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Oral Histology > L3 > Flashcards

L3 Flashcards

1
Q

22 pairs of

A

autosomes

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2
Q

Germ cells (gametes) =

A

spermatozoa and ova

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3
Q

Osteogenesis imperfecta (OI) =

A

Hereditary disease affecting bones and teeth
Mutations in COL1A1 (type I collagen)
Autosomal dominant = 1 mutant allele is enough to cause OI phenotype
AD: Usually shows up in every generation, 50% chance to show up in offspring

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4
Q

Supernumerary incisor

A

Autosomal recessive = Need 2 mutant alleles to change phenotype

AR: Two “carriers” necessary to contribute 2 mutant alleles to offspring
AR: Does not show up every generation, beware of consanguineous unions

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5
Q

Amelogenesis imperfecta (AI)

A

Mutations in AMELX gene on X chromosome

X-linked

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6
Q

Induction: The process that initiates

A

differentiation.
An inducer is an agent that provides cells with a signal to differentiate
BUT, cell must be competent to receive the signal

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7
Q

Competence: Ability of cell to receive and respond to a

A

molecular signal
Receptors
Internal machinery

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8
Q

Signaling affects…

A

Cell differentiation
Cell proliferation: Dividing into more cells
Cell migration: Moving to a new location

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9
Q

Transcription factors (TFs):

A

Controlling gene expression

Proteins that control whether genes will be transcribed into mRNA (to be translated into proteins)
One TF can control expression of dozens, hundreds of genes
TFs can activate or repress expression of target genes

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10
Q

DLX3: Distal-less Homeobox 3

A

214 amino acid TF in DLX family
Mutations in DLX3 lead to TDO syndrome

Tricho-dento-osseous (TDO) syndrome
(Hair-teeth-bone)

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11
Q

TDO syndrome

A

DLX3 regulates…
Hair follicle differentiation
BMP signaling

Enamel genes
Amelogenin
Enamelin
Kallikrein 4

Bone
Formation
Resorption
Homeostasis

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12
Q

Fetus

A

8-40 weeks

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13
Q

0 to 4 weeks Mostly

A

proliferation and migration, some differentiation

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14
Q

4-8 weeks

A

Cell differentiation, formation of major external and internal structures (morphogenesis)

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15
Q

Blastocyst stage

A

Embryoblast= Inner cell mass (ICM)
ICM forms ALL tissues of the embryo = embryonic stem cells
Other cells = trophoblast layer

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16
Q

Bilaminar (2 layer) embryo

A

2 germ layers: primary cell layers
Ectoderm dorsal
Endoderm ventral

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17
Q

Ectodermal cells converge toward the

A

midline to form the primitive streak

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18
Q

Ectodermal cells migrate through the

A

streak between ectoderm and endoderm

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19
Q

New mesoderm layer

Gastrulation: Conversion to

A

trilaminar embryo (3rd week)

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20
Q

Gastrulation

New

A

mesoderm layer separates ectoderm and endoderm (3rd germ layer)

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21
Q

Cephalic (more rostral) migrating cells form

A

notochord to support the embryo

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22
Q

Buccopharyngeal membrane remains

A

bilayer of ectoderm and endoderm – NO mesoderm

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23
Q

Weeks 4-8

A

Differentiation

Major structures

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24
Q

Rostro-caudal (front-back) folding –

A

Happening during week 4

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25
Q

One consequence of rostral-caudal folding – a !

A

MOUTH

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26
Q

Stomatodeum =

A

primitive oral cavity

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27
Q

Buccopharyngeal membrane defines most

A

rostral boundary of primitive gut

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28
Q

Buccopharyngeal membrane =

A

Bilayer of ectoderm and endoderm

Breaks down to allow stomatodeum to communicate with foregut

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29
Q

Cranial neural crest cells (NCCs)

A

Ectoderm in origin

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30
Q

Cranial neural crest cells (NCCs): Adjacent to

A

neural tube – separate from neural plate when neural tube closes (~ day 22/end of 3rd week)

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31
Q

Cranial neural crest cells (NCCs): Capacity to

A

migrate and differentiate extensively

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32
Q

Cranial neural crest cells (NCCs): Induced to undergo

A

epithelial-mesenchymal transformation- they are referred to as ectomesenchymal cells

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33
Q

Cranial neural crest cells (NCCs): Acting as

A

mesenchyme, NCC ectomesenchymal cells form most of the connective tissues of the head, including teeth and their supportive tissues

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34
Q

Some craniofacial bones come from

A

ectomesenchyme

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35
Q

During brain development, the neural tube expands as

A

forebrain, midbrain, hindbrain

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36
Q

Hindbrain forms

A

8 rhombomeres = bulges

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37
Q

Rhombomeres define the origins of

A

distinct populations of NCCs

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38
Q

NCCs from midbrain and rhombomeres 1, 2 contribute to

A

branchial arch 1

Contribute to embryonic connective tissue for craniofacial development
First stream = Face
Second stream = First branchial arch

