Article ear, nose, throat

Delayed Tooth Emergence

Jeffrey M. Karp, DMD, MS*
Objectives After completing this article, readers should be able to:

1. Recognize abnormalities in tooth emergence timing and order based on oral inspection.
Author Disclosure 2. Discuss local and systemic causes of delayed tooth emergence.
Dr Karp has disclosed 3. List treatment modalities available for management of delayed tooth emergence.
no financial 4. Determine when timely referral to a dentist is necessary.
relationships relevant
to this article. This
Introduction
commentary does not
Delayed tooth emergence (DTE) is a clinical term used when exposure of a tooth or
contain a discussion multiple teeth through the oral mucosa is overdue, according to population norms based
of an unapproved/ on chronologic age. DTE is common in childhood and adolescence, yet it is often
investigative use of a overlooked or dismissed in pediatric primary care. Timely screening and recognition of
commercial product/ DTE by clinicians can minimize medical, developmental, functional, and esthetic prob-
device. lems resulting from untreated underlying local and systemic causes. This article provides
clinicians with an overview of conditions responsible for DTE in children. Multidisci-
plinary care for patients who experience DTE in medical, dental, and surgical settings also
is discussed.

Odontogenesis
Human teeth develop through a series of complex, reciprocal interactions between the oral
epithelium and migrating cranial neural crest ectomesenchymal cells of the first branchial
arch. This process is tightly regulated by more than 300 genes expressed temporospatially
within the jaws. Dental patterning of the primary and permanent dentition is expressed
in three dimensions, exerting morphogenetic controls over tooth number, position, size,
and shape. In the end, the normal primary dentition consists of three tooth classes (four
incisors, two canines, four molars) in each jaw, for a total of 20 teeth. Thirty-two teeth
distributed among four tooth classes (8 incisors, 4 canines, 8 premolars, 12 molars)
comprise the permanent dentition.

Tooth Eruption and Emergence

Tooth emergence, the clinical exposure of any part of a tooth through the oral mucosa, is
the culmination of numerous developmental processes occurring within the jaws. Bony
crypts house developing teeth during crown morphogenesis (size and shape) as well as hard
tissue (eg, enamel, dentin) secretion and calcification. As
root development begins, teeth initiate a physiologic process
of vertical eruption through the overlying alveolar bone
Abbreviations toward the oral mucosa. Bone remodeling in the area is
DTE: delayed tooth emergence necessary for progression of tooth eruption. Root develop-
GE: gingival enlargement ment exceeds two thirds of its final length when the alveolar
HGF: hereditary gingival fibromatosis bone crest is reached. The primary dentition undergoes root
KCOT: keratocytic odontogenic tumor resorption, followed by crown exfoliation, to permit emer-
MPFM: maxillary permanent first molar gence of permanent incisors, canines, and premolars into the
Mx.C.P1: maxillary canine/first premolar proper position within the dental arch. Permanent molars
NBCCS: nevoid basal cell carcinoma syndrome do not replace primary teeth under normal circumstances.
PDC: palatally displaced canine Teeth make clinical emergence into the oral cavity when 75%
SP: supernumerary premolar of their roots’ length is achieved.
Numerous population studies conducted worldwide over

*Assistant Professor, Division of Pediatric Dentistry, Departments of Dentistry and Pediatrics, University of Rochester Medical
Center, Rochester, NY.

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 ear, nose, throat delayed tooth emergence

the past 100 years report marked variation in dental chro-
nology based on race, ethnicity, and sex as well as environ-
mental factors. Tooth development, eruption, and emer-
gence in healthy mouths are genetically controlled, with
high heritability scores reported in monozygotic twin stud-
ies. As seen in Table 1, tooth emergence and exfoliation
times are usually presented as ranges of chronologic age to
account for the previously mentioned factors. Clinicians
should recognize that teeth that fail to emerge within 12
months of the normal range are considered delayed. In
these cases, referral to a dentist is warranted for further
clinical and radiographic assessment. Some cases require
surgical treatment to permit tooth emergence.
Detection of DTE
DTE is a nonspecific clinical finding that can occur in a
localized or generalized distribution. Oral inspection
coupled with history can provide clinicians with substan-
tial information to define further the natural history and
clinical manifestations of the underlying condition. Oral
examination should consist of evaluation of the alveolar
ridges as well as the alignment and morphology of the
teeth that are present. The size and shape of the alveolar
ridges can help determine whether DTE is due to abnor-
malities in tooth development, eruption, or emergence.
Tooth eruption through alveolar bone causes expansion
and fullness of the alveolar ridge. On average, 2 months are
required for a tooth to progress from causing palpable
enlargement of the gingival tissues to overt clinical emer-
gence. Palpation of the oral mucosa in the area of erupting
teeth should cause localized tissue blanching if tooth emer-
gence is imminent. In addition, redness of the mucosa or an
eruption hematoma has been noted to precede tooth emer-
gence in more than 30% of cases. Thin, knife-edge alveolar
ridges suggest the absence of teeth in the area.
The dentition should be inspected systematically for
age-appropriate tooth counts (Figs. 1 and 2). Proper
inspection requires a working knowledge of the differ-
ences in tooth morphology among tooth classes and
between the two dentitions. Tooth counts should be
assessed for appropriateness in timing and order. For the
most part, the primary dentition adheres to the follow-
ing emergence order in each jaw: central incisors, lateral
incisors, first molars, canines, and second molars. Al-
though published emergence orders are available for the
permanent dentition, clinicians observe countless varia-
tions in order as a result of numerous genetic, anatomic,
and environmental influences.
Generalized timing delays in tooth emergence caused by
systemic disease do not usually result in changes in the order

