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Musculoskeletal > 1 + 3. Metabolic bone disease - histopathology + biochemistry > Flashcards

1 + 3. Metabolic bone disease - histopathology + biochemistry Flashcards

1
Q

What are 4 of the functions of bone?

A
  • Structure
  • Mechanical (support and site for muscle attachment)
  • Protective
  • Metabolic (reserve of calcium)
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2
Q

What is the bone composed of?

A

Inorganic (65%)
• Calcium hydroxyapatite
• Stores 99% of Ca, 85% of P, 65% of Na + Mg

Organic (35%)
• Bone cells
• Protein matrix
• (collagen, osteoid)

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3
Q

When does the epiphyseal line fuse and what does this mean?

A
  • Fusion of growth plate
  • Happens in early 20s
  • Until then, bone grows and elongates from the epiphysis (end of long bone)
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4
Q

What is the diaphysis?

A

Central, long part of the bone (shaft)

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5
Q

What is the metaphysis?

A

Slightly flared part of the bone below the growth plate (between epiphysis and diaphysis)

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6
Q

Which tissue does the blood supply to the bone come through?

A

Periosteum - dense layer of vascular connective tissue enveloping bones (not at joints)

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7
Q

What is cortical bone?

A
  • Long bones
  • 80% of skeleton
  • Appendicular (limbs)
  • 80-90% calcified
  • Mainly mechanical and protective
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8
Q

What is cancellous/trabecular bone?

A
  • Vertebrae + pelvis
  • 20% of skeleton
  • Axial (torso and head)
  • 15-25% calcified (shorter turnover)
  • Mainly metabolic function
  • Large SA - can be used as a mineral store
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9
Q

What does ‘anatomical bones’ describe as a level of classification?

A
  • Flat - protective e.g. cranial, ribs
  • Long - support weight, facilitate movement
  • Short/cuboid - stabilise and facilitate movement e.g. tarsals and carpals
  • Irregular - specific shape to protect organs e.g. vertebrae and pelvis
  • Sesamoid - embedded in tendons, protective e.g. patella
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10
Q

What does the macroscopic structure of bone describe?

A
  • Cancellous/trabecular/spongy - low strength and disorganised structure
  • Cortical/compact - makes up outside of the bone
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11
Q

What does the microscopic structure of bone describe?

A
  • Woven bone (immature) - low strength and disorganised structure
  • Lamellar bone (mature) - makes up most of the bone in the body
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12
Q

What are osteons?

A
  • Functional unit of bone
  • Circular regions formed of concentric layers of lamellar bone
  • Form in response to mechanical forces
  • Give the bone strength in cortical bone
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13
Q

Describe osteons

A

• Haversian canal at centre of each lamellae ring - contains blood vessels
• Circumferential lamellae on the outside of the bone
• Interstitial lamellae between osteons
(• Trabecular lamellae don’t have haversian canals and form layers)

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14
Q

Where are osteocytes located and how are they connected?

A
  • Sit between layers of lamellar bone
  • Contain dendritic processes which forms the canalicular network throughout the bone with other osteocytes
  • This forms mechano-sensory function to determine where bone needs to be repaired
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15
Q

Where are bone biopsies usually done and what are they done for?

A
  • Usually in ASIS area (transiliac)
  • Evaluate ongoing bone pain or tenderness
  • Investigate abnormality seen on X-ray
  • Bone tumour diagnosis
  • Determine cause of unexplained infection
  • Evaluate theraoy
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16
Q

What are the different types of bone biopsies?

A
  • Closed - needle: core biopsy (Jamshidi needle)

* Open - large sample of bone, for sclerotic or inaccessible lesions (requires general anaesthetic)

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17
Q

What stain do you use to look at bone?

A
  • Haematoxylin + eosin stain

* Can use Masson-Goldner Trichrome stain to look at mineralised and unmineralised bone

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18
Q

Describe the histology of the femoral head?

A
  • Trabecular bone on inside
  • Cortical bone on outside (thick + dense)
  • Cartilage on the surface between the two articular surfaces
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19
Q

What are the 3 main bone cells?

A
  • Osteoblasts - build bone
  • Osteoclasts - resorb bone (multinucleate, macrophage)
  • Osteocytes - osteoblast-like cells, sit in lacunae, look inert
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20
Q

What are osteoprogenitor cells and what do osteocytes do to them?

A
  • Stem cells in the marrow

* Osteocytes produce messengers to change them into osteoblasts or osteoclasts

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21
Q

What is ‘RANK’ and ‘OPG’?

A
  • RANK - receptor activator for nuclear factor kappa b

* OPG - osteoprotegerin

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22
Q

What does OPG do?

