ARTICLE IN PRESS

Ann Anat 188 (2006) 353—361

www.elsevier.de/aanat

Morphological and clinical considerations of first

and second permanent molar eruption disorders
Peter Proffa,, Thomas Bayerleina, Jochen Fanghänelb,
Sergio Allegrini Jr.b, Tomas Gedrangea

a
Poliklinik für Kieferorthopädie, Präventive Zahnmedizin und Kinderzahnheilkunde, Ernst-Moritz-Arndt-Universität
Greifswald, Rotgerberstraße 8, 17487 Greifswald, Germany
b
Abteilung für Oralanatomie im Zentrum für Zahn-, Mund- und Kieferheilkunde der Ernst-Moritz-Arndt-Universität
Greifswald, Rotgerberstraße 8, 17487 Greifswald, Germany

Received 11 January 2006; accepted 1 February 2006

KEYWORDS Summary
Eruption disorder of
Tooth eruption is a complex biological process which starts from the site of
permanent molars;
development in the jaw bone until the teeth reach their final functional position in
Theory of tooth
the chewing plane. Various factors can disturb this process. Besides mechanical
eruption;
obstacles on the eruption path, a pathological position or axial orientation of the
Aetiology;
tooth germ, morphological aberrations of the tooth or pathological alterations of the
Case reports;
periodontium, primary disorders of the eruption mechanism may lead to complete or
Therapeutical rele-
partial retention of the tooth in the jaw bone.
vance
These morphological features bear upon the prognosis of orthodontic correction
which is dependent upon the underlying cause. First and second molars are rarely
affected by eruption disorders, with a prevalence of 0.01 to 0.08 per cent, however,
marked consequences for function such as posterior open bite or elongation of the
antagonists may result. Following an overview of pathogenetic factors of tooth
eruption disorders, selected cases of impacted first and second permanent molars
are presented with respect to their morphological causes.
& 2006 Elsevier GmbH. All rights reserved.

Introduction

Tooth eruption is a multifactorial process de-

scribing the movement of teeth from their site of
Corresponding author. Tel.: +03834 867110; development in the jaw bone to their final
fax: +03834 867113. functional position in the chewing plane (Jung
E-mail address: proff@uni-greifswald.de (P. Proff). et al., 2003; Marks, 1995; Marks et al., 1996). This

