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Biochemistry (Cole) > Lecture 43 Chondrocytes and TMJ > Flashcards

Lecture 43 Chondrocytes and TMJ Flashcards

1
Q

Does cartilage contain blood vessels?

A
  • no its avascular
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2
Q

what makes up cartilage gelatinous ground substance?

A
  • predominantly proteoglycans that have collagen and and protein fibers embedded in it
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3
Q

Where is cartilage typically located?

A
  • locations where support, flexibility, and resistance to compression are important
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4
Q

What type of bone formation is cartilage important in?

A
  • embryonic bone formation (endochondral)
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5
Q

Growth plate cartilage is important for?

A
  • longitudinal bone growth
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6
Q

What are the types of cartilage?

A
  • hyaline
  • elastic
  • fibrous
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7
Q

What protein fibers make up hyaline cartilage?

A
  • II and X
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8
Q

What is the most abundant type of cartilage found in body?

A
  • hyaline

supportive connective tissue

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9
Q

What is the appearance of hyaline cartilage?

A
  • glossy appearance w/evenly dispersed chondrocytes
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10
Q

Where is hyaline cartilage found in?

A
  • growth plate
  • precursor to bone in embryonic skeleton
  • joint articular surfaces (reduces friction/act as shock absorber)
  • costal rib cartilages
  • cartilage in nose ears trachea larynx and smaller respiratory tubes
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11
Q

_________ has type II collagen together with a lot of elastic fibers (elastin) making it more flexible

A
  • elastic cartilage
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12
Q

Elastic cartilage is found in what structures?

A
  • pharyngotympanic (eustachian) tubes
  • epiglottis
  • ear lobes`
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13
Q

_________ is a mixture of fibrous tissue (type I collagen containing) and hyaline cartilage

A
  • fibrocartilage

- (also has chondrocytes dispersed among fine collagen fibers in arrays)

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14
Q

What cartilage is spongy and a good shock absorber?

A
  • fibrocartilage
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15
Q

Where is fibrocartilage found?

A
  • pubic symphysis
  • intervertebral disks
  • Temporomandibular joint
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16
Q

ECM of _______ contains both type I and type II collagen?

A
  • fibrocartilage
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17
Q

What is the precursor of chondrocytes?

A
  • mesenchymal progenitors ( same precursor as osteoblasts)
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18
Q

What are the steps of endochondral bone formation?

A
  1. mesenchymal condensation
  2. differentiation
  3. blood vessels initiate cartilage destruction/bone formation in center of developing element (VEGF)
  4. secondary ossification centers formed following vascular invasion
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19
Q

What cells do mesenchymal differentiate into as it results to endochondral bone formation?

A
  • proliferating
  • prehypertrophic
  • perichondrium
  • periosteal bone collar
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20
Q

What are the zones of the epiphyseal growth plate?

A
  • resting zone (contains stem cells)
  • proliferating zone (columnar organization)
  • maturing chondrocytes (prehypertrophic)
  • hypertrophic zone (where length happens from swelling chondrocytes)
  • bone
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21
Q

What is the principle engine for longitudinal bone growth? ðŸĶī

A
  • proliferation of columnar chondrocytes and expansion of chondrocyte (10-15 fold) in hypertrophic region
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22
Q

What are the transcription factors in chondrocyte differentiation?

A
  • SOX9
  • RUNX2
  • OSX (osterix)
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23
Q

what is the master regulator of chondrocyte differentiation?

A
  • SOX9
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24
Q

What are the signaling molecules for chondrocyte differentiation?

A
  • indian hedgehog
  • PTHrP
  • Fibrolblast
    (VEGF is marker of prehypertrophic chondrocytes)
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25
Q

Receptors for signaling molecules in chondrocyte differentiation?

A
  • PTC1 (Patched Ihh receptor)
  • Fibroblast growth factor receptor 3 (FGFR3)
  • PTH1R receptor
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26
Q

What are the extracellular matrix components involved in chondrocyte differentiation?

A
  • Type II Collagen
  • Aggrecan
  • Type X collagen
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27
Q

What enzymes or proteases are involved in chondrocyte differentiation?

A
  • TNSALP (tissue non specific alkaline phosphatase)

- MMP13 ( matrix metalloproteinase 13)

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28
Q

What is the transcription factor in the proliferation phase of cartilage growth?

A
  • SOX9
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29
Q

What transcription factors come into play during prehypertrophic and hypertrophic growth?

A
  • OSX

- RUNX2

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30
Q

Why must you down regulate SOX9?

A
  • it inhibits RUNX2 which is an important regulator of hypertrophy
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31
Q

What happens when RUNX2 is homozygous deleted?

