Session 9 - Cartilage and Bone Flashcards

1
Q

What are the 3 main types of cartilage?

A

Hyaline - Collagen 2 - tough dense tissue often containing fluid (around 70%)
Elastic - Elastic fibres and Collagen 2 - tough but flexible tissue
Fibrocartilage - Collagen 1 mainly, small amounts of collagen 2 - such as in intervertebral discs

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2
Q

Describe the main features of hyaline cartilage

A
  • Chondrocytes are the only cell present. They can be present as single cells or, if recently divided, in small clusters called isogenous groups
  • Chondrocytes lay down extracellular matrix containing collagen 2, Hyaluronic acid and Proteoglycans.
  • Avascular
  • High water content increases resilience to pressure
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3
Q

Describe the ground substance and extracellular matrix in cartilage

A
  • About 100 hyaluronate proteoglycan aggregates per collagen fibre
  • Makes a very “stiff” gel-like substance
  • Attracts a lot of water-preventing compression
  • Hyaluronic acid together with its attached proteoglycan monomers, forms hyaluronate proteoglycan aggregate
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4
Q

Describe chondrocytes and how they lay down the extracellular matrix

A
  • Each chondrocyte lies within a lacuna

- When placed under pressure, mechanical signals increase synthetic activity to lay down more extracellular matrix

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5
Q

What is the difference between appositional and interstitial growth?

A
  • Appositional growth - growth from the periphery

- Interstitial growth - growth from the centre

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6
Q

Describe the growth of hyaline cartilage

A

It shows appositional growth. The perichondrium covers the top and bottom of the cartilage which is where fibroblast like cells develop into chondroblasts and progress inwards to the maturing chondral region to become chondrocytes. Which lay down and maintain the extra cellular matrix.

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7
Q

Describe the structure of the hyaline cartilage found in the trachea and on articular surfaces

A

Trachea/tracheal wall - The lumen of the trachea is maintained by C shaped tracheal cartilages. It prevents collapse. It is lined with pseudostratified ciliated epithelium
Articular Surfaces - Provides smooth surface for movement. In the adult cells don’t proliferate enough to repair damage. Fibroblasts lay down scar tissue instead. Calcifies with age. Also only in articular hyaline cartilage there is no perichondrium on the articular surface. This surface has more type 3 collagen than normal as it provides for an even smoother surface

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8
Q

Outline the structure and distribution of elastic cartilage

A
  • Only chondrocytes present
    • contain elastic fibres as well as collagen 2 conferring elasticity
  • It is found in 3 places:
    • The pinna of the ear
    • Eustachian tube
    • Epiglottis
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9
Q

Outline the structure and distribution of fibrocartilage

A
  • Contains chondrocytes and fibroblasts
  • It’s a combination of dense regular connective tissue and hyaline cartilage
  • cells distributed in rows, no surrounding perichondrium
    It can be found in:
    • Intervertebral discs
    • Articular discs of sternoclavicular and temporomandibular joints
    • Menisci of knee joint
    • Pubic symphysis
  • They act as a shock absorber and to resist shearing forces
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10
Q

Explain what is involved in bone development and growth and what is this process called?

A

1) Initial hyaline model (embryo 5-6 weeks)
2) collar of the periosteal bone appears in the shaft (embryo 6-8 weeks)
3) Central cartilage calcifies. Nutrient artery penetrates. supplying bone - depositing osteogenic cells. Primary ossification center formed (8-12 weeks)
4) Medulla becomes cancellous bone. Cartilage form epiphyseal growth plates. Epiphyses develop secondary centers of ossification (post natal)
5) Epiphyses ossify and growth plate continues t0 move apart, lengthening bone (prepubertal)
6) Epiphyseal growth plates replaces by bone. Hyaline articular cartilage persists.

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11
Q

What is the composition of bone (matrix and cells)?

A

Matrix:
- 65% inorganic:
- Calcium hydroxyapatite and magnesium/aluminium salts
- resists bending and compression
- 35% organic:
- 1) Collagen 1
- 2) GAGs and proteoglycans
- 3) Non-collagenous proteins
- resists pulling and tension forces
Cells:
- Osteoprogenitor cells:
- undifferentiated- stem cell
- Inner later of endosteum and periosteum
- Osteoblast:
- Intermediate cells that can’t divide
- Inner layer of endosteum and spicules
- lay down new bone
- Osteocyte:
- Terminally differentiated bone cell
- Trapped within osteon
- No longer lay down matrix - tissue maintenance (stress and strain sensed)
- Osteoclast:
- Huge cell (up to 50 nuclei)
- Fused monocytes (WBCs)
- Surface of cortical bone (endosteum)
- Resorption of existing bone

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12
Q

Describe the structure of compact bone

A

The functional unit (the osteon):

  • Made from layers (lamellae) of compact mineralised collagen
  • Trap osteoblasts that produce the bone, osteocytes are terminally differentiated
  • They sit in small depressions called lacunae
  • send out long filipodia to “communicate” with other osteocytes
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13
Q

What is the difference between osteoarthritis and rheumatoid arthritis?

A

Osteoarthritis - is a degenerative disease as a result of over use. It is the mechanical failure of the articular cartilage narrowing the joint space.
Rheumatoid Arthritis - is an autoimmune disease which results in the inflammation of the synovial membrane and thickening of the joint capsule

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14
Q

Name 3 different functions of bone

A

Mechanical - protect delicate organs, framework for shape of body, leaver for movement
Synthetic - Heamopoeisis
Metabolic - Mineral storage (calcium and phosphorus), fat storage (yellow bone marrow), acid base regulation (absorbs/releases alkaline salts for pH regulation)

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15
Q

What are the 2 ossification types?