0940-9602/$ - see front matter & 2006 Elsevier GmbH. All rights reserved.
doi:10.1016/j.aanat.2006.02.003
 ARTICLE IN PRESS
354
process continues over a relatively long period of
time, depends upon genetic and individual factors
and influences the development of the whole
stomatognathic system (Nolla, 1960; Radlanski et
al., 1999). Population studies have provided aver-
age eruption times depending on chronological age
(Harzer and Hetzer, 1987). Nevertheless, marked
interindividual differences may exist even in
absence of a respective anatomical aberration.
Premature or delayed tooth eruption is assumed, if
the eruption time lies outside 2 standard deviations
of the respective population mean expected for
chronological age (Rasmussen and Kotsaki, 1997).
Exact diagnostic and therapeutic appraisal, how-
ever, implies biological age which is assessed from
clinical and radiological examination (Becker,
1998). Skeletal maturity and tooth development
may be determined by means of a hand X-ray and a
panoramic X-ray respectively. Physiological erup-
tion time is defined as the time when about 23 to 34 of
the final root length of the tooth have developed
(Gron, 1962). Retention occurs when root growth
has advanced or been completed without eruption.
A primary retention of a normally shaped tooth
without discernible cause is clinically distinguished
from a secondary retention due to a physical
barrier or tooth malformation or malposition
(Raghoebar et al., 1991; Andreason et al., 1997).
In the literature, numerous technical terms such as
impaction, depression, reinclusion, or pseudo-
anodontia partly are used synonymously for de-
layed or incomplete tooth eruption (Suri et al.,
2004). Even though first and second molars are
rarely affected by eruption disorders, severe
consequences for the patients may result from
failing orthodontic mobilization and alignment.
Pathogenesis of tooth eruption
Various classical theories have dealt with the
mechanisms of tooth eruption. Root theory (Tomes,
1872, and others) implies that the growing root
pushes the tooth away from the alveolar bottom
towards the oral cavity. The alveolar theory (Groß,
1934, and others) is based on the idea that the pre-
eruptive growth and transformation processes
within the alveolar bones (apposition) move the
tooth germs in the oral direction. Pulp theory
(v. Korff, 1935, and others) suggests that the tooth
is moved lingually by pressure from the pulpal
bulge. The explosive effect of the pulpal bulge is
produced by the osmotic pressure of the briskly
proliferating and differentiating mesenchymal
cells. The mitotic activity concentrates at the
apical end. The pulp theory has many supporters,
P. Proff et al.
however, the eruption process has to be regarded
as multicausal.
The knowledge of the physiological and patholo-
gical mechanisms of tooth eruption in genetic,
cellular and particularly molecular terms has been
vastly expanded during recent years, partly owing
to the increased use of molecular biological
techniques, albeit to date the exact mutual
relationships and interactions of single molecules
in the signal cascade have not yet been decoded
(Wise et al., 2002). The established fundamentals
reflecting the assured preconditions of the complex
eruption process comprise the chronological inter-
play and the mutual interaction of single cells of
the enamel organ, the alveolar bone and the dental
follicle. That the tooth roots themselves are not
involved in active tooth eruption, has been estab-
lished for a fairly long time (Gowgiel, 1961). The
relevance of the dental sac for tooth eruption was
demonstrated by Cahill and Marks in 1980 in an
experimental study in dogs. Surgical removal of the
dental follicle of premolars prior to their regular
eruption prevented the latter (Cahill and Marks,
1980). At the cellular level, the active eruption
phase begins with the immigration of mononuclear
cells (monocytes) to the coronal part of the dental
sac, accompanied by a parallel increase of osteo-
clasts in the coronal part of the covering alveolar
bone, and followed by a decrease of both cell types
(Marks et al., 1983). The immigration of monocytes
is a precondition of the subsequent formation of
multinucleate osteoclasts which leads to resorption
of the alveolar bone and formation of an eruption
path (Wise and Fan, 1989). Interestingly, the
formation of this eruption path is a genetically
determined event proceeding independently of
possible pressure components of the erupting
tooth. The retention of teeth in the absence of
osteoclasts was confirmed by several studies in
osteopetrotic rats (Cotton et al., 1974; Marks et
al., 1994). Osteoclastogenesis requires the pre-
sence of osteoblasts. In mouse studies, the pheno-
typical occurrence of Cbfa1 (+/
), the most
important transcription factor for osteoblast dif-
ferentiation, led—besides numerous other skele-
ton-associated symptoms—to retardation or even
failure of tooth eruption due to the absence of
osteoblasts (Wise et al., 2002). The processes at
the molecular level run parallel to the cellular
processes. The basic reaction pathways on the one
hand lead to the above-mentioned accumulation of
monocytes in the dental follicle (Diagram 1) and on
the other hand to subsequent osteoclastogenesis
(Diagram 2). The molecule probably playing the
most important role during initiation of the cellular
processes is the (macrophage) colony-stimulating
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Morphological and clinical considerations of first and second permanent molar eruption disorders 355

Alveolar protein (PTHrP), as well as by control of the

Bone
Osteoclast
epidermal growth factor (EGF) and CSF-1 within
the dental sac itself. Following immigration of the
mononuclear cells, the fusion and formation of
Dental Fusion osteoclasts occurs in a favourable environment.
Follicle This process is influenced by transcription factors
Mononuclear
Recruitment Cells Recruitment
such as c-fos and NFkB in the dental follicle, and
MCP-1 CSF-1
the osteoclast-differentiating factor (ODF) in the
Enhances alveolar bone which was demonstrated in knock-
Enhances MCP-1 mRNA CSF-1 mRNA out mice by several studies (Grigoriadis et al.,

