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OSR basic science Flashcards

1
Q

From which cells do osteoblasts arise?

A

Undifferentiated mesenchymal stem cells (MSCs)

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2
Q

What seven growth factors influence osteoblast differentiation?

A

Interleukins (ILs); Insulin-like growth factor (IGF-I); Platelet-derived growth factor (PDGF); Bone morphogenic proteins (BMPs); Transforming growth factor-_ (TGF-_); Osterix; Runx 2 (formerly Cbfa 1)

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3
Q

What is the function of IGF?

A

Osteosynthesis

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4
Q

Through what intracellular signaling pathway does it work?

A

Tyrosine kinase

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5
Q

What is the function of PDGF?

A

Chemotaxis

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6
Q

Through what intracellular signaling pathway does it work?

A

Tyrosine kinase

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7
Q

What is the function of BMP?

A

Stimulates mesenchymal cell differentiation

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8
Q

Through what intracellular signaling pathway does it work?

A

Serine/threonine kinase through SMAD proteins

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9
Q

Is BMP osteoinductive or osteoconductive?

A

Osteoinductive

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10
Q

TGF-b stimulates mesenchymal cells to produce what two substances?

A

Type II collagen; Proteoglycans

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11
Q

TGF-b also indirectly stimulates osteoblasts to produce what?

A

Type I collagen

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12
Q

Through what intracellular signaling pathway does it work?

A

Serine/threonine kinase

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13
Q

What four substances do osteoblasts produce?

A

Alkaline phosphate; Type I collagen; Osteocalcin; RANK ligand

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14
Q

Osteoblasts respond directly to what five factors?

A

Parathyroid hormone (PTH); Glucocorticoids; Prostaglandins; 1,25-vitamin D; Estrogen

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15
Q

Which two of these favor osteogenesis?

A

1,25-vitamin D; Estrogen

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16
Q

Which three favor resorption?

A

PTH (resorption releases calcium); Glucocorticoids; Prostaglandins

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17
Q

What two factors upregulate adenylate cyclase at the cellular level?

A

PTH; Prostaglandins

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18
Q

What factor downregulates adenylate cyclase?

A

Estrogen

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19
Q

What factor also decreases calcium absorption at the level of the gut?

A

Glucocorticoids

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20
Q

From what cells do osteoclasts arise?

A

Monocyte progenitors

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21
Q

How do osteoclasts bind to the surface of bone?

A

With integrins (vibronectin)

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22
Q

Where does resorption occur?

A

Howship’s lacunae

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23
Q

What are the two products of osteoclasts?

A

Hydrogen ions (through carbonic anhydrase); Tartrate resistant acid phosphatase

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24
Q

What do osteoclasts respond directly to?

A

Calcitonin

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25
Q

What is the effect of calcitonin on the osteoclast?

A

Inhibits osteoclast function

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26
Q

What is the effect of IL-1?

A

Stimulates osteoclast function

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27
Q

What is the effect of IL-10?

A

Inhibits osteoclast function

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28
Q

What is the effect of IL-11?

A

Increases production of RANK ligand

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29
Q

What is the function of RANK ligand?

A

Links osteoblast and osteoclast function

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30
Q

What cell contains RANK ligand?

A

Osteoblast

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31
Q

How does RANK ligand work?

A

Binds to and stimulates osteoclasts

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32
Q

What cofactor is required?

A

Macrophage colony-stimulating factor (M-CSF)

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33
Q

What inhibits the RANK stimulation of osteoclasts?

A

Osteoprotegerin

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34
Q

How?

A

Blocks RANK binding to the osteoclast, competitive inhibition

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35
Q

If considering estrogen replacement therapy, when should it be started for maximal benefit?

A

Within 5 to 10 years of menopause

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36
Q

Generally speaking, how does estrogen work?

A

Decreases both bony resorption and formation; But resorption is decreased much more than formation

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37
Q

What are two pharmacologic alternatives to estrogen therapy?

A

Alendronate; Raloxifene

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38
Q

What are osteocytes stimulated by?

A

Calcitonin

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39
Q

What are osteocytes inhibited by?

A

PTH

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40
Q

How does mechanical stimulation work?

A

Increases prostaglandin E2”_production (stimulus)

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41
Q

How are osteons connected to one another?

A

By haversian canals

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42
Q

What are the extensive networks of osteonal processes that allow communication?

A

Canaliculi

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43
Q

What is the outer osteonal border called?

A

Cement line

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44
Q

What lies in between osteons?

A

Interstitial lamellae

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45
Q

What is the principal organic component of bone?

A

Type I collagen

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46
Q

What is the composition of a collagen fibril?

A

Two _1”_chains; Two _2”_chains

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47
Q

How is collagen secreted?

A

Secreted as procollagen

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48
Q

Then what happens?

A

Cross-linked after secretion

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49
Q

What is the difference between a hole and a pore?

A

Holes are the spaces between the ends of collagen molecules; Pores are the spaces between the sides of the collagen molecules

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50
Q

What are the three noncollagenous matrix proteins of bone?

A

Osteocalcin; Osteonectin; Osteopontin

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51
Q

What stimulates osteocalcin production?

A

1,25-vitamin D

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52
Q

What inhibits osteocalcin production?

A

PTH

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53
Q

Osteocalcin attracts what cell type?

A

Osteoclasts

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54
Q

What are osteocalcin levels a marker of?

A

Bone metabolism

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55
Q

Bone mineralization consists of what two processes? What are the key features of each?

A

Initiation (sialoproteins, pores, high-energy requirement); Growth (osteocalcin, coalescing areas of mineralization)

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56
Q

What are the three laboratory markers of bone resorption?

A

Urinary hydroxyproline; Urinary pyridoline; N-telopeptide

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57
Q

What are the laboratory markers of bone formation?

A

Alkaline phosphate

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58
Q

Normal mature bone is of what type?

A

Lamellar

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59
Q

What is the defining characteristic of lamellar bone?

A

Remodeled along lines of stress

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60
Q

What are the two subtypes of lamellar bone?

A

Cortical; Cancellous

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61
Q

In contrast, immature or pathologic bone is of what type?

A

Woven

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62
Q

Bone is strongest in what direction? Weakest in what direction?

