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126 Cards in this Set

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Contents of haversian canals
Arterioles, Venules, Capillaries, Nerves, Lymphatics
Contents of canals/canaliculi
Osteocyte cell processes
Cement lines
Define border of osteon
Characteristics of cortical bone
Slow turnover, high Young modulus, higher resistance to torsion and bending
Characteristics of cancellous bone
Less dense, more remodeling according to Wolff's law, higher turnover, smaller Young modulus, more elastic
Characteristics of woven bone
Random organization (not oriented according to stress), increased turnover, weak, flexible. Can be immature or pathologic
Osteoblasts
Form bone by generating organic, non-mineralized matrix. Mesenchymal origin. More active cells line bone, less active trapped in resting regions- maintain ionic mileiu of bone.
Growth factor effects on osteoblasts
Differentiation increased by PDGF/ IDGF
PTH effects on osteoblasts
Secondary messenger-->activates adenyl cyclase-->Produce ALK Phos, type I collagen, osteocalcin, bone sialoprotein
Osteoblast receptors
1. PTH 2. 1,25- dihydroxyvitamin D 3. glucocorticoids 4. prostagalndins 5. estrogen
Osteocytes
Maintain bone. Most common cell in mature bone. Made from osteoblasts. Important for control of calcium/phosphorous balance. Stimulated by calcitonin/ inhibited by PTH
Osteoclasts
Resorb bone. Multinucleated giant cells. Monocyte origin. Ruffled brush border used for bone resorption. Osteoclast formation inhibited by IL-10
RANKL
On surface of osteoblasts and tumor cells. Stimulate RANK on osteoclasts--> differentiation into mature osteoclasts/ increases bone resorption. Inhibited by osteoprotegrin
Osteoclast bone resorption
Occurs in Howship's lacunae. Carbonic anhydrase creates H+ ions--> lower pH-->increases solubility of hydroxyapatite. Organic matrix removed via proteolytic digestion. Stimuated by IL-1.
Bisphosphonate effects
Inhibit osteoclast resorption. Prevents formation of ruffled border.
Osteoprogenitor differentiation in different environments
low strain/ high O2--> osteoblasts. Intermediate strain/low O2--> cartilage. High strain--> fibrous tissue
Calcitonin
From parafollicular cells of thyroid. Stimulated by high Ca+. Inhibits osteoclastic bone resorption-> transient decreased Ca+. Analgesic properties in pathologic fractures
Vitamin D3 effects on osteoblasts
stimulates matrix and ALK Phos synthesis/ bone protein synthesis
Glucocorticoid effects on bone
inhibits synthesis of DNA/ collagen production/protein synthesis by osteoblast. Cancellous affected more than cancellous.
Prostaglandin effects on osteoblasts
activates adenylyl cyclase--> stimulates resorption of bone
Estrogen effects on bone
Anabolic/ anticatabolic. Increases mRNA levels for ALK Phos and inhibits adenyly cyclase activation. Side effect: inc risk of heart disease/ breast CA
Collagen structure
Triple helix of one alpha 2/ 2 alpha 1 chains. Hole zone: within fibril between ends of molecules. Pores between sides of parallel molecules
Collagen cross-linking
decreases solubility/ increases strength
Most abundant non-collageneous protein in bone
Osteocalcin. Note: VERY popular question on OITE
Osteocalcin
Most abundant protein in bone (except collagen). Attracts osteoclasts, regulates bone density. Marker of bone turnover. Inhibited by PTH/ stimulated by vit D
Proteoglycans in bone
Compressive strength. Composed of GAG complexes. Inhibit mineralization
Osteonectin
Secreted by platelets and osteoblasts. Role in regulating calcium/ matrix
Osteopontin
Cell-binding protein similar to an integrin
Ca hydroxyapatite
Compressive strength. Most of inorganic matrix.
