Growth and Development Flashcards
Define: Growth Development Hypertrophy Hyperplasia Acretion
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
When is the embryonic period? What is the most prominent structure during this time?What is the fetus susceptible during this period?
First 8 weeks of life The head/face Fetal Alcohol Syndrome Infections (rubella, CMV) Radiation Nutrition deficiency
What are the facial prominences? What do they surround?
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
Branchial arch : 1- mandibular 2 - hyoid 3- glossopharyngeal 4 - plus
1- Meckel’s cartilage, malleus, incus and muscles of masicationg. Trigeminal nerve, maxillary artery
2- Hyoid: stapes, styloid, stapedius, Facial nerve, stapedial artery
- Glossopharyngeal : Greater cornu, stylopharyngeus muscle, glossopharyngeal arter
- Thyroid cartilage, vagus nerve, aorta
The facial processes either fuse or merge. Which ones merge? fuse? What occurs during this? Possible problems?
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
Which branchial arch anomalies are the most common? Examples of?
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.
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?
- between 3-11 weeks (the embryonic period)
- 1st branchial arch
- Trigeminal nerve, muscles of mastication, meckel’s cartilage
What are three 1st branchial arch syndromes? And one common manifestation?
Pierre Robin Sequence,
Hemifacial microsomia (goldenhar),
Mandibulofacial dysplasia (Treacher Collins)
- Cleft lip/palate
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?
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
Describe the Fetal development period
Begins 9th week in utero to birth
Characterized by more growth than development (size change)
Body grows more rapidly
Ossification begins
Dental anomalies frequently encountered with cleft/lip patients?
Ectopic eruption of maxillary 1st molars (30%)
Supernumerary teeth
morphologic anomalies
missing teeth
Palatal fusion is typically completed by?
11 weeks
Describe the order the palates “zip” together:
Primary palate zips from posterior to anterior
Secondary palate zips closed from anterior to posterior
Submucous palate occurs when?
What are some problems associated with submucous cleft?
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
Describe the triad of the submucous cleft
Bifid uvula
Palatal muscle diastasis
Notch in the posterior surface of the hard palate
Epidemiology of cleft lip and palate (prevalence, race, gender)
Prevalence 1/2000 (lip alone 1/1000)
Slightly higher in Asians
Slightly higher in females
Unilateral cleft lip and palate What percentage to each side?
Majority to the left- 2/3rds
Management of cleft at neonatal period: timing of each treatment 0-12 months
Obturation, tissue molding
5 weeks orthopedic appliances
7 weeks lip adhesion
5 months surgical lip repair
10 months: palate repair
Intramembranous bone formation describe - how its made, where its made
No cartilage precursor
Occurs at areas of tension
Bone formed by periosteum and sutures
What are the key concepts related to cleft management?
- Early Orthopedic tx: Retraction of premaxilla allows for lip closure
- Phase 1 Ortho: maxillary expansion which provides room for alveolar bone graft before maxillary canine eruption
- phase 2 Ortho
What embyronic structures give rise to the palate?
Median nasal process > primary palate
Maxillary processes > palatal shelves
- These structures fuse anteriorly and posteriorly from the area of the incisial foramen
Adult structure, name the embryonic precursors:
- Median tuberculum
- Lateral lip and maxilla
- Lower lip and mandible
- Palate
- Commisures of the mouth
- Median tuberculum - median nasal processes
- Lateral lip and maxilla - median nasal and maxillary
- Lower lip and mandible - mandibular processes
- Palate - primary palate and palatal shelves of max proces
- Commisures of the mouth - maxillary and mandibular processes
What is an example of an inherited defect of intramembranous bone formation?
Cleidocranial dysplasia
Endochondral bone formation: hows it made? where does it occur? What causes differentiation of the cells?
Cartilaginous precursors
Generally occurs in areas of pressure
Hypoxia and decreased vascular capacity result in differentiation of chondroblasts from stem cells
Example of an inherited defect of endochondral ossification?
Achondroplasia (dwarfism)
Cranial vault and base form how?
Cranial vault: intramembranous (sutures)
and cranial base: endochondral
An example of a disorder with failure of both intramembranous and endochondral bone formation?
osteogenesis imperfecta
Disorders of cranial sutures?
What does this look like radiographically?
Apert’s syndrome
Crouzon’s syndrome
-“Copper beaten skull- there is resuprtion on the inner however cannot expand
Of the cranial base synchondrosis, which remain active at birth? Which are active during childhood? What age does it close?
Active at birth: spheno-occipital, intersphenoidal
through childhood: spheno-occipital (closes at 13)
Maxilla and mandible form/grow how?
–bonus: clinical relevance for how the mandible grows relative to IAN
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
Alveolar bone growth occurs how?
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.
Orthodontic forces result in what kind of bone growth?
Intramembranous-
ortho is a tensions, intramembranous bone growth occurs where there is tension while endochondral occurs where there is pressure
Describe the Sutural push theory
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.
Nasal septum theory of facial growth
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
Functional matrix theory: why was this a paradigm shift? What does it determine
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
Servosystem theory (Petrovic) describe:
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
Today’s theory of facial growth summary
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