Table 1. Tooth Emergence and Exfoliation

PRIMARY DENTITION
Mandible Maxilla
Eruption Exfoliation Eruption Exfoliation
(months) (years) (months) (years)
Central incisors 5 to 8 6 to 7 6 to 10 7 to 8
Lateral incisors 7 to 10 7 to 8 8 to 12 8 to 9
Canines 16 to 20 9 to 11 16 to 20 11 to 12
First molars 11 to 18 10 to 12 11 to 18 9 to 11
Second molars 20 to 30 11 to 13 20 to 30 9 to 12
PERMANENT DENTITION
Mandible Maxilla
Eruption Root Complete Eruption Root Complete
(years) (years) (years) (years)
Central incisors 6 to 7 9 to 10 7 to 8 9 to 10
Lateral incisors 7 to 8 10 8 to 9 11
Canines 9 to 11 12 to 15 11 to 12 12 to 15
First premolars 10 to 12 12 to 13 10 to 11 12 to 13
Second premolars 11 to 13 12 to 14 10 to 12 12 to 14
First molars 5.5 to 7 9 to 10 5.5 to 7 9 to 10
Second molars 12 to 14 14 to 16 12 to 14 14 to 16
Third molars 17 to 30 18ⴙ 17 to 30 18ⴙ
Adapted from American Academy of Pediatric Dentistry, Guideline on management of the developing dentition and occlusion in pediatric dentistry. Reference
Manual. 2009;32(6). Copyright © American Dental Association. All rights reserved. Used with permission.

Pediatrics in Review Vol.32 No.1 January 2011 e5

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ear, nose, throat delayed tooth emergence
Figure 1. Development of the dentition from birth to 6 years
of age. Reprinted with permission from Logan WHG, Kronfeld
R. Development of the human jaws and surrounding structures
from birth to the age of fifteen years. JADA. 1933;20(3):379 –
427. Copyright © 1933 American Dental Association. All rights
reserved. Adapted 2010 with permission of the American
Dental Association. Schour L, Massler M. The development of
human dentition. JADA. 1941;28(7):1153–1160. Copyright
© 1941 American Dental Association. All rights reserved.
Adapted 2010 with permission of the American Dental Asso-
ciation.
of tooth emergence or exfoliation. In contrast, localized
disease should be investigated when the order of tooth
emergence is altered. Three general rules exist for normal
tooth development and emergence: 1) anterior teeth within
a specific tooth class (eg, first premolars) always precede
posterior teeth within the same class (eg, second premo-
lars), 2) mandibular teeth emerge earlier than their maxil-
lary counterparts, and 3) symmetric emergence of tooth
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Figure 2. Development of the dentition from age 7 to adult-
hood. Reprinted with permission from Logan WHG, Kronfeld R.
Development of the human jaws and surrounding structures
from birth to the age of fifteen years. JADA. 1933;20(3):379 –
427. Copyright © 1933 American Dental Association. All rights
reserved. Adapted 2010 with permission of the American
Dental Association. Schour L, Massler M. The development of
human dentition. JADA. 1941;28(7):1153–1160. Copyright
© 1941 American Dental Association. All rights reserved.
Adapted 2010 with permission of the American Dental Asso-
ciation.
antimeres (corresponding teeth on opposite side) usually
occurs.
Causes of DTE
Anomalies in Tooth Number
Tooth agenesis, one of the most common developmental
anomalies in humans, alters the order of tooth emer-
gence. Although missing teeth are noted in only 1% of
children in the primary dentition, approximately 30% of
the general population fails to develop a full complement
of primary and permanent teeth. Agenesis of one or more
permanent third molars (wisdom teeth) affects about