Enhances
Enhances

EGF Enhances
1994; Franzoso et al, 1997; Kong et al., 1999).
Enhances
Current concepts of osteoclast differentiation
Stellate
Enhances accredit three molecules with special roles.
Reticulum
TGF- 1 IL-1 PTHrP Besides the receptor activator of nuclear factor-
6B (RANKL) which has also been referred to as ODF
(as mentioned above) and co-induces osteoclasto-
genesis, the previously mentioned CSF-1 is an
Diagram 1. Schematic sketch of the signaling pathway important factor in osteoclast proliferation and
for recruitment of the mononuclear cells with regard to differentiation (Yasuda et al., 1998; Felix et al.,
the tissue segments involved (after Wise et al., 2002).
1990; Kodama et al., 1991). Amazingly, the
presence of osteoprotegrin (OPG), a RANKL inhi-
bitor blocking differentiation of osteoclasts from
Alveolar progenitor cells, is also an indispensable factor in
Bone tooth eruption (Kong et al., 1999).
RANKL Osteoclast
Stimulates
The complexity of these processes at the cellular
as well as the molecular level despite their high
Dental redundancy incurs various possible disturbances of
Follicle
Mononuclear Cell Fusion
physiological tooth eruption of local, systemic,
genetic or multicausal origin.
OPG
Stimulates

