DOI: 10.

1051/odfen/2018129 J Dentofacial Anom Orthod 2017;20:402

© The author

Tooth eruption disorders associated with

systemic and genetic diseases: clinical
guide
C. Choukroune
Qualified specialist in Dentofacial Orthopedics, former Hospital Resident, private practice in
­Boulogne-Billancourt

SUMMARY
Tooth eruption is defined as the movement of the dental root and the tooth from its original devel-
opment site in the alveolar process to its functional position in the oral cavity. Despite vast amounts of
research, the exact mechanism of tooth eruption remains unknown. The authors have shown that the
dental crown is not necessary for tooth eruption, whereas the dental follicle seems to be essential for
the process. The formation of an eruption pathway by bone resorption allows the root to breach the oral
cavity, at the same time, bone formation occurs at the basal level of the dental root. Multiples genetic
and molecular structures coordinate these events. Sometimes it is by studying pathological conditions
that we discover the essential interactions that occur during tooth eruption. Frequently, a delayed tooth
eruption (DTE) is the first, if not the only, expression of a local or general pathology. A DTE can affect
directly the diagnosis, the treatment planning, or the timing of the orthodontic treatment. Therefore, it
is essential for the orthodontist to identify the cause of a DTE for implementing the correct treatment.

KEY WORDS
Tooth eruption, genetic disease inborn, systemic disease, delayed tooth eruption

INTRODUCTION
Dental eruption is a unique physiolog- between osteoblasts, osteoclasts, and the
ical event; the tooth is the only organ to dental follicle (DF), involving many genet-
appear a few months or years after birth. ic factors. These studies have opened the
This c­ omplex and finely regulated process way for the discovery of multiple genetic,
influences the normal development of the molecular, and tissue interactions that oc-
craniofacial region. cur during dental eruption.
In the 1980s, many teams looked at the The study of genetic or acquired disorders
mechanisms behind dental eruption; their has made it possible, among other things,
work has highlighted complex interactions to understand the mechanisms involved in

Address for correspondence:

Chloé Choukroune
150, rue Gallieni – 92100 Boulogne-
Billancourt – France Article received: 20-04-2017.
Email: [email protected] Accepted for publication: 18-05-2017.

This is an Open Access article distributed under the terms of the Creative Commons Attribution
License (http://creativecommons.org/licenses/by/4.0),
which permits unrestricted use, distribution, and reproduction in any medium,
provided the original work is properly cited. 1

Article available at https://www.jdao-journal.org or https://doi.org/10.1051/odfen/2018129

 C. CHOUKROUNE

dental eruption and has shown how Although the development of the
these interactions are essential for craniofacial region is of interest to or-
the smooth running of the process. A thodontists, the clinical signs of sys-
disruption of the eruption process can temic and genetic disorders responsi-
occur in the context of systemic or ge- ble for eruptive disorders are still not
netic disorders; the clinical picture can fully understood by practitioners. This
range from a simple delay to a com- article summarizes the clinical signs
plete agenisis. Often, changes in the of the main disorders presenting as
eruption process are the first, if not eruption disorders after reviewing the
the only, manifestation of a systemic mechanisms which affect eruption.
or genetic pathology. The precise iden- This is to improve management and
tification of the cause of a disruption of diagnosis so that treatments can be
the eruption process helps refine the better adapted to meet the needs of
diagnosis, define the overall treatment patients and their families.
plan, and the orthodontic treatment
schedule.