Figure 3. An 8-year-old white boy who has bilateral agenesis
of the maxillary lateral incisors (3) causing a wide diastema
between the maxillary central incisors. Photograph courtesy of
Ryan Walker, DDS.
one in every five people. A recent meta-analysis reported
the prevalence of dental agenesis, excluding third mo-
lars, as 2.5% to 6.9%, depending on the race, sex, and
country of study. (1) Tooth agenesis is slightly more
common (1.3:1) in females versus males.
Hypodontia is defined as the absence of up to six
teeth. In more than 80% of patients, one or two teeth are
missing. After the third molars, the mandibular second
premolars, maxillary lateral incisors, and maxillary second
premolars are affected most frequently, with a 1.5% to
3.1% prevalence rate. Unilateral tooth agenesis is seen
more commonly, except for permanent maxillary lateral
incisors (Fig. 3), which have a propensity toward bilateral
agenesis.
Only 0.14% of the general population has oligo-
dontia, defined as the absence of six or more teeth.
Oligodontia following autosomal dominant inheritance
patterns can be indicative of PAX9, MSX1, or AXIN2
mutations. Ectodermal dysplasia should be considered
when underdeveloped alveolar ridges are seen in the
anterior jaws of predentate infants older than 7 months
of age, when multiple primary teeth are absent, or when
conical incisors are seen (Fig. 4).
Recognition of missing teeth by number and loca-
tion along with other physical findings can aid in the
diagnosis of numerous genetic diseases (Table 2). Clini-
cians should consider abnormal alignment and increased
spacing of teeth as well as localized delays in primary
tooth exfoliation as potential clinical manifestations of
hypodontia (Fig. 5). Patients who manifest hypodontia
may warrant consultation with a geneticist to rule out
associated syndromes.
Supernumerary teeth (hyperdontia) developing with
the jaws often delay the eruption and emergence of
permanent teeth. Hyperdontia is seen in 1.5% to 3.5% of
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ear, nose, throat delayed tooth emergence
Figure 4. A 9-year-old white girl who has ectodermal dys-
plasia. Agenesis of the permanent maxillary lateral incisors
and all mandibular incisors is seen, and a conical permanent
maxillary central incisor (*) is present. Photograph courtesy of
David Levy, DMD MS.
the general population. More than 80% of cases occur in
the anterior maxilla, and supernumerary teeth presenting
at this site can occur singly or in multiples, can have
normal incisor anatomy, can be conical (Fig. 6), or can
appear to have cuspal morphology. The teeth can emerge
into the mouth or be inverted within the maxilla. A single
supernumerary tooth that develops in the primary palate
directly behind the maxillary central incisors is called a
mesiodens. These teeth account for more than 50% of all
supernumerary teeth reported in epidemiologic studies.
Altered fusion between the medial nasal process and the
maxillary facial process during embryogenesis produces
the presence of two maxillary lateral incisors on the
affected side, as is seen occasionally in the general popu-
lation and more commonly in children born with isolated
cleft lip and cleft lip and palate.
Maxillary permanent fourth molars or rudimentary
paramolars constitute approximately 18% of all supernu-
merary teeth. Supernumerary premolars (SPs), on the
other hand, develop in 0.64% of the general population.
A 3:1 male-to-female distribution is seen. SPs are the
most common type of hyperdontia occurring in the
mandible. Their development appears to be genetically
controlled, although the pattern of inheritance remains
unclear. These teeth usually have normal premolar anat-
omy. Five out of every six SPs fail to emerge clinically,
and they can cause impaction of adjacent teeth (Fig. 7).
They are often incidental findings on panoramic radio-
graphs in adolescence. Many can develop after the emer-
gence of age-appropriate premolars.
Surgical removal of a supernumerary tooth becomes
necessary when it impedes or deflects age-appropriate
tooth eruption and emergence. One in four patients who
has a history of extra teeth in the anterior maxilla later
Pediatrics in Review Vol.32 No.1 January 2011 e7
 Table 2. Genetic Diseases With Anomalies in Tooth Number
Condition
Autosomal dominant
oligodontia
Witkop syndrome
Van der Woude
Down syndrome
e8 Pediatrics in Review Vol.32 No.1 January 2011
Ellis-van Creveld
Apert syndrome
Osteogenesis imperfecta
Incisor-premolar
hypodontia
Hutchinson-Guilford
progeria syndromes
Hypohidrotic ectodermal
dysplasia
Incontinentia pigmenti
Axenfeld-Rieger syndrome
Orofacial-digital syndrome
type 1
Holoprosencephaly
Cleidocranial dysplasia
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Gardner syndrome
AD⫽autosomal dominant, AR⫽autosomal recessive, Xd⫽X-linked
Gene Inheritance Dental Findings Other Findings
PAX9 AD Agenesis of permanent molars None documented
ear, nose, throat
AXIN2 Permanent tooth agenesis across tooth types Colon polyps and cancer, cleft lip and palate
MSX1 Agenesis of second premolars and third molars Cleft lip and palate
MSX1 AD Agenesis of permanent mandibular incisors and Nail hypoplasia (especially toenails)
second molars, maxillary permanent canines
IRF6 AD Permanent tooth agenesis, second premolars, Cleft lip and palate, mandibular lip pits
maxillary lateral incisors
Numerous Trisomy 21 Agenesis of incisors and second premolars, peg- Dysmorphic facies, congenital heart disease,
shaped lateral incisors, maxillary canine-first intellectual disability, leukemia, thyroid
premolar transposition dysfunction, hearing loss, maxillary hypoplasia
delayed tooth emergence
EVC AD Tooth agenesis, enamel hypoplasia, multiple oral Chondrodysplasia, polydactyly, congenital heart
frenula, premature exfoliation of primary defects
teeth
FGFR2 AD Permanent tooth agenesis Craniosynostosis, maxillary hypoplasia, hand
anomalies
COL1A1/2 AD Hypodontia, dentinogenesis imperfecta Blue sclera, multiple fractures
Unknown AD Agenesis of lateral incisors and second None documented
premolars, taurodontism, ectopic maxillary
canines
LMNA Sporadic Permanent tooth agenesis, ectopic eruption of Precocious senility, early death, coronary artery
permanent incisors disease, beaked nose, baldness, lipodystrophy,
short stature
EDA Xd Primary and permanent tooth agenesis, conical Defective hair, nails, skin; hypohidrosis; poor
EDAR AD, AR incisors, anodontia hearing; respiratory infections
EDARR AD, AR
IKK␥ Xd Permanent tooth agenesis, conical teeth, delayed Defective hair, nails, eyes; intellectual disability;
exfoliation of primary dentition autochthonous tattooing
NEMO Agenesis, conical teeth, delayed tooth Hypohidrosis, immunodeficiency
emergence
PITX2 AD Agenesis of incisors and canines, enamel Glaucoma, redundant periumbilical skin
hypoplasia, conical teeth
CXORF5 Xd Agenesis of incisors and canines Cleft palate, hand anomalies, intellectual disability
Numerous AD Solitary maxillary central incisor Seizures, syndromic facies, premaxillary agenesis,
cleft lip and palate, hypotelorism
RUNX2 AD Multiple supernumerary teeth, retained primary Hypoplastic calvaria, absent clavicles, midface
teeth, impacted permanent teeth hypoplasia, delayed fontanelle closure, short
stature, scoliosis, sinus/respiratory infections,
hearing loss
APC AD Supernumerary teeth, tooth agenesis, jaw Gastrointestinal polyps, multiple osteomas, skin and
osteomas, impacted teeth soft-tissue tumors, cancer in 50% by age 30