Location of mineralization of bone
Primary mineralizatin occurs in collagen gaps. Secondary at periphery
Osteocalcium phosphate
Remainder of inorganic matrix of bone
Wolff's Law
Bone remodels in response to mechanical stress. Increased stress--> increased bone density. Immobilization--> loss of bone mass
Ionic properties of bone
Compression side: electronegative--> stimulates osteoblasts. Tension side: electropositive--> stimulates osteoclasts
Hueter-Volkman law
remodeling occurs in basic multicellular units (BMU's) modulated by hormones/ cytokines. Compression inhibits growth/ tension facilitates growth
Cortical bone remodeling
Osteoclastic tunneling (cutting cones)--> layering of osteoblasts and deposition of laemllae. Head of cutting cone made of osteoclasts followed by capillaries/osteoblasts
Cancellous bone remodeling
Osteoclastic resorption--> osteoblastic formation
Blood flow to bone
5-10% of cardiac output
Nutrient artery
branch from major arteries--> diaphyseal cortex through nutrient foramen--> medullary canal-->arterioles in endosteal cortex. Suplly inner 2/3 of diaphyseal cortex. High pressure
Periosteal blood supply
Primarily capillaries--> outer 1/3 diaphyseal cortex. Low pressure
Direction of blood flow in bone
Normal bone: centifugal (in to out). Displaced fracture: centripetal (in to out)- disrupt high flow endosteal supply and flow reverses. Immature bone: centripetal (highly vascularized periosteum). Venous flow: centripetal
Physiologic states that increase blood flow to bone
hypoxia, hypercapnia, sympathectomy (SCI)
Effect of fracture on blood flow to bone
immediate: decreased. Hours-days: increases. 2wks: peak blood flow. 3-5 months: normal
Effect of reaming on endosteal blood supply
devascularizes inner 50-80%
Periosteum
Inner layer: cambium- loose/vascular/contains cells capable of becoming osteoblasts. Responsible for increaseing diameter o f bone/ forming callus. Outer layer: fibrous/less cellular/contiguous with joint capsules
Bone marrow
Red: Hematopoietic (40% H20/40%fat/20% protein). Changes to yellow marrow. Yellow marrow: inactive: 80% fat
Enchondral ossification
Replaces cartilage model. Locations: embryonic long bones. Physis. Callus. Disrupted in achondroplasia
Intramembranous ossification
Aggregates of undifferentiated mesenchymal cells become osteoblasts--> bone. Locations: embryonic flat bones. Distraction osteogenesis. Blastema bone. Disrupted in cledicranial dysostosis
Appositional ossification
Osteoblasts lay new bone on old bone. Locations: periosteal bone enlargement. Bone remodeling.
Physeal nutrition
primarily from perichondrial artery
Physis physiology: reserve zone
cells store material. Low O2 tension. Effected by lysosomal storage diseases
Physis physiology: proliferative zone
longitudinal growth. Increased O2 tension. Inc PG--> inhibits calcification. Effected by achondroplasia
Physis physiology: hypertrophic zone
Three zones. Maturation/degeneration/provisional calcification. Matrix mineralization occurs. Low O2 tension. Low PG. Widened in rickets
Indian hedgehog
produced by physeal chondrocytes. Regulates expression of PTHrP
Physeal layer affected by SCFE
Hypertrophic zone- idiopathic. Metaphyseal spongiosa- renal failure
Groove of Ranvier
supplies chondrocytes to periphery of growth plate--> increased width
Perichondrial ring of LaCroix
Dense fibrous tissue. Anchors and supports physeal periphery. Affected in Salter Harris VI injuries
Stages of fracture repair
Inflammation, repair, remodeling
Inflammatory phase of fracture healing
Hematoma--> cells release growth factors--> attract cells-->granulation tissue at fracture ends-->osteoblasts/fibroblasts proliferate
Repair phase of fracture healing
primary callus within 2wks. Soft callus replaced by hard callus by enchondral ossification. Cellular differentation depends on local strain and O2 tension.
Effects of ultrasound on fracture healing
Low intensity/ pulsed- accelerates healing and improves callus strength.
Electrical stimulation effects on bone
DC: stimulates inflammatory like response. AC: affects cAMP/colalgen synthesis/calcification during repair stage. Pulsed electromagnetic fields: initiate calcification of fibrocartilage
Location with highest risk of pathologic fracture
Subtrochanteric femur
Osteoconductive
scaffold for bone formation
Osteoinductive
Growth factures- stimulate bone formation
Osteogenic
Cells that make bones
Bone graft antigenicity
mediated by cell surface glycoproteins. Method of rejection: cellular
Cortical bone graft
Slower incorporation through remodeling of haversian systems. Resorption occurs first--> weakens graft.
