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Module 204 MSK & Immune system > T2 L12 Physiology of bone repair > Flashcards

T2 L12 Physiology of bone repair Flashcards

1
Q

What are the functions of the skeleton?

A 
Maintaining bone structure
Locomotion
Haematopoiesis
Ca2+ / mineral homeostasis
Protection of inner organs
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2
Q

What is the consequence of too much bone resorption?

A

Osteoporosis
Osteopenia
Rickets

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3
Q

What is the consequence of too little formation?

A

Osteopetrosis

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4
Q

What is the definition of bone resorption?

A

Solid bone dissolved by physiological processes

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5
Q

Why is bone resorption important?

A

Repair of broken bones
Remodelling of bones as person grows
Remodelling of bone for specific stresses

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6
Q

What is the definition of demineralisation?

A

Breaking down bone by making hydroxyapatite soluble

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7
Q

What is osteopenia?

A

Condition were bone mineral density is lower than normal

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8
Q

What are the uses of measuring bone mineral density?

A

Identify osteoporosis
Determine risk for fractures
Measure response to osteoporosis treatment

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9
Q

What is osteopetrosis?

A

One of several diseases where bones harden in excess
Bone becomes hard, lacks flexibility, easily fractures
Autosomal recessive disease

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10
Q

What is rickets?

A

Disease of bone development usually due to malnutrition

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11
Q

What does rickets result in?

A

Bone deformities
Increased tendencies for fractures
Spinal deformity

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12
Q

How is bone classified on macroscopic level?

A 
Cortical bone
Cancellous bone (spongy)
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13
Q

What is cortical bone?

A

Thick bone organised in osteons
Associated with or connected to outer surface of bone
High turnover to remodel according to stress across bone
Spicules
Trabeculae

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14
Q

What is cancellous bone?

A

Bony structs organised into loose network with blood / bone marrow between struts
30-90% is porous and contains bone marrow

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15
Q

What happens to cancellous bone in osteoporosis?

A

Increased porosity

Less strong, less ridge, more elastic

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16
Q

How is bone organised microscopically?

A

Lamellar

Woven

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17
Q

Describe lamellar organisation of bone?

A

Secondary bone which is created by remodelling woven bone
Organised and stress oriented
Stronger and less flexible than woven bone
Osteons

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18
Q

Describe woven organisation of bone

A

Immature
Disorganised
Not stress orientated
More osteocytes, higher rate turnover, weaker and more flexible than lamellar bone

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19
Q

What are the 3 principle cell types in bone?

A

Osteoblasts
Osteocytes
Osteoclasts

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20
Q

Describe osteoblasts

A

Form new bone and release signalling substances
Produce protein components of acellular matrix which regulates bone growth and degradation
Located on developing bone surfaces
Post-mitotic - most will undergo apoptosis

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21
Q

What are osteoblasts derived from?

A

From mesenchyme

Precursor cells in bone marrow storm

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22
Q

Describe the histology of osteoblasts

A

20-25 microns
Round and regular shape
Mononucleate

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23
Q

Describe osteocytes

A

Quiescent mature cells embedded in bone matrix
Function is maintenance and detection of environmental and ageing stresses
Within osteoid

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24
Q

What are osteocytes derived from?

