1

•Introduction
•Definition
•Theories of eruption
•Anatomic stages in the eruption of the teeth
•Nolla’s stages of tooth development
•Patterns of tooth movement
•Shedding of teeth
•Sequence of tooth eruption
•Molecular determinants of tooth eruption
•Teeth and teething difficulties
•Management of teething
•Problems in primary tooth eruption
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•The word ‘eruption’ properly refers to the cutting of the tooth
through the gum.

•It is derived from the Latin word ‘Erumpere’, meaning “The

Breaking Out”.

•It can also be interpreted as eruption means the axial or occlusal

movement of the tooth form its development position in occlusal
plane.

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Maury Massler and Schour (1941) :
“Eruption is a process whereby the forming tooth migrates
from its intraosseous location in the jaws to its functional
position within the oral cavity.”

Osborne :
“Eruptive movement is defined as the axial movement of the
tooth which brings the crown of the tooth from its
developmental position within the bone of the jaw to its
functional position within the oral cavity”.

James K Avery :
“Eruption is the movement of the teeth from the bone of the
jaws and the overlying mucosa to appear and function in the
oral cavity.” 4
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• There are many theories that explain the mechanism of tooth
eruption:

1. VASCULARITY THEORY
2. PRESSURE THEORY/ CELLULAR PROLIFERATION THEORY
3. ROOT FORMATION THEORY/ ROOT ELONGATION THEORY
4. BONE REMODELLING THEORY
5. DENTAL FOLLICE THEORY
6. PERIODONTAL LIGAMENT THEORY/ GROWTH OF
PERIODONTAL TISSUES
7. FORCE THEORY / PRESSURE FROM MUSCULAR ACTION
8. HYDROSTATIC PRESSURE THEORY/ BLOOD PRESSURE THRUST
THEORY 7
9. PULPAL CONSTRICTION THEORY
10. PERIODONTAL LIGAMENT CONTRACTION THEORY
11. RESORPTION OF THE ALVEOLAR CREST
12. HORMONAL THEORY
13. FOREIGN BODY THEORY

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1. Vascularity
Vascularity plays an important role in tooth eruption
Sufficient blood supply to the tooth germ has proven to cause
eruptive tooth movement
 Localized hyperaemia has shown to causes increased vascularity of
the periodontal tissue and also increased eruption of adjacent tooth.
Evidence for the theory- Submerged teeth often erupt under the
influence of hyperaemia, the hyperaemia in periodontitis causes a
supra-eruption of teeth.

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2. Pressure / Cellular Proliferation Theory
Decreased pressure overlying a tooth and increased
pressure around the tooth are major factors in tooth eruption.

When the root formation begins an eruption pathway

develops overlying the tooth, just like a growing plant.

Remodelling of tissue around the developing tooth brings

about an increase in pressure tooth which causes the tooth
movement.

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3. Root formation
Root formation causes an overall increase in the length of the
tooth.

It produces enough force that leads to the resorption of bone.

However, this force in itself does not cause tooth movement.

Evidence against the theory - Rootless teeth also erupt.

One point of importance is that, the tissue beneath the growing

root resists the apical movement of the developing root. This
resistance results in the occlusal movement of the tooth crown as the
root lengthens.

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4.Bone remodelling
The selective resorption and formation of bone surrounding the
tooth cause its movement.

This theory also explains the tooth movement during pre-eruptive

phase.

 Bone formation also occurs apical to the developing tooth

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5. Dental Follicle
There is signalling between the reduced enamel epithelium and the
dental follicle.

This signalling regulates the timing of eruption of teeth – known as

‘biologic clock’.

 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 animal models and human

diseases that cause a defect in osteoclasts differentiation.

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6. Periodontal ligament
The remodelling of PDL has also been considered as a factor for
tooth eruption.

The fibroblasts possess traction power that causes tooth

movement.

The PDL helps lift the tooth to its occlusal plane during the
supraosseous phase of eruption

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 PDL

Root

Bone

Force theory
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7. Force theory / Pressure from Muscular Action

•Berten suggested that the action of the musculature of the cheeks

and lips upon the alveolar process might serve to squeeze the crown
of the tooth out into the oral cavity like a pumpkin seed from
between the fingers

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 8. Hydrostatic Pressure

• A number of studies exist to demonstrate that there is a

hydrostatic pressure difference between the tissue around
the erupting crown and its apical extent

• The hydrostatic theory was investigated by Hassel and

McMinn (1972) who demonstrated that the tissue pressure
apically was greater than occlusally theoretically
generating an eruptive force.

• No association was found between the rate of eruption and

the pressure gradient.

• Modification of the pressure changed the rate of eruption

in rabbits which somewhat supported the theory.
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9. PULPAL CONSTRICTION

•This theory states that the growth of the root dentin and the
subsequent constriction of the pulp may cause sufficient pressure to
move the tooth occlusally.

