Review Article

The tooth eruption and its abnormalities - A narrative

review
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Sai Charan K V, Sangeetha R, N. Santana, Hema Priya G, Kumari M, Murali P, Gayathri V S

Department of Oral Medicine and Radiology, Ragas Dental College and Hospital, Chennai, Tamil Nadu, India
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ABSTRACT
Background: The process of tooth eruption is influenced by local, systemic, and genetic
factors. Any disturbances in these factors might lead to abnormalities in the eruption of
the tooth. Aim: The aim of this narrative review is to classify and discuss the eruption
and its abnormality in detail. Methods: This narrative review was performed through
an electronic search of data for the articles dealing with eruption, theories of eruption,
and eruption abnormalities from the following databases such as PubMed, Scopus,
Medknow, WebMD, and IndMed. Results: Based on our search, we were able to
retrieve the information from 15 articles. Conclusion: A mastered eye in evaluating
the radiographs, the practitioner’s acquaintance with associated abnormalities, and
the patient’s clear history including familial and traumatic history might pave the way in
arriving at an approximate diagnosis.

Key words: Eruption abnormalities, osteoprotegerin, rank, receptor activator of nuclear

factor‑ kappa‑b ligand, syndromes, systemic factors

INTRODUCTION
Tooth eruption is a complex procedure in which the germ
of the tooth erupts in the oral cavity in a synchronized
manner through the available space.[1] The tooth traces
its pathway through the alveolus toward the epithelium
of the oral cavity and then reaches its ultimate position in
the plane of occlusion.[2] The mechanism behind the tooth
eruption is an interaction between osteoblasts, osteoclasts
and the dental follicle, with the presence of genetically
influenced factors.[3] Hence, there are various systemic,
local, and genetic factors responsible for tooth eruption, any
disturbances in these factors might lead to abnormalities
in eruption.[2] Any disturbances in these factors might lead
to abnormalities in the eruption of the tooth.
This article intends to discuss the theories of tooth eruption,
classification of eruption abnormalities, a key significant
reason behind eruption abnormality, their etiology, and a
route map for diagnosing the type of abnormality.
METHODS

This narrative review was performed through an electronic

Address for correspondence:
Dr. Sai Charan K V,
Ragas Dental College and Hospital, Chennai, Tamil Nadu, India.
E‑mail: kvss1996@gmail.com
Received: 13‑06‑2022,
Accepted: 18‑07‑2022,
Access this article online
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search of data for the articles dealing with eruption, theories
of eruption, and eruption abnormalities from the following
Revised: 14‑07‑2022, This is an open access journal, and articles are distributed under the
Published: 09-09-2022
terms of the Creative Commons Attribution‑NonCommercial‑ShareAlike
4.0 License, which allows others to remix, tweak, and build upon the
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the new creations are licensed under the identical terms.
Website:
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For reprints contact: WKHLRPMedknow_reprints@wolterskluwer.com

DOI: How to cite this article: Sai Charan KV, Sangeetha R, Santana N,
10.4103/srmjrds.srmjrds_83_22 Priya GH, Kumari M, Murali P, et al. The tooth eruption and its
abnormalities - A narrative review. SRM J Res Dent Sci 2022;13:109-14.

109
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 Charan, et al.: Tooth eruption and its abnormalities

databases: PubMed, Scopus, Medknow, WebMD, and
IndMed.
RESULTS
As a result of our search, 15 articles were included, but
we could not find a complete classification of eruption
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normal eruption of teeth. This hypothesis briefly deals with
the blood flow from the vascular channels to the pulp and the
adjacent tissues which creates the kinematic and hydrostatic
force in the vascular channels that creates a resultant force
that causes the tooth to erupt.[3]

