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Oral Histology Exam 1 > Molecular and Genetic Basis of Tooth Development > Flashcards

Molecular and Genetic Basis of Tooth Development Flashcards

1
Q

where are cranial neural crest cells formed?

A

at back of the neural tube

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2
Q

when do cranial neural crest cells start migrating? where do they migrate to?

A

when the neural tube closes

migrate a long distance through defined paths to reach the branchial arches

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3
Q

what are stem cells and what can they do?

A

a single cell that can replicate itself and differentiate into many cell types

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4
Q

what allows for structure development such as odontogenesis at the right location and time?

A

tissue-tissue interaction

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5
Q

how does ectoderm help ncc?

A

regulates ncc cells during morphogenesis

controls the position size and shape of organs

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6
Q

how does mesoderm help ncc?

A

provides environment for ncc cells to populate

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7
Q

how does endoderm help ncc?

A

develops pharyngeal pouch- generated organs: thyroid, parathyroid and thymus

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8
Q

how many streams do hindbrain derived neural crest cells migrate?

A

3 streams
1st branchial arch- r1-2
2nd branchial arch- r4
3rd branchial arch r6-7

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9
Q

how does branchiomotor nerves exit the hindbrain?

A

collect axons from cell bodies but exit the hindbrain only from (orange balls) the even numbered segments (oral ovals) to innervate peripheral target structures
trigeminal nerve: r1-3- 1st branchial arch including teeth
facial nerve: r4-5
glossopharyngeal nerve: r6-7

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10
Q

what are hox genes?

A

a group of homeobox genes, which possess a unique homeobox (DNA sequence), which encodes a conservative homeodomain (protein segment)
if a hox gene is expressed, its protein product functions as transcription factor, which controls other gene expression

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11
Q

which arch nccs are hox free?

A

1st branchial arch. carry the genes but don’t express them

nccs involved in tooth development do not express hox genes

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12
Q

what are dlx genes

A

within each branchial arch, specific dlx gene codes are expressed to produce regional differences such as between maxilla and mandible
it is another homeobox gene- 7 members of fam have been identified
vertebrates -4,7,8,9 are the same gene

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13
Q

what are the dlx combinations for branchial arch 1?

A

dlx 1/2 combo required for development of proximal portion (maxillary process)
dlx 5/6 combo required for development of the distal portion (mandibular process)

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14
Q

what do dlx 1/2 double mutants lack?

A

all maxillary molars- mandibular structures not affected

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15
Q

what do dlx 5/6 mutants develop?

A

lower jaws like mirror images of the upper jaw

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16
Q

among cells required for tooth development which ones have ncc origin?

A

odontoblast, cementoblast, fibroblast, osteoblast, chondroblast

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17
Q

which homeobox gene differentiates nccs migrated to different branchial arches?

A

hox

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18
Q

what does normal tooth development involve?

A

process with precisely arranged/regulated cell and tissue interactions
initated by the epithelium, followed by epithelium-mesenchyme interaction through the entire processs of tooth development

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19
Q

what are the four major signaling pathways of the extoderm-derived epithelium?

A

bmp: bone morphogenic protein
fgf: fibroblast growth factor
wnt: wingless (drosophila) and int (mouse)
shh: sonic hedgehog
all four molecules bind to cell membrane receptors and eventually impact on gene regulation through varied intracellular pathways
these molecular signals are also important for the development of other ectodermal organs, such as hair, nails and glands

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20
Q

what enamel knots?

A

epithelial aggregates function as signal centers for tooth morphogenesis and odontoblast differentiation

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21
Q

what does primary enamel knots do?

A

appear at the end of bud stage
closely interact with the mesenchyme
strongly stimulate proliferation of adjacent cells
essential for bud to cap stage transition; without it, tooth development will be arrested
disappear by cell apoptosis

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22
Q

what does secondary enamel knots do?

A

appear at the locations of future molar cusps at the bell stage
stimulate terminal differentiation of odontoblasts at the end of bud stage, which always occur first at the location of future cusp tips
determine the number and locations of molar cusps
no present in incisors

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23
Q

what determines cusp patterns?

