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Applied Biochemistry > Chondrocytes and TMJ > Flashcards

Chondrocytes and TMJ Flashcards

1
Q

what is cartilage?

A

specialized connective tissue

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2
Q

is cartilage vascular?

A

no, avascular

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3
Q

cartilage has limited — capacity

A

regenerative

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4
Q

Cartilage contains — ground substance

predominantly proteoglycans

A

gelatinous

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5
Q

(2)

embedded in ground substance

A

Collagen and elastic protein fibers

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6
Q

where is cartilage found?

A

in locations where support,
flexibility, resistance to compression
are important.

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7
Q

cartilage is important in embryonic — —

A

bone formation (endochondral)

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8
Q

growth plate cartilage is important for

A

longitudinal bone growth

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9
Q

in hyaline cartilage, protein fibers are predominantly

A

collagen (2 and ten)

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10
Q

appearance of hyaline cartilage

A

glossy with evenly dispersed chondrocytes

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11
Q

hyaline cartilage is a — connective tissue

A

supportive

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12
Q

most abundant cartilage type in the body

A

hyaline

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13
Q

where is hyaline cartilage found (5)

A

− Growth plate
− Precursor to bone in embryonic skeleton
− Joint articular surfaces (reduces
friction/acts as shock absorber)
− Costal (rib) cartilages
− Cartilage in nose, ears, trachea, larynx,
smaller respiratory tubes

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14
Q

type of fibers in elastic cartilage

A

type 2 collagen together with a lot of elastic fibers (elastin), making it more flexible

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15
Q

where is elastic cartilage found? (3)

A

pharngotympanic (Eustachian tubes)
epiglottis
ear lobes

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16
Q

fibrocartilage

A

mixture of fibrous tissue (type

I collagen containing) and hyaline cartilage

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17
Q

structure of fibrocartilage

A

Chondrocytes dispersed among fine collagen

fibers in layered arrays

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18
Q

fibrocartilage is —, making it a good — absorber

A

spongy

shock

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19
Q

where is fibrocartilage found? (3)

A

public symphysis
intervertebral disks
TMJ

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20
Q

ECM is fibrocartilage contains what type of cartilage?

A

type 1 and 2

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21
Q

Osteoblasts, Chondrocytes, Myoblasts and Adipocytes Differentiate from a Common — Precursor

A

Mesenchymal

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22
Q

what is the principle engine for longitudinal bone growth?

A

proliferation of columnar chondrocytes

and expansion of chondrocyte size (10-15 fold) in hypertrophic region

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23
Q

genes/markers importnat in chondrocyte differentiation: TF (3)

A

SOX9 SRY-box 9 (master regulator)
RUNX2 Runt related transcription factor 2
OSX Osterix

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24
Q

genes/markers importnat in chondrocyte differentiation: signaling molecules (4)

A

IHH Indian hedgehog
PTHrP Parathyroid hormone related protein
FGFs Fibroblast growth factors
(VEGF Vascular endothelial growth factor)

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25
Q

genes/markers importnat in chondrocyte differentiation: receptors for signaling molecules (3)

A

PTC1 Patched (Ihh receptor)
PTH1R PTH/PTHrP receptor
FGFR3 Fibroblast growth factor receptor 3

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26
Q

genes/markers importnat in chondrocyte differentiation: ECM components (3)

A

COL2A1 Type II collagen
ACAN Aggrecan
COL10A1 Type X collagen

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27
Q

genes/markers importnat in chondrocyte differentiation: enzymes/proteases (2)

A

TNSALP Tissue non specific alkaline phosphatase

MMP13 Matrix metalloproteinase 13

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28
Q

SOX9 is a master transcription factor which drives

differentiation down —- pathway

A

chondrocyte

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29
Q

where is SOX9 expressed?

A

in chondroprogenitors/ proliferating chondrocytes (not hypertrophic chondrocytes)

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30
Q

SOX 9 must be

downregulated to allow

A

chondrocytes to mature

SOX 9 inhibits RUNX2

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31
Q

where is RUNX2/OSX expressed?

