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ESA1 - Tissues Of The Body > Ossification And Bone Disease > Flashcards

Ossification And Bone Disease Flashcards

1
Q

Where are the growth plates of bones located?

A

EPIPHYSIS

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2
Q

Briefly explain the development of long bones

A
  • Periosteal collar forms on initial hyaline cartilage template by endochondral ossification
  • Central cartilage CALCIFIES and nutrient artery penetrates to supply osteogenic cells (PRIMARY OSSIFICATION CENTRE)
  • Medulla becomes cancellous bone and cartilage forms at EPIPHYSEAL growth plates (SECONDARY OSSIFICATION CENTRE)
  • Epiphyseal growth plates ossify and continue to move apart, lengthening the bone
  • Hyaline cartilage remains at articulating surfaces
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3
Q

Explain how growth occurs at the EPIPHYSEAL GROWTH PLATE

A
  • Zone of PROLIFERATION -> chondrocytes actively divide forming columns and secreting matrix
  • Zone of HYPERTROPHY -> cells enlarge and matrix is compressed into linear bands between cell columns
  • Zone of CALCIFIED CARTILAGE -> enlarged cells degenerate and matrix calcifies (hydroxyapatite)
  • Zone of RESORPTION -> small blood vessels invade region occupied by dying cells (calcified cartilage forms spicules between them and new bone is laid down by osteoblasts)
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4
Q

What is the zone of reserve cartilage?

A

Zone above the zone of proliferation where no cellular proliferation or active matrix production occurs

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5
Q

What is INTRAMEMBRANEOUS OSSIFICATION?

A

New bone is formed by condensations of MESENCHYMAL TISSUE

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6
Q

What type of bones form by intramembraneous ossification?

A

FLAT BONES such as skull, pelvis and clavicle

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7
Q

How does intramembraneous ossification contribute to growth of long bones?

A

Thickening of long bones by ossification of the periosteum

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8
Q

What is osteoid?

A
  • Unmineralised component of bone (non calcified matrix)
  • Precursor laid down by osteoblasts
  • Formed by lack of vitamin D
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9
Q

Describe the cause(s) of OSTEOGENISIS IMPERFECTA

A
  • Autosomal recessive (RARE 1 in 10000)
  • Mutation in gene coding for TYPE I COLLAGEN (most abundant protein in body and present in matrix)
  • Results in brittle bones that are prone to fractures
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10
Q

What is the medico-legal importance of osteogenesis imperfecta?

A

Possible confusion of multiple fractures caused by deliberate injury

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11
Q

What group of people are more susceptible to osteoporosis?

A
  • Most common bone condition affecting the elderly

- Affects 1 in 3 women and 1 in 12 men in UK over the age of 50

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12
Q

What are the risk factors associated with osteoporosis?

A
  • Age
  • Menopause
  • Hypogonadism
  • Long term steroid treatment
  • Poor dietary calcium and vitamin D
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13
Q

Why are females more susceptible to osteoporosis than men?

A
  • Oestrogen and testosterone promote osteoblasts and suppress osteoclasts
  • Loss of oestrogen post-menopause
  • Less suppression of osteoclast activity and less promotion of osteoblast activity
  • Rate of regeneration
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14
Q

Explain how steroids can be considered a risk factor for osteoporosis

A
  • Steroids inhibit osteoblasts

- Regeneration

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15
Q

Describe the changes of bone mass that occur with ageing

A
  • Bone mass density rises and peaks at mid-20s
  • Slowly begins to decline
  • Women have accelerated decline of bone mass post-menopause
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16
Q

What is the difference between osteoporosis and osteomalacia in regards to bone mass and density?

A
  • Osteoporosis -> decrease in bone mass, same bone density

- Osteomalacia -> same bone mass, decrease in bone density

17
Q

Explain the importance of vitamin D in ossification and bone strength

A
  • Essential for normal ossification
  • Absence causes formation of osteoid (poorly mineralised, pliable matrix)
  • Affected bones are unable to support body weight and bend, as well as being prone to fractures
18
Q

Give 2 examples of bone diseases that can occur due to lack of dietary vitamin D

A
  • RICKETS in growing children as there is insufficient calcium to mineralise bone trabeculae (bones are weakened and bend as a result)
  • OSTEOMALACIA in adults occurs similarly and results in decrease in bone mass
19
Q

Outline 5 common fracture sites and explain why these bones are more susceptible to fractures

A 
- Common sites are: 
> Neck of femur
> Vertebrae (spine)
> Ribs
> Pubic ramus
> Distal radius
- More spongy cancellous bone in these areas (contain weakened trabeculae due to insufficient mineralisation)
20
Q

What is the role of vitamin D in the mineralisation of bone?

