3: Principles of Bone Healing - Carnevale Flashcards
(26 cards)
breakdown of bone
- 35% organic
- 65% inorganic
matrix of bone
95% collagen type I
5% non-collagenous prtns
unmineralized bone =
osteoid
pluripotent mesenchymal cell that can form osteoblasts
osteoprogenitor
cells that initiate mineralization
osteoblasts
- synthesize and transport prtn (like type 1 collagen) and osteoprotegerin
what receptor on osteoclasts stimulates osteoclastic bone resorption
RANK receptor
- RANK ligand is produced by osteoblasts
become osteocytes when surrounded by matrix
osteoblasts
- osteocytes are matured osteoblasts that regulate daily serum calcium and phosphorus
responsible for bone resorption
osteoclasts
- mutliple nuclei
- live in howship lacunae
osteoprotegerin
acts as decoy on RANK receptor on osteoclast
what are osteoclasts derived from?
hematopoietic progenitor cells
role of estrogen in bone growth
- increases bone formation by increasing collagen synthesis by osteoblasts
- prevents bone resorption by inhibiting osteoclast differentiation
when is woven bone normal?
- fetal skeleton
- growth plates
- pathologic in adults almost always
only type of normal bone in adults
lamellar bone
- highly orderly
terms
- end of long bone
- growth plate
- next to growth plate
- shaft
- bone covering (blood vessels, nerves)
epiphysis epiphyseal plate metaphsis diaphysis periosteum
describe bone remodeling cycle
- osteoclast precursors recruited to bone surface, where thy fuse, differentiate, and mature
- osteoclasts resorb both organic and inorganic bone matrix
- resorption phase ends with osteoclast apoptosis
- in reversal phase, osteoblasts differentiate from mesenchymal precursors, under influence of factros from osteoclasts, and secrete new bone matrix (osteoid)
- at end of cycle, some osteoblasts have been incorporated into bone as osteocytes and others remain on the surface as quiescent bone-lining cells
why do we need vit C for bones?
- maintenance of normal connective tissue
- synthesizes collagen
- responsible for bone formation –> synthesizes organic matrix
- inorganic calcified portion of capillary walls
clinical syndrome related to problems with osteoid synthesis AND collagen support of blood vessels
scurvy (vit C deficiency)
- note hemorrhages found around corkscrew hairs
- poor wound healing
- subperiosteal hemorrhage
three phases of fracture healing
1 = organization of hematoma at fracture site –> soft, organizing PROCALLUS (hematoma organizing by end of 1st wk, anchorage, no structural rigidity)
- conversion of procallus to FIBROCARTILAGINOUS CALLUS : reactive mesenchymal cells (deposition of woven bone and new cartilage); 3rd wk; max enlargement
- replacement of mesencymal cells by OSSEOUS CALLUS; eventually remodeled along lines of weight bearing; completes repair (endochondral ossification forms bony networl; fractured ends bridged by bone callus)
“callus”
orderly progression of cartilage into microtrabecular new bone
inhibitory factors to fracture healing
- infection
- non union
- inadequate immobilization
- poor circulation, poor nutriton
- drugs (corticosteroids, immunosuppressives, cytotoxic therapy)
- systemic abnormality
mechanisms of avascualr necrosis (infarction of bone and marrow resulting from ischemia)
- fracture
- corticosteroids
- uncertain cause idiopathic
- sickle cell disease
most common route of osteomyelitis
hematogenous
most common agents of osteomyelitis
pyogenic (staph aureus) agents or mycobacterium tuberculosis
cause of osteomyelitis in sickle cell patients
salmonella
