Module 1 Overall Flash Cards

Phases of tooth formation

1. Initiation

2. Eruption

3. Development

When is initiation complete for the primary dentition?

6 weeks in utero

When does eruption into the oral cavity occur for the primary dentition?

6 - 30 months of age

When does the development phase occur for the primary dentition

6 months - 6 years of age

When is the initiation phase complete for the permanent dentition

4 months in utero

When does eruption occur for the permanent dentition

6 years to 21 years old (typically 18-21 for the wisdom teeth)

When is the development stage complete for the permanent dentition

13 years and onwards

When can the mixed dentition be found

between 6 and 13 years old

What two types of cells give rise to the tooth

Epithelial Cells

Neural Crest Cells

What do tooth epithelial cells give rise to

Enamel

What do neural crest cells give rise to

dentine, pulp, cementum, periodontal ligament, alveolar bone

What are the stages of tooth development

1. Initiation

2. Bud stage

3. Cap stage

4. Early bell stage

5. Late bell stage

6. Root formation

Describe the initiation stage of tooth development

Starts at 6 weeks in utero

Formation of the dental lamina on the maxillary and mandibular processes in oral epithelium

Dental lamina → dental placode (the region where the tooth will form)

• thickens as a result of reciprocal induction

The thickening of dental lamina forms tooth buds in the dental placodes

Reciprocal induction

interaction between epithelial cells and neural crest cells - mediated by growth factors

What happens to the oral epithelium after 11 weeks in utero

it loses its ability to form teeth and undergoes further differentiation

Describe the bud stage

Further differentiation of epithelial and neural crest cells

Epithelial cells proliferate into mesenchymal tissue inside the dental lamina

• Epithelial peripheries develop faster than interior causing invagination of the tooth bud into the cap structure

NCC will condense around the tooth bud (thickened dental lamina)

Epithelial and NCC separated by basement membrane, but growth factors continue to mediate interactions - reciprocal induction

Describe the cap stage

The cap structure = the enamel organ

Epithelial cells differentiate into:

• Inner enamel epithelium (IEE) - located on concave area of enamel organ [near dental papilla] - forms ameloblasts

• Outer enamel epithelial (OEE) - line left and right walls of enamel organ [near dental follicle] - maintains enamel organ shape, responsible for exchange of substances

Neural crest cells differentiate into:

• Dental papilla - forms dentin and pulp

• Dental follicle - forms cementum, periodontium, alveolar bone

What components comprise the tooth germ

The tooth germ is composed of the enamel organ, dental papilla, and dental follicle.

Describe the transitory structures

1. Enamel knot (EK)

   • undefined cells that aggregate at centre of tooth cusp - regulate signals that help transition tooth from cap to bud stage

2. Enamel Niche

   • tooth germ may show double attachment to oral epithelium, ie. two dental lamina

3. Enamel cord

   • strand of cells from the stellate reticulum to the outer enamel epithelium that supplies nutrients to the enamel knot

Describe the early bell stage

Enamel organ begins to resemble bell-shape as the cap deepens - cells form final shape

Shape of epithelial cells:

• OEE = low cuboidal shape

• IEE = short columnar

IEE and OEE meet at Cervical Loop

Stratum Intermedium forms above IEE

Stellate Reticulum forms

What two types of lamina enable the formation of permanent teeth

Successional Lamina

Accessional Lamina

Successional Lamina

forms from dental lamina and gives rise to permanent teeth that replace primary teeth.

Primary incisors → permanent incisors

Primary canines → permanent canines

Primary molars → permanent premolars**

Accessional Lamina

forms from the dental lamina and contributes to the development of permanent molars that do not replace primary teeth.

