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 4th 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

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(1) Outer enamel epithelium (OEE) It’s a layer that is adjacent to the dental sac , it’s a single layer of cuboidal cells , prior to enamel formation capillaries in the connective tissue surrounding the enamel organ proliferate and protrude toward it to increase vascularity, they also have thin walls to enhance the process of diffusion by which nutrients will be reaching the enamel matrix. (2) Stellate reticulum (SR) -Forms the middle part of enamel organ, filled by a large amount on intracellular substance (fluid). - Cells are star-shaped with long processes reaching all directions; they are connected with each other and with the cells of outer enamel epithelium and cells of the stratum intermedium with desmosomes. -It’s a resistant and elastic structure so its act as a buffer against physical forces. - It also permits the flow of nutrients to formative cells, as it reduces in thickness. After first layers of dentine form cutting the inner enamel epithelium from its original supply which is the dental papilla. (3) Stratum intermedium (SI) These are flat to cuboidal in shape arranged in three layers, they are believed to play a role in enamel formation through control of fluid diffusion or by contribution of formative elements or enzymes. (4) 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 . These cells are continuous with the outer enamel epithelium at the border of the wide basal opening of the enamel organ thus, forming the cervical loop.

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Formation of hard tissues:
1- Dentinogenesis : in which the dentin is formed 2- Amelogenesis: in which the enamel is formed

(1) Dentinogenesis: dentine is the first tissue to be laid, its laid before enamel, once the dentin is laid it will induce the enamel formation, and then enamel will induce more dentin to be formed it’s like a mutual induction between the enamel and dentin. -the dentin formation occurs when the inner enamel epithelium (IEE) cells lengthen and induce differentiation (become ameloblasts), and when they become ameloblast they will induce the differentiation of the odontoblast (cells that are responsible for dentin formation) from dental papilla.

The first formed layer of dentin which is less mineralized is the mantle dentin its poorly mineralized because it’s the first layer to be formed ( the minerals are not enough in the blood) but the layers after that are much more mineralized and called circumpulpal dentin. So dentin formation like any other mineralized tissue its formation occurs in two steps: 1- Matrix formation 2-Mineralization of the matrix the matrix is called predentin before mineralization and after the mineralization it will called dentin.

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Odontoblast: it’s a big cell with long process. Mantle dentin: first layer to be formed above it there will be DEJ (its near the DEJ) Circumpulpul dentine: around the pulp.

Compostion of dentine: -Inorganic component is mainly hydroxyapatite crystals , and the organic component is mainly type I collagen. - Dentine is softer and less brittle than enamel because it contains more organic components and its less mineralized than enamel(has less hydroxyapatite crystals than enamel). So if you know any disease that affect type I collagen, dentin will also be affected so this is how you link syndrome and diseases.

**IMP** Principle of mutual induction: -only after the first layer of dentin is formed the ameloblasts can begin their secretory activity as we said IEE will differentiate into ameloblast this will induce the differentiation of odontoblast, odontoblasts will lay down mantle dentin, and this will induce ameloblasts to lay down enamel. -its amazing how this mutual induction occurs between the epithelial cells (ameloblasts) and mesenchymal cells(odontoblasts) and that each one depends on the other .

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(2) Amelogenesis: Formation of enamel occurs in three stages: 1- Enamel matrix formation. 2-Calcification. 3-Maturation (Its beyond calcification its like the perfection of the calcification).

(1)Enamel matrix formation: in which the proteins involved in amelogenesis are produced, these enamel proteins are : Amelogenin, Ameloblastin, Enamelin . (2) Calcification: - Immediate partial mineralization occurs. -Most of the original proteins are removed. that means that the proteins are removed from the matrix and these proteins are replaced by minerals(calcium and phosphate) . -Proteins are removed by enzymes (proteolytic/degrading enzymes) . -Minerals come from the blood stream. (3)Maturation: -Characterized by gradual completion of mineralization and further remaining proteins are removed, the gaps are refilled by minerals (calcium and phosphate) this starts from the height of the crown and progresses cervicaly . -Its characterized by growth of hydroxyapatite crystals. -Fluoride is incorporated into the structure during this stage

Development of primary and permanent teeth: As jaws grow in length, the dental lamina penetrate posteriorly to form the buds of the permanent molar developed in mesiodistal sequence (the 6,7 and 8 developed in this manner) initially within the ramus of the jaw and later in the body of the jaw after the resorption of the anterior body of coronoid process.
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-From each tooth buds a successional lamina grows lingually to form the permanent successor tooth. That’s why the permanent tooth is usually lingual to primary tooth.