Cancellous bone grafts
Revascularize and incorporate quickly. Osteoblasts lay down new boneon old trabeculae (creeping substitution)
Silicate grafts
bioactive glasses
Ca-phosphate based grafts
capable of osseoconduction/ osseointegration. Biodegrade at very slow rate. Ceramics
BMP effects on bone
Osteoinductive. Induces metaplasia of mesenchymal cells into osteoblasts. Target cesll: undifferentiated perivascular mesenchymal cells. Signal via serine/threonine kinase
TGF-beta effects on bone
induces production of type II collagen/ PG. Induces osteoblasts to synthesize collagen. Regulates cartilage/bone formation in fracture callus. Serine/threonine kinase signalling
IGF-II effects on bone
Stimulates type I collagen/ cellular proliferation/cartilage matrix and bone formation. Tyrosine kinase signalling
PDGF effects on bone
Chemotactic for inflammatory cells to fracture site. Released by platelets. Tyrosine kinase signalling
Distraction osteogenesis phaes
Latency: 5-7 days. Distraction: 1mm/day. Consolidation: 2x duration of distraction phase
Most osteoconduction bone graft
cancellous autograft
Most osteogenic bone graft
cancellous autograft
Best structuaral bone graft
cortical autograft
Effects of bisphosphonates on HO
inhibits mineralization but does not prevent osteoid matrix. Will mineralize when medication stopped
Calcium metabolism
Absorbed in duodenum (active transport-regulated by vit D3) and passive diffusion in jejunum. Kidney resorbs most Ca @ proximal tubules.
Calcium intake needs
600mg/day- kids. 1300 mg/day- adolescents. 750mg/day- adults. 1500mg/day-pregnant. 2000mg/day- lactating. 1500mg/day- healing fracture
PTH
Secreted by chief cells in parathyroid glands. Stimulated by low Ca conc. Inhibited by high Ca/ high 1,25(OH)2 vit D. Directly activates osteoblasts/modulates renal phosphate filtration. Stimulates 1,25(OH)2 vit D production in kidney, increaes renal Ca resorption, increases excretion of Phos. Net: inc Ca/dec Phos
1,25(OH)2 vit D
Secreted by proximal tubule of kidney. Stimulated by PTH. Inhibited by low PTH/high Ca/high phos. Stimulates intestinal absorption of Ca/phos. Stimulates osteoclastic resorption of bone.
Phenytoin effects on bone
impairs vitamin D metabolizms
Effects of menopause on calcium
decreased intestinal absorption/ increased urinary excretion
Markers of bone resorption.
Urinary hydroxyproline, pyridinoline cross-links.
Markers of bone formation
Serum alk phos.
Hypercalcemia symptoms
polyuria/polydipsia/nephrolithiasis/osteotis fibrosa cystica/confusion/constipation/anorexia/nausea
Primary hyperparathyroidism
Usually due to parathyroid adenoma. Result: inc Ca/dec phos. Increased bone resorption/ poor mineralization. Labs: high ca/PTH/urinary phos. Bony changes: osteopenia/fibrous replacement of marrow/brown tumors- destructive metaphyseal lesiosn.
Pseudohypoparathyroidism
PTH receptor abnormality. Decreased levels of active form of vitamin D. Normal serum Ca
hypoparathyroidism
low ca/ high phos. Low 1,25(OH)2 vit D. Usually iatrogenic
Renal osteodystrophy- high turnover
Decreased renal phos excretion-->hyperphosphatemia--> low Ca/ high PTH--> secondary hyperparathyroidism. Osteitis fibrosa cystica/amyloidosis. Tx: treat renal dz, restrict dietary phos, phosphate biding antacids, 1,25(OH)2 vit D supplementation
Renal osteodystrophy- low turnover
secondary to aluminum toxicity. No hyperparathyroidism
Hypophosphatemic rickets
Most common type. Inborn error in phosphate transport--> renal phosphate loss. Ca nml/PTH nml/vit D nml. Classic triad: hypophosphatemia/lower limb deformities/ stunted growth
Hypophosphatasia
Inborn error in alkaline phosphatase. High Ca/phos. Low serum alk phos. Osteomalacia. Early loss of teeth. Dx: elevated urinary phosphoethanolamine. Tx: none available
Nutritional rickets
low or nml ca/high phos. Hihg alk phos/PTH. Sx: Osteomalacia/hypotonia/weakness/tetany. Bowing of long bones. Tx: vitamin D/Ca/Phos supplementation depending on etiology
Vitamin D dependent rickets- type I
Pseudo vitamin D deficiency. Defect in renal 25-(OH) vatimin D 1alpha hydroxylase-->inhibits activation of vitamin D. More severe than vit D deficiency rickets
Vitamin D dependent rickets- type II
intracellular receptor deficit for 1,25 (OH)2. Very very high levels of vitamin D diagnostic
treatment of hypercalcemia
1. Saline hydration 2. loop diuretics 3. dialysis-severe
Hypocalcemia sx
increased neuromuscular irritability (tetany/seizures/Chvostek's sign). Cataracts. Onychomycosis. Prolonged QT.
