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non neoplastic bone disorders


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cells that make transport and arrange matrix proteins, have hormone receptors, involved in bone formation
mature blone cells surrounded by matrix
multinucleated cells derived from heatopoetic cells which are involved in bone resorption
gene mutated in achondroplasia
FGFR3 which normally inhibits cartilage formaition, when mutated it is always on-->decreased chondrocytes
histological appearance of achondroplasia
abnormal clusters of chondrocytes at growth plate instead of normal columns
mutation in osteogenesis imperfecta
deficiency in synthesis of type I collagen due to mutation in gene coding for alpha 1 and alpha 2 chains of collagen
definition of osteoporosis
increased porosity of skeleoton due to reductrion in bone mass, making bone susceptible to fracture
osteomalacia/rickets cause, histology
increased osteoid and less mineralized mature bone
caused by deficiency of vitamine D, calcium, phosphate, genetic abnormalities,
Rickets is undermineralization of bone in children
Hyperparathyroidism/osteitis fibrosa cystica
too much parathyroid hormone, can be primary or spurred on be prolonged calcium dec in serum
renal osteodystrophy, wtf is it
skeletal changes from chronic renal disease, loss of kidney fnx in phosphate retention and decreaced vitamin d result in fucked up shit
osteopetrosis (marble bone disease)
hereditary osteoclast dysfunction from absence of carbonic anydrase II, ostclasts cannot resorb bone. bone fills up marrow and is brittle. present soon after birth
paget's disease of bone (osteitis deformans). what? cause?
disease of abnormal/ increased bone remodeling. age over 40. common in northern europe. triggered by virus
3 phases of paget's disease of bone
initial osteolytic phase, abnormal large osteoclasts up to 100 nuclei
mixed osteoclastic osteoblastic phase, linging of osteoblasts around trabeculae, osteoclasts still present with loose connective tissue and vessels inmarrow space
burnt out osteosclerotic phase, larger coarse trabeculae, cortex soft, porous and weak
lab findings in paget's disease
elevated alkaline phosphatase and increased urinary hydroxyproline and deoxyproline
four phases of normal fracture healing
1 formation of hematoma/fibrin mesh, interleukins from platelets activate progenitor cells and inc osteoblastic and clastic activity
2 1 week later soft tissue callus
3 2-3 weeks later, woven bone laid down, forms fibrocartilage, undergoes endochondral ossification to form a bony callus
4 remodeling of these areas continues to accomodate stress and weight
osteonecrosis presentation, 2 types
subchondral pain and may predispose to arthtritis
medulary may be asymptomatic
osteomyelitis common bacterial infectious agents, modes of infection
staph aureus 80-90%, contigous or hematogenous spread
e coli, pseudomonas, klebsiella: pts with uti's, IV drugs
H influenza, group B strep: neonates
salmonella: sickle cell
mixed: surgery, open fractures

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