A

Endochondral Ossification:
- formation of long bones from a cartilage template
- continued lengthening by ossification at epiphyseal plate
- appositional growth (growth at edges; grows in one direction, Which pushes out in the opposite)
Intramembranous ossification:
- formation of bone from clusters of MSC (mesenchymal stem cell) in the center of bone - trabecular bone
- interstitial growth (growth in the middle pushing out)

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16
Q

What are the stages of intramembranous ossification - flat bone?

A

1) Mesenchymal stem cells form a tight cluster
2) The MSCs transform to osteoblasts.
3) Osteoblasts lay down osteoid (extracellular matrix containing type 1 collagen)
4) The osteoid mineralises (crystals of calcium form in and around it) to form rudimentary bone tissue spicules [surrounded by osteoblasts and containing osteocytes]
5) The spicules join to form trabeculae, which merge to form woven bone
6) Trabeculae replaced by the lamellae of mature compact bone

17
Q

How can you identify mature and immature bone?

A
  • Immature bone has osteocytes in random arrangements
  • Mature bone has osteocytes arranged in concentric lamellae of osteons
  • Resorption canals in mature bone run parallel with the osteons’ long axes
18
Q

What are Haversian and Volkmann’s canals?

A

Haversian canals run parallel with the osteons and are found centrally within them. They are a hollow tube that has, blood and lymph vessels and nerve fibres running through them.
Volkmann’s canals run perpendicular to these and link Haversian canals allowing blood and lymph vessels and nerves through

19
Q

What factors affect bone stability and how are they modulated?

A

Activity of osteocytes (osteoid recycling):

  • can act like osteoblasts laying down “scavenged” osteoid into their lacunae (increased by oestrogen/thyroid hormone)
  • can act like osteoclasts and degrade bone (a little) (increased PTH, parathyroid hormone)

Activity of osteoblasts (bone deposition)
- Stimulated by calcitonin, GH (via IGF-1), oestrogen and testosterone, thyroid hormones, Vit A

Activity of osteoclasts (bone resorption)

  • Increased by PTH - releases Ca2+ ion into the blood
  • Calcitonin blocks the action of PTH at the PTH receptor

Nutrition:

  • Vitamin D3 - needed for calcium absorption from the gut
  • Vitamin C - Synthesis of collagen
  • Vitamin A and B12 - synthesis of bone proteins
20
Q

Detail the stages of bone fracture repair

A

1) A blood clot (haematoma) is formed in which granulation tissue arises. This is where granulocytes enter the site and swelling and inflammation occurs. Phagocytic cells and osteoclasts begin to remove dead and damaged tissue
2) The procallus of granulation tissue is replaces by a fibrocartilaginous callus in which bony trabeculae are developing. New blood vessels infiltrate.
3) Endochondral (replacing the cartilage) and intramembranous (filling any gaps) ossification gives rise to a bony callus of spongy/cancellous bone.
4) Cancellous bone is replaces by compact cortical bone until remodelling is complete. The material bulging out and into the medulla is removed by osteoclasts. The final shape is the same as the original bone as it responds to the same set of mechanical stressors

21
Q

What are the 2 main stages in bone remodelling?

A

1) Osteoclasts make a wide tunnel in the bone (cutting cone)

2) Osteoblasts make a smaller tunnel of cortical bone (closing cone)

22
Q

Name 5 bone diseases

A
  • Osteogenesis imperfecta
  • Rickets
  • Osteomalacia
  • Osteoporosis
  • Achondroplasia
23
Q

What causes osteogenesis imperfecta?

A
  • A mutation in the COL1A gene
  • Incorrect production of collagen 1 fibres
  • weak bones and increased fracture risk
  • shortened height and stature
  • mainly affects neonates and children
24
Q

What causes rickets?

A
  • Vitamin D deficiency resulting in poor calcium mobilisation and absorption in the intestine.
  • As such there is ineffective mineralisation of the collagen fibres that forms bones
  • This ultimately causes, weakened bone development, soft bones and shortened height and stature, painful to walk and the characteristic bowed legs
25
Q

What is osteomalacia?

A

AKA “rickets in adults”
- caused by a vitamin D deficiency and as such there is lower mineralisation and increased osteoid (un-mineralised/ calcified bone matrix)
This lack of Vitamin D can be caused by:
- Kidney disease - activates Vitamin D
- Protection from sunlight - produces D3
- Surgery of stomach and intestine - Ca2+ absorption hindered
- Drugs - phenytoin prevents Vitamin D absorption

26
Q

What causes Achondroplasia?

A
  • It is an inherited mutation in the FGF3 receptor gene
  • FGF promotes collagen formation from cartilage (endochondral ossification affected, intramembrane isn’t)
  • Results in short stature but normal head and torso (long bones can’t lengthen properly)
27
Q

What is osteoporosis and how does it come about?

A

Primary:
- Type 1: occurs to postmenopausal women, due to an increase in osteoclast number (controlled by oestrogen), loss of oestrogen after the menopause
- Type 2: Occurs in (older) men and women, due to loss of both oestrogen and androgen
Secondary:
- Result of drug therapy
- Malnutrition, prolonged immobilisation, weightlessness (processes that affect bone remodelling)
- Metabolic bone diseases (hyperparathyroidism, metastatic cancers)

28
Q

Name some modifiable risk factors for osteoporosis

A
  • Insufficient calcium intake: recommended value for post menopausal women is 700mg a day
  • Exercise: immolation of bone
  • Cigarette smoking - in women - smoking correlates with increased incidence of osteoporosis