CTB Theme 3 Flashcards
1
Q
what is involved in the establishment of the ‘body plan’
A
- Fertilisation
- Initially the cells proliferate
- Organisation into a body- gastrulation
- 3 sheets of cells develop- ecoderm, mesorderm and endoderm
- Forms a primitive embryo where a head develops at one end and a tail at the other.
- Correct folding is governed my mesenchymal- epithelial interaction
- Organogenesis- organs form
2
Q
what are the derivatives of the ectoderm (outer layer)
A
epidermal cells of skin and oral/dental epithelium
cns- neurone of brain
neural crest- pigment cell and CRANIOFACIAL TISSUES (cartilages, bone, teeth)
3
Q
what are the derivatives of the mesoderm (middle layer)
A
notochord bone tissue tubule cell of the kidney red blood cells facial muscle
4
Q
what are the derivatives of the endoderm (internal layer)
A
digestive tube
pharynx
respiratory tube
5
Q
what are the derivatives of germ cells
A
sperm
egg
6
Q
what is the period where the embryo is subjected to teratogens which can causes malformations in organ systems
A
4-12 weeks
7
Q
what are examples of early head formation defects
A
Holoprosencephaly
•Facial midline defect due to deficiency in forebrain tissue.
•Caused by mutations in Shh pathway genes.
Anencephaly
•Abnormal brain development due to failure of neural tube closure- c
•Caused by teratogens or malnutrition, e.g.:
-High retinoic acid (Vitamin A) levels can interfere with Hox gene expression
-Folic acid (Vitamin B9) deficiency- can prevent craniofacial diseases
8
Q
why is folic acid advised for pregnant women
A
(Vitamin B9)
can prevent craniofacial diseases
9
Q
outline the development of the head fold
A
21 day human embryo
The folding of the early embryo is a crucial developmental event. (e.g. head formation).
The plate of the 3 germ layers can be seen, structures start to form.
10
Q
outline the development of the head and mouth for a 16 day old embryo (1/4)
A
Three germ layers: Ectoderm, Mesoderm, Endoderm
Expansion of the neural plate- formation of head fold
Cells proliferate
11
Q
outline the development of the head and mouth for a 18 day old embryo (2/4)
A
Oropharyngeal membrane develops.
It separates the future mouth (stomodeum) from the pharynx and acts as a transient cell signalling centre to “pattern” the oral cavity- It breaks down eventually so it doesn’t interfere with other development
12
Q
outline the development of the head and mouth for a 22 day old embryo (3/4)
A
Formation of the future mouth (stomodeum).
Note the rotation of the heart- more inwards
13
Q
outline the development of the head and mouth for a 30 day old embryo (4mm) (4/4)
A
Rudiments (anlagen) of most organs are established!
Oropharyngeal membrane starts to break down.
Yellow tube forms the oesophagus
Pharyngeal arches 1,2,3 become prominent
14
Q
outline the basic structure of the pharyngeal arches
A
Each arch is covered externally by ectoderm and internally by endoderm.
The internal mesodermal core becomes infiltrated by migrating cranial neural crest cells that migrate into the pharyngeal arches .
=> 1 nerve, 1 cartilage, 1 artery per arch
15
Q
outline the formation of neural crest cells
A
- Neural crest cells are induced molecularly at the border between neuroectoderm (forms brain and spinal cord) and epidermis (forms skin)
- Neural plate invagination and formation of neural folds (spinal column) generates an “open tube”.
- Neural folds fuse to form the neural tube. Neural crest cells begin to migrate along pre-determined pathways.
- Neural crest cells continue migration to their pre- determined destinations and become specialised cell types.
16
Q
outline how NCCs are specified by opposing gradients of signalling molecules
A
Neural crest cells are specified at the border between neuroectoderm and epidermis.
Overlapping gradients of BMP4 and WNT6 signalling proteins (“morphogens”) induce the expression of FoxD3 and Slug, two transcription factors necessary for neural crest cell specification and migration.
2 opposing gradients- each cells get different gradients. The cells that get intermediate signals are the neural crest cells
17
Q
outline how Cranial neural crest cells (CNCs) migrate into pharyngeal arches
A
The cells at each level of the neural tube know where to migrate
Molecular subdivision- cells express different genes that instruct them to migrate to target region
CNCs migrate along specific pathways from the early brain into the pharyngeal
arches.
Genetic codes (overlapping expression of homeobox transcription factors) determine the identity of CNCs. (pre-patterning vs. local specification of cell fates)
In the head region there are other Homeobox genes
18
Q
what are the embryonic features involved in facial development
A
lateral nasal process
medial nasal processes
maxillary process
mandibular process
19
Q
what is the difference between merger and fusion
A
Merger: Elimination of a furrow between two processes (by mesenchymal cell proliferation). The cells appear as one continuous structure as it expands, its not 2 things coming together. (e.g. mandibular process)
Fusion: Contact between epithelial cells of two processes triggers fusion of epithelial cell sheets and subsequent elimination of epithelial cells. These are 2 different things
20
Q
what are the key events in the development of the face (4-5 weeks) (1/3)
A
Formation and growth of an unpaired frontonasal prominence -
Formation of 2 nasal placodes (epithelial thickenings)
Nasal pit:
Formation of paired nasomedial (medionasal) processes
Formation of paired nasolateral (lateronasal) processes
Formation, growth and merger of the paired mandibular processes- this has already merged in the middle so its one continuous process
Formation and growth of paired maxillary processes (small!)- only grow to the inside
21
Q
what are the key event in the development of the face (5.5-6 weeks) (2/3)
A
Recession of frontonasal prominence
Due to strong forward growth of nasomedial (medionasal) processes- causes a relocation back wards of the frontonasal prominence
Growth of nasolateral (lateronasal) processes
Strong growth of maxillary processes
-Formation of nasolacrimal duct, cheek and alar base of nose
22
Q
what are the key event in the development of the face (7-8 weeks) (3/3)
A
Merger of nasomedial (medionasal) processes- still like two separate processes.
Further growth of maxillary processes and fusion with nasomedial processes
- Formation of central part of nose, upper lip and primary palate
- Upper lip is formed from maxillary processes laterally and in the midline from the nasomedial processes (philtrum).
23
Q
Outline a summary of the Contributions to face from facial processes summary
A
A: Maxillary processes
- Maxilla
- Lateral part of upper lip
B: Mandibular processes
- Mandible
- Lower lip
C: Medial nasal processes
- Medial part of nose
- Medial part of upper lip
- Primary palate
D: Lateral nasal processes
- Lateral part of nose
24
Q
what causes a median cleft lip (rare)
A
Failure of merger of medial nasal processes.
25
what causes a (Bi)lateral cleft lip (rare)
Failure of fusion between maxillary processes and medial nasal processes. (Persistence of bucconasal grooves.)
26
what causes an Oblique facial cleft (rare)
Failure of fusion between maxillary process and lateral nasal process. (Persistence of nasolacrimal groove).
27
what causes a Lateral facial cleft (macrostomia)
Failure of merger between mandibular and maxillary process.
Mouth is too big (it is underdevelopled)
28
what causes a Median mandibular cleft
Failure of merger of mandibular processes
Mild form: Chin dimple!
