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Development and eruption of the

teeth

Dr: Abdullah Sharaf


Introduction
• An accurate chronology of primary and
permanent teeth calcification is of clinical
significance to the dentist.
• It is often necessary to explain to parents the
time sequence of calcification in utero and
during infancy.
• The common observations of tetracycline
pigmentation, developmental enamel defects,
and generalized hereditary anomalies can be
explained if the calcification schedule is known.
• The development and subsequent eruption
of the teeth is a complex procedure that
occurs simultaneously with the growth and
development of the entire facial complex.
th
• The development of teeth starts at about 6
intrauterine week
• The locations of teeth are established with
the appearance of tooth germ
LIFE CYCLE OF THE TOOTH
Initiation (bud stage)

The first epithelial invasion into the


mesenchyme of the jaw to form a tooth
occurs that resembles a bud and is called
as enamel organ.

Bud stage of tooth development


• Different teeth are initiated at different
and definite time.
• Enamel organ forms the enamel of the
tooth. Lack of initiation or an arrest in
the proliferation of cells results in the
absence of tooth development leading to
congenitally missing tooth and
conversely abnormal initiation may lead
to supernumerary teeth as well.
• The initiation processes occurs along
each jaws which marks the beginning of
development of deciduous teeth.
• The timing will differ for anterior teeth
and the posterior teeth.
• Anterior teeth develop earlier than the
posterior teeth.
Proliferation (Cap Stage)

As the growth continues regular changes


in the size and proportion of the growing
tooth germ is seen leading to the
formation of a cap shaped enamel organ
• The dental papilla shows active budding
of capillaries.
• The peripheral cells adjacent to inner
enamel epithelium enlarge and later
differentiate into odontoblasts.
• A deficiency in proliferation results in
failure of the tooth germ to develop and
in fewer than the normal numbers of
teeth
◻ Excessive proliferation of cells may
result in epithelial rests. These rests
may remain inactive or become
activated due to an irritation or
stimulus.
◻ If the cells become partially
differentiated or detached from the
enamel organ in their partially
differentiated state, they assume the
secretory functions common to all
◻ If the cells become more fully
differentiated or detached from the
enamel organ, they produce enamel
and dentin, which results in an
odontoma or a supernumerary teeth
Histodifferentiation and
Morphodifferentiation (Bell Stage)

• The epithelium continues to invaginate


and deepen until the enamel organ
takes on the shape of a bell
• It is during this stage that the cells of the
dental papilla differentiate into
odontoblasts and those of the inner
enamel epithelium differentiate into
ameloblasts.
• Histodifferentiation marks the end of
the proliferative stage as the cells lose
their capacity to multiply.
• Disturbances in the differentiation of the
formative cells of the tooth germ result
• One clinical example of the failure of
ameloblasts to differentiate properly is
amelogenesis imperfecta
• The failure of the odontoblasts to
differentiate properly, with the resultant
abnormal dentin structure, results in
dentinogenesis imperfecta
In the morphodifferentiation stage, the
formative cells are arranged to outline the
form and size of the tooth.

Disturbances and aberrations in


morphodifferentiation lead to abnormal
forms and sizes of teeth, resulting in
conditions such as peg teeth, other types of
microdontia, and macrodontia
Apposition
• Appositional growth is the result of a layer-like
deposition of a nonvital extracellular secretion
in the form of a tissue matrix. This matrix is
deposited by the formative cells, ameloblasts,
and odontoblasts, which line up along the future
dentinoenamel and dentinocemental junction at
the stage of morphodifferentiation.
• These cells deposit the enamel and dentin
matrix in a definite pattern and at a definite rate.
• Any systemic disturbance or local trauma that
injures the ameloblasts during enamel
formation can cause an interruption or an
arrest in matrix apposition, which results in
enamel hypoplasia.
• Hypoplasia of the dentin is less common than
enamel hypoplasia and occurs only after severe
systemic disturbances.
Early development and calcification of the
anterior primary teeth

