankylosis is
unknown at present, and treatment
attempts such as breaking the ankylosis
sites by tooth luxation have not proved
successful. Thus, in most cases, the
tooth has to be removed in order to
prevent further complications.

Amelogenesis Imperfecta
In this hereditary condition it is known
that the tooth follicle is defective, and this
may lead to tooth retention
So far, no systematic treatment
approaches have been published, and in all
the reported cases the impacted teeth have
been removed.
However, considering that the defect is
most likely situated in the enamel
epithelium, surgical exposure of the tooth
should be a treatment possibility


Cleidocranial Dysplasia
In this hereditary condition, folliclemediated osteoclast
activation is deficient, leading to severe disturbances in
eruption .
The treatment of choice for this condition is either
surgical uncovering with enamel exposure or surgical
repositioning.
Follicular Cysts:
A follicular cyst is one that encloses the crown of an
unerupted tooth and is attached to its neck
Seen mostly between10 40 years
Cyst development can lead to displacement of the
impacted tooth as well as neighboring teeth
Treatment of choice for follicular cysts is usually a
fenestration, which after 612 months leads to eruption of
the displaced tooth germ

The treatment regimen depends entirely on the cause of
impaction or retention.
The following treatments have been found effective in
activating eruption in the clinical situations.
Ectopic Position of the Tooth Germ
Extraction of primary predecessor
Surgical uncovering with or without
enamel exposure
Surgical repositioning
Obstruction of the Eruption Pathway
Crowding
Orthodontic expansion
Extraction of the unerupted tooth or an
adjacent tooth

Follicle collision
Removal of one of the colliding tooth
germs

Compact bone
Surgical uncovering with or without enamel exposure
Scar tissue, giant cell fibromatosis, unattached oral
mucosa, odontogenic tumors
Surgical uncovering with enamel
Exposure
Supernumerary teeth or odontomas
Removal of the hard tissue obstacle
Follicle or PDL Defects
Surgical uncovering exposure
Surgical repositioning with enamel exposure

Summary:
It is essentail to diagnose and treat
eruption disturbances as early as possible
because treatment at a later stage is usually
more complicated due to the tendency of
malocclusion to increase with time and
reduced ability of remaining dentition to
adjust.


References:
1.V. Ravinder, Nikhar Verma. Ashima Valiathan: 3
Dimensional Computed TomographyA new method for
localization of Impacted Canines,JIOS 2002 page 7375
2.A Nagpal, Gsharma. A Sarkar and KM Pai: Eruption
Disturbances: an etiologicalcummanagement
perspective(Case Report),Dentomaxilofacial Radiology
2005 page 59 63
3.L. Suri, E.Gagari, H.Vastardis:Delayed tooth eruption:
Pathogenesis,Diagnosis, and treatment. A literature
Review, AJO DO October 2004,vol 126, number 4,
page433445.
4.Arathi R, Ashwini R :Supernumerary teeth: A case
report, JIPDS 2005 vol23 page 103105

5.Andreason, Petersen, Laskin DM. Normal and disturbed
eruptions in humans. Textbook and colour Atlas of
Tooth Impactions, 1997 Page 4964
6.H.L Craddock, C.C. Youngson: Eruptive tooth
movement The current state of Knowledge.BDJ
October 2004 vol 197 page385391
7.Tencate A.R. Oral Histology:Physiologic tooth
movement: Eruption and shedding , 7th edition
2005,page 276 297
8.J. Kurol, Early treatment of tooth eruption disturbances,
AJO DO June 2002 vol 121 number 6 page 588591.
9.Becktor et al: Association between ectopic eruption of
maxillary canines and first molars, EJO 2005 vol27 page
186 189

10.William Proffit: Contemporary Orthodontics:3rd edition,
2000 page 430 432, 471
11.L.Mitchell, T.G Bennett: Supernumerary teeth causing
delayed Eruption A retrospective Study, EJO February 1992
page 56 62
12. MG, Barry HJ, Blake M. Supernumerary Teeth An
Overview of Classification, Diagnosis and Management, J
Can Dent Assoc 1999;65:6126.
13.Regezi and Sciubb. Oral Pathology, W. B. Saunders Co.
2nd Ed. 1993.
14.Brook AH. Dental anomalies of number, form and size:
Their prevalence in British schoolchildren. J Int Assoc Dent
Child 1974;5:37
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15. Kinirons MJ. Unerupted premaxillary
supernumerary teeth. A study of their occurrence in
males and females. Br Dent J 1982;153:110.
16.RamosGomez FJ, Petru A, Hilton JF, Canchola
AJ, Wara D,Greenspan JS. Oral manifestations and
dental status in paediatric HIV infection. Int J Paediatr
Dent 2000;10:311.
17. Pope JE, Curzon ME. The dental status of cerebral
palsied, children. Pediatr Dent 1991;13:15662
18.B. Neville, D.Damm,C.Allen,J.Bouquot:Oral and
Maxillofacial Pathology, 2nd Edition, 2004 page
40,41,598

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Leader in continuing dental education


Dental education guide on tooth eruption problems

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