A

in prehypertrophic and hypertrophic chondrocytes

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32
Q

RUNX2/OSX is an important regulator of

A

hypertrophy

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33
Q

RUNX2 homozygous deletion results in (2)

A

delayed chondrocyte maturation, failure to form bone

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34
Q

Hypertrophy:
• Chondrocytes — in size (10-15 fold)
• Express type – collagen
• Express — —-, which promotes mineralization
• Express —. which promotes vascular invasion
• Eventually undergo —

A 
swell
10
alkaline phosphatase
MMP13/VEGF (vascular endothelial growth factor)
apoptosis (programmed cell death)
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35
Q

key regulators of chondrogenesis (2)

A

Ihh

PTHrP

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36
Q

Co-ordinated actions of Ihh and PTHrP signaling

through their receptors (PTC1 and PTH1R) regulate

A

chondrocyte proliferation/differentiation and determine length of the proliferating columns of chondrocytes

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37
Q

Co-ordinated actions of Ihh and PTHrP signaling
through their receptors (PTC1 and PTH1R) regulate
chondrocyte proliferation/differentiation and determine length of the proliferating columns of chondrocytes
• Also determines when chondrocytes enter —

A

hypertrophy

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38
Q

principle engine for bone

growth

A

chondrocyte hypertrophy

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39
Q

Ihh/PTHrP axis is very important

in regulating

A

bone longitudinal bone growth

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40
Q

PTHrP produced by early proliferative

chondrocytes near

A

ends of bone/growth plate

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41
Q

PTHrP then acts on PTH1R receptor in late

proliferating/prehypertrophic chondrocytes to

A

keep
them proliferating (stops them entering
hypertrophy)

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42
Q

When chondrocytes are far enough away from

source they are no longer stimulated by PTHrP, they (3)

A

stop proliferating → become prehypertrophic →

synthesize Ihh

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43
Q

what does Ihh stimulate?

A

chondrocyte proliferation

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44
Q

Ihh diffuses to ends of bones and acts on early

proliferating cells, stimulating them to

A

produce

more PTHrP

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45
Q

Ihh also induces periosteal cells to

A

form the

mineralized bone collar

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46
Q

feedback loop ensures once cells enter hypertrophy (a one way trip eventually resulting in apoptosis!) they

A

produce Ihh then PTHrP to ensure proliferation of a continual supply of chondrocytes to replace them

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47
Q

critical regulator of chondrocyte proliferation/differentiation

A

FGF signaling

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48
Q

– FGF genes and – FGF receptor genes

A

23

4

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49
Q

many FGF and FGFr genes are expressed in

A

cartilage

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50
Q

Complete story of which
ligands/receptors are important
not fully determined, however — is very important

A

FGFR3

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51
Q

where is FGFR3 expressed?

A

in proliferating/prehypertrophic chondrocytes

52
Q

FGFR3 also suppresses —

A

Ihh

53
Q

Major fibrillar collagen in cartilage, vitreous humor, inner ear

A

type 2 collagen

54
Q

structure of type 2 cartilage

encoded by

A

Homotrimer of α1(II) chains (encoded by COL2A1 gene)

55
Q

Major collagen expressed in hypertrophic cartilage

A

type 10 cartilage

56
Q

structure of type 10 cartilage

encoded by

A

Homotrimer of α1(X) chains (encoded by COL10A1 gene)

57
Q

GAGs

A

Unbranched polysaccharide chains composed of repeating

disaccharide units

58
Q

1st sugar residue =

A 
amino sugar (N-acetylglucosamine or
N-acetylgalactosamine)
59
Q

2nd sugar residue =

A

uronic acid (glucuronic or iduronic)

60
Q

GAGs are usually highly —-, and — charged

A

sulffonated

highly

61
Q

4 main groups of GAGS:

A

hyaluronan
chondroitin sulfate and dermatan sulfate
heparan sulfate and heparin
keratan sulfate

62
Q

Most GAGs found covalently attached to a protein core in the form of —

A

proteoglycans

63
Q

Major proteoglycans of skeletal tissues: (2)

A

aggrecan

versican

64
Q

small leucine rich proteoglycans (SLRPs) (4)