Stimulates

Enhances

EGF C-Fos NFkB Local factors

Enhances

Enhances

CSF-1 Local alterations frequently form a physical

barrier to normal tooth eruption. In the gingiva,
Enhances

Stellate
Reticulum
PTHrP
Diagram 2. Schematic sketch of the signaling pathway
for osteoclastogenesis with regard to the tissue segments
involved (after Wise et al., 2002).
factor one (CSF-1) (Wise et al., 1995). Together
with the monocyte chemotactic protein (MCP 1),
CSF-1 fulfills a chemotactic function attracting
mononuclear cells to the dental follicle, with the
redundancy serving to assure their effect on the
osteoclast progenitor cells in this critical process
during tooth eruption (Wise et al., 2002). Synthesis
and secretion of both chemokines are regulated by
the paracrine signaling pathway between the
dental follicle and the stellate reticulum involving
transforming growth factor beta (TGF-b), inter-
leukin-1a (IL-1a) and parathyroid-hormone-related
Enhances scar tissue resulting from trauma or surgery,
IL-α1 TGF- β1 fibromatous or hyperplastic alterations may ham-
per the eruption of the underlying tooth (Di Biase,
1971; Goho, 1987; Kratz et al., 2002). In the bone,
supernumeraries, odontogenous or non-odontogen-
ous tumours, cysts or cleft anomalies may interfere
with proper eruption (Mitchell and Bennett, 1992;
Duque et al., 2004; Kupietzky et al., 2003; Flaitz
et al., 2001; McGuinness et al., 2001).
The fusion of cementum or dentine with alveolar
bone producing an ankylotic union of tooth and
bone is the most frequent local cause of disturbed
eruption (Raghoebar et al., 1991; Suri et al., 2004;
Alexander et al., 1980). The erupting tooth itself
may show anomalies of shape or structure of its
crown or root, or eruption may be delayed or
hampered by germ displacement or dispersion (Suri
et al., 2004; Diab and elBadrawy, 2000). Inflamma-
tion, disturbed resorption, premature loss or
traumata of primary teeth can cause eruption
disorders of the corresponding permanent teeth
 ARTICLE IN PRESS
356
(Johnsen et al., 1977; Northway et al., 2000;
Yawaka et al., 2002; Diab and elBadrawy, 2000).
Space shortage within the dental arch may lead to
disturbed eruption in addition to crowding (Pulver,
1968; Bjerklin and Kurol, 1983).
Systemic factors
Many systemic causes of delayed tooth eruption
are well established. The numerous associations
between dentition and other physical features have
been subsumed under the heading of ‘‘dento-
somatic correlation’’ (Weyers, 1968). Of great
importance are factors that exert influence on
growth and development of the skeletal system
(Weyers, 1968; Schumacher et al., 1986). Extreme
malnourishment bears on tooth calcification and is
a rare systemic cause of delayed tooth eruption
(Alvarez and Navia, 1989). Endocrine dysfunction
such as hypothyreosis, lack of parathyroid hormone
or growth hormone can affect tooth development
and eruption (Suri et al., 2004; Barberia Leache
et al., 1988; Pirinen, 1995).
Drugs such as chemotherapeutic agents or antic-
onvulsants, or exposure to noxae such as tobacco
smoke or radioactive radiation have an impact on
tooth development and eruption (Minicucci et al.,
2003; Appleton and Leach, 1991; Kieser et al.,
1996). Animal studies suggest that hypoxia, ane-
mia, or renal failure may have an effect on human
tooth development and eruption (Suri et al., 2004).
Genetic factors
Disturbed tooth eruption occurs in numerous
syndromal diseases or hereditary disorders of tooth
development (Suri et al., 2004). Various mechan-
isms are blamed for manifestation of the disorder.
On the one hand, secondary physical obstacles
occurring in the context of syndromal diseases may
interfere with timely tooth eruption, e.g., multiple
cysts in the Gorlin-Goltz syndrome or in cherubism,
or supernumerary teeth in cleido-cranial dysostosis
or Apert syndrome (Rosenblum, 1998; Schultze-
Mosgau et al., 2003; Jensen et al., 1990; Kaloust
et al., 1997). On the other hand, deformities or
dysfunctions of the tissues and cells involved in
tooth eruption can be part of a genetic disease
(Rasmussen and Kotsaki, 1997; Zou et al., 2003;
Marks, 1995; Marks et al., 1996). Also, a combina-
tion of physical barrier and direct disturbance of
tooth eruption is frequent in syndromal diseases.
Suri et al., have tabulated hereditary diseases
involving disturbed tooth eruption.
P. Proff et al.
Findings and discussion
Impacted first and second molars are a relatively
rare finding, with prevalence rates ranging from
0.01 to 0.08 per cent (Valmaseda-Castellon et al.,
1999). However, the consequences of first or second
molar retention are severe, if orthodontic therapy
fails. The loss leads to a restricted chewing
function and, in case of an impacted or missing
wisdom tooth, to a prosthetic free-end gap.
A marked vertical bone deficit makes prosthodontic
treatment, e.g., using implants, difficult and
requires augmentative bone surgery. Development
of a posterior open bite results in failing support
and consecutive elongation of the antagonists.
Partial molar retention poses the risk of a pericor-
onal infection with abscess formation.
In the following sections, four different cases of
impacted permanent molars are presented. The
tooth formulae are given according to the FDI
(Fédération Dentaire Internationale).
Case 1
The patient presented for orthodontic consulta-
tion at the age of 10 years. The family history was
inconspicuous. The clinical examination produced
evidence of a marked distal bite with increased
overjet and a deep bite with retained tooth 36 and
elongated 26. The panoramic image reveals a late
second stage mixed dentition (Fig. 1). The teeth 75
and 85 have not yet exfoliated, while 17,27,37, and
47 have already erupted. Tooth 36 is partially
impacted, the periodontal gap is invisible, root
growth is almost completed. Tooth 75 displays
distal tipping, with its distal bulge overlapping the
mesial shoulder of 36. After removal of tooth 75
and eruption of 35 and 45, a fixed orthodontic
appliance was inserted. The panoramic X-ray taken
after two years shows the partially impacted tooth
36 with a mesial and distal vertical bone deficit and
halted root growth (Fig. 2). Orthodontic traction
was impossible. Complete ankylosis was revealed
upon extraction. Prosthodontic treatment of the
tooth gap was called for in view of the occlusal
situation.
Case 2
The patient presented at the age of 10 with the
main problem of an intraorally invisible tooth 46.
Family history was positive for Angle class III
anomalies (mesial occlusion). The clinical examina-
tion revealed a mesial bite with reduced overbite,
right-hand crossbite, invisible 46 and elongated 26.
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Morphological and clinical considerations of first and second permanent molar eruption disorders 357

Figure 1. Orthopantomogram, Case 1.

