Eruption of Teeth / orthodontic courses by Indian dental academy

I. INTRODUCTION

Tooth eruption is an essential process for the survival of many species

and although the movement of teeth into function has been the subject of

extensive research, there is no consensus as to the mechanisms involved.

The term tooth “tooth eruption” generally refers to the appearance of

some part of the tooth above the surface of the gingiva. However, eruption

actually includes the entire embryological process from the formation of the

tooth germs, in the mandible and maxilla, to calcification, crown formation and

root formation. The root is only about 1/3rd formed when the crown begins to

erupt into the oral cavity. Not only is this embryological process a part of the

eruption, so is the long process of occlusal development. Thus, the emergence

of teeth into the oral cavity is only a part of the total eruption process.

I. TOOTH MOVEMENTS

The teeth develop within the tissues of the jaw. Thus for the teeth to

become functional, considerable movement is required to bring them into the

occlusal plane. The movements teeth make, are complex and may be described

in general terms under the following headings:

1. Pre-eruptive tooth movement - which is made by both the deciduous and

permanent tooth germs within the tissues of the jaw before they begin to

erupt.

2. Eruptive tooth movement - made by a tooth to move from its position

within the bone of the jaw to its functional position in occlusion.

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3. Post-eruptive tooth movement - those which maintains the position of

the erupted tooth in occlusion while the jaws continue to grow and to

compensate for occlusal and proximal wear of the tooth.

Although this categorization of tooth movement is convenient for

descriptive purposes, it must be recognized that, what is being described is a

complex series of events occurring in a continuous process. As a result, other

categorizations exist. For instance, some describe tooth movement as having

pre-functional and functional phases.

1. Pre-Eruptive Tooth Movements

When the deciduous tooth germs first differentiate, they are extremely

small and there is a good deal of space for them in the developing jaw. Because

the tooth germs grow rapidly, however they become crowded together,

particularly in the anterior region of the jaw. This crowding is gradually

alleviated by the lengthening of the jaws, which permits the second deciduous

molar tooth to move backward and the anterior tooth germs to move forward.

At the same time, the tooth germs are also moving bodily outward and upward

or downward as the case may be, as the jaws increase in length as well as in

width and height.

The permanent tooth germs develop on the lingual aspect of their

deciduous predecessors in the same bony crypt. From this position, the tooth

germs shift considerably as the jaws develop. For example, the incisors and the

canines eventually come to occupy a position, in their own bony crypts, on the

lingual of the roots of their deciduous predecessors, while the premolar tooth

germs, also in their own crypts, are finally positioned between the divergent

roots of the deciduous molars.

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The permanent molar tooth germs which have no predecessors, develop

from the backward extension of the dental lamina. At first there is little room in

the jaws to accommodate those tooth germs, so that in the upper jaw the molar

tooth germs first develop with their occlusal surfaces facing distally and can

swing into position only when the maxilla has grown sufficiently to provide

room for such movement. In the mandible, the permanent molars develop with

their axis showing a mesial inclination which becomes vertical only when

sufficient jaw growth has occurred.

These pre-eruptive movements of both deciduous and permanent tooth

germs are best thought of as the movements required to place the teeth within

the jaw in a position for eruptive tooth movement. Analysis has shown that

these pre-eruptive movements of the tooth are a combination of two factors.

The first factor is the total bodily movement of the tooth germs and the

second factor is growth, in which one part of the tooth germ remains fixed

while the rest continues to grow, leading to a change in the centre of the tooth

germ. This growth explains, for example, how the deciduous incisors maintain

their position relative to the oral mucosa as the jaws increase in height.

As pre-eruptive movement occur in an intraosseous location, such

movement is reflected in the patterns of bony remodeling within the crypt wall.

For example during bodily movements in a mesial direction, bone resorption

occurs on the mesial surface of the crypt wall and bone deposition occurs on

the distal wall as a filling in process. During eccentric growth, only bony

resorption occurs, thus altering the shape of the crypt to accommodate the

altering shape of the tooth germ.

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2. Eruptive Tooth Movement

During the eruptive phase of physiologic tooth movement, significant

developmental changes occur, including the formation of roots, periodontal

ligament and dentogingival junction of the tooth.

Root formation is initiated by the proliferation of Hertwig’s epithelial

root sheath. The forming root first grows toward the floor of the bony crypt and

as a result, there is resorption of bone in this location to provide room for the

advancing root tip. However, with the onset of eruptive tooth movement,

(probably coincident with the periodontal ligament formation) space is created

for the forming root and resorption no longer occurs on the floor of the crypt.

Indeed, in some instances the distance moved by the tooth outstrips the rate of

root formation and bone deposition occurs on the crypt floor.

As the roots of the tooth form, important changes associated with the

development of the supporting apparatus of the tooth occur in the dental

follicle.

- There is bone deposition on the crypt wall.

- Cement deposition on the newly formed root surface.

- Organization of a periodontal ligament from the dental follicle.

These changes lag behind root formation. There are a number of

important histologic features in the periodontal ligament that are important in

explaining eruptive tooth movement. First, is the occurrence of cell to cell

contacts of the adherens type between periodontal ligament fibroblasts. Second,

is the demonstrated presence of contractile elements in ligament fibroblasts.

Third, is the occurrence of a structure called fibronexus. This describes a

morphologic relationship between intracellular microfilaments in the fibroblast,

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a corresponding increased density of fibroblast cell membrane, extracellular

filaments and fibronectin.

Fibronectin is a sticky glycoprotein which sticks to a number of

extracellular components including collagen. Fourth, is the active ingestion and

degradation of old collagen fibrils by many of the fibroblasts of the ligament

and the convenient formation of new collagen fibrils. Thus the continual

degradation and synthesis of collagen by fibroblasts permit the remodeling of

the principal fibre bundles of the periodontal ligament.

