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Craniofacial & tooth biology > Theme II: Development of dental & tooth attachment tissues > Flashcards

Theme II: Development of dental & tooth attachment tissues Flashcards

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AP® Biology flashcards
1
Q

The key stages of initiation, morphogenesis and histogenesis in tooth development What each stage determines about the teeth

A
  1. Initiation: determines tooth identity/ type and position.
    - Primary epithelial band
  2. Morphogenesis: determines tooth shape, size and number.
    - Bud
    - Cap
    - Early Bell
  3. Histogenesis: formation of dental hard tissues. Differentiation.
    - Late bell
    - Eruption
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2
Q

What happens during initiation

A
  • Primary epithelial band forms. This is the thickening of the oral epithelium.
  • It results in a change of orientation of the cleavage plane of the dividing cells, from horizontal to vertically.
  • Invaginates down into the mesenchyme so it condenses.
  • The band continues to proliferate then bifurcates into dental lamina and vestibular lamina.
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3
Q

What happens during morphogenesis

A

1-Bud: Dental lamina elongates. Local swelling at the deep surface and condensation of surrounding mesenchyme.

2-Cap: Bigger swelling of the bud. More invagination into mesenchyme. Enamel organ, enamel knot, dental papilla and follicle form.

3-Early bell stage: Lots of cell layers develop: OEE, stellate reticulum, IEE, stratum intermedium.

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4
Q

What are the cell types and layers in the early bell stage of the tooth germ and mention their functions or shapes

A
  • Dental follicle
  • OEE: cuboidal, exchanges substances with follicle, barrier and maintains shape
  • Stellate reticulum: star shaped cells separated by glycosaminoglycans and collagen for cushioning/ protection and maintain tooth shape. Cells connected by desmosomes - (the part inside the germ)
  • Dental papilla - will form the pulp
  • IEE: columnar, signals to papilla to induce differentiation of odontoblasts
  • Stratum intermedium: flat, produces alkaline phosphatase and proteins which mineralise enamel. Support ameloblast function by transporting substances to and from IEE
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5
Q

What is the enamel knot. When does it form

A
  • Formed in Late cap stage of morphogenesis
  • A group of non-dividing epithelial cells, formed by mesenchyme.
  • It is a transient molecular signalling centre that secretes signalling molecules to induce cell proliferation during cap stage
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6
Q

What happens during histogenesis (late bell and eruption)

A

1-late bell stage: Cervical loop develops new layers of ameloblasts, odontoblasts, enamel, dentine.

  • Stellate reticulum moves downwards to protect the cellular area of the developing tooth.
  • Dental lamina is broken down.
  • Crown completed, REE forms, root begins to form

2-Eruption. Once crown is complete and the root is beginning to develop. REE fuses with the oral epithelium, which will form the dent-gingival junction

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7
Q

What is the cervical loop

A
  • Where the OEE and IEE meet. It is the growing end of the enamel organ
  • IEE and OEE communicate and coordinate the differentiation of odontoblasts and ameloblasts.
  • Later involved in root formation. Will form the epithelial diaphragm and HERS.

-a problem in this region results in crown not developing properly

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8
Q

What are the cell types and layers of the late bell stage (from papilla to OEE)

A
  • Dental papilla
  • Odontoblasts
  • Dentine
  • Separation artefact
  • Enamel
  • Ameloblasts
  • Stratum intermedium
  • Stellate reticulum
  • (OEE)
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9
Q

What is the reduced enamel epithelium and its functions. What will its fusion with the oral epithelium make

A
  • Formed from the flattened ameloblasts and the remnants of SR, SI, OEE.
  • In the late bell stage, after enamel maturation
  • Initiates bone remodelling for eruption
  • Protects unmineralised enamel before eruption.
  • Protects the enamel during eruption from being attacked and absorbed by osteoclasts.
  • Also will fuse with oral epithelium when it erupts to prevent bleeding. forms the dent-ginigval junction
  • Forms Nasmyth’s membrane
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10
Q