Root growth theory

abnormalities, and then we worked toward defining and
Growth of the root in the apical direction creates a force
classifying the eruption abnormalities and correlating the
which in turn drives the tooth axially leading to the tooth
information gathered from the various articles and framed a
eruption.[3] This hypothesis states that proliferating root
definition and classification based on the resource available
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exerts a force on a fixed base that results in a coronal

till date.
DISCUSSION
Molecular characteristics of tooth eruption
Many signalling processes and components (cytokines/
growth factors) are involved in triggering the bone
resorption around the crown of the tooth during the
eruption process. Monocytes are osteoclast precursors and
recruitment of monocytes to areas of tooth eruption has
been linked to osteoclastogenesis and bone resorption.
Macrophage colony‑stimulating factor‑1 (CSF‑1),
monocyte chemoattractant protein‑1 (MCP‑1), and
nuclear factor‑ kappa‑B light chain enhancer of activated
B‑cells (NF‑kB) act directly on monocytes. Whereas,
parathyroid hormone (PTH)‑related protein, receptor
activator of NF‑kB ligand (RANKL), and interferon‑1α act
indirectly on the recruitment of monocytes in the area of
resorption. Bone morphogenetic protein and Runt‑related
transcription factor are the osteogenic molecules responsible
for the formation of bone at the base of alveolus during
the eruptive process.[3] Transforming growth factor – β1,
interleukin‑1α, and parathormone‑related protein in the
stellate reticulum enhance the MCP‑1 and CSF‑1. Due to
the presence of enhanced CSF‑1 and MCP‑1, the dental
follicle itself acts as a chemotactant which attracts monocytes.
These enhanced factors also have a regulatory effect on
osteoprotegerin, thus stimulate bone resorption and favors
eruption [Figure 1]. Apart from this molecular aspect, several
questions regarding the eruption process remain unanswered,
which include the following: (1) What is the significant
mechanism allowing tooth germ to rise? (2) what is the
factor which remains behind the tissue resistance during
the upward movement? (3) how the functional integrity of
the tooth is maintained throughout life? To answer these
questions, various theories have been put‑put forth by various
researchers, which have their own merits and demerits.
Theories of tooth eruption
Blood pressure theory
A tissue surrounding the erupting end of the root comprises
of abundant vascular supply and the pressure from that rich
vascularity is supposed to cause the movement of the tooth
axially. This theory deals with the force which causes the
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movement of the tooth. However, when the tooth hits on a
fixed base, it might lead to resorption of the root rather than
a coronal eruption. Teeth without roots have also erupted.
Teeth can erupt even after the complete root formation,
sometimes, the teeth can even erupt to a greater distance
when compared to their root length. All these valid points
made this theory unacceptable.
Hammock ligament theory
Band of fibrous tissue exists underneath the apex of the
root and consists of fluid droplets. The erupting end of the
root forces itself against the fibrous band and thus initiates
eruption. Hammock ligament act as a cushion that straddles
the base of the socket from one bony wall to the other like
a sling that runs across the tooth apex and has no bony
attachment. Sicher observed this ligament below the tooth
in the histologic section and reported that it is merely an
artifact created in the process of histologic preparation.[4]
Periodontal traction theory
Periodontal ligament fibers are rich in fibroblast, which
contains contractile tissue, contraction of oblique fibers
results in axial movement of the teeth. Formation and
renewal of fibers of periodontal ligament are considered to be
key factors in eruption. Therefore, the force transmitted from
the extracellular compartment to oblique fibers brings about
the tooth eruption. However, the contraindicating point
for this theory is, that even impacted tooth has periodontal
ligament fibers but why it is not erupting and even rootless
teeth erupt.
Alveolar bone growth theory
Deposition of bone beneath the erupting tooth is responsible