A

Strongest in compression; Weakest in shear

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63
Q

When bone is under torsion, where is the greatest load experienced?

A

Maximum load experienced at 45 degrees to the long axis of the bone

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64
Q

What is the basic premise of Wolff’s law?

A

Increased stress leads to increased bone formation

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65
Q

Piezoelectric charges: is compression electropositive or negative?

A

Compression results in a negative charge

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66
Q

The negative charge then leads to what process?

A

Bone formation

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67
Q

Is tension electropositive or negative?

A

Positive charge

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68
Q

What does the positive charge lead to?

A

Bone resorption

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69
Q

What is the Heuter-Volkmann law? Give an example of where this law applies.

A

Compression inhibits growth; Tension stimulates growth; Example: scoliosis

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70
Q

At what age is peak bone mass achieved?

A

End of the third decade of life (the 20s)

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71
Q

What is the annual rate of bone loss after peak?

A

0.3 to 0.5% per year

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72
Q

What is the annual rate of bone loss after menopause, without treatment?

A

2 to 3% per year for 6 to 10 years after menopause

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73
Q

Is the observed postmenopausal decline simply estrogen related?

A

Not just estrogen, but changes in calcium metabolism also; Decreased intestinal calcium absorption; Increased calcium losses

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74
Q

Is the nutrient system high or low pressure?

A

High pressure

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75
Q

What does it supply?

A

Inner two thirds of bone

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76
Q

Is the periosteal system high or low pressure?

A

Low pressure

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77
Q

What does it supply?

A

Outer one third of bone

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78
Q

In what direction does blood flow in the adult?

A

Nutrient to periosteal

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79
Q

In what direction does blood flow in immature bone?

A

Opposite direction of flow

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80
Q

What is the principal determinant of fracture healing?

A

Blood supply

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81
Q

What are the three components of the sequence of changes in blood supply after fracture?

A

Immediate decrease in blood supply; Increased vascularity (maximal at 2 weeks); Return to normal by 3 to 5 months

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82
Q

What is the effect of reaming?

A

Destroys endosteal blood supply

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83
Q

What are the three effects of nicotine on fracture healing?

A

Increased time to fracture healing; Increased risk of nonunion; Decreased fracture callus strength

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84
Q

Nicotine use is associated with increased risk of fractures at which locations?

A

Increases risk of wrist and hip fractures

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85
Q

How does smoking affect lumbar fusion rates?

A

Increases the pseudarthrosis rate of lumbar fusion by 500%

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86
Q

What is the two-step sequence of callus types formed after fracture?

A

Bridging (soft) callus within 2 weeks; Replaced by woven bone (hard callus)

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87
Q

Callus is ultimately remodeled over what period?

A

Remodeled to lamellar bone within 7 years

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88
Q

What two types of bone formation are seen with cast treatment of fracture?

A

Periosteal bridging callus; Enchondral ossification

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89
Q

Is there any difference with intramedullary (IM) nail treatment?

A

IM nail treatment also results in medullary callus formation late

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90
Q

Under what two conditions can intramembranous bone formation (no cartilage precursor) be seen after fracture?

A

Low strain; High oxygen tension

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91
Q

What type of chondrocytes are present in the first 10 days after fracture?

A

Proliferative chondrocytes

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92
Q

What collagen type do they produce?

A

Type II

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93
Q

What other collagen type is present in the chondroid phase?

A

Type IX: cross-linking function

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94
Q

After 14 days, what chondrocyte type is present?

A

Hypertrophic chondrocytes

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95
Q

What type of collagen do they produce?

A

Type X

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96
Q

What are the next three steps?

A

Calcification; Osteoclasts resorb matrix; Osteoblasts lay down new bone

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97
Q

How do hypertrophic nonunions heal?

A

Mineralization of fibrocartilage

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98
Q

What other treatment modality has a similar mechanism?

A

Pulsed electromagnetic field treatment (bone stimulator)

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99
Q

Rate the four tissue types from highest to lowest strain tolerances?

A

Granulation tissue (100% strain tolerance); Fibrous tissue; Cartilage; Bone

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100
Q

At what phase of fracture healing does direct current exert an effect?

A

Inflammatory-response phase

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101
Q

At what phase of fracture healing does alternating current exert an effect?

A

Repair phase (callus)

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102
Q

What is the effect of pulsed electromagnetic fields?

A

Initiates fibrocartilage calcification

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103
Q

What is the classic application of this technology?

A

Nonhealing pseudo-Jones fracture

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104
Q

What are the two benefits of pulsed low-intensity ultrasound?

A

Accelerated fracture healing; Increased callus strength

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105
Q

What are the two detrimental effects of radiation?

A

Decreased cellularity; Decreased callus strength

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106
Q

How long should the latency phase last?

A

5 to 7 days

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107
Q

What is the desired rate of distraction during distraction phase?

A

1 mm/day

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108
Q

What is the duration of the consolidation phase?

A

Twice as long as the distraction phase

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109
Q

What is the weight-bearing status throughout treatment?

A

Weight-bearing as tolerated (WBAT)

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110
Q

What changes are seen in blood vessels?

A

Proliferation of vasa vasorum

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111
Q

What is the oxygen tension with distraction osteogenesis?

A

High oxygen tension

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112
Q

So what type of bone formation is seen under these low-strain, high oxygen tension conditions?

A

Intramembranous bone formation (no cartilage precursor)

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113
Q

What is the daily calcium intake recommendation for healthy children and adults?

A

750 mg

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114
Q

What is the daily calcium intake recommendation for teenagers, pregnant women, and individuals with healing fractures?

A

1500 mg

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115
Q

What is the daily calcium intake recommendation for lactating mothers?

A

2000 mg

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116
Q

What is the mechanism of calcium absorption in the duodenum?

A

Active transport

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117
Q

What is the mechanism of calcium absorption in the jejunum?

A

Passive diffusion

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118
Q

What is the mechanism of calcium absorption in the kidney?

A

Proximal tubular resorption

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119
Q

What percentage of total body calcium is within plasma?

A

1.00%

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120
Q

What are the relative proportions of bound vs. unbound plasma calcium?