Successional teeth development from the dental lamina

A
  • Tooth germs of the incisors, canines and premolars of permanent teeth bud off lingually from the dental lamina of the primary
  • Molars have no primary predecessors. Formed by posterior growth of the dental lamina.
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11
Q

Function of the dental papilla and the follicle, and what they will form

A
  • Papilla: condensed mesenchymal cells underlying the enamel organ. Generates fibroblasts, odontoblasts and mesenchymal stem cells of the pulp. [Adjacent to IEE]
  • Follicle: Mesenchyme cells surrounding the organ, associated with OEE. Nourishes the tooth germ as vascular, protective and maintains its shape. Later generates the PDL, cementoblasts, osteoblasts, bone.
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12
Q

What gene mutations cause hypodontia. And at what stage in development

A
  • PAX9 and Msx1

- Morphogenesis, between bud and cap stage, as this affects the number of teeth

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13
Q

What gene mutations cause ectodermal dysplasia and at which stage in development

A

EDA1/ EDAR

  • Abnormal or missing teeth. Cone/ peg shaped.
  • Mutations during Initiation phase of development
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14
Q

What is the odontogenic potential. And describe when it switches

A

-The capacity of dental tissues/ cells to regulate and guide further tooth development. At different stages during development different cell types secrete signal molecules to regulate other surrounding cells.

1-During Initiation= epithelial cells. Secrete signal molecules to induce response in mesenchyme
2-Bud stage= Mesenchymal cells. Induce formation of enamel knot
3-Cap stage= enamel knot. Induce cell proliferation in surrounding cells causing down growth of enamel organ.

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15
Q

What is the odontogenic homeobox code. What genes encode incisor and molar regions

A
  • Shows which homeobox transcription factors are expressed in different regions of the upper and lower jaw.
  • Overlapping shows that a combination of genes result in specific teeth found in the region
  • Different homeobox code differ in mandible and maxilla
  • Incisors: Msx 1, Msx 2
  • Molar: Dix1, Dix2, Barx 1
  • Absence of genes causes of absence of teeth
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16
Q

What defects occur when mutations occur during the initiation stage of tooth development. Give examples of disorders.

A
  • Affects Tooth identity and number

- Ectodermal dysplasia, hyperdontia

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17
Q

What defects occur when mutations occur during the histogenesis stage of tooth development. Give examples of disorders.

A
  • Affects hard tissue formation

- Amelogenesis imperfecta, dentinogenesis imperfecta

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18
Q

What defects occur when mutations occur during the morphogenesis stage of tooth development. Give examples of disorders.

A
  • Tooth number, shape and size

- Hypodontia, hyperdontia

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19
Q

List examples of syndromic disorders associated with hypodontia

A
  • Ectodermal dysplasia
  • Treacher-collins syndrome
  • Apert syndrome
  • Rieger syndrome
  • Van der Woude syndrome
  • Oligodontia-colorectal cancer syndrome
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20
Q

3 things that can disrupt the eruption of teeth. And how delayed eruption affects the teeth.

A
  • Osteoperosis (bone disease)
  • Eruption cysts/ serre’s/ pearls (keratin-like material that block the eruption pathway in the gubernacular canal)
  • Odontome (benign tumor.)

-Cause various cellular defects at later stages and can cause other dental abnormalities.

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21
Q

What causes hyperdontia. What disorder is associated with this.