29
what is a cleft lip and how can it be managed by Multidisciplinary team approach
associated with cleft palate (because the medionasal process also contributes to the primary palate;
Note protrusion of premaxilla in bilateral cleft lip patient.
Clinical management: Multidisciplinary team approach (Oral surgeon, Orthodontist, Speech therapist, Specialist nurse, Psychologist)
30
what are the clinical features of Frontonasal dysplasia:
Too much tissue in the frontnasal process
Frontonasal separation
various degrees of excessive tissue in the frontonasal process
31
what are the clinical features of Treacher Collins syndrome (Mandibulofacial dysostosis)
Hypoplasia of mandible and facial bones (e.g. cheek bones), macrostomia (big mouth), ear malformations, cleft palate, abnormal dentition, slanting of palpebral fissures, eyelid coloboma.
32
how is Treacher Collins syndrome caused
Failure of neural crest cells to migrate into the craniofacial region. Cells die by apoptosis.
-Heterozygous mutations in Tcof1 geneinvolved in ribosome biogenesis – making of ribsomones that produce proteins.
33
outline the development of the primary palate from
5-6 weeks
6.5 weeks
7 weeks
5-6 weeks: Nasal pits are relocated inwards towards the oral cavity. (Primary palate forms indirectly by relocation of the nasal pits)
6.5 weeks: A thin oronasal membrane separates the nasal and oral cavities. Brings the 2 epithelia together. Molecular signal centre that needs to be removed once development to be complete.
7 weeks: The oronasal membrane disintegrates and nasal choanae (space that forms the nasal and oral cavities) form.
- Continuous nasal and oral cavities
- The primary palate is formed by the merged medial nasal processes (“intermaxillary process”) that continue to grow inwards into the oral cavity.
34
what is choanal atresia
Persistence of oronasal membrane
Narrowing or blockage of the nasal airway by tissue-
•Incidence: 1:7,000
-Most common nasal abnormality
* Unknown cause
* Part of syndromes, e.g. CHARGE syndrome
* Variability:
- Unilateral (more common) or bilateral
- Blockage by soft tissue or bone
- Partial (stenosis) or complete
•Treatment:
- At birth: Babies Resuscitation, Intubation, Tracheostomy
- Later: Surgical correction
35
outline the overview of the development of the secondary palate
•The secondary palate is formed by lateral outgrowths of the maxillary processes
(6-10 weeks) and closes the space between nasal and oral cavities.
•12 weeks: Secondary palate has formed completely and is fused to primary palate.
- Nasal and oral cavities are completely separated allowing breathing and eating.
- Babies with cleft palate can’t breathe while feeding! -cant breathe through their nose
36
outline the development of the secondary palate at 6 weeks and 7-8 weeks (1/2)
* 6 weeks: The median palatal process (primary palate) has formed as an ingrowth of the merged medionasal processes.
* The lateral palatine processes (palatal shelves) appear as outgrowths from the maxillary processes. They grow downwards on either side of the tongue.
* 7-8 weeks: The palatal shelves elevate above the tongue, but are not fused.
* Downgrowth of the nasal septum (formed from frontonasal prominence and tectoseptal process; primary & secondary nasal septum).
37
outline the development of the secondary palate at 9 weeks and 12 weeks (2/2)
* 9 weeks: Fusion of palatal shelves in anterior part and fusion with primary palate. Fusion of nasal septum with palatal shelves.
* 12 weeks: Fusion of palatal shelves in posterior part and formation of palatine raphe. Incisive foramen remains for blood vessels and nerves. Uvula forms as posterior projection from the medial soft palate (swallowing; speech; gag reflex; breathing).
38
outline the Development of the secondary palate – Frontal view
* A: 7 weeks: shelf down-growth on both sides of the tongue.
* B: 8 weeks: shelf elevation (but not fusion) & nasal septum down-growth Hypothesised mechanism: Tongue movement, selective tissue hydration- structure can flip up (GAGs)
* C: 9 weeks: shelf fusion (anterior region) & fusion with nasal septum.
* 10 weeks: Developing palatine processes of maxilla and palatine bone rudiments start to ossify and grow towards the midline (arrows).
* 12 weeks: Palatal bone rudiments meet in midline and fuse. - continuous hard palate
39
outline the Fusion of palatal shelves
Palatal shelves meet through growth of palatal mesenchymal cells.
- Fusion of the two epithelia to form MES (medial epithelial seam)
- Need to happen only between the 2 palatal shelves
- Palatal shelve epithelia fuse randomly with other palates in the mouth cleft lip
Removal of MES by apoptosis of epithelial cells.
All epithelial cell remnants are re-moved resulting in a continuous secondary palate.
40
what does Incomplete removal of epithelial remnants result in
palatal cysts- Filled with keratin/soft mucous
Could interfere with denture
41
outline Developmental causes for cleft secondary palate
Early growth or morphogenetic defect :
- Reduced cell proliferation of mesenchymal cells
- If they elevate they can’t fuse
Premature epithelial fusion:
-Epithelium of palatal shelves fuses with other oral epithelia
Failure of palatal shelf elevation:
-Mechanical obstruction or abnormal cell differentiation in ‘hinge’ region of palatal shelves
Late growth defect:
-Reduced cell proliferation of mesenchymal cells
Secondary effects:
-e.g. abnormally wide head (in craniosynostosis)
Epithelial fusion defects:
-Failure of the epithelium to break down during fusion
42
what are Common varieties of cleft palate
Most common birth defect:
- Cleft lip (CL/P): 1:1000
- Cleft palate only (CP): 1:2500
Unilateral cleft passing through lip and primary palate.
Bilateral cleft lip and cleft primary palate
Cleft secondary palate only (CP)
- C1: Unilateral (cleft on one side of NS)
- C2: Bilateral (cleft on both sides of NS)
- They relate to the fusion with nasal septum
Bilateral cleft lip and cleft primary& secondary palate
* C1: Unilateral: One shelf fused to nasal septum
* C2: Bilateral: Both palatal shelves not fused with nasal septum (NS)
43
what are the bones of the hard palate
3 bones that form hard palate: premaxilla palatine process of maxilla and horizontal late of palatine bone
* The primary palate bears the incisor teeth and forms the premaxilla bone.
* The premaxilla fuses with the palatine processes of the maxilla bone (arrows).
* The incisive foramen allows for passage of blood vessels and nerves.
* The palatine processes of the maxilla fuse with the horizontal plates of the palatine bone (arrowheads).
44
Which teeth are most likely to be missing in the cleft lip area
- Upper lateral incisors- they are closely located to the cleft -no space
- Canines??? – its rarely affected by developmental conditions
- The second premolars are next likely to be missing
45
what is Torus palatinus
* Benign bone overgrowth; usually in the midline of the hard palate
* No treatment required although ulcers are possible; impact on dentures!
46
what is the Aetiology of syndromic and isolated CL/P and CP
* 30% of cleft cases are associated with another disease (syndromic)- due to single gene mutation in coding regions
* 70% isolated- genetic predisposition, SNP in gene regulatory region
47
what are Isolated cases of CLP are usually explained by:
Multifactorial complex aetiology
•Interaction between multiple genes (polygenic)
•Interactions between genetic and environmental factors
-High variability of clinical manifestations (mild to severe)
48
what are Environmental risk factors for cleft lip/palate
* Deficiencies in maternal diet
* Excessive or insufficient vitamin intake e.g. folic acid
* Alcohol abuse
* Tobacco smoking
* Hypoxia (e.g. living at high altitude) – not enough oxygen increased incidence of clefting disorder- the embryo doesn’t get enough oxygen = underdevelopment .