A
  • delayed chondrocyte maturation - failure to form bone
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32
Q

What cells express RUNX2/OSX?

A
  • prehypertrophic and hypertrophic chondrocytes
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33
Q

What happens during the hypertrophy phase?

A
  • chondrocytes swell in size (10-15 fold)
  • type X collagen is expressed
  • Alkaline phosphatase is expressed (mineralizes into bone)
  • MMP13/VEGF are expressed (promote cascular invasion)
  • eventually undergo apoptosis
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34
Q

______ and _______ are key regulators of chondrogenesis?

A
  • Ihh and PTHrP
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35
Q

What do Ihh and PTHrP do?

A
  • regulate chondrocyte proliferation/differentiation and determine length of the proliferating columns of chondrocytes
  • also determine when chondrocytes enter hypertrophy
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36
Q

What is the principle engine for bone growth?

A
  • chondrocyte hypertrophy
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37
Q

Ihh/PTHrP axis is?

A
  • very important in regulating longitudinal bone growth bc of its involvement with chondrocyte hypertrophy
38
Q

Describe the feedback loop of PTHrp/Ihh

A
  • feedback loop ensures once cells enter hypertrophy (a one way trip eventually resulting in apoptosis) they produce Ihh then PTHrP to ensure proliferation of a continual supply of chondrocytes to replace them
39
Q

What is PTHrP role in the chondrocyte differentiation?

A
  • acts on PTH1R receptor in late proliferating/prehypertrophic chondrocytes to keep them proliferating (prevents them from entering hypertrophy)
40
Q

What happens when chondroctyes are far enough away from source they are no longer stimulated by PTHrP

A
  • stop proliferating and become prehypertrophic and synthesize Ihh
41
Q

What does ihh do?

A
  • stimulates chondrocyte proliferation by telling early proliferating cells to produce more PTHrP
42
Q

What is the other function of ihh?

A
  • induces periosteal cells to form the mineralized bone collar
43
Q

What is FGFR3 role?

A
  • FGFR3 signaling is important additional regulatory step that limits chondrocyte proliferation
  • (also suppresses Ihh)
44
Q

What type of collagen is expressed in the proliferative phase of cartilage growth?

A
  • type 2 collagen (COL2A1 gene)

- and aggrecan

45
Q

What type of collagen is expressed in the hypertrophic part of growth?

A
  • type X collagen (COL10A1 gene)
46
Q

What is the major fibrillar collagen in cartilage, vireous humor, and inner ear?

A
  • type II collagen
47
Q

_ what is the structure of type II collagen?

A
  • homotrimer of a1(II) chains encoded by the COL2A1 gene
48
Q

What is the collagen expressed in hypertrophic cartilage?

A
  • type x collagen
49
Q

What is the structure of type X collagen?

A
  • homotrimer of a1(X) chains (encoded by COL10a1 gene)
50
Q

Unbranched polysacccharide chains composed of repeating disaccharide units are?

A
  • glycosaminoglycans (GAGs)
51
Q

what is the structure of GAGs)

A
  • 1st sugar residue is an amino sugar (N-acetylglucosamine or N- acetylgalactosamine)
  • 2nd sugar residue is uronic acid (glucuronic or iduronic)
  • usually highly sulfated i.e negatively charged
52
Q

What are 4 main groups of GAGS:

A
  • hyaluronan
  • chondroitin sulfate and dermatan sulfate
  • heparan sulfate and heparin
  • keratan sulfate
53
Q

What are the major proteoglycans of skeletal tissues?

A
  • aggrecan

- versican

54
Q

Most GAGS are found covalently attached to what?

A
  • a protein core in the form of proteoglycans
55
Q

What is the major proteoglycan found in cartilage?

A
  • aggrecan

produced in large amounts of proliferating and prehypertrophic chondrocytes

56
Q

Aggregan core protein has _______ and _____ sulfate GAG chains

A
  • keratan sulphate

- chondroitin

57
Q

What does aggrecan assemble with to form huge aggregates?

A
  • hyaluronan
58
Q

What is the function of aggrecan?

A
  • binds high amounts of water due to negative charge (cartilage is hydrated, resilient)
  • may regulate calcification
59
Q

_________ are hereditary skeletal disorders characterized by abnormal growth plate function leading to skeletal deformities/growth defects (often dwarfism)

A
  • chondroysplasias
60
Q

What condrodysplasia is associated by a heterozygous loss of function mutation in SOX9?

A
  • camplomelic dysplasia

often life threating in neonatal period

61
Q

Is campolimelic dysplasia AD or AR?

A
  • Autosomal dominant
62
Q

What happens to mice if they have homozygous loss os SOX9?

