Delayed Tooth Emergence

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DOI: 10.1542/pir.32-1-e42011;32;e4Pediatrics in Review

Jeffrey M. KarpDelayed Tooth Emergence

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DelayedTooth EmergenceJeffrey M. Karp, DMD, MS*

Author Disclosure

Dr Karp has disclosed

no financial

relationships relevant

to this article. This

commentary does not

contain a discussion

of an unapproved/

investigative use of a

commercial product/device.

Objectives After completing this article, readers should be able to:

1. Recognize abnormalities in tooth emergence timing and order based on oral inspection.

2. Discuss local and systemic causes of delayed tooth emergence.

3. List treatment modalities available for management of delayed tooth emergence.

4. Determine when timely referral to a dentist is necessary.

IntroductionDelayed tooth emergence (DTE) is a clinical term used when exposure of a tooth or

multiple teeth through the oral mucosa is overdue, according to population norms based

on chronologic age. DTE is common in childhood and adolescence, yet it is often

overlooked or dismissed in pediatric primary care. Timely screening and recognition of

DTE by clinicians can minimize medical, developmental, functional, and esthetic prob-

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.

OdontogenesisHuman 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 teethdistributed among four tooth classes (8 incisors, 4 canines, 8 premolars, 12 molars)

comprise the permanent dentition.

Tooth Eruption and EmergenceTooth 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

toward the oral mucosa. Bone remodeling in the area is

necessary for progression of tooth eruption. Root develop-ment exceeds two thirds of its final length when the alveolar

bone crest is reached. The primary dentition undergoes root

resorption, followed by crown exfoliation, to permit emer-

gence of permanent incisors, canines, and premolars into the

proper position within the dental arch. Permanent molars

do not replace primary teeth under normal circumstances.

Teeth make clinical emergence into the oral cavity when 75%

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.

Abbreviations

DTE: delayed tooth emergence

GE: gingival enlargement

HGF: hereditary gingival fibromatosis

KCOT: keratocytic odontogenic tumor

MPFM: maxillary permanent first molar

Mx.C.P1: maxillary canine/first premolar

NBCCS: nevoid basal cell carcinoma syndrome

PDC: palatally displaced canine

SP: supernumerary premolar

Article ear, nose, throat

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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 DTEDTE 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 beassessed 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 delaysin tooth emergence causedby

systemic disease do notusually result in changes in theorder

Table 1.Tooth Emergence and ExfoliationPRIMARY DENTITION

Mandible Maxilla

Eruption(months)

Exfoliation(years)

Eruption(months)

Exfoliation(years)

Central incisors 5 to 8 6 to 7 6 to 10 7 to 8Lateral incisors 7 to 10 7 to 8 8 to 12 8 to 9Canines 16 to 20 9 to 11 16 to 20 11 to 12First molars 11 to 18 10 to 12 11 to 18 9 to 11Second molars 20 to 30 11 to 13 20 to 30 9 to 12

PERMANENT DENTITION

Mandible Maxilla

Eruption(years)

Root Complete(years)

Eruption(years)

Root Complete(years)

Central incisors 6 to 7 9 to 10 7 to 8 9 to 10Lateral incisors 7 to 8 10 8 to 9 11Canines 9 to 11 12 to 15 11 to 12 12 to 15First premolars 10 to 12 12 to 13 10 to 11 12 to 13Second premolars 11 to 13 12 to 14 10 to 12 12 to 14First molars 5.5 to 7 9 to 10 5.5 to 7 9 to 10Second molars 12 to 14 14 to 16 12 to 14 14 to 16Third molars 17 to 30 18 17 to 30 18

Adapted from American Academy of Pediatric Dentistry, Guideline on management of the developing dentition and occlusion in pediatric dentistry. ReferenceManual.2009;32(6). Copyright American Dental Association. All rights reserved. Used with permission.

ear, nose, throat delayed tooth emergence

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



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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

antimeres (corresponding teeth on opposite side) usually

occurs.

