Anatomy, Head and Neck, Tooth Eruption


Tooth eruption is the movement of the developing tooth from its non-functional position in the alveolar bone to its final functional position in the oral cavity (occlusal plane).[1] The term eruption differs from emergence as the latter refers to the moment of appearance of any aspect of the crown through the gingiva.[2]

In general, teeth eruption involves bone remodeling mechanisms regulated by the dental follicle. The dental follicle regulates the metabolic changes in alveolar bone that mediate tooth eruption (bone formation and resorption) and gives rise to the periodontal ligament (believed to contribute to tooth eruption in the supraosseous stage).[1] Bone resorption forms an eruption pathway first, and the developing tooth follows this path; bone apposition apical to the developing tooth is believed to be the propulsion force that moves the tooth in an occlusal direction along this path.[3] The beginning of eruptive movements coincides with the start of root formation.[3] Root growth may contribute, but it is not the cause of tooth eruption - teeth with no roots do erupt.[3] The periodontal ligament potentially mediates supraosseous events.[1] Intraosseous events are not related to the periodontal ligament.[1]

Structure and Function

Two things are required for the eruption of a tooth to occur: removal of bone, primary roots, and later soft tissues, and a force that moves the tooth in an occlusal direction following the eruption pathway.[4] The process through which these events take place is still a subject of study, but the most likely mechanisms will be explained in this review.

The steps leading to tooth eruption can be generally divided into intraosseous and supraosseous. In the intraosseous stage, bone resorption and movement of the tooth within the bone occurs. The supraosseous stage begins when part of the erupting crown is above the alveolar crest.[1] Tooth eruption is further subdivided into five stages: pre-eruptive movements, intraosseous eruption, mucosal penetration, pre-occlusal eruption, and post-occlusal eruption.[3]

Preeruptive Movements

Crown development happens within the alveolar bone, during which small, random movements occur before the eruption. These movements are local and not in an axial eruption direction.[3] It is unknown if the movements of the developing crown are the result of the growth and maturation of the jaws or are caused by follicular events.[3]

The Intraosseous Stage of Tooth Eruption 

The first eruption movements begin when the crown finishes its development and root formation begins.[4] During this stage, an eruption pathway is cleared by bone resorption through which the tooth erupts.[4] It would be reasonable to believe that pressure from the developing tooth could initiate the osteoclastic activity and consequent eruption pathway.[4] However, studies on premolars of dogs demonstrated that an eruption path (alveolar resorption occlusal to the tooth) was formed despite immobilizing the tooth bud by ligating it to the mandible's lower border.[5] Furthermore, when a tooth bud was unintentionally ligated during the management of a jaw fracture, resorptive activity created this eruption pathway for the immobile tooth bud anyway.[4] Therefore, the alveolar resorption that creates the eruption path occurs first, independent of the developing tooth force.[4]

Different areas of the dental follicle are believed to initiate bone resorption occlusal to the developing crown and induce alveolar bone formation apical to the developing root, contributing to the translocation of the tooth to the alveolar crest.[3]

The dental follicle is an organized connective tissue surrounding the tooth germ in the early stages of tooth formation.[1] It also gives rise to the periodontal ligament, believed to mediate tooth eruption in the supraosseous stage.[1] The resorptive cellular activity in the dental follicle begins after the crown fully develops, involving signals from the enamel epithelium.[3] Possible mediators include interleukin-1, epidermal growth factor-1, matrix metalloproteinases, and some unknown proteins in the enamel organ and the dental follicle.[3]

Root formation happens at the same time as eruption, which may accelerate the eruption's speed.[3] However, root formation alone is not responsible for tooth eruption, e.g., teeth with no roots do erupt, like in dysplasia Type I,[3] and teeth with closed apices can erupt.

Mucosal Penetration and Eruption to the Occlusal Plane 

After the cusps reach the alveolar crest, the eruption pathway is completed, and the eruption rate accelerates, which will slow down again when the tooth reaches the occlusal plane.[3] The enamel epithelium thickens, transforms, and fuses with the oral epithelium thanks to the proliferation of the external enamel epithelium and proteolytic events.[3]

Proteins from the enamel matrix are released before and during the penetration of the oral mucosa, which is thought to be responsible for a hypersensitivity reaction that triggers the common symptoms of teething: fever, rhinitis, and local erythema.[3] Another important event during mucosal penetration is the formation of the junctional epithelium on the tooth surface.[3]