pseudo-pseudohypoparathyroidism
looks like pseudoparathyroidism except Ca normal and normal response to PTH
Amyloidosis
Accumulation of beta-2-microglobulin. Assocaited with carpal tunnel syndrome, arthropathy, pathologic fractures.
Definition of osteoporosis/osteopenia
WHO: L2-L4 density at least 2.5 SD below peak bone mass of 25yo. Osteopenia- 1.0-2.5 SD
Risk factors osteoporosis
sedentary thin caucasian female age smokers heavy drinkers northern european h/o breast feeding poor diet phenytoin use
Strongets predictor of future vertebral fracture
2+ prior vertebral fractures
Type I osteoporosis
Postmenopausal. Primarily affects trabecular bone. Vertebral/distal radius fractures
Type II osteoporosis
Age related. >75yo. Affects trabecular and cortical bone. Related to poor calcium absorption. Hip/pelvic fractures.
Degree of osteoporosis necessary to be visible on XR
>30%
Idiopathic transient osteoporosis of hip
third trimester of pregnancy. Presents with groin pain/ dec ROM/ localized osteopenia. Tx: PWB. Resolves after 6-8mo.
Osteomalacia
Defect in mineralization. Qualitative deficit. Associated with Vit d deficiency/ GI disorders/ phenytoin/alcoholism. RA: Looser's zones, biconcave vertebral bodies, trefoil pelvis. Bx: widened osteoid seams. Tx: high dose vitamin D theraphy
Scurvy
Vitamin C deficiency-->dec chondroitin sulfate synthesis--> defective collagen growth/impaired hydroxylation of collagen. Sx: gum bleeding/ecchymosis/joint effusion/iron deficiency. RAD: thin cortices. Histo: widened zone of provisional calcification. Metaphyseal bone affected first
Osteopetrosis
Decreased osteoclast/chondroclast function-->failure in bone resorption. Histo: osteoclasts lack ruffled border/clear zone. Marrow filled with necrotic calcified cartilage.
Infantile AR form of osteopetrosis
Most severe form. Bone within bone appearance. Hepatosplenomegoly. Aplastic anemia. Fatal during infancy. Tx: BMT. High dose calcitriol +/- steroids
AD form of osteopetrosis
Albers-Schonberg disease. Generalized osteosclerosis. Rugger jersey spine. Pathologic fractures
Osteopoikolosis
Spotted bone disease. Islands of deep cortical bone within medullary cavity and cancellous bone. Asymptomatic. No malignant degeneration
Paget's disease
Dx: Elevated alk phos/urinary hydroxyproline/ virus-like inclusion bodies in osteoclasts. Active phase: intense resorption. Mixed phase. Sclerotic phase: osteoblastic formation. Inactive phase.
Caisson's disease
osteonecrosis secondary to dysbarism (SCUBA)
Osteonecrosis
Bony necrosis due to loss of blood supply. Hip commonly affected. Associated with steroid use/alcoholism/blood dyscrasias/radiation. Path: grossly necrotic bone. Bilateral in hip in 50% (80% if associated with steroids). MRI best study- most sens/spec and positive earliest. Pressure measurements: >30mmHg abnormal
Legg-Calve-Perthe's disease
osteonecrosis of femoral head
Osgood-Schlatter disease
Osteochondrosis of tibial tuberosity
Sinding-Larsen-Johannson disease
Osteochondrosis of inferior pole of patella
Blount disease
Osteochondrosis of proximal tibial epiphysis
Sever's disease
Osteochondrosis of calcaneus
Kohler's disease
Osteochondrosis of tarsal navicular
Freiberg's infarction
Osteochondrosis of metatarsal head
Kienbock's disease
osteochondrosis of lunate