* Anticonvulsant drugs (epilepsy, neuropathic pain)
* Retinoids (medication, e.g. acne cream)
```
Teratogens
• Nitrate compounds
• Organic solvents
• Exposure to pesticides
• Exposure to lead
• Recreational drug use (cocaine, heroin)
```
49
what is the pathogenic mechanism associated with syndromic forms
• Mutations in coding sequences usually affect gene function more strongly (including pleiotropic effects in other organs) than mutations in gene-regualtory DNA regions that affect tissue-specific gene expression
50
what is the signifcance of mutations in the coding sequence
• Genetic modules regulating facial development are re-used during tooth development
51
outline the Development of the Tongue (1/2)
* Appearance of three PA1-derived swellings in floor of the mouth (4-5th week): The medial tuberculum impar (TI) and two lateral lingual swellings (LLS).
* The LLS quickly enlarge and merge with each other and the TI to form the anterior tongue (66% of tongue mass).
•Posterior tongue (34% of tongue mass) forms from hypobranchial eminence (PA3, PA4) that rapidly overgrows the copula ( a transient swelling of PA2; not visible on this image).
-Terminal sulcus: border between oral (anterior) and pharyngeal (posterior) tongue.
52
where are the anterior and posterior epitehliums of the tongue derived from
Anterior part- ectoderm
| Posterior part-endoderm
53
outline the Development of the Tongue (2/2)
• The foramen caecum marks the original location of the thyroid primordium at the border between TI and copula.
• 7th week: The thyroid primordium migrates downwards towards the 3rd tracheal cartilage (and stays connected by the thyroglossal duct - during migration. ).
• Epiglottis is formed from posterior part of PA4.
• Tongue muscles are derived from occipital somites which have migrated forward into the tongue. Innervation is in accordance with the origin of pharyngeal arches.
- Tongue muscles formed from the mesoderm
54
what are the Developmental defects of the tongue
Ankyloglossia (‘Tongue tie’)- Failure of lingual frenulum to regress
Macroglossia
55
what is Ankyloglossia
```
(‘Tongue tie’)- Failure of lingual frenulum to regress
• Connects tongue to floor of mouth
• Impaired tongue movement
• Impaired speech and feeding
• Surgical correction
• Van der Woude Syndrome
• Tbx22 gene mutations
```
56
what is Macroglossia
* Tongue hyperplasia (too large tongue): Down-Syndrome
* Beckwith-Wiedemann Syndrome
* Acromegaly
* Hypothyroidisms (often associated with)
* Microglossia: Tongue hypoplasia (too small): Less common
57
what are some Developmental defects of thyroid migration
lingual thyroid-the cells need to migrate downwatds into the neck however some of the cells become stuck-
thyroid tissue
thyroglossal duct sinus
ectopic thyroid tissue - check slides for Common points where the thyroid can get stuck in it’s migration pathway
58
outline the development of the mandible (1/3)
1: Meckels cartilage has formed ~6 weeks i.u.: two hyaline cartilage rods on either side of the jaw surrounded by fibrous tissue extending from the otic capsule (arrow) to the midline of the merged mandibular arches (arrowhead).
- Provides a framework around which the mandible can form but Meckels cartilage actually contributes little to the mature mandible!
2: Ossification starts at 7 weeks i.u. in a lateral mesenchymal cell condensation near the future mental foramen. Ossification rapidly spreads forwards, upwards and backwards.
59
outline the development of the mandible (2/3)
3: Ossification of mandible body proceeds. Note the tooth germ
4: Mandible takes the shape of a trough underneath the incisive nerve. Meckel’s cartilage is smaller and alveolar process grows to surround the tooth germ.
5: Meckel’s cartilage is resorbed. Incisive nerve now enclosed in bony canal .
Alveolar process almost surrounds incisor tooth germ
Mandibular bones are not fused in the midline (→ symphysis develops ~10 weeks i.u.).
60
outline the development of the mandible (3/3)
* Ossification proceeds backwards (“posterior”) to form the ramus (R) of the mandible.- In utero not fused
* Mandible direction diverts from Meckel’s cartilage at the level of the lingula.
(Lingula: Mandibular spine attaching to the sphenomandibular ligament. Located near the entry of inferior alveolar nerve into the body (B) of the mandible (mandibular foramen)).
61
what is the Fate of Meckel’s cartilage
Most of Meckel’s cartilage eventually degrades and the space is filled with bone, BUT... …it is not endochondral ossification!
62
What structures are formed from Meckel’s cartilage remnants?
Dorsal remnants ossify to form:
- Incus
- Malleus
- Spine of sphenoid bone – remanants of meckels cartilage (→S-man lig)
Ventral remnants ossify to form:
- Lingula (→S-man lig)
- Mental ossicles (→ Mental protuberance)
63
what are the Sphenomandibular ligament (S-man lig)
| and Sphenomalleolar ligament (S-mall lig) ligaments formed from
perichondrium
64
what are Secondary cartilages (how do they appear histologically)
Secondary cartilages form later in development (always associated with a membranous bone such as the mandible) and appear histologically different from primary cartilages
-More ecm – specialised function of condoyle
65
how does meckels cartilage appear histologically
larger cells and less extracellular matrix
66
what Three secondary cartilages develop (10-14 weeks in utero):
Condylar: ( endo- chondral growth plate)
oGrowth potential until 16-20 years of age
oRole in mandibular growth
Coronoid
(transient: ossified before birth)
Symphyseal
o(“mental ossicle”)
o(ossified within 1-2 years of birth)
67
outline the Postnatal development of the mandible at birth (1/3)
- Ramus comparatively underdeveloped, mandible not fused, no distinct chin
- mandibular “symphysis” – where 2 mandibular bones meet(not a true symphyseal joint! More like a suture!!)
- no distinct chin
68
outline the Postnatal development of the mandible at 6 years old (2/3)
- Symphysis completely ossified (closed) (by ~1-2 years); mandible fused (single bone)
- Ramus has grown
69
outline the Postnatal development of the mandible in an adult (3/3)
- Mental protuberance forms prominent chin after puberty (especially in males)
- Growth by bone remodelling
- Prominent chin
70
what are the types of joints
Fibrous joint
Cartilaginous joint
Synovial joint
71
what is a fibrous joint and examples
* Two bones connected by fibres e.g sutures
* Sutures: little or no movement (stability & growth)
* Tooth attachment to alveolar bone by periodontal ligament (=> intrusion and recovery in response to biting forces; “shock absorber”)
72
what is a Cartilaginous joint and examples
2 types
•Primary: Costochondral junction
-Ribs connected to sternum
-bone and cartilage directly apposed
•Secondary: Pubic symphysis
-Piece of fibre inserted - bone-cartilage-fibres-cartilage-bone
73
what is a synovial joint and examples
Two bones (each with an articular surface covered by hyaline cartilage) are surrounded by a fibrous capsule that creates a joint cavity filled with synovial fluid.