Figure 5. A 14-year-old African American boy who has
hypodontia. The mandibular right second premolar (**) did not
develop. Clinically, the mandibular right second primary molar
(3) shows delayed exfoliation. The permanent third molars
continue to develop in the jaws (*). Photograph courtesy of
Aliakbar Bahreman, DDS, MS.
develops SPs. Moreover, SPs, unlike other supernumer-
ary teeth, recur in 8% of patients. Of note, natal and
neonatal teeth should be maintained when possible be-
cause they not supernumerary in more than 90% of cases.
Clinicians who suspect the presence of a supernumerary
tooth should refer the child to a dentist for radiographic
examination.
Delayed Dental Age
Biologic delays in dental development generally retard
emergence of the primary and permanent dentitions.
Delayed dental age has been studied using tooth counts
from clinical inspection as well as the stage of tooth
formation on panoramic radiography. As mentioned,
DTE using clinical tooth counts is an inexact measure of
dental age due to a host of local factors. Dental age scores
Figure 6. A conical mesiodens (3) has emerged into the
anterior maxilla, causing the permanent maxillary right cen-
tral incisor (*) to emerge late and out of position. Surgical
removal of the mesiodens is recommended. Photograph cour-
tesy of Aliakbar Bahreman, DDS, MS.
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ear, nose, throat delayed tooth emergence
Figure 7. A 15-year-old Hispanic boy who has delayed exfo-
liation of the mandibular right primary molars (3) as well as
delayed emergence of the mandibular left premolars (*). An
age-appropriate set of permanent teeth is present in the
maxillary arch. Four supernumerary mandibular premolars,
two on each side, are the cause for the delayed emergence of
the mandibular premolars. Photograph courtesy of Aliakbar
Bahreman, DDS, MS.
are best determined using radiographic stages of tooth
formation.
Few studies have focused on the primary dentition
because radiography is limited by patient cooperation.
However, numerous methods have been proposed to
score dental age using a variety of statistical methods
based on scores of crown and root formation for the
permanent teeth. The Demirjian method, originally
studied in a French Canadian pediatric population, is
used most commonly. (2) This method scores the man-
dibular left permanent teeth, excluding the third molars,
according to eight developmental stages. More than
100 studies have used the Demirjian method and modi-
fications of it to compare dental age to the chronologic
age of a population. This method, although validated
through epidemiologic studies, gives varied results by
sex, race, and ethnicity of the population of study. Dental
age scoring using these methods is used commonly in
forensics and immigration proceedings for unaccompa-
nied minors as a means of age estimation when additional
information is not available.
Dental age does not consistently correlate with skele-
tal age and the timing of puberty. However, the mandib-
ular canine has been shown to be the best indicator of
pubertal onset using tooth formation stages. In general,
skeletal age delayed by systemic disease or malnutrition is
often two to six times more severe than the delay noted in
dental age.
Using the Demirjian method and others in conjunc-
tion with clinical tooth counts, patients who have a host
of systemic diseases have been found to have delayed
dental age. Most studies, however, involve a limited
Pediatrics in Review Vol.32 No.1 January 2011 e9
ear, nose, throat delayed tooth emergence
number of affected individuals, lending poor statistical
power. In addition, numerous genetic syndromes have
DTE (also described as delayed tooth eruption) listed as
a clinical finding. Case reports and studies involving these
patients do not usually assess dental age based on radio-
graphic parameters.
Nonetheless, oral inspection of children who have
Down syndrome, hypothyroidism, growth hormone de-
ficiency, hypopituitarism, and chronic malnutrition often
results in a finding of DTE. In small case-control studies,
patients who have hypodontia and those who have pala-
tally displaced canines (PDCs) are also noted to have
delayed dental age. DTE resulting from delayed dental
age in children who have Down syndrome remains un-
treatable. In contrast, growth hormone therapy has been
shown in preliminary studies to accelerate dental matu-
ration and improve the timing of tooth emergence. (3)
Although preterm birth has been associated with de-
layed dental age according to chronologic age, dental age
normalizes when the child’s term age is used. (4) Simi-
larly, children who have enamel and dentin anomalies
due to X-linked hypophosphatemic rickets do not
present initially with delayed dental age. They do, how-
ever, develop spontaneous dental abscesses due to micro-
scopic abnormalities in the mineralized dental tissues
that allow ingress of microorganisms and pulpal necrosis.
Early primary tooth loss due to infection can slow the
dental development of the permanent successors and
lead to DTE.
Dental Crowding
Insufficient space in the jaws for eruption and emergence
of teeth constitutes the most benign, yet common,
Figure 8. Space loss in the maxillary left quadrant is seen
when compared with the contralateral side due to early
extraction of the maxillary left primary molars because of
dental caries. The maxillary permanent first molar (bottom
right) has migrated into the space previously occupied by the
primary molars due to the lack of a space maintenance
appliance.
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source of DTE in children. A tooth-to-jaw size discrep-
ancy is often responsible for dental crowding. This dis-
harmony occurs as a result of: 1) normal-size teeth in
small jaws, 2) larger-size teeth in normal-size jaws, or 3) a
combination of both. Children who have constricted,
V-shaped alignment of the teeth are more likely have
tooth crowding than those in whom the dental arch is
U-shaped. Dental crowding among primary incisors pre-
dicts moderate-to-severe crowding in the permanent
dentition.
Early tooth loss due to dental caries raises a child’s risk
for dental crowding and delayed emergence of perma-
nent teeth. Primary teeth serve as placeholders for their
successors. Premature extraction of primary canines or
molars results in migration of adjacent teeth (Fig. 8), loss
of dental arch length and circumference, and shift of
dental midlines toward the side of early tooth loss. Pedi-
atric dentists and orthodontists attach appliances to teeth
adjacent to tooth extraction sites to maintain space for
later permanent tooth emergence.
The presence of supernumerary teeth as well as fused
teeth (Fig. 9) can exacerbate dental crowding. Later
developing teeth can remain unerupted in the jaws or be
forced to emerge ectopically when adjacent teeth are
impediments to the normal eruption path. Odontogenic
pathology and jaw bone disorders also worsen dental
crowding through displacement of unerupted and
emerged teeth into compact areas of the jaws.
Dental crowding can be alleviated by transverse ex-
pansion of the jaws. Posterior retraction of medially
positioned molars also increases the amount of space for
future tooth emergence. In some cases, dental crowding
necessitates the removal (serial extraction) of healthy
primary canines and molars as well as permanent first
premolars sequentially to allow proper alignment of the
permanent dentition in adolescence and adulthood.
Dentists, orthodontists, and oral maxillofacial surgeons
Figure 9. A 6-year-old African American girl who has a
maxillary left primary incisor fused (**) to a supernumerary
tooth. Photograph courtesy of Aliakbar Bahreman, DDS, MS.