•Evidence for the theory- The pulp is progressively constricted by

growth of root dentin

•Evidence against the theory - Pulpless teeth erupts at the same rate
as the normal teeth, premolar will often “jump” into occlusion after
the premature extraction of the deciduous molar without any
appreciable growth of dentine or pulpal constriction.

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10. PERIODONTAL LIGAMENT CONTRACTION THEORY

•Suggests that the contractile element within the periodontal

ligament, collagen constriction due to fibroblasts are responsible.

•Evidence to this theory - The actual force required to move the tooth
is linked to the contractility of fibroblasts. When fibroblasts are plated
onto silicone rubber, they crawl about and doing so create wrinkles
or folds in the rubber indicating that tractions forces are associated
with locomotion.

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11. RESORPTION OF ALVEOLAR CREST THEORY

•Resorption of the alveolar crest would serve to expose the crown of

the tooth into the oral cavity. This theory is not tenable since
histological examination shows that the alveolar crest is the site of
the most rapid and continuous growth of bone.

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12. HORMONAL THEORY

•Sir Arthur Keith suggested that the hormones secreted by the

thyroids and pituitary glands might govern the eruption of the teeth.
This theory does not attempt to explain the mechanism of the
eruption of the teeth, and only points out the fact the hormones may
affect the eruption of the teeth.

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13. FOREIGN BODY THEORY

•Gottlieb’s foreign body theory, states that a calcified body such as

the tooth tends to be exfoliated by the tissues just as does any
foreign body.

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Given by Noyes and Schour :

Stage I : Preparatory stage (opening of the bone crypt)

Stage II: Migration of the tooth toward the oral epithelium

Stage III: Emergence of crown tip into the oral cavity. (Beginning
of clinical eruption)

Stage IV: First occlusal contact

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Phase 1: The Pre-eruptive phase

Phase 2: The Pre-functional eruptive or eruptive

phase

Phase 3: The Functional eruptive or post eruptive

phase

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 Pre-Eruptive Phase
 All movements of primary and permanent tooth crowns
from the time of their early initiation and formation to the
time of crown completion.

 Eccentric growth is accompanied with bone resorption

altering the shape of the crypt

 The phase is finished with early initiation of root formation.

 Early in the stage, the permanent anterior teeth begin

developing lingual to the incisal level of the primary teeth.
Later, as the primary teeth erupt, the secondary teeth are
positioned lingual to the apical third of their roots.

 Permanent premolars shift from a location near the occlusal

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Permanent molars have no predecessors

Maxillary molars develop within the maxillary tuberosity with their

occlusal surfaces slanted distally

Mandibular molars develop in the ramus with the occlusal surfaces

slanting mesially

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Pre-eruptive tooth movement: Why do developing crowns
move constantly in the jaws during the pre-eruptive phase?

To place teeth in position for eruptive tooth movement

1.To alleviate the problems of jaw growth which allows second molar to
move backward and anterior teeth to move forward

2.Developing crown move constantly during the pre-eruptive phase as

they respond to positional changes of the neighboring crowns and to
changes in the mandible and maxilla

3.Permanent teeth develop lingual to the incisal level of the primary

anterior teeth and later as primary teeth erupt, the permanent crowns
are lingual to the apical 3rd of primary roots

4.Permanent premolars move from occlusal level of primary molars to a

position enclosed within the primary tooth roots

5.All movements in the preruptive phase occur within the crypts of the
developing crowns 30
Two types of tooth movement in pre-eruptive phase:

1. Total bodily movement

2. Movement where one part remains fixed while the rest

continues to grow leading to change in the center of the
tooth germ

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Figure from Ten Cate’s Oral Histology,
Ed., Antonio Nanci, 6th edition

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 Pre-Functional Eruptive
 Starts with the initiation of root formation and ends when
the teeth reach occlusal contact

 Four major events occur during this phase:

1. Root formation

2. Movement occurs incisally or occlusally through the bony

crypt to reach the oral mucosa

3. Penetration of the tooth crown tip into the oral cavity

4. Intraoral movement occlusally and incisally until clinical

contact with the opposing crown occurs.
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Eruptive Tooth Movement

4 major events occur:

1. Root formation. Space is required for root formation
Proliferation of epithelial root sheath
Initiation of root dentin and pulp
Increase in fibrous tissue of the follicle
2. Movement. Occurs incisally or occlusally
The main reason for movement is so that the
roots can form normally
Reduced enamel epithelium fuses and contacts
the oral epithelium
3. Penetration of the tooth’s crown tip through the fused
epithelial layers allowing entrance of the crown into the
oral cavity