A

Bound = unbound

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121
Q

What are the two principal regulators of plasma calcium concentration?

A

PTH; 1,25-vitamin D

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122
Q

What are the relative proportions of bound vs. unbound plasma phosphate?

A

Unbound predominates

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123
Q

What is the principal site of phosphate resorption within the kidney?

A

Proximal tubule

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124
Q

What type of molecule is parathyroid hormone (PTH)?

A

Peptide

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125
Q

Where is PTH produced?

A

Chief cells of the parathyroid gland

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126
Q

What is the stimulus for release of PTH?

A

Low plasma calcium concentration

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127
Q

What receptor detects calcium concentration?

A

Calcium sensing receptor (CaSR)

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128
Q

In what organ and gland can this receptor be found?

A

Kidney; Parathyroid gland

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129
Q

What type of receptor is CaSR?

A

G-protein-coupled receptor

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130
Q

What are the three effects of CaSR activation within the parathyroid gland?

A

PTH secretion; PTH gene expression; Cellular proliferation

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131
Q

In what organ and in what cells can PTH receptors be found?

A

Kidney; Osteoblasts

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132
Q

What are PTH’s two actions on the kidney?

A

Increase 1,25-vitamin D production; Decrease resorption of renal phosphate

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133
Q

What are PTH’s three actions on the bone?

A

Stimulate osteoblasts; Osteoblasts produce RANK ligand; RANK ligand stimulates osteoclasts

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134
Q

What is the net effect of PTH on plasma calcium and phosphate concentrations?

A

Increased plasma calcium; Decreased plasma phosphate

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135
Q

What type of molecule is 1,25-vitamin D?

A

Steroid

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136
Q

As vitamin D is activated to 1,25-vitamin D, what are the two sites of hydroxylation?

A

First: liver; Second: kidney

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137
Q

What are the three stimuli for release of 1,25-vitamin D?

A

Low serum calcium concentration; Low serum phosphate concentration; Elevated PTH levels

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138
Q

What are the two effects of 1,25-vitamin D?

A

Increased intestinal absorption of calcium and phosphate; Increased osteoclast activity

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139
Q

What is the net effect of 1,25-vitamin D on plasma calcium and phosphate concentrations?

A

Increased plasma calcium; Increased plasma phosphate

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140
Q

What type of molecule is calcitonin?

A

Peptide

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141
Q

Where is calcitonin produced?

A

Clear cells (parafollicular cells) of the thyroid gland

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142
Q

What is the stimulus for release of calcitonin?

A

Elevated serum calcium

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143
Q

What is the effect of calcitonin?

A

Inhibits osteoclast activity

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144
Q

What is a common cause of primary hyperparathyroidism?

A

Adenoma of one parathyroid gland

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145
Q

If four glands are affected, what diagnosis must be considered?

A

Multiple endocrine neoplasia (MEN) syndrome

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146
Q

What is the effect of primary hyperparathyroidism on 1,25-vitamin D levels?

A

Increased 1,25-vitamin D

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147
Q

What is the effect of primary hyperparathyroidism on serum calcium concentration?

A

Increased serum calcium

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148
Q

What is the effect of primary hyperparathyroidism on serum phosphate concentration?

A

Decreased serum phosphate

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149
Q

What is the hydration status of hypercalcemic patients?

A

Generally dehydrated as hypercalcemia leads to polyuria

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150
Q

What is osteitis fibrosa cystica?

A

Resorption of bone due to PTH overactivity and replacement with fibrous tissue

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151
Q

What are the two characteristic histologic features of brown tumors?

A

Giant cells; Hemosiderin

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152
Q

What are the other systemic effects of hypercalcemia?

A

Renal stones; Psychiatric disorders; Abdominal pain

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153
Q

What are the four available hypercalcemia treatment methods?

A

Saline hydration; Loop diuretics; Dialysis; Mobilization

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154
Q

What is the most common cause of hypoparathyroidism?

A

Iatrogenic

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155
Q

What is the effect on serum calcium concentration?

A

Decreased serum calcium

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156
Q

What is the effect on serum phosphate concentration?

A

Increased serum phosphate (because low PTH levels)

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157
Q

What is the effect on 1,25-vitamin D levels?

A

Decreased 1,25-vitamin D

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158
Q

What is the characteristic radiographic finding on skull films?

A

Calcification of the basal ganglia

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159
Q

What is the cause of pseudohypoparathyroidism?

A

No PTH effect at target cells

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160
Q

Inheritance?

A

X-linked dominant (XLD)

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161
Q

Quick review: what other disorder has a similar inheritance pattern?

A

Hypophosphatemic rickets

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162
Q

What gene is involved?

A

GNAS1

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163
Q

Mutation?

A

G_ subunit

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164
Q

Quick review: in what two other clinical situations do G-proteins play a vital role?

A

Fibrous dysplasia; CaSR function

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165
Q

What is the PTH level in pseudohypoparathyroidism?

A

Normal or high

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166
Q

What is the serum calcium concentration?

A

Low serum calcium

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167
Q

What is the serum phosphate concentration?

A

Elevated serum phosphate (again, no PTH effect)

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168
Q

What is the effect on 1,25-vitamin D levels?

A

Low 1,25-vitamin D

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169
Q

Give an example of a disorder associated with pseudohypoparathyroidism?

A

Albright syndrome

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170
Q

What are the four characteristic features of pseudohypoparathyroidism?

A

Short metacarpals; Bony exostoses; Obesity; Mental retardation

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171
Q

Quick review: what is another disorder that is associated with obesity and mental retardation?

A

Prader-Willi

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172
Q

Pseudopseudohypoparathyroidism is phenotypically similar to what?

A

Pseudohypoparathyroidism

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173
Q

What is the serum calcium concentration?

A

Normal

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174
Q

What is the target cell response to PTH?

A

Normal

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175
Q

What are the two general types of renal failure osteodystrophy?

A

High turnover; Low turnover (excess aluminum leads to decreased metabolic activity)

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176
Q

With the high turnover type, what is the serum phosphate level?

A

Elevated due to renal failure/inability to dump phosphate

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177
Q

_ the serum calcium level?

A

Low because with elevated phosphate, calcium precipitates out of solution

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178
Q

_ the PTH level?