Significant changes occur within the tissues that cover the erupting

tooth. There is a loss of intervening connective tissue between the reduced

enamel epithelium covering the crown of the tooth and the overlying oral

epithelium. Because of this loss, the two epithelia proliferate and form a solid

plug of cells in advance of the erupting tooth. The central cells of this epithelial

mass degenerate and form an epithelium lined canal through which the tooth

erupts without any haemorrhage. This epithelial cell mass is also involved in

the formation of the dentogingival junction.

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Interestingly, once the tooth erupts into the oral cavity, it continues to

erupt at the same rate of about 1mm every 3 months, only slowing as it meets

its antagonist in the opposing arch. This suggests that the resistance to the force

of tooth eruption provided by the overlying connective tissue is minimal. Root

formation, however, is not yet complete, and because further occlusal

movement is restricted, additional root growth is accommodated by removal of

bone on the socket floor.

The above description generally applies to all the teeth. Successional

teeth, however possess an additional anatomic feature, the gubernacular canal

and its contents, the gubernacular cord which may have an influence on

eruptive tooth movement. When the successional tooth germ first develops

within the same crypt as its deciduous predecessor, bone surrounds both tooth

germs but does not complete close over them. As the deciduous tooth erupts,

the permanent tooth germ becomes situated apically and entirely enclosed by

bone, except for a small canal that is filled with connective tissue and often

contains epithelial remnants of the dental lamina. This connective tissue mass

is termed the ‘gubernacular cord’ and it may have a function in guiding the

permanent tooth as it erupts.

Once the erupting tooth appears in the oral cavity, it is subjected to

environmental factors that help determine its final position in the dental arch.

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Muscle forces from the tongue, the cheeks, and the lips play on the tooth, as do

the forces of contact of the erupting tooth with other erupted teeth. A sustained

muscular force of only 4 to 5 grams is sufficient to move a tooth. The

childhood habit of thumb sucking is an obvious example of environmental

determination of tooth position.

3. Post Eruptive Movement

Post eruptive movements are those made by the tooth after it has

reached its functional position in the occlusal plane. They may be divided into

three categories:

1. movements made to accommodate the growing jaws.

2. those made to compensate for continued occlusal wear.

3. those made to accommodate interproximal wear.

a. Accommodation for growth

They are seen histologically as a readjustment of the position of the

tooth socket, achieved by the formation of new bone at the alveolar crest and

on the socket floor to keep pace with the increasing height of the jaws. Recent

studies have shown that this readjustment occurs between the ages of 14 to 18,

when active movement of the tooth takes place. The apices of the teeth move 2

to 3 mm away from the inferior dental canal (regarded as a relatively fixed

reference point). This movement occurs earlier in girls than in boys and is

related to the burst of condylar growth that separates the jaws and teeth,

permitting further eruptive movement. Although this movement is seen as

remodeling of the socket, it must not be assumed that this bony remodeling

brings about tooth movement.

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b. Compensation for occlusal wear

The axial movement a tooth makes to compensate for occlusal wear is

most likely achieved by the same mechanism as eruptive tooth movement. It is

often stated that the compensation for occlusal wear is achieved by continued

cementum deposition around the apex of the tooth, but the deposition of

cementum in this location occurs only after the tooth has moved.

c. Accommodation for interproximal wear

Wear also occurs at the contact points between teeth on their proximal

surfaces the extent of this wear can be considerable (more than 7 mm in the

mandible). This interproximal wear is compensated for, by a process known as

mesial or approximal drift. There are two, possibly three factors that bring

about mesial drift. They are: i. occlusal force ii. ligament contraction and

possibly iii. soft tissue pressures.

i. Anterior component of occlusal force

When the teeth are brought into contact, for example, when the jaws are

clenched, a forwardly directed force is generated. That this is so can be easily

demonstrated by placing a steel strip between the teeth and showing that more

force is required to remove it when the jaws are clenched. The anterior force is

the result of the mesial inclination of most teeth and the summation of the

intercuspal planes producing a forwardly directed force. In the case of incisors

which are inclined labially, it would be expected that any anterior component

of force would move them in the same direction. Incisors in fact moves

mesially but this can be explained by the billiard ball analogy.

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That cuspal inclination is a significant factor can be demonstrated by

selectively grinding cusps in such a way so as to either enhance or reverse the

direction of the occlusal force.

When opposing teeth were removed thereby eliminating the biting force,

the mesial migration of teeth were slowed but not halted indicating the

presence of some other force, and here the transseptal fibres of the periodontal

ligament have been implicated.

ii. Contraction of transseptal fibres

The periodontal ligament has an important role in maintaining tooth

position, and it is suggested that its transseptal fibres running between adjacent

teeth across the alveolar process draw neighbouring teeth together and maintain

them in contact. There is some evidence to support this. For example, it is

known that relapse of orthodontically moved teeth is much reduced if

gingivectomy is done, that is the transseptal ligament is removed. It has been

demonstrated experimentally that in bisected teeth, the two halves separate

from each other. If however, the transseptal ligaments are previously cut, this

separation does not occur. By disking away proximal contacts, room is

provided for the tooth to move to reestablish contact.

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iii. Soft tissue pressures

It does not have a major role in tooth movement. The pressures

generated influence tooth position, even if it does not cause tooth movement.

III. THEORIES OF TOOTH ERUPTION

The mechanism that brings about tooth movement is debatable. There

are numerous theories of tooth eruption which is usually a reflection of

incomplete understanding. All these theories have contributed to and provoked

research into various aspects, to support or refute hypotheses which are now

briefly reviewed.

1. Pulp Theory

This theory suggests that a propulsive force is generated by extrusion of

the pulp through three mechanisms; first growth of dentin, secondly, interstitial

pulp growth and thirdly, hydraulic effects within the vasculature. Perhaps the

most damning evidence against this theory is the work of Herzberg and Schour

(1941) who removed the pulp of rodent incisors and found that its eruption

rates were unaffected.

