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IHP 1001 > Bone Histology > Flashcards

Bone Histology Flashcards

1
Q

Connective tissue characterized by a mineralized extracellular matrix

A

Bone

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2
Q

What make up the primary mineralization of bone?

A

Hydroxyapotite crystals

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3
Q

What is the primary collagen in bone?

A

Type I collagen fibers

90% of total weight of bone matrix protiens

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4
Q

Also contains
Proteoglycan macromolecules, multiadhesive glycoproteins, Vitamin-K dependent proteins, growth factors; make up small compoenent

A

Bone

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5
Q
  • bone cells, connected via canaliculi.
  • Survive 10-20 years.
  • Important for maintaining overall structure
  • Sense for adaptation
A

Osteocytes

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6
Q

1 cause of morbitiy in ppl over 80 occurs after what?

A

bone breakage, seditary

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7
Q

Excersise places pressure on bones causing ____ to secrete more hydroxyappotite making bones denser and stronger

A

Osteocytes

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8
Q

gives rise to osteoblasts. Respond to markers in ECM, causing htem to differentiaie into osteoblast.

A

Osteoprogenitor cells

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9
Q

Differentiated bone-forming cell which secretes bone matrix (osteoid matrix)

A

Osteoblasts

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10
Q

Osteoblasts fo to where the Bone matrix is produced and secretes a _____

A

Osteoid matrix

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11
Q

Consist of collagen, glycoproteins etc

A

Osteoid matrix secreted by osteoblasts

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12
Q

Once osteoid matrix is down, ____ is secreted and traps osteoblast in matrix converting them to ___

A

Hydroxyapotitie, converting to osteocytes

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13
Q
  • found on bone surface, derived from osteoblasts.
  • Provide a foundation of cells that can quicly differentiate into osteoblasts.
  • Bones always under stress microfractures, these cell fix these
A

Bone lining Cells

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14
Q
  • resorb bone they are specialized with enzyme TRAP
A

Osteoclasts

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15
Q

What is the physiological marker of osteoclasts?

A

Enzyme TRAP

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16
Q

How do osteoclast function?

A
  1. Seal themselves on bone surface
  2. Clear zone on edge
  3. Ruffle zone in center, acid released to break down HA, and TRAP breaks down the rest of the EC components.
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17
Q

two types of bone

A
  1. Compact (dense)
  2. Spongey (cancellous
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18
Q

4 classifications of bone

A
  1. Long (femur)
  2. Short (carpals)
  3. Flat (hip)
  4. Irregular (vertebrae)
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19
Q

Explain three parts of long bone

A
  1. Diaphysis; main shaft
  2. Metaphysis on middle end
  3. Epiphysis; on either end lined with articular cartilage to reduce friction.
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20
Q

what part of long bone is cut off with joing replacments?

A

Metaphysis cut off and replaced with prosthetic

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21
Q

the outer covering of bones

A

Periosteum

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22
Q

articulating surfaces – then covering is ____; reduce fricion

A

cartilage

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23
Q

the main component of the periosteum in non-growing bones

A

Fibrous Layer

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24
Q
  • may become osteoblasts with appropriate stimulus
  • Important with repair, major break, disrupt periosteal layer, they can differentiatin into osteoblast. Bone producton
A

Periosteal Cells

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25
Q

In long bones, the bone cavites are line with ____ which contains ___ cells

A

Endosteum, osteoprogenitor cells

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26
Q

What marrow?

blood producing
Contains blood cells in different stages of development

A

red marrow cavity

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27
Q

What marrow?

found in adults, mostly fat cells
Can revert to blood producing in cases of extreme blood loss (trauma)

A

Yellow marrow cavity

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28
Q

organized in concentric lamina called ____ (nerve, artery, vein)

A

osteon

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29
Q
  • Perpendicular to long axis
  • Channal where blood vessle and nerve travel through
  • Connect to haversian canal
  • Metabolic transfer in/out
  • Growth factors in
  • Calcium control with blood
A

Volkmann Canals

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30
Q
  • parallel with long axis to bone
  • Connected to inner and outer surfaces
A

Haverisian Canal

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31
Q

Where do the nutrient diaphyseal and epiphyseal arteries arise from?

A

arise from the periosteal buds

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32
Q

Where do the nutrient metaphyseal arterry arise from?

A

From periosteal vessels during bone widening

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33
Q

Lymphatic drainage only occurs from the ___

A

Only in the periosteum

No lymphatic vessels in bone tissues

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34
Q
  • Not organized – nonlamellar
  • More cells per unit area than mature
  • Random arrangement
  • More ground substance
A

Immature bone

During development & repair x4

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35
Q

?

A

**Immature bone **
*lack of mineralization

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36
Q

?