work collaboratively on these cases to obtain optimal
treatment outcomes.
Ectopic Tooth Eruption
Abnormalities in the path of tooth eruption also can
cause delayed tooth emergence in the permanent denti-
tion. The literature suggests that 2% to 6% of children
demonstrate ectopic tooth eruption. The maxillary per-
manent first molars and canines are affected most com-
monly. The prevalence of ectopic eruption is substan-
tially higher (⬎20%) in children born with cleft lip and
palate, likely due to genetic and anatomic differences.
Under normal circumstances, the maxillary perma-
nent first molar (MPFM) follows an eruption path pos-
terior to the maxillary second primary molar. It emerges
through the gingival tissues and uses the posterior sur-
face of the primary molar to guide its eruption into
functional occlusion with teeth in the opposing jaw.
Ectopic MPFMs take a medial eruption course, leading
them under the crown of the second primary molar
(Fig. 10). This eruption disturbance, often detected on
dental radiographs between 5 and 7 years of age, delays
MPFM emergence and often causes root resorption of
the primary second molar, with some cases persisting
until the primary tooth is exfoliated prematurely. Two
thirds of ectopic MPFMs self-correct, usually by 7 years
of age. For the remaining cases, orthodontic manage-
ment is necessary to prevent anterior migration of the
ectopic MPFM and future impaction of the ipsilateral
maxillary second premolar. Clinically, this anomaly can
be detected through premature mobility of the primary
second molar or mesial angulation of the MPFM, with
emergence of the distal (away from midline) cusps only.
PDCs in the maxilla should be suspected in children
Figure 10. The maxillary permanent first molars (*) are erupt-
ing in an ectopic position under the crowns of the maxillary
primary second molars. Root resorption of the primary second
molars is also occurring. Photograph courtesy of Aliakbar
Bahreman, DDS, MS.
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ear, nose, throat delayed tooth emergence
Figure 11. Asymmetric expansion of the anterior palate (3).
The maxillary primary canine on the ipsilateral side (*) has
been exfoliated. This clinical presentation is indicative of an
untreated palatally displaced canine. Photograph courtesy of
Aliakbar Bahreman, DDS, MS.
older than 9 years of age when alveolar ridge palpation
adjacent to the buccal vestibule lacks a canine bulge, a
clinical finding suggestive of normal canine eruption.
The early manifestations of PDCs can be detected on
panoramic radiography because ectopic maxillary canines
often appear more horizontal on the film and tend to
overlap the root of the mature ipsilateral lateral incisor.
Early extraction of the adjacent maxillary primary canine
corrects the eruption path and spatial orientation of
PDCs in almost 70% of cases. PDCs are associated with
other dental anomalies (small-size maxillary permanent
lateral incisors, infraocclusion of primary molars, and
enamel hypoplasia) that can be detected by clinicians
through oral inspection. Delayed exfoliation of the ipsi-
lateral maxillary primary canine or asymmetric anterior
palatal enlargement with or without primary canine loss
(Fig. 11) are late clinical manifestations of PDCs. If left
untreated, ectopic eruption of the maxillary canine leads
to tooth impaction in the hard palate. Surgical tooth
exposure, forced orthodontic traction, and space regain-
ing in the maxillary anterior segment through fixed orth-
odontic appliances (braces) becomes necessary.
Tooth transposition also results in delayed tooth
emergence in many cases. This abnormality of dental
position occurs more frequently in the maxilla than the
mandible. Maxillary canine/first premolar (Mx.C.P1)
transposition cases (Fig. 12) occur most commonly, with
a prevalence of 0.25%. Based on a review of 143 cases,
Mx.C.P1 transposition appears to be polygenic, with a
propensity for occurrence in females. (5) A higher prev-
alence of Mx.C.P1 transposition is seen among children
who have Down syndrome. Clinically, agenesis of the
ipsilateral lateral incisor is common. Twenty-seven per-
cent of published Mx.C.P1 cases occur bilaterally.
Pediatrics in Review Vol.32 No.1 January 2011 e11
ear, nose, throat delayed tooth emergence
Figure 12. Maxillary permanent left canine with left first
premolar transposition. In this case, reshaping of the teeth
with dental composite restorations can permit normal func-
tion and satisfactory esthetics. Photograph courtesy of Aliak-
bar Bahreman, DDS, MS.
Early permanent tooth loss due to dental caries or
trauma as well as traumatic displacement of developing,
unerupted teeth within the jaws accounts for most other
cases of transposition in the maxilla, including canine/
lateral incisor, canine/first molar, lateral incisor/central
incisor, and canine/central incisor patterns. Mandib-
ular canine/lateral incisor transposition, identified in
0.03% of dental patients, often is seen in conjunction
with permanent third molar agenesis, suggestive of ge-
netic influences. Transposition cases, if recognized early
enough, usually can be managed effectively with inter-
ceptive orthodontics without surgery.
Delayed Exfoliation of Primary Teeth
Delayed exfoliation of primary teeth is intimately associ-
ated with delayed root development and eruption of
their permanent successors. As a result, permanent tooth
agenesis or delayed dental maturity typically results in
delayed exfoliation of primary teeth according to chro-
nologic age. In these cases, the timing of primary tooth
root resorption is appropriate from a biologic standpoint.
In contrast, primary tooth exfoliation is considered bio-
logically delayed when the primary tooth remains in place
despite permanent tooth root length greater than 75% of
its expected final length.
Primary teeth that appear biologically ready for exfo-
liation are common in primary care. These teeth are
usually retained in soft tissue or interlocked between
adjacent teeth, limiting their ability to be removed at
home. Children also tend to delay tooth removal if they
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Figure 13. The maxillary primary central incisors are delayed
in exfoliation. They are forcing the maxillary permanent
central incisors to erupt in the anterior palate. When the child
occludes his teeth, the maxillary permanent central incisors
are behind (crossbite) the mandibular incisors (3). Orthodon-
tic correction of this condition becomes necessary. Photo-
graph courtesy of Aliakbar Bahreman, DDS, MS.
feel that pain is likely. Timely extraction of over-retained
primary teeth is indicated if maxillary permanent incisors
will be deflected palatally and malocclusion such as ante-
rior crossbite (Fig. 13) is likely to occur.
Soft-tissue infection is another indication for tooth ex-
traction when food becomes impacted under the exfoliat-
ing primary tooth. Lingual emergence of mandibular per-
manent incisors is common but rarely a cause for concern.
In these cases, further emergence of the permanent teeth
ultimately causes exfoliation of their predecessors, followed
by anterior repositioning of the permanent incisors within
the dental arch by tongue pressure. Extraction of over-
retained mandibular primary incisors is needed more fre-
quently in cases of severe dental crowding.
Infraoccluded primary molars (teeth that fail to reach
the normal occlusal plane) are reported to occur in 5% of
the general population. These teeth often appear to be
ankylosed on clinical examination because they are im-
mobile to palpation and tend to be submerged in the
gingival tissues compared with continually erupting ad-
jacent teeth (Fig. 14). Nonetheless, infraoccluded pri-
mary molars usually exfoliate within 1 year of the normal
range as long as the permanent tooth successor is present
with adequate root formation.
Infraoccluded primary molars can become surgical
problems if the crowns of the adjacent teeth are allowed
to migrate over top of them. In addition, alveolar bone
levels surrounding the adjacent teeth can approximate
the crown of the infraoccluded molar, leading to im-

