Bone and Ossification Flashcards

1
Q

What are some characteristics of bone?

A
  • can withstand compression, stress and deformation
  • dynamic
  • vascular (blood and lymph vessels supplied)
  • sensitive to pain, especially in periosteum
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2
Q

What are the functions of bone?

A

Support, protection, mineral storage, haemopoiesis.

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3
Q

What is the composition of the bone matrix?

A
  • It is 65% inorganic (calcium phosphate, calcium carbonate etc)
  • it is 35% organic (collagen, water, 2% non collagen)
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4
Q

What causes bone to be hard?

A

Hardness and rigidity is due to interaction between inorganic salts and collagen. Flexibility is due to collagen.

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5
Q

Where are the calcium and phosphate stored?

A

Either in matrix or released into blood to maintain proper level

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6
Q

What is the effect of parathyroid hormone on bone?

A

Parathyroid hormone stimulates the osteoclasts to break down bone matrix leading to calcium in the blood. When blood calcium levels are higher than normal calcitonin is released, which inhibits osteoclast activity and decreases bone reabsorption.

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7
Q

Which type of cells do osteogenitor cells become?

A

Osteoblasts

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8
Q

What is the function of osteoblasts?

A

They synthesise organic components of cells making bone. They produce osteoid matrix.

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9
Q

What is the function of osteocytes and where are they found?

A

They’re found embedded within lacunae cavities. They are entombed osteoblasts. They maintain the bone matrix.

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10
Q

What are osteoclasts?

A

They are large multinucleated cells, formed from monocytes, that digest bone

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11
Q

What is the structure of compact bone?

A

Concentric Iamellae with central microvascular (haversian) canal, which communicate via Volkmann’s canals. The Haversian system is a system of interconnecting canals present in compact bone.

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12
Q

What is the structure of spongy bone?

A

It is a meshwork of trabeculae filled in with marrow.

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13
Q

What is the function of red bone marrow?

A

Red blood cell synthesis

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14
Q

What is the function of yellow bone marrow?

A

Contains adipose tissue

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15
Q

What is the marrow lined with?

A

Endosteum

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16
Q

What is the primary microstructure of bone?

A

It is woven/immature born that will eventually be replaced by mature bone. Collagen fibres arranged randomly. More cells and less minerals

17
Q

What is the secondary microstructure of bone?

A

Series of Haversian systems consisting of concentric lamellae of bone laid around central canal containing blood vessels. Spaces between haversian systems are interstitial lamellae and whole bone surrounded by circumferential lamellae

18
Q

Which types of bones are formed via endochondral ossification?

A

Long bones

19
Q

Which types of bones are formed via intramembranous ossification?

A

Flat bones develop by intramembranous ossification, examples being:

  • skull bones
  • maxilla
  • mandible
  • pelvis
  • clavicle
20
Q

Describe the condition of Osteogenesis Imperfecta

A
  • Autosomal Dominant disease resulting in type 1 collagen deformity/deficiency, major component in ground substance of bone.
  • Brittle bone disease
  • Most severe case leads to no conversion of feotal (hyaline) skeleton, incompatible with life. In most cases, repeated fractures lead to bowed long bones.
  • Blue sclera due to unknown cause, possibly thinning of cornea due to issues with collagen that forms it.
21
Q

Describe the condition of Rickets disease

A
  • Deficiency in vitamin D
  • less absorption of Ca2+ by small bowel -> less rigid bones. -bowed bones in children as they’re still growing.
  • more common in dark skinned people as fair skin synthesises vit D better than dark skin.
22
Q

Describe the condition of osteoporosis

A

Type 1 (menopausal) due to oestrogen no longer mediating osteoclast function – 2x more likely to fracture hip and 8x more likely to fracture vertebrae.

Type 2 (old age) due to loss of osteoblast function – no remodelling. Both due to clast > blast action.

Bone density decreases to the point of fracture risk. Medullar canals in centre of bone become enlarged and gaps develop in lamellae.

23
Q

Describe the condition of osteomalasia

A
  • Deficiency in vitamin D
  • less absorption of Ca2+ by small bowel -> less rigid bones.
  • bone/back ache, and can be secondary to impaired hepatic/renal function (less absorption).
  • more common in dark skinned people as fair skin synthesises vit D better than dark skin.
24
Q

What is the relavance of Vitamin D to bone development?

A
  • precursor for calcitriol
  • D3 absorbed from sunlight
  • essential for calcium and phosphate absorption in small intestine
  • in its absence, unclassified matrix is formed
  • osteoblasts don’t become osteoclasts
25
Q

Describe the condition of achondroplasia

A

-congenital, often hereditary skeletal disorder

  • few cells in proliferating zone of end plate
  • hypertrophic cartilage cells form irregular columns,
  • results in small zone of provisionally calcified cartilage meaning there isn’t adequate scaffolding for bone matrix deposition by osteoblasts
26
Q

Describe the role of Growth Hormone in bone development

A
  • Lack of GH affects epiphyseal cartilage causing pituitary dwarfism
  • Excess GH causes gigantism
  • in adults too much GH leads to increase in bone width from intramembranous growth (periosteal), big jaw (adults) – epiphyseal plates fuse end of puberty so no lengthening.
27
Q

Describe the role of sex hormones in bone development

A
  • they influence timing and development of ossification centres
  • precocious sexual development (due to tumour for example) retard body growth because of premature closure of epiphyses
  • thyroid hormone deficiency leads to cretinism
28
Q

Describe the role of growth plates in growing bones past the embryonic stage

A
  • The plate’s chondrocytes are under constant division by mitosis. These daughter cells stack facing the epiphysis while the older cells are pushed towards the diaphysis. As the older chondrocytes degenerate, osteoblasts ossify the remains to form new bone.
  • In puberty increasing levels of estrogen, in both females and males, leads to increased apoptosis of chondrocytes in the epiphyseal plate. Depletion of chondrocytes due to apoptosis leads to less ossification and growth slows down and later stops when the entire cartilage have become replaced by bone, leaving only a thin epiphyseal scar which later disappears.