ERUPTION STAGES
Eruption is defined as the movement Pre-eruptive phase
of the tooth germ from its site of devel-
opment in the alveolar processes to its Long before eruption, the tooth germ
functional position in the oral cavity22. will undergo intra-alveolar movements
Before teeth achieve their functional during its development, which do not
placement on the arch, they undergo affect the direction of eruption6,7,45.
many movements. According to Ten Because of the rapid development of
Cate, these complex movements can the deciduous teeth (DT), their germs
be organized into three phases25: will overlap at a given moment within
the maxillae. Maxillary growth will force
– Pre-eruptive movements: undergone the roots of the second deciduous mo-
by deciduous and permanent teeth lars to move backward the roots of the
within the tissues before the onset front teeth to move forward to prevent
of eruption; cluttering.
– Eruptive movements: when the tooth The permanent teeth (PT) germs are
moves from its intraosseous position initially in the same bony crypt as the
to its functional position on the arch. deciduous teeth but are located on
This phase can be divided into intra-al- their lingual slope25.
veolar and supra-alveolar eruption; After DT eruption, PT occupy their own
– Posteruptive movements: the tooth crypts. They will move considerably dur-
remains in its functional position and ing growth, for example from a lingual
adapts to the growth of the jaw and position for premolar germs to a more
proximal and occlusal wear.

2 Choukroune C. Tooth eruption disorders associated with systemic and genetic diseases: clinical guide
 Tooth eruption disorders associated with systemic and genetic diseases: clinical guide

Figure 1
Panoramic view of a 9-year-old boy showing mandibular premolar germs
located between the roots of deciduous molars. Note the mesial inclination of the second man-
dibular permanent molar (ODF service, Pitié-Salpêtrière Hospital).

Figure 2
Panoramic view of a 9-year-old child showing bone resorption that occurs over 37/47 germs and
the formation of an “eruption path” across the bone (ODF service, Pitié-Salpêtrière Hospital).

vestibular position between the roots of before initiating the eruptive move-
the deciduous molars (Figure 1). ment. They result from the combination
These pre-eruptive movements aim of two factors: on the one hand, the
to position the germ in its final position movements made by the germ itself,

J Dentofacial Anom Orthod 2017;20:402 3

 C. CHOUKROUNE

and on the other hand, the “passive” The supraosseous phase is the pro-
movements of the germ because of cess by which the tooth emerges into
maxillary growth25. A lack of maxillary the oral cavity. When the deciduous
growth can disrupt these movements. tooth falls out, the bone that surrounds
Few things are known about these the root is reabsorbed. With the erup-
pre-eruptive mechanisms and it is tion of the permanent tooth, the alveo-
difficult to know if they are predeter- lar bone is reconstructed thanks to the
mined or if they represent an adaptive osteogenic activity of the periodontal
response. They are used to correctly ligament. Then, the gingival defect is
position the germ and its bone crypt repaired progressively, and the alveolar
before the actual eruption begins6. process is built44.
When teeth appear in the oral cavity,
Eruptive phase they are subject to environmental fac-
tors such as the muscular pressures of
The eruptive phase can itself be di- the cheeks, tongue, and lips, as well as
vided into three stages: intraosse- the eruptive forces of adjacent teeth,25
ous phase, supraosseous phase, and which will continue until the teeth
posteruptive phase. reach their final position on the dental
Intraosseous eruption begins as soon arch. The displacement of the teeth to
as crown formation is complete7. It cor- the occlusal plane is ensured by root
responds to the entire germ eruption elongation and bone formation at the
phase through bone and occurs with apical level and at the level of the in-
mainly axial movements6 (Fig. 2). ter-radicular septa22.
It is similar for both teeth. Numerous Finally, the posteruptive phase includes
other events accompany the intraosse- all movements made after the teeth have
ous eruption of the germ: root elonga- reached the occlusal plane. They include
tion is initiated as well as the develop- adaptive growth movements of the jaw
ment of the periodontal ligament and as well as compensatory movements
the gingival junction. caused by occlusal and proximal wear.

PHYSIOLOGY OF ERUPTION
For over 70 years, multiple theories The authors examined the proposed
have been proposed to explain the eruption mechanisms and tested mul-
eruptive phenomenon. It must be said tiple hypotheses:
that despite numerous studies and
publications on the subject, the pre- – Collagen contraction of the periodon-
cise mechanism of the eruption is still tal ligament has been proposed to
unknown. explain the eruptive phenomenon.
Eruption could be attributed to many However, no cause-effect relationship
factors that have been studied, ap- was found between the eruption rate
proved, and then disapproved over and collagen turnover rate43. Many
time. experiments have been performed in

4 Choukroune C. Tooth eruption disorders associated with systemic and genetic diseases: clinical guide
 Tooth eruption disorders associated with systemic and genetic diseases: clinical guide

This indicates that the root is not the

motor of dental eruption (Fig. 3).