A
  • Overactivity of the dental lamina
  • Duplication of the dental lamina can cause multiple rows of teeth to form

-Cleidocranial dysplasia (RUNX2 mutation): associated with multiple extra teeth, bone defects, delayed eruption, malocclusion

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22
Q

What 3 defects does incomplete break down of the dental lamina at the late bell stage cause

A
  • Supernumerary teeth
  • Eruption cysts that block the eruption pathway causing delay
  • Odontomes (benign tumours, calcified masses)
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23
Q

What are eruption cysts / epithelial pearls. How do they form

A
  • Aka serre’s pearls
  • They are filled with keratin-like material arranged in concentric lamella.
  • They obstruct the eruption pathway (gubernacular canal) so delay eruption
  • Form from remnants of the dental lamina.
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24
Q

What happens to the stellate reticulum during late bell stage and why

A

-It relocates from overlying the mineralised region of the cusp to the lower regions that are more cellular and need more protection

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25
Q

What is the function of Tome’s processes. What are they

A
  • Extensions of ameloblasts
  • Enamel matrix secretion: Distal portion secrete enamel rods. Proximal portion secrete inter-rods. (Same composition but orientated differently)
  • Secrete enamel prisms at an oblique angle relative to ameloblasts position
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26
Q

2 Key enamel proteins in the enamel matrix and describe their function

A
  1. Amelogenins: 90% of matrix. Hydrophobic. Form nanospheres which surround the forming crystals to prevent them fusing and to prevent growth until there is enough ions. *Regulates growth and thickness of crystals
  2. Non-amelogenins (enamelin & ameloblastin etc.): 10%. First secreted. Hydrophilic and acidic so have a role in Ca and PO4 conc and crystal formation
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27
Q

What is HERS. How does it form. What is its fate

A
  • After crown completion, IEE and OEE proliferate downwards from the cervical loop to form the double cell layered HERS
  • IEE induce odontoblast differentiation to make root dentine
  • stretch by tooth dentine. Forms epithelial cells around root
  • May differentiate into cementoblasts.
  • Eventually disintegrates once root is complete. Remaining cells appear as rest of Malassez, which incorporate into the cementum.
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28
Q

Origins of cementoblasts

A
  • Formed during root development by dental follicle cells.

- Perhaps also from HERS

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29
Q

How enamel pearls develop (2 theories)

A
  • Rest cells of malassez (remnants of HERS) attach to predentine. Predentine signals differentiation of ameloblasts
  • OR, intermedium or reticulum cells may become trapped in rest cells which can initiate IEE differentiating into ameloblasts.
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30
Q

What causes lateral accessory root canals in the dentine. Why are they bad

A
  • If HERS is interrupted too early from capillaries in the papilla or follicle, it interferes with local formation of odontoblasts
  • It connects the pulp and PDL, so infection can spread
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31
Q

How dentine differs to enamel. Its properties.

A
  • Less HA so less brittle and softer
  • More organic matrix of collagen I (and III), glycoproteins, phosphoproteins.
  • Higher tensile strength, more resilient & elastic to support the enamel
  • Sensitive, due to innervation from the pulp (tubules wider closer to pulp).
  • Repairs itself
  • Less radiopaque than enamel due to less mineral content.
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32
Q

When does dentinogenesis occur and how. What do odontoblasts secrete

A
  • Late bell stage
  • Pre-amaeloblasts (derived from IEE) signal undifferentiated mesenchymal cells of the dental papilla to differentiate into odontoblasts.
  • Odontoblasts secrete predentine (unmineralised matrix), type I and III collagen and matrix vesicles.
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33
Q

What are matrix vesicles. What do they contain

A
  • Small membrane-covered vesicles produced by odontoblasts and secreted into dentine matrix, involved in mantle dentine mineralisation
  • They contain phosphoporyn that bind to Ca, and alkaline phosphatase that increases phosphate concentration
  • Crystallites burst out the vesicles to form the mineralising front
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34
Q

How does the thickness of predentine change during development and during ageing

A
  • Thickness is constant because the amount that calcifies/ mineralises is balanced by the addition of new unmineralised matrix by odontoblasts
  • During ageing it diminishes in thickness
35
Q

Describe globular and linear mineralisation of dentine. Fast or slow. Which regions they occur (mantle and circumpulpal)

A
  • Linear calcification- slow
  • Globular= fast.