The eruption movement that takes the tooth from the gingival plane to the occlusal plane is believed to be generated primarily by the periodontal ligament collagen fibers: collagen maturation involves a cross-linking and shortening process, providing a propulsive eruptive mechanism.[4] Oral forces would change the orientation and number of fibers, activating this mechanism.[4] Drugs that interrupt collagen maturation also interrupt tooth eruption, indicating that the collagen fibers of the periodontal ligament are the primary mechanism of post-emergent axial movement.[4][6]

Root growth and bone apposition at the crypt's base and interradicular septa contribute to the propulsive force that moves the erupting tooth from its gingival emergence to the occlusal plane.[3]. Studies have demonstrated that this eruption stage occurs only during a few critical hours of the early evening when growth hormone levels are at their highest.[4] Furthermore, blood flow fluctuations in the periodontal ligament seem to affect the eruption rate during this period.[4]

Post-occlusal Eruption

After the tooth reaches its functional position in the occlusal plane, events to stabilize the tooth in its new position occur. This is done by bone activities like forming circumferential bone and lamina dura visible in x-rays and maturation of periodontal ligament fibers.[3] Also, during the post-occlusal stage, the roots finish their development.[3]

There is still the question of how horizontal movements take place. Possibly teeth move in the horizontal plane, e.g., buccally, through bone resorption and formation and cementum apposition in a coordinated effort.[3] Cementum apposition may also be partly responsible for the compensatory eruption seen in tooth wear.[3] A tooth can continue to erupt later in life to compensate for the loss of an antagonist, demonstrating that eruption activity continues during adulthood.[4] 

Tooth Eruption Theories

Numerous mechanisms to explain tooth eruption have been hypothesized. Marks and Schroeder suggested that for a theory to be valid, it should fulfill three eruption facts: 1) teeth are moved axially but also three-dimensionally, 2) teeth erupt with different characteristics and at a stage-specific speed, and 3) the functional position of teeth is inheritable.[3]

A brief description of past and newer tooth eruption theories is given below:

Cushioned Hammock Theory

According to this theory, proposed by Harry Sicher, a cushioned hammock ligament below a tooth is responsible for its eruption.

Root Formation Theory

According to this theory, the apically directed force by the proliferating root exerts a reactive occlusal force resulting in the coronal movement of the erupting tooth. However, as previously mentioned, teeth without roots can erupt, and the teeth erupt even after the completion of their root formation. Also, some teeth erupt to a distance greater than their total root length. Moreover, the newly formed dentin at the apex of the root is unmineralized and is vulnerable to trauma.[7]

Vascular/Hydrostatic Pressure theory

The local increase in tissue fluid pressure in the vessels of the dental pulp and the periapical region are believed to exert hydrodynamic and hydrostatic pressure within the vessels resulting in tooth eruption.[8]

Bone Remodeling Theory/Dental follicle theory

Osteoblasts and osteoclasts from the dental follicle cause bone remodeling via resorption in the coronal area and bone apposition in the apical region, thereby forming a pathway through which the tooth can passively erupt.[5][9][5]

Periodontal Ligament Traction Theory

According to this theory, the periodontal ligaments-dental follicle complex exerts eruptive force via the traction power of the fibroblasts when they contract.[10]

More Recent Theories of Eruption

Bite Forces Theory

The soft tissues of the dental follicle are believed to detect bite forces, which in turn direct bone remodeling and tooth eruption.[11]

Innervation-Provoked Pressure Theory

This theory postulates that the innervation in the root membrane causes pressure in the apical aspect of the tooth resulting in tooth eruption.[12]

The Equilibrium Theory

Once the tooth reaches its functional plane, further eruption occurs in response to the vertical growth of the lower jaw away from the maxilla. As the teeth get more space, they erupt occlusally to maintain occlusal contact with the tooth in the opposing arch.

Neuromuscular Theory

This theory states that the simultaneous and balanced forces of the orofacial muscles under the control of the central nervous system are responsible for the active eruption of a tooth. The coordinated neuromuscular forces convert into electrical, electrochemical, and biomechanical energies to stimulate cellular and molecular responses within and around the dental follicle and enamel organ. This action prepares a pathway and other cellular functions for the eruption of a developing tooth.