4. Intraoral incisal or occlusal movement of the erupting tooth

continues until clinical contact with the opposing crown occurs
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Essentials of Oral Histology and Embryology. James Avery, 2nd edition

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Essentials of Oral Histology and Embryology. James Avery, 2nd edition

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Clinical crown: During eruption, the exposed crown extending
from the cusp tip to the area of the gingival attachment

Anatomic crown: Entire crown, extending from cusp tip to the

cementoenamel (CE) junction

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 Histology – changes that occur in tissues overlying
erupting teeth
Degeneration of connective tissue (decrease in blood vessels and
degeneration of nerves) immediately overlying the erupting teeth

Eruption pathway – altered tissue area overlying the teeth

Macrophages destroy cells and fibers by secreting hydrolytic

enzymes

Gubernacular cord: The connective tissue overlying a

successional tooth that connects with the lamina propria of the oral
mucosa by means of a strand of fibrous connective tissue that
contains remnants of dental lamina

Gubernacular canal: Holes noted in a dry skull noted lingual to

primary teeth in jaws that represent openings of Gubernacular cord

As the successional teeth erupt, Gubernacular canal widens 42

Essentials of Oral Histology and Embryology. James Avery,
2nd edition

Figure from Ten Cate’s Oral Histology, Ed., Anton

6th edition
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Essentials of Oral Histology and Embryology. James Avery, 2nd edition

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Figure from Ten Cate’s Oral Histology, Ed., Antonio Nanci, 6th edition

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 Stages of tooth eruption

Essentials of Oral Histology and Embryology. James Avery, 2nd edition

46
 Histology – Surrounding tissues
•The surrounding fibers change from being parallel to the tooth surface
to bundles that are attached to the tooth surface and extending
towards the periodontium (bone)

•The periodontal ligament have contractile properties and changes

drastically during eruption

•During eruption, collagen fiber formation and turnover are rapid

enabling fibers to attach and release and attach in rapid succession.

•Some fibers may attach and reattach later while the tooth moves
occlusally as new bone forms around it and the fibers will organize
and increase in number and density as the tooth erupts

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Essentials of Oral Histology and Embryology. James Avery, 2nd edition

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Essentials of Oral Histology and Embryology. James Avery, 2nd edition

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The rate of tooth eruption depends on the phase of movement

Intraosseous phase: 1 to 10 µm/day

Extra osseous phase: 75 μm/day

Environmental factors affecting the final position of the tooth:

Muscular forces
Thumb-sucking

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 Functional Eruptive Phase
1. Movements to accommodate the growing jaws. Mostly occurs
between 14 and 18 years by formation of new bone at the alveolar
crest and base of socket to keep pace wit increasing height of jaws.

2. Movements to compensate for continued occlusal wear.

Compensation primarily occurs by continuous deposition of
cementum around the apex of the tooth. However, this
deposition occurs only after tooth moves. Similar to eruptive tooth
movement.

3. Movements to accommodate interproximal wear. Compensated by

mesial or approximal drift. Mesial drift is the lateral bodily
movement of teeth on both sides of the mouth.
Very important in orthodontics.
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Several factors control mesial drift:
(a) Contraction of the transseptal fibers: As the proximal tooth surfaces
of adjacent teeth become worn from functional tooth movement,
the transseptal fibers of the periodontal ligament become shorter
(due to contraction) and thereby maintain tooth contact.

(b) Adaptability of bone tissue: The side of pressure on PDL fibers

causes bone resorption, whereas pull on the fibers causes bone
apposition (formation). Therefore, as the contact areas of the crowns
wear, the teeth tend to move mesially, thereby
maintaining contact

(c) Anterior compartment of occlusal force: An anteriorly directed force

is generated when teeth are clenched, due to the mesial inclination
of most teeth and the forward-directed force generated from inter-
cuspal forces. Eliminating opposing teeth results in elimination of
biting forces, causing a slowing down of the mesial migration
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Active eruption: to compensate incisal and occlusal wear

Passive eruption: gradual recession of the gingiva and the

underlying alveolar bone

Both active and passive eruption leads to lengthening of clinical

crown

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 Shedding of Teeth

1. Osteoclast/bone remodeling
2. Odontoclast (cementoclast; dentinoclast)
3. Resorption of soft tissues

Pressure from successional teeth

Odontoclast

Figure Source: Dr. Sandra Meyers

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Osteoclasts are bone resorbing cells derived form monocyte-
macrophage lineage

Giant multinuclear cells with 4-20 nuclei

Osteoclasts resorb hard tissue by separating mineral from the collagen

matrix through the action of hydrolytic enzymes

Resorption occurs at the ruffled border which greatly increases the

surface area of the Osteoclast in contact with bone

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 Shedding of Mandibular incisor