Calcospherites form within the collagen matrix then increase in size and fuse together to form a single calcified mass

  • Mantle dentine= globular
  • Circumpulpal= Linear and globular
36
Q

What are calcospherites. What does incomplete fusion result in

A
  • Calcospherites: mineral spheres that form in the predentine. They fuse together during calcification.
  • If calcification is fast, incomplete fusion of calcospherites results in interglobular dentine which is hypominerlaised. Found in upper third of coronal dentine
37
Q

Difference between enamel spindles, tufts and lamella. How they form

A
  • Spindles: formed from an odontoblast process that has intercalated between 2 ameloblasts, during early stages of development (before hard tissues are formed) and it becomes trapped in the enamel. Small. Orientation doesn’t follow prism direction.
  • Tufts: hypomineralised voids that contain organic material (mainly tuftelin that hasn’t been removed) Project from EDJ to inner third of enamel and branch, following prism decussation.
  • Lamella: pass through the entire thickness of enamel. Look like cracks, but these are filled with organic material. Hypomineralised.. Could increase caries risk as bacteria could invade here.
38
Q

Why are dentinal tubules branched

A

-Decussation is higher in the region of the EDJ where tufts occur, helping to prevent crack propagation from enamel into dentine

39
Q

Describe the primary curvature and secondary curvature of dentine

A
  • Primary: S shaped tubules in coronal region due to overcrowding of odontoblasts
  • Secondary: changes in tubule direction during dentine deposition, due to stress and disturbances in formation, creating wavy tubules. =Contour line of Owen forms (Neonatal line in enamel)
40
Q

What are the dentine and enamel incremental growth lines called

A

Dentine:

  • Short period (dentine deposited daily) = von Ebner Lines
  • Long period= Anderson lines

Enamel

  • Short= cross striation
  • Long= Striae of Retzius
41
Q

When is primary, secondary and tertiary dentine made. Explain the 2 types of tertiary

A
  • Primary= during tooth development, until root completion
  • Secondary= after root completion and throughout life
  • Tertiary= made in response to stimuli
    1. Reactionary: weak stimulus, slow response (attrition) Original odontoblast still functioning so make new dentine, with fewer tubules
    2. Reparative. Strong stimulus, fast. Cells die so odontoblast-like cells deposit new dentine. No tubules
42
Q

What is intertubular and intratubular dentine. Which is more mineralised

A
  • Intertubular: between tubules. Less mineralised

- Intratubular: lines the inner surface of the tubules. Hypermineralised.

43
Q

What is sclerotic dentine

A
  • appears translucent in a ground section because increased deposition of peritubular dentine completely occludes the dentinal tubules
  • hypermineralised
  • Increases with age in areas of attrition and caries.
  • Protects the pulp against invading bacteria. Less tubules so less pathways for bacteria to get to pulp
44
Q

What are dead tracts in dentine

A
  • When odontoblasts die due to stimulus, the tubules lose their odontoblast processes. Tubules becomes empty and air-filled and appear as dark bands on ground sections
  • due to ageing or caries
45
Q

2 explanation of how Tome’s granular layer forms, and where is it.

A

-It is between the outer Hyaline dentine layer and the inner root dentine

1- incomplete fusion of calcospherites (similar to interglobular dentine in crown)

  1. or from extensive branching and backward looping of odontoblast processes
    - Hypomineralised
46
Q

Balance between fluoridation and fluorosis. Who is at risk

A
  • Water fluoridation (1ppm) makes fluoride hydroxyapatite which is less soluble. So enamel is more resistant to acid and demineralisation, reducing caries risk
  • Fluorosis: long term risk of Fluoride as it can disturb the ameloblasts during development causing mottling and staining. Only children under 8 are at risk because this is when permanent teeth are developing.
47
Q

What is acid-etching

A

-etching enamel with acid improves adhesion of restorative materials. It removes plaque and other debris and thin layer of enamel which appears matt and whiter. Increases surface area for retention of materials

48
Q

When does amelogenesis occur and the main steps in presecretory and secretory phase.