A

Elevated, because high phosphate levels lead to secondary hyperparathyroidism

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179
Q

What are the two components of the treatment for high turnover renal osteodystrophy?

A

Phosphate binders (antacids); Activated oral vitamin D

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180
Q

With the low turnover type, what is the serum calcium level?

A

Normal

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181
Q

_ the serum phosphate level?

A

Normal

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182
Q

_ the PTH level?

A

Low

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183
Q

_ the 1,25-vitamin D level?

A

Low because of impaired renal hydroxylase

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184
Q

With renal osteodystrophy, what is the clinical appearance of the spine?

A

Rugger jersey spine

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185
Q

What other disorder also exhibits a rugger jersey spine?

A

Osteopetrosis

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186
Q

What other generalized bony changes are present?

A

Osteitis fibrosa cystica due to secondary hypoparathyroidism

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187
Q

Chronic dialysis treatment also leads to what disorder?

A

Amyloidosis

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188
Q

With renal tubular acidosis, what two ions are lost in the urine?

A

Sodium; Calcium

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189
Q

What is the key lab value for diagnosis?

A

Urine calcium > serum calcium

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190
Q

What is the treatment of renal tubular acidosis?

A

Alkalinize the urine

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191
Q

Renal tubular acidosis is phenotypically similar to what disorder?

A

Rickets

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192
Q

Quick review: What are three other situations in which calcium losses can exceed intake?

A

Postmenopausal woman (increased urine calcium, decreased absorption); Elevated glucocorticoids (increased urine calcium); Osteogenic rickets (fibroblast growth factor-23 [FGF-23])

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193
Q

What is the suggested daily intake of vitamin D for healthy adults?

A

200 international units (IU)

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194
Q

What is the suggested daily intake of vitamin D for children, pregnant women, and lactating mothers?

A

400 IU

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195
Q

What is the only natural dietary source of vitamin D?

A

Oily fish

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196
Q

What is the serum calcium level with vitamin D deficiency?

A

Decreased (due to decreased absorption)

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197
Q

What is the resulting effect on PTH?

A

Increased (in response to low calcium)

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198
Q

What two clinical features of nutritional rickets are most sensitive and specific?

A

Wrist enlargement; Costochondral enlargement

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199
Q

What is the serum phosphate level?

A

Decreased (due to high PTH)

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200
Q

What does treatment of vitamin D deficiency rickets consist of?

A

5000 IU per day of vitamin D

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201
Q

Deficient calcium intake has what effect on PTH levels?

A

PTH levels become elevated

202
Q

What effect does this have on vitamin D levels?

A

Increases vitamin D levels (attempt to absorb greater amounts of calcium, phosphate)

203
Q

What are serum phosphate levels?

A

May actually be low (due to elevated PTH)

204
Q

What is the treatment of calcium deficiency rickets?

A

750 mg/day of calcium

205
Q

Deficient phosphate intake has what effect on PTH levels?

A

None (PTH responds only to high phosphate)

206
Q

What effect does low serum phosphate have on vitamin D levels?

A

Increases vitamin D levels (attempt to absorb greater amounts of phosphate)

207
Q

What is the treatment of phosphate deficiency rickets?

A

Oral phosphate supplementation

208
Q

Inheritance?

A

Autosomal recessive (AR)

209
Q

Mutation?

A

Defect in renal 1,25-hydroxylase

210
Q

What is the effect of defective hydroxylase?

A

No conversion of inactive vitamin D to active form

211
Q

What is the characteristic clinical feature?

A

Rachitic rosary responsive to vitamin D

212
Q

What is the resulting serum calcium level?

A

Decreased

213
Q

What is the resulting serum phosphate level?

A

Decreased (due to decreased absorption)

214
Q

What is the resulting serum PTH level?

A

Elevated (in response to low calcium)

215
Q

What is the treatment of vitamin D-dependent rickets (VDDR) type I?

A

Oral activated vitamin D

216
Q

Defect?

A

No receptor for 1,25-vitamin D at target cells

217
Q

What is the serum level of 1,25-vitamin D?

A

Very high

218
Q

What is the serum level of active vitamin D in type I?

A

Very low in type I

219
Q

What are the two characteristic clinical features?

A

Alopecia; Rachitic rosary unresponsive to vitamin D therapy

220
Q

What is the treatment of VDDR type II?

A

Vitamin D analogue

221
Q

What is the relative severity of both types of vitamin D dependent rickets vs. nutritional rickets?

A

Vitamin D dependent rickets I and II are more severe

222
Q

What is the relative frequency of hypophosphatemic rickets as a cause of rickets?

A

Most common cause in the United States

223
Q

What is the inheritance?

A

XLD

224
Q

What is the mutation?

A

Impaired renal tubular absorption of phosphate

225
Q

What is the gene?

A

PHEX

226
Q

This disorder is also known as what?

A

Vitamin D resistant rickets

227
Q

What is the serum phosphate level?

A

Low, because a lot of phosphate is lost in the urine

228
Q

What is the resulting PTH level?

A

Normal (no PTH response to low serum phosphate)

229
Q

What is the serum calcium level?

A

Normal

230
Q

What is the classic triad of clinical features?

A

Short child; Lower limb deformities; Low serum phosphate

231
Q

What are the two components of treatment of hypophosphatemic rickets?

A

High-dose phosphate replacement; High-dose vitamin D (to facilitate phosphate absorption)

232
Q

What is the inheritance?

A

AR

233
Q

What is the defect?

A

Enzymatic deficiency leads to low levels of alkaline phosphate

234
Q

Clinical features are similar to what group of disorders?

A

Nutritional rickets

235
Q

How is hypophosphatasia diagnosed?

A

Elevated urinary phosphoethanolamine

236
Q

What is the treatment of hypophosphatasia?

A

No good options exist

237
Q

High-turnover renal osteodystrophy displays clinical features similar to what other disorder?

A

Primary hyperparathyroidism (for example, osteitis fibrosa cystica)

238
Q

The renal osteodystrophy spine has what appearance?

A

Rugger jersey spine

239
Q

This spine appearance is also associated with what other disorder?