A

decorin
biglycan
fibromodulin
osteoglycin

65
Q

Major proteoglycan in cartilage – produced in large amounts by proliferating and prehypertrophic chondrocytes

A

aggrecan

66
Q

Aggrecan core protein has (2) GAG chains

A

keratan sulphate and chondroitin sulfate

67
Q

aggrecan assembles with hyaluronan to form

A 
huge aggregates (hyaluronan
disaccharide chains can be as long as 50,000 repeats)
68
Q

aggrecan binds high amounts of — due to negative charge (cartilage is hydrated, resilient)

A

water

69
Q

aggrecan may regulate —

A

calcification

70
Q

What happens when there are
mutations in genes involved
with cartilage differentiation
and function?

A

Chondrodysplasias

71
Q

Chondrodysplasias

A

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

72
Q

sometimes skeletal dysplasia or osteochondrodysplasia are used
somewhat interchangeably with chondrodysplasia - these terms encompass

A

dysplasias of both cartilage and bone.

73
Q

Camplomelic Dysplasia

A 
Rare human syndrome caused by 
heterozygous loss of function mutation 
in SOX9 (haploinsufficiency)
74
Q

camplomelic dysplasia is

A

autosomal dominant

75
Q

camplomelic dysplasia affects development of skeleton/reproductive system, such as (8)

A
  • Hypoplasia of skeletal elements
  • Bowing of limbs
  • Shortened limbs/dislocated hips
  • Underdeveloped shoulder blades
  • 11 pairs of ribs instead of 12
  • Clubfoot
  • Ambiguous genitalia
  • Craniofacial abnormalities
76
Q

camplomelic dysplasia is often threatening in

A

neonatal period

77
Q

In mice - homozygous loss of Sox9 -

A

completely inhibits chondrogenesis

78
Q

Impaired PTHrP signaling –

A 
late
proliferating/prehypertrophic chondrocytes
will enter hypertrophy too soon
(premature growth plate
maturation/skeletal maturation)
79
Q

Impaired Ihh signaling –

A

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

80
Q

Ihh/PTHrP Signaling is Required for Normal — in Humans

A

Chondrocyte Differentiation/Bone Development

81
Q

Inactivating Mutations in PTHrP (loss of function)

A

Brachydactyly type E2

82
Q

Brachydactyly type E2

A

shortened digits; short stature; delayed tooth eruption in some patients

83
Q

Inactivating Mutations in IHH (loss of function) (2)

A

Brachydactyly type A1

Acrocapitofemoral Dysplasia

84
Q

Brachydactyly type A1

A

shortened digits; short stature; premature fusion

of growth plates

85
Q

Acrocapitofemoral Dysplasia

A

short stature; cone shaped epiphyses in

the hands, hips; premature fusion of growth plates

86
Q

Mutations in PTH1R

Inactivating mutations (loss of function)- (1)
Activating mutations (gain of function) – (2)
A

Blomstrand Lethal Chondrodysplasia

Jansen’s metaphyseal chondrodysplasia, Eiken Syndrome

87
Q

Blomstrand Lethal Chondrodysplasia:

A

premature growth plate maturation; premature skeletal maturation; increased bone density; joint fusion; short stature (perinatal lethal)

88
Q

Jansen’s metaphyseal chondrodysplasia, Eiken Syndrome:

A

delayed
growth plate maturation/delayed skeletal maturation/ossification; short
stature; malpositioning of teeth (also hypercalcemia, hypophosphatemia)

89
Q

Activating point mutations in FGFR3 in humans –

associated with —

A

Achondroplasia

90
Q

Achondroplasia

A

shortened, disorganized columns of chondrocytes in growth plate – FGFR3 signaling normally acting to limit chondrocyte proliferation

91
Q

most common form of short limbed dwarfism (1 in 15,000-40,000)

A

achondroplasia

92
Q

achondroplasia avg height in M and F

A

M: 4’4”
F: 4’1”

