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Growth and development > Lec5&6 > Flashcards

Lec5&6 Flashcards

1
Q

when a baby is just born, what are their head and tooth development like?

A
  1. head is about half of total body mass
  2. no maxi or mandi alveolar process
  3. natal tooth can be at present (either supernumerary or normal central incisor)
  4. first primary teeth not until 6 months
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2
Q

what happens during the first 6 months after a baby is born?

A
  1. tongue grows down/forward (need airway for milk), so does palatal width
  2. overjet (maxi way front before mandi) decreases as lower jaw grows faster than upper
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3
Q

baby teeth eruption sequence (6mo to 30 mo)?

A
  1. L central (8mo)
  2. U central
  3. U lateral
  4. L lateral
  5. U 1st M
  6. L 1st M
  7. U cuspid* (19mo)
  8. L cuspid * (20mo)
  9. L 2nd M (27mo)
  10. U 2nd M (29mo)
  • cuspids are the ones that most variable
  • timing can be vary, but the sequence is important
  • big time gap (about 7 mo) btwn L cuspid and L 2nd M
  • all primary teeth should be out by age 3
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4
Q

what is primary space and why is it important?

A
  1. space btwn lateral and canine in maxi
  2. space btwn canine and 1st M in mandi
  • very important for proper alignment of the permanent teeth
  • no space with deciduous teeth, very likely to have the same problem with permanent teeth (teeth crowded)
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5
Q

By age 3, what happens?

A
  1. all primary teeth are out
  2. maxi and mandi relationship settle down
    * prog-nathism: growing forward
    * retro-nathism
    * maxi prognathism can be the same issue with or caused by mandible retronathism
  3. the relationship of distal end of opposing secondary primary molar to one another is established and we can expect how it will grow later
    1) distal step (later Class II, 14%)– mandi 2nd M toward more distal
    2) flush terminal plane (later Class I or end-to-end, 37%)– good match
    3) mesial step (later Class I or III, 49%)– mandi 2nd M toward more mesial
    * Class II need to be corrected big time!
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6
Q

By age 6, 1st permeant M erupts. What is the ideal angle of 1st M and what are 3 types of malocclusions?

A
  • . Class I molar (ideal, 30%): MB cusp of maxi 1st M occludes in buccal groove of mandi 1st and perfect alignment of other teeth
    1. Class I (55%): molar relationship good (MB cusp of maxi 1st M occludes in buccal groove of mandi 1st ) but some significant malposition of other teeth. Maxi canine sits in sits in canine and 1st M in mandi
    2. Class II (15%): MB cusp of maxi 1st is mesial to buccal groove of mandi 1st M (overjet looking)
    3. Class III (1%): opposite Class II
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7
Q

What can causes Class II or III?

A

Class II (convex)– maxi jaw forward and/or mandi jaw retro

Class III (concave)– opposite of Class II

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8
Q

How would primary teeth grow into permeant teeth (in molar relations)?

A
  1. Distal step (mandi distal)
    - w/ minimal grow: Class II
    - mandible forward: end-to-end
  2. Flush terminal plane
    - w/ minimal grow: end-to-end
    - mandible forward: Class I
  3. Mesial step (mandi mesial)
    - w/ minimal grow: Class I
    - mandible forward: Class III
  • End-to-end is perfect alignment btwn the molars
  • Class I has mandi molar just a little more mesial
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9
Q

what is ideal teeth?

A
  1. Class I molar and canine (upper canine sits distal to the lower canine– btw 1st PM and canine)
  2. 2mm anterior and posterior overjet
  3. 2mm anteior overbite
  4. co-incident dental midlines
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10
Q

what is the typical eruption sequence of mandible?

A 
1st M (6)
central incisor (6)
lateral incisor (7.5)
cuspid (10.5)
1st PM (10.5)
2nd PM (11)
2nd M (12)
3rd M (20)
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11
Q

what is the typical eruption sequence of maxi?

A

same as maxi but cuspid AFTER 1st and 2nd premolars!

1st M (6)
central incisor (7)
lateral incisor (8)
1st PM (10)
2nd PM (11)
cuspid (11.5)
2nd M (12.5)
3rd M (20)
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12
Q

what are the characteristics of the transition from primary to permanent?

A
  • permanent first molars and incisors erupt first!
  • primary molars and canines replaced with permanent premolars and canines respectively
  • full permanent dentition includes 2nd and 3rd molars
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13
Q

dental age 6, 7, 8?

A

Dental age 6?

  • mandi center incisor out
  • mandi 1st M
  • maxi 1st M

Dental age 7?

  • maxi centrals and mandi laterals
  • root of maxi laterals keep advancing till 8
  • canines and premolar crowns are still growing or root just beginning

Dental age 8?

  • maxi lateral out
  • 2~3 year delay before any more permeant teeth to be out (during age 9~10 – prep time for canines and 1/2 premolars)
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14
Q

dental age 9, 10?

A

Dental age 9?

  • still primary teeth (canines, first/second molars)
  • 1/3 of mandi canine root and mandi premolar root is completed

Dental age 10?

  • primary canines and molars root gets resorb and their permanent successors bone develop
  • half of mandi canine and 1st PM completed
  • half of maxi 1st PM root completed
  • teeth usually emerge when 2/4 of the root is complete ***
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15
Q

dental age 11~15?

A

Dental age 11?
- eruption of another group: mandi canine, mandi 1st PM, maxi 1st PM all simultaneously

Dental age 12?

  • all succadaneous teeth erupt
  • 2nd M normally erupt by end of the time

Dental age 13-15?

