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Tooth Eruption

Tooth Eruption
Tooth eruption and the shedding of primary teeth are important events in the life of a child, and teething
in very young children often results in slight increases in temperature, generally less than 0.2 F.,
irritability etc. However, high fever or other signs of illness should never be assumed to be related to
tooth eruption. In the middle of the 19th century, teething was considered one of the leading causes of
childhood mortality, simply because of the coincidence of severe childhood illnesses, such as
diphtheria, with the onset of tooth eruption.
There is a predictable pattern to the eruption of teeth. With a few exceptions, tooth eruption begins in
the anterior and proceeds posteriorly, and mandibular teeth appear before their maxillary counterparts.
More importantly there is a fairly predictable timing to the sequence of eruption. This has had
considerable significance for determining both the age at which children could be employed in the 18th
and 19th centuries, and unfortunately in our time, for forensic medicine. While the timing of tooth
eruption is predictable, the is considerable variability. For example, the normal age of eruption for the
primary central incisors is usually given as 6 months of age, but it is perfectly normal for eruption to
occur as early as 3 months and as late as 12 months after birth. Dental age may be assessed clinically
by visually determining the number of teeth present, but a radiographic assessment of both the stages
of crown and root development, as well as the stages of eruption, is much more reliable
How you go about remembering the sequence and timing of eruption (and shedding of primary teeth) is
up to you, but here are some rules of thumb that I use to help me.
1. The primary teeth begin to erupt between the ages of 4 and 8 months, and every 4-6 months
thereafter 4 more teeth will have emerged. All the primary teeth will have erupted by about 2
years of age.
2. In the case of permanent teeth, the time between the beginning of crown formation, i.e. the
apposition of enamel and dentin, and the emergence of the tooth into the oral cavity is about 5 to
6 years.
3. With the exception of the 3rd molars, eruption of permanent teeth begins about age 7 and the
mixed dentition phase is finished between the ages of 12 and 14 years.
4. 1st primary molars erupt before primary canines.
5. 6 year (1st permanent) and 12 year (2nd permanent) molars explain themselves.
6. Maxillary 1st premolars erupt shortly before mandibular 1st premolar well before maxillary
Abnormalities of eruption can occur, and these include delayed eruption, ectopic eruption and
impaction. In addition, other clinical conditions (early loss of a primary tooth, hypo- and hyperdontia, lack
of space) all must be dealt with in the context of tooth eruption.

Active versus Passive Eruption

Active Eruption
Active eruption is defined as the bodily movement of a tooth from its site of development to its functional
position in the oral cavity. Although tooth eruption is traditionally though of as a tooth moving in an axial
direction from its position within a bony crypt of alveolar bone to its final place in functional occlusion,
eruption is in fact a life long process. Further, teeth erupt in three-dimensions (due to the growth of the
jaws) and at varying speeds. The rate of eruption also depends on the balance of forces that tend to
move the tooth axially, or to impede that movement.

Prior to emergence the rate of eruption may be quite slow, and it may take 2-4 years for a tooth

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to reach the oral cavity.

Upon entering the oral cavity, however, the rate of movement can be very rapid (~ 1mm per
month). Nevertheless, it may take the tooth 1-2 years to fully reach the occlusal plane.
Finally, the forces imposed by contact with opposing teeth dramatically slow the rate of
movement (compensatory eruption related to attrition).

The process of eruption can be divided into five stages:


Preeruptive movements -- movements prior to completion of the crown

Intraosseous eruption -- formation of an eruption pathway through the bone
Mucosal penetration -- formation of primary junctional epithelium
Preocclusal eruption -- post-emergence prior to reaching functional occlusion
Postocclusal eruption -- occurs thoughout the life of the tooth

Passive Eruption
In contrast to active eruption, passive eruption is the apparent lengthening of the crown due to the loss
of attachment, or recession of the gingiva. In most adults both active and passive eruption occur to
some extent, and the active eruption is compensated for in part by the addition of alveolar bone at the
crest of the alveolar bone and at the base of the socket, and by the deposition of cementum on the root

Non-Eruptive Tooth Movement

Other movements also occur, and the most important one is mesial drift, which compensates for
interproximal wear. The forces that lead to mesial drift include:
1. Contraction of the transeptal ligament
2. Anterior component of occlusal forces
3. Soft tissue pressure generated by the cheeks and tongue.

