Karim abdelhamid mahmoud
Mechanism of tooth eruption
Tooth eruption is traditionally considered to be a developmental process whereby the tooth
moves in an axial direction from its location within the alveolar crypt of the jaw into a functional
position within the oral cavity.
Tooth eruption is a more general process, however, which includes certain posteruptive tooth
movements. These movements following eruption 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, and
(3) those made to accommodate interproximal wear.
This article examines the possible mechanisms of tooth eruption. Remarkably, for so basic a
process, the mechanisms of tooth eruption are not well understood. Numerous theories of
tooth eruption have been proposed. These theories have involved almost all of the tissues in or
near an erupting tooth. None of the theories can alone account for all of the movements made
by a tooth during its lifetime. In order to be clinically valid, a theory of tooth eruption must
accommodate the following observations about the eruptive process:
(1) teeth are moved in three dimensions of space,
(2) teeth arrive at a functional position that is heritable, and
(3) teeth erupt at varying, characteristic stage-specific speeds.
First we will briefly review theories that are not serious contenders to satisfactorily explain
1. Vascular pressure and blood vessel thrust. It is known that the teeth move in their sockets in
synchrony with the arterial pulse, so local volume changes can produce limited tooth
movement. Furthermore, spontaneous changes in blood pressure have been shown to influence
eruptive behavior. Ground substance can swell from 30% to 50% by retaining additional water,
so this to could create pressure. But since surgical excision of the growing root and associated
tissues eliminates the periapical vasculature without stopping eruption, this means that the
local vessels are not absolutely necessary for tooth eruption.
2. Pulpal pressure and pulpal growth. This theory says that the force exerted by the growth of
cells is the result of multiplication of cells--analogous to the roots of a growing plant forcing
pebbles aside. Yet, when a developing tooth is surgically removed and replaced by a silicone
replica, that replica will erupt provided that the dental follicle is retained.
3. Traction by periodontal fibroblasts. Administration of lathyrogens show no disruption of the
eruption of teeth in experimental animals. Lathryogens are drugs that specifically inhibit the
formation of collagen crosslinks. The implication is that the eruptive force is unlikely to involve a
tractional element that pulls the tooth toward the oral cavity.
In this next section, we review the theories that provide the most convincing data to explain
tooth eruption in man and other mammalian species. These should be seriously considered.
1. Root elongation. Root formation would appear to be the obvious cause of tooth eruption
since it undoubtedly causes an overall increase in the length of the tooth along with the crown
moving occlusally. Yet, clinical observation, experimental studies, and histologic analysis argue
strongly against such a conclusion. Remarkably, rootless teeth do erupt. This is most obvious in
cases of dentin dysplasia Type I and following irradiation. Some teeth erupt a greater distance
than the total length of their roots, and teeth will still erupt after the completion of root
formation or when the tissues forming the root--the apical papilla, Hertwig's epithelial root
sheath, and periapical tissue--are surgically removed.
2. Alveolar bone remodeling. Alveolar bone growth, tooth development, and eruption of the
teeth are interdependent. It is observed that the alveolar process forms during tooth
development and is locally deficient in sites where primary or permanent teeth fail to develop.
Similarly, alveolar bone loss is a consistent clinical finding in the edentulous patient.
Formation of bone apical to developing teeth has long been proposed as one mechanism for
eruption. There is no doubt that bone forms in these sites, but bone formation per se is not
sufficient for tooth eruption. A good example to illustrate this is the presence of an unerupted
dentition in osteopetrotic mutation in which bone formation is nearly normal or elevated and
bone resorption greatly reduced. Osteopetrosis, sometimes called 'marble bones' is
disseminated condensing osteopathy, a genetic disorder marked by bone sclerosis or defective
skeletal remodeling. The same applies for cases of cleidocranial dysotosis in which deciduous
teeth erupt and persist while permanent teeth erupt late or ectopically. Cleidocranial dysotosis
is a familial disease characterized by abnormalities of the skull, teeth, and jaws.