2. Vascular Theory

The mechanisms behind this theory to some extent overlaps the pulp

theory. The force of eruption comes from the pressure in the blood vessels

within or below the tooth. This theory has been discounted by some for the

same reasons as the pulp theory. In addition, use of hypotensive drugs appears

to have no effect on the eruption rates. However, a critical review by Moxham

suggests that at least part of the eruptive force is generated by a non-functional

force.

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3. Root elongation theory

This theory attributes tooth eruption to elongation of the roots. It

suggests that the tooth erupts as a result of root pushing against an immovable

base. Root formation appears to be the obvious cause of tooth eruption, since it

undoubtedly causes an overall increase in the length of the tooth which must be

accommodated either by the root growing into bone of the jaw, by increase in

height of the jaw, or by crown of the tooth moving occlusally. It is the latter

movement, of course that occurs but it does not follow that root growth is

responsible. If a continuously erupting tooth, such as a rodent incisor or a

guinea pig molar is prevented from erupting by pinning the tooth to the bone,

root growth continues and is accommondated by resorption of some bone at the

base of the socket and a buckling of the newly formed root. Such a simple

experiment yields two conclusions: first, that root growth produces a force;

second, that this force is sufficient to produce bone resorption.

At one time, it was proposed that a structure called “Cushion hammock”

ligament was strung across the base of the socket and when the growing root

impinged on it. This structure acted as a sling, translating downward root

growth into eruptive tooth movement. Careful histologic study has found no

such ligament. It must therefore be concluded that some force other than root

growth is moving the tooth to provide room for the newly formed root tissue.

Furthermore, Marks and Cahill (Arch. Oral Biol.; 1984) using young

dogs, took teeth at the beginning of eruption, removed their pulps and killed the

periodontal ligament cells by freeze thawing. These inert rootless teeth with no

periodontal ligaments were reimplanted and still managed to erupt by

compensatory bone growth. Thus, although root growth can produce a force, it

cannot be translated into eruptive tooth movement unless there is some

structure at the base of the tooth capable of withstanding the force.

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4. Alveolar bone growth

The importance of bone growth in tooth eruption was demonstrated with

a series of classical experiments by Brash (1928) using madder fed pigs.

Madder is a dye which binds to newly formed bone and Brash noticed large

amounts of bone laid down between the crypts of erupting teeth. These

observations have been confirmed (Marks and Cahill 1980), but although bone

formation is clearly involved in tooth eruption, cause and effect are still at the

phenomenology stage.

5. Periodontal ligament theory

This theory suggests that the impetus for tooth eruption is derived from

the periodontal ligament. Evidence for this came from some brief observations

by Moxham and Berkovitz (Arch. Oral Biol.; 1974) where root transsection

failed to prevent the incisor segment superfacial to the transsection from

erupting. This strongly implicates the periodontal ligament in the eruption

process, and suggests that there is little contribution from alveolar bone, root

growth and indeed pulp pressure. Evidence against this theory includes studies

with lachyritic compounds, such as -aminoproprionitrile. They inhibit

intermolecular crosslinking of the polypeptide chains in the collagen molecule

and should therefore inhibit the teeth from erupting. Despite adminstration of

these drugs, rat incisors continue to erupt normally.

It has already been indicated that fibroblasts have the ability to contract,

but for such contractions to bring about tooth movement, a number of other

conditions must be met. There must be some mechanism to summate the

contractile forces of a number of fibroblasts; the fibroblasts must have

something to pull on (collagen fibre bundles?) which must also be firmly

attached to the tooth and be correctly oriented. The numerous cell to cell

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contact between fibroblasts could be involved in summating contractile force.

The fibronexus and associated fibronectin could transmit this force to the

collagen fibre bundles. These bundles in turn are firmly attached to the bone

and the tooth in the correct position to bring about tooth movement. Finally,

they have the ability to remodel after the tooth moves.

In summary, then the force moving the tooth is most likely generated by

the contractile property of the ligament fibroblast, but a number of other

conditions must exist to translate this contraction into tooth movement.

Eruption must therefore be considered a multifactorial phenomenon.

The periodontal ligament theory has also gained some support from

tissue culture experiments. If a fibroblast is cultured on a substrate on which it

can move, it vibrates using contractile mechanisms generated by its

cytoskeleton. The actin molecule has a particularly prominent role. As the

fibroblast moves, it elongates on the leading edge and leaves the trailing end of

the cell adherent to the substrate. Eventually the latter edge will detach. If these

cells are cultured on thin silicon sheets, then as they move, the contractile

element is sufficiently strong to cause the rubber to wrinkle. This effect can

also be demonstrated when these cells are embedded in three dimensional gels

and this is true for fibroblasts derived from the periodontal ligament. This

model has been adapted to show that periodontal ligament fibroblasts are

capable of generating sufficient contractile force to lift a piece of root, against

gravity, towards the top of a tissue culture well (Arch. Oral Biol.; 1983). Direct

evidence of this tractional effect is not available but these models prove that

periodontal ligament has some role in the process of eruption.

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6. Genetic input

If tooth eruption is to be explained at the cellular and molecular level, a

degree of genetic control is highly likely in normal development of occlusion.

Incisors erupt before premolars and this process of eruption is often disturbed

in a number of genetic disorders. A classification of this has been presented by

Caulk (1988). These comprise:

a. inhibited defects, primarily involving enamel - amelogenesis

imperfecta.

b. syndromes with enamel involvement.

c. disorders associated with supernumerary teeth and / or crowding of

teeth.

d. growth retardation syndromes.

e. conditions associated with tissue overgrowth of the gingiva and

hyperplastic frenula.

f. miscellaneous disorders (these include premature exfoliation such as

Hypophosphatasia, Juvenile Periodontosis and Papillon Lefevre

Syndrome).

