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Flashcards in Metabolic Bone Disease Deck (20):
1

Bone remodeling

-osteoclasts: make resorption pits using enz/acid
-osteoblasts: fill pit back up with osteoid (bone specific collagen, high affinity for Ca phosphate crystal): calcifying osteoid: Ca x PO4 greater than 24

Osteoclasts have RANK, which binds RANK-L
lots of RANK L and not much OPG: bone resorption high (high OPG bone resorption low)

2

Sclerostin

prevents new bone formations

3

Promotion of osteoblasts (signaling)

Wnt
Frizzled/LRP5
B-catening

4

Osteoporosis

compromised bone strength, increased risk of fragility fractures

5

Types of fragility fractures and RFs

spine, most (only 1/3 cause pain)
hip
wrist

fragility fractures= osteoporosis

RFs:
age
falls
low bone mass
previous fractures

6

T score

SDs below peak bone mass
-1-2.5 below peak bone mass: osteopenia
-2.5 and further below: osteoporosis

7

abnormal bone remodeling

increased resorption or decreased formation: bone mass lost

8

Non modifiable RFs fro low bone mass

Age
Race
Gender
Family History
Early Menopause

9

Modifiable

Low Calcium Intake
Low Vitamin D Intake
Estrogen Deficiency
Sedentary Lifestyle
Cigarette Smoking
Excess Alcohol (greater than 2/day)
Excess Caffeine (greater than 2/day)
Medications: Glucocorticoids, Excess Thyroid Hormone, Anticonvulsants
Probable/Possible: Thiazolidinediones, SGLT2-I’s, SSRI’s, PPI’s

10

Osteoporosis Prevention and Tx

1000-1500 mg Ca/d
Vit D: 1000units/d
exercise: aerobic, resistance
falls: assess/prevent

11

Osteomalacia and rickets

impaired bone mineralization resulting in soft, weak bones

Osteomalacia: adults
rickets: kids

*inadequate ca x phosphate product for bone mineralization (should be above 24)

12

Phosphate disorders

Acquired Hypophosphatemia
Poor Oral Intake
Renal Phosphate Wasting

Congenital Hypophosphatemic Rickets
“Vitamin D Resistant Rickets”
Renal Phosphate Wasting
Impaired 1,25 (OH)2 Vitamin D Formation

13

Osteomalacia features, and readiology

pain
deformities
fractures

Radiology:
fractures
pseudofractures (Milkman's Fractures; Looser's Lines)

14

Rickets features and radiology

pain
deformities
muscle weakness
short stature

Radiology
bowing of long bones
flaring ends of long bones
-delayed epiphyseal calcification

15

Paget's Disease of Bone

-an idiopathic bone condition characterized by excessive/unregulated bone resorption and formation

-genetic (familial aggregation; 18q linkage; mutation of osteoprotegerin gene; mut of sequestosome 1/P62 gene)
-chronic paramyxovirus infection
-viral disorder evidence (geographic variation; dog ownership; time trends; viral studies)

16

Sequestosome I

SQSTMI: ubiquitin binding protein. Forms ubiquitinated chains that function as protein scaffolds for IL-1 and TNF induced NF-kB activation, which regulates RANK signaling that controls osteoclast differentiation, activity and survival.
SQSTMI mutations: linked to Paget’s Disease

17

clinical features of Paget's disease

Skeletal:
Pain
Deformity
Fractures
Osteoarthritis
Hypervascularity
Acetabular Protrusion
Osteogenic Sarcoma

Neuro:
deafness (8th n, ossicles)
CN compression (bony)
spinal cord compression (vascular)

CV:
atherosclerosis
aortic stenosis
CHF (high output)

Common sites of involvement:
pelvis
skull
vert
femur
tibia

18

Paget's progression

1st 10 yrs: osteoclastic (increase NTX/CTX)

Then: osteoclastic/osteoblastic mixed phase (high NTX/CTX); alk phos high

After 20 years: osteoblastic (NTX/CTX low) alk phos high or low

19

Dx of Paget's disease

remodeling markers: elevated
XR feat: very specific
(osteolytic lesions: blades of grass on long bones and resorption frot in flat bones; osteosclerotic lesions; thickened disorg trabeculae; thick, expanded cortex; expansion of bone size)
bone scan: very sensitive (intense uptake in osteoblastic stage)
bone biopsy: occasionally needed

20

Histology of Paget's

Increased Osteoclast Numbers
Increased Osteoclast Nuclei (20-100 per cell)
Increased Osteoblasts in Periphery
Disorganized, Mosaic, Woven Bone