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**Pediatric Dentistry Boards 2019 > Growth and Development > Flashcards

Growth and Development Flashcards

1
Q 
Define:
Growth
Development
Hypertrophy
Hyperplasia
Acretion
A

Growth: increase in size
Development: increase in complexity
Hypertrophy: increase in size of individual cells
Hyperplasia: increase in # of cells
Acretion: increase in non-cellular material

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2
Q

When is the embryonic period? What is the most prominent structure during this time?What is the fetus susceptible during this period?

A 
First 8 weeks of life
The head/face 
Fetal Alcohol Syndrome
Infections (rubella, CMV)
Radiation
Nutrition deficiency
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3
Q

What are the facial prominences? What do they surround?

A

The 5 prominences surround the stomoadeum/mouth :
Single median frontonasal (includes the Median nasal process and Lateral Nasal processes)
Paired maxillary process
and paired mandibular process

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4
Q 
Branchial arch : 
1- mandibular
2 - hyoid
3- glossopharyngeal
4 - plus
A

1- Meckel’s cartilage, malleus, incus and muscles of masicationg. Trigeminal nerve, maxillary artery

2- Hyoid: stapes, styloid, stapedius, Facial nerve, stapedial artery

  1. Glossopharyngeal : Greater cornu, stylopharyngeus muscle, glossopharyngeal arter
  2. Thyroid cartilage, vagus nerve, aorta
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5
Q

The facial processes either fuse or merge. Which ones merge? fuse? What occurs during this? Possible problems?

A

Merge (median nasal process-philtrum/tip of nose/primary palate; Mandibular process-lower lip/mandible; maxillary and mand processes- comissures of the mouth): midline, incomplete separation of these structures, the underlying mesenchyme migrates

Fusion (median nasal and maxillary process-lateral lip and maxilla; Primary palate and palatal shelves- palate): more complex, surface epithelium needs to disintegrate, defects are more likely to occur where processes fuse as opposed to merge

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6
Q

Which branchial arch anomalies are the most common? Examples of?

A

2nd branchial arch anomalies (90-95%)
These are all soft tissue defects.

1st branchial arch anomalies are next common at 1% and involve hard tissues.

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7
Q

When are facial structures “defined” during in utero development?
What branchial arch is the major contributor to the facial structures?
What nerve, muscle group and cartilage are associated w/ this branchial arch?

A
  • between 3-11 weeks (the embryonic period)
  • 1st branchial arch
  • Trigeminal nerve, muscles of mastication, meckel’s cartilage
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8
Q

What are three 1st branchial arch syndromes? And one common manifestation?

A

Pierre Robin Sequence,
Hemifacial microsomia (goldenhar),
Mandibulofacial dysplasia (Treacher Collins)
- Cleft lip/palate

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9
Q

What percentage of branchial arch anomalies are due to the 2nd branchial arch? What types are there?
-What kind of lesions are they? and when do they present?

A

90-95%

  • Type 1: sternocleidomastoid muscle
  • Type 2: near the great vessels
  • Type 3: near the in/external carotid arteries
  • Type 4: (rare) next to the pharyngeal wall

Cystic lesions are commonly found.
Typically present in the 2nd decade of life

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10
Q

Describe the Fetal development period

A

Begins 9th week in utero to birth
Characterized by more growth than development (size change)
Body grows more rapidly
Ossification begins

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11
Q

Dental anomalies frequently encountered with cleft/lip patients?

A

Ectopic eruption of maxillary 1st molars (30%)
Supernumerary teeth
morphologic anomalies
missing teeth

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12
Q

Palatal fusion is typically completed by?

A

11 weeks

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13
Q

Describe the order the palates “zip” together:

A

Primary palate zips from posterior to anterior

Secondary palate zips closed from anterior to posterior

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14
Q

Submucous palate occurs when?

What are some problems associated with submucous cleft?

A

The hard tissue closure is incomplete, but the soft tissue is complete.
- Nasal speech due to lack of muscle attachment, increased incidence of otitis media, “tenting” of the soft palate

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15
Q

Describe the triad of the submucous cleft

A

Bifid uvula
Palatal muscle diastasis
Notch in the posterior surface of the hard palate

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16
Q

Epidemiology of cleft lip and palate (prevalence, race, gender)

A

Prevalence 1/2000 (lip alone 1/1000)
Slightly higher in Asians
Slightly higher in females

17
Q

Unilateral cleft lip and palate What percentage to each side?