Role of the dental crown

Another hypothesis was that eruption
depended on the dental organ itself,
and particularly on the crown. A series
of excellent experiments conducted by
Marks and Cahill in the 1980s focused
on showing the role of the crown and
DF during eruption.
In one of their experiments, they
Figure 3
show that DF is essential to the erup-
Tooth 45 having erupted in the absence
of root elongation (ODF service, Pit- tion, whereas the crown is not. Indeed,
ié-Salpêtrière Hospital). by replacing a premolar crown in dogs
with a metal object, but leaving DF in
the presence of a ­collagen inhibitor place, the metal object still erupted. In
and show that the teeth retain similar contrast, in another study group, they
eruption rates42. removed DF and left the crown in place.
– It has also been hypothesized that In this group, eruption did not occur
vascular pressure may be responsi- and ankylosis plaques were identified
ble for the eruptive force. In 1985, around the germ19. They therefore con-
authors drained the dental alveoli be- cluded that the dental crown is abso-
low the incisors of rats whose root lutely unnecessary to the eruptive pro-
ends had been removed. Therefore, cess. On the other hand, DF seems to
increasing interstitial fluid pressure play a primordial role and, in particular,
is impossible. They then observed a protective role.
a significant decrease in the rate of In addition to the eruption of the me-
eruption and conclude that intersti- tallic replica, the authors note the for-
tial fluid pressure is necessary for mation of an “eruption path” above the
the eruption2. To date, there is a lack replica and basal bone apposition. This
of high-level studies to conclude that suggests that remodeling of the bone
tissue and vascular pressure play a is also involved in dental eruption.
role in eruptive phenomena. How is bone modeling involved dur-
– The periodontal ligament was hypo- ing dental eruption and which parts de-
thetically implicated as well. Marks pend on it?
showed in his study that in individuals
with osteopetrosis, the periodontal Role of DF
ligament is present, but the teeth do
not erupt18. On the other hand, in in- In 1983, Marks et al. studied the
dividuals with type-I dentinal dysplasia c­ ytology of the bone crypt and DF to
(with teeth without roots and there- qualify and quantify cell populations
fore no ligament), eruption still occurs. present before and during eruption21.