Differences between primary and permanent teeth (the dr. Explained them before so she didn’t mention the slide’s details, so these note s are from the handout). - The first difference is in size : permanent teeth are bigger than primary teeth. - A,B : Enamel and dentin are thinner - C: pulp chamber bigger, horns higher - D : cervical ridge more pronounced - E : Enamel rods slope occlusally - F: constricted neck - G: C-R ratio less - H : roots more flared & furcation closer to cervix. ->The crowns of primary teeth differ from one on the left is primary, and the one on the right is permanent. those of permanent teeth, by: -Shorter -Narrower occlusal table -More constricted cervically -Broad, flat contact areas -Lighter in color - Enamel rods slope occlussaly in gingival third, but slope apically in permanent teeth. ->The roots of primary teeth differ from those of permanent teeth by: -Narower mesiodistally -Longer and slender in relation to crown size -Flare towards apex to accommodate permanent tooth buds ->The pulp of primary teeth differs from those of permanent teeth, by: - Larger in relation to crown size
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-Horns closer to outer surface - Mesial pulp horn higher than distal -Mn molar has larger pulp than Mx -Form of pulp chamber follows shape of the crown - Usually pulp horn under each cusp. ->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 development inside 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
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within the PDL, three possible agents have been identified to explain the eruptive force: (1) Collagen contraction- tensional force : Collagen contract and pushes the tooth upward to oral cavity. (2) Fibroblast traction- tensional force .

(3) Tissue fluid hydrostatic pressure- compressional force: tissue fluid that’s around the tooth bud. -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 no extracellular 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 a rigid 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 happ en before calcification in order to maintain the morphology of the tooth.
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Chronology of human dentition : primary teeth: - Appear between 6 month-2.5 years - Called deciduous , baby and milk teeth - 20 teeth in number: A ,B, C, D, E. - Sequence of eruption: A, B, D, C, E. - Sequence of calcification: A,=B,D=C,E - Root formation: 18 months post eruption. -Importance: mastication,esthetics,speech,avoid infection —turner’s spots, space maintenance& arch continuity. permanent teeth: - Appears between 6-12 years - 28-32 in number - Sequence of eruption: * Mx : 6,1,2,4,5,3,7,8 * Mn: 6,1,2,3,4,5,7,8 -Sequence of calcification: * Mx: 6,1,3,2,4,5,7 * Mn: 6,1=2,3,4,5,7 -Root formation: 3 years post-eruption.

Eruption principles: (1) Sequence is more important than the timing of eruption . that means if the upper central incisor should erupt at the age of 8 years old and the patient now is 9 years old and his central incisor didn’t appear , so you get shocked and you start asking why, so first of all you look at the lower incisors and the first molars have they erupted?? Cause the upper centrals usually erupt after them , so if
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the lower incisors and molars still not erupted its not the time of upper centrals eruption and we should focus on why they are not erupted yet because the sequence of teeth eruption is more important . Sometimes there will be delay in tooth eruption, because the dates that we study are average dates and they are not necessary apply to all patients. There are many big range of differences between different races or ethnic groups. (2) Mandibular teeth erupt first. (3) symmetrical eruption on both sides of the jaw: always check eruption on both sides, so if the six (first molar) erupted in the right side it should also appear in the left side if not , there is a problem. So always check for : timing and symmetry End of part 1 DONE BY: Gewanna J. Ghazal

Here's an example: The premolar has erupted on one side; it's Almost in full occlusion, while it hasn't Erupted on the other side. Here we're Concerned about symmetry. The premolar that hasn't erupted is dilacerated because of an infection in the primary tooth .