• Central incisor begin to develop


morphologic characteristics 11 weeks in
utero
• Lateral incisors begin to develop
morphologic characteristics between
13-14 weeks in utero.
• Canines begin to develop morphologic
characteristics between 14-16 weeks in
• Initial calcification of central incisors 14
weeks in utero
• Initial calcification of lateral incisors 16
weeks in utero
• Initial calcification of canines 17 weeks in
utero
Early development and calcification
of the posterior primary teeth

• First evidence of calcification of first


primary molar 15 1/2 weeks in utero
• First evidence of calcification of second
primary molar between 18-19 weeks in
utero
Eruption of the teeth

• The process of tooth eruption can be


defined as the movement of the tooth
through the tissues of the jaw towards
occlusion into the oral cavity until it
achieves occlusal contact with adjacent and
opposing teeth
• Each tooth starts to move toward occlusion
at approximately the time of crown
Factors Influence the Timing of Eruption

1. Genetic factor
2. Sex
3. Socioeconomic conditions
4. Birth weight
5. Systemic disorders
6. Hormones and vitamins
7. Local causes
1. Genetic factor

• Genes play a definite role in tooth


eruption and have been estimated to
be about 78%
2. Sex
◻ Teeth of girls erupt slightly earlier than those of
boys
◻ The average amount of tooth development for
girls is about 3% ahead that of boys.
◻ The difference may vary from 2 months [First
molar] to 10 months [maxillary canine].
◻ Initially during the formation stage, there was no
sex difference up to the stage of calcification, and
the difference begins only from the crown
completion stage.
3. Socioeconomic Condition
◻ Socioeconomic levels are known to affect
eruption.
◻ Retarded eruption of anterior teeth and
accelerated emergences of the posterior
dentition has been linked to low
socioeconomic status in all racial groups.
4. Birth Weight
◻ Low birth weight has been associated with
delayed emergence of permanent teeth and
conversely early eruption has been associated
with increased birth weight.
5. Systemic Disorders
◻ Precocious eruption is rare and is observed less
commonly than retarded eruption.
◻ Delay in permanent tooth eruption is associated
with Down’s syndrome, cleidocranial dysostosis,
hypothyroidism, hypopituitarism and hemifacial
atrophy.
◻ Precocious eruption is seen in precocious
puberty, hyperthyroidism, hemifacial
hypertrophy, Sturge-Weber syndrome and
hyperpituitarism.
6. Hormones and Vitamins
◻ Thyroid, Pituitary [Growth Hormone],
and Parathyroid hormones are essential
for normal eruption of teeth.

◻ Vitamins like Vitamin B Complex, A, C


and D aid either directly or indirectly for
tooth eruption.
7. Local Causes
◻ Ankylosis of primary teeth, delays the
eruption of permanent tooth.

◻ Very early extraction of a primary molar,


delays gingival eruption of the successor.
Chronology of eruption of primary
teeth

Maxillary Mandibular
Central 6-10 months 5-8 months
incisors
Lateral 9 months 7-10 months
incisors
Canines 16-20 months 16-20 months
First molars 11-18 months 11-16 months
Second molars 20-30 months 20-30 months
Chronology of eruption of
permanent teeth
Eruption sequence

Primary
◻ Maxillary Teeth A B C D E

◻ Mandibular Teeth: A B D C E

Permanent
◻ Maxillary Teeth: 6124537

◻ Mandibular Teeth: 6123457


Pattern of tooth movement
◻ A considerable movements are required to
bring the tooth to the occlusal plane and then
into functional occlusion.
Types of tooth movements:
1. Pre-eruptive tooth movement

2. Eruptive movements

3. Post-eruptive tooth movements


1. Pre-eruptive Movements

◻ Includes all movements of the deciduous


and permanent tooth germs within the
tissues of the jaw, from the time of early
initiation and formation to the time of
crown completion and this phase
terminates with the initiation of root
development
◻ During this phase the growing tooth
moves in two directions to maintain its
position in the expanding jaws (outward
and upward in the mandible and outward
and downward in maxilla).
2. Eruptive tooth movement
It is the axial movement of the tooth from
its crypt within the bone of the jaw to its
functional position in occlusion (to occlude
with its antagonist)
3. Post-eruptive tooth movement
◻ It occurs primarily to maintain the
position of the erupted tooth while the
jaw continues to grow and to compensate
for the occlusal and proximal wear.