Alveolar bone growth involving turnover (resorption and formation) is required during tooth
eruption. Bone resorption and bone formation are polarized around erupting teeth. These
metabolic events depend upon the adjacent parts of the dental follicle. Thus, it appears that
tooth eruption is a localized, bilaterally symmetrical event in alveolar bone that is regulated by
the dental follicle proper, a derivative of cranial ectomesenchyme (neural crest).
The strengths of this theory lie in explanations for the early events of tooth eruption since part
of the follicle is lost after mucosal penetration. Nevertheless, the periodontal ligament,
cementum, and alveolar bone proper are derivatives in part of the follicle, so that later events
could be controlled by these and other related tissues. Then dental follicle proper is the thin,
dense, ectomesenchymeal connective tissue investment of a developing tooth which surrounds
the enamel organ.
The fact that active eruption begins only after crown formation is complete suggests a role also
for the enamel organ and its proteases in the early signaling of eruption. In addition, the
proximity of the enamel organ and the dental follicle and their tight adherence in surgical
manipulations indicate that many effects attributed above to the dental follicle proper may
indeed be events initiated or controlled by the enamel organ or the reduced enamel epithelium.
If this is the case, tooth eruption may be yet another example of collaborative epithelialmesenchymal interactions in development.
3. Periodontal ligament. Formation and renewal of the periodontal ligament is associated with
the continuous eruption of permanently growing rodent incisors. (Note well: continuously
growing rat incisors are different than human teeth that have a limited period of growth.)
For teeth with a limited period of growth, the presence of a periodontal ligament does not
assure eruption. In the case of osteopetrotic mutations, a periodontal ligament is present, but
teeth do not erupt. Therefore, the periodontal ligament cannot be essential for tooth eruption
in man. Its role has been largely overstated due to experiments performed on continuously
erupting rodent teeth.
II. Clinical and Experimental Data on Tooth Eruption
Developing teeth must erupt through diverse mineralized and unmineralized connective tissues.
This movement requires resorption of bone, and often roots of primary teeth, in the direction of
movement and formation of bone and roots in the opposite direction. The height of the alveolar
process increases during eruption, and there are regional differences in the rates of growth
during this period.
In 1944 Carlson published a comprehensive radiographic analysis of the eruption of different
types of permanent teeth. He showed that for the human permanent premolars:
1) eruption begins only after crown formation in complete,
2) root formation occurs initially at the expense of basal bone without movement of the crown,
3) most root growth occurs during the stage of rapid preocclusal eruption to the occlusal plane,
4) the completion of the root, like its initial growth, is at the expense of basal bone, and
5) teeth continue to erupt slowly or move with growth of the alveolar process throughout life.
Use of metallic implants on facial bones to serve as fixed reference points studied in a series of
sequential radiographs has shown that differential growth of the jaws produced a rotation
around a center in their anterior part. Remodeling of the inferior border of the mandible
obscured much of this differential growth in jaws traced without internal reference points.
These positional changes of the jaws during the period of tooth eruption mean that most
erupting teeth must fit into a rotating occlusal plane while moving between and amongst their
neighbors. With this formidable complexity. one is hardly surprised that tooth eruption is
III. Preeruptive Movements of Developing Teeth
During crown development, small preeruptive random movements of the forming tooth do
occur. Whether they are mediated by the follicular events accompanying eruption or reflect
regional differences in the growth and maturation of the jaws is not known. At any rate, these
small movements of the developing crown are local and are not in the direction of eruption.
Premolar tooth germs develop initially lingual to the crowns of the primary molars. Later, when
the primary molars erupt, they move labially to grow and erupt in the interradicular space of
IV. The Interosseous Stage of Eruption
All teeth develop within the alveolar bone of the jaws. The challenge of the intraosseous stage
of tooth eruption is to escape from the bone surrounding the crown and to redirect the growth
of the alveolar bone proper to surround and support a developing root. The former involves
bone resorption and the latter bone formation on opposite sides of the erupting tooth. These
activities have been shown to depend upon the adjacent parts of the true dental follicle.
