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What is endochondral ossification?

- Replacement of a pre-existing hyaline cartilage template by bone
- Most bones of the body develop in the this way

1

Describe the development of long bones by endochrondral ossification

- Embryo 5-6 weeks: Cartilage models develops
- Embryo 6-8 weeks: Collar of periosteal bone forms around the diaphysis (shaft) (intramembranous ossification)
- Fetus 8-12 weeks: Central cartilage calcifies; nutrient artery penetrates which supplies bone-depositing osteogenic cells; primary ossification centre forms
- Postnatal: Medulla becomes cancellous bone; cartilage forms the epiphyseal growth plates; secondary centres of ossification develop in the epiphyses
- Prepubertal: Epiphyses ossify and growth plates continue to move apart which lengthens the bone
- Mature adult: Epiphyseal growth plates replaced by bone; hyaline cartilage persists at edge of epiphyses

2

What are the zones of the epiphyseal growth plate?

- Zone of reserve cartilage
- Zone of proliferation
- Zone of hypertrophy
- Zone of calcified cartilage
- Zone of resorption

3

What is the zone of reserve cartilage?

- No cellular proliferation or active matrix production

4

What is the zone of proliferation?

- Cartilage cells divide and organise into distinct columns
- Cells enlarge and secrete matrix (collagen-mainly type II and XI, and other cartilage matrix proteins)

5

What is the zone of hypertrophy?

- Cells enlarge greatly
- Matrix is compressed into linear bands between cell columns

6

What is the zone of calcified cartilage?

- Enlarged cells begins to degenerate
- Matrix calcifies (initial scaffold for new bone)

7

What is the zone of resorption?

- Calcified cartilage is in direct contact with the connective tissue of the
marrow cavity
- Small blood vessels and connective tissue invade the region previously occupied by dying chondrocytes
- This leaves the calcified cartilage as spicules, onto which bone is laid down

8

What is intramembranous ossification?

- Condensations of mesenchymal tissue, not the replacement of a pre-existing hyaline cartilage template

9

What bones develop by intramembranous ossification?

- Flat bones:
~ Skull bones (eg parietal, occipital, temporal, frontal)
~ Maxilla
~ Mandible
~ Pelvis
~ Clavicle
- Also contributes to thickening if long bones

10

How does intramembranous ossification occur?

- Mineral deposits within trabeculae radiate from a central point (primary ossification centre)

11

What is osteogenesis imperfecta?

- Autosomal dominant group of heritable disorders of connective tissue
- Caused by mutations in the gene for type I collagen - abnormal collagen synthesis by osteoblasts and fibroblasts
- Affects the skeleton, joints, ears, ligaments, teeth, sclerae and skin
- Leads to 'brittle bones' - bone fragility which causes predisposition to fractures and deformity
- Multiple fractures are usually present at/before birth and are often fatal

12

Where is growth hormone synthesised and stored?

- Anterior pituitary gland

13

What are the effects of growth hormone on bones before puberty?

- Excessive: Gigantism (promotion of epiphyseal growth plate)
- Insufficient: Pituitary dwarfism (affects epiphyseal cartilage)

14

What are the effects of growth hormone on bone as an adult?

- Excessive: cannot cause gigantism as there are no longer epiphyseal growth plates
- Insufficient: Acromegaly (promotion of periosteal growth by increase in bone width)

15

What is the effect of sex hormones on bone?

- Influence the development of ossification centres
- Induce secondary sexual characteristics and pubertal growth spurt
- Bone growth is retarded because of premature closure (fusion) of epiphyses as a result of precocious sexual maturity (can be caused by tumours producing sex hormone)
- Prolonged bone growth and tall stature can result if epiphyseal growth plates persist later into life that normal because of sex hormone deficiency

16

What is the effect of thyroid hormone on bone?

- Thyroid hormone deficiency can lead to an infant with cretinism (permanent neurological/intellectual damage) and other abnormalities eg short stature
- Effects of neonatal hypothyroidism can be reversed with prompt administration of thyroxine

17

What is osteoporosis?

- Metabolic bone disease where bone mass decreases so that it cannot provide adequate mechanical support
- Incomplete filling of osteoclasts resorption bays
- Osteoclasts activity is more than osteoblast activity

18

What is the most common type of osteoporosis?

- Primary osteoporosis
~ Type 1: occurs in postmenopausal women; caused by an increase in osteoclasts number (result of oestrogen withdrawal)
~ Type 2: occurs in the elderly of both sexes (senile osteoporosis) generally occurs after age 70; reflects attenuated osteoblasts function

19

What are some osteoporosis risk factors?

- Genetic: peak bone mass is higher in blacks that whites or Asians
- Insufficient calcium intake: 800 mg/day is recommended for postmenopausal women
- Insufficient calcium absorption and vitamin D: decreased renal activation of vitamin D with age (occurs in populations without vitamin D supplementation or elderly confined indoors)
- Exercise: immobilisation of bone (eg prolonged bed rest/cast) leads to accelerated bone loss as physical activity is needed to maintain bone mass
- Cigarette smoking: has been correlated with increased incidence of osteoporosis in women

20

What is achondroplasia caused by?

- Autosomal dominant point mutation in the fibroblast growth receptor-3 gene

21

What does the mutation in the gene that causes achondroplasia do?

- Decreased endochondral ossification
- Inhibited proliferation of chondrocytes in growth plate cartilage
- Decreased cellular hypertrophy
- Decreased cartilage matrix production

22

What is achondroplasia?

- Short limb dwarfism
- Have a normal intelligence and an average lifespan
- Is heritable

23

Where do we get Vitamin D from?

- Dietary eg fish
- Synthesised by skin using UV ligh

24

What happens to Vitamin D in the body and where?

- Is hydroxylated in the liver
- Undergoes more hydroxylation in the kidney to form active 1,25-dihydroxyvitamion D3

25

What does the hydroxylated, active form of vitamin D do?

- Increase calcium absorption by the small bowel
- Promotes mineralisation of bone

26

What is rickets?

- A childhood disease where bones do not harden due to a deficiency of vitamin D

27

What causes rickets?

- Insufficient calcium deposition for adequate bone rigidity
- Bones (especially long bones) become soft and malformed
- Distortion of skull bone (leading to 'bossing')
- Enlargement of costochondral junctions of ribs (rickety rosary)

28

What osteomalacia?

- Adult counterpart of rickets
- Caused by significant calcium deficiency or a lack of vitamin D (eg because of poor diet, lack of sunshine, intestinal malabsorption, liver/kidney disease

29

What are common symptoms of osteomalacia?

- Bone pain
- Back ache
- Muscle weakness

30

What happens to the bone in osteomalacia?

- Trabeculae of cancellous bone have an abnormally large amount of non-mineralised bone (osteoid-uncalcified matrix secreted by osteoblasts) covering the trabecular surface
- The trabeculae are weakened by insufficient mineralisation