Eruption Patterns

The age at which deciduous and permanent teeth erupt can vary extensively. The sequence of eruption is more significant than the timing, which may differ in both deciduous and permanent teeth. Generally, a variation of 6 months on either side of the usual eruption date is considered normal. The first teeth to erupt in the oral cavity are the deciduous mandibular central incisors at approximately 5 to 8 months of age, followed by maxillary central incisors a month or two later. In general, by the age of 19 months, the child has a total of 12 erupted deciduous teeth. By 23 months, children should have 16 deciduous teeth, and by 27 months, all the deciduous teeth should have erupted.

The first permanent teeth that emerge in the oral cavity are the maxillary and mandibular first molars at around six years of age (six-year molars). They erupt distally to the deciduous second molars. Their eruption is accompanied by or preceded by the exfoliation of the deciduous mandibular central incisors. Between 6 to 7 years of age, the permanent mandibular incisors erupt, followed by the permanent maxillary incisors between 7 to 9 years of age. The permanent anterior teeth develop lingual or palatal to the deciduous teeth, whereas the permanent premolars develop between and beneath the roots of the deciduous molars they replace.

Clinical Significance

Tooth eruption is a very complex and finely regulated process that influences the healthy development of the craniofacial region. Factors such as eruption timing, sequence, direction, rate, position, and morphology of teeth are crucial for facial esthetics and phonetics.[13] Estimation of the eruption schedule is a valuable tool in planning a child's dental health that includes diagnostic, preventive, and therapeutic measures.[14] It is also a key indicator when diagnosing certain growth disturbances and estimating the chronological age of the child with unknown birth records in forensic dentistry.[15] Moreover, it can also aid in interceptive guidance of occlusion, especially when determining the timing of eventual extractions of deciduous teeth and the timing of orthodontic treatment.[16]

Disturbances in tooth eruption are a common problem in dental practice. Tooth eruption may be delayed, completely impaired, or premature, and teeth may also erupt in an ectopic position. This article intends to elucidate what is known about the physiology of normal tooth eruption, but a summary of the common eruption complications is provided below.

Ectopic Eruption

When a tooth does not follow its usual course, it is known as an ectopic eruption.[17] An early diagnosis and management of ectopic teeth will prevent future malocclusion. Variation in position is influenced by various factors such as ethnicity, sex, and individual characteristics. Local traumatic injury may displace one or more tooth buds resulting in an ectopic eruption of the affected teeth. Other local factors include the presence of fibrous tissue, supernumerary teeth, arch length deficiency, and retained or prematurely lost deciduous teeth.

Reports also exist of nasal teeth, which are teeth that appear in the nasal cavity as supernumerary.[18] Nasal teeth may be asymptomatic or lead to facial pain, nasal cavity obstruction, headache, epistaxis, foul-smelling rhinorrhea, external nasal deformities, and nasolacrimal duct obstruction.[18]

Delayed Eruption

When the emergence timing deviates significantly from the established norms assigned to ethnicity and sex, the condition is known as a delayed eruption.[2] Emergence refers to the moment of appearance of any aspect of the tooth in the oral cavity.[2]

It may occur due to local factors (mucosal barrier, gingival fibromatosis, odontogenic and non-odontogenic tumors, premature loss of a primary tooth, radiation damage), systemic conditions, and endocrinal disorders (hypothyroidism,[19] hypopituitarism, and hypoparathyroidism) and medications.[2]

Long-term chemotherapy or drugs (aspirin, acetaminophen, ibuprofen, indomethacin, bisphosphonates) may inhibit the prostaglandins pathway resulting in decreased osteoclastic activity in periodontal tissues, thus, slowing down the rate of eruption. 

Chronic and prolonged malnutrition (vitamin deficiencies) during childhood also correlates with delayed eruption.[2] Various syndromes have been shown to cause a delayed eruption, including Down syndrome, Gardner syndrome, Cleidocranial dysostosis, Anhidrotic ectodermal dysplasia, Hutchinson–Gilford syndrome, Bloch–Sulzberger, Apert syndrome, and Axenfeld–Rieger Syndrome.[2]

Impacted Teeth

These teeth cannot erupt due to a physical barrier preventing their eruption.[2] Mandibular third molars are the most commonly impacted teeth.