Describe the late bell stage

mineralization of the enamel organ and development of the shape of the tooth bud into the future crown

Epithelial cells

• IEE → pre-ameloblasts → ameloblasts → enamel

NCC

• dental papilla → pre-odontoblasts → odontoblasts → dentine

• remaining dental papilla will form pulp

Mineralization of the tooth

Breaking of the basement membrane in late bell stage allows for Epithelial-NCC signaling and enables direct signaling between pre-ameloblasts and pre-odontoblasts

What proteins do ameloblasts secrete

enamelin and amelogenin

Cell rests of Serres

remnants of leftover dental lamina as the lamina disintegrates

cell rests usually disappear after 5 years, but can be tumorgenic if they persist

Reduced enamel epithelium

Following the crown formation, the IEE and OEE form the REE that plays a role in tooth eruption

Describe the Root Formation stage

OEE and IEE form the Hertwig’s Epithelial Root Sheath (HERS) - separates the dental pulp from the dental follicle.

HERS dictates the number of roots a tooth will have

HERS will disintegrate and dental follicle will interact with dentine to form cementum

Cell Rests of Malassez

remnants of the disintegrated HERS

can form cysts and tumors

What does the dental follicle differentiate into

1. Cementum (create root surface)

2. Fibroblasts (create collagen and PDL)

3. Osteoblasts (create alveolar bone)

Composition of enamel

96% mineral

• calcium hydroxyapatite [Ca10(PO4)6(OH)2]

4% organic material

• protein matrix and water

• protein matrix = amelogenin

Enamel is acellular = no capacity to repair itself

What are the stages of enamel formation

1. Initiation

2. Secretion

   • ameloblasts secrete enamelin and amelogenin

3. Mineralization

   • deposits of Ca and PO4

4. Maturation

   • enamel becomes more dense

I See Many Teeth (initiation, secretion, mineralization, thickening [maturation])

Structure of Enamel

Rods and interrods arranged in a prism - formed by ameloblasts

Rods run perpendicular to the dentinoenamel junction (DEJ)

Rods: long cylinders (~4 micro m)

Interrods: crystals oriented obliquely

Rod Sheath: space between rods and interrods - made of highly organic material

Tomes’ process

cytoplasmic projection from the ameloblast that produces rod enamel fibers (distal end) and interrod enamel fibers (proximal end)

Short term incremental bands (Cross Striations)

short lines (perpendicular to enamel rods) that show the rhythmic daily production of enamel

Each group of 1 light band and dark band = one day of enamel growth

Diurnal Rhythm

the varying levels of enamel production creates light and dark bands

light bands = more mineralized (day time)

dark bands = less mineralized (night time)

Long term incremental lines (Striae of Retzius)

longer cycles of enamel production (7-11 day intervals)

line deformities can be seen in the enamel, indicating periods of stress or disturbance during enamel formation.

Lamellae, Tufts, and Spindles

Lamellae: extend from enamel surface to DEJ - contain large amounts of organic material (black) - offer channel for bacteria to pass through

“Line from Lid (enamel surface)”

Tufts: extend partially from DEJ into the enamel. No significance

“Tucked at DEJ”

Spindles: trapped extensions of odontoblasts near DEJ

“Spin up from pulp”

Hunter-Schreger Bands

Highly mineralized (white) bands that extend from DEJ to 2/3 into the enamel

Provide anti-fracturing strength

Gnarled Enamel

found in pointed regions of enamel (cusps)

complex enamel structures that increase strength and crack resistance

Types of cementoenamel junctions

Overlapping: 60%

Edge-to-edge: 30%

Gap: 10%

Dentine composition

70% mineral

20% organic material

• collagen type 1

10% water

** Dentine has regenerative ability

Dentinal Tubules

produce the organic matrix in dentine

odontoblasts reside in pulp-dentine margin

• body of odontoblasts is in pulp - odontoblasts extension protrude into dentine

Peritubular Dentine

Highly mineralized dentine that surrounds the dentinal tubules, providing structural support and influencing the mechanical properties of dentine.

Intertubular dentine

the less mineralized space between dentine tubules

Types of dentine

1. Mantle dentine

   • forms first, smallest in size, perpendicular to DEJ, less mineralized with more collagen

2. Primary dentine

   • bulk of dentine, forms during tooth development

3. Secondary dentine

   • forms at slower rate after root formation, surround pulp chamber

4. Tertiary dentine

   • repairs damaged dentine in localized regions

Circumpulpal dentine

primary + secondary dentine

Globular dentine

normally dentine is mineralized linearly but in globular dentine, mineralization occurs in a more irregular pattern, leading to areas of incomplete mineralization.

hypomineralization can cause interglobular dentine = less mineralization of dentine in specific areas, affecting tooth strength and health.