A

Osteopetrosis

240
Q

Hypophosphatasia displays clinical features similar to what other disorder?

A

Nutritional rickets

241
Q

The spine has what appearance in hypophosphatasia?

A

Rachitic rosary (like rickets)

242
Q

What are three proposed viral etiologies for Paget’s disease?

A

Respiratory syncytial virus (RSV); Paramyxovirus; Canine distemper virus

243
Q

What is the typical clinical presentation of Paget’s?

A

Bone pain

244
Q

Within a given bone, how does Paget’s progress?

A

Starts at one end and progresses to the other

245
Q

What is the radiographic appearance of progression?

A

Leading lytic flame

246
Q

Laboratory findings include increased levels of what four substances?

A

Alkaline phosphate; Urinary hydroxyproline; Osteocalcin; N-telopeptide

247
Q

What are the three key histologic features?

A

Osteoclasts with viral inclusion bodies (paramyxovirus); Cement lines; Relative osteoblastic or osteoclastic appearance depends on phase of disease

248
Q

What is the treatment of Paget’s disease?

A

Bisphosphonates

249
Q

What other clinical conditions occur secondary to Paget’s disease in the spine?

A

Spinal stenosis

250
Q

What other clinical conditions occur secondary to Paget’s disease in the heart?

A

High output cardiac failure

251
Q

What other clinical conditions occur secondary to Paget’s disease in the auditory system?

A

Deafness

252
Q

What does the new onset of severe pain and swelling in a patient with known Paget’s suggest?

A

Malignant osteosarcoma

253
Q

How often does this occur?

A

In 10% of patients

254
Q

What effect does aging have on stomach acidity?

A

Decreased acidity

255
Q

What effect does the change in acidity have on calcium absorption?

A

Decreased calcium absorption

256
Q

What effect does aging have on vitamin D requirements?

A

Increased vitamin D requirements with age

257
Q

Is osteoporosis a quantitative or qualitative deficiency of bone?

A

Quantitative (not enough bone)

258
Q

What are the common laboratory findings in patients with osteoporosis?

A

Generally normal

259
Q

What is the definition of osteoporosis in terms of T-score?

A

T-score of -2.5 or less

260
Q

What are the two indications for treatment of osteoporosis?

A

T score of -2.5

261
Q

Compare the definitions of T-score and Z-score?

A

T-score is the number of standard deviations away from mean peak bone mass (comparison to 25-year-old population)

262
Q

What two imaging modalities are most commonly used to arrive at a T-score?

A

Dual-energy x-ray absorptiometry (DEXA) scan

263
Q

How much bone must be lost before a change in plain x-ray appearance is evident?

A

30.0%

264
Q

Does a DEXA scan evaluate cancellous and cortical bone individually?

A

No, together

265
Q

Does a quantitative CT scan evaluate cancellous and cortical bone individually?

A

Yes, can separate

266
Q

What is the downside of quantitative CT?

A

Increased radiation

267
Q

What test is the most accurate for determining bone density?

A

Quantitative CT

268
Q

What test is the most reliable for predicting fracture risk?

A

DEXA scan

269
Q

What are the two general types of osteoporosis?

A

Type I: postmenopausal

270
Q

With type I osteoporosis, what type of bone is principally affected?

A

Trabecular bone (cancellous)

271
Q

Give two examples of typical type I fractures?

A

Vertebral body fractures

272
Q

With type II osteoporosis, what type of bone is principally affected?

A

Trabecular and cortical bone

273
Q

Give two examples of typical type II fractures?

A

Hip fracture

274
Q

How do bisphosphonates affect osteoclast microstructure?

A

Disrupt microtubules within the ruffled border

275
Q

How do they disrupt macrostructure?

A

Disrupt protein prenylation

276
Q

What disadvantageous effect do high-dose bisphosphonates have?

A

Disrupt calcium deposition also, not just resorption

277
Q

Over what period of time does the peak bone loss occur?

A

First 16 months after injury

278
Q

After that period of time, how much bone mass remains?

A

Two thirds of the preinjury bone mass

279
Q

What anatomic region is most affected by bone loss?

A

Knee

280
Q

What anatomic region is most spared by bone loss?

A

Skull

281
Q

What are the two products of stem cell division?

A

Another stem cell

282
Q

Why is it desirable to select out stem cells from other cells within grafts?

A

Because the greater the total number of cells, the greater the metabolic needs

283
Q

What is the main advantage of fresh allograft?

A

Contains osteoinductive BMPs

284
Q

What is the main disadvantage?

A

Immunogenic

285
Q

Is fresh allograft osteoconductive or inductive?

A

Both

286
Q

What are the two advantages of fresh frozen allograft?

A

Still contains osteoinductive BMPs

287
Q

Is fresh frozen allograft osteoconductive or inductive?

A

Both

288
Q

What is the main advantage of freeze-dried allograft?

A

Lowest immunogenicity

289
Q

What are the two main disadvantages?

A

Does not contain BMPs

290
Q

How does freeze-dried stiffness and compactability compare to fresh allograft?

A

Same maximal stiffness

291
Q

Based on recent literature, what type of allograft results in superior stem fixation?

A

Freeze-dried has superior stem fixation

292
Q

What does the recent literature on use of freeze-dried allograft in adolescent idiopathic scoliosis surgery indicate?

A

Significantly lowers fusion rates

293
Q

What is demineralized bone matrix?

A

Digested allograft and BMP

294
Q

Is it osteoconductive or inductive?

A

Both

295
Q

What are the three key points to know about BMP mechanism of osteoinductivity?

A

Serine/threonine kinase intracellular signaling pathway

296
Q

What is the main disadvantage of osteochondral allografts?

A

Cartilage is immunogenic

297
Q

How does cryogenic preservation affect chondrocyte number?

A

Very few remain

298
Q

After implantation of osteochondral allograft, what happens to host chondrocytes?

A

Not preserved

299
Q

How long is transplanted cartilage preserved?

A

2 to 3 years

300
Q

What is the histological appearance thereafter?

A

Transplanted cartilage covered by fibrocartilage

301
Q

Bottom line: How does the strength of cortical and cancellous grafts change over time?