There is no simple explanation of tooth eruption and this biological

phenomenon is a multifactorial event. Biological sciences are more likely to

offer clear, rational approaches to improve our understanding of tooth eruption.

7. Hydrostatic pressure.

This theory requires a higher pressure system, either within or around

the base of the tooth. It is known that teeth move in their sockets in synchrony

with the arterial pulse, so local volume changes can produce limited tooth

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movement. Ground substance can swell from 30%-50% by retaining additional

water, so this too could create pressure. But, since surgical excision of the

growing root and associated tissue eliminate the periapical vasculature without

stopping eruption, this means that the local vessels are not absolutely necessary

for tooth eruption.

8. Follicular Theory

This theory attributes a critical role to the dental follicle for the eruption

of teeth. It seems unlikely that the dental follicle provides the eruptive force

since fibre transsection fails to prevent eruptive movement. It seems more

probable that the loose connective tissue of the dental follicle is a rich source of

factors which are responsible for bone formation and resorption. Indeed, the

follicle is capable of releasing cytokines, ericunosoids and growth factors but

as our understanding of these factors increases, we’re likely to explain tooth

eruption in terms of cellular and molecular interactions.

Follicular Theory – Molecular Biology of Initiation of Tooth Eruption

Further studies have been done regarding Follicular Theory through

recent advances in Molecular Biology.

Thanks to the pioneering experiments of Marks and Cahill, it was

established that, in teeth of limited eruption, a tissue required for eruption is the

dental follicle, a loose connective tissue sac that surrounds the tooth prior to

eruption. Their studies showed that surgical removal of the follicle prevents

eruption whereas leaving the follicle intact but substituting an inert object for

the tooth results in eruption of the inert object (Marks & Cahill; 1984).

At the cellular level there is an influx of mononuclear cells (monocytes)

in the dental follicle which is the onset of active eruption (Marks et al.; 1983

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Wise et al.; 1985). Concurrent with the monocyte influx is an increase in the

number of osteoclasts on the coronal positions of the bony crypt followed by a

decrease that parallels monocyte decrease. Studies by Wise and Lan (1989)

suggests that the influx of the monocytes contributes to the formation of

osteoclasts to resorb alveolar bone for the tooth to escape its bony crypt.

What is / are the molecular signal(s) that ultimately initiate the onset of

tooth eruption as seen by the above cellular changes?. At least 4 molecules

emerge as potential candidates because of their ability to accelerate eruption,

their immuno localization, their gene expression or a combination of these.

Perhaps the molecule that plays the most direct role in initating the

cellular events of eruption is colony stimulating factor one (CSF-1). When

these were injected into osteopetrotic (toothless) rats, the incisors erupted

(Ilizuka et al.; 1992) and injection of CSF-1 in normal rats lead to eruption of

first molars with increase in numbers of monocytes and osteoclasts (Cielinski

et al.; 1995).

A cascade of molecular signals is probably involved in stimulating the

expression of CSF-1 for the onset of eruption. In particular, interleukin-1

(1L-1 ) enhances the transcription of CSF-1 gene in rat dental follicle cells

(Wise and Lin; 1994). Immunolocalization studies have shown that 1L-1 is

present in the stellate reticulum (Wise et al.; 1995), the portion of enamel organ

that is immediately adjacent to the dental follicle. Thus the 1L-1 might diffuse

into the dental follicle to stimulate the dental follicle cells to express the CSF-1

gene.

The expression of the 1L-1 gene may be regulated by epidermal

growth factor (EGF). EGF, long known for its ability to stimulate precocious

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eruption of incisors in rodents (Cohen; 1962), also increases the amount of

1L-1 in the stellate reticulum following injection into rats (Wise et al.; 1995).

Another molecule that might be

involved in a cascade of signals leading to

tooth eruption is transforming growth

factor (TGF- 1). Like 1L-1 TGF 1

immunolocalizes to the stellate reticulum

and in vitro, its mRNA expression is

enhanced by incubation with EGF.

Because TGF- 1 is a chemoattractant

for monocytes, it is possible that TGF-

1 could enter the capillaries adjacent

to the dental follicle and attract monocytes

to the follicle.

Based on these above studies, a

hypothesis of the molecular events of tooth

eruption can be presented:

1. If EGF were the first signal there are at least three ways it could initiate

eruption.

2. If EGF were not required, however, eruption could begin with a signal

from TGF- 1.

3. Should EGF and TGF-1 both not be required, eruption could begin

with 1L-1 enhancing CSF-1 mRNA expression.

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IV. PATTERN OF ERUPTION OF TEETH

The teeth of the deciduous dentition begin to appear in the mouth at

about 6 months of age and the dentition is complete by 3 years. A majority of

the permanent teeth appear in the mouth between 6 and 12 years of age, during

this time teeth from both dentitions are present in the mouth, a phase known as

mixed dentition.

The teeth of both dentitions develop initially within the bones of the

jaws and have to move bodily through the jaws to reach the oral cavity by the

process of eruption. In addition, the deciduous teeth have to be shed or

exfoliated to make room for their permanent successors.

In the deciduous dentition, calcification of the crowns commences about

a month after the completion of cytodifferentiation of the tooth germ.

Calcification of all deciduous teeth begins before birth. Crown formation takes

about 6 months to complete and the tooth appears in the mouth some 6 months

after crown formation is achieved. When the teeth first appear, their roots are

incomplete and are not fully formed until 18 months later.

In the permanent dentition, the tooth germs are fully formed before birth

for all but the second and third molars. Crown formation begins at varying

times thereafter. In general, for the teeth of the permanent dentition, crown

formation takes 3 years and the teeth appear in the oral cavity about 3 years

after the crown is complete. Root completion is achieved about 3 years after

eruption.

