Ossification of bone and disease Flashcards Preview

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Flashcards in Ossification of bone and disease Deck (41)
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0
Q

What is intramembranous ossification?

A

-The replacement of mesenchyme with bone

1
Q

What is endochondral ossification?

A

-The replacement of hyaline cartilage template with bone

2
Q

Where does intramembraneous ossification occur?

A
  • In the formation of flat bones

- In the widening of long bones

3
Q

Describe intramembraneous ossification

A
  • Mesenchyme template of flat bones is invaded by osteoblasts from the periosteum
  • Osteoid becomes mineralised and forms bone tissue spicules
  • These bone tissue spicules develop to form trabeculae which radiate out from a central point which used to be the primary ossification centre
4
Q

In endochondral ossification of long bones, does all the cartilage get replaced to bone immediately?

A

-No the epiphyseal growth plates remain to allow development of long bones

5
Q

Describe endochondral ossification

A
  • Initial cartilage model in embryo
  • Collar of periosteal bone appears at the shaft
  • Central cartilage calcifies, nutrient artery penetrates supplying osteogenic cells, primary ossification centre formed
  • (postnatal) Medulla becomes cancellous, cartilage forms epiphyseal growth plates and epiphyses develop secondary ossification centres
  • (pre-puberty) Epiphyses ossify and growth plates continue to move apart, lengthening bone
  • (mature) Epiphyseal growth plate replaced by bone, articular cartilage remains
6
Q

Describe how growth occurs at the epiphyseal growth plates (think zones)

A
  • Zone of reserve cartilage
  • Zone of proliferation-> Chondrocytes proliferate, enlarge and secrete matrix
  • Zone of hypertrophy-> Chondrocytes become very large
  • Zone of calcified cartilage -> Chondrocytes degrade and the matrix calcifies
  • Zone of resorption-> Columns of calcified cartilage becomes mineralised forming bony spicules which develop into bone
7
Q

Can you tell the difference histologically between intramembraneous and endochondral ossification?

A

-No they are both arranged in the same way with haversian systems

8
Q

What inheritance pattern is osteogenesis imperfecta?

A

-Autosomal dominant

9
Q

What is the cause of osteogenesis imperfecta?

A

-Mutation in the TI collagen gene

10
Q

What morphological and mechanical abnormalities can bones show in osteogenesis imperfecta?

A
  • Bones are often thin and bowed/curved with growth retardation
  • Bones are highly susceptible to fracture due to the weakened structure of collagen fibres
11
Q

How is osteogenesis imperfecta treated?

A

-Orthopaedic devices such as rods being insterted into the medulla

12
Q

Why does ostogenesis imperfecta have medicolegal importance?

A

-The recurrent fractures can look like deliberate harm to the child

13
Q

What is achondroplasia?

A

-Short-limbed dwarfism

14
Q

What is the cause of achondroplasia?

A

-An autosomal dominant point mutation in the fibroblast growth factor receptor gene which results in a gain of function

15
Q

How does the gain of function of the FGFR gene in achondroplasia result in short-limbed dwarfism?

A

Stops the action of the growth plates by:

  • Decreased endochondral ossification
  • Inhibited proliferation of cartilage in growth plates
  • Decreased cellular hypertrophy
  • Decreased cartilage matrix production
16
Q

Can you be homozygous in achondroplasia?

A

-No it is fatal

17
Q

What is the result of excessive growth hormone before puberty?

A

-Gigantism

18
Q

How does excessive GH cause gigantism?

A

-Promotion of epiphyseal growth plate activity

19
Q

What is the result of excessive GH in an adult?

A

-Acromegaly (widening of bone through increased periosteal growth)

20
Q

What is the result of decreased GH before puberty?

A

-Pituitary dwarfism

21
Q

What is the most common cause of altered GH levels?

A

-Benign pituitary tumour (adenoma)

22
Q

How do sex hormones influence growth?

A
  • Influence the development of ossification centres

- Control pubertal growth spurt

23
Q

What is the result of excessive sex hormones in puberty?

A

-Retards bone growth due to early closure of the epiphyseal growth plates

24
Q

What is the result of deficient sex hormones in puberty?

A

-Prolonged bone growth and tall stature as epiphyseal growth plates persist till later in life

25
Q

What is the cause of cretinism?

A

-Untreated thyroxine deficiency during development

26
Q

Can thyroxine deficiency damage be reversed in neonates?

A

-Yes with prompt administration of thyroxine within a time-window

27
Q

What is rickets?

A

-A childhood bone disease characterised by soft bones due to lack of vitamin D

28
Q

What are the characteristics of rickets?

A
  • Insufficient calcium deposition for rigidity
  • Soft and malformed bones
  • Distortion of the skull bone (bossing)
  • Enlargement of the costochondral junctions in ribs
29
Q

What is the cause of osteomalacia?

A

-Lack of calcium or vitamin D in adults

30
Q

What are the common causes of osteomalacia? (what causes lack of vit D)

A
  • Poor diet
  • Lack of sunlight
  • Intestinal malabsorption
  • Liver/kidney damage
31
Q

What are the common symptoms of osteomalacia?

A
  • Bone pain
  • Back pain
  • Muscle weakness
32
Q

What are the characteristics of the trabeculae like in osteomalacia?

A

-Trabeculae have large amounts of non-mineralised bone (osteoid) making them weaker

33
Q

What sites are commonly effected in osteomalacia?

A
  • Neck of femur
  • Ribs
  • Spine
34
Q

What is osteoporosis?

A

-A metabolic bone disease caused by a decrease in bone mass to the point where bone no longer provides adequate mechanical support

35
Q

What is the cause of decreased bone mass in osteoporosis?

A

-Enhanced bone resorption relative to deposition

36
Q

Why are bones susceptible to fracture in osteoporosis?

A

-Increased resorption causes thin traneculae, making them more prone to fracture

37
Q

Why is osteoporosis associated with age?

A

-Outer surfaces of trabeculae are constantly remodelled, with ageing the resorption bays formed by osteoclasts are incompletely filled

38
Q

What are the two types of postmenopausal causes of osteoporosis?

A
  • T1-> Increased osteoclast activity due to oestrogen withdrawal
  • T2-> generally occurs over 70 due to attenuated osteoblast function
39
Q

How do genetic factors play a role in osteoporosis risk factors?

A

-Bone density is higher in black races

40
Q

Why can lack of exercise be a risk factor for osteoporosis?

A

-If the bones are immobilised there is an acceleration of bone loss