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Y2 LCRS 2 - Musculoskeletal > 1. Metabolic Bone Disease – Histopathology > Flashcards

1. Metabolic Bone Disease – Histopathology Flashcards

1
Q

What are the three main functions of bones?

A

Mechanical – support and site for muscle attachment
Protective
Metabolic – reserve of calcium

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2
Q

What are the two main components of bone and what are their relative proportions?

A

Inorganic (65%) – calcium hydroxyapatite (store of 99% of the body’s calcium, 85% of the phosphorous and 65% of Na and Mg)
Organic (35%) – bone cells and protein matrix

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3
Q

Describe the classification of bone as cortical and cancellous.

A 
Cortical  
 Long bones 
 80% of skeleton 
 Appendicular skeleton 
80-90% calcified 
 Mainly mechanical and protective role 
Cancellous 
 Vertebrae and pelvis  
 20% of skeleton  
 Axial  
15-25% calcified  
 Mainly metabolic 
 Large surface
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4
Q

What are the indications for bone biopsy?

A 
Evaluate bone pain or tenderness 
Investigate abnormality seen on X-ray  
For bone tumour diagnosis  
To determine the cause of unexplained infection  
To evaluate therapy
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5
Q

What are the two types of bone biopsy?

A

Closed – needle – core biopsy with Jamshidi needle

Open – for sclerotic or inaccessible lesions

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6
Q

What are the three types of bone cell?

A

Osteoblast – build bone by laying down osteoid
Osteoclast – multinucleate cells of the macrophage family that resorb bone
Osteocyte – osteoblast like cells

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7
Q

Where are osteocytes found?

A

Lacunae

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8
Q

What cytokine is important for stimulating the differentiation of osteoclast precursors into pre-osteoclasts?

A

M-CSF (this is produced by osteoblasts)

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9
Q

Which cells produce RANKL and what is its effect?

A

Pre-osteoblasts

It stimulates the maturation of osteoclasts

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10
Q

What do mature osteoblasts produce that blocks the RANK/RANKL binding?

A

Osteoprotegrin

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11
Q

How are bones classified anatomically?

A

Flat
Long
Cuboid

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12
Q

What type of ossification leads to the formation of:

a. Long Bones
b. Flat Bones

A

a. Long bones
Endochondral ossification
b. Flat bones
Intramembranous ossification

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13
Q

How else can bone be classified?

A

Trabecular (cancellous) or compact (cortical)

Woven (immature) or lamellar (mature)

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14
Q

What is metabolic bone disease?

A
  • Disordered bone turnover due to imbalance of various chemicals in the body (vitamins, hormones, minerals etc.)
  • Overall effect is reduced bone mass (osteopaenia) + strength often resulting in fractures from little or no trauma
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15
Q

What are the three main categories of metabolic bone disease?

A

Related to endocrine abnormality (e.g. Vit D and PTH)
Non-endocrine (e.g. age-related osteoporosis)
Disuse osteopaenia

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16
Q

Describe the staining of calcified and uncalcified bone.

A

Calcified – green

Uncalcified – orange

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17
Q

What are the primary causes of osteoporosis?

A

Age

Post-menopause

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18
Q

What are the secondary causes of osteoporosis?

A

Drugs

Systemic disease

19
Q

Describe the histology of osteoporotic bone.

A

Weak trabecular bridging

Holes and cysts

20
Q

What is osteomalacia and what can it be caused by?

A

Defective mineralisation of normally synthesized bone matrix
(Rickets in children)

caused by:

  • Vitamin D deficiency
  • Phosphate deficiency (usually related to chronic renal disease)
21
Q

What are the metabolic and endocrine consequences of vitamin D deficiency (Osteomalacia)?

A

Secondary hyperparathyroidism –> increased bone resorption

Hypocalcaemia – neuronal excitability causing muscle twitching, spasms, tingling and numbness

22
Q

Describe the histology of osteomalacia.

A

No calcification of bone
More uncalcified osteoid
Bones are very bendy and cannot carry musculature very easily

23
Q

What are the clinical consequences of osteomalacia?

A
  • Bone pain/tenderness
  • Fracture (horizontal fractures at Looser’s zone at the neck of the femur are commonly seen)
  • Proximal weakness
  • Bone deformity
24
Q

What is used to investigate mineralisation?

A

Fluorescent tetracycline labelling

25
Q

What are the consequences of hyperparathyroidism?

