Hypotheses for the Tooth Eruption Mechanism

Table of Contents


Tooth eruption, the movement of the tooth germ from its non-functional position in the alveolar processes to its final function position in the oral cavity, is a little-known mechanism despite being highly documented. Many theories try to explain the mechanism of the eruption of the tooth; however, none succeed to define the event in its entirety. This essay discusses the different theories and confronts them to question their relative plausibility.


Every species has one or more sets of teeth specially adapted to their dietary needs as well as their current mouth morphology. We, humans, are used to having one change of teeth, namely from milk teeth to adult teeth. However, some species have many more sets of teeth, like crocodiles who can change all their teeth more than 46 times! Either way, a species equipped with teeth must have an impeccable tooth eruption mechanism otherwise its ability to feed itself, and hence to stay alive, is compromised. Despite the primordial importance of teeth eruption for survival, this mechanism is still unknown in the medical sphere. Even if tooth formation, tooth histology and tooth cells no longer hold any secrets for researchers, the tooth eruption system is still a subject full of unknowns and speculations. The objective of this paper is to go over the main hypotheses for the tooth eruption mechanism and analyze which one of them are the more plausible. However, to understand those intricate hypotheses, it is essential to first take a look at tooth formation and histology to acquire some basic tooth knowledge.

Embryonic Tooth Formation

It all starts from the primitive oral epithelial band, which is a tissue layer in the future mouth of the embryo. The tooth development is regulated by this primitive oral epithelium and cells called ectomesenchymal (derived from neural crest cells).  Interaction between the dental epithelium and ectomesenchyme induces the three following different stages of tooth production: bud stage, cap stage and bell stage (“Development of the Teeth” | Osmosis | YouTube, 2020).

Bud Stage

The oral epithelial band thickens as a result of signaling proteins that trigger epithelial cells to proliferate and transport themselves to the location of the future teeth. These locations are called dental placodes (“Development of the Teeth” | Osmosis | YouTube, 2020). The thickened primitive oral epithelium is now referred to as the dental lamina, and it is on this dental lamina that the teeth will form, which is now only in the shape of a bud. Ectomesenchymal cells appear below the tip of these buds while groups of epithelial cells at the tip of each bud form what is called the “primary enamel knot”, which has a role intricately linked with tooth shape regulation (“Development of the Teeth” | Osmosis | YouTube, 2020).

Cap stage

The primary enamel knot continues to proliferate and evolve until it forms the enamel organ, which is cap shaped. Indeed, the tooth has now begun to invaginate, meaning it has a deepening below, like a bottle of wine (“Development of the Teeth” | Osmosis | YouTube, 2020). Meanwhile, the ectomesenchymal cells that continued to agglomerate near the tip of the bud are now in the invagination of the cap and form what is referred to as the “dental papilla”. These cells begin to proliferate elsewhere than below the cap, and start to encapsulate the enamel organ, to form what is called the dental follicle (“Development of the Teeth” | Osmosis | YouTube, 2020).

Bell Stage

As the enamel organ continues to grow and the invagination deepens even more, a cervical loop begins to form at the end of the invaginating epithelium, which will provide the basis for the root of the tooth (“Development of the Teeth” | Osmosis | YouTube, 2020). It is at the bell stage that morphodifferentiation, differentiation of the shape of the tooth, as well as histodifferentiation, differentiation of cells into specialized cells, occurs. Indeed, we introduced a lot of various cell and organ terms in the cap stage, and it is in the bell stage that these cells differentiate into specialized cells which will give rise to tissues as we know them in mature teeth (“Development of the Teeth” | Osmosis | YouTube, 2020). The differentiation occurs as follows:

  • Epithelial cells of the enamel organ differentiate into ameloblasts, which are cells responsible for enamel production.
  • Ectomesenchymal cells of the dental papilla will differentiate into odontoblasts, which are cells responsible for the dentin-pulp complex.
  • Ectomesenchymal cells of the dental follicle will differentiate into three kinds of cells:
    • cementoblasts (responsible for production of dentin),
    • osteoblast (give rise to alveolar bone in which sits the tooth) and
    • fibroblasts (which develop the periodontal ligament)

These many cell and tissue names may seem daunting, but they will be revised and further explained in the next few paragraphs.