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The primary tooth was eventually extracted; a space maintainer was placed to allow the permanent tooth to erupt, which it did. It was rotated when it erupted because of the dilaceration; and so it was aligned orthodontically.

Eruption patterns in primary teeth
Usually at 6 months of age, the 71 and 81 appear. At 7 months, 51 and 61 appear. You have to keep in mind that there are differences between people. A total of 4 teeth will have erupted within the first year (between 6-12 months) of age.

 The "7 + 4" guideline
You add 4 to each side of the table to get a rough estimation of eruption times. (It's not necessarily accurate.) Age 7 11 15 19 23 27 Erupted teeth 0 4 8 12 16 20

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Teething problems:
 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 biting on 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. Immunoglobulins are present in breast milk, and are provided to the child by the mother up to the age of 6 months. After that, the child has to depend on his/her own immunity. At this stage, the child is exposed to many microorganisms, and, since the child moves (crawls) around and then bites his/her fingers, he/she will get lots of infections.

 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 7 to 10 days.
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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 healthy individuals) 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.

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Premature exfoliation of primary teeth It's mainly caused by caries, periapical infections, and, sometimes, trauma. Other causes include hormonal causes (like hypophosphatasia), tumors (like histiocytosis X), and some syndromes. This condition will cause space problems.

Causes of delayed and accelerated eruption:  Systemic causes: hormonal, syndromes.  Local causes: early loss of primary tooth, tumors, trauma, severe periodontal disease, presence of obstacles.

Ectopic eruption The tooth erupts in a site other than its normal position . Permanent maxillary canines are the teeth most commonly erupted ectopically (they might go palatally or buccally). It may involve permanent mandibular central incisors (which erupt lingually), or permanent maxillary central/lateral incisors (which erupt palatally), which might erupt lingually. It might also involve first molars. The guidance theory and the genetic theory are theories pertaining to the etiology of this condition.

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Impaction It's when the tooth is stuck inside and doesn't erupt. Usually permanent maxillary canines and third molars get impacted. Most (85%) impacted permanent maxillary canines have palatal impaction, the rest (15%) are impacted buccally. Impaction is usually unilateral.

Infraocclusion (submerged teeth) It's when the tooth fails to maintain its position relative to the adjacent teeth of the dentition, and it gets submerged (below the occlusal level). It occurs most commonly in the mandibular D's at the age of 8-9 years. The most common cause is ankylosis. Possible sequelae include interference with eruption of the premolar, tilting or overeruption of the adjacent teeth, space loss, and destruction of the occlusal plane. We usually monitor and await normal exfoliation: if the ankylosis rate is minimal, we can leave the tooth as it is; if the ankylosis rate is quicker, we go for restoring the tooth to the level of the occlusal plane; if it's too quick, we extract the tooth. Treatment depends on the presence or absence of the permanent tooth , the onset and time of diagnosis, the resorption rate, rate of progression of infraocclusion, and the risk of adverse effects over time.

Tooth transposition It's when two teeth exchange positions. It's not very common. It's caused by intraosseous migration of the tooth buds, and eruption of the tooth bud into an ectopic position ordinarily occupied by a nonadjacent tooth. Seven types have been identified in the human dentition: five in the maxilla; two in the mandible.

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Maxillary: - Canine and first premolar. (Most common.) - Canine and lateral incisor. - Canine and first molar. - Lateral incisor and central incisor. - Canine and central incisor. Mandibular: - Lateral incisor and canine. - Canine transmigrated/erupted.

Natal teeth 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. (Cysts form because of the delay in eruption.)
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 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. The problem 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 important growth 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 .