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The sequence of eruption is an important aide memoire; the first

permanent molars erupt first at 6 years of age. The other teeth appear at

approximately yearly intervals corresponding to their sequence of eruption. If

the sequence and dates of eruption are remembered, the timing of other events

may be calculated by simple addition or subtraction.

Birth to Two Years

The permanent incisors and canines first develop lingual to the

deciduous tooth germs at the level of their occlusal surfaces and in the same

bony crypt. As their deciduous predecessors erupt, they move to a more apical

position and occupy their own bony crypts. First teeth to erupt are the

mandibular central incisors.

The usual eruption sequence in the primary dentition is as follows. First

the central incisors, followed in order by the lateral incisors, first molars,

canines and second molars. Mandibular teeth usually precede the maxillary

teeth. This sequence is not always followed.

Time of eruption is usually stated as 6 months of age for the maxillary

primary centrals, 7-8 months for the mandibular primary laterals and 8 or 9

months for the maxillary primary laterals. At about 1 year, the first primary

molars erupt. At around 16 months, the primary cuspids appear. Two years is

usually given as the age for the second primary molars to appear.

Two Years to Six Years

By two and a half years of age, the deciduous dentition is usually

complete and in full function. By three years of age, the roots of all deciduous

teeth are complete. First permanent molar crowns are fully developed and the

roots are starting to form. The crypts of the developing permanent second

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molars are now definite and can be seen in the space formerly occupied by the

developing first permanent molars.

Between three and six years of age, the development of the permanent

teeth continues, with the maxillary and mandibular incisor teeth more

advanced. From five to six years, just before the shedding of the deciduous

incisors, there are more teeth in the jaws than at any other time. Space is quite

critical within both the alveolar process and the deciduous dental arches

themselves. Developing permanent teeth are shifting close to the alveolar

border, the apices of the deciduous incisors are being resorbed; the first

permanent molars are about ready to erupt.

Very little bone exists between the permanent teeth and their crypts and

the “front line” of deciduous teeth. [A cross section of the maxilla and

mandible illustrates this remarkable phenomenon]. The complex interplay of

forces makes it imperative that the integrity of the dental arch be maintained at

this time. Loss of arch length through caries may make the difference between

normal occlusion and malocclusion. It does not take very much to upset the

delicate timetable of tooth formation, eruption and resorption within a viable

osseous medium.

Six Years to Ten Years

Between six and seven years of age, the first permanent molars erupt

into the mouth. As the upper and lower first permanent molars erupt, a pad of

tissue overlying them creates a premature contact. Proprioceptive response

conditions the patient against biting on this natural “bite opener” and thus the

deciduous teeth anterior to the first permanent molar area erupt, reducing the

overbite. About this time, the deciduous central incisors are lost and their

permanent successors start their eruptive path toward contact with the incisors

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of the opposing arch. Usually the mandibular central incisors erupt first,

followed by the maxillary permanent central incisors. These teeth frequently

erupt lingual to their deciduous counterparts and move forward under the

influence of tongue pressure as they erupt. The maxillary central incisors

appear as large bulges in the mucobuccal vestibule above the deciduous

incisors before they erupt.

Calendric age is even less

reliable as a bases for projection

of eruption of maxillary and

mandibular incisors. More

sophisticated research and the

accumulation of precise

developmental data from several

“growth centres” has indicated

that the physiologic age provides

a better yard stick. Those neat and

simplified “tooth eruption charts”

based on specific ages, posted in

schools, physicians offices etc.

with no indication of range,

standard deviation or standard

error provide little useful

information. By themselves, these

charts are often misleading and

can delude an inquiring parent

into a sense of false security.

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The period from eruption of the lateral incisors to the eruption of canine

is termed by Broadbent as the “ugly duckling stage”. It is an apt term, implying

an unaesthetic metamorphosis leading to an esthetic result. During this period

parents become worried. A space may develop between the maxillary central

crowns. The lateral crowns may flare. Frenums are often sacrificed in an effort

to remove the cause of the space between the centrals.

Actually, the crowns of the cuspids in the young jaw impinge as the

developing roots of the lateral incisors, driving the roots medially and causing

the crowns to flare laterally. The roots of the centrals are also forced towards

each other. As the laterals erupt further, narrower portions of their roots are in

proximity to the developing canines. Margolis has called the alveolar process

“the servant of the tooth”. At this stage the maxilla is bulging in the canine

region as the alveolar process develops around the forming canine. With the

further migration of the canine occlusally, with its servant the alveolar process,

the point of influence of the canine on the laterals shifts incisally so that

eventually, the lateral crowns are driven medially, also effecting closure of the

space between the centrals.

Eruption of the incisors is usually completed by eight and a half years of

age. Even though the central and lateral incisors erupt into the normal position,

root formation is not complete. The apices are wide open and do not close for

at least another year. Between nine and ten years of age, the apices in the

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deciduous canines and molars begin to resorb. Individual variation is great

here. Girls are usually a year to a year and a half ahead of boys.

After Ten Years

Between 10 and 12 years of age, there is considerable variability in the

sequence of eruption of the canines and premolars. In about half the cases, the

mandibular canines erupt ahead of the mandibular first and second premolars.

In the maxilla, the first premolar usually erupts before the canine. The first

premolar usually erupts before the canine. The maxillary second premolar and

the maxillary canine erupt at about the same time. At times, deciduous teeth are

retained beyond the time that they should normally be shed. A good rule of

thumb is to try and maintain the left and right sides on approximately the same

schedule. If the upper left deciduous molar is lost naturally and the upper right

first deciduous molar is still firm, radiographic evidence may show that the

mesial or distal root has not resorbed properly. It is then advisable to assist the

removal of the tooth.

Eruption of the second molar teeth usually occur shortly after the

appearance of the second premolars. Since the second premolar and second

molar teeth show the greatest variability in order of eruption of any of the teeth

(third molars excepted), the second molar teeth may be expected to erupt

before the second premolar teeth in 17% of cases in Caucasians.