A
  • Found on osteoblasts
  • Competes with RANK for RANKL, preventing it from binding
  • Therefore inhibits osteoclastogenesis
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23
Q

What can cause an up-regulation of RANKL?

A

Many stimuli e.g. infection or trauma

=> differentiation of osteoclast

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24
Q

What happens to OPG in menopause?

A
  • Oestrogen levels fall
  • OPG levels fall
  • More resorption
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25
Q

Where are osteocytes and osteoblasts located in the bone?

A
  • Osteocytes - bone matrix
  • Osteoblasts - surface of the bone
  • Osteoclasts - Howship’s lacunae
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26
Q

What are reversal lines?

A

Lines left when the bone is remodelled

27
Q

What are lamellae?

A

Lines that form in response to gravity

28
Q

What is tetracycline labelling?

A
  • Give tetracycline antibiotic, related to a fluorescent stain
  • Look at bone turnover and growth
  • Forms a bright green layer on the slide
  • Normally give 2 doses a few days apart then can measure the average distance between the layer to calculary bone growth
  • Contraindicated in children - turn teeth black
29
Q

How does reduction in calcium affect the kidneys?

A 
• More PTH release
• PTH activates 1-α hydroxylase in the kidney
(• Hydroxylated vitamin D)
• Stimulated reabsorption of calcium
• Inhibited reabsorption of phosphate
30
Q

What is the rank system?

A
  • Receptor Activator of a Nuclear Factor Kappa
  • PTH causes bone resorption through the RANK system
  • Ligand on osteoblasts is RANK-L (RANK of osteoclasts)
  • Binding causes activation and differentiation of osteoclasts
  • Slowed down by a dummy receptor - OPG - blocks ligand but has no effect
31
Q

What happens in metabolic bone disease and what causes it?

A
  • Disordered bone turnover
  • Imbalance of various chemicals in the body (vitamins, hormones, minerals etc.)
  • Can altered bone cell activity, rate of mineralisation and changes in bone structure
  • Overall reduced bone mass (osteopenia) => fractures with little or no trauma
  • Patients present with bone pain and difficulty performing normal tasks
32
Q

Name some common metabolic bone diseases?

A
  • Osteoporosis
  • Rickets/osteomalacia
  • Primary hyperparathyroidism
  • Renal osteodystrophy
  • Paget’s disease
33
Q

What are the 3 main categories of bone disease?

A

1) Related to endocrine abnormality
2) Non-endocrine e.g. age related
3) Disuse osteopenia (reduced use of bones)

34
Q

What is secondary hyperparathyroidism caused by?

A

Vitamin D deficiency
=> hypocalcaemia
=> excessive PTH

35
Q

What defines osteoporosis and what are the different types?

A

Bone mineral density T-score of 2.5 or more SD below average

  • Primary - age related/due to post-menopausal changes
  • Secondary - seen with drugs and in systemic disease
  • High turnover - increased activity of osteoblasts/clasts (more osteoclasts)
  • Low turnover - decreased activity of osteoblasts/clasts (more osteoblasts)
36
Q

How does mineralisation change in osteoporosis

A

It doesn’t

37
Q

How does the calcium:phosphate:protein ratio change in osteoporosis?

A

It doesn’t

38
Q

How much of the bone is calcified and osteoid in a normal bone biopsy and osteoporosis biopsy?

A

Both normal and osteoporosis
• 2/3 calcified
• 1/3 osteoid
• Only less bone in total in osteoporosis

39
Q

What proportion of the bone is calcified in osteomalacia?

A
  • 1/3 calcified (as opposed to 2/3 normally)

* Less bone in total as well

40
Q

Describe the main tool to assess for osteoporosis

A
  • BMD (bone mineral density)
  • Represents 70% of total fracture risk
  • Measured using X-rays ‘DEXA’ bone scan
  • T-score = (measured BMD - young adult mean BMD)/young adult SD
  • Anything above -1 is normal (average 25 year old in UK is 0)
  • Between -1 and -2.5 is osteopenia
  • Anything below -2.5 is osteoporosis
  • z-score compares you to average person of the same age
41
Q

Describe osteomalacia?

A
  • Defective bone mineralisation
  • Bendy bone, which is mostly osteoid
  • Can result from deficiency of vitamin D or phosphate
42
Q

What are the sequelae (consequences) of osteomalacia?

A
  • Bone pain/tenderness
  • Fracture and microfracture
  • Proximal weakness
  • Bone deformity
43
Q

How do bone changes differ in rickets compared to osteomalacia?