Phases of Tooth Life

The tooth is now created, but it remains in the gums. From this stage to the completely developed tooth, we will pass through the following three stages:

  • Pre-eruptive phase
  • Eruptive phase
  • Post-eruptive phase

The pre-eruptive phase is the phase during which the set of teeth will prepare to erupt via bodily movement and eccentric growth (Chu and Yeung, 2014). Bodily movement is the displacement of the tooth within the gingiva so that it erupts at the right place. Eccentric growth, on the other hand, is the irregular growth of the tooth (some parts grow more than others) to achieve the desired shape of the tooth (Chu and Yeung, 2014). The eruptive phase is the phase in which the tooth erupts, via many factors such as eruptive forces. The post-eruptive phase describes the time from which the tooth erupts onwards. It details the wear and occlusion that the tooth must maintain to achieve and preserve dental health (Chu and Yeung, 2014).

The following section will present an overview of tooth composition and structure in terms of tissues as well as cell types so that the hypotheses might be clearer.

Overview of Tooth Histology and Cellular Composition

The different structural parts of the tooth are the crown, located above the gingiva, emerging from the latter, and the root, located beneath the gingiva. The gum line, where the crown and the root meet, is called the neck of the tooth (“Tooth” | American Dental Association, n.d.).

The three tissues that compose the crown are, from the innermost to outermost layer, the pulp, the dentin, and the enamel. The root of the tooth has the same histology except enamel is replaced with a hard substance called cementum, produced by cells referred to as cementoblasts (“Tooth” | American Dental Association, n.d.).

Fig. 1 Diagram showing a teeth’s principal tissues and components. [Adapted from “Tooth” | American Dental Association, n.d.]
Tooth AreasTissueProducer Cells
Pulp ( in the pulp chamber)N/A
RootCementum Cementoblasts
Pulp (in the cementum)N/A
Table 1 Tooth tissues and their producer cells. [Information retrieved from Peckham et al., “The Mouth”]

Below are a few key characteristics of each of the tissues mentioned in Table 1.


Enamel is the outermost protective layer of the tooth. It is its most calcified and hard tissue (“Tooth” | American Dental Association, n.d.). Those properties of enamel, namely the mineralization and the hardness, are reminiscent of another tissue of the body: bone tissue. However, enamel differs from bone tissue in many ways, amongst other that it is not vascularized, and it does not have collagen as its main constituent. Enamel is made exclusively of inorganic material, except for a few regulatory proteins. Therefore, it makes sense that the cells producing enamel – the tall columnar cells called ameloblasts – are not embedded in enamel but are rather found covering the exterior of enamel, as Fig. 2 shows (Shotgun Histology Tooth Eruption” | WashingtonDeceit | YouTube, 2007). When the tooth erupts, the ameloblasts die and no longer exist on the exterior of the tooth and thus, enamel cannot regenerate or be repaired once the tooth has erupted (Peckham et al., “The Mouth”).

Fig. 2 Photomicrograph showing a tooth prior to eruption. [Adapted from “Shotgun Histology Tooth Eruption” | WashingtonDeceit | YouTube, 2007]


Dentin makes up the bulk of the inorganic teeth. Even though this tissue is nine times softer than enamel, it is still a hard, calcified tissue (“The Anatomy of a Tooth” | Coast Dental Blog | Coast Dental & Orthodontics, n.d.). It is composed of thousands of microscopic tubules, that are made mostly of collagen and hydroxyapatite (“Shotgun Histology Tooth Eruption” | WashingtonDeceit | YouTube, 2007). This explains why, when the enamel layer is lost, the exposed dentine tubules can conduct heat, cold or sticky food to the vascularized and innervated part of the tooth – the pulp – which causes sensibility (Peckham et al., “The Mouth”). Like enamel, the cells that are responsible for the production of this tissue lie on its exterior, as the tissue is almost exclusively inorganic. In the case of dentin, the cells producing it are tall columnar cells called odontoblast (situated on dentin’s innermost border) (Peckham et al., “The Mouth”). Dentin is first produced by odontoblasts, and then calcified.