5 months
At birth 1 year

2 years 3.5 years 4.5 years

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Figure Source: Dr. Sandra Meyers
Deciduous 1st molar

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Figure from Ten Cate’s Oral Histology, Ed., Antonio Nanci, 6th edition
 Shed element following “shedding of primary incisor

Complete resorption of roots

Resorption lacunae seen (arrow)

Most of coronal pulp is intact

Figure Source: Dr. Sandra Meyers

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7 years-functional occlusion attained
15 years – incisal wear
but root apex is still not fully formed
Figure Source: Dr. Sandra Meyers

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Sequence and chronology of tooth eruption

Source: http://www.columbia.edu/itc/hs/dental/d9903/lectures/lecture4.pdf

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 The six/four rule for primary tooth emergence
Four teeth emerge for each 6 months of age

1. 6 months: 4 teeth (lower centrals & upper centrals)

2. 12 months: 8 teeth (1. + upper laterals & lower laterals)
3. 18 months: 12 teeth (2. + upper 1st molars & lower 1st molars)
4. 24 months: 16 teeth (3. + upper canines & lower canines)
5. 30 months: 20 teeth (4. + lower 2nd molars & upper 2nd molars)

Summary
1. By 5 months in utero, all crowns started calcification
2. By 1 year old, all crowns completed formation
3. By 2.5 years, all primary teeth erupted
4. By 4 years old, all primary teeth completed root formation

Source: http://www.columbia.edu/itc/hs/dental/d9903/lectures/lecture4.pdf
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 The rules of “Fours” for permanent tooth
development (3rd molars not included)

At birth, four 1st molars have initiated calcification

At 4 years of age, all crowns have initiated calcification
At 8 years, all crowns are completed
At 12 years, all crowns emerge
At 16 years, all roots are complete

Source: http://www.columbia.edu/itc/hs/dental/d9903/lectures/lecture4.pdf

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 Rules of “sixes” in dental development

6 weeks old in utero: beginning of dental development

6 months old: emergence of the first primary tooth
6 years old: emergence of first permanent tooth

Source: http://www.columbia.edu/itc/hs/dental/d9903/lectures/lecture4.pdf

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 Molecular Determinants of
•
Tooth Eruption
A review article by Wise et al
(2002) stated that tooth
eruption is a complex and
tightly regulated process.
• Mononuclear cells
(Osteoclast precursors) must
be recruited into the dental
follicle prior to onset of
eruption. Recruitment may
require colony stimulating
factor 1 and monocyte
chemotactic protein 1
• Parathyroid hormone related
protein and interleukin 1
produced in the stellate 67
reticulum are also involved
 Control of Eruption
• Eruption occurs only during a critical period between 8pm
and midnight or 1am.
• During the morning, tooth eruption ceases or even the
tooth intrudes a bit. This reflects Circadian Rhythm
reflecting the possible involvement and control of growth
hormone and thyroid hormone.
Hormonal Control Mechanisms
• A study by Leache et al (1988) of children with growth deficit
concluded that children with delayed growth due to growth
hormone deficiency or low genetically determined height had
delayed tooth eruption. However those with delayed growth
for other reasons show normal dental development.
• This was a large study of children who were shorter than
average for their chronological age, although the numbers of
children in each group studies were relatively small. 68
• The time of eruption for primary and
permanent teeth varies greatly. A variation of
6 months on either side of the usual eruption
date may be considered normal for a given
child.

69
 Teething and teething
• difficulties
According to Macknin et al the teething period was defined
as the 8-day period beginning 4 days before a tooth
emergence and extending 3 days after the event.
• Over half of babies have one or more problems during
teething.
• In a prospective study by Seward, mothers of 224 infants
reported 74% and 100% to suffer at least one local
disturbance during the eruption of the front and back teeth,
respectively.
• In the past, a variety of physical disturbances such as croup,
diarrhea, fever, convulsions, primary herpetic gingivo-
stomatitis, and even death have been incorrectly attributed
to eruption. Many of these are common in early childhood,
and there is no evidence to support an association with
dental eruption . It is now accepted that the localized
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 Extra oral & Intraoral
• Finger chewing symptoms
• Gum rubbing
• Lip biting • Inflammation/gingival
• Object biting redness over erupting
tooth
• Irritability/restlessness
• Tender swollen gums
• Night crying
• Tooth erupting
• Drooling
• Circumoral rash and
inflammation
• Appetite loss
• Flushed cheeks
• Mild temperature
elevation
• Ear rubbing 71
 Myths and Realities
• Although many studies have suggested associations
between teething and a range of signs and symptoms; both
local and systemic, the level of evidence remains poor for
any cause-effect relationship.