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Chronology table

Checked by:salam bataieneh Very especial thanks for Gewanna J. Ghazal for her effort  thank u

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Summary for this lecture
Tooth development  Dental epithelium consists of: 1- enamel organ (ectoderm) 2- dental papilla (ectomesenchyme) 3-dental follicle.  Tooth formation (8 weeks intrauterine), tooth mineralization (4 months intrauterine). 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-shaped with 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 form cervical 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 cells ameloplastodontoplastsecretion dentine ameloplast  and so on.
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 Amelogenesis: happened in 3 stages: 1. Enamel matrix formation: (Amelogenin, Ameloblastin, Enamelin ) 2. Calcification: (partially mineralized) the proteins are removed from the matrix and these proteins are replaced by minerals (calcium and phosphate). Minerals come from the blood stream. 3. Maturation: Characterized by gradual completion of mineralization and further remaining proteins are removed.

Development of primary and permanent teeth:
  As jaws grow in length, the dental lamina penetrate posteriorly to form the buds of the permanent molar From each tooth buds a successional lamina grows lingually to form the permanent successor tooth.

Differences between primary and permanent teeth:
  Permanent teeth are bigger than primary teeth. those of permanent teeth, by: shorter, Narrower occlusal table, More constricted cervically, Broad, Lighter in color, Enamel rods slope occlussaly in gingival third, but slope apically in permanent teeth. The roots of primary teeth differ from those of permanent teeth by: Narower mesiodistally, Longer and slender in relation to crown size, Flare towards apex to accommodate permanent tooth buds. The pulp of primary teeth differs from those of permanent teeth, by: Larger in relation to crown size, Horns closer to outer surface, Mesial pulp horn higher than distal, Mn molar has larger pulp than Mx , Form of pulp chamber follows shape of the crown, Usually pulp horn under each cusp.

Eruption: (The main direction of movement is axially, the fastest rates of eruption are seen
following the crown emergence) its accrue in 5 stages: 12345Pre eruptive- when it is still tooth bud Intraosseous- when it is inside the bone Mucosal penetration- this is actually where the child starts feeling some sort of discomfort Pre-occlusal- after penetrating the mucosa but still not reaching its final position Post-occlusal- if there is no opposing tooth the tooth will keep on erupting.

Theories of eruption: Theories of eruption: within the PDL, three possible agents have been
identified to explain the eruptive force:
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(1) Collagen contraction- tensional. (2)Fibroblast traction- tensional force. (3) Tissue fluid 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 calcified crown. 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 posteruption.
- Sequence of eruption: * Mx : 6,1,2,4,5,3,7,8 * Mn: 6,1,2,3,4,5,7,8 -Sequence of calcification: * Mx: 6,1,3,2,4,5,7 * Mn: 6, 1=2, 3,4,5,7

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
Age 7 11 15 19 23 27 Erupted teeth 0 4 8 12 16 20

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 include inflammation 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
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asymptomatic bluish swelling that is occasionally filled with blood. The cyst is treated by marsupialization or excision of the overlying tissue to expose the crown and drain the fluid. 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. Premature exfoliation of primary teeth: It's mainly caused by caries, periapical infections, and, sometimes, trauma.
Causes of delayed and accelerated eruption:  Systemic causes: hormonal, syndromes. Local causes: early loss of primary tooth, tumors, trauma, severe periodontal disease, presence of obstacles.

Ectopic eruption: The tooth erupts in a site other than its normal position. Permanent maxillary canines are the teeth most commonly erupted ectopically Impaction: Permanent maxillary canines are the teeth most commonly stuck apically. Infraocclusion (submerged teeth): tooth fails to maintain its, It occurs most commonly in the mandibular D's at the age of 8-9 years. Tooth transposition: It's when two teeth exchange positions. It's not very common Natal teeth: They are displaced superficially, very close to the mucosa, so they erupt very early (in the uterus), Most commonly affected teeth are mandibular central incisors, followed by the maxillary incisors.

Eruption problems associated with syndromes
Cleidocranial dysplasia: (dental aspect) Multiple supernumerary teeth, Delayed dental development and complete primary dentition up to the age of 15 years

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.

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.

NOTE: go to the table’s page 18 and memorize them. Summary done by: HEBAH R3D RAMADNEH 
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