A

Majority to the left- 2/3rds

18
Q

Management of cleft at neonatal period: timing of each treatment 0-12 months

A

Obturation, tissue molding
5 weeks orthopedic appliances
7 weeks lip adhesion

5 months surgical lip repair
10 months: palate repair

19
Q

Intramembranous bone formation describe - how its made, where its made

A

No cartilage precursor
Occurs at areas of tension
Bone formed by periosteum and sutures

20
Q

What are the key concepts related to cleft management?

A
  1. Early Orthopedic tx: Retraction of premaxilla allows for lip closure
  2. Phase 1 Ortho: maxillary expansion which provides room for alveolar bone graft before maxillary canine eruption
  3. phase 2 Ortho
21
Q

What embyronic structures give rise to the palate?

A

Median nasal process > primary palate
Maxillary processes > palatal shelves

  • These structures fuse anteriorly and posteriorly from the area of the incisial foramen
22
Q

Adult structure, name the embryonic precursors:

  1. Median tuberculum
  2. Lateral lip and maxilla
  3. Lower lip and mandible
  4. Palate
  5. Commisures of the mouth
A
  1. Median tuberculum - median nasal processes
  2. Lateral lip and maxilla - median nasal and maxillary
  3. Lower lip and mandible - mandibular processes
  4. Palate - primary palate and palatal shelves of max proces
  5. Commisures of the mouth - maxillary and mandibular processes
23
Q

What is an example of an inherited defect of intramembranous bone formation?

A

Cleidocranial dysplasia

24
Q

Endochondral bone formation: hows it made? where does it occur? What causes differentiation of the cells?

A

Cartilaginous precursors
Generally occurs in areas of pressure
Hypoxia and decreased vascular capacity result in differentiation of chondroblasts from stem cells

25
Q

Example of an inherited defect of endochondral ossification?

A

Achondroplasia (dwarfism)

26
Q

Cranial vault and base form how?

A

Cranial vault: intramembranous (sutures)

and cranial base: endochondral

27
Q

An example of a disorder with failure of both intramembranous and endochondral bone formation?

A

osteogenesis imperfecta

28
Q

Disorders of cranial sutures?

What does this look like radiographically?

A

Apert’s syndrome
Crouzon’s syndrome
-“Copper beaten skull- there is resuprtion on the inner however cannot expand

29
Q

Of the cranial base synchondrosis, which remain active at birth? Which are active during childhood? What age does it close?

A

Active at birth: spheno-occipital, intersphenoidal

through childhood: spheno-occipital (closes at 13)

30
Q

Maxilla and mandible form/grow how?

–bonus: clinical relevance for how the mandible grows relative to IAN

A

Maxilla: intramembranous
Mandible: endochondral and intramembranous
–Condyle-intramembranous.
– All of the growth occurs posterior to the 2nd primary molar the relative position of lingual foramen moves up and back w/age (older people aim higher for IAN)
- and mandibular processes fuse at 12 months, therefore any mandibular expansion that occurs after is dentoalveolar

31
Q

Alveolar bone growth occurs how?

A

Intramembranous bone growth
Periodontal ligament acts similar to suture
no teeth- no bone
Clinical relevancy: if primary tooth present maintain utnil ready to place implant.

32
Q

Orthodontic forces result in what kind of bone growth?

A

Intramembranous-
ortho is a tensions, intramembranous bone growth occurs where there is tension while endochondral occurs where there is pressure

33
Q

Describe the Sutural push theory

A

Bone form, shape etc is controlled by genetics/intrinsically
- in order for sutures to push the face down and forward (like we observe) they would be responding to pressure–however sutures only respond to tension.

34
Q

Nasal septum theory of facial growth

A

Cartilaginous growht is the primary determinant of craniofacial growth

  • Nasal septum exerts downward and forward influence on growth of the maxillary complex
  • Truth: there is some role of the nasal cartilage
35
Q

Functional matrix theory: why was this a paradigm shift? What does it determine

A

All the previous theories focused on hard tissues directing growth whereas Dr. Moss believed soft tissues to direct growth.
- “Functional demands of the craniofacial complex control growth.” Ex

36
Q

Servosystem theory (Petrovic) describe:

A

All facial growth is controlled by the midface.

  • With maxillary growth there is a change in the occlusion, max/mandible relationship leads to muscular repositioning of the mandible and the condylar cartilage responds
  • Big fan of functional appliances
  • Theory is rejected; lack of mandible response in studies
37
Q

Today’s theory of facial growth summary

A

Overall growth potential is determined by intrinsic (genetic) factors
- The extent to which this growth potential is realized can be determined by extrinsic (environmental) factors

**Pediatric Dentistry Boards 2019 (23 decks)

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