Both maxillary and mandibular second molars erupt at about the same

time. Here again, we are confronted with the raising of the bite that is the

gingival pads overlying the upper second molars contact prematurely, blocking

open the bite anteriorly allowing eruption of teeth anterior to second molar, for

a couple of weeks.

23

If the second molars exfoliate before the second premolars, occasionally

the first permanent molars may tip to the mesial. This is especially true in

patients with premature loss of second deciduous molars. If the molars are

tipped mesially, the eruption of the second premolar is further delayed, it may

erupt lingually or may not erupt at all.

Radiographs taken shortly after

eruption of second molar teeth often show

an image of the developing third molar

teeth that are difficult to interpret. This is

especially true of the mandibular third

molars. Since the alveolar process curves

lingually at the point of juncture with the

anterior border of the ramus, the 3rd

molars (which are seen to be in the ramus

but actually present lingual to the ramus)

may erupt lingually. Although maxillary

second molars erupt in a downward and

forward direction, the maxillary third

molars erupt downward and backwards.

To this might be added the term

‘outward’. It is not possible to estimate a

definite time of eruption of third molars.

Hume estimates the median time of

eruption of 20.5 yrs. Eruption of 3rd

molars is seen more rapidly in girls than

in boys. By 20 yrs of age must females

have their 3rd molars if they have going to

have them. This is not true for males.

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It is easy to understand that problems arise frequently in the third molar

area considering the initial deficiency in arch length, the tendencies for the

maxillary and mandibular molars to bypass each other, their varying axial

inclination and the unpredictable timing of eruption of these teeth. The 3rd

molar problem can be not only be a painful experience but can cause functional

disturbance which can affect longevity of the dentition and create and

aggravate TMJ pathology.

Chronology of the human dentitionTeeth Hard tissue

formation beginsAmount of enamel

formed at birthEnamel

completedEruption Root

completedDeciduous dentitionMaxillaryCentral incisorLateral incisor Cuspid First molarSecond molar

MandibularCentral incisorLateral incisorCuspidFirst molarSecond molar

Permanent dentitionMaxillaryCentral incisorLateral incisor Cuspid First bicuspidSecond bicuspidFirst molarSecond molarThird molar

MandibularCentral incisorLateral incisor Cuspid First bicuspidSecond bicuspidFirst molarSecond molarThird molar

4 mo in utero4 ½ mo in utero5 mo in utero5 mo in utero6 mo in utero

4 ½ mo in utero4 ½ mo in utero5 mo in utero5 mo in utero6 mo in utero

3-4 mo10-12 mo4-5 mo1 ½ - 1 ¼ yr2-2 ¼ yrAt birth 2 ½ - 3 yr7-9 yr

3-4 mo3-4 mo4-5 mo1 ¼-2 yr2 ¼ - 1 ½ yrAt birth2 ½-3 yr8-10 yr

Five sixthsTwo thirdsOne thirdCusps unitedCusp tips still isolated

Three fifthsThree fifthsOne thirdCusps unitedCusp tips still isolated

Sometimes a trace

Sometimes a trace

1 ½ mo2 ½ mo9 mo6 mo11 mo

2 ½ mo3 mo9 mo5 ½ mo10 mo

4-5 yr4-5 yr6-7 yr5-6 yr6-7 yr2 ½ - 3 yr7-8 yr12-16 yr

4-5 yr4-5 yr6-7 yr5-6 yr6-7 yr2 ½-3 yr7-8 yr12-16 yr

7 ½ mo9 mo18 mo14 mo24 mo

6 mo7 mo16 mo12 mo20 mo

7-8 yr8-9 yr11-12 yr10-11 yr10-12 yr6-7 yr12-13 yr17-21 yr

6-7 yr7-8 yr9-10 yr10-12 yr11-12 yr6-7 yr11-13 yr17-21 yr

1 ½ yr2 yr3 ¼ yr2 ½ yr3 yr

1 ½ yr1 ½ yr3 ¼ yr2 ¼ yr3 yr

10 yr11 yr13-15 yr12-13 yr12-14 yr9-10 yr14-16 yr18-25 yr

9 yr10 yr12-14 yr12-13 yr13-14 yr9-10 yr14-15 yr18-25 yr

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V. ACTIVE AND PASSIVE ERUPTION

According to the concept of continuous eruption (Orbans, Gottlieb J.

Dent. Res. 13 ; 214 ; 1933), eruption does not cease when the teeth meet their

functional antagonists but continues throughout life. It consists of an active and

passive phase.

Active eruption – is the movement of the teeth in the direction of the occlusal

plane.

Passive eruption – is the exposure of the teeth by the apical migration of the

gingiva.

This concept distinguishes between the:

Anatomic crown - the portion of the tooth covered by enamel.

Anatomic root - the portion of tooth covered by cementum.

Clinical crown - the part of the tooth that has been derived of its gingiva and

projects into the oral cavity.

Clinical root - that portion of the tooth covered by periodontal tissues.

When the teeth reach their functional antagonists, the gingival sulcus

and junctional epithelium are still on the enamel, and the clinical crown is

approximately two thirds of the anatomic crown.

Active and passive eruption were believed by Gottlieb to proceed

together. Active eruption is coordinated with attrition. The teeth erupt to

compensate for tooth substance worn away by attrition. Attrition reduces the

clinical crown and prevents it from being disproportionately long in relation to

the clinical root, thus avoiding excess leverage in the periodontal tissues.

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Ideally, the rate of active eruption keeps pace with tooth wear, preserving the

vertical dimension of the dentition.

As the teeth erupt, cementum is deposited at the apices and furcations of

the roots, and bone is formed along the fundus of the alveolus and at the crest

of the alveolar bone.