J Dentofacial Anom Orthod 2017;20:402 5

 C. CHOUKROUNE

Regarding the bone crypt, they found However, no part of the follicle can
the following: support the eruption alone.
The eruption is therefore a polarized
– During the pre-eruptive period: os- phenomenon, coordinated by DF in
teoblasts distributed on all surfaces time and space.
of the crypt; osteoclasts present in Recently, Sarrafpour et al. have pro-
small numbers and concentrated in posed a new theory of eruption, in
the coronal region; which DF is central to the initiation of
– During the eruption: abundant osteo- the phenomenon36. Their theory is that
blasts located in the basal and apical the mastication forces between the
parts of the crypt; osteoclasts located bone and the soft tissues surround-
almost exclusively in the coronal part ing the erupting tooth lead to tissue
of the bone crypt and exhibiting char- remodeling, which results in tooth
acteristics of osteoclastic activity; eruption. Therefore, dental tissues are
– Monocytes (osteoclast precursors): supposed to be sensitive and able to
located in the coronal part of the crypt; respond to functional stress.
they were small at the start of erup- Using finite element analysis, they
tion whereas they were large and ad- showed that DF is the most likely tis-
jacent to osteoclasts during eruption. sue to act as a mechanoreceptor. Their
analysis also showed that DFs of the
The populations of osteoclasts and erupting teeth all undergo the same
monocytes increase simultaneous- forces during mastication: the coronal
ly just before the eruption, coinciding part of DF experiences compressive
with the start of eruption path forma- forces whereas the basal part experi-
tion. ences tension forces. This is consist-
Later, they show that DF mono- ent with bone apposition/resorption
cytes appear through the bloodstream observations in the basal and coronal
and then migrate into the bone crypt, parts of bone crypts during the intraos-
where they fuse to form osteoclasts. seous phase of eruption.
At the basal level of the germ, there To conclude, Cahill and Marks, at
is significant proliferative activity both the end of one of their experiments,
in the follicle and in the adjacent bone54. expressed the idea that “the eruption
In an experiment conducted in the consists of a series of metabolic events
late 1980s, Marks and Cahill examine within the bone characterized by appo-
the effects of selectively removing sition and resorption ­coordinated by DF.”
certain parts of the follicle20. When
the coronal portion of the follicle was Molecular aspects of the eruption
removed, neither bone resorption nor
eruption path formation occurred. In Multiple processes and components
contrast, the eruption pathway formed are involved in triggering the bone re-
when the basal portion of the follicle sorption necessary for the formation
was removed, but no basal bone for- of the eruption pathway. These have
mation was detected. been discovered over several years of
Bone formation and resorption there- research and some signaling paths are
fore occur independently of each o ­ ther. still unclear.

6 Choukroune C. Tooth eruption disorders associated with systemic and genetic diseases: clinical guide
 Tooth eruption disorders associated with systemic and genetic diseases: clinical guide

We can discuss the molecules acting and throughout life to maintain the
directly on the formation of monocytes: functional integrity of the system;
CSF-131,52, MCP-131,32, and NF-κB30. – A process of tissue resistance dur-
­Other molecules, such as PTH-rP28,55,56, ing the upward movement.
RANKL8,16,40,58, IL-1α47,53, or TGF-β46,49, will
act indirectly on monocyte recruitment Current and future research must
by stimulating the expression of the take into account all these ideas to up-
above-mentioned molecules or by act- date the processes involved.
ing directly on the osteoclasts (Figure 4). Although many advances have been
A small part of the research focused made in understanding the eruption
on the no less essential phase of bone process, there are still many unclear
formation occurring at the alveolar areas. Is there a force which leads
base during eruption. Osteogenic mol- to eruption? What causes the tooth
ecules have been highlighted, these to erupt? What is the trigger for this
are BMP48,51,56,57, from Runx250,59, or movement? What are the phenomena
MMP4. responsible for supraosseous erup-
The design of a multifactorial eruptive tion and adaptation to occlusal wear
process must include the following: throughout life?
The understanding of the eruptive
– A mechanism capable of allowing phenomenon, sometimes through the
the germ to rise; observation of pathological conditions,
– A process of bone and periodontal will allow targeted treatments to be
remodeling during this movement used in cases of eruption alterations.

Coronal rt of DF

Figure 4
Diagram representing the main molecular components of the coronal part of DF during dental
eruption. A green arrow indicates a stimulating action, a red arrow an inhibiting action.

