1 | Page Tooth development, Eruption and development of occlusion Tooth development- At 8 weeks intrauterine the epithelium of the oral cavity bulges into the mesoderm forming the horseshoe shaped dental lamina in each jaw, from this dental lamina buds evolve to form tooth bud. The tooth bud is organized into three parts: 1- Enamel organ– originates from ectoderm. 2- Dental papilla - originates from ectomesenchyme. 3- Dental follicle. - Tooth formation begins at 8 weeks intrauterine, and mineralization begins later at the 4 th month intrauterine. -The dental lamina goes through three stages of maturity to start secretory functions to form different dental tissues: Enamel, Dentin and Cementum these stages are: 1-Bud stage Consists of the ectodermal outgrowth of the dental lamina with the adjacent mesenchyme. 2-Cap stage Is where you have the enamel organ growing from the dental lamina around the dental papilla like a cap. 3-Bell stage Is where the enamel organ will differentiate into four different histological layers: 1-Outer enamel epithelium 2-Stellate reticulum 3-Stratum intermedium 4-Inner enamel epithelium
->Contact with neighboring tooth: it is an area(contact area) in primary teeth but a
point (contact point) in permanent teeth.
Eruption
-Tooth eruption is defined as the movement of the tooth from the site of developmentinside the alveolar process to its functional position in the oral cavity,
- The main direction of movement is axially.
-The fastest rates of eruption are seen following the crown emergence, once the
crown emerged through the gingiva (tooth is shown in the mouth) it erupts quickly.
Tooth eruption can arbitrarily divided into five stages:
1- Pre eruptive- when it is still tooth bud
2- Intraosseous- when it is inside the bone
3- Mucosal penetration- this is actually where the child starts feeling some sort of
discomfort
4-Pre-occlusal- after penetrating the mucosa but still not reaching its final position
5- Post-occlusal- if there is no opposing tooth the tooth will keep on erupting.
Theories of eruption:
Many clinical studies have been done to evaluate how eruption occurs; most of these
studies were done on animals so they came up with many ideas and thoughts on how
eruption occurs.
-Components of dental follicle have been implicated as source of eruptive force
-Proposes that eruptive force is derived from the hydrostatic pressure of the tissues
surrounding the tooth (I.e. of the PDL) , this pressure comes from the pulse – the heart
cause some sort of pressure inside the arteries and veins and this pressure reaches to
extracellular fluids and causes this hydrostatic pressure that will make the tooth erupt.
- The Key components of the process are :
*the presence of the continual pulsatile force “ as long as there is blood vessels the
force is continual”
*Calcification of the tooth and extracellular matrix through which the tooth can
move.
Tooth usually erupt after calcification, so when there is no calcification there is noextracellular matrix so there will be no support for this tooth to erupt.
-Bone resorption along gubernacular canal precedes emergence into oral cavity for
tooth
-The first evidence of eruption radiographicaly is bone resorption beneath the calcified
crown.
- Calcification of the crown is a critical step for the eruptive process since it provides arigid mass against which the forces within the follicle can act.
Imagine if the tooth bud wasn’t calcified and these compressive forces are acting on it,
it will be very soft and can change in shape so eruption shouldn’t happen before
calcification in order to maintain the morphology of the tooth.
Teething: is a natural physiologic process. It causes some irritation and
discomfort, though. So the pain (or discomfort) is not pathological. During
this period the child has a desire to chew or bite; the child is always bitingon something: his/her fingers, toys, etc. Drooling is also common at this
stage.
Other problems may coincide with this stage due to lack of maternal
immunity, which is lost after 6 months of age. The child might get
diarrhea, throat infections, tonsillitis, cold, or any other bacterial or viral
infections that coincide with teething. Most of the time, people will
wrongly think that teething causes the infection.
Other symptoms wrongly assumed to be caused by teething include
inflammation of the mucous membrane overlying teeth, general irritability,
malaise, disturbed sleep, facial flushing, drooling, diarrhea, loss of appetite,
and ear rubbing.
Primary herpetic gingivostomatitis
This is one of the viral infections that coincide with teething. It is caused by herpes
simplex virus type I. It causes fever, loss of appetite, and irritability. It is characterized
by vesicles that erupt and then rupture into ulcers. And it's usually self-limiting within
The treatment is symptomatic: bed rest, antipyretics, analgesics, and fluid intake to
prevent dehydration. The child should be isolated from peers (child is not sent to
kindergarten) and siblings. If the child is immunocompromised , antibiotics are
prescribed.
Ulcers usually heal without scars. Antibiotics are contraindicated (in healthyindividuals) unless there are signs of secondary infection. Steroids are also
contraindicated.
Eruption hematoma (eruption cyst)It's a variation of the dentigerous cyst with the same microscopic features, except that
it's associated with the crown of an erupting primary or permanent molar. It usually
occurs in the maxilla; because the maxilla is more vascular than the mandible. The cyst
develops from the accumulation of fluid or blood in the dilated follicle.
It appears as an asymptomatic bluish swelling that is occasionally filled with blood.Most of the time, the tooth will erupt without the need for intervention (just review
and observation). If the underlying tooth is not erupted, however, or if it is very painful
or causes eating difficulties.
The cyst is treated by marsupialization or excision of the overlying tissue to expose
the crown and drain the fluid. It should also be drained if it causes difficulty in eating
or severe pain.
Delayed exfoliation of primary teeth (retained primary teeth)
The causes of delayed exfoliation could be agenesis of the permanent tooth bud,
ankylosis, and bruxism. Most affected teeth are D's and E's.
