Embryology Flashcards

(42 cards)

1
Q

Neural crest cells develop from ________. Name some structures that neural crests are responsible for forming.

A

1) ectoderm on the lateral border of the neural plate. 2) bone, cartilage, dentin, dermis (not enamel)

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2
Q

Dental lamina begins formation at _______ embryonic age.

A

6 weeks

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3
Q

From what structure does dental lamina form?

A

basal layer of oral epithelium

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4
Q

What structures form from dental lamina?

A

tooth buds

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5
Q

At what age does the permanent first molar begin initiation? At what age does the permanent 2nd molar begin initiation?

A

1) 16 weeks in utero 2) 4-5 years

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6
Q

Name the components of the tooth bud.

A

enamel organ, dental papilla, dental sac

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7
Q

Name the components of the enamel organ.

A

Inner enamel epithelium (concavity), outer enamel epithelium (convexity), stellate reticulum (center)

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8
Q

The dental papilla forms from ________.

A

neural crest

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9
Q

Name the stages of tooth development in order.

A

Bud stage, cap stage, bell stage, advanced bell stage

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10
Q

Hertwig’s epithelial root sheath is composed of what structures?

A

inner and outer enamel epithelia (not stratum intermedium or stellate reticulum)

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11
Q

The remnants of Hertwig’s root sheath persist as _____.

A

rests of Malassez

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12
Q

Problems in the initiation stage of tooth development lead to anomalies of __________.

A

Tooth number

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13
Q

Problems in the proliferation stage of tooth development lead to anomalies of __________.

A

size, proportion, number, twinning

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14
Q

Problems in the histodifferentiation stage of tooth development lead to anomalies of ____________.

A

anomalies of enamel and dentin (enamel hypoplasia, AI, DI, DD)

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15
Q

Problems in the morphodifferentiation stage of tooth development lead to _____________.

A

Anomalies of enamel, dentin, and cementum

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16
Q

Is hyperdontia more common in males or females?

A

males (2:1)

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17
Q

Is hyperdontia more common in primary or permanent dentition?

A

permanent dentition (5:1)

18
Q

Is hyperdontia more common in the maxilla or the mandible?

A

maxilla (9:1)

19
Q

Name the most common teeth affected by hypodontia in order of frequency.

A

3rd molars, mandibular 2nd premolar, maxillary lateral, maxillary 2nd premolar

20
Q

Name (9) syndromes associated with hyperdontia.

A

Apert’s, cleidocranial dysplasia, Gardner syndrome, Crouzon syndrome, Sturge-Weber syndrome, Orofaciodigital syndrome I, Hallerman-Strieff syndrome, cleft lip and palate, Down syndrome

21
Q

Describe features of Apert Syndrome.

A

supernumerary teeth, cleft palate, delayed/ectopic eruption, shovel shaped incisors, hypoplastic midface, syndactyly, craniosynostosis, hypertelorism, class III with anterior openbite, crowded dentition

22
Q

Is gemination more common in the primary or permanent dentition?

23
Q

Describe twinning.

A

Complete cleavage of a single tooth bud which results in a supernumerary mirror image tooth.

24
Q

What is the cause of taurodontism?

A

failure of normal invagination of Hertwig’s epithelial root sheath

25
Name 6 diseases associated with taurodontism.
Klinefelter syndrome, tricho-dento-osseous syndrome, Mohr syndrome (aka orofaciodigital syndrome II), ectodermal dysplasia, Down syndrome, amelogenesis imperfecta type IV
26
The most common type of amelogenesis imperfecta is :
type I- hypoplastic
27
What type of amelogenesis imperfecta is associated with taurodontism?
AI type IV with taurodontism (hypomaturation-hypoplastic)
28
Dentinogenesis imperfecta is a defect of what structure?
Predentin matrix (normal mantle dentin)
29
Which type of Dentinogenesis imperfecta occurs along with osteogenesis imperfecta?
Shields Type I
30
Describe Shields Type I dentinogenesis imperfecta.
Occurs with osteogenesis imperfecta, primary teeth more severely affected, permanent first molars and central incisors most often affected, amber translucence, periapical radiolucencies without caries, autosomal dominant, rapid attrition
31
Describe Shields type II dentinogenesis imperfecta
no OI, hereditary opalescent dentin, both primary and permanent dentitions equally affected, periapical radiolucencies, rapid attrition, pulp chamber obliteration, autosomal dominant
32
Describe Shields Type III dentinogenesis imperfecta.
"bell-shaped crowns, ""shell teeth"", short roots, enlarged pulp chambers, enamel pitting, rare, pulp exposures"
33
What type of osteogenesis imperfecta is the most common?
OI type I
34
What type of osteogenesis imperfecta is lethal in the perinatal period?
OI type II
35
What types of amelogenesis imperfecta are most commonly associated with dentinogenesis imperfecta?
Types III and IV
36
Describe the features of osteogenesis imperfecta.
bone fractures, bowing of legs, blue sclera, bitemporal bossing, loose ligaments, impaired hearing, macrocephaly, autosomal dominant, may be treated with bisphosponates, capillary fragility, cardiac defects
37
Name some systemic causes of acquired enamel hypoplasia.
Deficient vitamin A, C, D, calcium, phosphate; infection of rubella, syphilis, cytomegalovirus, radiation, fluorosis, Celiac disease
38
Names of syndromes associated with acquired enamel hypoplasia.
Down syndrome, tuberous sclerosis, epidermolysis bullosa, Hurler syndrome, Hunter syndrome, Treacher-Collins syndrome, hypoparathyroidism, tricho-dento-osseous syndrome, Vitamin D-dependent rickets, Lesch-Nyhan syndrome, Fanconi syndrome, Sturge-Weber syndrome, Turner syndrome
39
Describe Shields type I dentin dysplasia.
normal color, short roots or rootless, pulp obliteration, severe mobility, autosomal dominant
40
Describe Shields type II dentin dysplasia.
primary teeth affected, amber-colored teeth, permanent teeth look normal but radiographically demonstrate thistle-tube shaped pulps with multiple pulp stones;
41
Describe regional odontodysplasia.
"""ghost teeth"", thin enamel, diffuse shell appearance, both dentitions affected"
42
Describe vitamin D-resistant rickets.
hypophosphatemic rickets, hypomineralized dentin, enlarged pulp and pulp horns