Metabolic bone disease: Histopathology Flashcards

(28 cards)

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
What is renal osteodystrophy?
Chronic renal disease resulting in skeletal changes: ``` Increased bone resorption (OFC) Osteomalacia Osteosclerosis Growth retardation Osteoporosis ```
26
What is Paget's disease? What are the 3 stages?
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
Clinical symptoms of Paget's disease?
``` Often asymptomatic Pain Microfractures Nerve compression Deafness ```
28
Histology of Paget's disease?
Thickening of cortex (sclerosis) Cavity in middle of bone (osteolytic black spots) Mix of osteoblasts/osteoclasts forming/resorbing bone Mosaic pattern - disorganised bone structure