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Musculoskeletal > Metabolic bone disease: Histopathology > Flashcards

Metabolic bone disease: Histopathology Flashcards

1
Q

Give 4 functions of bone

A

Structural
Mechanical
Protective
Metabolic

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2
Q

Describe the composition of bone

A

65% inorganic - Calcium hydroxyapatite
(Stores 99% of body calcium, 85% of phosphorus, 65% sodium)

35% organic

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3
Q

What are the main anatomical regions of the bone

A

Diaphysis - Medulla, cortex, periosteum

Metaphysis - joins diaphysis to epiphysis (epiphyseal line where growth plate would have been during growth)

Epiphysis - Articular cartilages, chondyles

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4
Q

What % of bone must be mineralised to show up on X-ray?

A

50%

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5
Q

What are the bone types/classifications?

A

Anatomical bones - flat, long, short, irregular, sesamoid
Macroscopic structure - cancellous/cortical/spongy bone, trabeculae
Microscopic structure - Woven bone (immature), Lamellar bone (mature)

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6
Q

What are cortical bones?

A 
Long bones
80% of skeleton
Appendicular
Long turnover, 80-90% calcified
Mainly structural/mechanical/protective
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7
Q

What are cancellous bones?

A 
Vertebrae + pelvis
20% of skeleton
Axial
Fast turnover, 15-25% calcified
Mainly METABOLIC
Large SA
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8
Q

What are the different bone cells?

A

Osteoclasts - multinuclear, resorb bone
Osteoblasts - thin cuboid shape, produce osteoid to form new bone
Osteocytes - mechanosensory network embedded in mature bone

Osteoblasts can become embedded in bone to become osteocytes

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9
Q

Describe bone remodelling cycle

A

Osteocyte apoptosis -> release of RANKL
RANKL binds to RANK on osteoclast precursor, forming mature osteoclast -> bone resorption

When osteoclasts die they are replaced by Reversal cells which trigger the formation of mature osteoblasts -> bone formation

Osteoblasts also regulate formation of osteoclasts

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10
Q

Why would you perform bone biopsy?

A 
Confirm diagnosis
Find cause of bone pain/tenderness
Investigate abnormality seen on x-ray
Bone tumour diagnosis (benign vs malignant)
Evaluate therapy performance
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11
Q

Types of bone biopsy?

A

Closed (common) - core biopsy using needle

Open - for sclerotic (very hard) bone or inaccessible lesions

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12
Q

What type of biopsy would be used to determine condition of whole skeleton or to monitor treatment?

A

Transiliac bone biopsy

Core consisting of cortical bone on either end AND cancellous/trabecullar bone in the middle

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13
Q

What histological stains do you use for bone biopsy?

A

H&E staining - basic

Masson - Goldner Trichrome staining: can distinguish mineralised (green) and unmineralised bone (orange)

Tetracycline/Calcein labelling: Fluorescent labelling of newly forming bone, GOLD STANDARD for assessing bone turnover)

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14
Q

What is metabolic bone disease?

A

Reduced bone mass/strength
Due to imbalance of chemicals in the body
This causes altered bone cell activity, rate of mineralisation or changes in bone structure

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15
Q

List common metabolic bone diseases

A 
Osteoporosis
Osteomalacia/Rickets
Primary hyperparathyroidism
Renal osteodystrophy
Paget's disease
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16
Q

Mechanism and causes of osteoporosis?

A

Bone mineral density T-score of -2.5 or lower
PRIMARY = age, menopause
SECONDARY = drugs, systemic disease

Rapid turnover of trabecullar bone (which is highly metabolic)

17
Q

How would osteoporosis look under Masson-Goldner trichrome staining?

A

Less/thinner trabecullar bone (less green)

Comparatively more unmineralised osteoid (more orange)

18
Q

Mechanism and causes of osteomalacia? What are the types?

A

Defect in mineralisation of normally synthesised bone matrix
In children = RICKETS
Two types: Vit. D deficiency OR phosphate deficiency

19
Q

How does Vit D deficiency cause osteoporosis?

A

Less Calcium absorption/reabsorption

20
Q

How would osteomalacia look under trichrome staining?

A

LOTS of orange (unmineralised osteoid due to lack of calcium)

Hardly any green (mineralised bone)

21
Q

Clinical features of osteomalacia?

A 
Bone/pain
Fracture
Proximal weakness
Bone deformity
Looser's zone fracture at areas of high tensile stress (occurs at right angle to cortex)
22
Q

Mechanism and causes of hyperparathyroidism?

A

Excess PTH leading to increase calcium reabsorption + phosphate excretion in urine (hypercalcaemia + hypophosphatemia)

PTH indirectly stimulates osteoclast activity (by binding to osteoblasts and increasing RANKL)
This leads to increased bone resorption -> release of Ca (hypercalcaemia)

Results in osteitis fibrosa cystica

Primary hyperparathyroidism: parathyroid adenoma
Secondary hyperparathyroidism: chronic renal deficiency, vitamin D deficiency

23
Q

Which organs are affected by PTH and how do they control calcium metabolism?

A

Parathyroid glands (release PTH)
Bones (PTH -> release of Ca)
Kidneys (absorption of Ca)
Proximal Small Intestine (reabsorption of Ca)

24
Q

Histology of hyperparathyroidism?

A

You would be able to see sub-periosteal bone erosions as a result of osteitis fibrosa cystica

Also see tunnelling erosions where center of trabecullae are eroded

May also see Brown cell tumours, where bone has been replaced by fibrous tissue

25
Q

What is renal osteodystrophy?

A

Chronic renal disease resulting in skeletal changes:

Increased bone resorption (OFC)
Osteomalacia
Osteosclerosis
Growth retardation
Osteoporosis
26
Q

What is Paget’s disease? What are the 3 stages?

A

Disorder of bone turnover

  1. Osteolytic phase - rapid breakdown of bone
  2. Mixed phase - osteoblasts + osteoclasts
  3. Osteosclerotic phase - osteoblasts form disorganised mosaic-patterned bone

Aetiology unknown

27
Q

Clinical symptoms of Paget’s disease?

A 
Often asymptomatic
Pain
Microfractures
Nerve compression
Deafness
28
Q

Histology of Paget’s disease?

A

Thickening of cortex (sclerosis)
Cavity in middle of bone (osteolytic black spots)
Mix of osteoblasts/osteoclasts forming/resorbing bone
Mosaic pattern - disorganised bone structure

Musculoskeletal (11 decks)

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