93
Q

achondroplasia is caused by activating mutations in

A

FGFR3

constitutive ligand independent activation

94
Q

achondroplasia is

A

autosomal dominant

80% of vases are sporadic mutation

95
Q

prognosis for homozygous achondroplasia

A

severe disease

usually still born or die shortly after birth from respiratory failure

96
Q

Achondroplasia Features: (6)

A 
• Short stature w/ 
disproportionately short limbs 
(trunk relatively normal)
• Short fingers/toes
• Large head/prominent forehead
• Small midface/flattened nasal 
bridge
• Spinal kyphosis (convex 
curvature) or lordosis (concave 
curvature)
• Varus (bowleg) or valgus (knock 
knee) deformities
97
Q

Type II collagen mutations - wide spectrum of

clinical severity ranging from:

A

lethal, severe, mild

98
Q

Lethal -
Severe-
Mild-

A

achondrogenesis type II/hypochondrogenesis
spondyloepiphyseal dysplasia (SED),
spondyloepimetaphyseal dysplasia congenita, Marshall syndrome
Stickler syndrome and early onset osteoarthritis

99
Q

Spondyloepiphyseal Dysplasia (SED) is from mutations in — gene

A

COL2A1

100
Q

SED is

A

autosomal dominant

101
Q

SED features (5)

A

• Short stature from birth - height reaches 2– 4.5ft
• Kyphoscoliosis (curved spine) / vertebral defects
(e.g. flattened vertebrae)
• Short trunk, neck, limbs
• Hands/feet less affected
• Hip deformities/clubfoot

102
Q

Type X Collagen Mutations Associated with

A

Schmid-Type Metaphyseal Chondrodysplasia

103
Q

Mutations in — gene associated
with Schmid-type metaphyseal
chondrodysplasia

A

COL10A1

104
Q

features/symptoms of schemed-type metaphysical chondrodysplasia

A

Short stature, bowing of the long
bones, widening/irregularity of growth
plates

105
Q

TMJ has – articulation surfaces

A

3

106
Q

why is TMJ a unique joint

A

articular surfaces dont come into contact with each other

107
Q

TMJ is separated by

A

articular disk

108
Q

articular disk

A

cushioning function - prevents bone on bone wear

109
Q

— — splits the joint into two synovial joint cavities

A

articular disk

110
Q

Articular surfaces of bones covered in

— rather than hyaline

A

fibrocartilage

111
Q

TMJ enclosed in a — capsule

A

fibrous

112
Q

— — surround joint

capsule (adds stability)

A

Thick ligaments

113
Q

Upper head of — — muscle inserts onto articular disk

A

lateral pterygoid

114
Q

Disk =

A

fibrous/avascular (fibrocartilage)

115
Q

Composed of dense fibrous tissue containing

A

−Tightly packed collagen fibers
−Proteoglycans
−Elastic fibers

116
Q

Central part of disk =

A

avascular

117
Q

Some —like cells appear with age

A

chondrocyte

118
Q

Opening and Closing of the TMJ (3)

A

• First 20mm opening involves rotational
movement of the joint in the socket
• To open mouth wider, the condyle and disc
have to move out of the socket, forward and
down the articular eminence
• Disc = avascular and lacking innervation –
cushions joint

119
Q

Partly due to unique anatomy, disorders of TMJ =

A

common

prevalence > 5% of population

120
Q

Most common TMJ disorder is

A

disc displacement

121
Q

disc displacement

A

disc is displaced
anteriorly, pulling vascularized/innervated retrodiscal tissue into the
joint (painful)

122
Q

TMJ can lead to — — if disc degenerates

A 
bone contact 
(wearing of joint surfaces)
123
Q

TMJ is more prevalent in — than —

A

women

men

124
Q

peak occurrence of TMJ

A

20-40 years

125
Q

Temporomandibular disorder (TMD) -

A

thought to be a multifactorial
process secondary to muscle hyperfunction, traumatic injuries,
hormonal influences, articular changes (e.g. osteoarthritis)

126
Q

— thought to be a contributing factor

A

Malocclusion

127
Q

Symptoms of TMD/TMJ (3)

A

decreased mandibular range of motion
muscle/joint pain
functional limitation/deviation of the jaw opening

Applied Biochemistry (52 decks)

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