Pulp Cavity

The pulp cavity, or dental pulp is the most sensitive part of the tooth as it contains the nerves and blood supply of the tooth (“The Anatomy of a Tooth” | Coast Dental Blog | Coast Dental & Orthodontics, n.d.). As mentioned, when enamel is worn down, the pulp is less protected and thus vulnerable, which can create uncomfortable sensations when eating. As the pulp contains all the vessels and nerves, a lot of factors such as alteration in capillary filtration or inflammation will cause a change in pressure in the pulp chamber, known as the intrapulpal pressure (“Shotgun Histology Tooth Eruption” | WashingtonDeceit | YouTube, 2007). This intrapulpal pressure variance can lead to pain and even complicated pulpal disease but is also hypothesized to play a role in tooth eruption. As we descend from the crown to the root, the pulp cavity thins and elongates until it becomes the root canal, a passageway between the dental pulp and the rest of the body to conduct nerves and blood vessels (“Shotgun Histology Tooth Eruption” | WashingtonDeceit | YouTube, 2007).

Fig. 3 Photomicrograph showing a tooth prior to eruption. [Adapted from “Shotgun Histology Tooth Eruption” | WashingtonDeceit | YouTube, 2007]


The cementum, produced by cementoblasts, is what replaces enamel once the tooth is immersed in the gum. Cementum is a hard, calcified, vascularized substance that will help the rest of the tooth to anchor itself to the alveolar bone, by way of the periodontal ligament: cementum is attached to the periodontal ligament on one side of the root, and to the dentin on the other side (“Histology of the Tooth” | PathologyNOW | YouTube, 2017).

Tooth Eruption Theories

The eruption of the tooth is a complicated and uncertain process which is subject to many hypotheses and assumptions including the alveolar bone remodeling theory, the root formation theory, the periodontal traction theory, the dental follicle theory and the hydrostatic pressure theory. These assumptions are based on different cellular, molecular, and mechanical mechanisms that will be described in more detail. More recent theories also exist and will be presented but, in less detail, because they are not common.

Dental Follicle Theory

The dental follicle theory relies on the assumption that the dental follicle, a vascular fibrous sac containing the developing tooth, is capable of inducing, guiding, and coordinating the bone resorption above the crown and bone apposition (Rabea, 2018).

Fig. 4 Photomicrograph of a developing dog tooth, with the dental follicle (F) around the developing tooth, the alveolar bone (M), and overlying oral epithelium (E). [Adapted from Nel et al., 2015]

The bone resorption creates an eruptive pass through which the tooth is conducted (Rabea, 2018). To support this theory, studies have shown that in osteoporotic animals, which refers to a genetic condition characterized by an increased bone density, the lack of factor that stimulates differentiation of osteoclasts (the mediator of bone destruction) prevents the tooth eruption (Rabea, 2018).

The role of the dental follicle in the resorption of the alveolar bone is to serve as a target tissue to attract mononuclear cells and serve as a repository for these cells to fuse and form osteoclasts (Wise et al., “Cellular, Molecular, and Genetic Determinants of Tooth Eruption”). These osteoclasts are responsible for resorbing the bone and creating an eruption pathway. The dental follicle is at a strategic location, between the alveolar bone and the tooth, to regulate the cellular event of the eruption (Wise et al., “Cellular, Molecular, and Genetic Determinants of Tooth Eruption”).

The eruption is regulated by molecular signals. Those signals originate from the dental follicle (Nel et al., 2015). The coronal aspect of the dental follicle regulates bone resorption (osteoclastogenesis) and the basal regulates bone formation (osteogenesis). RANKL gene, a marker for bone resorption has been found in the coronal aspect of the dental follicle whereas BMP2, a gene marker for bone formation, has been found in the basal aspect of the dental follicle (Nel et al., 2015).