Figure 14. The mandibular left primary first molar is infra-
occluded. The adjacent teeth continue to erupt while it
remains stationary, creating the clinical appearance of a tooth
submerging into the gingiva. Photograph courtesy of Aliakbar
Bahreman, DDS, MS.
paired exfoliation and delayed premolar emergence (Fig.
15). Close monitoring of infraoccluded primary molars
by dentists is recommended to avoid these complications.
Trauma
Tooth development, eruption, and emergence can be
altered by dental or maxillofacial trauma in infancy or
childhood. Trauma to developing primary teeth is rela-
tively rare. Extreme root curvature (aka dilaceration) and
eruption failure of maxillary incisors have been reported
Figure 15. A 12-year-old white boy who has infraoccluded
maxillary second primary molars (*). The adjacent teeth have
erupted over the top of the infraoccluded teeth, causing them
to become impacted in the jaw. This condition impedes the
maxillary second premolars from erupting into the mouth.
Photograph courtesy of Aliakbar Bahreman, DDS, MS.
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ear, nose, throat delayed tooth emergence
Figure 16. A 6-year-old boy born in Uganda presents with
malformed mandibular primary canines (*) and missing max-
illary primary canines (ⴙ). His history corroborates that canine
extirpation was completed before emigration from Uganda.
Photograph courtesy of Terry Farquhar, RN, DDS.
as sequelae of traumatic laryngoscopy and prolonged
endotracheal intubation in infancy. Clinicians also may
encounter children who have emigrated from Eastern
Africa and appear to have DTE of the primary canines or
other adjacent teeth on clinical inspection (Fig. 16). This
finding is consistent with the practice of ebinyo, in which
tribal healers remove these teeth in infancy to prevent
or treat high fevers, vomiting, or diarrhea in the child.
Damage, displacement, or extraction of adjacent primary
and permanent teeth also can be seen.
Mandibular fractures due to falls, motor vehicle crashes,
or child abuse can disturb teeth developing along the line
of fracture. Infection and inadvertent placement of plates
and screws during jaw fixation also jeopardizes adjacent
developing teeth. Similarly, children born with microgna-
thia (eg, Pierre Robin sequence, Goldenhar syndrome)
who require mandibular distraction osteogenesis to prevent
long-term tracheostomy can have permanent molar tooth
germs displaced or destroyed during mandibular osteot-
omy and placement of the internal distraction device. Pro-
phylactic enucleation of tooth germs in planned sites of
distractor pins is advocated by some surgeons to improve
bone volume and treatment outcomes.
Intrusion of primary incisors into the dental alveolus
commonly results in developmental changes to their
permanent successors. The amount of internal displace-
ment and direction of primary tooth displacement cou-
pled with the age of the child aid clinicians in deter-
mining whether enamel hypoplasia, root dilaceration, or
tooth germ displacement are possible sequelae. Reim-
Pediatrics in Review Vol.32 No.1 January 2011 e13
ear, nose, throat delayed tooth emergence
Figure 17. A 9-year-old African American girl who has
delayed exfoliation of the maxillary right primary central
incisor (#). This tooth is discolored due to dental trauma. Her
permanent incisor emergence order is affected. Extraction of
the over-retained primary incisor is indicated. Photograph
courtesy of Aliakbar Bahreman, DDS, MS.
plantation of avulsed primary incisors after trauma pre-
disposes them to delayed tooth exfoliation because de-
struction of the periodontal ligament apparatus and
ankylosis between the alveolar bone and the tooth’s root
often occur. In these cases, ectopic permanent incisor
eruption occurs along with rotation of adjacent teeth
(Fig. 17). This problem is seen infrequently because
dentists and first responders at accident sites are educated
to avoid replantation of avulsed primary teeth.
Jaw Bone Pathology
Tooth development and emergence often are affected by
jaw pathology. In some cases, dental abnormalities occur
as a result of inadequate bone remodeling, and in other
disorders, displacement of developing teeth is caused by
expanding jaw lesions.
Children who have infantile osteopetrosis experience
marked delays in tooth emergence as well as tooth agenesis
and enamel hypoplasia. These clinical manifestations are
directly related to osteoclast dysfunction. Stem cell rescue of
those who have osteopetrosis can restitute normal tooth
eruption and emergence of the permanent dentition.
Various types of osteogenesis imperfecta present with
dental developmental anomalies. Delayed tooth emergence
is seen in 20% of patients who have osteogenesis imperfecta
type III. Ectopic tooth eruption is another common finding
in affected individuals. Bisphosphonate therapy used in the
management of osteogenesis imperfecta can cause delayed
tooth emergence of 1.6 years relative to matched controls.
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To date, bisphosphonate therapy has not been associated
with osteonecrosis of the jaws, as is reported in adult pa-
tients using these medications.
McCune-Albright syndrome is a sporadic multisystem
disease characterized by polyostotic fibrous dysplasia, café
au lait hyperpigmentation, and precocious puberty. Cranio-
facial forms of fibrous dysplasia result in progressive facial,
palatal, and jaw asymmetries. The maxilla is affected more
commonly than the mandible, with a ground-glass appear-
ance of the lesion noted through panoramic radiography or
computed tomography scans. Oligodontia as well as tooth
impaction, displacement, and rotations are common in
affected patients.
Jaw osteomas and supernumerary teeth often are the
first manifestations of Gardner syndrome in puberty. Early
recognition is necessary to permit monitoring of gastroin-
testinal polyps because malignant transformation occurs in
50% of patients by age 30.
Permanent teeth often fail to erupt in patients born with
cleidocranial dysplasia because the teeth lack secondary
cementum. Extraction of primary teeth that have failed to
exfoliate normally does not promote eruption of their per-
manent successors. In addition, supernumerary teeth can
impede tooth emergence. Surgical exposure of unerupted
teeth followed by orthodontic traction has limited success.
Oral rehabilitation for these patients often centers on jaw
reconstruction and the use of dental prostheses.
Cherubism is a rare autosomal dominant disease that
affects the jaws. The condition is characterized by bilateral
expansion of the posterior mandible and, in some cases,
the maxilla and facial bones. Bony expansion of the jaws
causes the individual to have a “chubby cheeked,” cherubic
appearance. The osseous lesions are usually multilocular
radiolucencies affecting the angles and ascending rami of
the mandible. They are histologically defined by multinu-
cleated giant cells in a loose fibrous stroma. The lesions tend
to increase in size until puberty, after which lesion stabiliza-
tion or even regression is noted. Bilateral expansion of these
lesions causes marked displacement of developing and
emerged teeth. Failure of tooth eruption due to severe
dental crowding and malocclusion is common. Watchful
monitoring is the usual course of action unless expansion
progresses rapidly.
Odontogenic Cysts and Tumors
Epithelial-lined jaw cysts derived from odontogenic epi-
thelium commonly impair eruption of developing teeth,
producing alterations in tooth emergence timing or or-
der. Dentigerous cysts, originating from a separation of
the follicle around the crown of an unerupted tooth,
comprise approximately 20% of all odontogenic cysts.

