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Z MD1 locomotor and exercise block > histology and pathology of bone and other connective tissue > Flashcards

histology and pathology of bone and other connective tissue Flashcards

0
Q

what does the ECM of hyaline cartilage consist of

A
  • collagen type 2
  • aggrecans
  • hyaluronic acid
  • chondronectin
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1
Q

what are the types of connective tissue

A

connective tissue proper
cartilage
bone

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2
Q

what is chondronectin

A

a glycoprotein that binds together the collagen, aggrecans, and integrins together

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3
Q

what are the 2 main aggrecans of hyaline cartilage

A

chondroitin sulphate

heparin sulphate

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4
Q

where is hyaline cartilage found

A

ribs, trachea, joints

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5
Q

what is elastic cartilage

A

modified hyaline cartilage

hyaline cartilage with elastin fibres

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6
Q

where is elastic cartilage found

A

ears, ear canal, epiglottis and larynx

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7
Q

what is the added benefit of elastic cartilage over hyaline cartilage

A

flexible, but maintains shape

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8
Q

where is fibrocartilage found

A
  • binds solid joints
  • intervertebral discs
  • minisci
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9
Q

what is fibrocartilage

A

mixture of dense fibrous CT made of type 1 collagen, and isolate islands of cartilage

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10
Q

describe the structure of intervertebral discs as you age

A

initially: fibrocartilage around the periphery (type 1 collagen), surrounding gelatinous nucleus pulposis (type 2 collagen)
as you age: the nucleus pulposis becomes replaced with fibrocartilage until you have a solid disc of fibrocartilage

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11
Q

explain the different parts of a long bone

A

diaphysis = shaft
metaphysis
epiphysis

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12
Q

where is compact bone found

A

forms the outside of bone

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13
Q

where is trabecular bone found

A

in the centre of long bones

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14
Q

what fills the gaps in the trabecular bone

A

yellow/red marrow and blood vessels

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15
Q

what are special about the blood vessels in the bone

A

they include sinusoids - Large diameter and can have pores

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16
Q

explain the inner and outer layers of periosteum

A 
outer fibrous (fibroblasts, blood vessels and collagen)
inner layer cellular (osteoprogenitor cells)
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17
Q

is the periosteum or endosteum thicker

A

periosteum

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18
Q

what are sharpey’s fibres

A

collagen fibres of a tendon that penetrate into the bone for connection, –> the collagen of the tendon and bone become continuous

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19
Q

what are the branches of blood vessels that supply the long bones

A

epiphyseal artery
metaphyseal artery
nutrient artery (to supply diaphyses)
periosteal arteries

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20
Q

in what two places is there no periosteum on the bones

A
  • articular surface

- where tendon inserts into bone

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21
Q

explain the type of cell of the synovial membrane

A
  • very leaky cells (lack BM, tight junctions, desmosomes) - NOT epithelium
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22
Q

explain the intima of the synovial membrane

A

2-3 layers thick - mix of fibroblast-like cells and macrophage-like cells

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23
Q

explain the sub-intimal layer of the synovial membrane

A

fibrous CT

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24
Q

what is synovial fluid

A

an ultrafiltrate of synovial blood plus proteoglycan

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25
Q

explain the histological structure of dense bone

A

organised into Haversion systems (organised along the lines of stress)
- centre has the blood vessels

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26
Q

where are osteoprogenitor cells found

A

in periosteum and endosteum

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27
Q

function of osteoprogenitor cells

A

can give rise to new osteoblasts to grow or repair bone

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28
Q

what is the origin of osteoprogenitor cells

A

from mesenchymal stem cells in bone marrow

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29
Q

function of osteoblasts

A

makes osteoid

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30
Q

what is osteoid

A

the organic ECM of bone (collagen type 1 and bone matrix proteins)

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31
Q

function of osteocyte

A
  • maintain bone in its vicinity in response to loading

- mechanotransduction (can tell where the stresses are)