A

Cortical grafts are strongest day 1; then resorbed and remodeled

302
Q

What is the two-step sequence of chemical conversion of tricalcium phosphate (TCP)?

A

TCP rapidly broken down

303
Q

Is TCP osteoconductive or inductive?

A

Osteoconductive only

304
Q

Is TCP immunogenic?

A

No

305
Q

What is the ideal ceramic pore size?

A

150 _m

306
Q

What two factors determine the extent of allograft incorporation?

A

Cellularity

307
Q

What cells mediate the immune response?

A

T cells

308
Q

What surface structure on transplanted cells is recognized by host immune cells?

A

Surface glycoprotein

309
Q

Mechanical properties of allograft change at what dose of radiation?

A

3 Mrad

310
Q

What four growth factors act on chondrocytes?

A

IGF-I

311
Q

What is the effect of IGF-I on the chondrocyte?

A

Stimulates matrix production

312
Q

TGF-_ has what three effects on the chondrocyte?

A

Stimulates production of proteoglycans

313
Q

Quick review: what other commonly tested role do Smads have?

A

Facilitate signaling and activity of BMPs

314
Q

What are the two other key points about BMP?

A

Intracellular signaling through serine/ threonine kinase pathway

315
Q

What is the net effect of FGF on chondrocytes?

A

Synthetic

316
Q

PDGF is particularly important in what clinical situation?

A

Osteoarthritis

317
Q

What is the predominant collagen type in articular cartilage?

A

Type II

318
Q

What is the principal function of type II collagen?

A

Provides tensile strength

319
Q

What three other collagen types may also be present in articular cartilage?

A

Type VI

320
Q

Are type VI collagen levels higher with normal aging or with osteoarthritis?

A

Osteoarthritis

321
Q

In what situation are type X collagen levels particularly elevated?

A

During enchondral ossification

322
Q

Type X collagen is produced by what cells?

A

Hypertrophic chondrocytes

323
Q

When does this occur?

A

> 14 days after fracture

324
Q

Type X collagen is generally associated with what process?

A

Calcification of cartilage

325
Q

Type X collagen is deficient in what inherited syndrome?

A

Schmid metaphyseal chondrodysplasia

326
Q

What is the principal function of type XI collagen?

A

Acts as an adhesive holding collagen together

327
Q

What is the principal function of proteoglycans?

A

Provide compressive strength

328
Q

How do they achieve this function?

A

By maintaining water within the matrix

329
Q

What limits the total water content of normal cartilage?

A

The ordered structure of proteoglycan and collagen

330
Q

What are proteoglycan subunits called?

A

Glycosaminoglycans (GAGs)

331
Q

What are three commonly tested GAGs?

A

Chondroitin 4 sulfate

332
Q

What GAG increases most significantly in concentration with normal aging?

A

Keratan sulfate

333
Q

What GAG increases most significantly with osteoarthritis development?

A

Chondroitin 4 sulfate

334
Q

What GAG concentration remains relatively constant despite aging or osteoarthritis?

A

Chondroitin 6 sulfate

335
Q

How are GAGs bound to the protein core?

A

Sugar bonds

336
Q

GAGs and the protein core form what molecules?

A

Aggrecan

337
Q

What is the role of link proteins?

A

Stabilize aggrecan molecules to hyaluronic acid (HA)

338
Q

Several aggrecan molecules stabilized to HA form what?

A

Proteoglycan aggregate

339
Q

What is the half-life of a proteoglycan aggregate?

A

3 months

340
Q

How can mature cartilage be differentiated from immature cartilage?

A

Mature cartilage has no stem cell population

341
Q

What are the five zones of articular cartilage?

A

Gliding zone (superficial)

342
Q

In general, where is water content the highest?

A

At the surface

343
Q

In general, where is proteoglycan concentration the highest?

A

In the deep layers

344
Q

Within the gliding zone, what is the fiber orientation?

A

Tangential

345
Q

What is the function of this zone?

A

Resists shear

346
Q

What is the level of metabolic activity?

A

Low

347
Q

Within the transitional zone, what is the fiber orientation?

A

Oblique

348
Q

What is the function of this zone?

A

Resists compression

349
Q

What is the level of metabolic activity?

A

High

350
Q

Within the radial zone, what is the fiber orientation?

A

Vertical

351
Q

What is the function of this zone?

A

Resists compression

352
Q

What is the collagen size?

A

Large

353
Q

Within the tidemark, what is the fiber orientation?

A

Tangential

354
Q

What are the two functions of this zone?

A

Resists shear

355
Q

Is the tidemark seen best in adults or children?

A

Adults

356
Q

Is the tidemark present in cartilaginous exostoses?

A

No, joints only (articular cartilage)

357
Q

In the calcified zone, what is the key component?

A

Hydroxyapatite crystals

358
Q

What is the function?

A

Acts as an anchor

359
Q

How do these zones make cartilage biphasic?

A

Fluid layers shield solid matrix from stress

360
Q

What two cell types are present within synovium?

A

Type A: responsible for phagocytosis

361
Q

Does synovium have a basement membrane?

A

No; facilitates fluid transport

362
Q

What three components of plasma are absent in synovial fluid?

A

Red blood cells

363
Q

Compare complement levels in synovial fluid with rheumatoid arthritis and ankylosing spondylitis.

A

Rheumatoid arthritis: decreased levels of complement

364
Q

How does the viscosity of synovial fluid change with shear? What does that say about synovial fluid?

A

Viscosity increases as shear decreases

365
Q

Under conditions of high strain, what two things happen to the hyaluronan within synovial fluid?

A

Becomes entangled and forms a relatively solid cushion

366
Q

Under conditions of instability, what happens to the hyaluronan within synovial fluid?

A

Hyaluronan content and efficacy decrease

367
Q

Under conditions of disuse, what happens to the hyaluronan within synovial fluid?

A

No change

368
Q

What are the two key lubricating components of synovial fluid?

A

Lubricin: a glycoprotein

369
Q

What is hydrodynamic lubrication?

A

A thin film completely separates two articulating surfaces

370
Q

What is elastic lubrication?

A

Articular surfaces deform slightly when loaded to create pockets of fluid

371
Q

What is the primary method by which normal articular cartilage is lubricated?

