3: Principles of Bone Healing - Carnevale Flashcards
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
sequestrum
residual necrotic bone post osteomyelitis - may be resorbed or surrounded by rim of reactive bone called involucrum
brodie abscess
when well-defined rim of sclerotic bone surrounds residual abscess - viable organisms may persist
