bone 2

Question 1

bone development in the embryo

Answer 1

2 types:

• intramembranous
• endochondral

both involve replacing a connective tissue template

Question 2

intramembranous bone development

Answer 2

Sheets of mesenchymal cells
Differentiation to osteoblasts in centres of ossification. These merge to form trabecular bone that is remodelled
Remaining mesenchyme makes bone marrow and periosteum
Flat bones of skull, maxilla and mandible

Question 3

endochondral bone development

Answer 3

Cartilage template
Blood supply to shaft of bone causes osteoblast differentiation: primary centre of ossification
At birth blood supply to the epiphyses instigate secondary centres of ossification
Cartilage growth plate remains to allow the bone to lengthen
Long bones and base of skull

Question 4

bone growth

Answer 4

Epiphyseal end: Proliferation

Diaphyseal end: chondrocytes mature and die and are replaced by bone

In long bones bone grows in length via the epiphyseal growth plate
This fuses in adulthood.
Other bones grow by coordinated appositional growth at periosteum and resorption at inner surface (long bones gain in circumference by this method also)

Question 5

achondroplasia

Answer 5

Congenital bone disease: Dwarfism
Caused by mutation on the fibroblast growth factor receptor 3: activation
Activation of FGFR3 inhibits chondrocyte proliferation: affects growth plates
They are disorganised and hypoplastic: long bone growth is stunted:
Lordosis (back), bowed legs and stunted extremities (especailly proximal)

Question 6

bone metabolism

Answer 6

Bone contributes to calcium homeostasis under the influence of:
PTH
Calcitonin
Vitamin D

PTH (parathyroid hormone) increases blood calcium levels and regulates phosphate
By releasing calcium from bone
By stimulating vitamin D:
enhances uptake of calcium in the gut
Increases Ca and PO reabsorption from bone (increased Oc, decreased Ob)
By conserving calcium in the kidney while reducing reabsorption of phosphate
Calcitonin (thyroid C cells)decreases blood calcium levels
By inhibiting osteoclast activity
By reducing calcium reabsorption in the kidney

Question 7

metabolic bone disease

Answer 7

Result from an imbalance between bone formation and resorption 
Four main diseases:
Osteoporosis
Rickets and osteomalacia
Paget’s disease
Hyperparathyroidism

Question 8

osteoporosis

Answer 8

• metabolic disease.
  Increased bone erosion due to imbalance of osteoblasts and clasts causes loss of bone mass. . This leads to thinner trabeculae initially and then thinned cortical bone. Bone tissue is normal. Fracture risk.

Question 9

osteomalacia

Answer 9

• metabolic disease.
  Lack of vitamin D leads to inadequate mineralisation of bone –weak and soft. Osteoid is normal. Bowing of bones and bone pain.

Question 10

paget’s disease

Answer 10

• metabolic disease.
  Overactive osteoclasts. These destroy bone and result in osteoblasts responding by laying down bone rapidly-immature woven bone. Therefore bone mass is increased but it is weak. Metabolic consequences due to energy demands of the disease.

Question 11

hyperparathyroidism

Answer 11

• metabolic disease.
  Increased osteoclast activity as a result of increased levels of PTH due to renal disease or tumour. Destruction of cortical and trabecular bone. Inadequate compensation by osteoblasts leads to loss of bone mass. Fracture risk.

Question 12

bone fracture

Answer 12

Periosteum is breached, haematoma, blood clot forms
Replaced by vascular collagenous tissue (granulation tissue) which becomes increasingly fibrous: fibrous granulation tissue
Replaced by hyaline cartilage: firm, flexible provisional callus
Osteoprogenitor cells from peri and endosteum differentiate onto osteoblasts and lay down new woven bone: bony callus
Site completely bridged by bone: bony union
Slowly remodelled to form oriented lamellar bone