Globular is Great; Interglobular is Incomplete

Granular layer of tomes

black granules found in root dentine - hypomineralized clusters

Diurnal Dentine Lines

perpendicular lines to dentine tubules - 5 day lines made of collagen

Biomineralization Types

Amorphous: granules of crystals with no defined morphology

Crystallized: clusters of granules with a defined morphology

Amorphous is Awkward, Crystalline is Clean

Biomineralization of dentine

Matrix-mediated

Matrix proteins (collagen type 1 and fibroblasts) develop backbone of matrix

Odontoblasts release Ca and PO4 through dentinal tubules

Biomineralization of enamel

Hydroxyapatite grows first due to a lack of collagen

Enamel grows faster laterally than it does thick

No elaborate matrix

Proteins involved in Enamel mineralization

Enamelin - coats surface of mature HA

Amelogenin - regulates HA growth

Nonamelogenins - initially deposited but degrade quickly to have compact crystals

Tuftelin - localizes at the DEJ and enables the establishment of the DEJ

Enzymes - enamelysin (MMP20; short term break down of enamel), serine proteinase (bulk degradation of enamel)

Aunt Emily Never Touches Emus

Types of congenital dental malformations

isolated (non-syndromic) or syndromic

Isolated

65% unknown aetiology, environmental, trauma or infection, genetics 5-10% (causes amelogenesis/dentinogenesis imperfecta).

Syndromic

genetic mutations (inherited), chromosomal malformation, isolated mutations, mitochondrial defects, epigenetic influences

What type of abnormalities occur at the initiation/bud phase

tooth number anomalies

What type of abnormalities occur at the cap/early bell phase

shape/size anomalies

What type of abnormalities occur at the late bell/root phase

hypomineralization/tooth discolouration

Hormones involved in tooth development (Initiation through Cap stage)

FGFs

BMP

EDA

WNT

MSX1

Activin

Fancy Baby Enamel Wants More Activation

Hormones involved in tooth development (Early bell through root formation stage)

Enamel matrix proteins

DSPP

Collagen

Hypodontia

Missing teeth caused by Ectodermal Dysplasia; 7 in 1000 births

Mutations in:

• ectodysplasin A

• MSX1

• AXIN2

Most likely to be missing 3rd molars, 2nd premolars, maxillary lateral incisors

Typically autosomal dominant

Oligodontia

Hypodontia where more than 6 teeth are missing

Ectodysplasin A

gene that regulates ectodermal tissue growth

MSX1

multiple epithelial-mesenchymal interactions

AXIN2

cell apoptosis; most likely to cause oligodontia

Cleidocranial Dysplasia

a type of hyperdontia

caused by RUNX2 mutation (FGF regulator in bone and teeth)

Other Features:

• clavicles missing

• enlarged mandible

• reduced maxilla

• enlarged frontal bone

Dental Features

• supernumerary teeth

• delayed eruption

Gardner’s Syndrome

APC (tumor suppressing gene) mutation

creates multiple jaw osteomas that give a “cotton wool” appearance to the jaws

causes impacted and supernumerary teeth

Shape and size abnormalities

Macrodontia: larger teeth

Microdontia: smaller teeth

Peg shaped teeth

Invaginated odontoma or Den invaginatus

Evaginated odontoma or Den evaginatus

Amelogenesis Imperfecta

1:700 to 1:1400 people affected

Mutations in enamel matrix genes:

• ameloblastin

• enamelin (most common)

• tuftelin

• amelogenin

• FAM83H

Can be autosomal dominant (mutation in enamelin or FAM83H); autosomal recessive (ameloblastin mutation); X-linked dominant (amelogenin mutation)

defect in the mineralization of the enamel

Amelogenesis Imperfecta (Hypoclastic)

deposition of enamel matrix is defective, mineralization is normal

• Smooth - not much enamel, so the tooth is soft and smooth, can also give incisors a chisel-like appearance

• Rough - surface enamel is thin

Clastic, Like Plastic = Thin

Amelogenesis Imperfecta (Hypocalcified)

defect in the mineralisation of matrix

• Normal thickness of the enamel, less mineralised, but has more organic materials and proteins.

