|Year : 2022 | Volume
| Issue : 3 | Page : 109-114
The tooth eruption and its abnormalities - A narrative review
KV Sai Charan, R Sangeetha, N Santana, G Hema Priya, M Kumari, P Murali, VS Gayathri
Department of Oral Medicine and Radiology, Ragas Dental College and Hospital, Chennai, Tamil Nadu, India
|Date of Submission||13-Jun-2022|
|Date of Decision||14-Jul-2022|
|Date of Acceptance||18-Jul-2022|
|Date of Web Publication||09-Sep-2022|
Dr. K V Sai Charan
Ragas Dental College and Hospital, Chennai, Tamil Nadu
Source of Support: None, Conflict of Interest: None
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.
Keywords: Eruption abnormalities, osteoprotegerin, rank, receptor activator of nuclear factor- kappa-b ligand, syndromes, systemic factors
|How to cite this article:|
Sai Charan K V, Sangeetha R, Santana N, Priya G H, Kumari M, Murali P, Gayathri V S. The tooth eruption and its abnormalities - A narrative review. SRM J Res Dent Sci 2022;13:109-14
|How to cite this URL:|
Sai Charan K V, Sangeetha R, Santana N, Priya G H, Kumari M, Murali P, Gayathri V S. The tooth eruption and its abnormalities - A narrative review. SRM J Res Dent Sci [serial online] 2022 [cited 2022 Nov 26];13:109-14. Available from: https://www.srmjrds.in/text.asp?2022/13/3/109/355829
| 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. 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. The mechanism behind the tooth eruption is an interaction between osteoblasts, osteoclasts and the dental follicle, with the presence of genetically influenced factors. Hence, there are various systemic, local, and genetic factors responsible for tooth eruption, any disturbances in these factors might lead to abnormalities in eruption. 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 search of data for the articles dealing with eruption, theories of eruption, and eruption abnormalities from the following 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 abnormalities, and then we worked toward defining and classifying the eruption abnormalities and correlating the information gathered from the various articles and framed a definition and classification based on the resource available 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. 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.
|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|
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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 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.
Root growth theory
Growth of the root in the apical direction creates a force which in turn drives the tooth axially leading to the tooth eruption. This hypothesis states that proliferating root exerts a force on a fixed base that results in a coronal 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.
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.
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. Cahill and Marks in 1980 reported that the removal 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.
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.
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.
The neuromuscular theory also known as the unification theory postulates that a coordinated force from the oro-facial 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.
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. 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.
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. 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.
“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 the position, shape, and size of the tooth.” Tooth eruption anomalies might occur due to various reasons. A complete understanding of the growth and development of an individual is crucial for the management of eruption abnormalities. 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 tooth eruption is the most commonly encountered situation. Regularly, a delayed eruption is the first and foremost, or sometimes the only, manifestation of local or systemic conditions. When there is delayed eruption concerning a group of teeth or whole teeth, the etiology could be either systemic or genetic (might be most commonly associated with syndromes or not associated with a syndrome).
Classification of eruption abnormality
- Eary tooth eruption
- Delayed tooth eruption (DTE),
Early tooth eruption
Taking into consideration, the time of eruption as the reference, Massler and Savara defined the early-erupted teeth as natal (present at the time of birth) and neonatal teeth (erupt into an oral cavity within 30 days of life). Synonyms of these teeth include congenital teeth, fetal teeth, precocious teeth, dens cannatalis, dentition praecox, etc.
Spoug and feasby classification
- Based on the degree of maturity:
- Mature natal/neonatal tooth
- Immature natal/neonatal tooth.
Based on appearance:
- Shell-shaped crown (absence of root)
- Solid – crown (little or no crown)
- Unerupted – tooth (edema of the gingival tissue but the tooth is palpable)
- Eruption of just a portion of the tooth (incisal margin).
Etiology for early tooth eruption
Hereditary transmission of an autosomal dominant gene (Msx 1 and Msx 2 gene). Mutation in activity-dependent neuroprotective protein most commonly encountered in autism children, the mutation of this particular gene causes premature primary tooth eruption.
Increase in the secretion of pituitary hormones including thyroid and androgens.
Nutritional deficiency during pregnancy, which in turn is the cause for various other problems including maternal health, issues, pyelitis, febrile episodes (exanthema and fever might tend to accelerate the eruption).
Superficial position of tooth germ.
Delayed tooth eruption classification based on various factors,,
Delayed tooth eruption due to systemic conditions
Deficiency of the certain hormones may have an indirect impact on the tooth development, thus delaying the tooth eruption. These conditions include the following (a) Hypothyroidisim, (b) Hypopitutarism, (c) hypo-parathyroidism, (d) Hypo-vitaminosis A and D, and (e) Calcium imbalance (osteoporosis). RANKL is expressed in the plasma membrane of osteoclast progenitor. RANK binds to RANKL leading to the signalling reaction thus resulting in the differentiation and fusion of osteoclast precursor. Osteoclast secretes osteoprotegerin, which prevents binding of RANKL and RANK, thus interfering in osteoclast formation. Thyroid, PTH, growth hormone, glucocorticoid, estrogen, Vitamin D, and cytokines regulate the RANKL-OPG pathway. Low serum/blood levels of these hormones interfere with the osteoclast formation, thus retarding eruption. In osteopetrosis, the number of osteoclasts may be reduced/ normal/increased. The deficiency of an enzyme carbonic anhydrase in osteoclast inhibits hydrogen ion pumping which in turn leads to defective bone resorption, despite the bone formation. The bone formed is brittle, which delays dental development and eruption.
Delayed tooth eruption due to local factors
The following entities may obstruct the tooth from erupting: (a) Eruption cyst, (b) dentigerous cyst, (c) replacemental 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)., 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
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.
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.
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.
Multiple jaw osteomas, supernumerary teeth, and odontomas are the common features of Gardner syndrome. Eruption abnormalities are seen mostly in patients with multiple osteomas.
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.
Growth retardation, alopecia, pseudo-anodontia, and optic atrophy syndrome
it is characterized by growth retardation, alopecia, pseudo-anodontia, and optic atrophy.
The diagnostic approach for the eruption abnormalities is tabulated in [Figure 2].
| 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. This manuscript may serve as an eyeopener for students at the undergraduate level regarding eruption abnormality.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]
[Table 1], [Table 2]