4th Exam: Bone & Joint Disease Flashcards
Shaft of bone:
diaphesis
Center of long bone:
spicules of bone, aka cancellous bone
Outer shell of long bone:
compact bone, cortex
Smoothest part of long bone:
articulating ends
Bone building molecules, etc.:
Vit D, Ca2+, Calcitonin, PTH
What is the bone covered by:
periosteum
Are there blood vessels in the periosteum?
yes
Osteoblast progenitors give rise to:
-blasts, -cytes, -oclasts
Mineralized osteoblast:
Osteocyte
These make osteoid:
osteoblasts
Osteoblasts have ____ receptors, secrete osteoclasts stimulating factor, bone break down.
PTH
Histology of -blasts:
blue stain: calcified bone, red stain: in bw osteoblast, mineralization front
Where is the inorganic material found?
ECM
What inorganic material is found in the ECM?
Hydroxyapatite crystals (calcium phosphate)
Organic material found in matrix:
collagen, proteoglycan, glycoprotein
What stimulates glycoprotein synthesis?
Vit D
How many days after matrix deposition does mineralization occur?
12-15d
Where is the mineralization front?
At osteoid-mineralization bone interface
What controls the mineralization front?
under osteoblast/osteocyte influence
When does mineralization occur?
if Ca2+ and PO4 adequate (need to crystalize), they displace H2 → Ca-OH apatite crystals
Lamellar:
mature, strong bone, parallel lines
Woven bone:
weaker than lamellar, fibers don’t look parallel
The osteon is part of what type of bone?
compact bone
Cancellous bone viewed thru polarized light:
bone breaks into spicules, not as dense, bone marrow in space
Osteoclasts:
multinucleated, form from macs
-
How do -clasts break up bone?
Burrow into calcified bone (blue), liberate calcium, demineralization
How do -Blasts signal -clasts:
RANK-RANK ligand receptors. Receptor on -clast precursor, -blast binds -clast receptor to tell it to break bone down, PTH: stimulates -blasts via its receptors, calcitonin: turns off -clasts
PTH, turns on or off -clasts?
turns off, stimulates -blasts via its receptors, calcitonin:
-clasts are derived from:
monocyte/mac system
-clasts secrete:
carbonic anhydrase → carbonic acid
TF? Exercise can stimulate new bone formation
T.
Types of fractures:
simple, displaced, comminuted, open (compound), compression, pathologic
Simple fracture:
unsially transvers, bone still aligned
Displaced fracture:
bone not aligned
Comminuted fracutre:
splintered, multiple pieces, crushing injury, longer to heal, bring pieces together surgically
Open fracture:
through skin
Compression fracture:
ex: mainly vertebra, and pt looses height- osteoporosis
Pathologic fracture:
pre-existing disease- bone wouldn’t fracture otherwise
Fracture complications
Infection, delayed union and nonunion, avascular necrosis
Fracture type most prone to infection:
compound
Most common cause of delayed healing:
Infection
What causes avascular necrosis?
loss of blood supply
What typically causes kyphosis?
spine disease: osteoporosis, disc disease, osteoarthritis
Metabolic bone diseases:
osteogenesis imperfect, osteoporosis, osteomalacia, Paget’s disease, Rickets
primary osteoporosis:
classic disease, post-menopausal or senile
secondary osteoporosis:
can cause or complicate primary osteoporosis
Cause and tx for secondary osteoporosis:
iatrogenic, corticosteroid therapy
Most cases found in this population:
post-menopausal elderly women
First signs of osteoporosis after possibly remaining silent for yrs:
bone pain, gradual loss in heigh
Most common fracture site due to osteoporosis:
hip
Who are more affected by osteoporosis, white or black women?
white, 1:2, vs 1:5
osteoprosis fractures are due to:
peak bone mass
Osteoporotic hip fractures mortality:
25%, high
Gross appearance of osteoporosis fracture:
a depression, dec bone density
Osteoporosis risk factors:
Female, age, asian, white, early menopaus, low peak bone mass, inadequate Ca2+ intake, lack of exercise, alcohol, smoking, steroids
There is low ___ activity and high ___ activity in osteoporosis:
blast, clast
Which types of bone are thin in osteoporosis?
cortical and trabecular
Common fracture sites:
Femoral neck, Colles’ fractures (distal radius) in the hand in the wrist
At what age do women meet their peak bone mass?