J Dentofacial Anom Orthod 2017;20:402 7

 C. CHOUKROUNE

PATHOLOGIES ASSOCIATED WITH ERUPTION DISORDERS

Regularly, there is clinical evidence superficial anomalies of the face (nasol-
of deviations from the “normal” age abial cleft, frontal aplasia, nasofrontal
of eruption. Although premature teeth plane angioma) and deep (velo-palatal
eruption is observed occasionally, de- cleft, choanal atresia) and dental anom-
layed eruption is observed most of the alies (additional or missing teeth and
time. enamel structure anomalies)5.
Frequently, a delayed eruption is the Children have delayed bone matura-
first, or even the only, manifestation tion, decreased skull base and facial
of a local or systemic pathology. A de- bones, small sella turcica, a basicrani-
layed eruption may directly affect the al angle opening, facial retrognathism,
diagnosis, treatment plan, and ortho- decreased maxillary and mandibular
dontic treatment schedule. dimensions, maxillary and mandibular
retroposition, decreased lower facial
– The etiology is local when the erup- height, increased mandibular diver-
tion delays concern a tooth. These gence, as well as delayed tooth min-
are the most common cases. eralization, maturation, and eruption5,15.
– When eruption delays concern a group In practice, when faced with the dis-
of teeth or all the teeth, the etiology is covery of facial and/or dental abnormal-
systemic or genetic (associated or not ities in a small child, it is appropriate to
associated with a syndrome). ask for an endocrine assessment.
Growth hormone (GH) supplementa-
Systemic diseases associated with tion restores normal growth. However,
eruption disorders it is possible that maxillomandibular
imbalances will persist or worsen dur-
Endocrinal disease ing treatment, requiring regular ortho-
Hypothyroidism, hypopituitarism, dontic follow-ups5.
and hypoparathyroidism are endocrine
disorders often associated with erup- Drug treatments
tion delays41. Many treatments, such as long-term
Hypothyroidism is an abnormality of chemotherapy or drugs that inhibit the
thyroid metabolism characterized by a prostaglandins pathway, can slow the
thyroid hormone deficiency. It affects rate of eruption by decreasing osteo-
1/5,000 to 1/10,000 children in Europe. clastic activity in periodontal tissues
It includes in its symptomatology a (aspirin, acetaminophen, ibuprofen, in-
densification of the skeleton affecting domethacin, clodronate).
the long bones and the skull, a retarda- Bisphosphonate administration also
tion of maturation and a varying scale causes a delayed eruption. Bisphos-
of mental retardation5. The eruption of phonates are usually used in the treat-
DT and PT is delayed, these teeth can ment of certain bone cancers, osteo-
also present anomalies in the enamel genesis imperfecta, and osteoporosis
structure5. to decrease bone fragility. A study on
Congenital pituitary insufficiencies rats confirmed that bisphosphonates
(hypopituitarism) are characterized by cause eruption delays14. Some authors

8 Choukroune C. Tooth eruption disorders associated with systemic and genetic diseases: clinical guide
 Tooth eruption disorders associated with systemic and genetic diseases: clinical guide

have reported an average delayed on- Vitamin deficiencies are also associ-
set of eruption of 1.6 years in young pa- ated with eruption delays. In fact, rats
tients treated with bisphosphonates11. for which vitamin A has been removed
from the diet show eruption delays,
PREMATURE BIRTH the alveolar bone is delayed in its for-
Delays in growth and dental develop- mation and the gingival tissues are hy-
ment in premature infants have been perplastic38. According to Moulis et al.,
identified by Seow and have been vitamin A and D (rickets) deficiencies
linked to DTE37. are among the most common system-
In 2010, Aktoren et al. showed that ic causes of eruption delay in perma-
children weighing <2.5 kg at birth had nent dentition24.
an eruption delay of about 2 months
compared to children weighing <2.5 kg1. Genetic diseases associated with
In addition to the eruption delay, there eruption disorders
are enamel abnormalities and maxillary
growth defects notably related to intu- Structural anomalies
bation duration37. Hereditary amelogenesis imperfecta
(HAI) is a group of inherited disorders
Malnutrition that affect the enamel quantitatively
Chronic and prolonged malnutrition and/or qualitatively. It exists in isolation
during childhood is linked to delays in or associated with certain syndromes.
eruption27. The authors report delays Most amelogenesis imperfecta are
ranging from 1–4 months compared to transmitted in an autosomal dominant
normal eruption ages. fashion with variable severity.

Figure 5
Panoramic view of a 9-year-old patient with hypocalcified amelogenesis imperfecta. We noted
the eruption delay of 36 (courtesy of Dr. De La Dure Molla - Center of reference of malforma-
tions of the face, Rothschild Hospital).