The cellular movements rely on molecular events, controlled by the dental follicle. Tooth eruption is programmed and localized even initiated by interactions between the dental follicle, the reduced enamel epithelium, and the stellate reticulum (Nel et al., 2015).

Fig. 5 Paracrine signaling of the coronal half of the eruption tooth. [Adapted from Nel et al., 2015]

The paracrine signaling process starts with the apoptosis of epithelial cells during stages of enamel secretion which influences bone resorption (osteoclastogenesis) through the release of interleukin-1a by stellate reticulum cells (Nel et al., 2015). The receptor of the interleukin-1a is in the dental follicle, which stimulates the expression of CSF-1 and monocyte chemotactic protein-1 (MCP-1). The dental follicle acts as a chemoattractant for monocytes. The stellate reticulum also releases PTHrp (parathyroid hormone-related protein) which increases the expression of MCP-1 and CSF-1 (Nel et al., 2015). CSF-1 down-regulates the expression of the receptor for RANKL which inhibits osteoclast differentiation. The cells of the reduced enamel organ and the stellate reticulum are responsible for the paracrine effect on the dental follicle. The dental follicle thus attracts the monocytes which will form osteoclasts (Nel et al., 2015). However, bone resorption is not sufficient for the displacement of the tooth which leads us to a second theory.

Root Formation Theory

The essential idea of root formation theory is that the root of the tooth grows larger eventually making contact with a hard fixed surface. It continues to grow, the normal force pushing the root in the occlusal direction, eventually pushing the corona of the erupting tooth in that direction during tooth eruption (Nanci, 2013).

Fig. 6 Photomicrograph showing root formation. [Adapted from Nanci, 2013]

This hypothesis has multiple questionable aspects to it. Tooth eruption can occur with rootless teeth, or after the root tissue has been removed (Rabea, 2018). In addition, teeth often erupt further than the length of the root, which should be impossible by this hypothesis. Teeth can even erupt after the root has stopped growing and the timing of root formation and tooth eruption does not match. The freshly formed dentin on the base of the erupting tooth is not yet hardened by mineralization, and is prone to trauma from this pressure which could mangle the tooth (Rabea, 2018).

During periods of root formation, combined with jaw growth, the compression caused by this on the tissue between the tooth and jaw can cause hydrostatic stress in the cells of the dental follicle and stellate reticulum (Nanci, 2013). They react by releasing bone resorption mediators. The idea is that they are combating excessive bone growth with the mediators they secrete causing the calcium of nearby bone to resorb into the bloodstream (Nanci, 2013). Combined with the stress on the tooth germ caused by the hydrostatic pressure this results in bone deposition of the tooth (Rabea, 2018).

Though root formation may play a minor role, it clearly is not the central mechanism of tooth eruption, and as shown by rootless tooth eruption, it is likely not even a necessary component of tooth eruption.

Alveolar Bone Remodeling Theory

As stated in the dental follicular theory, tooth eruption requires the dental follicle to regulate the resorption of the alveolar bone. However, it is not sufficient for the teeth to erupt; The alveolar bone growth at the base of the crypt occurring during eruption could create a motive force that pushes the tooth through the pathway. To determine if it is a plausible mechanism, experiments were designed in which “the expression of an osteogenic gene in the dental follicle, bone morphogenetic protein 6 was inhibited by injection of siRNA” (Wise et al., “Requirement of alveolar bone formation”). The results showed that the eruption was delayed or completely inhibited in impacted molars, the eruption pathways were formed but the bone growth at the base of the crypt was reduced. The alveolar bone growth at the base of the crypt is necessary for tooth eruption (Wise et al., “Requirement of alveolar bone formation”).  The tooth is then moved out of its alveolar socket by the alveolar bone growth (osteogenesis) at the base of the crypt. The bone growth is then the motive force of the eruption (Wise et al., “Requirement of alveolar bone formation”).