for eruption. Even though the growth of the alveolar bone,
development of teeth, and eruption are closely related, the
formation of bone as such is not adequate for eruption.[3]
Dental follicle and tooth eruption
Dental follicle acts as a chemoattractant and recruits the
monocytes (osteoclast precursor) and leads to resorption
of the bone surrounding the tooth which paves way for
eruption.[3] Cahill and Marks in 1980 reported that the removal
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Figure 1: Molecular mechanism of tooth eruption (Macrophage‑CSF‑1, MCP‑1, TGF– β1, IL‑1α, PTHrP, EGF, OPG). CSF‑1:
Colony‑stimulating factor‑1, MCP‑1: Monocyte chemoattractant protein‑1, TGF– β1: Transforming growth factor– β1, IL‑1α:
Interleukin‑1α, PTHrP: Parathormone‑related protein, EGF: Epidermal growth factor, OPG: Osteoprotegerin
of the dental follicle in the premolar region before eruption
prevented unerupted tooth from erupting into the oral cavity.
In 1984, Cahill and Mark removed the tooth bud with the
dental follicle intact and implanted an artificial replicate of a
tooth, which resulted in an eruption of the artificial tooth.[5]
Recent concepts of tooth eruption
Bite force theory
This theory states that “functional bite‑force induces a
jaw‑strain which accounts for tooth eruption.” According
to this theory, the follicular tissue detects the bite forces
and directs the bone remodeling which enables the tooth
eruption. Various researchers reported that when the bite
force in periodontal ligament and dental follicle persuades a
strain, it resulted in a widespread area of compression in the
superimposing crowns, and wide zones of tension in the follicle
below the apices of the root. Follicular tissues perceive the bite
force, induce bone strain, and lead to direct bone remodeling
within the inner surface of the adjacent bony crypt.[6]
Innervation‑provoked pressure theory
According to this theory, the membrane of the root persists
as the glandular membrane. Therefore, the innervation in
this glandular membrane creates pressure in the tooth apices
which paves way for an eruption of the tooth. It is assumed
that the tooth eruption depends on the following factors (1)
Persistence of sufficient space in the eruption pathway, (2)
Pressure from underneath for upward movement, and (3)
functional adaptation of the periodontal membrane along
the eruption pathway.[6]
Neuromuscular theory
The neuromuscular theory also known as the unification
theory postulates that a coordinated force from the oro‑facial
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musculature, underneath the influence of the central
nervous system, is accountable for tooth movements and
the molecular signaling events are planned according to the
regulation of this co‑ordinated forces.[6]
Equilibrium theory
According to this theory, when the functional occlusal plane
is reached, a supplementary eruption becomes apparent in
response to the vertical growth of the mandible. The teeth
tend to acquire further space, then it erupts in an occlusal
direction to sustain occlusal contact with the teeth in the
opposing arch.[7] The gubernacular cord is the structure that
comprises of connective tissue, which connects the dental
follicle to the gingiva overlying the follicle, thus steering the
course of the tooth eruption.[7]
Among these theories mentioned above, some are discounted
and others are accepted [Table 1].
Sequence of eruption
The sequence/order of eruption of the primary tooth is as
follows: central incisor, lateral incisor, 1st molar, canine, and
2nd molar. Whereas, the order of eruption of a permanent
tooth is as follows: 1st molar, central incisor, lateral incisor,
1st premolar, 2nd premolar, canine, 2nd molar, and 3rdmolar.[8]
The time required for the development of the primary and
permanent tooth is represented in Table 2.
• Primary tooth: order of eruption: ABDCE
• Permanent tooth: order of eruption: 61245378.[8]
Eruption abnormalities
“Eruption abnormalities may be defined as an irregularities
in eruption influenced by various conditions which include
hormonal imbalance, local factors, and genetical inheritance,
causing premature/delayed type of eruption irrespective of
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 Charan, et al.: Tooth eruption and its abnormalities