Figure 18. A 13-year-old white girl presents with delayed
exfoliation of the maxillary right primary canine (*). On dental
radiography, a large unilocular cyst is present around the
crown of the unerupted permanent canine. Histopathologic
examination reveals a dentigerous cyst.
Mandibular third molars, followed by maxillary perma-
nent canines (Fig. 18), are affected most commonly.
Dentigerous cysts around supernumerary teeth and
odontomas also are seen frequently. Usually, the lesion
should measure at least 3 to 4 mm in diameter on
radiograph to be called a dentigerous cyst rather than a
variation in normal follicular anatomy. These lesions are
found more often in the second decade, with the highest
prevalence noted in white patients. Dentigerous cysts can
grow very large and have a tendency to displace the involved
tooth within the jaw (Fig. 19). Treatment of these lesions
involves either marsupialization or enucleation of the cyst
with or without removal of the unerupted tooth. Recur-
rence is rare after complete removal of the cyst.
Keratocytic odontogenic tumors (KCOTs), previously
known as odontogenic keratocysts, have been reported to
account for 2% of all oral biopsies performed in children
younger than 16 years of age, according to retrospective
review of a United States dental school biopsy service. (6)
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ear, nose, throat delayed tooth emergence
Figure 19. A 17-year-old white girl who presents with painless
swelling of the mandibular left posterior jaw has age-appropriate
dentition on clinical examination. On panoramic radiography, a
large unilocular radiolucency is seen along with marked displace-
ment of the unerupted third molar. Histopathologic examination
confirmed the lesion to be a dentigerous cyst.
KCOTs are aggressive tumors that have a marked tendency
for development in the posterior body and ascending ramus
of the mandible. An unerupted tooth is involved in 25% to
40% of cases, mimicking a dentigerous cyst. KCOTs have
thin, friable walls that make complete enucleation and thor-
ough curettage difficult. As a result, recurrence is common.
In locally aggressive cases, jaw resection followed by bone
grafting may be necessary.
The presence of multiple KCOTs warrants further
testing for nevoid basal cell carcinoma syndrome
(NBCCS). Gorlin syndrome, as it also is called, is char-
acterized by multiple KCOTs as well as multiple basal cell
carcinomas, hyperkeratosis of the palms and soles, skele-
tal abnormalities, intracranial ectopic calcifications, and
facial dysmorphia. NBCCS is caused by mutations in the
PTCH1 gene. It is transmitted as an autosomal dominant
trait and is reported in fewer than 1 in 57,000 individu-
als, with a 1:1 male-to-female ratio. Multidisciplinary
care by dental professionals, pediatricians, dermatolo-
gists, and neurologists is recommended.
Ameloblastomas have been described as the most
clinically significant odontogenic tumor. They arise from
cells of odontogenic epithelial origin. Multicystic lesions
are seen most commonly across the lifespan. However,
only 8.7% to 15% of all ameloblastomas in Western
countries develop in the pediatric population. Fifty per-
cent of unicystic intraosseous ameloblastomas are diag-
nosed in the second decade of life. Most of these tumors
develop as asymptomatic lesions in the posterior mandi-
Pediatrics in Review Vol.32 No.1 January 2011 e15
ear, nose, throat delayed tooth emergence