A

-Late bell stage of histogenesis, shortly after dentine formation
1-Short columnar IEE cells lining the basal lamina become taller preameloblasts and establish polarity. They make proteins and the basal lamina becomes fragmented and is resorbed.
2-Elongated ameloblasts secrete enamel matrix - First makes partially mineralised rodless enamel. And then they develop Tome’s processes, which secretes the mineralised enamel rods and inter-rods.

49
Q

What are Tome’s processes. How they form. What is their role. How the rod sheath is formed

A
  • The secretory processes of ameloblasts. Have a distal and proximal portions (Same composition but orientated differently)
  • Form when preameloblasts elongate (in bell stage)
  • Distal portion forms the enamel rods
  • Proximal forms the interrod.

-As enamel rods grow, distal portion elongates and is squeezed between the rod and interrod, creating a narrow space between them that fills with organic material and forms the rod sheath (boundary between rod and interrod.)

50
Q

Explain the maturation phase of amelogenesis.

A
  • Matrix dissembles where the nanospheres collapse and crystals and thicken, but decrease in height.
  • 50% of ameloblasts die.
  • Ruffled and smooth ended ameloblasts.
  • Ruffled: transport calcium into matrix
  • Smooth: remove water and protein
  • Alterations in permeability of enamel organ
  • Protective stage where REE and Nasmyth’s membrane develop to protect the tooth during eruption.

-Primary teeth less mineralised as less time in maturation phase

51
Q

What is the papillary layer, primary enamel cuticle, REE and Nasmyth’s membrane. Their functions and fates

A
  • Papillary layer = SR + SI + OEE
  • Primary enamel cuticle is secreted by ameloblasts and after eruption will interact with saliva to form the pellicle.
  • REE= ameloblasts + PEC. Protects crown from resorption by osteoclasts during eruption. Will form the junctional epithelium.
  • Nasmyth’s membrane is made of REE and PEC. Covers the enamel of unerupted teeth to prevent bleeding during eruption, and it is leaky so allows trace elements into the enamel.
52
Q

What are the properties of enamel

A
  • 96% hydroxyapatite by weight
  • Hard so resistant to abrasion and high forces
  • Brittle and likely to shatter so soft dentine supports it
  • Transparent
  • Non-living, cannot repair
53
Q

How the thickness of enamel varies in primary/ permanent and cusps/ cervical area. Which molars are thicker

A
  • Thicker in permanent
  • Thicker over cusps than cervical margin
  • Thickness increases from 1st to 3rd molars
54
Q

Enamel prism direction in primary and permanent teeth at cervical region

A

=Primary: obliquely orientated towards the oral cavity, upwards
=Permanent: obliquely orientated downwards towards the alveolar crest.
-So important to follow direction of prisms when making a cavity so no enamel is left unsupported

55
Q

What does the keyhole pattern of enamel prisms look like, how many ameloblasts make it, and its role.

A
  • A head and a tail, with different crystallite orientation. Each keyhole is made of 4 ameloblasts.
  • Head = rod. Direction of prisms is parallel to the long axis (1 ameloblast)
  • Long Tail= interrod, inter prismatic enamel which is oblique to the long axis (3 ameloblasts)
  • This pattern along with decussation strengthen the enamel structure and prevents cracks propagating into deeper areas. Improves resistance to fractures.
56
Q

What are Hunter-schreger bands

A
  • Optical phenomenan in the inner two thirds of the enamel. Alternating bands of light (parazones) and dark (diazones)
  • Due to the decussation (S shaped) of prisms
57
Q

What is gnarled enamel and how it forms

A

-ameloblasts are adapting to the fast development of crown and are displaced apically by their own enamel production.
=area of exaggerated decussation so the rods look angular and twisted
- Appears in the cusps so may be a functional adaptation to protect the tooth against strong masticatory forces, as decussation prevents propagation of cracks into deeper areas.