• Historically, teething has often been blamed when

diagnostic ability has failed . Since the eruption of teeth is a
normal physiologic process, the association with fever and
systemic disturbances is not justified. A fever or respiratory
tract infection during this time should be considered
coincidental to the eruption process rather than related to
it.

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• High temperature (higher than 39°C) should not be attributed
to teething, and should be investigated

• Since eruption takes place over a period of two and a half

years, it is not surprising that these coincidental factors
emerge. If attention is given to these symptoms, it is often
recognized that some other coincidental mild infection is
present, usually gastro-intestinal or upper respiratory.

• An undiagnosed primary herpetic infection (primary herpetic

gingivo-stomatitis) could be responsible for the symptoms of
fever, irritability and appetite loss

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• Reassurance of the parents regarding teething
signs and symptoms by the pediatrician, dentist or
auxiliary staff is necessary.
• Steward recommended a sequential approach to
the management of teething ranging from giving
the child objects to bite on through topical and
systemic medications.
• Biting on these chilled objects may give some relief
from soreness by the pressure of biting, or hasten
the eruption process.
• Hard vegetables such as chilled carrots or celery
may be used.
• Teething rusks or biscuit preparations are available,
consisting mainly of flour or fat.
• Care should be taken that these do not contain 74
• If the pain is troublesome, the appropriate dose of paracetamol elixir,
preferably sugar-free may be given regularly, every 4-6 hours.
• Topical medications include gels containing choline salicylate,
lidocaine HCl and powders containing benzocaine and paracetamol
for temporary relief
• Uncontrolled application Iatrogenic oral mucosal trauma
• (chemical
Bonjela®, burns at the site
an analgesic drugofcontaining
application8.7%
on the mucosa
choline in a 10-
salicylate in a
month-old
flavored gelboy
basein Malta)
• Choline salicylate is a synthetic non-steroidal anti-inflammatory
based on aspirin,
• Indicated for mild oral and perioral lesions and 1/4-1/2 inch is
applied topically 3-hourly, up to a maximum of six applications per
day.
• The drug has a local analgesic effect although the pressure of
application may be the true mechanism of action.
• Less adverse effects when compared to aspirin, however, according to
Sarll and Duxbury, it has been reported to cause salicylate
intoxication when applied topically in a child. 75
•Paediatric Paracetamol Elixir BP
•Each 5ml contain 120 mg of paracetamol

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• ERUPTION HEMATOMA

•ERUPTION SEQUESTRUM

•ECTOPIC ERUPTION

•NATAL AND NEONATAL TEETH

•NON ERUPTION OF TEETH

• LOCAL FACTORS INFLUENCING TOOTH ERUPTION

•SYSTEMIC FACTORS INFLUENCING TOOTH ERUPTION

•EARLY EXFOLIATION OF TEETH

•AGENESIS OF TEETH
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•HYPOPHOSPHATASIA

•CHERUBISM

•ACRODYNIA

•HYPOPHOSPHATEMIA

•CYCLIC NEUTROPENIA

•OTHER DISORDERS LIKE: Acatalasia, Chediak-Higashi Syndrome,

Coffin Lowry Syndrome, Down’s Syndrome, Ehler’s-Danlos Syndrome,
Hajdu-Cheney Syndrome, Hyperpituitarism, Hyperthyroidism,
Juvennille Diabetes, Papillon-Lefevre Syndrome, Progeria,Singleton-
Merten Syndrome, and some mlignant diaseases like Histiocytosis,
and Leukemias.

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80
 Eruption hematoma/Eruption
cyst
• A bluish purple, elevated area of tissue, occasionally develops
a few weeks before the eruption of a primary or permanent
tooth.
• Blood filled cyst mostly associated with primary second molar
or first permanent molar
• ? Trauma during function
• Self-limiting: usually within a few days, the tooth breaks
through the tissues and the hematoma subsides
• Surgical uncovering

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 Eruption Sequestrum
• Occasionally occurs at the time of eruption of the
permanent molars.
• Starkey et al. (1963) were the first to report the presence
of small fragments of calcified tissue overlying the
crowns of erupting molar teeth. Generally, these pieces
directly overlay the central occlusal fossa, while
remaining within the soft tissue and, as the molar tooth
erupts through the bone, a small osseous fragment is
lost.

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 Ectopic Eruption of First Molars

• Ectopic eruption is defined as the abnormal eruption of a

permanent tooth out of position and causing the resorption
of a primary tooth in an abnormal fashion.

• A disturbance of the path of eruption in a position

different to its normal path

• In reference to the first molar, the definition is: an ectopic

molar erupts at an angle mesial to the normal path of
eruption and atypical resorption of the distal surface of the
neighbouring primary second molar.