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32
Q

loss of osteocytes leads to

A

bone resorption and release of free calcium

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33
Q

function of osteoclasts

A

destroys/remodels bone in growth, repair and normal turnover

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34
Q

explain the “look” of osteoclasts

A

giant multinuclear cells

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35
Q

explain the steps in how osteoclasts destroy bone

A
  1. seals itself to bone
  2. secretes H+, Cl- from H2CO3 breakdown to dissolve CaP
  3. secretes proteases to destroy to collagen
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36
Q

what molecule is a marker of osteoclast activity

A

tartrate-resistant acid phosphatase

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37
Q

origin of osteoclasts

A

related to granulocytes/macrophages

not related to osteoblasts

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38
Q

which hormones affect osteoclast activity

A

parathyroid hormone - increases activity
calcitonin - decreases activity
(opposite for osteoblasts)

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39
Q

what happens to osteoclasts when not required

A

they apoptose

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40
Q

during the development of bone.. what two types of bone can be made

A

membrane bone

endochondral bone

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41
Q

how does membrane bone form

A

forms directly from mesenchyme

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42
Q

where does membrane bone form

A

the skull and flat bones of the face, the mandible and clavicles

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43
Q

which bones form by endochondral ossification

A

weight bearing bones and bones of the extremities

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44
Q

what is the endochondral ossification method of making bone

A

a cartilage model of the bone is produced and then the cartilage is replaced by bone

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45
Q

what are the 5 steps in endochondral ossification

A
  1. bone collar forms around the diaphysis
  2. the cartilage beneath the collar degenerates
  3. BVs invade, and bring in bone cell progenitors
  4. a second nucleus of ossification appears in each epiphysis
  5. zones of ossification grow together, but leave a thin zone of cartilage, the growth plate
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46
Q

what are the 5 zones of the growth plate in bones

A 
resting zone
proliferation zone
maturation zone
hypertrophic zone
ossification zone
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47
Q

what is the resting zone of the growth plate in bones

A

zone of normal hyaline cartilage

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48
Q

what is the proliferation zone of the growth plate in bones

A

zone of dividing chondrocytes

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49
Q

what is the maturation zone of the growth plate in bones

A

a zone of mature chondrocytes

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50
Q

what is the hypertrophic zone of the growth plate in bones

A

a zone of hypertrophic (dying chondrocytes)

51
Q

what is the ossification zone of the growth plate in bones

A

zone of bone laid down

52
Q

when is woven bone made

A

during development or repair

53
Q

what is different about woven bone

A

it is more cellular, has more collagen and has no Haversian systems

54
Q

how is woven bone made into lamellar bone

A

remodelled by osteoclasts and osteoblasts

55
Q

explain the layering of the bone in Haversian canals

A

the collagen alternate in different directions in each layer and is laid down from outside inside, leaving only a small narrow space around the blood vessel (Haversian canal)

56
Q

where do osteocytes live

A

in lacunae within the Haversian systems

57
Q

how do osteocytes receive/gain nutrients

A

via their canaliculae

58
Q

explain the “look” of osteoblasts

A

amphophilic cytoplasm
perinuclear hoff
(either resting - thin, or active - fat)

59
Q

are osteoblasts or osteoclasts faster

A

osteoclasts

60
Q

how does PTH cause an increased activity of osteoclasts

A

PTH causes an increase in the expression of RANKL and a decrease in the expression of osteoprotegrin on the osteoclast progenitor–> differentiation to osteoclast

61
Q

where does the RANKL ligand come from

A

ligand on osteoblast

receptor on osteoclast

62
Q

what is the action of osteoprotgrin

A

blocks the RANK receptor

63
Q

what are the steps in normal osteoid mineralisation

A
  1. osteoblasts secrete collage and secretory vesicles

2. increase in conc of Ca and PO locally causes precipitation around the vesicles

64
Q

what do the vesicles contain which the osteoblasts secrete

A

alkaline phosphatase and pyrophosphatase

65
Q

what are the two types of “incomplete” fractures

A

greenstick - break only part way through

torus - compression fracture

66
Q

what is the normal annual bone turnover in adults?