A

Elastohydrodynamic: a combination of elastic and hydrodynamic lubrication

372
Q

Comparison/review: What is the primary lubrication method for hard-on-soft articular bearings?

A

Boundary method

373
Q

Comparison/review: What is the primary lubrication method for hard-on-hard articular bearings?

A

Mixed: hydrodynamic and boundary methods

374
Q

What does weeping refer to?

A

Under conditions of loading, fluid shifts to loaded areas of articular cartilage

375
Q

What is the half-life of articular cartilage?

A

117 years

376
Q

Because cartilage has such a long half-life, what is the rate of cartilage synthesis in adulthood?

A

Markedly diminished relative to earlier in life

377
Q

What is the basic mechanism by which normal cartilage ages?

A

Passive glycation

378
Q

What is the net effect of this process?

A

Increased cartilage stiffness (modulus of elasticity)

379
Q

With aging, what changes are seen in chondrocyte number?

A

Decreases

380
Q

What changes are seen in chondrocyte size?

A

Increases

381
Q

What changes are seen in collagen variability?

A

Increases

382
Q

What changes are seen in total proteoglycan concentration?

A

Decreases

383
Q

What is the corresponding change in water content?

A

Decreases

384
Q

In normal aging, what happens to chondroitin 4 concentration as a percentage of total chondroitin?

A

Decreases

385
Q

What happens to keratan sulfate concentration?

A

Increases

386
Q

Again, what is the net effect on modulus of elasticity?

A

Increased (increased cartilage stiffness)

387
Q

Do superficial cartilage lacerations heal?

A

No, because cartilage is avascular

388
Q

Do lacerations deep to the tidemark heal?

A

Yes, blood supply is available

389
Q

What cell type is involved in healing?

A

Mesenchymal cells produce fibrocartilage

390
Q

Is motion beneficial or detrimental to the healing of deep lacerations?

A

Beneficial

391
Q

After BMP-7 application, what effect is seen at 4 weeks? At 8 months?

A

4 weeks: accelerated healing observed

392
Q

Is there an observed difference in outcomes between microfracture and autologous chondrocyte implantation?

A

No demonstrated difference

393
Q

What sequence of three steps is involved in autologous chondrocyte implantation?

A

Harvest cartilage

394
Q

What is the maximum defect area for which this technology is applicable?

A

8 cm

395
Q

What are the two potential benefits of hyaluronic acid injection?

A

Stimulation of fibroblasts

396
Q

Have any chondroprotective effects been proven?

A

No

397
Q

What location is the most reliable for successful injection into the knee?

A

Superolaterally

398
Q

What two families of enzymes are involved with the development of osteoarthritis?

A

Metalloproteinases

399
Q

What are three examples of metalloproteinases? What is a common factor among them?

A

Collagenase

400
Q

What are the roles of tumor necrosis factor-a (TNF-a) and interleukin-1 (IL-1)?

A

Catabolic

401
Q

What is more detrimental to articular cartilage: shear or compression?

A

Shear (e.g., instability)

402
Q

With osteoarthritis development, what changes are seen in collagen order and relative concentration?

A

Increasingly disordered

403
Q

What changes are seen in DNA within the chondrocytes?

A

No change; remains essentially normal

404
Q

What changes are seen in rate of proteoglycan degradation?

A

Markedly increased

405
Q

What changes are seen in proteoglycan concentration?

A

Decreases

406
Q

What changes are seen in water content?

A

Increases

407
Q

So, if a proteoglycan concentration determines water content, why does the water content increase in osteoarthritis when proteoglycan concentration decreases?

A

Because the ordered structure of proteoglycan and cartilage in normal cartilage limits total water content

408
Q

In osteoarthritis, what happens to chondroitin 4 concentration as a percentage of total chondroitin?

A

Increases

409
Q

What happens to keratan sulfate concentration?

A

Decreases

410
Q

What happens to modulus of elasticity?

A

Decreases (decreased stiffness)

411
Q

What joint is most commonly affected by osteoarthritis?

A

Knee

412
Q

What are two subchondral changes?

A

Sclerosis

413
Q

How do gross changes in cartilage appear?

A

As microfractures

414
Q

What is the four-part Outerbridge classification of cartilage injury?

A

I: cartilage softening

415
Q

With rheumatoid arthritis, what are the two key associated enzymes?

A

IL-1

416
Q

What are the two key human leukocyte antigen (HLA) associations?

A

DR4

417
Q

What virus may possibly be associated with rheumatoid arthritis development?

A

Epstein-Barr virus

418
Q

What cell type is responsible for inciting inflammatory response?

A

T-cell

419
Q

What cell type is responsible for the associated destruction?

A

Monocyte

420
Q

What are the two key elements of the history and exam?

A

Morning stiffness

421
Q

What four laboratory findings may be present in rheumatoid arthritis?

A

Elevated erythrocyte sedimentation rate (ESR)

422
Q

What is rheumatoid factor?

A

An immunoglobulin M (IgM) antibody against IgG

423
Q

What are the two classic radiographic findings of rheumatoid arthritis?

A

Periarticular erosions

424
Q

What are the four classic disease-modifying antirheumatologic agents (DMARDs)?

A

Methotrexate

425
Q

What drug is anti IL-1?

A

Anakinra

426
Q

What three drugs are anti-TNF-a?

A

Etanercept: may be associated with demyelination as side effect

427
Q

What drug is anti-B-cell?

A

Rituximab

428
Q

What are the three characteristics of Felty’s syndrome?

A

Rheumatoid arthritis

429
Q

What are the three characteristics of Still’s disease?

A

Acute fever

430
Q

By definition, symptoms must last for how long to be considered juvenile rheumatoid arthritis (JRA)?

A

At least 6 weeks

431
Q

What is the age criterion for JRA diagnosis?

A

16 years old or less

432
Q

What joint is most commonly affected?

A

Knee

433
Q

Are most JRA patients rheumatoid factor positive or negative?

A

Negative

434
Q

What is the significance of rheumatoid factor positive JRA?

A

Increased likelihood of developing adult form of rheumatoid arthritis

435
Q

How many joints must be affected for JRA to be considered polyarticular?

A

Five

436
Q

What gender is most affected by early-onset pauciarticular JRA?