Causes of DTEAnomalies 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 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):379427. 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):11531160. Copyright

1941 American Dental Association. All rights reserved.Adapted 2010 with permission of the American Dental Asso-

ciation.

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 rightsreserved. Adapted 2010 with permission of the American

Dental Association. Schour L, Massler M. The development of

human dentition. JADA. 1941;28(7):11531160. Copyright

1941 American Dental Association. All rights reserved.

Adapted 2010 with permission of the American Dental Asso-

ciation.





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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 seenmore 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 ofPAX9, 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

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 themandible. 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

Figure 3. An 8-year-old white boy who has bilateral agenesis

of the maxillary lateral incisors (3) causing a wide diastemabetween the maxillary central incisors. Photograph courtesy of

Ryan Walker, DDS.

Figure 4. A 9-year-old white girl who has ectodermal dys-

plasia. Agenesis of the permanent maxillary lateral incisorsand all mandibular incisors is seen, and a conical permanent

maxillary central incisor (*) is present. Photograph courtesy of

David Levy, DMD MS.





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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 AgeBiologic 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

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, originallystudied 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 additionalinformation 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 sixtimes more severe than the delaynoted 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

Figure 5. A 14-year-old African American boy who has

hypodontia. The mandibular right second premolar (**) did notdevelop. 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.

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.

Figure 7. A 15-year-old Hispanic boy who has delayed exfo-

liation of the mandibular right primary molars (3) as well asdelayed 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 AliakbarBahreman, DDS, MS.





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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 beenshown 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 childs 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 thedental development of the permanent successors and

lead to DTE.

Dental CrowdingInsufficient space in the jaws for eruption and emergence

of teeth constitutes the most benign, yet common,

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 childs 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), lossof 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 andemerged 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 8. Space loss in the maxillary left quadrant is seen

when compared with the contralateral side due to earlyextraction 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.

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.





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work collaboratively on these cases to obtain optimal

treatment outcomes.

Ectopic Tooth EruptionAbnormalities 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 emergesthrough 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

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 withother 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.

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.

Figure 11. Asymmetric expansion of the anterior palate (3).

The maxillary primary canine on the ipsilateral side (*) hasbeen exfoliated. This clinical presentation is indicative of an

untreated palatally displaced canine. Photograph courtesy of

Aliakbar Bahreman, DDS, MS.





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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 TeethDelayed 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 indelayed 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

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 beankylosed 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 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.

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.





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paired exfoliation and delayed premolar emergence (Fig.

15). Close monitoring of infraoccluded primary molars

by dentists is recommended to avoid these complications.

TraumaTooth development, eruption, and emergence can be

altered by dental or maxillofacial trauma in infancy orchildhood. Trauma to developing primary teeth is rela-

tively rare. Extreme root curvature (aka dilaceration) and

eruption failure of maxillary incisors have been reported

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 ofebinyo, in whichtribal 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 toothgerms 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-

Figure 15. A 12-year-old white boy who has infraoccludedmaxillary 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.

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.

Figure 16. A 6-year-old boy born in Uganda presents with

malformed mandibular primary canines (*) and missing max-

illary primary canines (). His history corroborates that canine

extirpation was completed before emigration from Uganda.

Photograph courtesy of Terry Farquhar, RN, DDS.





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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 tooths root

often occur. In these cases, ectopic permanent incisoreruption 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 PathologyTooth 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 experiencemarked delays in tooth emergence as well as tooth agenesis

and enamel hypoplasia. These clinical manifestations are

directlyrelated to osteoclast dysfunction. Stemcellrescue 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 commonfinding

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.

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, cafe

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. Earlyrecognition 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 giantcells 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 andemerged 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 TumorsEpithelial-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 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. Photographcourtesy of Aliakbar Bahreman, DDS, MS.