A

Osteoblasts

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25
Describe the histology of osteocytes
Long and thin Extensive branches that travel through canaliculi Main cell body inside lacunae is 20x5microns Mononucleate
26
Describe osteoclasts
Function is bone degradation and remodelling bone | Can proliferate
27
What are osteoclasts derived from?
Same precursor as monocytes (haematopoietic stem cells)
28
Describe the histology of osteoclasts
40-100micrometre diameter 15-20 closely packed oval-shaped nuclei Regular, cube-like shape with ruffled border
29
What does the ruffled border on osteoclasts do?
Has integrins to surround region of resorption Prevents dilution of acid Prevents loss of proteases
30
What is an osteoid?
Unmineralised, organic portion of bone matrix that forms prior to maturation of bone tissue
31
What are the organic components that make up the matrix?
Proteins e.g. collagen and elastin Polysaccharides Glycosaminoglycans
32
What are the inorganic components that make up the matrix?
Ca2+ Phosphate Hydroxyapatite Magnesium
33
Wha types of components are found in the matrix?
Organic components Inorganic components Growth factors
34
Describe glycosaminoglycans
Long unbranched polysaccharides Highly negative Resist compression Abundant in cartilage
35
Describe the role of growth factors
Revealed by osteoclast action which stimulates and attracts osteoblasts leading to proliferation and mineralisation Bone remodelling leading to bone turnover and activation-resorption-formation sequence
36
What is the Haversian system?
One type of microscopic organisation of bone tissue | Communication system between cells is immobilised in bone matrix
37
What is the Haversian canal?
Longitudinal canal within bone tissue Runs parallel to surface and along long-axis of bone Surrounded by lamellae to form Haversian system
38
What are canaliculi?
Microscopic canals between lacunae of ossified bone | Radiating processes of osteocytes projects into these canals
39
What is compressive strength?
Ability to resist compression without collapsing or expanding to point of failure
40
What provides compressive strength in bone?
Hydroxyapatite
41
What is tensile strength?
Ability to resist stretching without breaking
42
What provides tensile strength?
Collagen
43
Where do osteoclasts resorb bone?
In Howship's lacunae
44
What is Howship's lacunae?
Space on edge of bony spicule which has been made by and contains osteoclast
45
What controls activation-resorption-remineralisation sequence?
Surface osteoblasts | Detect mechanical factors (stresses on that bone) and hormonal factors that initially trigger bone remodelling
46
What are the 2 ways bone can form?
Intramembranous | Endochondral
47
What is intramembranous bone formation?
Bone formation without cartilage model
48
Describe the mechanism of intramembranous bone formation
Osteoblasts lay down osteoid and bone mineralisation Form tiny bony spicules Join with nearby spicules Form trabeculae (woven bone)
49
What is endochrondral bone formation?
Bone formation based on cartilage model. Cartilaginous template made from mesenchyme
50
Describe the mechanism of endochondral bone formation
Chondrocytes proliferate and secrete extracellular matrix and proteoglycans Osteoblasts arrive Osteoid laid down Mineralisation begins
51
What factors govern bone remodelling?
Recurrent mechanical stress | Calcium homeostasis
52
What happens to bone trabeculae under recurrent mechanical stress?
Becomes dense and prominent to strengthen bone
53
How does recurrent mechanical stress govern remodelling?
Surface osteoblasts and osteocyte network detect stresses | Inhibits bone resorption and promotes deposition
54
What are bisphosphonates used for?
Osteoporosis to diminish bone resorption by osteoclasts
55
Give an example of a bisphosphonae
Alendronate
56
What is the mechanism of bisphosphonates?
Inhibit osteoclast-mediated bone resorption Related to inorganic pyrophosphate - pyrophosphate is endogenous regulator of bone turnover - accumulates on bone as it binds to calcium, ingested by osteoclasts which interferes with osteoclast metabolism
57
Give an example of a drug that encourages osteoblast formation of bone
Teriparatide
58
What drug prevents osteoclast maturation?
Denosumab
59
What is densoumab?
Monoclonal antibody that targets RANK ligand | - mimics action of OPG to prevent activation and differentiation of osteoclasts
60
What is RANK ligand?
Member of TNF cytokine family | Functions as key factor for osteoclast differentiation and activation
61
What is the molecular mechanisms in osteopetrosis?
Osteoclasts can't remodel bone Defective vacuolar proton pump which can't make Howship's lacuna acidic so bone isn't resorbed Defective chloride channel
62
What are the consequences of osteopetrosis?
``` Fatal within 10 years Brittle (dense) bones Blindness Deafness Severe anaemia ```
63
What is the treatment for osteopetrosis?
Bone marrow transplant - only partially effective