•TMJ: articular surface covered by fibrous tissue joint cavity is divided by articular disk.
-Allows for significant movement in various directions
74
what can be seen on the External view of temporomandibular joint (TMJ)
* Condyle- secondary cartilage ossified
* Articular disk- not labelled, divides into compartments
* Disk connected to the lateral ptyergoid which enable translation movements of the TMJ
75
what are the TMJ motions
Rotation (horizontal) and Translation (forwards-backwards)
76
outline the movements of the TMJ during
- closed mouth
- opening of mouth
- fully open mouth
Closed mouth: Posterior band of disk is situated above the condyle
Opening of mouth: Condyle translates forward and the intermediate zone becomes the articulating surface.
Fully open mouth: Anterior band of disk may be situated above the condyle-
77
where does the TMJ develop from
from mesenchymal cells located between mandibular condyle
and mandibular fossa in the temporal bone
- Condensation of mesenchymal cells (like dental papilla)
78
outline the development of the TMJ
At 12 weeks, two clefts appear in the mesenchyme and form the upper and lower joint cavities (D).
-The intervening mesenchyme becomes the articular disk (arrow).
The joint capsule develops from a mesenchymal condensation surrounding the developing joint.
Initially, the mandibular fossa (C) is flat. (The articular eminence becomes prominent only after tooth eruption)
Clefting of mesenchyme to form the lower joint cavity
Articular eminence fully formed and the mandibular fossa no longer flat
developmental processes assoociated with function
79
what do Variations of TMJ anatomy depend on
functional requirements for mastication! (e.g. tiger the TMJ looks like a door hinge- they need a strong bite, badger, humans)
80
outline the features of the TMJ
* A: articular disk
* B: mandibular (glenoid) fossa
* C: condyle
* D: joint capsule
* E: lateral pterygoid muscle
* F: articular eminence
(see image)
81
outline the Histology of the growing TMJ
Fibrous layer of the condyle provides progenitor cells that form chondrocytes that undergo endochondral ossification (similar to perichondrium in epiphyseal/growth plate).
Fibrous layer of the mandibular fossa contains outer layer (more fibrous → articulation) and inner layer (more cellular);
Articular disc- fibrocartilage, made of fibres with chondrocytes interspaced in the middle - more mobility and stability than a typical fibrous tissue
82
outline the Growth of the condyle
The cells of the proliferative layer divide and produce new chondrocytes enabling condylar growth.
-Grow rapidly and differentiate into mature chondrocytes that produce cartilage.
Endochondral ossification is similar to the epiphyseal/growth plate. Condylar cartilage can grow up to the age of 16-20 years, and is then fully calcified.
-Chondrocytes will die and osteoblasts move in and deposit bone matrix on top of the cartilage matrix
83
outline development of The condyle at the end of the growth period
Growing condyle (13 years): enlarged proliferative cell layer
Adult condyle: reduced proliferative cell layer
- Cells of the proliferative layer persist throughout life and can respond to functional changes (“masticatory stress”) by reactivating condylar growth-
- Basis for remodelling of articular surfaces by orthodontic treatment.- most efficient in teenage period when this cell layer is thick and can grow rapidly, it is still possible.
84
what layers form in the adult condyle
Fibrocartilage and calcified cartilage
85
outline the The articular eminence formation in adults
Similar organisation as in the condyle but no endochondrally ossified cartilage
- Proliferative zone can also respond to functional changes and induce remodelling
- Note: Thick layer of fibres covering the articular eminence potentially involved in ensuring articulation.(→ articulation)
86
what is the Synovial membrane
Lines the capsule
Bilayered with folds/villi that protrude into joint cavity and produce synovial fluid. (more folds with increasing age and in pathological conditions- to compensate for production of more fluid if there is an issue in the joint
87
what is the function of the Temporomandibular ligament
The temporomandibular ligament prevents posterior, inferior, lateral and medial displacement.
- Dislocation can only occur in a forward direction (by slipping of the condyle head over the articular eminence).
88
what are the muscles of mastication
```
infrahyoid
lateral pterygoid
masseter;
medial pterygoid
suprahyoid
temporalis
```
89
where does the Temporalis attach and what are clinical issues associated with it
Temporal fossa → Coronoid process & Ramus
Bruxism → Jaw pain
Seizure → Rupture of myotendon at coronoid due to clenching of the jaws
90
where does the masseter attach and what are clinical issues associated with it
(superficial, deep)
- Zygomatic arch → Ramus & Angle
- Bruxism → Hypertrophy- enlarges (asymmetric face; do not confuse with other diseases such as ankylosis!)
91
where does the medial pterygoid attach
Superficial: Maxillary tuberosity/pyramidal process → Ramus
Deep: Sphenoid → Ramus
92
where does the Lateral Pterygoid attach
Superior: Sphenoid (greater wing) → Condyle (neck), TMJ capsule
Inferior: Sphenoid (lateral pterygoid plate) → Condyle (neck), TMJ capsule
93
what is the Innervation of the TMJ
mandibular branch of trigeminal nerve (CN V)
94
what do Free nerve endings (most abundant) in the TMJ do
Free ending
Widely distributed
Sense pain (nociception: “sense harm”) → joint protection
95
what do Ruffini’s corpuscles do in the TMJ do
Encapsulated ending
Associated with joint capsule
Sense joint posture (proprioception: “sense position”)
96
what do Golgi tendon organs do in the TMJ do
Encapsulated ending (appear similar to Ruffini’s corpuscles)
Associated with joint ligaments
Sense only extreme joint movements → ligament protection
97
what do Pacini’s corpuscles (least abundant) do in the TMJ
Encapsulated ending
Associated with joint capsule
Sense pressure and vibration
98
what are Clinical considerations for the Mandible
* Treacher Collins syndrome (Small mandible; ‘Micrognathia’)- absence of zygoma
* Pierre Robin sequence (Small mandible, cleft palate, glossoptosis- base of the tongue od too far back obstructing the airways)
* Other: Russell-Silver syndrome, Seckel syndrome, Cri-du-chat syndrome
* Acromegaly (Large mandible)-
99
what is Acromegaly caused by
over production of growth hormones (pituitary tumours)
Excessive growth hormone production (often caused by pituitary tumour), often associated with gigantism: general soft tissue swelling, frontal bossing, mandibular protrusion, macroglossia.
100
what is Hemifacial microsomia
can be associated with Goldenhar syndrome: eye tumours)
• Second most common birth defect
• The lower half of one side of the face is underdeveloped (mandibular, maxillary hypoplasia) => Facial asymmetry Ear abnormalities (microtia, anotia)
• Variable phenotype
• Unknown aetiology (genetics?; impaired blood supply to area?; teratogens? => 4-8 weeks in utero)
• Treatment: Surgery (bone graft)
101
what are TMJ disorders and symptoms
pain and dysfunction of TMJ and masticatory muscles (5-12% prevalence; more common in young people and women)
symptoms- Pain (most common cause of orofacial pain after toothache), swellings, restricted jaw movements, noises (‘clicking’ or ‘grating’ sounds).
not well understood condition
Can become chronic and is difficult to manage
102
what can TMJ disorders cause
* Trauma and infection can cause ankylosis (stiff joints; difficulties opening the mouth; can create facial asymmetry due to asymmetric jaw growth)
* Bone cancer: Osteosarcoma of jaw (8%)
103
what does the Anterior displacement (AP) of the articular disk do
positions the posterior band in front of the condyle. As the condyle and disk translate forward, the bilaminar zone becomes abnormally stretched
104
what can the The displaced posterior band do in anterior displacement
Return to its position (AP with reduction) → “popping/clicking” sound
Not return to its position (AP without reduction) → “grinding” sound Patients often cannot fully open their mouth- condyle head makes direct contact with the mandibular fossa creating a grinding sound
105
what is Eagle (Stylohyoid) syndrome
Elongated process (>3 cm) or calcified stylohyoid ligament
Rare condition (4% of population have enlarged styloid process but no symptoms!)