A

**Mature bone **
*extensive secondary mineralization, organized

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37
Q

Derived from Mesenchymal stem cells
Can differentiate into many cell types: fibroblasts, osteoblasts, chondrocytes, muscle cells

A

Osteprogenitor cells

Located on internal and external bone surfaces

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38
Q

Osteoblast are responsible for what?

A

Calcification of the bone matric

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39
Q

How to osteoblast communicate?

A

Via gap junctions through canaliculi

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40
Q

How do osteocytes connect to one another?

A

Canaliculi

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41
Q

Mature bone cell enclosed in bone matrix occupying the lacuna

A

Osteocytes

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42
Q

Osteocytes respond to what?

A

Mechanical forces via mechanotransduction

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43
Q

Mechanotransduction in osteocytes with cause what?

A

Bone remodeling in response to pressure changes

44
Q

Derived from osteoblast, cover non-remodeling bone surfaces

A

Bone lining cells

45
Q

what cells?

External bone surfaces

A

Periosteal cells

46
Q

What cells?

Internal bone surfaes

A

Endosteal cells

47
Q

Large multinucleated cellss responsible for bone resorbtion

A

Osteoclasts

47
Q

what forms as a result of osteoclast activity?

A

Howship Lacuna
Resorbtion bay

48
Q

What is the purpoe of enzyme Tartrate-resistant acid phosphatase (TRAP)

A

Primary enzyme of bone resorbtion and organic digestion.

acids digest inorganic element

49
Q

What cells are osteoclast derived from?

A

Mononuclear hematopoetic progenitor cells

50
Q

What receptor is found in immature inactive osteoclasts?

A

RANK

51
Q

Explain osteoclast activation

A
  1. RANK receptor on immature oseoclasts
  2. RankLigand comes and binds
  3. Activates NF-KB
  4. Differentiates to mature osteoclasts and commences resorbtion
52
Q

RANK activation can be blocked how?

A

Osteoprotegerin which binds RANK and blocks RL from binding and activating

53
Q

Osteoclast activation depends on amount of what?

A

Amount of RANKL and Osteoprotegerin

54
Q

Treatment of osteoperosis?

A

Use OPG to prevent activation of osteoclasrs, less destructuin

55
Q

Osteoclast bone resorbtion

increases surface area and increases efficiency of enzyme release and bone resorption

A

Ruffle boarder of cell

56
Q

Edge of osteoclast, area of attachment to site being resorbed.

Targeted, controlled digestion

A

Clear Zone

sealing zone

57
Q

Inflammation of joints

A

Arthritis

58
Q

characterized by progressive loss of normal bone density accompanied by the deterioration of its microarchitecture.

A

Osteoperosis

59
Q

Occurs in post menopausal women, occurs earlier in life so long term effect is more severe.

A

Type 1 osteoperosis

60
Q
  • occurs in the 7th - 8th decade of life
  • Leading cause of serious morbidity and functional loss in the elderly
  • Due to loss of osteoblastic activity with age.
A

Type 2 osteoperosis

61
Q

result of drug therapy (corticosteroids)or disease process (malnutrition, immobilization, weightlessness, hyperparathyroidism, cancer)

A

Secondary Osteoperosis

62
Q

What is first line Tx of osteoporosis

A
  • Supplement with VitD & Calcium
  • Excersive to increse pressure on bone
63
Q

What is 2nd line Tx for osteoporosis ?

A

Pharmacologic therapy

64
Q
  • For postmenopausal women (estrogen and progesterone)
  • Increase of risk of CVD, blood clots, breast cancer
A

HRT tx of osteoporosis

65
Q

** inhibit osteoclastic activity**
* oral vs IV can have increase in osteonecrosis of the jaw following tooth extraction

A

Bisphosphates

66
Q

neutralizes RANKL;
* inhibit osteoclastic acivity act like OPG and block!

A

Monoclonal antibody therapy (Denosumab)

67
Q

Osteoclast Function Regulation

What does parathyroid hormone do?
(PTH)

A

Indirect effect, stimulates RankL production in lymphocytes and osteoblast.

More osteoclast act.
* increases blood calcium levels

68
Q

Osteoclast Function Regulation

What does Calcitonin do?

A

Reduce osteoclastic activity
* decreases blood calcium levels

69
Q

look

A

look

70
Q

look

A
71
Q

requires Cartilage model precursor

A

Endochondral Ossification

72
Q

No cartilage model precursor

A

Intramembranous ossification

73
Q

Expain intramembranous ossification

A
  1. Increased vascularity
  2. Mesenchymal cells condens
  3. Differentiation into osteogenic cells and then osteoblasts
  4. Osteoblasts deposit osteoid
  5. Osteoblasts become surrounded (now osteocytes)
  6. Osteoid calcifies into spicules forming trabeculae
  7. Salts deposited as HA with cartilage fibers
  8. Periostieum & compact bone ofrmed
74
Q

As condensationof bone occurs what penetrates?

