L16- Bone function and repair Flashcards

1
Q

a) How to bones grow in length?

b) How do bones grow in width?

A

a)
Interstitial growth: Endochondral ossification- activity in the epiphyseal plate: there are 5 zones
1. Zone of resting cartilage: matrix production
2. Zone of proliferation; new chondrocytes made
3. Zone of hypertrophy
4. Zone of calcification: matrix calcified and chondrocytes die
5. ossifciation zone

b) Appositional growth: intramembranous ossification
- occurs at endosterum or periosteum
- osteoblasts in the periosteum deposit new bone matrix layers onto already-formed layers of the outer surface of bone.
- At the same time, osteoclasts on the endosteum break bone tissue down.
- bone moves sideways

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2
Q

What are the 3 main functions of bones ?

A
  1. MECHANICAL
    - protect important tissues and organs
    - provide a framework for the overall shape of the human body
    - form the basis of levers involved in movement
  2. Synthetic
    - Haemopoiesis (holds and protects red bone marrow)
  3. Metabolic
    - mineral storage (calcium and phosphorus)
    - fat storage (yellow bone marrow)
    - acid-base homeostasis (absorbs or releases alkaline salts to help regulate blood pH)
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3
Q

Bone is constantly being made and resorbed.

a) Reasons for bone synthesis?
b) Reasons for bone resorption?
c) What do the two together do for bone?

A

a) Bone synthesis- the need to store excess calcium or increase the length of bone during development
b) Bone resorption- triggered when blood calcium levels fall and calcium needs to be released from bone
c) maintain integrity

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4
Q

a) What is bone modelling?
b) What is bone remodelling?
c) Differences?

A

a) reshapes bone to increase the mechanical strength of bone and to react to changes in the amount or direction of mechanical stress
b) replaces old, damaged bone with new bone to maintain the mechanical integrity of bone
c) Modeling: osteoblasts and clasts work on opposite surfaces of the bone where as during remodelling they work on a common surface

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5
Q

How come a bone can resist fracture?

A
  • It has great tensile and compressive strength, a degree of flexibility
  • main force lines are through the cortical bone as lamallae are thought to be able to slip, relative to each other to resist fracture, excessive load causes fracture
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6
Q

The activity of the bone cells affect bone stability.

What factors can affect the activity of:

a) osteocytes
b) osteoblasts
c) osteoclasts

A

A)

  • Oestrogen/ thyroid hormone: stimulate these cells to act like osteoblasts and lay down osteoid in lacunae
  • PTH: stimulate them to degrade a little bone in a process known as osteocytic osteolysis

b) Stimulated by calcitonin, GH, oestrogen and testeosterone, thyroid hormones, vitamin A

c)
- Stimulated by PTH: releases calcium ions in the blood
- calcitonin blcoks the action of PTH

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7
Q

What vitamins are important for bone stability and why?

A
  1. Vitamin D3 (either absorbed from gut or synthesised in skin): produces calcitriol (calcium absorption)
  2. Vitamin C: synthesis of collagen
  3. Vitamin K and B12: synthesis of bone proteins
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8
Q

What are the steps of fracture repair?

A
  1. Haematoma (blood clot) is formed: granulation tissue arises
  2. Fibrocartilaginous callus formation: procallus of granulation tissue is replaced by a fibrocartilaginous callus in which bony trabeculae (spongy) are developing
  3. Bony callus formation: endochondral and intramembranous ossification give rise to a bony callus of spongy/cancellous bone
  4. Bone remodeling: cancellous bone is replaced by compact cortical bone until remodelling is complete
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9
Q

Outline the process of Haematoma formation.

What step is this in fracture repair?

A

Step 1

  • Blood vessels in bone and periosteum break
  • mass of clotted blood (haematoma) form
  • bone cells at the fracture edge die
  • swelling and inflammation occurs (granulocytes enter)
  • phagocytic cells and osteoclasts begin to remove dead and damaged tissue
  • macrophages will eventually remove clot
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10
Q

Outline the process of fibrocartilaginous callus formation.

What step is this in fracture repair?

A

Step 2

  • new blood vessels infiltrate the fracture
  • a procallus of granulation tissue (rich in capilarries and fibroblasts) develops
  • fibroblasts: produce collagen fibres that span the break, others differentiate into chondroblasts that give rise to hyaline cartilage
  • osteoblasts from the nearby periosteum and endosteum invade and begin bone reconstruction by forming spongy/trabecular bone
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11
Q

Outline the process of Bony callus formation.

What step is this in fracture repair?

A

step 3

  • within a week new bone trabeculae begin to appear in the fibrocartilaginous (soft) callus
  • the trabeculae develop as the former callus is converted to hard bony callus of cancellous bone
  • endochondral ossification replaces all cartilage with cancellous bone
  • intramembranous ossification produces new cancellous bone in any gaps
  • bony callus formation continues for about 2 months until a firm union across the fracture site is formed
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12
Q

Outline the process of bone remodelling.