Symptoms: Orofacial pain, tinnitus, sore throat, swallowing difficulties (dysphagia)
Diagnosis: palpation, radiograph, CT scan. Treatment: analgesics; styloidectomy
106
what are the mechanisms of bone formation
Endochondral ossification
Intramembranous ossification
Sutural ossification
107
what is involved in Endochondral ossification and which bones are formed from this
•Bones made from a cartilage model (Chondrocytes produce cartilage that is replaced by osteoid/bone produced by osteoblasts)- migrate towards the cartilage and deposit bone on top of the cartilage
•e.g. Long bones (epiphyseal growth plate), mandibular condyle (secondary cartilage), all bones base of skull (synchondrosis)
(Most bones from head down apart from clavicle )
108
What is involved in intramembranous ossification and which bones are formed from this
* Bones made by osteoblasts that have differentiated from mesenchymal stem cells
* Direct process
* e.g. Flat skull bones; Facial bones: mandible, maxilla
109
What is involved in sutural ossification and which bones are formed from this
Similar to intramembranous ossification but with fibrous connection
providing stability during growth
sutures- fibrous connections between bones
e.g. Postnatal growth of skull bones
110
outline the development of the endochondral bones (1/2)
Early perichondrium (source of the stem cells that from chondrocytes) is formed by chondroblasts that are derived from condensed mesenchymal cells.
Cartilage model assumes shape of the future bone and the perichondrium becomes prominent.
In the diaphysis (central) region, the perichondrium becomes a periosteum. -Osteoblasts differentiate from osteoprogenitor cells in the periosteum (making osteoblast) and produce a collar of bone (cortical bone; intramembranous)
Cartilage matrix begins to calcify (dots) on the inside- osteoblasts deposit on the cartilage
111
outline the development of the endochondral bones (2/2)
Blood vessels invade the cartilage model through the bone collar and introduce osteoblasts and osteoclasts through the blood. Osteoblasts form of primary ossification centre – small area that is mineralised and this mineralisation spreads out
Bone trabeculae are formed and link to the bone collar, later the spaces between the trabecular fill with bone marrow- not yet though!
Secondary ossification centres are established in the epiphysis.
112
where are the primary and secondary ossification centres located during the development of endochondral bones
primary ossification centres- DIAPHYSEAL (centre)
secondary ossification centres- EPIPHYSEAL (towards ends)
113
what is growth in length in endochondral bones mediated by
Epiphyseal growth plate – occurs in the small area between 2 already calcified part of the bone
114
what is growth in thickness in endochondral bones mediated by
periosteum
115
what are the types of chondrocytes in the epiphyseal/growth plate of growing endochrondral bones
resting chondrocytes
proliferating chondrocytes
prehypertrophic chondrocytes
hypertrophic chondrocytes
116
what are resting chondrocytes
Reservoir of chondrocytes to replenish lost chondrocytes
117
what are Proliferating chondrocytes
- Chondrocytes align in columns and divide (secrete cartilage matrix; collagen type II)
- Allows growth in one direction
118
what are Prehypertrophic chondrocytes
Chondrocytes begin to swell; increased production of cartilage matrix (collagen type X) (Start to mature )
119
what are hypertrophic chondrocytes
- Fully matured chondrocytes; eventually die by apoptosis
| - Filled with cartilage matrix
120
what is the calcification zone in the growth plate of growing endochondral bones
Cartilage matrix being replaced by osteoblasts
121
what are Synchondroses and examples
Cartilaginous joints of the cranial base
•Mirror image of two epiphyseal/growth plates (stippled line)
•Example: Synchondrosis between sphenoid and occipital bone
-Enables growth of cranial base in both directions
122
what is epiphyseal cartilage
•Mediates growth of endochondral bones: Cartilage formed by chondrocyte proliferation, maturation& hypertrophy; Alignment in cell columns reflects growth in length.
123
what is condylar cartilage
* Mediates growth of an intramembranous bone: Mesenchymal cells respond to functional loading, proliferate and differentiate into chondrocytes. Random arrangement reflects multidirectional growth capacity!
* Chondrocytes not in columns- needs to grow in all directions – intramembranous bone does not have the capacity to grow as much as an endochrondral bone.
124
what are sutures and what do the allow
Fibrous joints between skull bones
- Enable skull bone growth in response to brain growth
- Respond to mechanical stress
- Pulling on sutures by underlying brain induces bone formation
125
outline the Organisation of the suture and the histological sequence
Cambrian layer: cellular → bone growth
-Mediated by osteoblasts
Capsular layer: fibrous → stability
-Mediated by fibroblasts
Bone – Cells – Fibres – Cells – Bone
126
what is the neurocranium and what type of ossification takes place
Neurocranium = Cranial vault + cranial base
- the bones that completely encase the brain
- intramembranous or cartilaginous ossification
- Surrounds the brain
127
what is the visocranium
= Facial skeleton
| Surrounds oral cavity, pharynx, upper respiratory tract
128
what bones from the visocranium and the neurocranium are formed by endochrondral ossification
visocranium- cartilaginous viscerocranium
neuocranium- chondrocranium
129
what bones from the visocranium and the neurocranium are formed by intramembranous ossification
membranous neurocranium
| membranous viscerocranium
130
whah is the origin of posterior and anterior bones of the skull
posterior- mesoderm
anterior- neural crest cells
131
outline the development of the cranial vault
1. Bones develop ~ 5 weeks i.u.:
- Frontal Parietal
- Temporal (squamous)
- Occipital (squamous)
- Intramembranous bones
- Small condensation of menenchymal cells
2. ossification progresses until the bones meet at ~7 months i.u. – fully formed
3. Sutures and Fontanelles are formed
- Specialised growth centres
- Fibrous connections between the 2 bones
132
what are sutures and frontanelles and the function
Sutures coordinate skull bone growth in response to brain growth. (→ CTB 38)
Fontanelles are enlarged sutures (where three or more calvarial bones meet)
-Flexibility to pass down birth canal
* Required to enable birth of the babies- bones compressed so the head can get out- bones slide over each other and are compressed.