Table 1: Discounted and accepted theories of tooth
eruption
Discounted
Blood pressure theory
Root growth theory
Hammock ligament theory
Periodontal traction theory
Alveolar bone growth theory
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Etiology for early tooth eruption
Accepted Genetic causes
Dental follicle theory Hereditary transmission of an autosomal dominant
Equilibrium theory gene (Msx 1 and Msx 2 gene). Mutation in activity‑dependent
Bite‑force theory neuroprotective protein most commonly encountered in
Neuromuscular theory
autism children, the mutation of this particular gene causes
Innervation‑provoked pressure theory

premature primary tooth eruption.[11]

Table 2: The time required for development[8]

Developmental Primary tooth Permanent Endocrine causes
process tooth Increase in the secretion of pituitary hormones including
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Eruption Incisors: 4-6 months after Incisors, canine, thyroid and androgens.
crown completion and molars:
Canine and molars: 6-12 3-4 years after
months after crown completion crown completion Infectious causes
Root 1 year after the eruption 3 years after the Syphilis.
completion eruption

Malnutrition
the position, shape, and size of the tooth.” Tooth eruption
Nutritional deficiency during pregnancy, which in turn is the
anomalies might occur due to various reasons. A complete
cause for various other problems including maternal health,
understanding of the growth and development of an individual
issues, pyelitis, febrile episodes (exanthema and fever might
is crucial for the management of eruption abnormalities.[9]
tend to accelerate the eruption).
Frequently, there is the clinical scenario of eccentricities in
an eruption from normal age. While premature eruption is
detected occasionally in some individuals, delayed type of Superficial position of tooth germ.[10]
tooth eruption is the most commonly encountered situation.
Regularly, a delayed eruption is the first and foremost, or Delayed tooth eruption classification based on
sometimes the only, manifestation of local or systemic various factors[12‑14]
conditions. When there is delayed eruption concerning a Delayed tooth eruption due to systemic conditions
group of teeth or whole teeth, the etiology could be either Deficiency of the certain hormones may have an indirect
systemic or genetic (might be most commonly associated with impact on the tooth development, thus delaying the
syndromes or not associated with a syndrome).[3] tooth eruption. These conditions include the following
(a) Hypothyroidisim, (b) Hypopitutarism, (c)
Classification of eruption abnormality
hypo‑parathyroidism, (d) Hypo‑vitaminosis A and D,
• Eary tooth eruption
and (e) Calcium imbalance (osteoporosis).[12] RANKL is
• Delayed tooth eruption (DTE),
expressed in the plasma membrane of osteoclast progenitor.
RANK binds to RANKL leading to the signalling reaction
Early tooth eruption
thus resulting in the differentiation and fusion of osteoclast
Taking into consideration, the time of eruption as the
precursor. Osteoclast secretes osteoprotegerin, which
reference, Massler and Savara defined the early‑erupted
prevents binding of RANKL and RANK, thus interfering
teeth as natal (present at the time of birth) and neonatal
in osteoclast formation. Thyroid, PTH, growth hormone,
teeth (erupt into an oral cavity within 30 days of life).
glucocorticoid, estrogen, Vitamin D, and cytokines regulate
Synonyms of these teeth include congenital teeth, fetal teeth,
the RANKL‑OPG pathway. Low serum/blood levels of
precocious teeth, dens cannatalis, dentition praecox, etc.
these hormones interfere with the osteoclast formation,
thus retarding eruption.[3] In osteopetrosis, the number
Spoug and feasby classification
of osteoclasts may be reduced/ normal/increased. The
I. Based on the degree of maturity:
deficiency of an enzyme carbonic anhydrase in osteoclast
• Mature natal/neonatal tooth
inhibits hydrogen ion pumping which in turn leads to
• Immature natal/neonatal tooth.
defective bone resorption, despite the bone formation. The
II. Based on appearance:
bone formed is brittle, which delays dental development
• Shell‑shaped crown (absence of root)
and eruption.