A
  • completely inhibits chondrogenesis
63
Q

What are the symptoms of camplomelic dysplasia?

A
  • hypoplasia of skeletal elements
  • bowing of limbs
  • shortened limbs/dislocated hips
  • underdeveloped shoulder blades
  • 11 pairs of ribs instead of 12
  • clubfoot
  • ambigous genitalia
  • craniofacial abnormalities
64
Q

What happens with impaired PTHrP signaling?

A
  • late proliferating/prehypertrophic chondrocytes will enter hypertrophy too soon (premature growth plate maturation/skeletal maturation)
65
Q

What happens with Impaired Ihh signaling?

A
  • no replacement of proliferating cells once they have gone into hypertrophy (premature closing of the growth plate)
66
Q

Both impaired PTHrP and Ihh signaling lead to?

A
  • Growth retardation (DWARFISM)
67
Q

What do inactivating mutations in PTH1R lead to?

A
  • Blomstrand lethal chondrodysplasia
68
Q

What is blomstrand lethal chondrodysplasia?

A
  • premature growth plate maturation; premature skeletal maturation, increased bone density, joint fusion; short stature (perinatal lethal)
69
Q

What do activating mutations in PTH1R cause?

A
  • Jansens metaphyseal chondrodsplasia, Eiken syndrome
70
Q

What are symptoms of jansens metaphyseal chondrodsplasia, Eiken syndrome?

A
  • delayed growth plate maturation/delayed skeletal maturation/ossification; short staure; malpositioning of teeth
71
Q

What do inactivating mutations of PTHrP cause?

A
  • Bradhydactlyly type e2 (shortened digits; short stature; delayed tooth eruption in some patients)
72
Q

What do inactivating mutations in Ihh cause?

A
  • brachydactyly type A1

- Acrocapitofemoral dysplasia

73
Q

Brachydactyly type A1

A
  • caused by inactiving mutations in Ihh

- shortened digits, short stature, premature fusion of growth plates

74
Q

Acrocapitofemral dysplasia

A
  • caused by inactivating mutations in Ihh

- short stature; cone shaped epiphyses in hands, hips; premature fusion of growth plates

75
Q

What are activating point mutations in FGFR3 associated with?

A
  • Achondroplasia
76
Q

Achondroplasia

A
  • shortened disorganized columns of chondrocytes in growth plate
77
Q

What is the most ocmmon form of short limbed dwarfism?

A
  • achondroplasia
78
Q

What causes achondroplasia?

A
  • activating mutations in FGF receptor 3 gene (FGFR3)

- (constituitve ligand independent activation)

79
Q

Is achondroplasia AR or AD?

A
  • autosomal dominant

- (homozygotes have severe disease usually still born or die shortly after birth form respiratory failure)

80
Q

What are the lethal type II collagen mutations?

A
  • ahcondrogenesis type II/hypochondrogenesis
81
Q

What are the severe type II collagen mutations?

A
  • spondyloepiphyseal dysplasia (SED)
  • spondyloepimetaphyseal dysplasia congenita
  • marshall syndrome
82
Q

What are the mild type II collagen mutations?

A
  • stickler syndrome and early onset osteoarthritis
83
Q

There are over 10 mutations causing ACGII-HCG reported and all involve replacement of ________ by a bulkier amino acid in triple helical region of a1(II) chain?

A
  • glycine
84
Q

Spondyloepiphyseal Dysplasia (SED)

A
  • mutations in COL2A1 gene
  • AD
  • short stature from birth (2-4.5ft)
  • kyphoscoliosis (curved spine)/ vertebral defects (e.g. flatttened vertebrae)
  • short trunk, neck, limbs
  • hands/feet less affected
  • hip deformities/clubfoot
85
Q

What causes shmid type metaphyseal chondrodysplasia?

A
  • type X collagen mutation

results in short stature bowing of the long bones, widening/irregularity of growth plates

86
Q

autosomal recessive spondyloepimetaphyseal dyslplasia

A
  • aggrecan type
  • pretty severe
  • height 2’2 - 2’4
87
Q

What type of cartilage covers the TMJ?

A
  • fibrocartilage
88
Q

______ thought to be a multifactoral process secondary to muscle hyperfunction traumatic injuries hormonal influences articular changes

A
  • Temporomandibular disorder
89
Q

Articular disorders of TMJ

A
  • Inflammation related - Rhuematoid arthritis
  • non - inflammatory - Osteoarthristis joint damage from trauma/ surgery
  • disc displacement (most common)
90
Q

Non-articular disorders

A
  • extracapsular
  • myofascial pain in muscles of mastication fibromyalgia, muscle strain
  • myopathies- may arise from clenching/bruxism

Biochemistry (Cole) (25 decks)

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