Figure 2. Orthopantomogram, Case 1.

The orthopantomogram showed a late second stage
mixed dentition (Fig. 3). Tooth 46 is completely
retained in the jaw with pericoronal radiolucency.
The apex of the shortened root displays hook-
shaped deviations. Tooth 46 was extracted for
infaust prognosis with orthodontic gap closure from
distal.
Case 3
At the age of 9 12 years, the patient presented for
orthodontic consultation. Family history was insig-
nificant. Examination revealed an Angle class II/2
anomaly (distal occlusion with steep upper incisor
position). Intraorally, the teeth 16 and 26 were
palpable under the mucosa, the mesiobuccal cusp
tip of 36 was visible, 46 was invisible and not
palpable. The panoramic image showed a mid
mixed dentition, with presence of all permanent
tooth germs except the third molars (Fig. 4). Since
root growth of the lower 6-year molars is almost
completed, disturbed eruption is assumed instead
of a deviant order of eruption. The anatomical
shape of the second milk molar with its distal bulge
may be a mechanical obstacle to the 6-year molars.
After removal of the barrier by exfoliation of the
second milk molars, the 6-year molars appear.
Case 4
The patient presented for orthodontic consulta-
tion at the age of 10 for aesthetic impairment due
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358 P. Proff et al.

Figure 3. Orthopantomogram, Case 2.

Figure 4. Orthopantomogram, Case 3.

to the invisible tooth 21. Family history revealed
that two molars of the mother had not erupted.
Examination showed a distal occlusion with in-
creased overjet and bilateral posterior open bite.
Intraorally, the teeth 21, 26 and 36 were invisible,
while 64, 65, 74, 75, and 84 presented infraocclu-
sion. A tongue dysfunction existed. The panoramic
X-ray displayed a second stage mixed dentition
with impacted 21, 26, and 36, and deficient
posterior vertical development of all quadrants
(Fig. 5). After paediatric consultation for exclusion
of a syndromal disease, the radiographically non-
ankylosed impacted teeth indicated a primary
idiopathic eruption disorder (40). First of all,
orthodontic treatment of the distal occlusion was
carried out using removable appliances. Radio-
graphic follow-up at the age of 12 additionally
reveals impaction of 17, 27, 37, and 47 (Fig. 6).
Tooth 21 was surgically exposed and provided with
an attachment. Subsequently, mobilization of 21
will be attempted at minimum.
Concluding considerations
Disturbed eruption of permanent molars does not
lead to marked aesthetic impairment such as
retained incisors or canines, yet functional dis-
orders may develop quite rapidly depending on the
number of teeth affected. Morphology, topop-
graphic-anatomical position, and axial orientation
of the affected tooth, mechanical obstacles on the
eruption path, and the condition of the period-
ontium play an important role for the prognosis of
possible tooth conservation and orthodontic align-
ment. If the eruption mechanism of the permanent
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Morphological and clinical considerations of first and second permanent molar eruption disorders 359

Figure 5. Orthopantomogram, Case 4.

Figure 6. Orthopantomogram, Case 4.

molars is primarily disturbed, orthodontic treat-
ment is almost futile even with normal molar
morphology (Proffit and Vig, 1981). In such cases,
treatment options are, besides prosthodontic care,
restricted to surgical tooth alignment using seg-
mental or distraction osteotomy. The limited
therapeutic options for eruption disorders raise
the question of more efficient treatment alter-
natives. A method of resolution may be provided by
oral molecular biology. The prospect of better
understanding of molecular biological interactions
and the timing of the eruptive structures, together
with the hope of causal treatment approaches
leading to initiation or resumption of lacking or
prematurely halted eruption, underpin the need for
continuing research in this complex and difficult
branch of oral biology.
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