  • all remaining roots complete
  • by age 15, third molar should be visible on radiograph
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16
Q

what is incisor liability and why is it important?

A
  • permanent tooth buds like lingual and apical to the primary incisors
  • so when permeant incisors erupt, it can be crowded (space problem)
  • space problem can be more prevalent in lower arch because primary incisors usually 3mm when permanent incisors are usually 5.5mm
  • when mandi lateral incisors erupt, usually “1.6mm” space deficiency called “incisor liability”
17
Q

what is leeway space?

what is late mesial shift?

A
  • leeway space is due to the difference in size btw primary canine, 1st and 2nd M, and permanent canine and 1st and 2nd PM
  • 1.5mm per side in upper arch– total 3 mm
  • 2.5 m per side in lower arch– total 5mm
  • leeway space closes when “late mesial shift” occurs
  • the late mesial shift is when lower first permeant molar move forward relative to the upper 70% because the lower primary 2nd molar is larger than upper primary 2nd molar
  • this would make the incisors to be more crowded
  • need a lower mandi 1st molar holder (so it won’t move mesially)
18
Q

what is special about late childhood (5~6 yrs)?

A
  • by 7 yrs, neural growth is complete

- lymphoid tissue in body proliferated a lot (large adenoids and tonsils)

19
Q

what is pre-emergent eruption?

A
  • eruption soon after root beings forming
  • resorption of bone and primary tooth roots
  • eruption in the direction of the resorption path
  • what causes the pre-eruption remains unknown, but it’s localized force within PDL
  • eg. Cleidocranial dysplasia
20
Q

What is Cleidocranial dysplasia?

A
  • example of a defective eruption process (pre-mature eruption)
  • heavy fibrous tissue (bone is resorbed)
  • missing or underdeveloped clavicles
    dental implication: multiple supernumerary teeth can impede normal eruption due to the thick soft/fibrous tissue (keep plucking them out as they come)
21
Q

what is post-emergent eruption?

A
  • when a tooth breaks through the gingiva and erupts rapidly until it reaches occlusion (mastication) and gets slows down
  • it goes through “juvenile occlusal equilibrium” that is a very slow process of eruption
  • teeth usually stops during the day time
  • 8~midnight: teeth are erupting slightly (related to the GH release cycle)
22
Q

what is juvenile occlusal equilibrium?

A
  • a post-emergently erupted tooth goes though very slow process of eruption after it hits occlusion
  • when the teeth is in function, eruption now parallels the vertical growth of the mandiblular ramus (eruption and jaw growth together)
  • first permeant molar erupt 2.5mm and half of that is after the tooth reaches occlusion
  • pubertal spurt
  • after a tooth is in occlusion, the rate of eruption is controlled by the force that oppose the eruption rather than promoting it
  • this means that if there is no opposing tooth in contact (eg. missing tooth), it can keep growing occlusally
23
Q

what is SHH (sonic hedgehog)?

A

gene necessary for growth of the fronto-nasal complex

24
Q

etiology of malocclusion (in America)?

A

60% mal of unknown cause
5% mal of known cause
35% normal occlusion

malocclusion can be from

  • single or complex factor
  • congenital
  • developmental or environmental
25
Q

5 stages of abnormal craniofacial development?

A
  1. germ layer formation and initial organization of craniofacial structure
  2. neural tube formation and initial oropharynx formation
  3. origins, migrations, and interactions of cell populations
  4. formation of organ systems
  5. final differentiation of tissues
26
Q

fetal alcohol synddrome?

A
  1. defects during stage 1 (germ layer formation and initial organization of craniofacial structure)
  2. first three brain ventricles fail to separate
  3. deficient medial nasal prominence
  4. no nose or midface deficiency
    (eg. small eye openings, smooth philtrum, thin upper lip)
27
Q

retinoic acid and thalidomide teratology?

A
  • congenital
  • underdeveloped mandi
  • cleft palate
  • brain abnormal
28
Q

hemifacial microsomia?

A
  • half face is lack of tissue (deformed)
  • usually in mandible and ear area affected
  • due to the early loss of neural crest cells
  • cleft lip/palate 6~22%
  • renal abnormal 5%
  • possible to be treated by functional appliance
  • 2 or more surgical interventions maybe
29
Q

mandibulofacial dysostosis (=treacher-collins syndrome)?

A
  • missing facial tissues bilaterally
  • zygomatic arch and lateral orbit rim deficient
  • absent or rudimentary condyle
  • severe retrogenia or antegonial notching (very short ramie)
  • due to excessive dell death in the trigeminal ganglion that affects neural crest derived cells
  • treatment options
  • at age 8: only bone grafting the orbital and zygomatic regions
  • at age 14: surgery to reposition jaws
30
Q

how is primary palate formed and what could damage to it (cleft)?

A
  • primary palate is formed when the lateral edge of the olfactory placed is curling forward
  • lateral nasal process develops and makes contact with median nasal process
  • any interference in this process can cause primary palate cleft
  • maternal cigarette smoking can fail the process
31
Q

how can secondary palate cleft occur?

A
  • might be genetic predisposition
  • 1/3 of the cases due to a single recessive gene
  • tongue cannot get out
32
Q

dental arch growth and numbers?

A

Maxi

  • canine to canine: +5
  • arch perimeter: +1

Mandi

  • canine to canine: +3
  • arch perimeter: -4 (due to late mesial shift)
  • 2mm space as teeth grows upward and outward
  • maxi gains more space
  • boys gains more space (girls have more incisor liability)
  • mandi canines both widens out and move back into the primate space, giving 1 mm

Growth and development (3 decks)

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