A

Nutrient vessles

75
Q

Explain Endochondra ossification

within 1 year of birth

A
  1. Start with** hyaline cartilage** model in shape of bone
  2. Form primary ossification center
  3. Enlargement of chondrocytes reults in increase length at epiphyseal plate
  4. Secondary oss. centers establish
76
Q

Endochondra ossificationn

Increase in length is attributed to interstitial growth of ____, forces to either end.

A

chondorocytes

77
Q

Endochondra ossificationn

Increase in width result of addition of ____ on outside.

A

cartilage matrix

78
Q

By the late teens to early 20s, all remaining ____ in the epiphyseal plate is generally consumed

A

cartilage
* Gap btwn epihysease and diaphysis closes
* primary & secondary marro cavities unite
* bone can no longer grow in lenght

79
Q

Excess of growth hormone before closure of epiphyseal plate

A

Gigantism

80
Q

Once epiphyseal plate closes, lots of growth hormone

A

Acromegaly, bones expand in width.

Jaws, fingers, larger.

81
Q

what are the 5 zones of epiphyseal cartilage?

A
  1. Reserve Cartilage
  2. Proliferation
  3. Hypertrophy
  4. Calcified cartilage
  5. Resorption
82
Q

zone where# of chondrocyes increases vastly

A

Zone of proliferation

83
Q

zone where chrondrocytes grow in size

A

Zone of hypertrophy

84
Q

What two cartilage zones are where length of bones originates from?

A
  1. Zone of proliferation
  2. Zone of hypertrophy
85
Q

Zone is where calcification of cartilage occurs, bone is still weak, 1st step in formation of dense bone

A

Zone of calcified cartilage

86
Q

Zone where you have turnover, resorb of calcified cartilage by osteoclast that ends depostion of dense bone by osteoblast

A

Zone of resorbtion

equals zone of proliferation

87
Q

Zone where you havr restin halyine cartilage

A

Zone of reserved cartilage

88
Q
A
89
Q

Responsible for maintaining growth process

A

Epiphyseal growth plate

Thickness constant until maturity then it shrinks

90
Q

Resorbed cartilage is replaced with ____

A

spongy bone

91
Q
  • Cutting cone (osteoclast)
  • Closing cone (osteoblasts)
A

Bone remodeling unit

92
Q

How is the bone remodeling unit initiatted?

A
  • Microcrack
  • Osteocytes signal
  • Locak hormones and GF released
93
Q

What are the 3 phases of active bone remodeling unit

A
  1. Cellular actication (recurited at cutting edge)
  2. Resorbtion
  3. Formation and mineralization
94
Q

Active Bone-Remodeling Unit

Osteovclasts are active for 12 days and then die, what cleans them?
* death releases IGF, FGF, which recruits what?

A

PMNL
recruits osteoblasts

95
Q

Active Bone-Remodeling Unit

Osetoid is formed by ____ mineralization begins ____ days later until eroded volume is filled

A

Formed by osteoblast, mindelization 13 days after, takes uo to 3 months

96
Q

produced by osteoblasts
Regulates energy and glucose metabolism through effects on adipocytes and the pancreas

A

Osteocalcin

97
Q

bone matrix does not calcify normally
* Insufficient calcium or Vitamin D
* Results in short stature and skeletal deformities (major is bow legged)

A

Rickets

98
Q

insufficient calcium or vitamin D in adults typically due to improper resorption and malnutrition.

A

Osteomalacia

99
Q

Lack of vitamin C it reduces calcification due to collagen synthesis errors catalyzes hydroxylincine
* VitC is not addition of hydroxylicine bad collage synth bad calcification.

A

Scurvy

100
Q

suppresses endochondral bone growth
* Fragility and fractures of long bones

A

Vitamin A deficiency

101
Q

fractured bone is surgically stabilized (screws/ rods)
* Bone undergoes internal remodeling like that of mature bone

A

Direct primary bone healing

102
Q

responses to signals from the periosteum and surrounding soft tissues
* Fractures are treated with nonrigid or semirigid bone fixation; bone respond to changes in pressure.

A

Indirect secondary bone healing

103
Q

Summary of bone healing

6-12 week process

A
  1. Disruption of blood supply due to** trauma,** etc
  2. Blood clot stimulates formation of soft callus (fibrocartilage scaffold) (2-3 weeks post fx)
  3. Granulation tissue form
  4. Inflammatory response(weak immune system inhibit formation of soft callus) (1 week)
  5. Osteoblast come in and deposite bone on soft callus to est. spongey bone; hard callus (3-4 months)
  6. Months later, spongey bone replaced with compact bone, **osteocyte network rest. **
104
Q

What helps expidite bone healing process?

A

Setting bone!

IHP 1001 (18 decks)

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