64
How long does fracture healing take in adults?
2 to 3 weeks in upper body | At least 4 weeks in lower body
65
What are the 4 phases of fracture healing?
1) Reactive phase - haematoma and inflammation 2) Soft callus formation 3) Hard callus formation 4) Remodelling
66
Describe the reactive phase of fracture healing
Blood cells enter wound and haematoma forms Inflammatory cells invade to form granulation Bone precursor cells arrive from periosteum
67
Describe the soft callus formation stage of fracture healing
Woven bone (or hyaline cartilage) joints pieces of broken bone - woven bone is near blood vessels - fibrocartilage is further away Fast process
68
Describe the hard callus formation stage of fracture healing
Lamellar bone replaces woven bone | Slow process resulting in stronger bones
69
Describe the remodelling phase of fracture healing
Endochondral (lamellar) bone is replaced by trabecular bone | Trabecular bone is remodelled into original bone shape
70
Where is calcium stored?
``` Bone Sequestered inside cells / SR Protein bound Complexed with anions Free calcium ```
71
Where is PTH made?
By parathyroid chief cells
72
What does PTH do to calcium?
Increases plasma calcium
73
Where does PTH act?
Bone Kidney Gastrointestinal tract
74
What effect does PTH have on kidney?
Reduces kidney secretion of calcium and increases secretion of phosphate
75
What effect does PTH have on bone?
Stimulates bone to mobilise calcium Detected by osteoblasts and osteocytes --> mobilise sequestered calcium and release cytokines Increased differentiation and activity e.g. osteoclasts
76
Where is vitamin D made?
Skin Liver Kidney
77
What effect does vitamin D have on calcium?
Increases plasma Ca2+ for longer time than PTH
78
Where is calcitonin made?
Thyroid C cells
79
What effect does calcitonin have on calcium?
Decreases blood calcium as more is taken up by bone
80
What does OPG (osteoprotegrin) do?
Binds to RANK ligand to prevent RANK binding | Inhibits differentiation of precursor osteoclast into mature osteoclast
81
Describe the negative feedback of calcium in lactation
Lactation --> low plasma Ca2+ Calcium-sensitive receptor in parathyroid chief cells detect low calcium Chief cells release PTH Kidney increases Ca resorption at DCT, enterocytes increase calbindin --> Ca absorption, bone mobilises Ca to plasma Plasma calcium increases
82
Describe the steps of vitamin D production and activation
1) Cholecalciferol in skin 2) 25-OH cholecalciferol 3) 1,25-di-OH-cholecalciferol (calcitriol) 4) Increase calbindin in gut enterocytes 5) Increase intestinal absorption of calcium 6) Increase calcium reabsorption in kidney 7) Increase plasma Ca2+
83
What are the effects of vitamin D?
Increase intestinal calcium absorption - increases calbindin Stimulates kidneys to reabsorb calcium Indirectly stimulates osteoclasts Facilitates bone remodelling
84
What is calbindin?
Calcium-binding protein that increases intestinal calcium absorption
85
How is vitamin D production controlled via negative feedback?
25-OH-cholecalciferol feeds back on liver to reduce production of 25-OH-cholecalciferol from cholecalciferol Calcium feeds back on parathyroid gland to reduce PTH production --> reduces kidney's activation of 25-OH-cholecalciferol to 1,25-di-OH-cholecalciferol
86
What are the causes of low plasma calcium?
``` Pregnancy, lactation Kidney dysfunction Low intake Parathyroid dysfunction Drugs ```
87
What drugs can cause low calcium?
Magnesium | Anticonvulsants
88
What are the consequences of chronic hypocalcaemia?
``` Skeletal deformities Increased tendency towards bone fractures Impaired growth Short stature Dental deformities ```
89
Describe the skeletal deformities in chronic hypocalcaemia
``` Bowlegs Forward projection breastbone Asymmetrical or odd-shaped skull Soine deformities e.g. scoliosis Pelvic deformities ```
90
What are the consequences of acute hypocalcaemia?
Convulsions Arrhythmias Tetany
91
What is Chvostek's sign?
Latent tetany | Tapping master leads to twitch on same side of face
92
What is Trousseau's sign?
Carpopedal spasm with lateral tetany
93
What is DiGeorge syndrome?
Rare genetic anomaly | Typically has issues with mediastinum that lead to absent thymus and underdeveloped parathyroid glands
94
Why does hypocalcaemia make membranes less stable?
More excitable Sodium is more able to leak through Explains late tetany
95
Why does hypercalcaemia make membranes more stable?
Reduces excitability | Increases intracellular calcium which inactivates channels to reduce calcium inflow in muscle cells
96
What are the signs and symptoms of hypercalcaemia?
``` Can be asymptomatic Reduced excitability - constipation - depression - confusion - kidney stones Abnormal heart rhythms - short QT interval - no ST segment - widened T wave ```
97
What are the signs of severe hypercalcaemia?
Coma | Cardiac arrest

Module 204 MSK & Immune system (44 decks)

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