Theories of tooth eruption

No one theory of how the forces might be generated to cause tooth movement has been put forward
that can account for all aspects of eruption. Nevertheless, available data demonstrate that the
mechanism of eruption is 1) a property of the periodontal ligament or its developmental precursor, the
dental follicle and 2) is probably multifactorial in that more than one mechanism may be involved. The
leading candidate theories include:
1. Root elongation
The major support for the theory of tooth movement involving root growth is that the intraosseous
phase of eruption does not begin until root formation has begun. In addition, the root is only 2/3
formed at the time of emergence into the oral cavity. However, rootless teeth do erupt and the
length of the eruption pathway taken by some teeth is longer than the root itself. This theory also
requires that the bone at the base of the alveolar crypt be more stable (resistant to pressure
resorption) that the overlying bone or primary tooth. However, once the eruption pathway has
been formed, the resistance to movement is presumably reduced and root growth may play a
2. Alveolar bone remodeling
The remodeling of alveolar bone (resorption 'above' and apposition 'below') has received
considerable attention. The cells of dental follicle and the reduced enamel epithelium interact to
recruit monocytes that differentiate into osteoclasts. These osteoclasts then function to form the
eruption pathway.

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Several lines of evidence support this primary role of the dental follicle in tooth eruption. First,
artificial teeth will erupt if placed within a dental follicle. Second, damage to the dental follicle will
arrest eruption. Finally, experimental animals in which osteoclast differentiation or function is
defective exhibit delayed eruption. In contrast, little data is available to demonstrate how the
compensatory apposition of bone at the base of the crypt may be regulated.
For permanent anterioir teeth, the role of the dental follicle may be to simply widen a pre-existing
eruption pathway. Unlike all the primary teeth and all the other permanent teeth, the developing
toothbuds for the incisors maintain their connection to the oral mucosa via a band of connective
tissue (gubernacular cord) that connects of the dental follicle and the lamina propria via the
gubernacular canal.
3. Periodontal ligament formation and renewal
The third major theory of tooth eruption involves the periodontal ligament, and two separate
mechanisms have been proposed. The first is dependent on the constant turnover (remodeling)
of collagen fibers in the ligament. During maturation, collagen fibers 'shrink' in length by about
10%. Because of the orientation of these oblique collagen fibers, the vector of force generated in
aggregate is directed occlusally.
The second mechanism involves a small, but measurable, contractile force that can be
generated by fibroblasts. Fibroblasts are the most numerous cell type in the periodontal ligament,
and they can "attach" to collagen type I fibers via fibronectin and integrins. The difficulty with the
periodontal ligament theory is that the periodontal ligament does not become highly organized
until after the tooth begins to come into functional occlusion. Therefore, the periodontal ligament
theory is unlikely to explain either the intraosseous or mucosal phases of eruption.
4. Periodontal ligament hydrostatic pressure
One final theory of tooth eruption has been proposed, which involves periodontal/tissue vascular
pressure. This theory requires that eruptive movements are maintained by pressure differentials
along the periodontal ligament space, and that periodontal tissue pressures are high. Support for
this mechanism includes 1) the predictable effects of vasoactive drugs on eruption behavior, 2)
the distribution of fenestrations in alveolar bone proper (greater number at the base) and 3)
changes in the number of fenestrations during different phases of eruption.

Formation of primary junctional epithelium

As the tooth nears the oral mucosa, or as the resorption of the roots of the primary teeth is nearly
complete, the reduced enamel epithelium plays the last role in the life history of the enamel organ. It
forms the primary junctional epithelium by fusing with the basal layer of the oral epithelium. The
epithelium overlying the enamel crown undergoes apoptosis and is lost. This leaves the occlusal surface
exposed to the oral cavity, but the lateral surfaces of the enamel remain covered by a tightly adherent
layer of cells. Thus a biological seal is formed that prevents bacteria and food debris from entering the
connective tissue space. In the case of permanent teeth replacing their deciduous precursors, the
junctional epithelium of the primary tooth proliferates apically to merge with the reduced enamel

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