A
  • Hypercalcaemia (increased Ca2+ reabsorption)
  • Hypophosphataemia (increased phosphate excretion in the urine)
  • Osteitis fibrosa cystica (due to increased osteoclast activity)
  • Overall increased Ca, and PO4 excretion in urine
26
Q

List the four organs that are directly or indirectly affected by parathyroid hormone to control calcium metabolism.

A

Parathyroid glands
Bones
Kidneys
Proximal small intestine

27
Q

State some causes of primary hyperparathyroidism.

A

Parathyroid adenoma

Chief cell hyperplasia

28
Q

State some causes of secondary hyperparathyroidism.

A

Chronic renal insufficiency

Vitamin D deficiency

29
Q

What are the symptoms of hyperparathyroidism?

A 
Stones, Bones, Abdominal Groans and Psychic Moans 
Stones – calcium oxalate renal stones  
Bones – osteitis fibrosa cystica  
Abdominal Groans – acute pancreatitis  
Psychic Moans – psychosis and depression
30
Q

What is the most important investigation for hyperparathyroidism and what will it show in someone with hyperparathyroidism?

A

X-ray of the hand
Subperiosteal bone erosions
Brown cell tumours – small areas of resorption in the long bones of the fingers that are filled with osteoclasts

31
Q

What are the five features of renal osteodystrophy?

A

Skeletal changes resulting from chronic renal disease

  • Increased bone resorption (osteitis fibrosa cystica)
  • Osteomalacia
  • Osteoporosis
  • Osteosclerosis
  • Growth retardation
32
Q

What are the consequences of renal osteodystrophy?

A 
Hyperphosphataemia 
Hypocalcaemia as a result of a decrease in vitamin D metabolism 
Secondary hyperparathyroidism 
Metabolic acidosis  
Aluminium deposition
33
Q

What is Paget’s disease?

A

Disorder of bone turnover (there is a lack of proper communication between the cells)

34
Q

What are the three stages of Paget’s disease?

A
  1. Osteolytic
  2. Osteolytic-osteosclerotic
  3. Quiescent osteosclerotic
35
Q

Describe the histology of Paget’s disease.

A

Prominent reversal lines

Masses of osteoclasts in the same site as osteoblasts

36
Q

In which ethnicities is Paget’s disease rare?

A

Asian

African

37
Q

Which sites does Paget’s disease most commonly affect?

A 
Skull 
Sternum 
Spine 
Humerus 
Pelvis 
Femur  
Tibia
38
Q

List some clinical features of Paget’s disease.

A 
Pain 
Microfractures  
Nerve compression  
Skull changes (may put medulla at risk)
Deafness  
Haemodynamic changes  
Cardiac failure  
Hypercalcaemias 
Development of sarcoma in the area of involvement
39
Q

What are Howship’s Lacunae?

A

Pits in the bone surface where osteoclasts are found (also called resorption bays)

40
Q

Describe cortical bone microanatomy.
What are the different lamellae?
What is a Haversian canal?

A
  • cortical bone is made of parallel osteons (0.2mm diameter), which are structured circular layers of lamellar bone surrounding a haversian canal/ central canal containing blood vessels
  • Circumferential lamellae: at periosteum, goes aorund whole bone
  • Interstitial lamellar: between osteons
  • Trabecular lamellae: do not surround central channels but are organized into layers
  • Osteocytes in lacunae have dendritic structures
41
Q

Describe bone remodelling cycle.

A
  • osteoblasts regulate osteoclast formation and activity by producing RANK-L and M-CSF, and RANKL decoy receptor OPG
  • osteocytes sense damage and signal to osteoclasts by producing RANKL as they apoptose
  • reversal phase
42
Q

When is transilliac bone biopsy used?

A
  • If reason to get tissue is general and not bone specific

- transiliac biopsy allows core sample with plenty of cortical and trabecular bone

43
Q

List the histological stains and explain when they are used.

A
  1. H&E- for majority, staining on decalcified samples
  2. Masson-Goldner Trichrome- amount of mineralised (green) vs unmineralised bone (orange)
  3. Tetracycline/Calcein labelling- allow dynamic histomorphometry to measure rates of bone formation and turnover
44
Q

Which mutations can cause Paget’s Disease?

Describe its pattern of inheritance.

A

SQSTM1/ RANK

Autosomal with incomplete penetrance

Y2 LCRS 2 - Musculoskeletal (10 decks)

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