A

5-10%

67
Q

what is a comminuted fracture

A

a fracture where there are more than 2 fragments

68
Q

what is a butterfly fracture

A

where the fracture is triangular shaped (3 fragments)

69
Q

what causes a stress fracture

A

repeated low force injury to a normal bone

70
Q

what causes a pathological fracture

A

a normal amount of force on an abnormal bone

71
Q

what are the 3 stages of healing bone

A

inflammatory phase
reparative phase
remodelling phase

72
Q

what occurs in the inflammatory phase of bone healing

A
  • haematoma formation and granulation tissue (fibrin creates framework, platelets and leukocytes release inflammatory cytokines and bone cells activated to start repair)
  • granulation tissue formation
73
Q

what is the time frame for the inflammatory phase of bone healing

A

first few days

74
Q

what are the two subphases of the reparative phase of bone healing

A

soft callus formation

hard callus formation

75
Q

at what time frame is the soft callus formation of bone healing

A

days-weeks

76
Q

what occurs during the soft callus formation of bone healing

A
  • cartilage formation to hold the fractured ends together

- periosteum repairs itself over the outside due to osteoporgenitor cells

77
Q

at what time frame is the hard callus formation of bone healing

A

weeks-months

78
Q

what occurs during the hard callus formation of bone healing

A

osteoid formation and ossification (firstly woven bone or endochondral ossification)

79
Q

at what time frame is the remodelling phase of bone healing

A

months-years

80
Q

what occurs during the remodelling phase of bone healing

A

bone remodelling of woven bone to lamellar bone along the lines of stress

81
Q

which type of fracture may not need a soft callus to form in the healing process of bone

A

if the ends are closely apposed

82
Q

what is the advantage and disadvantage of not having to form a soft callus during bone fracture healing

A

healing will be faster

but not as strong

83
Q

what is the goal of fracture management

A

union of the broken bone to allow healing as fast as possible and without complications

84
Q

how is ‘union’ of fractures performed

A
  • reduction - minimize the gap
  • fixation - minimize the strain or movement (cast)
  • minimize any other factors that slow healing
85
Q

what are the factors that slow fracture healing

A
  • advanced age
  • multiple medical comorbidities
  • NSAIDs, corticosteroids
  • smoking
  • poor nutrition
  • open fracture with poor blood supply
  • multiple traumatic injuries
  • local infetion
86
Q

what are the complications of bone fracture

A
  • non-union
  • delayed union
  • mal-union
  • infection
  • osteonecrosis/AVN
87
Q

most upper limb fractures in adults repair completely in …

A

6-8 weeks

88
Q

most lower limb fractures in adults repair completely in…

A

12-16 weeks

89
Q

what is mal-union

A

healing of a bone in anunacceptable position

90
Q

what are the potential problems of mal-union

A
  • disability
  • post-traumatic osteoarthritis
  • cosmetic
91
Q

what is the most common cause of osteomyelitis

A

staph aureus

92
Q

what are the common sites of osteonecrosis after fracture

A

neck of femur (blood supply is via neck)

scaphoid (blood supply is via distal end)

93
Q

why can osteonecrosis occur after bone fracture

A

because fractures can interrupt the blood supply and leave part of the bone ischaemic

94
Q

what is osteoporosis

A

reduced mass of otherwise normal bone

95
Q

how can menopause lead to osteoporosis

A

decreased serum oestrogen and increased IL-1, IL-6 and TNF levels leads to increased expression of RANK and RANKL –> increased osteoclast activity