ble. An unerupted third molar as well as teeth adjacent

to it often can become involved. These tumors resemble
cysts on surgical exposure. As such, they usually are
treated by enucleation with curettage. Recurrence rates
ranging from 10% to 20% are seen. Block resection can
become necessary in select cases. On very rare occasions,
ameloblastomas act as malignant tumors, with hematog-
enous spread of metastatic disease.
Odontomas are the most common odontogenic tu-
mors, accounting for approximately 30% of lesions. They
develop in both jaws, with greater prevalence in the
maxilla. They are equally distributed between both sexes.
Two types, compound and complex, are seen. Com-
pound odontomas are well-circumscribed masses of tiny
teeth of various numbers. The teeth are usually cone-
Figure 20. An 8-year-old white boy who has a history of trauma
shaped and have normal delineation of tooth layers.
to the maxillary anterior teeth presents with delayed emergence
Complex odontomas are similar but do not have orga- of the maxillary permanent right central and lateral incisors. The
nized dental structures. They are easily removed by enu- contralateral permanent incisors are already present. The outline
cleation and do not recur. Fifty-five percent of them are of the unerupted teeth can be seen within the gingiva. Surgical
diagnosed when delayed permanent tooth emergence or exposure was necessary to permit tooth emergence.
delayed exfoliation of a primary tooth is seen.
More than 20 other types of odontogenic cysts and
terized by proliferation of connective tissue extracellular
tumors can develop in the jaws. Histopathologic exami-
matrix in response to gingival drug metabolism. Phenytoin,
nation is necessary to discriminate these lesions, includ-
nifedipine, and cyclosporine are the most common catalysts
ing identification of specific odontogenic elements and
of the condition. Poor oral hygiene exacerbates GE
mineralized tissue. If left untreated, odontogenic disease
through inflammatory mechanisms. The anterior gingival
can cause displacement and mobility of teeth, delayed
tissues are involved more frequently. Males tend to be more
tooth emergence, root resorption, pain, jaw swelling,
severely affected for poorly understood reasons. The use of
and paresthesia. Large cystic lesions in the posterior
multiple anticonvulsant medications in addition to phenyt-
mandible can lead to pathologic jaw fractures.
oin increases the severity of phenytoin-induced GE. Addi-
Gingival Enlargements
The gingiva and oral mucosa provide the last barrier to
tooth emergence when sufficient space is present in the
dental arch. Under normal circumstances, reduced enamel
epithelium of erupting teeth fuses with the oral mucosa,
permitting emergence of the dentition. Gingival remodel-
ing also is necessary for emergence and continued tooth
eruption over time. A variety of genetic and environmental
conditions active in the gingival tissues can preclude either
localized or generalized tooth emergence.
Tooth emergence can be delayed when the gingival
tissue becomes scarred as a result of oral trauma (Fig. 20).
Eruption cysts can form over emerging teeth when fluid
extravasation occurs between the tooth crown and the
overlying gingival tissues. These conditions are usually self-
limiting with time and optimal oral hygiene. If persistence Figure 21. An 8-year-old African American boy who has
of the lesions affects normal emergence and alignment of hereditary gingival fibromatosis. Marked gingival enlargement
adjacent teeth, surgical excision may become necessary. with delayed tooth emergence can be seen. Surgical resection
Drug-induced gingival enlargement (GE) in severe cases of the gingiva is necessary to permit tooth emergence.
can impair tooth emergence. Drug-induced GE is charac- Photograph courtesy of Paul Romano, DDS, MS.

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tive effects are seen when nifedipine and cyclosporine are
used in organ transplant patients. Cyclosporine also has
been implicated in the development of oral eruption cysts
in select cases. Tacrolimus, another immunosuppressive
agent, has not been found to cause GE after organ and
hematopoietic stem cell transplantation. In fact, some clini-
cians believe that substitution of cyclosporine with tacroli-
mus can reverse GE in these patients. Surgical management
of GE through gingival resection may become necessary if
mastication, speech, and esthetics become problematic.
Hereditary gingival fibromatosis (HGF) is a rare con-
dition affecting 1 in 350,000 individuals that has no sex
predilection. Clinically, HGF affects the emergence of
the permanent teeth. The clinical manifestations of HGF
vary, with malpositioned teeth, delayed exfoliation of
primary teeth, delayed emergence of permanent teeth,
malocclusion, and open lip posture seen (Fig. 21). HGF
is usually managed through optimal oral hygiene prac-
tices and surgical resection if esthetics and function are
compromised.
Summary
• The presence of DTE, a commonly overlooked finding
in primary care, signals abnormalities in tooth
formation, eruption, or emergence.
• DTE often occurs through benign acquired processes
such as tooth loss due to dental caries or tooth-jaw
size discrepancy. However, the detection of DTE is
important because early identification can minimize
the comorbidity associated with systemic disease,
genetic syndromes, or odontogenic pathology.
• Pediatricians can reduce the burden of care related
to DTE through appropriate history taking and oral
inspection during health supervision visits.
• Children awaiting emergence of teeth for more than
12 months beyond normal chronologic ranges or
those who experience localized alterations in the
normal emergence order should be referred to a
dentist for further evaluation.
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ear, nose, throat delayed tooth emergence
References
1. Polder BJ, Van’t Hof MA, Van der Linden FPGM, Kuijpers-
Jagtman AM. A meta-analysis of the prevalence of dental agenesis in
permanent teeth. Community Dent Oral Epidemiol. 2004;32:
217–226
2. Demirjian A, Goldstein H, Tanner JM. A new system of dental
age assessment. Hum Biol. 1973;45:211–227
3. Krekmanova L, Carlstedt-Duke J, Dahllöf MC. Dental maturity
in children of short stature—a two-year longitudinal study of
growth hormone substitution. Acta Odontol Scand. 1999;57:
93–96
4. Paulsson L, Bondemark L, Söderfeldt B. A systematic review of
the consequences of premature birth on palatal morphology, dental
occlusion, tooth-crown dimensions, and tooth maturity and erup-
tion. Angle Orthod. 2004;74:269 –279
5. Peck S, Peck L. Classification of maxillary tooth transpositions.
Am J Orthod Dentofac Orthop. 1995;107:505–517
6. Shah SK, Le MC, Carpenter WM. Retrospective review of
pediatric oral lesions from a dental school biopsy service. Pediatr
Dent. 2009;31:14 –19
Suggested Reading
American Academy of Pediatric Dentistry. Guideline on manage-
ment of the developing dentition and occlusion in pediatric
dentistry. Reference Manual. 2009;32(6). Accessed August
2009 at: http://www.aapd.org/media/Policies_Guidelines/
G_DevelopDentition.pdf
Bailleul-Forestier I, Berdal A, Vinckier F, et al. The genetic basis
of inherited anomalies of the teeth. Part 2: syndromes with
significant dental involvement. Eur J Med Genet. 2008;51:
383– 408
Bailleul-Forestier I, Molla M, Verloes A, Berdal A. The genetic basis
of inherited anomalies of the teeth: Part 1: clinical and molecular
aspects of non-syndromic dental disorders. Eur J Med Genet.
2008;51:273–291
Frank CA. Treatment options for impacted teeth. JADA. 2000;
131:623– 632
Huber KL, Suri L, Taneja P. Eruption disturbances of the maxillary
incisors: a literature review. J Clin Pediatr Dent. 2008;32:
221–230
Slootweg PJ. Lesions of the jaws. Histopathology. 2009;54:
401– 418
Pediatrics in Review Vol.32 No.1 January 2011 e17
 Delayed Tooth Emergence
Jeffrey M. Karp
Pediatrics in Review 2011;32;e4
DOI: 10.1542/pir.32-1-e4

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 Delayed Tooth Emergence
Jeffrey M. Karp
Pediatrics in Review 2011;32;e4
DOI: 10.1542/pir.32-1-e4

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
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