58
Q

Function of pulp. What % is water

A
  • Provides vitality to the tooth
  • Nourishment to the odontoblasts and other pulp cells via blood vessels
  • Protects by sensing external stimuli via nerve endings
  • Defense: producing tertiary dentine in response to external stimuli. And activates immune cells
  • 75% water, 25% organic material
59
Q

What cells are in the pulp and their functions

A
  • Odontoblasts: Makes unmineralised predentine which then mineralises to form dentine
  • Fibroblasts: produce collagen and ground substance. Also degrades collagen
  • Undifferentiated mesenchymal cells
  • Multipotent Pulp stem cells: can differentiate into odontoblasts, chondrocytes, osteoblasts, neutrons
  • Macrophages: remove dead cells and bacteria. Release cytokines as immune response
  • Lymphocytes, neutrophils and eosinophils
  • Dendritic cells: present foreign antigens to T cells
60
Q

How do the shapes of coronal and root odontoblasts differ

A
  • Coronal: columnar

- Root: more cuboidal and shorter

61
Q

Function of lymph vessels in the pulp and how they differ to blood vessels

A
  • Drain tissue fluid
  • Enter apical foramen
  • Thinner walls and contain no red blood cells
62
Q

What makes up the extracellular matrix of the pulp

A

1-Collagen Type I and III to provide stability

2-Ground substance (non-fibrous matrix):

  • Glycosaminoglycans, proteoglycans, glycoproteins and mainly water
  • Reservoir for growth factors which transport nutrients and metabolites
63
Q

What nerve types are found in the pulp and what is their role.

A
  • myelinated A delta= sharp fast pain and extend into tubules. Detect pain, mechanical, thermal and tactile stimulus
  • Unmyelinated C fibers= slow dull pain.
  • Autonomic fibers regulate blood flow by causing vasoconstriction or vasodilation for immune response
64
Q

When does root formation start and how

A

-Formation begins after crown completion
-IEE and OEE proliferate downwards from the cervical loop to form a double layer of cells called HERS
-IEE of HERS induces odontoblast differentiation to form root dentine. No ameloblast differentiation occurs.
-HERS encloses the pulp and appears as a curtain hanging down from the crown
-Curved end of HERS is termed the epithelial diaphragm which outlines the primary apical foramen
-HERS then disintegrates
[-Apex remains open during eruption]

65
Q

Does the position of HERS remain stationary while the root forms

A

-Yes. It does not grow downwards as new cells proliferate. The formation of dentine pushes the tooth root upwards

66
Q

How long does it take for root completion of primary and permanent teeth after eruption

A
  • Primary: 1.5 years

- Permanent: 3 years (2 years for incisors)

67
Q

How do multiple tooth roots form

A

1-HERS encloses the root, hanging from crown. It grows and produces root dentine to form a single root
2-The primary apical foramen can divide by fusion of epithelial folds (ingrowths) from HERS to form secondary apical foramen = 2 roots
3-If fusion occurs at 3 points it results in 3 roots.

68
Q

What are the 4 layers of the root

A
  • Cementum: acellular
  • Hyaline dentine: outermost dentine layer. Non-tubular layer, first dentine formed
  • Tome’s granular layer: incomplete fusion of calcospheres or backward looping of odontoblasts
  • Root dentine
69
Q

What is the difference between root and coronal dentine

A

1-Root dentine=collagen fibers parallel to basal lamina of HERS.

  • less mineralised. Less phosphoporyn that binds Ca
  • mineralises faster
  • Cuboidal odontoblasts

2-Coronal: collagen perpendicular to HERS. Mineralises slower.
-columnar odontoblasts

70
Q

Properties and contents of cementum

A
  • Avascular connective tissue covering the roots
  • Acellualr or cellular
  • Formed from cementoblasts in the PDL
  • Attachment of dentine to PDL and an attachment for sharpy’s fibers to bone.
  • 45-50% HA
  • Harder and more mineralised than bone
  • Collagen type I (and some III)
  • Alkaline phosphatase and other proteins similar to in dentine and bone
71
Q