Fig. 7 Photomicrograph showing bone remodeling. [Adapted from Nanci, 2013]

The growth of the alveolar bone is regulated by a molecular event. As stated in the experiment, bone morphogenetic protein 6 promotes growth. Moreover, the expression of the bone morphogenetic protein-2 BMP-2, the gene marker for bone growth is expressed more strongly in the basal aspect of the dental follicle in the first days after birth. BMP-2 and BMP-6 enhance the growth of the alveolar bone (Wise et al., “Requirement of alveolar bone formation”).

The role of the dental follicle and the alveolar bone are interdependent. However, bone formation is not sufficient for tooth eruption either and imply other mechanisms, such as the periodontal ligament traction.

Periodontal Ligament Traction Theory

The periodontal ligament is particularly associated with the eruption of ever-growing teeth such as rodent incisors, while it does not assure eruption for teeth with limited growth (Marks Jr. and Schroeder, 1996). For this section, we will focus on the role of the periodontal ligament for permanently growing teeth.

Periodontal ligament traction theory relies on the force provided by the fibroblasts developing in the dental follicle, for the eruption (Chu and Yeung, 2014). The fibroblasts of the tooth-related part of the periodontal ligament pull the tooth with them thanks to the collagenous framework. The fibroblasts synthesize collagen and degrade collagen fibers, which maintain a dynamic situation in the periodontal ligament. In the rat, the periodontal ligament is involved in the eruption of the incisor (Beertsen et al., 1974). The fibroblasts contract and pull the erupting tooth during the eruption, thanks to a system of microfilaments and microtubules. The cytoplasm of fibroblasts in the periodontal ligament of the incisor contains microfilaments (Beertsen et al., 1974). In the alveolar zone, the microfilaments are “arranged in small bundles” and in the tooth-related part of the ligament, the fibroblasts “contain two types of microfilament system” (Beertsen et al., 1974). The fibroblasts in the tooth-related part of the periodontal ligament, whose cytoplasm consists of microfilaments and microtubules, migrate in the occlusal direction. Oxytalan fibers parallel to the tooth surface guide the fibroblasts, and the collagen fibrils inserted in the cementum of the fibroblasts draw the tooth axially (Beertsen et al., 1974). The movement of both cells and collagen equals the rate of the eruption. Moreover, the force generated by the periodontal ligament traction seems able to generate tooth eruption (Kasugai et al., 1990). In an experiment with root resection and root transaction, it has been shown that fibroblasts can generate tensional forces in a 3D collagen gel matrix. The force necessary to prevent the eruption of the rat incisors is 2 to 5 x 10-2 N and it was estimated that the force generated by 104 fibroblasts was 5 x 10-4 N (Kasugai et al., 1990). However, an estimation of 106 fibroblasts is in the tooth-related part of the periodontal ligament of the rat incisor, therefore the fibroblasts could generate enough force for tooth eruption. However, the traction force seems to be present only after the commencement of the eruption (Chu and Yeung, 2014). This mechanism alone cannot be the only mechanism behind tooth eruption.

 Blood Vessel Thrust/Hydrostatic Theory

The blood-vessel thrust theory for teeth eruption mechanism was suggested by Sutton. He believed that the blood flow in the blood vessels of the dental pulp and periodontal ligament will produce two forces: the hydrodynamic force and the hydrostatic force caused by the blood pressure. These forces produce a resultant force causing the teeth to erupt and migrate through bones (Sutton and Graze, 1985).

The forces generated in the pulpal vessels by blood can be considered as the forces generated in a U-shaped tube by a fluid with controlled volume, since the blood vessels are curved into a shape similar to the letter “U” (Sutton and Graze, 1985). Even though they do not represent a perfect ideal U-shaped tube, the hydrodynamic and hydrostatic forces in the tube can still be applied to the blood supply in the pulp (Sutton and Graze, 1985).

Fig. 8 Schematic drawing of the cross-section of an adult human molar. [Adapted from Editors of Encyclopedia Britannica, “Tooth”] (right) The blue shaded area represents a U-shaped tube. A hydrodynamic force is generated toward the crown at the first 90-degree bend (Site A). A reaction force of the hydrodynamic force generated by the blood flow at Site B is also acting toward the crown.