• Yellow-brown discolouration, loss in biting force, but doesn’t break because it’s very soft.

Calcified = Chalky and Soft

Amelogenesis Imperfecta (Hypomaturated)

maturation of enamel is affected

• Hard, but brittle enamel → can cause enamel chipping.

• Inner enamel is less mineralised than the surface enamel (inner is less dense)

Dentinogenesis Imperfecta (DI)

1:6000 to 1:8000 people affected

defect in the mineralization of the dentin

teeth appear translucent and thin - easily chipped

Dentinogenesis Imperfecta Type 1

combined with osteogenesis imperfecta

caused by collagen gene mutation (COL1A1 and COL1A2)

80% autosomal dominant

20% autosomal recessive

Dentinogenesis Imperfecta Type 2 and 3

caused by dentin sialophosphoprotein (DSPP) mutation

autosomal dominant

Dentin dysplasia type 1

Autosomal dominant condition - 1:100 000

Also known as radicular dentin dysplasia (rootless tooth, but crown is preserved)

High tooth mobility (loose) and premature exfoliation

Wide variation in root formation and shapes based on the stage of tooth development

Shape and colour looks normal

Microscope: stream flowing around boulders

Dentin dysplasia type 2

Thought to be a variation of dentinogenesis imperfecta

Affects both primary and permanent teeth

Clinical signs: discolouration in primary, no discolouration in permanent

Xray: similar to dentinogenesis imperfecta for primary teeth, enlargement of the pulp - flame shaped for permanent teeth

Regional Odontodysplasia (Ghost Teeth)

• Localised and nonhereditary - affects dentine, enamel and dentinal pulp

• Idiopathic origin, associated with other conditions

• Affects both dentitions

• >in Females, > in anterior maxilla

• Affected teeth fail to erupt and cause infection

• Crown is disfigured, yellow-brown, caries

• Ghost: dentine and enamel are hypomineralised - hard to distinguish between them

• Regional - affects many teeth

• Microscope: defective dentine, lack of dentinotubules

Gemination

single tooth bud where the crown of the tooth is bifurcated into two bifid crowns

affects primary and permanent teeth

generally affects maxillary incisors and canines

Fusion

two tooth buds fuse into one single tooth at the crown

generally affects mandibular teeth

Concrescence

two developed adjacent teeth are fused at the root by cementum

generally affects posterior maxillary teeth

can be developmental (entire roots are fused) or Post-inflammatory (only tips of the root are fused)

Cusp of Carabelli

extra mesiolingual cusp on the maxillary molar (near the palate)

Talon Cusp

“sharp” extra cusp on lingual side of anterior teeth (more common in the maxillary incisors)

Dens Evaginatus

Cusp like elevation on the occlusal surface of premolars (more common) and molars

Dens Invaginatus

folding of the crown into the root during tooth development

More common in permanent lateral incisors and maxilla

Looks like one tooth is sitting within another tooth (right on figure below)

1. Type I: Invagination confined to crown

2. Type II: Invagination extends to root

3. Type III/IV: Invagination extends through root apex

Enamel Pearl

pearl shaped structure on root of upper permanent molars (near furcation)

Cervical enamel extensions

extra enamel extending into the root of mandibular molars on the buccal surface towards the furcation

• common in the the 3rd molar

Taurodontism

enlargement of the pulp chamber

3 classifications: mild, moderate, severe

can be unilateral or bilateral

can be associated with AI or down syndrome

Hypercementosis

excessive deposition of cementum on roots of teeth

Dilaceration

unusual bending of the root or crown

often caused by injury or due to location (adjacent to cyst/tumor)

affects impaction

more common in mandibular third molars and anterior teeth