* Variable postnatal closure of fontanelles (by 18 months) and sutures (adulthood apart from metopic)
133
how is craniosynostosis
Premature fusion of sutures
Caused by dominant-negative FGFR2 mutations- this regulates osteoblasts and fibroblasts. mutation causes overactivity so lots of osteoblasts are formed hence premature suture closing
134
what is the name of the defect caused by Premature closure of Sagittal suture and what does it cause
Scaphocephaly
- Long, narrow skull
- Frontal and occipital bossing
135
what is the name of the defect caused by Premature closure of coronal suture and what does it cause
Brachycephaly
- Skull can only grow upwards, not sideways
- Tall, short skull
- Flat frontal and occipital regions
Plagiocephaly: Closure of coronal suture only on one side
136
outline Development of the cranial base
•A. Paired cartilages develop ~ 6 weeks i.u.:
-Extending from cranial end of the notochord to the nasal capsule
•B. Cartilages grow towards each other, fuse (~ 8 weeks i.u.) and form characteristic endochondral bones-
137
outline the Development of the cranial base (midline)
* Occipital sclerotomes & parachordal cartilage → basilar & condylar parts of occipital
* Hypophyseal & trabecular cartilages → body of the sphenoid
* Trabecular & nasal cartilages come together and form → perpendicular plate & crista galli of the ethmoid
138
outline the Development of the cranial base (lateral)
* Ala orbitalis & ala temporalis → lesser & greater wings of the sphenoid
* Otic capsule & lateral part of parachordal cartilage → petrous (very hard) & mastoid temporal
* Paired nasal cartilages & prechordal cartilage (anteriorly) → nasal cavity
139
outline the Histology of the developing cranial base
see image
| Basal plate- forms part of the occipital and sphenoid- pituirary gland sits in the sella turcica.
140
what are Synchondroses
-Cartilaginous joints
-Important growth centres
• Their development and growth influences the structure and dimensions of the craniofacial skeleton.
141
what are the Synchondroses of the cranial base
* Intersphenoidal synchondrosis: Ossifies ~ 7 months i.u.
* Spheno-ethmoidal synchondrosis: Ossifies ~ 7 years of age
* Spheno-occipital synchondrosis: Ossifies ~ 13-17 years of age
142
outline the Development of the facial skeleton
Ossification starts ~ 7 weeks i.u.:
- Maxilla (near primary canine)
- Mandible (lateral to Meckel’s cartilage between the mental & incisive branches of the inferior alveolar nerve).
2. Ossification spreads rapidly in all directions.
3. Meckels cartilage starts getting resorbed.
143
outline the Mode of ossification of:
- medial pterygoid plate of sphenoid
- interparietal bone of occipital bone
intramembranous
144
outline the Mode of ossification of:
- body of sphenois
- greater and lesser wing of sphenoid
- lateral pterygoid plate of sphenoid
- surpaoccipital
- exocciptals
- basioccipital
endochrondral
145
outline the features of simple bone
Formed by ossification of a single element
-Endochondral: e.g. malleus
• OR
- Intramembranous: e.g. zygomatic
146
outline the features of compound bone
Formed by fusion of two or more ossifying elements
-Two or more endochondral elements: e.g. ethmoid
OR
-Two or more intramembranous elements: e.g. maxilla
OR
-Endochondral and Intramembranous elements: e.g. sphenoid
147
outline how Sphenoid = Compound Bone
1. Body:
- Two parts ossify endochondrally ~7 months i.u.
2. Lesser wing:
- Ossifies endochondrally before birth
3. Greater wing and lateral pterygoid plate:
- Ossification initiates endochondrally from alisphenoid cartilage but spreads intramembranously
4.Medial pterygoid plate ossifies intramembranously
148
outline the features of a newborn skull
Large anterior frontonell
Mandible not fused yet
Hard palate- can see fusion
Massive imbalce in the facial structure- e.g. comparatively large skull due to well developed brain. And face is small. Relates to function. Face grows rapidly in post natal development
149
Why is understanding of the mechanisms underlying craniofacial growth important for an orthodontist?
* Facial growth directly influences the skeletal relationship between the jaws.
* Orthodontic treatment is often carried out during the period of craniofacial growth and often attempts to modify the pattern of jaw growth.
* Previous patterns of facial growth can be useful for predicting future growth.
150
outline the Principles of crraniofacial growth and development
A: Bones do not grow by simple symmetrical enlargement!
B: The mandible grows by elongation of condyle and ramus in a posterior and superior direction, and the body of the mandible lengthens
151
How does the human skull grow after birth?
```
Growth at cartilaginous joints:
• Synchondroses (cranial base)
• Condyle
Growth at sutures:
• Cranial vault
• Naso-maxillary complex
Remodelling of bone surfaces:
• All bones
• Safe answer in exam
```
152
what are the Mechanisms of bone growth and development: defined by Cobourne and DiBiase
* Relocation: Bone deposition and resorption on opposing surfaces causes a bone to move (“drift”) in space (→ towards the side of deposition).
* Displacement: External forces generated by growing soft tissues separate the bones from each other allowing for compensatory bone growth into the space.
153
what are the Mechanisms of bone growth and development: defined by Nanci (Ten Cate’s Oral Histology)
* Bone remodelling can also lead to an increase in bone size if deposition is higher on one end than resorption on the other end.
* Size increase and remodelling
154
what are the Mechanisms of bone growth and development: defined by Lieberman
Drift: Equal bone deposition and resorption on opposing surfaces causes a
bone to move in space (→ Cobourne’s Relocation), e.g. downward drift of palate.
Displacement: Growth in one location causes the bone to be pushed away from other structures; e.g. condyle growth. As the condyle grows the mandible moves further from the cranial base
Rotation: Result of reversed depository and resorptive fields on either side of a central axis
155
what is secondary displacement
Relocation of bones that are not growing themselves; e.g. displacement of the toes from the pelvis as the femur grows.
156
what involved in the growth of the cranial base
Remodelling & growth of synchondrosis
157
How does the cranial base grow?
Spheno-ethmoidal and spheno-occipital synchondroses mainly contribute to cranial base growth. Doesn’t need stimulation to grow
158
What is a synchondrosis?
Cartilaginous joint with the ability to grow
Spheno-ethmoidal (anterior cranial base) 7 years
Spheno-occipital (posterior cranial base) 13-17 years
159
where does the sphenoidal synchronsosis sit
in the body
160
what is involved in Bone remodelling in the cranial base
get apposition of the underside of it
get deposition on the upper surfaces
this allows growth in volume
8 (see image) resorption and deposition- changes the position
161
what does Growth at the spheno-occipital synchondrosis influence
angle of the cranial base (→ flexion)
Influences facial form
162
what does Growth at the spheno-occipital synchondrosis regulate
Regulates jaw relationships:
Class I: Orthognathic
Class II: Retrognathic
Class III: Prognathic
163
what is Enlow’s hypothesis
Craniofacial development is integrated (parts of the craniofacial complex are co-dependent) - one thing changes and another also changes
164
outline Cranial base flexion and skeletal patterns
class II: Retroganthic profile
Cranial base angle more open (obtuse)
-Backward rotation of the mandible
Class III: Prognathic profile
Cranial base angle more closed (acute)
-Forward rotation of the mandible
As the condyl joins to the back part of the cranial base -more obtuse angle means that the mandible is set further back
Acute angle - the mandible will be set further forward due to the condyl joining to the cranial base
165
what ate the different facial profiles
```
Orthognathic: mandible soft tissue is slightly behind maxillary (class I)
Retro: much further behind (Class II)
Pro: much further forward (class III)
```
166
what is Class II: Retrognathic profile Associated with
* Associated with dolichocephalic head (another word)
| * Most common in Caucasian populations: N/S-Europe, North Africa, Middle East
167
what is Class III: Prognathic profile Associated with
* Associated with brachycephalic head
| * Most common in Asian populations: Middle Europe, East Asia
168
what is a Dolicocephalic head form like
* Long and narrow => leptoprosopic face
* Convex profile; retrognathic mandible
* Forehead slopes
* Glabella & supraorbital ridges prominent
* Close-set eyes
* Nose: long & thin, aquiline (“Roman”)
169
what is a Brachycephalic head form like
* Round and wide => euryprosopic face
* Flat profile; ortho-/prognathic mandible
* Forehead upright and bulbous
* Glabella & supraorbital ridges inconspicuous
* Wide-set eyes
* Nose: short & wide, (“pug-like”)
170
what are the Causes of mandibular rotation
1) Growth of cervical region of vertebral column (neck) displaces the head from the shoulder girdle.