• Solid – crown (little or no crown)
• Unerupted – tooth (edema of the gingival tissue
but the tooth is palpable) Delayed tooth eruption due to local factors
• Eruption of just a portion of the tooth (incisal The following entities may obstruct the tooth from erupting:
margin).[10] (a) Eruption cyst, (b) dentigerous cyst, (c) replacemental
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 Charan, et al.: Tooth eruption and its abnormalities
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Figure 2: Diagnostic approaches toward eruption abnormalities
variety of odontogenic keratocyst (OKC), (d) ameloblastoma,
and (e) Odontomes
Genetic disorders influenced delayed tooth eruption
The following genitic condition has the regulating influence
on tooth eruption which includes (a) amelogenesis
imperfecta, (b) cherubism, (c) cleidocranial dysplasia,
(d) ectodermal dysplasia, (e) congenital hypertrichiosis
lanugionosa, (f) Gaucher disease, etc.,
Drug‑induced delayed tooth eruption
Long‑term use of the following drugs influences
the retardation of tooth eruption, (a) aspirin, (b)
acetaminophen, (c) ibuprofen, (d) indomethacin, and
(e) clodronate (Bisphosphonate). [12,13] Prostaglandins
have a direct role in bone resorption. Nonsteroidal
anti‑inflammatory drugs block Prostaglandin E2 synthesis
which lead to failure of bone resorption resulting in DTE.
Immunosuppressors may persuade severe hypertrophy of
the gingiva. In children, it might delay the eruption/cause
eruption cyst.
Delayed tooth eruption related to syndromes
There are various syndromes associated with DTE, which
include the following: (a) Down’s syndrome, (b) Turner’s
syndrome, (c) Gardner’s syndrome, (d) Cleidocranial
dysplasia, (e) ectodermal dysplasia, (f) Hutchinson-
Gilford syndrome, (g) Bloch‑Sulzberger syndrome, (h)
Apert syndrome, (i) Axenfeld-Rieger syndrome, (j)
growth retardation, alopecia, pseudo‑anodontia, optic
atrophy syndrome (k) Goltz-Gorlin syndrome and (l)
Mucopolysaccharidosis
SRM Journal of Research in Dental Sciences | Volume 13 | Issue 3 | July-September 2022
Apert syndrome
Anomalies in the shape of the molar are often encountered
in this syndrome, which might lead to a lack of space for the
adjacent tooth to erupt in the oral cavity.[12]
Down syndrome
Vascularity of peri‑radicular connective tissue is suppressed
which leads to poor peripheral circulation which in turn
leads to retarded growth of maxilla and mandible owing to
improper bone formation thus resulting in the absence of
scaffold for tooth germ to stabilize leading to abnormalities
in tooth eruption.[13]
Turners syndrome
Defects in x‑chromosomes, X‑chromosomes determine tooth
size and shape, and root morphology. Taurodontism has
been reported in this condition (more or less 60%), which
might be the local factor leading to the lack of space and
thus retarded eruption.
Gardner syndrome
Multiple jaw osteomas, supernumerary teeth, and odontomas
are the common features of Gardner syndrome. Eruption
abnormalities are seen mostly in patients with multiple
osteomas.
Oculo‑facio‑cardio‑dental syndrome
It is an x‑linked inherited disorder with characteristic
anomalies eye, face, heart, and teeth, most commonly
affecting the female gender. The more common dental
anomaly is radiculomegaly (enlarged roots) of canines.
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 Charan, et al.: Tooth eruption and its abnormalities
Growth retardation, alopecia, pseudo‑anodontia, and optic
atrophy syndrome
it is characterized by growth retardation, alopecia,
pseudo‑anodontia, and optic atrophy.
Diagnostic approach[9,12‑16]
The diagnostic approach for the eruption abnormalities is
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tabulated in Figure 2.
CONCLUSION
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A mastered eye in evaluating the radiographs, the
practitioner’s acquaintance with associated abnormalities,
and the patient’s clear history including familial and
traumatic history might pave the way in arriving at an
approximate diagnosis. This manuscript may serve as an
eyeopener for students at the undergraduate level regarding
eruption abnormality.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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