96
Q

how can aging lead to osteoporosis

A
  • decreased replicative activity of osteoprogenitor cells
  • decreased synthetic activity of osteoblasts
  • decreased biological activity of matrix-bound growth factors
  • reduced physical activity
97
Q

what causes Paget’s disease

A

large, overactive osteoclasts and osteoblasts that produce more bone

98
Q

what is the result of Paget’s disease

A
  • thick soft cortex
  • coarse trabeculae
  • easily fractured
  • can compress nerves
99
Q

what are the 3 stages of Paget’s disease

A

osteolytic - osteoclasts
mixed - osteoclasts and osteoblasts
osteosclerotic - osteoblasts

100
Q

what are the primary and secondary causes of hyperparathyroidism

A

primary - parathyroid hyperplasia or tumour

secondary - prolonged hypocalcaemia or hyperphosphataemia

101
Q

what are the effects of hyperparathyroidism

A
  • increased osteoclastic activity (RANK-L) with associated compensatory increase in osteoblastic activity
  • -> dissecting osteitis
  • -> osteitis fibros cystica
102
Q

what histological features do you see in dissecting osteitis

A

osteoclasts in trabeculae

103
Q

what do you see in osteitis fibrosa cystica

A

microfractures and granulation tissue

104
Q

what are the presenting symptoms of bony mets

A
  • pathological fractures
  • hypercalcaemia
  • bone marrow failure
  • bone pain
105
Q

how do the malignant cells influence bone

A

they produce RANK-L an PTHrP

they dont influence bone directly

106
Q

which primary tumours can lead to bony metastases

A 
breast
lung
thyroid
kidney
prostate
bowel
107
Q

what are the disorders of bone metabolism

A 
hypocalcaemia
hypercalcaemia
hypophosphataemia
hyperphosphataemia
osteoporosis
108
Q

what causes hyperphosphataemia

A

renal failure

109
Q

what percentage of trabecular bone and cortical bone is remodelled per year

A

trabecular - 25%

cortical - 3%

110
Q

which bones in particular are affected by bone remodelling

A

femoral neck and vertebral bodies (trabecular bone)

111
Q

what things affect bone remodelling

A

ageing
physical factors (exercise, loaing)
hormones (oestrogen)
drugs

112
Q

what causes the expression of RANKL by osteoblasts

A

active vitamin D (calcitriol) and PTH

113
Q

what are the components of synovium

A
  • macrophage like cells
  • fibroblast like cells
  • blood vessels and lymphatics
114
Q

from what is synovial fluid derived

A
  • a transudate of plasma from synovial capillaries

- hyaluronic acid produced by synovial cells

115
Q

what is in the ECM of hyaline cartilage

A
  • collagen type 2
  • hyaluronic acid produced by chondrocytes
  • proteoglycans - aggrecan
  • glycosaminoglycans such as chondroitin sulphate
  • water
116
Q

what is in the Haversian canal

A

blood vessels, nerves, lymphatics and connective tissue

117
Q

what structures link the lacunae of Haversian systems

A

canaliculi

118
Q

what are the 2 main types of ossification

A

endochondral

intramembranous

119
Q

what causes osteophytes in a joint with OA

A

calcification of periarticular cartilage and synovium

120
Q

what causes subchondral cysts in a joint with OA

A

synovial fluid entering bone through microfractures

121
Q

what causes subchondral sclerosis in a joint with OA

A

thickening of subchondral bone and trabeculae

122
Q

what causes a loss of joint space in a joint with OA

A

fibrillation and sloughing of articular cartilage

123
Q

what is the precursor protein of the amyloid deposition that occurs in rheumatoid arthritis

A

serum amyloid associated protein

124
Q

what other diseases are associated with serum amyloid associated protein

A

TB
IBD
bronchiectasis
chronic osteomyelitis

125
Q

which cytokines are involved in fracture healing and what do they do

A

TGF-b, PGDF, FGF - activate osteoprogenitor cells in the periosteum and activate OB and OC

126
Q

what does the haematoma provide during fracture healing

A
  • stops the bleeding

- provides a framework for fibroblasts and inflammatory cells

Z MD1 locomotor and exercise block (13 decks)

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