J Dentofacial Anom Orthod 2017;20:402 9

 C. CHOUKROUNE

The multiplicity of clinical forms O’Connell et al. report a delay in den-

makes their classification difficult, but tal maturation of >12 months in 21%
Witkop classification is commonly patients with type-3 OI, whereas pa-
used to describe this disease23. The ab- tients with type-4 OI exhibit an accel-
normalities are classified as hypoplas- eration of dental development26.
tic, hypocalcified, or hypomatic.
HAI clinical forms can vary among Syndromes
families carrying different mutations of Many syndromes are associated
the same gene, within the same fami- with eruption delays in permanent den-
ly, and even within a single dental arch tition24:
between teeth from different areas.
Orally, HAI is accompanied by other – Down syndrome or trisomy 21;
abnormalities such as taurodontism, – Turner syndrome (XO);
pulp calcifications, eruption defects, – Gardner syndrome or familial adeno-
skeletal abnormalities (open bite, class matous polyposis;
III, etc.; Figure 5). One study identified – Cleidocranial dysostosis or Pierre–
the anomalies associated with HAI in Marie Foy and Sainton’s disease;
1999, Seow, cited by these authors, – Anhidrotic ectodermal dysplasia or
assessed the risk of delayed eruption Christ–Siemens–Touraine disease;
in HAI patients as six times higher – Hutchinson–Gilford syndrome or pr-
compared to the healthy population. ogeria (dwarfism and pseudosenility,
Cases with the most severe eruption often associated with dental delays,
delays were associated with recessive dentinal dysplasias and abnormal po-
hypoplastic forms of HAI9. sition, dysplasia);
– Bloch–Sulzberger syndrome or In-
• Dentinogenesis imperfecta (DI) continentia pigmenti: a condition
associated with osteogenesis that is transmitted according to the
­imperfecta dominant X-linked mode and associ-
Osteogenesis imperfecta (OI) is a ates dental delays with oligodontia;
heterogeneous group of genetic dis- – Apert syndrome or acrocephalosyn-
eases characterized by bone fragility, dactylyia: associated craniosynos-
low bone mass, and a tendency for tosis, syndactlylia of the feet and
fractures of varying severity. hands, various synostoses, as well
Dental manifestations include: pos- as frequent dental congestion;
terior open bite, bulbous teeth, pul- – Axenfeld–Rieger Syndrome: asso-
pal obliterations, short and fine roots, ciated oligodontia, multiple dental
brown or gray discolorations of the delays and primary mesodermal dys-
crown, bluish tint when OI is asso- genesis of the iris.
ciated with DI, ectopic eruptions or
molar impactions, and agenesis. Very Primary failure of eruption (PFE)
frequently, in all types of OI, a class The term PFE, was first proposed by
III is present, more or less associated Proffitt and Vig in 1981 following a find-
with anterior open bite and/or laterally ing of posterior open bites in several
inverted articulations3,17. patients29. It attests to a nonsyndromic

10 Choukroune C. Tooth eruption disorders associated with systemic and genetic diseases: clinical guide
 Tooth eruption disorders associated with systemic and genetic diseases: clinical guide

Figure 6
33-year-old patient with DPE.
The gap is not due to lingual interposition (ODF service, Pitié-Salpêtrière Hospital).

state in which the tooth fails to erupt. The result of these eruption defects
The tooth/teeth concerned is (are) not is severe lateral obstruction and growth
ankylosed, but its (their) eruption is not of the alveolar process is deficient on
due to a malfunction of the eruption the affected side (Fig. 6).
mechanism. Note that deciduous teeth are often
The eruption path forms well but ankylosed and a family history of erup-
the tooth does not erupt, or only par- tion failure is present in many cases35.
tially. It suddenly stops its movement Case analysis suggested autosomal
and is sometimes submerged or dominant familial transmission with
“­reincluded”39. variable penetrance.
The diagnosis is made on the basis of In 2008, a team discovered a muta-
the following symptoms: tion of the PTH1R gene in 15 distinct
patients. The nonsyndromic mutation
– The posterior teeth are most often results in a truncated PTH1R receptor
affected; leading to premature degradation of
– The teeth posterior to the first affect- the dysfunctional receptor. The hap-
ed tooth are generally affected; loinsufficiency of the PTH1R receptor
– The eruption path is formed but would therefore be the mechanism be-
eruption fails or only partially erupts; hind DPE10. To date, there are 14 muta-
– DTs and PTs can both be affected; tions of PTH1R associated with DPE34.
– The issue may be symmetrical or There is no explanation for the fact
asymmetrical; that posterior teeth are preferential-
– The affected teeth are not anky- ly affected, although the authors as-
losed, but tend to become anky- sume a chronologically and spatially
losed when applying an orthodontic regulated expression of PTH1R during
traction force. ­eruption13. They do not exclude any