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Classification
• The disorder was first described by Chapman (1923) and
later refined by Young (1957) describing two types of
ectopic molar eruption:
Jump-Reversible type
Hold-Irreversible type
• Jump: describes a reversible ectopic eruption typified by a
mild manifestation allowing the first permanent molar to
free itself from under the second primary molar and erupt
into normal position. Account for 66% of cases
• Hold: describes a permanent molar erupting with a mesial
inclination, causing resorption of the primary molar roots
such that the first permanent molar becomes trapped
under the second primary molar. The tooth will not erupt
until treatment is provided or until the primary molar
exfoliates causing further mesial tipping, space loss, 88
Aetiology
• Remains relatively unknown, however, a number of causes have
been suggested:

1. Genetic factors (familial)

2. Imbalance in the growth of the mandible in relation to the
eruption of the first permanent molar, which can encourage
continued mesial inclination of the molar and subsequent
entrapment under the bulge of the second primary molar
3. Arch length deficiency
4. Larger than normal sizes of all maxillary primary and permanent
teeth
5. Tendency towards a hypo plastic maxilla
6. Retrusive position of the maxilla in relation to the cranial base
7. Pronounced mesial inclination of the tooth by 15 degrees on
average
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8. Delayed calcification of the affected molar
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 What are natal and neonatal
teeth?
• Natal teeth- teeth that are already present at the time of
birth.

• Neonatal teeth- teeth which grow in during the first 30 days

after birth.

• Precocious Dentition- teeth erupting during the 3-5th month

of life

• Normal Dentition -8 months

95
85% are the deciduous mandibular
incisors

96
 Location
• 85% mandibular incisor
• <.01% lateral mandibular incisor
• 2.5% other mandibular teeth
• 4% upper central incisors
• <.01% other maxillary teeth

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 Embryology

 Derived from the ectoderm of the first branchial

arch, and the ectomesenchyme of the neural
crest.
• For human teeth to have a healthy oral
environment, enamel, dentin, cementum, and
the periodontium must all develop during
appropriate stages of fetal development.
• Primary (baby) teeth start to form between the
sixth and eighth weeks.
• Permanent teeth begin to form in the twentieth
week.

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 Embryology

1) Mandible
2) Anlage of the
permanent tooth
3) Enamel organ
4) Enamel
5) Dentin
6) Labiogingival
sulcus

100
 Etiology of Natal Teeth
also unknown

• Unknown.
• Possible genetic link, as often occurs in
same family.
• No clear genetic pattern has been
identified
• Gates thought it may be an irregular
dominant trait, perhaps associated with an
inhibitor gene, or the presence of two
genes. 101
 Problems

 Natal teeth are usually

not well formed, but they
are firm enough that,
because of their
placement, they may
cause irritation and
injury to the infant's
tongue when nursing.
 Natal teeth may also be
uncomfortable for a
nursing mother.

 Riga-Fede
102
 Solutions

• Frequently, natal teeth are removed

shortly after birth while the newborn infant
is still in the hospital.
• Must be removed if the tooth is loose and
the child runs a risk of aspiration, or
"breathing in" the tooth.

103
 Associations

• Most of the time, natal teeth are not

related to a medical condition. However,
sometimes they may be associated with:
• Ellis-van Creveld Syndrome
• Hallermann-Streiff syndrome
• Jadassohn-Lewandowski Syndrome
• Sotos syndrome

104
1. Ellison van Creveld Syndrome features:
• Cleft lip and palate
• Polydactyly
• Nail problems
• Short arms and legs
• Short height (b/w 3.5 – 5ft)
• Sparse , absent or fine textures hair
• Tooth abnormalities :
 Peg teeth
 Widely spaced teeth
 Natal teeth
 Delayed or missing teeth

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2. Hallerman-Streiff Syndrome :
 Malformations of skull and facial region
 Sparse hair
 Ocular abnormalities
 Degenerative skin atrophy
 Short stature
 Dental changes :
• Natal teeth
• Hypodontia or partial anodontia
• Malocclusion

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3. Jadassohn-Lewandowski Syndrome
Nail disorders
Blisters in the different parts of the foot
Excessive sweating of the feet
Excessive hair growth
Thick skin on palms and toes
Oral manifestations:
•Oral mucosal leukoplakia
•White tongue
•Natal teeth
•Premature eruption of primary teeth

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4. Soto's Syndrome
Macrocrania
Dolicocephaly
Prominent forehead
Apparent hypertelorism
High arched palate
Increased birth length and weight
Excessive growth in childhood
Disproportionately long hands and legs
Low muscle tone
Developmental delay
Expressive language delay
Teeth defects like natal teeth

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 Summary
 Natal teeth are relatively rare (1:3000 births), but you
WILL likely see it in your career
 We don’t know what causes it, possibly genetics.
 It’s awesome or scary, depending where you come from.
 The teeth are usually the lower incisors, and those are
the first teeth to erupt normally (8 mo)
 They are usually premature deciduous teeth and will fall
out, they have no roots, and are not well formed.
 You can pull them out if they are causing mouth ulcers,
or pain to mother.
 They may be associated with syndromes, so a good
physical exam is necessary.