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39
Q

NCCs from rhombomeres ≥ 3 express

A

Hox TFs

40
Q

Hox TF genes =

A

ancient rostral-caudal patterning genes that define body segments

41
Q

Craniofacial region is a more

A

recent evolutionary structure- developed new set of TFs (examples in figure)

42
Q

NCCs that migrate to the face and first branchial arch are

A

Hox-free

43
Q

All transcription factors include a

A

DNA-binding domain that allows them to interact with genes

44
Q

Homeobox TFs include a specific

A

~180 base pair “homeobox” with specific sequence

45
Q

Hox TFs are a subset of

A

Homeobox genes that were discovered to be very ancient body patterning directors

46
Q

HOM-C Homeobox gene

Controls formation of

A

legs during development

Loss-of-function: Legs → Antennae (loss of body patterning)
Gain-of-function (ectopic expression) : Antennae → Legs
Similar to legs exchanging with arms or molars with incisors

47
Q

What patterning TFs direct craniofacial development?

A

Otx2: Orthodenticle homeobox 2
Msx: Muscle segment homeobox (MSX1-3)
Dlx: Distal-less homeobox (DLX1-7)
Barx: BarH-like homeobox (BARX1-2)

48
Q

NCCs contribute to the

A

mesoderm in the branchial arches

49
Q

Arch =

A

External “bumps” (internally, a mix of NCC and mesoderm)
Groove/cleft = Separate arches externally
Pouch = Internal depression

50
Q

(recall stomatodeum was bilayer of

A

ectoderm and endoderm– as a result oral cavity is lined with ectoderm while rest of digestive tract is lined with endoderm)

51
Q

Dlx homeobox TFs

A 
Family Dlx1-7 in humans
How to understand functions?
Dlx1/2 mutant mice show 
altered craniofacial morphology 
lack of maxillary molars 
Dlx1/2 affects proximal BA1 (maxillary process)
52
Q

Treacher-Collins syndrome aka Mandibulofacial dysostosis

A

Underdevelopment of craniofacial region and mandible
Failure/impairment of NCC migration to the facial region
Mutations in TCOF1, POLR1C, or POLR1D (functions still unknown)

53
Q

Epithelial-mesenchymal interactions drive

A

tooth formation

Conserved mechanism for many ectodermal organs
For example, hair, mammary gland, feather
Placode – bud – morphogenesis
Both adjacent tissues are essential for the organ to form properly

54
Q

Molecular signaling during crown development:

A

Epithelial-mesenchymal (E-M) signaling
Reciprocal: E-M signals must continue back and forth to push tooth formation forward
Reiterative: Cells use same signaling pathways again and again at different stages (BMP, FGF, SHH, WNT, TNF)
Sequential: Orderly sequence of events determine whether cells are ready to receive the signal and how they respond

55
Q

Primary epithelial band – dental lamina

A

Proliferation of epithelial cells
Altered orientation of axis of division
Formation of dental lamina (=odontogenic bands) and 20 dental placodes (= local thickening of ectoderm for primary teeth)

56
Q

Which tissue holds the odontogenic potential?

A

Both actually…

** First epithelium, then mesenchyme

57
Q

If you combine odontogenic epithelium with 2nd BA mesenchyme, together they

A

still form a tooth

58
Q

If you combine molar mesenchyme with incisor epithelium, they form a

A

molariform tooth

59
Q

Tooth type determination (crown pattern)

A

Still not well understood
Epithelial signals (BMP4, FGF8) induce mesenchymal expression of homeobox TFs (**again, epithelium is first to initiate)
Mesenchymal homeobox TF expression in overlapping domains that direct tooth shape formation
E.g. Incisors directed by Msx1, Msx2, and Alx3 and molars guided by Barx1, Dlx1 and 2

60
Q

Down growth of dental lamina into a

A

bud

Up growth of mesenchyme packing into condensation

61
Q

Cap stage

A

Epithelial growth forms concave, cap-like structure
Condensed ectomesenchyme = dental papilla
Surrounding ectomesenchyme = dental follicle
Further separated in next stages…

62
Q

Signaling in the Cap stage: (

A

Primary) Enamel Knot

63
Q

Primary enamel knot

A

Non-dividing enamel organ cells in cap stage
Expresses numerous signaling molecules (FGF4 above, right)
Directs proliferation of surrounding epithelial cells
Essential for bud to cap transition by regulating cap morphology
Disappears by apoptosis (directed cell death)

64
Q

Transitioning to Bell stage

A 
Enamel organ has 4 components
Outer enamel epithelium (OEE)
Inner enamel epithelium (IEE)
Stratum intermedium (SI)
Stellate reticulum (SR)
65
Q

Late Bell stage

Signaling in the Bell stage:

A

(Secondary) Enamel Knot(s)

