-
primary v. secondary fracture healing
- primary: repair thru membrane of osteoprogenitor calls in periosteum - like intramembranous ossification
- secondary: cartilaginous intermediate endochondral ossification
-
secondary healing zones
- 1) resting zone
- 2) hypertrophic cartilage zone
- 3) mineralized cartilage zone
- 4) ossification zone
-
secondary healing phases
- inflammatory phase (48h): hemorrhage, vessel constriction, 2-5d hematoma (blood clot) seals site, necrotic bone, macrophages initiate and clean up
- reparative phase (bone callus): 2nd wk-months, neovascularization, granulation tissue forms as pluripotent cells differentiate into fibroblasts, chondroblasts, osteoblasts
- remodeling, osteoclasts remove matrix to form cartilage spicules, woven bone deposited, osteoblasts produce lamellar spicules
- remodeling
-
primary healing
- takes place where there is rigid internal fixation (pins etc)
- osteoprogenitor cells (periosteum) form membrane for bony spicule formation
-
risk factors for delayed healing
- delayed healing: 16-20wks
- nonunion: 9mo+
- smoking
- infection/bone pathology
- inadequate immobilization
- malnutrition, alcoholism, drug abuse
- NSAIDs during inflammatory phase
-
bones w/ poor blood supply, likely to have problems healing
- femoral neck
- scaphoid
- talus of foot
- dens of axis (C2)
-
fractures in children
- periosteum is thicker, more vascularized
- les underlying disease
- unless it occurs @physis, likely to heal faster
- physis = cartilage, weaker than bone, will break before ligaments will tear
-
epiphyseal fractures Salter-Harris classification
- type 1-5
- 1 is where the physis comes off w/the metaphysis
- 5 is a compression, most severe
-
compound v/ comminuted
- compound: breaks skin (eg GSW)
- comminuted: more than 2 fracture segments
-
diagnosis of hidden fracture
- fat pad sign on xray
- fat in joint aspirate
- fat leaks out of marrow
-
osteoid
- ECM produced by osteoblasts
- Fibers: type I collagen (90%), procollagen -procollagen peptidase-> tropocollagen-> collagen microfibrils-> collagen fiber
- Ground substance: hyaluronan (GAG), proteoglycans (GAG+core protein aggrecan), adhesion glycoprotein molecules osteocalcin/osteonectin/osteopontin
-
osteogenesis imperfecta
- deficiency of collagen type I synth, aka "brittle bone disease"
- Type I: normal life span, increased childhood fractures
- Type II: fractures in utero, death shortly after birth
-
mineralization
hydroxyapatite crystals formed by minerals attaching to osteoid
-
osteocytes
- osteoblasts trapped in lacuna of rigid bone matrix
- cell processes extend into canaliculi
-
regulation of osteoclast activity
- calcitonin (C cells of thyroid stroma): binds to osteoclast receptors to inhibit activity
- parathyroid hormone (chief cells of parathyroid gland): stimulate osteoclasts to produce RANKL, which binds to RANK receptors on other osteoclasts and activates them
-
bone resorption
- plamsa membrane of osteoclasts = ruffled border, increases SA for absorption
- resorption pit between ruffled border and Howship's lacuna on the bone
-
cancellous bone
- responds best to compression forces
- lamellar bone, shaped like bony spicules
-
cortical bone
- responds best to torsional forces
- lamellar bone in solid sheets
- circumferential lamellae: on inside and outside surfaces
- osteons: circles of lamellar bone, majority of bone, core is Haversian canal which is formed off of Volkmann's canals and lined w/endosteum
- interstitial lamellae: connects osteons
-
blood supply of long bones
- periosteal arteries: along ligament or tendon insertions
- nutrient artery: thru nutrient canal in diaphysis
- epiphyseal and metaphyseal arteries: unite when growth plate closes
- medullary vascular system: where nutrient artery and metaphyseal/epiphyseal arteries unite
-
intramembranous ossification
- takes place in a membrane of mesenchymal cells
- clavicle, flat bones of skull, some facial bones
- ossification centers w/osteoblasts producing woven bone spicules which are replaced w/lamellar bone
-
endochondral ossification
- primary ossification center forms in diaphysis of hyaline cartilage: chondrocytes hypertrophy, cartilage matrix becomes mineralized, chrondocytes die b/c fluid can't diffuse thru matrix
- blood vessels invade and bring osteoprogenitor cells
- collar of bone is formed
- in long bones, a secondary ossification center @ the epiphysis will form
- vertebra have multiple ossification centers
-
achondroplasia
- growth plate disease
- reduced chondrocyte differentiation
- very short arms and legs, normal otherwise
-
Paget's disease
- imbalance of remodeling process
- often asymptomatic
-
BMUs
- basic multicellular units remodel the bone
- osteoclasts tunnel in a cutting zone
- remodel or replace 10% of bone annually
- mechanical stress is needed for stimulation (can cause sclerosis)
- cement line = where reversal of degradation occured
|
|