J Dentofacial Anom Orthod 2017;20:402 11

 C. CHOUKROUNE

other genes that may be involved with arch if the chosen technique is a multi-
DPE. fastening/straight arch technique.
It is important to make the differential The infraocclusion generated by DPE
diagnosis between DPE and ankylosis. causes significant aesthetic and func-
It can be accomplished with three-di- tional damage. Using orthodontic forc-
mensional (3D) imaging, which greatly es on teeth with DPE leads to failure.
improves the visibility of pathological The choice of treatment for DPE is
areas compared to two-dimensional therefore complex.
(2D) radiography. In fact, only a genetic To date, few therapeutic options ex-
test for PTH1R mutations can identify ist to date to improve occlusion in pa-
with certainty the presence of DPE33. tients with DPE. The options are the
This will prevent the orthodontist following: therapeutic abstention for
from implementing a long and difficult the mildest cases, prosthetic (onlay,
treatment that will inevitably fail, as removable, or fixed prosthesis), or im-
teeth affected by DPE will become an- plant restorations12, or as a last resort,
kylosed and will affect the rest of the vertical segmental osteotomies.

CONCLUSION
Dental eruption is a very finely reg- alveolus during eruption. Osteogenic
ulated process. DF is a major compo- molecules have been highlighted: they
nent and many genes, molecules, and are BMP, Runx2, or MMP.
cells participate in this process. In the end, very few studies have
Eruption theories are unanimously been conducted on the supraosseous
agreed upon: osteolysis is necessary phase of eruption, although this is a
for successful dental eruption. Re- crucial stage in the process. Some au-
search has focused on this essential thors have suggested the involvement
phase of the eruption process, high- of the desmodontal ligament, a struc-
lighting the many molecules needed, ture derived from DF.
coming into play at different stages, Dental eruption can sometimes pres-
sometimes redundantly. We can dis- ent chronological anomalies. It can be
cuss the molecules acting directly on delayed or completely interrupted. Eti-
the recruitment of monocytes (os- ologies can be local (not detailed in this
teoclast precursors): CSF-1, MCP-1, work), systemic, or genetic.
and NF-κB. Other molecules, such as The orthodontist is involved in the
PTHrP, RANKL, IL-1a, or TGF-ββ, will act early detection of eruption delays,
indirectly on monocytotic recruitment which improves treatment success
by stimulating the expression of the rates. The cause of abnormal eruption
aforementioned molecules or by acting should always be sought, and the pa-
directly on the osteoclasts. tient referred to a geneticist if a doubt
A small part of the research focused arises.
on the no less essential phase of bone Current treatments are limited to a
formation occurring at the base of the purely mechanical traction of the in-

12 Choukroune C. Tooth eruption disorders associated with systemic and genetic diseases: clinical guide
 Tooth eruption disorders associated with systemic and genetic diseases: clinical guide

cluded teeth or a delayed eruption. to foresee new modes of treatment in

However, recent advances in molecular which genetic and/or molecular treat-
biology promise hope for a change in ments would fit into the treatment pro-
the practices of orthodontists. The re- cess.
search avenues opened by the under-
standing of the pathologies associated Conflict of interest: The author declares that
with eruption delays make it possible there is no conflict of interest.

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