A

Female

437
Q

What is the usual age at onset?

A

2 to 3 years old

438
Q

What are two associated conditions to watch for?

A

Iridocyclitis

439
Q

What gender is most affected by late-onset pauciarticular JRA?

A

Male

440
Q

What is the usual age at onset?

A

Teenage years

441
Q

What is the classic treatment for JRA?

A

High-dose aspirin

442
Q

Ankylosing spondylitis (AS) patients generally feel stiffest at what time of day?

A

Morning

443
Q

What joint is most often the first affected?

A

Sacroiliac joint

444
Q

What physical exam finding is most specific for AS?

A

Decreased chest wall expansion

445
Q

What are the two classic ocular findings?

A

Iritis

446
Q

What two associated conditions may also severely complicate AS?

A

Pulmonary fibrosis

447
Q

What two tests can be used to evaluate bone density in ankylosing spondylitis patients?

A

DEXA scan of the hip

448
Q

What are the three classic spine findings of AS?

A

Bamboo spine

449
Q

What is the two-part treatment for low-energy neck trauma in AS patients? Why?

A

Strict immobilization

450
Q

What additional test may be beneficial in excluding an occult fracture?

A

Bone scan

451
Q

Cervical spine fractures in AS patients may be associated with what complication? How can this be evaluated?

A

Epidural hemorrhage

452
Q

What are two treatment options for cervical fractures in ankylosing spondylitis?

A

Halo vest

453
Q

In general, surgical intervention on the spine of AS patients requires what approach?

A

Combined anterior and posterior approaches

454
Q

What is the preferred osteotomy for treatment of AS-related kyphosis?

A

Pedicle subtraction osteotomy

455
Q

What is the general rule for the amount of correction this osteotomy can give you?

A

30 degrees per level

456
Q

At which level should cervical kyphosis generally be corrected?

A

C7-T1

457
Q

At which levels should umbar kyphosis generally be corrected?

A

L2 or below

458
Q

Quick review of syndesmophytes: What are the two key characteristics of the syndesmophytes associated with AS and inflammatory bowel diseases?

A

Marginal

459
Q

What are the two key characteristics of the syndesmophytes associated with Reiter syndrome and psoriasis syndesmophytes?

A

Nonmarginal

460
Q

What are the two aspects of the classic radiographic appearance of disseminated idiopathic skeletal hyperostosis (DISH)?

A

Nonmarginal syndesmophytes

461
Q

What is the composition of the crystals associated with gout?

A

Monosodium urate

462
Q

What are the two aspects of the appearance of crystals under plane-polarized light?

A

Yellow

463
Q

Where do articular erosions generally appear in patients with gout?

A

Generally away from the joint surface itself

464
Q

What is the drug of choice to inhibit associated inflammatory mediators?

A

Colchicine

465
Q

What two drugs act to inhibit phagocytosis?

A

Phenylbutazone

466
Q

What is the mechanism of action of allopurinol? When it is indicated?

A

Xanthine oxidase inhibition

467
Q

What is the relationship between myeloproliferative syndrome (MPS) and gout?

A

Chemotherapy for MPS may precipitate an attack of gout

468
Q

What are five potential causes of chondrocalcinosis?

A

Calcium pyrophosphate deposition disease (CPPD, positively birefringent crystals)

469
Q

What is the primary site of arthritic involvement with systemic lupus erythematosus (SLE)?

A

Hands and wrists

470
Q

What is the classic clinical feature of SLE?

A

Malar (butterfly) rash

471
Q

What are the two key lab values?

A

Generally ANA+

472
Q

How is SLE treated?

A

Generally the same as rheumatoid arthritis

473
Q

Mortality from SLE is generally due to what?

A

Renal disease

474
Q

Quick review: In general, when given a patient with avascular necrosis (AVN), what should always be in the differential diagnosis?

A

AVN secondary to chronic steroid therapy

475
Q

What are two commonly tested disorders that may present this way?

A

Systemic lupus erythematosus

476
Q

What is the associated mutation?

A

Homogentisic acid oxidase deficiency

477
Q

This deficiency results in the accumulation of what substance?

A

Homogentisic acid, which is then deposited within joints

478
Q

In what two ways is alkaptonuria diagnosed?

A

Urine is black

479
Q

What are two characteristics of the associated spondylitis?

A

Disk space narrowing

480
Q

What is the classic clinical presentation of relapsing polychondritis?

A

Episodic attacks of arthritic pain

481
Q

What patient population is most commonly affected?

A

Elderly

482
Q

Other clinical manifestations include what two organs?

A

Ears

483
Q

What organism is responsible for acute rheumatic fever?

A

Group A streptococcus

484
Q

What are the two relevant diagnostic tests?

A

Antistreptolysin O (ASO) titer

485
Q

What is the key point about the resultant arthritis?

A

Migratory

486
Q

Acute rheumatic fever preferentially involves joints of what size?

A

Large

487
Q

Other systemic manifestations include what process in the heart?

A

Carditis

488
Q

_ in the skin?

A

Erythema marginatum

489
Q

_ in the neurologic system?

A

Chorea (movement disorder)

490
Q

What is the classic triad of Reiter’s syndrome?

A

Arthritis

491
Q

What is the key clinical feature of the hand and wrist?

A

Tenosynovitis of the dorsal hand and wrist (especially if gonorrhea)

492
Q

What is the key clinical feature of the skin?

A

Pustular lesions on palms and soles

493
Q

What is the key clinical feature of the mucosal surfaces?

A

Oral ulcers

494
Q

How frequently are the sacroiliac joints involved?

A

In 60% of patients

495
Q

How often are Reiter syndrome patients HLA-B27 positive?

A

80 to 90%

496
Q

What are the characteristic synovial fluid findings of tuberculosis?

A

Rice bodies (fibrin globules)

497
Q

What is the smallest functional unit of muscle?

A

The sarcomere

498
Q

What is the function of tropomyosin?

A

Prevents actin cross-bridge binding

499
Q

What is the function of troponin?

A

Modifies tropomyosin to allow cross-bridge binding

500
Q

Troponin function is sensitive to what?

A

Changes in calcium level

test (3 decks)

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