A

differential expression of signaling molecules in the enamel knots
fgf may function as a cusp activator while bmps and possily shh as well may function as an inhibitor to regulate the formation of inter-cusp distance

24
Q

does cranial neural crest cells directly contribute to the development of enamel?

A

no but contribute to dentin, cementum, pulp and periodontal ligaments

25
Q

what are the three stages of development of tooth crown?

A

initiation
morphogenesis
differentiation and mineralization
intense molecular interactions occur through all 3 stages

26
Q

what determines molecular control for tooth identity?

A

different molecular interactions are present at the anterior (distal, BMP4 interaction Msx1 and Msx2) and posterior regions (proximal: FGF interact with Barx 1, Dlx2, Lhx6/7) regions, which may control the development of incisors and molars repectively.

27
Q

innervation of tooth is from branches of which cranial nerve?

A

pioneer trigeminal axons penetrate into the dental pulp after the start of enamel formation

28
Q

what is the molecular level of innervation of tooth

A

through epithelial mesenchymal interaction, epithelium expresses sema 3a into the mesenchyme. sema 3a serves as a chemorepellent for the axons= thus controlling the timing and patterning of tooth inervation

29
Q

what are the common transcription factors produced by mesenchyme?
what are the common signalling molecules produced by mesenchyme?

A

msx1/2, dlx1/2, pax9, gli2/3, runx2, barx2, etc

BMP, FGF, Wnt and their inhibitors

30
Q

how does the root develop?

A

after crown development is nearly complete, the hertwig’s root sheath grows apically between two mesenchymal regions: dental papilla and dental follicle
immediated after hertwig root sheath formation, apical odontoblasts appear adjacent to the HERS on the papillar side
although enamel is not present in the root, induction from the epithelium is required for root development

31
Q

how does HERS induce dental papilla cells to differentiate into odontoblasts?

A

may be through lamini-5 and tgf beta secreted by the HERS
odontoblasts in the root region are much less elongated than those in the crown region
nuclear factor Ic (nfic) is essential for root dentin formation but not for crown dentin formation
without nfic, odontoblasts cannot normally form even when the HERS appear normal

32
Q

how is root cementum formed?

A 
cementum formation starts when HERS and dental follicle cells are in close proximity
both epithelial (hers) and mesenchymal (dental follicle) cells participate but their relative ccontributions remain unclear
33
Q

what are the interaction between the epithelium and mesenchyme during root development?

A

HERS (epithelium): tgf-b, nfic, insulinlike growth factors, wnts, fgf
mesenchyme: bmp and fgf
compared to the molecules involved in the crown development only several are the same

34
Q

what are the contribution of hers to root development?

A

HERS do not respond to signals from the mesenchyme and diffferentiate into ameloblasts
induce the differentiation of odontoblasts
induce the differentiation of cementoblasts or HERS cells may transdifferentiate into cementoblasts
determine the number of roots

35
Q

what is the fate of HERS?

A 
become the epithelial rest of Malassez
apoptosis
incorporated into the cemetum front
epithelial-mesenchymal transformation
migraton into the periodontal ligament
differentiation into cementoblasts
36
Q

what are the tissue and cell origins for root dentin and cementum?

A

mesenchyme

37
Q

is epithelium required to induce the formation of odontoblasts and cementoblasts for root dentin and cementum formation?

A

yes

38
Q

what is ectodermal dysplasia syndrome?

A

two or more ectodermal structures are affected

39
Q

what is the molecular mechanism of ectodermal dysplasia?

A

mutations of transcription factor or p63 is required for the normal function of fgf, bmp, shh. critical signaling pathways involved in epithelial-mesenchymal interaction

40
Q

what is a msx-1 mutation?