They are displaced primary tooth germs that erupt prematurely. They are displaced
superficially, very close to the mucosa, so they erupt very early (in the uterus).Incidence is 1 in 2000-3500 births. Females are more often affected than males. Most
commonly affected teeth are mandibular central incisors, followed by the maxillary
incisors. They are associated with several syndromes (like chondroectodermal
dysplasia, Noonan syndrome, and Turner syndrome).
Eruption problems associated with syndromes
Cleidocranial dysplasia
Dental aspects:
Multiple supernumerary teeth; persistence of primary teeth, multiple unerupted
permanent teeth, twisted roots, malformed crowns, and dentigerous cysts.
Delayed dental development and complete primary dentition up to the age of
15 years resulting from delayed resorption of deciduous teeth. Delayed eruption
of permanent teeth is not uncommon.
One of the most distinguishing features is the presence of supernumerary teeth. Theproblem with these patients is that the primary force of eruption is absent; so there's
nothing that drives the permanent tooth to erupt. Even if the primary teeth are
removed, the permanent teeth will take very long to erupt. Sometimes we need to
drag the tooth out of the bone (orthodontically).
Hormonal causes of eruption problems Thyroid and pituitary conditions are systemic (hormonal) problems that may manifest
some eruption problems.
Ex:Hyperthyroidism causes accelerated exfoliation/eruption; thyroxin is an importantgrowth hormone. Hypothyroidism causes delayed exfoliation/eruption. Same goes for
the pituitary glands, since it "controls everything."
Tumors related to teething problems Neoplasms, odontomes, cysts, ameloblastoma, fibro-osseous lesions. All are obstacles
that usually delay eruption. When there's a tumor causing bone resorption around the
area of a tooth bud, it causes accelerated eruption of that tooth.
Fin
End of part 2
Done by: Abdullah Khasawneh
This table is very important dr Saied that u must memorized it for now & for next year:
Its better if you study this table from Pinkham Book .
Dental lamina goes into 3 stages to form dental tissue:
1-Bud stage: the ectodermal outgrowth, with the adjacent mesenchyme.
2-cap stage: enamel organ growth around dental papilla like a cap.
3- Bell stage: enamel organ form 4 layers:
Outer enamel epithelium (OEE): it’s a single layer of cuboidal cells, prior to enamel
formation capillaries in the connective tissue, also have thin walls to enhance the
process of diffusion.
Stellate reticulum (SR): (in the middle part of enamel organ) Cells are star-shapedwith long processes reaching all directions. It’s a resistant and elastic structure so its
act as a buffer against physical forces.
Stratum intermedium (SI): flat to cuboidal in shape arranged in three layers, to play a
role in enamel formation through control of fluid diffusion or by contribution of
formative elements or enzymes.
Inner enamel epithelium (IEE): Derived from the basal cell layer of the oral
epithelium, before enamel formation begins, they become columnar and differentiate
into ameloblasts starting at the incisal or cuspal edges. They are continued to formcervical loop.
Formation of hard tissues: dentine forms (dentenogeneses) before enamel (amelogeneses) and
it are inducing enamel formation.
Dentinogenesis: its start when IEE cells lengthen and form ameloplast which induce
formation of odontoplast which form dentine. The 1st
layer to form is the mantle dentin its
poorly mineralized then more mineralized layer form called circumpulpal dentin. Each layer
forms as following: matrix formation then mineralized of the matrix.
Compostion of dentine: Inorganic component is mainly hydroxyapatite crystals, and
the organic component is mainly type I collagen. It’s softer than enamel bcz it’s less
mineralized.
(IMP)Principle of mutual induction: IEE cellsameloplastodontoplastsecretion
hydrostatic pressure- compressional force: this pressure comes from the pulse – the heart
cause some sort of pressure inside the arteries and veins and this pressure reaches to
extracellular fluids and causes this hydrostatic pressure that will make the tooth erupt.
NOTE: -The first evidence of eruption radiographicaly is bone resorption beneath the calcifiedcrown. Calcification of the crown is a critical step for the eruptive process since it provides a
rigid mass against which the forces within the follicle can act.
Chronology of human dentition:
primary teeth: Appear between 6 month-2.5 years, 20 in number, Sequence of eruption: A, B, D, C,
E, Sequence of calcification: A,=B,D=C,E.
Permanent teeth: Appears between 6-12 years, 28-32 in number, Root formation: 3 years post-
eruption.
Eruption principles:
(1) Sequence is more important than the timing of eruption. (2) Mandibular teeth erupt first.
(3) Symmetrical eruption on both sides of the jaw.
Eruption patterns in primary teeth: The "7 + 4" guideline
Teething problems: pain and discomfort aren’t pathological condition, so the child has
problem with chewing. Other problems may coincide with this stage due to lack of maternal
immunity,other symptoms wrongly assumed to be caused by teething includeinflammation of the mucous membrane overlying teeth.
Primary herpetic gingivostomatitis: This is one of the viral infections that coincide with
teething. It is caused by herpes simplex virus type I. If the child is immunocompromised ,
Antibiotics are prescribed. And the treatment is symptomatic. . It is characterized by vesicles
that erupt and then rupture into ulcers. And it's usually self-limiting within 7 to 10 days.
Eruption hematoma (eruption cyst): dentigerous cyst, it's associated with the crown of an
erupting primary or permanent molar. It usually occurs in the maxilla; it appears as an
Tumors related to teething problems Neoplasms, odontomes, cysts, ameloblastoma, fibro-osseous lesions. All are obstacles that usuallydelay eruption. When there's a tumor causing bone resorption around the area of a tooth bud, it causes
accelerated eruption of that tooth.
NOTE: go to the table’s page 18 and memorize them.
Summary done by: HEBAH R3D RAMADNEH
Causes of delayed and accelerated eruption:
Systemic causes: hormonal, syndromes.
Local causes: early loss of primary tooth, tumors,
