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Musculoskeletal > Metabolic Bone Disease – Histopathology > Flashcards

Metabolic Bone Disease – Histopathology Flashcards

1
Q

What are the three main functions of bones?

A

Mechanical – support and site for muscle attachment
Protective - vital organs and bone marrow
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
  1. Inorganic (65%) – calcium hydroxyapatite (store of 99% of the body’s calcium, 85% of the phosphorous and 65% of Na and Mg)
  2. 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 area
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4
Q

What are the indications for bone biopsy?

A
  1. Confirm the diagnosis of a bone disorder
  2. Find the cause of or evaluate ongoing bone pain or tenderness
  3. Investigate an abnormality seen on X-ray
  4. For bone tumour diagnosis (benign vs malignant)
  5. To determine the cause of an unexplained infection
  6. To evaluate therapy performance
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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
  1. Osteoblast – build bone by laying down osteoid
  2. Osteoclast – multinucleate cells of the macrophage family that resorb bone
  3. 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 RANKLigand 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

competitive inhibitor of RANK

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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

-functionally
Trabecular (cancellous) or compact (cortical)

-architecturally
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) 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
  1. Endocrine abnormality (e.g. Vit D and PTH)
  2. Non-endocrine (e.g. age-related osteoporosis)
  3. 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
(physiological)

18
Q

What are the secondary causes of osteoporosis?

A

Drugs
Systemic disease
(pathological)

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
causes:
1. Vitamin D deficiency
2. Phosphate deficiency (usually related to chronic renal disease)

21
Q

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

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
  1. Sequelae
  2. Bone pain/tenderness
  3. Fracture (horizontal fractures at Looser’s zone at the neck of the femur are commonly seen)
  4. Proximal weakness
  5. Bone deformity e.g rickets
24
Q

What is used to investigate mineralisation?

A

Fluorescent tetracycline labelling

  • can be used to asses the advance of bone growth over a period
  • care in giving to children as teeth turn black
25
Q

What are the consequences of hyperparathyroidism?

A
  1. Hypercalcaemia (increased Ca2+ reabsorption)
  2. Hypophosphataemia (increased phosphate excretion in the urine)
  3. Osteitis fibrosa cystica (due to increased osteoclast activity)
  4. Increased Ca + 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
  1. Parathyroid adenoma (85-90%)

2. Chief cell hyperplasia

28
Q

State some causes of secondary hyperparathyroidism.

A
  1. Chronic renal insufficiency

2. Vitamin D deficiency

29
Q

What are the symptoms of hyperparathyroidism?

A

Stones, Bones, Abdominal Groans and Psychic Moans

  1. Stones – calcium oxalate renal stones
  2. Bones – osteitis fibrosa cystica
  3. Abdominal Groans – acute pancreatitis
  4. Psychic Moans – psychosis and depression
30
Q

What X-ray is of importance in showing the earliest skeletal change sin hyperparathyroidism?

A

X-ray of the hand

Subperiosteal bone erosions

31
Q

What are the five features of renal osteodystrophy?

A
  1. Increased bone resorption (osteitis fibrosa cystica)
  2. Osteomalacia
  3. Osteoporosis
  4. Osteosclerosis
  5. Growth retardation
32
Q

What are the consequences of renal osteodystrophy?

A
  1. Hyperphosphataemia
  2. Hypocalcaemia as a result of a decrease in vitamin D metabolism
  3. Secondary hyperparathyroidism (low calcium due to low Vis D so reflex hyperparathyroidism)
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 - rapid breakdown of bone
  2. Osteolytic-osteosclerotic - bone formation
  3. Quiescent osteosclerotic - quiescent stage
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
(more common in caucasians, onset 40 years plus)

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  
Deafness  
Haemodynamic changes  
Cardiac failure  
Hypercalcaemias 
Development of sarcoma in the area of involvement
39
Q

What is a Haversian canal?

A

Channel that blood vessels run in within bone

40
Q

What are Howship’s Lacunae?

A

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

41
Q

Where is RANK found?

A

Receptor activator for nuclear factor Kappa B

- found on osteoclast precursors in response to stimulation via M-CSF

42
Q

Describe the aetiology of Paget’s

A

mainly unknown

  • Familial cases show autosomal pattern of inheritance with incomplete penetrance (mutations in SQSTM1 or RANK)
  • Parvomyxovirus type particles have been seen on EM in Pagetic bone – some doubt this is cause.
  • Overuse or previous bone injury (pool player w finger he rested on table)

Musculoskeletal (10 decks)

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