In this way, part of the tooth substance lost by attrition is replaced by

lengthening of the root and socket depth is maintained to support the root.

Passive eruption is divided

into four stages. Although this

was originally thought to be a

normal physiologic process, it is

currently considered a pathologic

process.

1. Stage one: The teeth reach the line of occlusion. The junctional

epithelium and the base of the gingival sulcus are one the

enamel.

2. Stage two: The junctional epithelium proliferates so that part is on

the enamel. The base of the sulcus is still on the enamel.

3. Stage three: The entire junctional epithelium is on the cementum, and

the base of the sulcus is at the cementoenamel junction.

As the junctional epithelium proliferates from the crown

onto the root, it remains at the CEJ no longer than any

other area on the tooth.

4. Stage four: The junctional epithelium has proliferated further on the

cementum. The base of the sulcus is on the cementum, a

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portion of which is exposed. Proliferation of the

junctional epithelium onto the root is accompanied by

degeneration of gingival and periodontal ligament fibres

and thin detachment from the tooth. The cause of this

degeneration is not understood. At present however, it is

believed to be the result of chronic inflammation and

therefore a pathologic process.

The distance between the apical end of the junctional epithelium and the

crest of the alveolus remains constant throughout continuous tooth eruption

(1.07mm).

Exposure of the tooth by the apical migration of the gingiva is called

gingival recession or atrophy. According to the concept of continuous eruption,

the gingival sulcus may be located on the crown, CEJ, or root depending on the

age of the patient and the stage of eruption. Therefore some root exposure with

age is considered normal and referred to as physiologic recession. As

mentioned previously, this concept is not accepted at present. Excessive

exposure is termed pathologic recession.

VI. SHEDDING OF DECIDUOUS TEETH

The physiologic process resulting in the elimination of the deciduous

dentition is called shedding or exfoliation. The eruptive pathway of the

permanent teeth is very much related to the shedding or exfoliation of the

deciduous teeth as pressure from the erupting successional tooth helps to

determine the pattern of deciduous tooth resorption.

Shedding of teeth can occur due to two factors:

1) Odontoclasts.

28

The resorption of the hard tissues of the tooth is achieved by cells that

have an identical histology to osteoclasts but which, because they are involved

in the removal of dental tissue, are sometimes called odontoclasts. The

odontoclasts are capable of resorbing all dental hard tissues, including enamel,

but it is most commonly found on the surface of roots, where it resorbs

cementum and dentin. It is also found on occasion within the pulp chamber,

resorbing coronal dentin. This variation in the pattern of the deciduous tooth

resorption depends very much on the position of the successional tooth in

relation to the deciduous tooth. Thus, since the permanent incisors and canine

develop lingually to the deciduous teeth and erupt in an occlusal and vestibular

direction, resorption occurs at the lingual surface of the root and the tooth is

shed with much of its pulp chamber intact. Permanent premolars, however,

develop between the divergent roots of the deciduous molars and erupt in an

occlusal direction. Hence the resorption of the with interradicular dentin occurs

with the resorption of the pulp chamber and coronal dentin.

While little is known about resorption of the dental hard tissues, even

less is known about the resorption of the soft tissues associated with them; such

as dental pulp and periodontal ligament.

Simple observation of histological sections shows that the loss of

periodontal ligament is abrupt. Electron microscopic examination confirms this

finding and also shows that cell death occurs in this region in the absence of

inflammation.

2) Pressure

Obviously, pressure from the erupting successional tooth plays a role in

the shedding of the deciduous dentition. For instance, if a successional tooth

germ is congenitally missing or occupies an aberrant position in the jaw,

29

shedding of the deciduous tooth is delayed. Yet the tooth is eventually shed.

Growth of the jaws and also the muscles of mastication also aid in resorption of

deciduous teeth.

Pattern of shedding

It has been seen that the pattern of exfoliation is symmetrical for the

right and left sides of the mouth. Girls exfoliate their teeth before boys. The

greatest discrepancy between the sexes is observed for the mandibular canines,

the least for the maxillary central incisors.

Clinically it has been noticed that human deciduous teeth are shed with

little bleeding, when the teeth naturally exfoliate. Immediately after teeth are

shed, stratified squamous epithelium present in the dentogingival junction

(DGJ) and gingiva were found in the underlying tissue indicating that DGJ

epithelium and gingival epithelium play an important role in the process of

exfoliation. Furthermore, wound healing after exfoliation is usually more rapid

than after eruption. A study by N. Sahara et al. showed migration appeared to

be further stimulated as a result of chronic inflammation by microorganisms

present adjacent to the DGJ. The most interesting finding of the study was the

evidence of the stratified squamous epithelium of the DGJ and gingiva

proliferated and migrated towards the inside of the crown and eventually ended

up under the deciduous crown.

VII. CLINICAL SIGNIFICANCE

1. Caries during Tooth Eruption (Particularly in First Molars)

Caries is a disease with many causal factors. It is known to occur very

often in the occlusal surfaces of the first molars. The risk of caries is highest

during the first two years after the eruption of the first molars (i.e. the first

30

molars’ first two years), which roughly corresponds to the one to three year

period during which the first molars complete their eruption.

Survey studies revealed that, during the first 12 months after the first

molars had started erupting, caries was found on 6% of the maxillary first

molars and almost 20% of the mandibular first molars. During the first 24

months this percentage jumped to 37% of the maxillary first molars and 62% of

mandibular first molars.

The four major types of caries causal factors are:

a. The susceptible tooth.

b. Cariogenic bacteria in plaque.

c. Substrates.

d. Time (long term accumulation of plaque etc.)