35yo, demineralization thereafter
Consequences of osteoporosis in the spine:
pain, compression fractures (fxs), loss of height, stooped posture, kyphosis
Therapy for osteoporosis:
Regular exercise, diet, Ca2+, vit D, Limit alcohol, smoking, estrogen supplements, bisphosphonates inhibit -clast activity
Cause of osteonecrosis of jaw:
bisphosphonate therapy, fewer -clasts interfere w bone remodellin
Osteonecrosis could easily be misdiagnosed as:
neuralgia inducing cavitating osetonecrosis (NICO_
NICO:
Due to avascular (ischemic) osteonecrosis (NOT bisphosphonate therapy), in any bone, more susceptible to fracture
Case: 60yo white man, head enlarging for past 2 years, bowing of tibias, X-ray: thickening of skull
Paget’s Disease
Paget’s Disease:
White, euro descent, < age 40, ocalized or generalized (85%), etiology – myxovirus particles in -clasts, cycles of bone resorption and reformation (Woven instead of lamellar bone formed), X-rays: lytic (more dense) & sclerotic (less dense) lesions, bones look thick, imbalance of breaking and creating bone
osteolytic phase of Paget’s Disease:
high lesion, less bone, bone breaking
Osteosclerotic phase of Paget’s diseases:
less lesions, more bone, looks thick, bone creation
Paget’s diseases happens here:
Tibia, ilium, femur, vertebra, skull
Symptoms of Paget’s disease:
Cranial nerve compression → VIII cranial nerve – deafness
Bone thickening in Paget’s disease happens here:
from OUTER cortex, so bone is not compressing brain
pattern of new bone
mosaic (woven)
How to see new, mosaic, woven bone best:
under polarized light
TF? lamellar bone is formed around mosaic bone:
F. not formed here
mosaic bone:
• Weak, woven, prone to fracture
Saber shin:
bowing of the tibia, the bone is soft
Calvarium:
osteosclerosis of the skull
Osteoarthritis:
Common in elderly, 90% > 60yo, morning stiffness, pain w use, improves w rest, related to physical stress, often weight bearing joints, exception is DIP (distal interphalangeal?) joints
Degeneration of articular cartilage:
Superficial layer flaking, fissuring of cartilage, then loss of cartilage. Resulting bone on bone, loss of articular surface, “Naked” bone against “naked” bone, abnormal bone growth → Osteophytes: bony outgrowth due to new stress on different part of bone, bone grows sideways), bone spurs, Heberden’s nodes
Diarthrodial joints involves:
synovial fluid
osteoarthritis histo:
Flaking at surface → fissures in the cartilage → loss of cartilage → bone on bone, he result is throwing the joint out of alignment → different forces on different parts of the bone → new bone formation, creating outgrowths (osteophytes)
Gray section of the gross view of a surface of a joint:
erosion of the articular cartilage, partial or total
Locations of arthritis:
Hip, distal joints of fingers
Arthridial knobs of fingers:
Heberden’s nodes
Heberden’s nodes, more common in men or women?
women
Case: 41 year old man in good health, awakes from sleep with pain in great toe, severe, pain, sudden onset, can’t tolerate bed covers on toe, on PE next day, MP joint very tender to touch, joint swollen, red
Gout-Acute Arthritis
Gout of the great toe
Podagra
Gout risk factors:
Middle age or older, male, obesity and “rich diet”, alcohol consumption, superior intelligence
Why does alcohol consumption lead to gout?
alcohol interferes with excretion of urates, purine metabolism issue
Hyperuricemia:
Excessive intake of purine – containing foods (beer, organ meats (liver), beans), Low renal urate excretion (24h urinary acid < 1000 gm (apparently don’t memorize this number)), Alcohol and other agents which retard excretion, makes disease worse
Uric acid, solubility level:
marginally soluble even at normal levels
Normal serum uric acid:
~ 7 mg/dl
Serum uric acid:
Tends to rise w age, rises at earlier age and faster in males
What causes gout, crystal formation or inflammatory reaction?
inflammatory reaction
Elevated serum acid:
o
Crystal form in joint fluid (especially at low temp), engulfed by polys → release lysosomal enzymes, synovitis and ultimate destruction of articular cartilage due to release of cytokines, crystals deposit in surrounding tissues → tendinitis, tophus formation (nodule, in soft tissue)
TF? Gout is an untreatable disease.
F.
How are urate crystals in joint fluid aspirate seen?
under polarized light
Histo of crystal-induced arthritis:
white deposits of urates below the articular cartilage
Histo of gouty arthritis:
White gout precipitating on destroyed articular cartilage
Histo of Tophi in soft tissue:
Common in the ear and adjacent to the involved joint, like in the toe
Second most common cause of facial pain:
TMJ
Causes of TMJ:
The joint, muscles, osteoarthritis, bruxism
Symptoms of TMJ:
Pain in muscles of mastication, headache
Benign bone tumor:
osteoma
Malignant bone tumor:
primary, metastatic
Osteoma:
-
Benign, slow growing, common locations sinuses, jaw, skull, mean age 35, often asymptomatic
Histology of osteoma:
Looks like normal bone, seems to arise from bone surface
