4/17 Osteoarthritis - Corbett Flashcards
key points in MSK history
- duration
- acute vs chronic
- number of joints affected
- monoarticular vs polyarticular
- inflammatory vs noninflammatory
- stiffness? swelling/arythema/warmth?
- symmetric vs asymmetric
monoarticular arthritis
need to confirm that its a JOINT issue (not soft tissue)
- aggravated by movement (passive ROM)
- assoc with loss of motion
- assoc with swelling/erythema
trauma, inf, crystal-induced arth, osteoarth, systemic rheumatic disease
polyarthritis ddx
SYNOVITIS
- soft tissue swelling
- warmth over joint
- joint effusion
- loss of motion
osteoarthritis
role/features of CARTILAGE
- MOST COMMON joint disease
- prevalence increases with age
- common cause of intractable pain → reason for seeking medical care
disease of articular cartilage
- cartilage lines articular area of synovial joints
- serves as self-lubricating shock absorber w low friction (synovial fluid adds viscosity)
- component of epiphyseal growth plate → allows for growth of long bones
- avascular : no blood supply, no nerve/lymph supply either
- synovial fluid provides nutrients to cartilage
- synovial membrane lacks basement membrane → allows for quick/easy exchange of nutrients
- ECM made of type II collagen plus proteoglycans
- proteoglycans: high capacity to absorb water → good shock absorber, flexible, elastic
osteoarthritis
pathophysiology: fundamental/minor components
causes
stepwise sequence
fundamental: DEGENERATION of articular cartilage
minor: also involves inflammation
either due to:
-
physical damage to normal cartilage (biomech/biochem)
- macrotraumas or repeated microtraumas resulting in:
- release of degradative enzymes
- inadequate repair responses
- macrotraumas or repeated microtraumas resulting in:
-
defective cartilage (defect in type II collagen gene)
- normal joint loading → failure = osteoarthritis
step-wise…
- damaged cartilage : chondrocyte enlargement, proliferation, disorganization
- chondrocyte repair
- repair fails →→→ vertical and horizontal vibrillation/cracking of matrix
- synovitis
…full thickness articular cartilage lost
structural changes with OA
progressive fracturing and loss of articular cartilage
- devpt of subchondral bone cysts
- incr subchondral bone thickness (subchondral sclerosis)
- formation of osteophytes (new bone at joint margins)
OA morphology/special features
full-thickness portions of cartilage get sloughed off and are loose in the joint → JOINT MICE
exposed subchondral bone plate becomes new articular surface, scrapes up → BONE EBURNATION
osteoarthritis risk factors
- AGE
- genetics
- congenital/devpt (hip)
- obesity (knee)
- weight management for prevention!
- trauma-induced mech jt instability
OA pain and sx and locations
PAIN in joints
- worse with activity
- relieved by rest
crepitus (cracking/popping) of joints
systemic manifestations are NOT features of primary OA
etiology of OA pain?
NOT from articular cartilage or menisci
why? no nerve endings!
pain from:
- periosteum
- subchondral bone
- synovium
- periarticular structures (ex. bursitis)
inflammatory vs mechanical/degenerative process
passive vs active vs resisted movement
OA vs rheumatoid arthritis
OA of knee
varus deformities (bow legged) more common
- preferential loss of articular cartilage on medial surface of tibio-femoral jt
- Baker’s cysts: large collection of fluid extended from synovial cavity
OA of hip
1. devptal deformities
- issues with blood supply to head of femur
- corticosteroids
- sickle cell
- posterior dislocaiton of hip
- femoral neck fracture
2. Legg Calve Perthes disease
- idiopathic avascular necrosis in femoral head of child
- boys age 4-10
3. slipped capital femoral epiphysis
- femoral head looks like it slipped off
OA hip dx: decr ROM with restriction in internal rotation
- hip pain + two of following:
- ESR < 20mm/hr
- radiographic evidence of femoral/acetabular osteophytes
- radiographic evidence of jt space narrowing
hand OA
DIP joints affected? NOT rheumatoid! prob OA
summary and management of OA