66
Q

Secondary enamel knots

A

Non-dividing enamel organ cells in bell stage, appearing at sites of cusps (NOT in incisors)
Express signaling molecules (FGF4 above, right)
Direct proliferation of surrounding epithelial cells → IEE completes folding, determines number and location of cusps
Stimulates terminal differentiation of odontoblasts to begin dentinogenesis (always begins at cusp tips)

67
Q

Late Bell stage

Zone of maturation occurs

A

Dental papilla → → → Odontoblasts
IEE → → → Ameloblasts
Crown patterning

68
Q

Anodontia:

A

Absence of all primary or secondary teeth; tooth agenesis

69
Q

Oliogodontia:

A

6 or more missing teeth

70
Q

Hypodontia:

A

1-5 missing teeth

71
Q

Hyperdontia:

A

More than the normal numbers of teeth (supernumerary teeth)

72
Q

Oligodontia: PAX9

A

Autosomal dominant mutations in PAX9 transcription factor
PAX9 expressed in dental mesenchyme early in development
Most affected individuals missing maxillary and mandibular 2nd and 3rd molars
Incisors much less affected

73
Q

Hyperdontia: RUNX2

A

Autosomal dominant mutations in RUNX2 transcription factor
RUNX2 expressed in dental mesenchyme
Supernumerary primary teeth
Why extra teeth? RUNX2 probably negatively regulates tooth-initiating signal like Wnt…

74
Q

Wnt signaling and tooth initiation

A

Constitutively active Wnt signaling in mouse
Supernumerary teeth
Ectopic enamel knots
Numerous and malformed teeth

75
Q

Pluripotent: Ability to differentiate to all

A

3 germ layers
Divide indefinitely
Pros: Ability to make any tissue, repair any defect
Cons: How to control induction? Teratoma tumor formation, ethical concerns

76
Q

Adult (postnatal) stem cells

A

Multipotent: Ability to differentiate within limits
Divide asymmetrically (not indefinitely)
Pros: Ability to make several types of tissues, easier to control induction
Cons: Limited differentiation and division, quality/quantity decrease with age

77
Q

Induced pluripotent stem (iPS) cells

A

Reprogram adult somatic (body) cells or postnatal stem cells
Provide signals/induction factors
Pros: Pluripotent cells made from adults, patient-matched ES cells, combine the best of embryonic and postnatal stem cells
Cons: Reprogramming slow, inefficient, and expensive, controlling induction to specific tissues may be challenging

78
Q

Dental stem cells?

A

Several populations of adult/postnatal stem cells
Dental pulp, Periodontal ligament (PDL), dental follicle, apical papilla
Potential for tooth repair or engineering (or other tissues)

79
Q

Successes with dental stem cells

A

Creating tooth buds or repairing tooth structure in animal models
Treating other conditions like multiple sclerosis (MS) or spinal cord injury

80
Q

Limitations with dental stem cells

A

Size and shape of engineered teeth poorly controlled
How to integrate an engineered tooth into the jaw?
Human teeth take months-years to form

81
Q

A mutation in gene FAM83H causes a hereditary condition where enamel is brown soft and rough. 3 gen of families display this in both male and females

A

Genotype, phenotype, heritable, recording a pedigree can help determine what this is genetically.

82
Q

When cell signaling is targeted to nearby adjacent cells, it is called

A

paracrine

83
Q

What are the proteins that regulate mRNA expression of other genes

A

transcription factors

84
Q

TDO syndrom features defects in hair, tooth, bone dev, because mutations deactivate DLX3, a TF that has multiple functions in these organs.

A

T

85
Q

During 4th week of dev, rostral-caudal folding of the trilaminar embryo is an essential process in…

A

formation of the stomodeum

86
Q

Transition from bilaminar to trilaminar embryo in week 3 of embryo is called

A

gastrulation

87
Q

Which statement about the oral cavity is false

A

Buccopharyngeal membrane is a trilayer

88
Q

Neural crest cells are derived from

A

Ectoderm

89
Q

Which one of these statements about the midbrain is true

A

Neural crest cells from this region will migrate to branchial arch 1.

90
Q

Choose the answer to the correct chronological sequence of events (earliest to latest)

A

Blastocyst, gastrulation, cells migrate to branchial arch 1

91
Q

Hox genes are expressed by neural crest cells that migrate to

A

branchial arch 2

92
Q

What types of cells signal back and forth to direct tooth formation

A

mesenchymal and epithelial

93
Q

Odontogenic potential lies first with the —– layer, but is later transferred to the —– layer

A

epithelial, mesenchymal

94
Q

signaling cell centers in the bell stage that control cusp formation is/are called

A

secondary enamel knots

95
Q

During week 4 of embryo, rostral caudal folding is an essential process in

A

stomodeum formation

96
Q

Dental stem cells are

A

multipotent

Oral Histology (14 decks)

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