Embryology Flashcards

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?

A

Primary

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
Q

Name 6 diseases associated with taurodontism.

A

Klinefelter syndrome, tricho-dento-osseous syndrome, Mohr syndrome (aka orofaciodigital syndrome II), ectodermal dysplasia, Down syndrome, amelogenesis imperfecta type IV

26
Q

The most common type of amelogenesis imperfecta is :

A

type I- hypoplastic

27
Q

What type of amelogenesis imperfecta is associated with taurodontism?

A

AI type IV with taurodontism (hypomaturation-hypoplastic)

28
Q

Dentinogenesis imperfecta is a defect of what structure?

A

Predentin matrix (normal mantle dentin)

29
Q

Which type of Dentinogenesis imperfecta occurs along with osteogenesis imperfecta?

A

Shields Type I

30
Q

Describe Shields Type I dentinogenesis imperfecta.

A

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
Q

Describe Shields type II dentinogenesis imperfecta

A

no OI, hereditary opalescent dentin, both primary and permanent dentitions equally affected, periapical radiolucencies, rapid attrition, pulp chamber obliteration, autosomal dominant

32
Q

Describe Shields Type III dentinogenesis imperfecta.

A

“bell-shaped crowns, ““shell teeth””, short roots, enlarged pulp chambers, enamel pitting, rare, pulp exposures”

33
Q

What type of osteogenesis imperfecta is the most common?

A

OI type I

34
Q

What type of osteogenesis imperfecta is lethal in the perinatal period?

A

OI type II

35
Q

What types of amelogenesis imperfecta are most commonly associated with dentinogenesis imperfecta?

A

Types III and IV

36
Q

Describe the features of osteogenesis imperfecta.

A

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
Q

Name some systemic causes of acquired enamel hypoplasia.

A

Deficient vitamin A, C, D, calcium, phosphate; infection of rubella, syphilis, cytomegalovirus, radiation, fluorosis, Celiac disease

38
Q

Names of syndromes associated with acquired enamel hypoplasia.

A

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
Q

Describe Shields type I dentin dysplasia.

A

normal color, short roots or rootless, pulp obliteration, severe mobility, autosomal dominant

40
Q

Describe Shields type II dentin dysplasia.

A

primary teeth affected, amber-colored teeth, permanent teeth look normal but radiographically demonstrate thistle-tube shaped pulps with multiple pulp stones;

41
Q

Describe regional odontodysplasia.

A

”"”ghost teeth””, thin enamel, diffuse shell appearance, both dentitions affected”

42
Q

Describe vitamin D-resistant rickets.

A

hypophosphatemic rickets, hypomineralized dentin, enlarged pulp and pulp horns