Let us briefly examine each of these 4 factors:

a. Susceptible tooth : susceptibility to caries is largely determined by

hereditary and environmental factors, and in the first molars is also

caused by such anatomical factors as the large occlusal surface and the

numerous deep sulci, grooves and fissures. In addition, a long period is

required for eruption and during this period, the tooth substance is still

young.

b. Cariogenic bacteria are also part of oral microbiota. Cariogenic bacteria

known to the present time are Streptococcus Mutans, Streptococcus

Sanguis, Lactobacillus Acidophilus, Actinomyces Viscosus and

Actinomyces Naeslundii.

31

c. Substrate (glucides) : adherence of plaque to teeth is a natural

consequence of the teeths’ role in eating.

d. Time : two temporal factors contribute to tooth decay. These are:

i. the time since eruption in which the teeth lay exposed in the mouth.

ii. the period of time that elapses before the plaque is removed.

Therefore, the environment most conducive to rapid outbreak of caries is

that found during the first molars eruption period.

However, when just about two thirds of occlusal surface has erupted, in

the 1st and 2nd molars, although gingiva still covers the crown edges which

makes them extremely conducive to decay and difficult to clean. Caries occur

quite easily during this stage and utmost caution must be taken to achieve

adequate oral hygiene. This can be achieved by fluoride treatment and use of

molar brushes.

It is also common for caries in primary second molars and in

neighbouring primary teeth, to spread to the permanent first molar, which then

leads to problems in the entire permanent dental arch. Therefore, it is very

important to protect the primary teeth from caries thereby allowing the

permanent to develop and erupt normally.

2. It is evident that the principal supporting tissue of the tooth, the periodontal

ligament and the bone of the jaw, possess a remarkable plasticity that

enable the tooth to react favourably or unfavourably to its immediate

environment. This plasticity of the supporting tissue is used by the

orthodontist to achieve a favourable clinical response. By applying forces

to the tooth and by relying on the biologic responses of bone and

periodontal ligament, malalignment of teeth can often be corrected.

32

3. Sometimes when trauma occurs to the tooth especially permanent

anteriors, before the root formation is complete, it results in the formation

of blunderbuss canals. At this time endodontic therapy namely

apexification or apexogenesis is advocated to stimulate completion form of

root apex.

4. Premature eruption of teeth occurs infrequently. Sometimes, infants are

born with “erupted” lower central incisors, but this is an example of gross

maldevelopment. Such teeth need to be extracted as soon as possible

because they prevent suckling. Premature loss of a deciduous tooth without

closure of the gap may lead to early eruption of its successor.

5. Far more common, however is the occurrence of delayed or retarded

eruption. This may be caused by localized or systemic factors. Systemic

factors include nutritional, genetic and endocrine deficiencies. Local

factors include, such situations as loss of a deciduous tooth and drifting of

opposing teeth to block eruptive pathways. Severe trauma may eliminate

the dental follicle and hence periodontal ligament formation is prevented.

When this happens, the bone of the jaw fuses with the tooth, a condition

known as ankylosis, and eruption is not possible.

6. Whites exhibit an evolutionary trend to a diminution in the size of the

jaws. This trend has not been accompanied by a corresponding decrease in

size of teeth and as a result crowding is a common occurrence. The third

molars are the last teeth to erupt and frequently all the available space has

been used. And as a result teeth become impacted. Canines are also often

impacted because of their late eruption time.

7. Finally, it has been shown that the moment a tooth breaks through the

oral epithelium, an acute inflammatory response occurs in the connective

33

tissue adjacent to the tooth. This is seen even in the germ-free animals and

is seen in varying degrees around all teeth throughout life. Clinically, as

teeth break through the oral mucosa, there is often some pain, slight fever

and general malaise, all signs of an inflammatory process. In infants, these

symptoms are popularly called “teething”.

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VIII. SUMMARY & CONCLUSION

The mechanism of tooth eruption is an enigma which has perplexed

many investigators. It is a process that has been the subject of scientific enquiry

since 1778 when Hunter attributed the mechanism to root elongation. Recent

reviews have concluded that there is no simple explanation for this biological

phenomenon which is not surprising since most teeth erupt during periods of

active craniofacial growth and therefore eruption should be considered as part

of a multifactorial event. Furthermore, some evidence suggests that different

mechanisms operate during various stages of eruption and for teeth which have

limited or continuous growth. Recent advances in biochemistry, immunology

and structural and molecular biology have renewed interest in understanding

the mechanisms of bone remodeling and tooth eruption because it is now

possible to localize and determine the activity of cytokines, membrane

receptors, signal transduction molecules and post activation intracellular

events.

IX. REFERENCES

1. Eruption of Permanent Teeth – A Colour Atlas – Sadakatsu Sato and

Patricia Parsons (Ishiyaku Euro America Inc.).

2. Oral Histology – A.R. Ten Cate, Mosby Publications (3rd edition).

3. Orban’s Oral Histology and Embryology – Mosby Publications

(10th edition).

4. Principles of Anatomy and Oral Anatomy for Dental Students – M.E.

Atkinson and F.H. White (1st edition) Churchill Livingstone

Publishers.

35

5. Orthodontics, Principles and Practice - T.M. Graber (3rd edition)

W.B. Saunders Publication.

6. Clinical Periodontology - Carranza and Newman (8 th edition)

W.B. Saunders Publication.

Journals

1. Mechanism of tooth eruption – T.B. Kandos.

B.D.J. Vol. 181, No. 3 Aug. 10 : 1996 (91-95).

2. Tooth eruption and orthodontic movements – J.R. Sandy.

B.D.J. Vol 172, No. 4 : Feb 22, 1992 (141-149).

The Molecular Biology of Initiation of Tooth Eruption - G.E. Wise and

F Lin.

J. Dent. Res. 74 (1) : 303-306 Jan 95.

3. A Histologic study of the Exfoliation of Human Deciduous Teeth –

N. Sahara, N. Okafuji, Y. Ashizawa and K. Suzuki.

J. Dent. Res. 72 (3) : 634-640, March 93.

36