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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 arefound more often in the second decade, with the highest

prevalence noted in white patients. Dentigerous cysts can

grow very large andhave a tendency to displace theinvolved

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)

KCOTs are aggressive tumors that have a marked tendency

fordevelopmentin theposterior body andascending 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 completeenucleation 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-

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 examinationconfirmed the lesion to be a dentigerous cyst.

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.





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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-shaped and have normal delineation of tooth layers.

Complex odontomas are similar but do not have orga-

nized dental structures. They are easily removed by enu-

cleation and do not recur. Fifty-five percent of them are

diagnosed when delayed permanent tooth emergence or

delayed exfoliation of a primary tooth is seen.

More than 20 other types of odontogenic cysts and

tumors can develop in the jaws. Histopathologic exami-

nation is necessary to discriminate these lesions, includ-

ing identification of specific odontogenic elements and

mineralized tissue. If left untreated, odontogenic disease

can cause displacement and mobility of teeth, delayedtooth emergence, root resorption, pain, jaw swelling,

and paresthesia. Large cystic lesions in the posterior

mandible can lead to pathologic jaw fractures.

Gingival EnlargementsThe 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 environmentalconditions 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

of the lesions affects normal emergence and alignment of

adjacent teeth, surgical excision may become necessary.

Drug-induced gingivalenlargement (GE)in severe cases

can impair tooth emergence. Drug-induced GE is charac-

terized by proliferation of connective tissue extracellular

matrix in response to gingival drug metabolism. Phenytoin,

nifedipine, and cyclosporine are themost common catalysts

of the condition. Poor oral hygiene exacerbates GE

through inflammatory mechanisms. The anterior gingivaltissues are involved more frequently. Males tend to be more

severely affected for poorly understood reasons. The use of

multiple anticonvulsant medications in addition to phenyt-

oin increases the severity of phenytoin-induced GE. Addi-

Figure 20. An 8-year-old white boy who has a history of trauma

to the maxillary anterior teeth presents with delayed emergence

of the maxillary permanent right central and lateral incisors. The

contralateral permanent incisors are already present. The outline

of the unerupted teeth can be seen within the gingiva. Surgicalexposure was necessary to permit tooth emergence.

Figure 21. An 8-year-old African American boy who has

hereditary gingival fibromatosis. Marked gingival enlargement

with delayed tooth emergence can be seen. Surgical resection

of the gingiva is necessary to permit tooth emergence.

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 ofprimary 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.

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permanent teeth. Community Dent Oral Epidemiol. 2004;32:

217226

2. Demirjian A, Goldstein H, Tanner JM. A new system of dentalage assessment.Hum Biol. 1973;45:211227

3. Krekmanova L, Carlstedt-Duke J, Dahllof MC. Dental maturityin children of short staturea two-year longitudinal study of

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4. Paulsson L, Bondemark L, Soderfeldt B. A systematic review ofthe consequences of premature birth on palatal morphology, dental

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Suggested ReadingAmerican 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 withsignificant dental involvement. Eur J Med Genet. 2008;51:

383408

Bailleul-ForestierI, Molla M, Verloes A, BerdalA. Thegenetic basis

of inheritedanomalies of theteeth: Part1: clinical andmolecular

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2008;51:273291

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401418

Summary The presence of DTE, a commonly overlooked finding

in primary care, signals abnormalities in toothformation, eruption, or emergence.

DTE often occurs through benign acquired processessuch as tooth loss due to dental caries or tooth-jawsize discrepancy. However, the detection of DTE isimportant because early identification can minimizethe comorbidity associated with systemic disease,genetic syndromes, or odontogenic pathology.

Pediatricians can reduce the burden of care relatedto DTE through appropriate history taking and oralinspection during health supervision visits.

Children awaiting emergence of teeth for more than12 months beyond normal chronologic ranges orthose who experience localized alterations in thenormal emergence order should be referred to adentist for further evaluation.





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DOI: 10.1542/pir.32-1-e42011;32;e4Pediatrics in Review

Jeffrey M. KarpDelayed Tooth Emergence

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