When a fluid is flowing in the 180 degrees U-shaped tube, at the site where the fluid enters the first 90-degree bend, a momentum flux will be generated in the y-direction (setting vertical axis as y-direction). The formula describing it is the following:



where ρ1 is the density of the fluid, V1 is the average velocity, and Q1 is the first derivative of the fluid volume (Sutton and Graze, 1985).

After entering the first 90-degree bend, because the y-direction velocity component has disappeared, there is no y-direction momentum. As the fluid leaves the second 90-degree bend, in the y-direction, a momentum flux with the following formula will be produced



where ρ2 is the destiny of the fluid, V2 is the average velocity, and Q2 is the first derivative of its volume at the leaving site. Consequently, the hydrodynamic force, caused by the change in the flow direction, will be generated upward and along the vertical direction (Sutton and Graze, 1985). The hydrodynamic force is given by the following formula:

F_d = ρ_1Q_1V_1 + ρ_2Q_2V_2


Besides, when fluid enters a 180 degrees U-shaped tube, a hydrostatic force will also be generated (Sutton and Graze, 1985). Let A1 be the cross-sectional area at the site where the fluid enters the tube and A2 be the cross-sectional area at the site where the fluid leaves the tube. As the fluid enters and leaves the tube, the pressure of P1 and P2 are produced respectively. The U-shaped tube bend will experience a total hydrostatic force of

F_s = P_1A_1 + P_2A_2


Consequently, the bend of the U-shaped tube will experience a total force (FT) upward in the vertical direction (Sutton and Graze, 1985). FT is given by the following formula:  

F_T = F_d + F_s = ρ_1Q_1V_1 + ρ_2Q_2V_2 + P_1A_1 + P_2A_2


This resultant force will produce pressure on overlying bones or the root of the overlying deciduous tooth and cause them to undergo resorption (Sutton and Graze, 1985). Then, this allows teeth to erupt and those that remain unerupted will migrate through the bones. When the direction of the blood flow changes at an angle other than 180 degrees, a sideway x-direction component of the resultant force will be produced, causing the teeth to move laterally during the eruption (Sutton and Graze, 1985).

Above, we have analyzed the hydrodynamic force and associated hydrostatic pressures generated by dental pulp vascular flow, but the analysis of the forces generated by the blood flow in periodontal ligament vessels is more complicated. There are abundant arteries in the alveolar bone. After they enter the periodontal ligament at approximately 90 degrees, they will travel along the periodontal ligament toward the root (Sutton and Graze, 1985). The blood will flow down through those “longitudinal vessels” (Sutton and Graze, 1985), then due to the presence of the root, the direction of the blood flow is forced to change about 90 degrees. This change in direction of the blood flow will generate a force exerted on the surface of the root. Part of the force is acting along the vertical axis toward the crow, and the other part will cancel out with a similar force generated at the other side of the root (Sutton and Graze, 1985). Consequently, the resultant force produced by the blood flow in the periodontal ligament will act towards the crown, also resulting in tooth eruption and migration (Sutton and Graze, 1985).

Since the blood derived from the heartbeat will be pumped to the arteries, capillaries, veins, and lymphatics vessels in the pulp (arteries in periodontal ligament) discontinuously, there will be a discontinuous increase in the blood pressure and blood flow. Therefore, the hydrodynamic and hydrostatic forces will not be produced continuously (Sutton and Graze, 1985). However, since a normal heart rate is between 60 – 100 beats per minute, the blood flow and blood pressure will increase 60-100 times per minute, 31 536 000-52 560 000 times a year. Therefore, biologically they can act as continuous forces to initiate the process of tooth eruption (Sutton and Graze, 1985).

The blood-vessel thrust theory was supported by several studies. A vasodilator and a vasoconstrictor were injected into the erupting second premolar of eight children to determine the effect of the vasodilator and vasoconstrictor during the post-emergent eruption state (Cheek et al., 2002). After receiving a vasodilator, which causes a widening of blood vessels, an increase in tooth eruption rate was noted. By contrast, in teeth that received a vasoconstrictor, which causes a narrowing of blood vessels, the eruption rate of the second molar decreased (Cheek et al., 2002). This observation has shown that changes in blood flow and blood pressure will indeed affect the eruption rate (Cheek et al., 2002).