A
  • Calcium (Ca2+) absorption in small intestine
  • Ca2+ resorption from bone (osteoclasts)
  • Ca2+ reabsorption in loop of Henle in kidneys
21
Q

Explain the homeostatic mechanisms involved in maintaining levels of Ca2+ ions

A
  • ⬆️Ca2+ levels -> CALCITONIN stimulates osteoblasts to absorb Ca2+ into bone matrix
  • ⬇️Ca2+ levels -> PARATHYROID HORMONE stimulates osteoclasts to break down bone matrix and release Ca2+
22
Q

Why is osteoporosis considered as a risk factor for fractures but not as cause?

A

Associated with fractures as there is an increased chance of fracture due to weakened bones but is not necessarily the cause of fractures (FALLS)

23
Q

Explain how HYPERGONADISM is considered a risk factor for osteoporosis

A
  • Hormones from gonads act on osteoblasts and osteoclasts
  • Lack of gonadal hormones decreases promotion of osteoblasts and decreases suppression of osteoclasts
  • Results in reduced peak bone mass and bone mass declines more rapidly
24
Q

How can conditions such as osteoporosis, rickets and osteomalacia be prevented?

A
  • Increased dietary calcium
  • Increased vitamin D from sunshine (early on in life)
  • Increased mobility and exercise
  • Management using hormone replacement (hypergonadism)
25
Q

Explain the effects of sex hormones on bone growth

A
  • Give rise to pubertal growth spurts
  • Overproduction (possibly due to tumours) retards bone growth (premature fusion of epiphysis)
  • Deficiency can mean epiphyseal plates persist later in life leading to prolonged bone growth - TALL STATURE
26
Q

Explain the effects of GROWTH HORMONE on bone growth before puberty

A
  • Excessive GH can cause GIGANTISM through promotion of epiphyseal growth plate activity
  • Insufficient GH can affect epiphyseal cartilage and cause PITUITARY DWARFISM
27
Q

Can GH effect bone growth in adults? If so, how?

A
  • Cannot cause gigantism as epiphyseal growth plates no longer exist
  • Excessive GH may increase bone width by promoting periosteum growth (ACROMEGALY)
28
Q

What is the cause of ACHONDROPLASIA?

A
  • Autosomal dominant point mutation in the fibroblast growth factor receptor-3-gene FGFR3
  • Mutation causes gain in function of gene
29
Q

What are the effects of a gain in function of FGFR3?

A
  • Decreased endochondral ossification
  • Inhibited proliferation of chondrocytes in growth plate cartilage
  • Decreased cellular hypertrophy and cartilage matrix production at epiphyseal growth plates
  • Results in a decrease in bone growth - short stature
30
Q

What is the phenotype of someone with achondroplasia?

A
  • Limbs are shortened
  • Vault of skull is enlarged
  • Small face with flattened bridge of nose
  • INTELLIGENCE IS NORMAL
31
Q

What are the chances of 2 parents with achondroplasia having a normal child?

A
  • 25% chance of being homozygous recessive, therefor normal
  • 50% chance of being heterozygous, therefore having achondroplasia
  • 25% child will die soon after birth as homozygous dominant condition is fatal
32
Q

What is ENDOCHONDRAL OSSIFICATION?

A
  • Replacement of pre-existing hyaline cartilage template with bone
  • Most common in body
33
Q

Explain how epiphyseal growth plates are affected in achondroplasia

A
  • Smaller growth plates due to inhibition of proliferation of cartilage and decreased cellular hypertrophy and calcium matrix production
  • Closing off of growth plates
34
Q

What is a NIDUS?

A

Small, tight cluster of mesenchymal cells

35
Q

Explain how intramembraneous ossification occurs

A
  • Mesenchymal cells cluster together forming a NIDUS
  • MSC cells become osteoprogenitor cells (developing more Golgi and RER)
  • Osteoprogenitor cells become osteoblasts and lay down OSTEOID
  • Osteoid mineralises to form bony spicules containing osteocytes (surrounded by osteoblasts)
  • Spicules merge to form trabeculae which are eventually replaced by lamellae forming compact bone

ESA1 - Tissues Of The Body (19 decks)

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