Embedded Teeth

These teeth with no physical obstruction in their path remain unerupted due to la ack of eruptive force.[2]

Submerged Teeth

Submerged teeth are those that, after the eruption, ankylose and lose their ability to maintain the continuous eruptive potential as the jaws grow.[2]

Primary Failure of Eruption

Primary failure of eruption refers to the partial or complete failure of the tooth's eruption.[20] The tooth's eruption path forms well, but the tooth does not erupt.[20]

Intraosseous Ectopic Migration of Unerupted Teeth

It is a rare occurrence reported in less than 1% of the population with an increased preference for females and the mandibular arch. It usually involves the mandibular second premolar or the mandibular canine.[21][22]

Premature Eruption

Premature eruption refers to teeth eruption before its stipulated time. Teeth present in the oral cavity at the time of birth are referred to as natal teeth, whereas the teeth that erupt within the first month of life are referred to as neonatal teeth.[23] The prevalence of natal teeth is three times more than neonatal teeth. They occur most commonly in the mandibular anterior area, particularly the central incisors, followed by maxillary incisors, mandibular canines or molars, and maxillary canines or molars. 

Premature eruption of teeth can occur due to several factors such as genetic abnormalities, endocrine disturbances (pituitary, thyroid, and gonads), congenital syphilis, local factors (excessive resorption of the overlying bone), environmental factors (environmental pollutants such as toxic polyhalogenated aromatic hydrocarbons, polychlorinated biphenyls, polychlorinated dibenzodioxins, and dibenzofurans), poor maternal health, and febrile episodes during pregnancy. 

Some syndromes are also reported to be associated with natal teeth and neonatal teeth, such as chondroectodermal dysplasia, Rubinstein-taybi, Pierre-robin, neonatal progeria, cleft lip/palate, ectodermal dysplasia, craniofacial dysostosis, and Down syndrome.

Natal/Neonatal Teeth

They may lead to ulceration on the ventral surface of the tongue due to the sharp incisal edge of the tooth.[24]

This condition is known as Riga-Fede disease/syndrome. As the root development of these teeth is incomplete, they are mobile, which increases the possibility of swallowing and aspiration of teeth. Other complications include injury to the mother's breast and difficulty in suckling.[24] The mobility has also been shown to cause degeneration of Hertwig's epithelial sheath, which is responsible for the formation of the root. Degeneration of the sheath results in further incomplete root development.

Eruption Cyst

An eruption hematoma over an erupting tooth that presents as a bluish swelling due to the filling of blood-tinged fluid in the follicle surrounding the erupting tooth is usually asymptomatic.[25] They typically rupture spontaneously without any treatment. But sometimes, the size of the cyst may cause pain and impair eating.

Detrimental Habits that Affect Tooth Eruption

Digit Sucking

This habit affects the eruption path of maxillary incisors resulting in their protrusion due to the disturbance in the balance between the outward force of the tongue musculature on the palate and the inward force of the cheek musculature.[26]

Tongue Thrust

In children with tongue thrust habit, greater outward force by the tongue musculature is applied, resulting in a change in the eruption pathway of maxillary incisors.[27]

Lip Habit 

Sucking or biting the lips, particularly the lower lip, results in more significant inward pressure by the lip musculature, which in turn leads to a change in the eruption path of the mandibular incisors.[28]

(Click Image to Enlarge)
Microscopic view of a tooth bud. A) enamel organ. B) dental papilla. C) dental follicle.
Microscopic view of a tooth bud. A) enamel organ. B) dental papilla. C) dental follicle.
Contributed from Wikimedia Commons; CC BY-SA 3.0,

(Click Image to Enlarge)
Teething baby: first sign of the lower right incisor breaking through the oral mucosa.
Teething baby: first sign of the lower right incisor breaking through the oral mucosa.
Contributed By Daniel Schwen - Own work, CC BY-SA 4.0,

(Click Image to Enlarge)
Teething baby: lower right incisor penetrating the oral mucosa.
Teething baby: lower right incisor penetrating the oral mucosa.
Contributed By Daniel Schwen - Own work, CC BY-SA 4.0,

(Click Image to Enlarge)
Intraoral Periapical Radiograph (IOPA) of a boy aged 5 years showing primary tooth #75 and developing crowns of permanent teeth 35, 36 and 37. Note the eruption path for 36 has been completed. The 36 is now in the post-emergence eruption stage.
Intraoral Periapical Radiograph (IOPA) of a boy aged 5 years showing primary tooth #75 and developing crowns of permanent teeth 35, 36 and 37. Note the eruption path for 36 has been completed. The 36 is now in the post-emergence eruption stage.
Contributed By Nizil Shah - Own work, CC BY-SA 4.0,
Article Details

Article Author

Prachi Jain

Article Editor:

Manu Rathee


6/20/2022 2:21:49 PM



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