Bone Abnormalities

Question 1

Osteoporosis =

Answer 1

Complex skeletal disease characterised by low bone density resulting in increased bone fragility and susceptibility to fractures (too little bone)

Question 2

Osteopetrosis =

Answer 2

Too much bone

Question 3

How can bone structure be assessed?

Answer 3

Blood tests: Calcium, Phosphate, Parathyroid Hormone, Vitamin D, Alkaline Phosphatase, Albumin

Imaging: X-ray, CT, MRI, Ultrasound

Bone biopsy/histology

Bone density DEXA scan

Question 4

What are wider implications of osteoporosis?

Risk factors?

Answer 4

Future fractures, pain, quality of life, long term admission, mortality
Old age, sex, ethnicity, low BMI, family hx, post-menopause, smoking, excessive alcohol use, steroids, immobility, Ca2+/Vit D deficiency

Question 5

What’s the pathophysiology of Osteoporosis?

Answer 5

Loss of balance between bone formation and resorption during remodelling
Osteoclasts make deeper holes; osteoblasts less efficient

Question 6

What’s the post menopause pathophysiology of osteoporosis?

Answer 6

Reduced serum Oestrogen
Increased IL-1, IL6 and TNF
Increased RANK and RANKL expression
Increased osteoclast activity

Question 7

How does ageing increase risk of osteoporosis?

Answer 7

Reduced replicative activity of osteoprogenitor cells
Reduced synthetic activity of osteoblasts
Reduced biologic activity of matrix-bound growth factors
Reduced physical activity

Question 8

How is osteoporosis managed?

Answer 8

Diet
Exercise
Supplements (Ca2+, PO4, Vitamin D)
Fall prevention
Pharmacologically: bisphosphonates, SERMs, PTH, Denosumab

Question 9

What are side effects of bisphosphonates?

Answer 9

Asymptomatic hypocalcaemia
General GI disturbances
Osteonecrosis of the jaw

Question 10

How does PTH work in the treatment of osteoporosis?

Answer 10

Administered SC injection
Promotes bone production
Continuous PTH causes bone loss but intermittent peaks cause osteoblast differentiation and activity

Question 11

What’s Rickets?

Answer 11

Defective mineralisation at the growth plate (characterised by inadequate mineralisation of bone)

Common in children - growth retardation and bony deformities

Question 12

Osteomalacia?

Answer 12

Defective mineralisation of osteoid - can happen in children or adults - characterised by bone pain, fractures, muscle weakness

Most common cause is vitamin D deficiency resulting in low Ca2+ and PO4

Question 13

Paget’s disease of the bone? How is it treated?

Answer 13

Characterised by increased bone turnover - increase in woven bone being laid down
Woven bone is disorganised and weak, results in overgrowth, bowing, pain, more fractures

Treated with walkers, sticks, analgesia, supplements, bisphosphonates, surgery

Question 14

How do bisphosphonates work in Paget’s disease?

Answer 14

Reduce osteoclast recruitment
Increase osteoclast apoptosis
Reduce depth of resorption site

Question 15

Osteogenesis Imperfecta?

Answer 15

Group of disorders characterised by defective production of type I collagen
Systemic disease: brittle bones, sclera of eyes have blue tint, growth retardation and more prone to fractures

Question 16

What are some symptoms of Paget’s disease other than pain and bowing of the bone - how are these symptoms explained?

Answer 16

Increase in hat size -> increased bone turnover of the skull
Auditory/visual problems -> overgrowth of bones impinging on auditory/occipital nerves
High output cardiac failure / raised JVP -> Pagetoid bone is hypervascular and sets up arteriovenous shunts to increase blood flow through remodelled bone

Question 17

What are complications of Paget’s disease?

Answer 17

Pagets osteosarcoma (bone cancer)
Hypercalcaemia
Heart failure
Fracture
Hearing loss
Osteoarthritis

Question 18

What are some radiological observations of bone abnormalities?

Answer 18

Bone resoprtion
Lytic lesions
Thick cortical bone and coarse trabeculae