A
  • Epiphyses haven’t fused in children - so they start to bend
  • Tibial bowing and wide wrists/ankles stay with patient for life
  • Permanent damage to growth plates
44
Q

What skeletal disease can hyperparathyroidism lead to if not treated?

A
  • Osteitis fibrosa cystica

* Replacement of bone with fibrous cyst-like tissue

45
Q

What are the symptoms of hyperparathyroidism?

A
  • Ca oxalate renal stones
  • Osteitis fibrosa cystica, bone resorption
  • Acute pancreatitis
  • Psychosis + depression

(stones, bones, abdominal groans, psychic moans)

46
Q

What did the test for suspected hyperparathyroidism use to involve?

A
  • X-ray of the hand

* Small, brown cell tumours (lytic lesions) on radial side of the digits and thumb

47
Q

What are the brown cell tumours of hyperparaythyroidism?

A
  • Composed of osteoclast cells

* Become out of control - form tumours on a background of fibrous tissue and blood

48
Q

What causes 80% of primary hyperparathyroidism cases?

A

Adenoma in just one gland

49
Q

What can happen if (too much) calcium enters the urine?

A
  • Nephrocalcinosis (renal parenchymal calcification)

* Renal colic (pain from stones any part of urinary tract, mainly ureter)

50
Q

What is renal osteodystrophy and what happens in the condition?

A

• Bone disease related to CKD (chronic kidney disease)
• Comprises all the skeletal changes of CKD
- increased bone resorption
- osteomalacia
- osteosclerosis (osteoblasts not functioning properly)
- growth retardation
- osteoporosis

  • PO4 retention - hyperphosphatemia
  • Hypocalcaemia (due to low vitamin D)
  • Secondary hyperparathyroidism
  • Metabolic acidosis
  • Aluminium deposition
51
Q

How does renal failure lead to renal osteodystrophy?

A
  • Renal failure
  • Less 1-α hydroxylase
  • Calcium levels fall
  • Secondary hyperparathyroidism (attempt to increase Ca and reduce PO4)
  • Kidneys fail to excrete PO4 => low Ca, high PO4, hight PTH
  • PTH becomes autonomous
  • Tertiary hyperparathyroidism
  • Leads to renal osteodystrophy over time (mainly due to low PO4 excretion)
52
Q

What affect will giving vitamin D supplements to someone with CKD have on calcium?

A

None, can’t be hydroxylated

53
Q

What is the deposition of calcium salts in tissues around the body called?

A

Metastatic calcification

54
Q

What are the 3 stages of Paget’s disease?

A

1) Osteolytic - osteoclast predominant
2) Osteolytic-osteosclerotic - osteoblasts try to build bone
3) Quiescent osteosclerotic - disorganised, mineralised bone

55
Q

Describe the histology of Paget’s disease?

A
  • Osteolytic phase - bone remodelled in disorganised way
  • Lots of osteoclast giant cells, and multinucleated osteoclasts
  • Osteoblasts fight back and build none
  • Left with paving pattern - reversal lines where bone is remodelled
56
Q

What is the usual age of onset for Paget’s disease?

A

Over 40

57
Q

What proportion of Paget’s disease are mono-ostotic?

A

15% (remainder is polyostotic)

58
Q

What causes Paget’s disease?

A
  • Aetiology unknown
  • Familial cases show autosomal pattern of inheritance with incomplete penetrance
  • Mutation 5q35-qter - sequestosome 1 gene (on long arm of chr5
  • Parvomyxovirus type particles have been seen on EM in Pagetic bone, but dismissed
59
Q

What is the site predilection in Paget’s disease?

A
  • Affects the skull quite often
  • Vertebrae (particularly lower)
  • Long bones in the leg
60
Q

What are the clinical symptoms in Paget’s disease?

A
  • Pain
  • Microfractures
  • Nerve compression
  • Skull changes - medullat risk
  • Deafness - temporal bone
  • Haemodynamic changes
  • Cardiac failure
  • Hypercalcaemia
  • Sarcoma in area of involvement
61
Q

How does cardiac output change in Paget’s disease?

A

If disease is extensive within skeleton, a lot of CO can go into the bones instead of around the body

62
Q

How can Paget’s diseas affect the tibia?

A
  • Bowing
  • Bone becomes osteomalacic - not mineralising properly
  • Bone can’t respond to gravitational forces
  • Looser’s zone fractures
63
Q

Summarise what happens to the bone in Paget’s disease?

A
  • Increased bone turnover
  • Increase osteoblast and osteoclast activity
  • Spreads around the body
  • High alkaline phosphatase (making lots of osteoblasts)
  • Normal calcium handling
  • Bones get bigger and weaker

Musculoskeletal (9 decks)

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