2) Associated with growth and stretch of a chain of muscle groups from:
a) Mandible to skull base
b) Mandible to hyoid bone
c) Hyoid bone to shoulder girdles
3) Descent of mandibular symphysis and hyoid bone relative to cranial base.
- Increased anterior face height. (part that you see – base of nose to the chin we measure this)
4) Posterior face height increases by growth of middle cranial fossa and condyle.
- Extreme growth in either dimension can lead to excessive anterior or posterior facial growth and cause rotation of the mandible.
171
what are the Consequences of mandibular rotation (what are the 2 type and what are they caused by)
Deep bite
- forward rotation (most common)
- caused by excess growth in posterior face height
Open Bite
- backward rotation
- caused by excess growth in anterior face height
172
how can mandibular rotation be restored
Mandibular and dentoalveolar compensation can restore normal occlusion
173
what is Mandibular (skeletal) compensation
B: A pronounced open angle of the cranial base causes the mandible to rotate backwards and downwards resulting in a downward inclined occlusal plane.
C: The retrognathism can be compensated during facial growth by the development of a wider ramus that places the mandible in a more forward position.
-Mandibular compensation can correct a predisposition for malocclusion.
174
what is Dentoalveolar compensation
Backward mandibular rotation results in anterior open bite. (cant bite sandwich) (caused by open cranial base angle or a lowered maxillary arch).
Mandibular incisors drift upwards and maxillary incisors downwards to compensate for malocclusion. This results in a curve of occlusion.
Note: Typical curve of occlusion (marked curve of Spe)
175
what are the Key craniofacial landmarks for Cephalometric tracing
* S: Sella turcica
* N: Nasion
* Po: Porion
* Or: Orbitale
* Ar: Articulare
* Me: Menton
* Go: Gonion
* Point A: Subspinale
* Point B: Supramentale
* ANS: Anterior nasal spine
* PNS: Posterior nasal spine
176
what does Cephalometric tracing determine and how
determine the skeletal pattern and the antero-posterior position of the dentition
Different reference planes are drawn through craniofacial landmarks and measurement of angles
Growth of the cranial vault, naso-maxillary complex and maxilla and mandible & Age- and sex-specific craniofacial features
177
what does the Maxillary-mandibular plane give an indication of
the way that the mandible is growing
Forward rotators – low angle
Backward rotators – high angle
178
what are the Bones and structures of the cranial vault
metopic suture: frontal-frontal
coronal suture: frontal-parietal
sagittal suture: parietal-parietal
lamboid suture: parietal-occipital
squamosal suture: parietal-temporal
occipitomastoid suture: temoral-occipital
179
what is the implications on class II and III occlusions due t the continuation of mandible growth after the maxilla has stopped
class 3 will keep getting worse,
class 2 will get better
180
what are sutures and why do they grow in the cranial vault
Fibrous joints between skull bones grow in response to tension -
cranial vault the tension is a result of soft tissue growth: brain and eyes
181
outline the growth of the cranial vault
Sutures:
Displacement of skull bones by brain growth induces periosteal bone deposition on both sides of the suture to maintain patency.
```
Remodelling:
Bone remodelling (deposition and resorption) occurs along external and internal surfaces of skull bones to reduce their curvature.
```
182
what occurs in Craniosynostosis
In craniosynostosis, brain expansion results in excess compensatory bone growth in other regions of the skull (usually in a parallel direction to the prematurely closed suture).
183
what happens if compensatory bone growth is insufficient in craniosynosis
If compensatory bone growth is insufficient, it can cause increased intracranial pressure and lead to impairment of mental development
184
what influences the growth of the nasomaxillary complex
Growth of eyes/cartilage
Soft tissue: nasal capsule, septal cartilage, brain growth, eyes
185
outline the Growth of the maxilla in height
Grows downwards and forwards
Increase of maxillary height (downward growth) by:
• Bone deposition at the zygomatic and frontal sutures
• Bone remodelling at alveolar processes (vertical tooth drift)
• Bone remodelling of the hard palate (deposition on inferior [palatal] surface and resorption at the superior surface [floor of the nose and maxillary sinuses].
186
outline the Growth of the maxilla in width
Increase of maxillary width (lateral growth) by:
• Growth at midpalatal suture
• Some external bone remodelling
187
outline the Growth of the maxilla in length
* Increase of maxillary length (“forward” growth [in relation to cranial base]) by:
* Growth at posterior surface of maxillary tuberosities (backward growth resulting in forward displacement of the maxilla)
* Resorption on the anterior surface to keep things in place
* Bone remodelling in area above maxillary incisors.
188
outline the features of the newborn mandible compared to adult
* Smaller and narrower mandible: relatively small ramus compared to body
* Obtuse mandibular angle
* No erupted teeth
* Symphysis (superiorly) and mental ossicles (inferiorly) are visible (complete fusion of symphysis occurs at 1-2 years of age)
189
what does the forward and downward displcement of the mandible result in
* Growth of the condylar cartilage- intramembranous (condyle under compression)
* Bone remodelling of the ramus (bone deposition and resorption along the posterior and anterior margins of the ramus, respectively)
* Body gets longer and ramus gets longer
Note: Forward and downward displacement of the mandible results in backward and upward growth of the condyle and the ramus.
190
outline the Lateral growth and shape change in the mandible
• Complex bone remodelling along lateral and lingual surfaces of the condyle, coronoid, ramus and angle.
191
outline Summary: 3-18 years of post-natal development
* Cranial vault changes little in size relative to the rest of the face
* Naso-maxillary process /mandible grow hugely
192
what are the Differences between neonatal and adult skull
Face: disproportionately small face
Large cranial vault and orbits
Bone size: smaller bones, except ear ossicles (same size)
Cranial vault:6 fontanelles (closed by 18 months)
Additional sutures: Metopic (closes at 7 years)
Symphyseal (closes at 1-2 years)
Cranial base: spheno-occipital synchondrosis
(ossifies at 13-15 years in girls and 15-17 years in boys)
193
outline Sex-specific changes in the female face
* Facial growth stops after puberty
* In class III the mandible continues to grow so they tend to get worse
* Flatter, more delicate
* Little overhang of supraorbital ridges
* Zygomatic bone more prominent
* Thinner and less prominent nose
194
outline Sex-specific changes in the male face
• Facial growth continues into 20’s
- Protuberant & bulky face
• Wide and long nose (=> larger airways)
(Maxillary/Palatal constraint on nasal growth can cause upper nose to bend (aquiline or “Roman nose”).