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 Lingual Eruption of Mandibular
Permanent Incisors
• Given enough space is present, if labial migration of the
permanent incisor had not occurred by 8.2 years for
central incisors and 8.4 for lateral incisors, over-retention
is suspected and removal of primary teeth is
recommended

(Gellin and Haley, 1982)

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 Primary Failure of Eruption
• Called primary retention, cessation of the tooth’s
movement in the pre-eruptive stage, results in a deeply
embedded tooth that fails to achieve emergence and
remains covered with a thick layer of alveolar bone. The
roots are fully formed and usually unresorbed.

• In primary teeth 1:10,000, females>males, mostly

mandibular primary second molars

• D/D: secondary failure of eruption (secondary retention,

infraocclusion, submergence)

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Aetiology:
• Genetic
• Hormonal disturbances
• Developmental syndrome (Cleidocranial
dysplasia)
• Impaired eruptive process due to abnormal bone
resorption, aberrant development of tooth germ,
displacement of follicle, physical barrier
(considered impaction in this case)
Sequelae:
• Inversion
• Impaction
Management: surgical removal 117
118
 Ankylosis

• Anatomical fusion of the tooth cementum or

dentine to the alveolar bone during or after the
active eruption of tooth. It may occur before the
emergence into the oral cavity or after the
eruption and before they make contact with the
opposing teeth.
• Clinically: tooth below the occlusal level,
immobile, dull percussion (high pitch)
• Radiographically: obliteration of periodontal
space and dipped in apically crestal bone
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(Teague et al, 1999)
Source: Color atlas of clinical oral pathology. Neville, Damm and W

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Aetiology:
• Intrinsic: Genetic or congenital gap in the PDL
• Extrinsic:
1. Local trauma
2. Local metabolic defect
3. Reimplantation
4. Deficient eruptive forces
5. Thermal and chemical insult
6. Facial morphology
7. Forces squeezing the arch
8. Localized infection
9. Abnormal tongue pressure

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• Incidence between 8 and 14%, higher among
Caucasians and Hispanics
• Can occur as early as 3 years
• Mandible> maxilla
• 10 times more common in primary teeth

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Possible complications:
• Delayed exfoliation
• Delayed eruption
• Malocclusion
• Tipping
• Over eruption of opposing tooth
• Loss of arch length
• Damage to adjacent teeth (alveolar bone and PDL)
• Denuded root surface
• Increase difficulty of extraction
• Decrease alveolar bone support and increased
submergence
• In severe cases adaptive tongue thrust
• Retained root fragments
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 Submerged primary teeth

Hyper or supra eruption

125
Retained Primary teeth

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• Fromm reported that clinically visible cysts were found in 1028 of
1367 newborn infants. He noted and classified the following three
types of inclusion cysts:

1. Epstein Pearls are formed along the midpalatine raphe. They are
considered remnants of the epithelial tissue trapped along the raphe
as the fetus grows.

2. Bohn Nodules are formed along the Buccal and lingual aspects of
the dental ridges and on the palate away from the raphe. The
nodules are considered as the remnants of mucous gland tissue and
are histologically different form Epstein pearls.

3. Dental Lamina Cysts are found on the crest of the maxillary and
mandibular dental ridges. The cysts apparently originated form the
remnants of the dental lamina 127
 Systemic conditions causing
delayed eruption of teeth
• Hereditary gingival fibromatosis
• Down Syndrome
• Cleidocranial dysplasia
• Hypothyroidism
• Hypopitutarism
• Achondroplastic dwarfism

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 Hereditary gingival
fibromatosis
• Rare, genetically inherited
overgrowth condition
• A benign fibrous enlargement of
maxillary and mandibular keratinized
gingival. The gingival enlargement
may cover the crowns of teeth and
cause severe functional and esthetic
concerns.
• Recurrent even following surgery

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 Down’s Syndrome
•Delayed eruption of both primary and permanent dentitions

•35-55% microdontia, clinical crowns are short, conical, small, roots

complete

•Enamel hypocalcificiation and hypoplasia common

•DS patients 50% more likely to have congenitally missing teeth,

taurodonts are frequent finding

•1/3 more caries resistant than their non-DS siblings

•Gingivitis develops earlier and more rapidly and extensively in persons

with DS, perhaps because of an abnormality in host defenses. Patients
with DS have altered microbiological composition of subgingival plaque,
including increased Actinomyces and Hemophilus strains.
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•V-shaped palate,