However, the blood-vessel thrust theory is still debatable since cutting off the root and local blood vessels could not prevent the teeth from erupting (Wang, “Tooth Eruption without Roots”). Besides, in the research from Van Hassel and McMinn (1972, p. 184), they had stated that this blood-vessel thrust theory “encounters their greatest difficulty in explaining the earliest eruptive movements of the partially formed tooth before any part of it has emerged into the oral cavity”.

Other Theories

Based on the theories mentioned above, new theories are beginning to emerge and elaborate from them.

The “bites forces sensed by soft tissue dental follicles” theory postulates that the follicular soft tissues can detect bite-forces and initiate bone remodeling (alveolar bone remodeling theory) which enables tooth eruption as stated before. This theory is based on examination of the soft tissue of the dental follicles, suggesting “broad areas of compression in overlying crowns, and wide zones of tension in follicle below root apices” and thus these soft tissues could act as stress sensors (Sarrafpour et al., 2013).

The “innervation-provoked pressure” theory postulates that the root membrane acts as a glandular membrane, hence the innervation in this membrane pressure the apical part of the tooth which results in tooth eruption (Kjaer, 2014).

The “neuromuscular theory” or “unification theory” postulates that the “synchronized forces of the orofacial muscles, under the control of the central nervous system, are responsible for the active movements of a tooth and the molecular events prepared a pathway under the control of these forces” (Rabea, 2018).

Engineering Matrix

TheoryDescriptionContradictory PointsPlausible or Not?
Dental FollicleDental follicle induces bone resorption and enables the formation of an eruptive path.Experiments show that tooth does not erupt without a dental follicle, hence there are no contradictory points for this theory.Tooth eruption and bone formation depend on the dental follicle. However, bone resorption is not sufficient for the displacement of the tooth.
Root FormationRoot grows until it hits a hard surface, pushing the tooth occlusally as it continues to grow, eventually erupting.Rootless teeth can erupt. Teeth erupt more than root grows. Pressure causes trauma to teeth. Timing of eruption and root growth does not match.Very unlikely that it even plays a significant role in causing tooth eruption. It can occur normally even without root present.
Alveolar Bone RemodelingFormation of bone apical to developing teeth.Presence of an unerupted dentition in osteopetrotic mutations in which bone formation is nearly normal and bone resorption reduced.Bone formation is not sufficient for tooth eruption.
Periodontal Ligament TractionPeriodontal ligament exerts traction on the tooth when fibroblasts contract.In the case of osteopetrotic mutations, the periodontal ligament is present but teeth do not erupt.The periodontal ligament cannot be essential for tooth eruption especially in man. Applies only to continuously growing teeth.
Blood Vessel Thrust/Hydrostatic TheoryForces generated by the blood flow in the blood vessels of dental pulp and periodontal ligament will cause teeth to erupt.Teeth can still erupt even if their roots and local blood vessels are cut off. Since these forces are always present, they cannot explain why human teeth will stop erupting eventually.Hydrodynamic and hydrostatic forces are not sufficient for tooth eruption. 
Table 2 Summary of the most common theories for the tooth eruption mechanism. [Original table. Information taken from various sources mentioned in the respective section for each theory.]


There are many competing hypotheses for the tooth eruption mechanism. Despite the importance of the tooth eruption mechanism, and how long it has been studied, there is still no clear single explanation for tooth eruption. This research paper described five of the major theories, with all of them having key fundamental contradictory points, making their validity questionable. It is entirely possible that all these theories are incorrect, partially, correct, or require each other in some way. It seems clear that none of the theories for tooth eruption covered here are sufficient explanations on their own. It is the opinion of this article that each theory of tooth eruption is likely applicable to some stage or part of the tooth eruption mechanism, that there are likely components of the mechanism that have not been explored or properly explained, and that aspects of the existing hypotheses may change with future studies.


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