What step is this in fracture repair?

A

STEP 4

  • cancellous bone begins to be remodelled into compact bone
  • the material bulging from the outside of the bone and inwards into the medullary cavity is removed by osteoclasts
  • the final shape of the remodelled area is the same as that of the original unbroken bone becuase it responsds to the same set of mechanical stressors
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13
Q

How is bone remodelled in

a) Cancellous/trabeculae bone
b) Compact/cortical bone

A

a) Osteoclasts become activated and begin to resorb old bone, osteoclasts undergo apoptosis and finally osteoblasts synthesise new bone to replace old bone and osteoid will calcify to form bone

b) Osteoclasts make a wide tunnel in the bone (cutting cone): they are in front resorbing old bone
Osteoblasts: make a smaller tunnel of cortical bone (closing cone): trail behind and synthesise new bone to replace the old bone
- vessels remain in the tunnel and the tunnel will eventually develop into haversian canal surrounded by lamellar bone

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14
Q

Osteogenesis Imperfecta

a) Cause
b) Signs and symptoms
c) who does it mainly affect?

A

a) Mutation in COL1A gene leads to incorrect production of collagen 1 fibres

b) - Fractures can occur with minimal force
- weak bones
- Discoloration of the sclera, giving them a blue-gray color. due to the underlying choroidal veins which show through. This is due to the sclera being thinner than normal because the defective Type I collagen is not forming correctly.
- shortened height and stature

c) Mainly affects neonates and children

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15
Q

A) Why is Vitamin D so important?
b) What are some bone diseases caused by vitamin d deficiency?

Causes
Symptoms
who it affects

A

a) Vit D needed to help your body absorb calcium and phosphorus
- If these are low your body produces hormones that cause calcium and phosphate to be released from your bones.
- When your bones lack these minerals, they become weak and soft.

b) Rickets: mainly affects children

Causes:

  • poor calcium mobilisation
  • ineffective mineralisation
  • weakened bone development, soft bones
  • shortened height and stature
  • characteristic bowed legs
  • painful to walk

Osteomalacia: rickets in adults

Causes:

  • impaired bone metabolism due to Vitamin D deficiency and hence low levels of phosphate, calcium
  • or because of resorption of calcium
  • leads to inadequate bone mineralization and increased osteoid

Symptoms: Same: muscle weakness, pain and easy fractures

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16
Q

What is bone resorption?

A

Bone resorption is resorption of bone tissue, that is, the process by which osteoclasts break down the tissue in bones and release the minerals, resulting in a transfer of calcium from bone tissue to the blood.

17
Q

a) What is osteoporosis?

b) What are the types?

A

a) Osteoporosis is a weakening of living bone that is already formed and being remodeled. Making them fragile and more likely to break.

b) Primary Osteoporosis:
1. Type 1: postmenopausal women
- decreased level of oestrogen after menopause
- increase in osteoclast number: increase in bone resorption and hence decrease in amt of trabecular bone

  1. Type 2: senile osteoporosis
    - occurs in older women and men (after age of 70)
    - loss of both oestrogen and androgen
    - due to loss of osteoblast function

Secondary osteoporosis: caused by certain medical conditions or treatments that interfere with the attainment of peak bone mass and cause bone loss

  • can be result of drug therapy: corticosteroids
  • processes that affect bone remodelling: malnutrition, prolonged immobilisation, weightlessness
  • metabolic bone diseases i.e. hyperparathyroidism, metastatic cancers
18
Q

A) Modifiable and B) non-modifiable risk factors for osteoporosis?

A

A)

  • Smoking: quit smoking
  • inadequate calcium intake
  • inadequate vitamin D intake
  • low body weight
  • estrogen deficiency
  • low physical activity: immobilisation of bone leads to accelerated bone loss.

B)

  • Advanced age
  • ethnicity
  • female gender
  • family history of fractures
  • low body mass index
19
Q

How could you prevent getting osteoporosis?

A
  • Ensure a nutritious diet and adequate calcium intake
  • avoid under nutrition, eating disorders
  • maintain adequate supply of vit d
  • participate in weight bearing activity
  • avoid smoking
  • avoid drinking
20
Q

What is one of the major risk factors for bone fracture in elderly?

A

Osteoporosis

21
Q

What is the recommended value of calcium intake a day for postmeonopausal women?

A

700mg/a day

22
Q

What is achondroplasia?

A
  • inherited mutation in the FGF3 receptor gene
  • FGF promotes collagen formation from cartilage an hence endochondral ossification affected
  • results in short stature but normal size head and toso
  • long bones cannot lengthen properly
  • dwarf
23
Q

What type of ossification is affected in achondroplasia?

A

ENDOCHONDral