• incomplete development of the midface complex,

• soft palate insufficiency

•Hypotonic O. Oris, Masseter, Zygomatic, Temporalis Muscles

•Absent incisors make articulation difficult

•High incidence of laryngeal-tracheal stenosis, also upper airway

obstruction and sleep apnea common

•Scalloped, fissured tongue with bifid uvula, cleft lip/palate, enlarged

tonsils/adenoids

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 Cleidocranial Dysplasia
• Retained primary teeth
• Delayed eruption of permanent teeth
• Impaction
• Abnormal or absent cellular cementum

133
Cleidocranial Dysplasia

134
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 Hypothyroidism

• Congenital hypothyroidism occurring at

birth or during rapid growth period usually
causes mental deficiency and dwarfism.
• The untreated child is usually small and
disproportionate person, with abnormally
short arms and legs.
• The dentition is delayed in all stages of
eruption.

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The occlusion was normal but with delayed in its development. The
maxillary midline supernumerary tooth is coincidental.

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The delayed development in the Juvenile Hypothyroidism patient

140
 Hypopituitarism

• A pronounced deceleration of the growth

of the bones and soft tissues of the body
will result from a deficiency in secretion of
the growth hormone.
• Delayed eruption of teeth

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Complete primary dentition at the age of 28- years o
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The roots of the primary teeth have not resorbed to that appreciable degree
though some permanent teeth show complete development
143
 Achondroplastic Dwarfism

• Autosomal dominant disorder

• The maxilla may be small, crowding of the teeth
and a tendency for open bite
• A chronic gingivitis is usually present
• Development of dentition is usually delayed

144
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146
• It implies complete failure of the teeth to develop, a rare condition.

•It is often referred to as Congenital absence.

• Gorlin and, Herman, and Moss noted that, when agenesis occurs as
an isolated trait, the primary dentition is not affected, and the
inheritance is normally autosomal recessive.

• Swallow reported on to an 11-year-old boy who had a complete

primary dentition but no permanent dentition.

• Schneider also observed a 7-year-old white female with primary

teeth but with missing permanent teeth.

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 Hypodontia (Oligodontia)
• Agenesis of some teeth is referred to as Hypodontia, which is
preferable to the term Partial Anodontia.

•Oligodontia is sometimes used when only a few teeth develop.

• Hypodontia occurs with no known family history, but be found

associated with some syndromes, esp. in Ectodermal Dysplasia .

• Any of the 32 permanent teeth may be missing. However the most

frequent missing in children are the mandibular second premolars,
maxillary lateral incisors, and maxillary second premolars .

• The absence may be unilateral or bilateral.

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• Glenn observed during an examination of 1702 children that
o 5% had a missing permanent tooth other than 3rd molar.
o In 97% the formation of 2nd premolar could not be detected
radiographically at the age of 5.5yrs and that of the lateral incisor
at the age of 3.5 yrs.

• Later further studies were done and the causes for the missing
tooth/teeth were found :
o Mutation in the MSX1 gene located at 4p16.1
o Mutation in the human PAX9 gene
o Consanguineous marriage

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 Ectodermal Dysplasia
• When a no. of the primary teeth fail to develop, other ectodermal
deficiencies are usually evident.

• There are more than 100 types of ectodermal dysplasia with varying
anomalies of ectodermal derivatives, including both the primary and
permanent teeth, hair nails, and skin.

• One of the more common types of ectodermal dysplasia is X-linked

recessive hypohidrotic ectodermal dysplasia (XLHED), also called as
Anhidrotic Ectodermal Dysplasia and Christ-Siemens-Touraine
Syndrome.

• Characteristic features of this are:

oHypodontia and dental hypoplasia
oHypotrichosis/ Anhidrosis
oAsteatosis . 152
• Secondary characteristics are:
oDeficiency in salivary flow
oProtuberant lips
oSaddle-nose appearance
oDry and scaly skin
oFissuring at the corners of the mouth
oPrimary teeth maybe of normal or reduced in size
oThe primary molars without permanent successors have a
tendency to be ankylosed.
• Development of skeletal structures is normal.

• Children presenting with this syndrome have normal mental growth

and a normal life expectancy.

• Consanguinity increases the likelihood of expression of a trait or

condition that is inherited in a recessive manner, and may be one way
that a female with a normal karyotype can be affected.
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155
•Textbook of Pediatric Dentistry - Nikhil Marwah
•Dentistry for the Child and Adolescent – Eighth Edition
•Ten Cate’s Oral Histology, Ed., Antonio Nanci, 6th edition
•Essentials of Oral Histology and Embryology. James Avery, 2nd
edition
•Color atlas of clinical oral pathology. Neville, Damm and White.
2nd edition

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