◻ This movement occur in axial direction.


◻ They are the movements made by the tooth
after it has reached its functional position in
the occlusal plane.
◻ Post-eruptive tooth movements helps in
readjustment of the tooth in the socket.
◻ This is 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. Such movements can be in axial,
Theories of Mechanism of Tooth
Eruption
1. Root formation
2. Bone Remodeling
3. Vascular pressure
4. Periodontal ligament
5. Dental follicle theory
1. Root formation
According to this theory, as the root grows
apically there is a force generated in an
opposite direction that propels the tooth
occlusally.
Root growth theory suggested the presence
of the cushion hammock ligament at the
base of the socket that transmits the force
to cause eruption but the ligament was
Why this theory is weak?
◻ Studies found that rootless teeth erupt and
some teeth erupt a greater distance more than
the length of their roots
◻ Teeth still erupt even following root
completion also when the tissues forming the
root are excised surgically teeth continue to
erupt (all these events mean that root
formation is not required for tooth eruption).
2. Bone Remodeling
◻ An inherent growth pattern of the maxilla
and mandible supposedly moves teeth by
selective deposition and resorption of bone.
◻ This theory is not accepted. Bone resorption
and formation occurred because of eruptive
forces applied by tooth over the bone (there
are some animal studies showed that bony
remodeling occurs around the dental follicle
regardless of the presence of a tooth).
3. Vascular pressure
◻ The vascular pressure theory supposes
that a local increase in tissue fluid or
blood pressure in the periapical region is
sufficient to move the tooth (states that
“the tissue pressure apical to the erupting
tooth was greater than occlusally,
theoretically generating an eruptive
force”).
◻ It mean that the hydrostatic pressure on
top of the tooth is less than hydrostatic
pressure underneath the tooth.
◻ This difference in pressure will push the
tooth occlusaly
However, since surgical excision of the
growing root and associated tissues
eliminates the periapical vasculature
without stopping eruption, this means that
the local vessels absolutely are not
necessary for tooth eruption.
4. Periodontal ligament
◻ Eruptive force reside in the dental follicle
periodontal ligament complex.
◻ Formation and renewal of the PDL has
been considered a factor in tooth
eruption because of the traction power
that fibroblasts have which may pull the
tooth out during eruption.
◻ “The periodontal ligament, which is derived
from the dental follicle, provides the force
required for eruption mainly by fibroblast
contraction”
◻ However in vitro tissues studies have
limitations concerning this theory
5. Dental follicle theory
◻ It is clear that the dental follicle is
essential to achieve the bony remodeling
required to accommodate tooth
movement, for it is from this tissue that
the osteoblasts differentiate.
◻ Note. Studies have shown that the reduced
dental epithelium initiates a cascade of
intercellular signals that recruit osteoclasts to
the follicle. By providing a signal and chemo
attractant for osteoclasts. It is possible that
the dental follicle can initiate bone remodeling
which goes with tooth eruption.
◻ Teeth eruption is delayed or absent in
animals models and human diseases that
cause a defect in osteoclast differentiation.
So !!!
◻ What actually happens when the tooth is
erupting, there are certain genes codes
certain proteins binds to certain cells of the
dental follicle stimulating these follicle to
differentiate into osteoclasts and osteoblasts
where bone resorption and bone apposition
occurs on both surfaces of the tooth occlusal
and apical, this actually will cause the tooth
to erupt. Therefore, the dental follicle is
mainly responsible for the process of

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