Studies in nonhuman primates have shown that rootless teeth can erupt and that the follicle is
important in eruption. Damage to the follicle was the most reliable predictor of failed eruption
in transplantation studies.
In periods of rapid root growth, bone formation occurs primarily in furcation areas. Bone growth
in the apical region occurs only if root growth is not fast enough to keep up with eruption. The
rate of eruption is the rate of formation of the eruption pathway and its coordination with bone
formation in selected areas of the crypt and the alveolar crest. Since rootless teeth can erupt,
foot formation is not considered the prime mover in tooth eruption.
Movement of the tooth through bone requires a coordinated resorption and formation of bone,
that this process can be plastic, and asymmetrical to accommodate root growth and tooth drift,
and that these metabolic events likely begin in the enamel epithelia and are continued and
coordinated by the dental follicle.
V. Mucosal Penetration and Preocclusal Eruption
Formation of the eruption pathway is completed soon after the cusps reach the alveolar crest.
At this point, the rate of eruption accelerates. As the erupting tooth approaches the surface
epithelium, there is a thickening and transformation of the enamel epithelium and fusion with
the oral epithelium.
A major accomplishment of mucosal penetration is formation of the junctional epithelium on
the tooth surface. The epithelial attachment (to the mineralized tooth surface) is continually
renewed over the tooth surface during eruption.
Preocclusal eruption from gingival emergence to the occlusal plane is accomplished by root
growth and formation of bone at the base of the crypt. Since the alveolar crest is itself growing
in height, the tooth must overtake this growth and continue eruption.
VI. Eruption at the Occlusal Plane
Once the occlusal plane is approached, tooth eruption slows dramatically but continues at a
slow pace through the fifth decade of life. Eruption to the occlusal plane is accomplished by root
growth and formation of bone at the base of the crypt and/or alveolar septa. Teeth continue to
erupt through later decades, and occlusal wear may be in part compensated for by cemental
apposition. The position of the alveolar crest appears to be constant in relation to the tooth,
though obscured by periodontal bone loss.
VII. Speeds of Tooth Eruption
Erupting teeth move at different speeds at different times. Initially, eruption is slow in bone. If
there are prolonged delays, ankylosis of tooth to bone can result. The rate of eruption increases
as the tooth is released from bone, penetrates the mucosa, and becomes very slow as it
approaches the occlusal plane. These shifts in speed are also seen in root formation. It is fast at
first, slows as the apical foramen narrows, and is very slow thereafter.
VIII. Basic Principles in Tooth Eruption
Active tooth eruption begins in an interosseous environment. Bone resorption, necessary for
eruption, is regulated by the dental follicle. Like bone resorption, alveolar bone formation
associated with tooth eruption depends upon the dental follicle and is associated with high cell
proliferation. The basic principles of tooth eruption can be summarized as follows:
(1) Any region of a dental follicle has the potential for initiating and regulating bone resorption
and bone formation or for not influencing bone metabolism.
(2) Movement of teeth during eruption consists of preparing a path through bone or soft tissues
and moving them along this path. There is a failure of eruption when an eruption pathway has
not been formed.
(3) Root formation is accomodated during tooth eruption and is a consequence, not a cause of
(4) Bone formation and root formation move an erupting tooth through the oral epithelium and
into its position within the dental arch at the occlusal plane. It is unlikely that the periodontal
ligament contributes substantially to eruption, but may have a role late in the process. Bone
formation and possibly formation of apical cementum maintain a slow eruptive movement
throughout the life of the tooth.
The key to the successful clinical management of tooth eruption consists of understanding that
this process consists largely of the local regulation of alveolar bone metabolism to produce bone
resorption in the direction of eruption and shift and formation of bone at the opposite side. Our
ability to selectively and discretely affect these process at present is limited and includes the
local stimulation by extraction of a primary tooth or surgical removal of bone and assisting
mucosal penetration by incising the gingiva. More understanding of the molecular basis may
offer new clinical options in the future.