A

a family with multiple members lacking both maxillary premolars and mandibular 2nd premolars
affected members have an G–>C transversion (arginine ->proline) mutation of the Msx 1 gene
MSX1 functions as an critical transcription factor (in the mesenchyme) involved in nromal tooth development. the mutation is at the homeodomain region, which affects the normal function of msx1 protein as a transcription factor

41
Q

what is a pax9 mutation?

A

most afffected fam members have no molar development
affected members have a guanine insertion (causing reading frame shift) of the pax9 gene
pax9 is another critical transcription factor (in the mesenchyme) involved in normal tooth development. the mutation is at its dna binding domain which affects the normal function of pax9 protein as a transctiption factor

42
Q

what is a axin 2 mutation?

A

affected members all have more than 8 permanent teeth undeveloped
affected members either have a misses (c->t) or insertion (g) mutation. both mutation introduce a premature stop codon to the axin2 gene
during tooth development, axin 2 is expressed intensively in the mesenchyme. loss of axin 2 function disrupts the wnt signalling, but axin2 does not function as a transctiption factor
some patients with this mutation may be prone to colorectal polyps and cancer

43
Q

eda mutation

A

affected members have multiple missing anterior teeth (x-lined dominant)
affected members either have a missense c–>g mutation resulting in a q to e substitudition in the EDA
the product of the eda gene is a transmembrane signaling molecule belonging to the tnf pathway but it does not function as a transcription factor
the finding of eda leads to the recognition that the tnf pathway is another molecular pathway (in addition to bmp, wnt, fgf, and shh) involved in tooth development

44
Q

what are the theories for the etiology of supernumery teeth

A

atavism (evolutionary throwback)
tooth germ dichotomy (like in a cleft region)
hyperactivity of the dental lamina
genetic and environmental factors

45
Q

what are the cases of supernumery teeth?

A 
most are isolated cases
multiple sueprnumerary teeth are relatively rare but can happen 
cleidocranial dysplasia
familial adenomatous polyposis (including gardner's syndrome)
ehlers-danlos syndrome
nance-horan syndrome
thichorhino phalagic syndrome
rainbow syndrome
46
Q

what is cleidocranial dysplasia

A

autosomal dominant, skeletal dystplasia in clavicles, patent sutures and fontanels, formation of eomian bones and short statue. dental anomalies: supernumerary teeth, delayed eruption and impaction of permanent teeth

47
Q

what mutation cause cleidocranial dystplania

A

runx2 mutations
encodes a transcription factor (in the mesenchyme) essential for tooth development
runx2 knockout mice have tooth agenesis rather than supernumery teeth so it is believed that runx2 is a positive rgulator for primary teeth but a negative regularotr for secondary teeth
identical runx 2 gene mutations showed a wide variation in supernumerary tooth formation- sugegsting epigenetic and environmental factors also play a role

48
Q

gardners syndrome

A

adenomatours of polyps of the gi tract, demoid tumors, osteomas
dental anomalies: super numerary teeth, impacted teeth, dentigerous cysts etc

49
Q

what causes gardners syndrome

A

apc gene mutation
in transgenic mice, effect of apc difiency is mediated by b-catenin (wnt pathway) the apc loss of function or b-catenin gain of function mice are consistent with dental anomalies of gardners syndrome
apc gene mutation may function through the ent signaling pathway and cause the formation of supernumerary teeth. but the detailed molecular mechanism are yet to be identified

50
Q

does msx1 encode transcription factors or signaling molecules?

A

transcription factor

51
Q

does pax 9 encode transcription factors or signaling molecules?

A

transcription factor

52
Q

does axin2 encode transcription factors or signaling molecules?

A

signaling molecule, wnt pathway

53
Q

does eda encode transcription factors or signaling molecules?

A

signaling molecule, tnf pathway

54
Q

does p63 encode transcription factors or signaling molecules?

A

transcription factor, critical for bmp, fgf, shh pathways

55
Q

is runx2 encode transcription factors or signaling molecules?

A

transcription factor

56
Q

does apc encode transcription factors or signaling molecules?

A

signalling molecule, likely impact through wnt pathway

Oral Histology Exam 1 (5 decks)

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