Difference between cellular and acellular cementum

  • rate of development
  • pre-cementum layer
  • Where it is found
  • structure
A
  1. Acellular: Slow rate of development
    - Incramental lines close together
    - Precementum layer not visible.
    - Covers the roots, attachment for PDL
  2. Cellular: Clear border with dentine
    - Fast rate of development
    - Incramental lines wide apart
    - Precemntum layer present
    - Found in apical or interradicular areas for repair.
    - Lacunae containing cementocytes, and have canaliculi processes directed towards vascular PDL to gain nutrients
    - More in older people to compensate tooth wear.
72
Q

How does cementum form (3 things)

A

[-HERS disintegrates after inducing dentine formation]
1-Dental follicle cells into osteoblasts, fibroblasts and CEMENTOBLASTS
2-Undifferentiated follicle cells could migrate through gaps in the disintegrating HERS and align on newly formed dentine and differentiate into cementoblasts
3-Or HERS become cementoblasts. And rest of malassez incorporated into cementum

73
Q

What incremental growth lines are present in cementum

A

Lines of Salter

Caused by pauses in cementum formation

74
Q

How common is it for cementum to overlap with enamel, to touch, and to not meet

A
  • Overlapping= 60%
  • Meets enamel= 30%
  • Don’t meet= 10% - exposed dentine so sensitivity and susceptible to caries
75
Q

Defects in cementum - cementicles, concrescence, enamel pearls, dilacerated roots, multiple roots, hypercementosis

A

1-Cementicles: detached groups of cementoblasts from trauma. Acellular
2-Concrescence: cementum of 2 teeth fuse due to trauma or overcrowding
3-Enamel pearls: Epithelial rests of Malassez attach to predentine and signal ameloblast differentiation, forming a pearl. Or SI and SR could become trapped in the rest cells
4-Dilacerated roots: curved roots caused by developmental trauma in children
5-Multiple roots: abnormal folding of HERS
6-Hypercementosis: abnormal increases in production to compensate loss of enamel or bone

76
Q

How is mantle dentine formed. How it compares to other dentine

A
  • first layer of dentine deposited
  • Made by matrix vesicles secreted by odontoblasts
  • Less mineralised as it has less phosphoproryn to attract Calcium
77
Q

Why you cannot see enamel on a H&E histological section

A

-Decalcification process so removes mineralised enamel. Remaining enamel proteins collapse and are removed. So cannot see enamel

78
Q

What is peritubular dentine

A
  • dense mineralised tissue lining tubules
  • increased production forms with increasing age in response to attrition
  • recession of odontoblast processes from the tubules causing narrowing or closure of tubules. Hypermineralised.
79
Q

Why EDJ is scalloped. How it differs in primary teeth

A
  • increases surface area for more odontoblasts.
  • Provides better attachment of enamel to dentine
  • Stabilises the EDJ below the cusps where high forces

-Primary teeth form faster so less scalloping

80
Q

What is the neonatal line in enamel. How does the neonatal line in primary 1st and 2nd molar differ

A
  • Alteration in mineralisation of enamel during birth
  • represents the position of the mineralising front in dentine or the position of the distal ends of ameloblasts in enamel at the time of birth.
  • First molar is more developed during birth so line is further from EDJ
81
Q

Give examples of genes that encode signalling molecules and genes for transcription factors in tooth development

A
  • Signalling molecules = Wnt, Fgf, Tgf-B, Bmp, Hh, Eda

- TFs = Hox, Msx, Dix, Barx, Pax

82
Q

Where are mesenchymal cells derived from

A

neural crest cells

83
Q

What is the function of the capillaries located in the dental follicle

A

Capillaries in the dental follicle are closely associated with the OEE. Provides nutrients and blood supply to stratum intermedium and ameloblasts. This is required because the hard enamel and dentine block access of supply from the papilla to the ameloblasts

Craniofacial & tooth biology (4 decks)

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