• Downward rotation causes nasal profile to
drop straight down (“Greek nose”)
195
outline Craniofacial variation across populations
* Components of the face appear to be integrated.
* But variation occurs along a continuum.
* Most variation is between individuals and not between populations
* Caucasians class 2 & Asians class 3
196
what is class II likely due to
Class III - Deficiency in maxilla rather than overgrowth in the mandible
197
•Occipital sclerotomes ¶chordal cartilage
basilar & condylar parts of occipital
198
•Hypophyseal &; trabecular cartilages
→ body of the sphenoid
199
•Trabecular &; nasal cartilages come together and form
perpendicular plate &; crista galli of the ethmoid
200
•Ala orbitalis & ala temporalis →
lesser & greater wings of the sphenoid
201
•Otic capsule & lateral part of parachordal cartilage
→ petrous (very hard) & mastoid temporal
202
•Paired nasal cartilages & prechordal cartilage (anteriorly)
→ nasal cavity
203
where does the maxilla form from
an ossification centre below the infraorbital canal in the maxillary process, associated with canine and posterior teeth;
204
where does the premaxilla form from
ossification centres in the frontonasal process, associated with incisor teeth.
205
outline the development of the LACRIMAL bone
Intramembranous development: Small bones associated with the nasolacrimal ducts.
206
outline the development of the nasal bone
Intramembranous ossification: These bones form the roof over the snout. They are reduced to insignificance in man where the snout has been shortened and overgrown by the brain and orbits.
207
outline the development of the zygomatic bone
Intramembranous development. [Also known as 'Jugal'].
208
outline the development of the frontal bone
Intramembranous ossification from two centres gives paired elements separated by the metopic suture. Fusion is highly variable; usually between 2-14 months after birth. In some cases, the metopic suture can persist into adulthood.
209
outline the development of the palatine bone X2
Intramembranous ossification from a centre in the perpendicular plate. Ossification spreads into the palatal plate after fusion of the palatal shelves.
210
outline the development of the vomer
Intramembranous ossification from paired centres arising beneath the primary nasal septum at 9 weeks i.u. This bone is much larger in animals without a secondary palate.
211
outline the development of the inferior nasal concha x2
Endochondral ossification of nasal capsule commencing 5 th month i.u.
May fuse to the maxilla in the adult.
212
outline the development of the ethmoid
Endochondral ossification of nasal capsule originating in three parts: [1] & [2] from centres in
the orbital plates ( ~5th month i.u.) and [3] in the perpendicular plate (1 st postnatal year).
Fusion occurs across the cribriform plate at 2 years. Anterior skull base is cartilaginous at birth.
213
outline the development of the sphenoidal concha
posterior part of the nasal capsule; contains the sphenoidal sinus. They fuse to the ethmoid at 4 years, but not to the sphenoid until 12 years, after which time the sinus begins to invade the body of the sphenoid.
214
outline the development of the OCCIPITAL bone (compound bone consisting of five parts)
The 'interparietal' develops intramembranously from paired centres above the highest nuchal line, the paired elements quickly uniting but their origin as a pair being clearly seen in the neonatal skull. It may remain as a separate bone throughout life.
[2] The 'supraoccipital' is an endochondral ossification of the posterior tectum, below the highest nuchal line. Supraoccipital and interparietal usually fuse in the 3rd month i.u. to form the 'squamous part of occipital', the line of fusion being clearly seen in the neonatal skull.
[3] The 'exoccipitals' (='lateral parts') [x2] are endochondral ossifications of the occipital arch cartilages. At birth they are separated from the squamous part by synchondroses: this line fuses at 2 years.
[4] The 'basioccipital' (='basilar part') is ossified endochondrally from the caudal end of the basal plate. At birth it is separated from the lateral parts by synchondroses: these elements fuse at ~7 years.
215
how is The occipital bone separated from the sphenoid
by the spheno-occipital synchondrosis. Fusion and termination of this synchondrosis commences cranially at puberty and is completed by about 17 years, after which time the sphenoidal sinus may invade the basioccipital part of the occipital.
216
outline the development of the SPHENOID
A complex of 10 separate embryological elements and arising from a total of 19
[or sometimes 21] ossification centres [if the 2 sphenoidal lingulae are included]:
[1] Body of sphenoid: Endochondral ossification of the basal plate in two parts, the 'presphenoid' and the 'postsphenoid', which fuse at 7 months i.u.
[2] Lesser wing [x2]: Endochondral ossification of the orbitosphenoid cartilage. They fuse to the body of the sphenoid before birth.
[3] Great wing and lateral pterygoid plate [x2]: Initiated by endochondral ossification of the alisphenoid cartilage. The tiny cartilage is quickly outgrown and the bone spreads by intramembranous ossification to form the great wing and lateral pterygoid plate.
[4] Medial pterygoid plate: Intramembranous ossification
217
how does the PARIETAL [x2] form
Intramembranous ossification. Radial growth in the parietals and frontals results in presence
of fontanelles at the angles of these bones at birth.
218
how does WORMIAN BONES form
These are supernumerary bones formed by irregular ossification. They commonly occur
in the lambdoid and sagittal sutures.
219
how does the TEMPORAL [x2] Compound bones consisting each of five parts form
The 'petrous part' is the endochondral ossification of the otic capsule and contains the semicircular canals and cochlea. After birth, it expands to produce the mastoid process. The cochlea, ear ossicles and tympanum are full adult size at birth due to the physical requirements of receiving airborne sound waves.
[2] The 'squamous part' ossifies intramembranously.
[3] The 'tympanic part' ossifies intramembranously. At birth, it is a simple U-shaped element supporting the tympanic membrane. The tubular external acoustic meatus develops postnatally.
[4+5] The 'tympanohyal' and 'stylohyal' are small endochondral ossifications of the proximal end of
Reichert's cartilage [2nd pharyngeal arch], and together they form the styloid process.
220
how does the MANDIBLE form
Intramembranous ossification initially produces paired elements. Their growth is subsequently aided by the (secondary) condylar cartilage which ossifies endochondrally. In the midline of the mandible, the mental ossicle cartilages undergo endochondral ossification to produce variable small spherical mental ossicles. At birth, the two mandibular bones meet superiorly at the symphysis but are separated inferiorly by the mental ossicles. Full fusion at the mandibular symphysis usually occurs during the first postnatal year.
221
how does stapes, incus and maelleus form
stapes X2 Endochondral ossification of stapedial cartilage [2nd pharyngeal arch].
INCUS [x2] Endochondral ossification of quadrate cartilage [1st pharyngeal arch].
MALLEUS [x2] Endochondral ossification of articular cartilage [1st pharyngeal arch].
Note: The joint between incus and malleus is the homologue of the fish and reptilian TMJ.
222
how does the hyoid form
The lesser horn develops endochondrally from Reichert's cartilage [2nd arch], the greater horn
endochondrally from the thyrohyal cartilage [3rd arch], and the body endochondrally from the fused distal ends of Reichert's and thyrohyal cartilages.
