Week 4: Synovial Fluid and OA

synovial fluid is made of

blood plasma with additions of proteins and hylauronic acid

analysis of synovial fluid involves

arthrocentesis, surgical withdrawl of fluid from cavity

5 categories of arthrocentesis

normal, group 1-4

group 1- non inflammatory

OA, early RA, trauma, SLE, aseptic necrosis, scleroderma

SLE

autoimmune disease causing widespread inflammation and tissue damage to organs

scleroderma

autoimmune connective tissue and rheumatic disease that causes inflammation of skin and other areas

group II-inflammatory

RA, gout, rheumatic fever, reiters syndrome

rheumatic fever

inflake or make heart/joints/brain/skin swell. immune response to earlier infection

Reiters syndrome

arthritis caused by infection

group III- purulent

infections- bacterial, viral, TB

group 4: hemmorhagic has presence of

blood in synovial fluid. if any blood is there, it is here.

group 4 consists of

trauma, charcot, fracture, hemophilia, tumor, joint prosthesis, sickle cell trait, internal derangement, major ligament tear

other category is

fat, which indiactes fractures

cloudy synovial fluid indicates

leukocytes, if more than 2000 be worried about inflammatory joint disease

treatment of arthrocentesis

antibiotics, drainage of fluid from joint

4 functions of hyaline articular cartilage

distribute forces across bone, transmit loads/shear forces to bone, protect subchondral bone, permit frictionless movement

HAC disease process as we age causes what 2 things

fibrillation(fracture of collagen), depletion of ground substacne

OA def

loss of articular cartilage with secondary changes in subchondral bone

Is OA inflammatory or noninflammatory?

noninflammatory but may have some subsets that have inflammatory episodes

primary OA (idiopathic)

develops spontaneously in middle age and progresses slowly, occurs without any preexisting joint disease

secondary OA

most common, follows joint dysfunction/trauma and abnormal stresses on joint, can be at any age

associated factors with secondary OA

obesity, high degree of activity, physical disabilities

pathology of OA

cartilage becomes worn, thin and frayed. Subchondral bone is exposed and compressed, has osteophyte formation, shape changes when new bone is formed

what 2 things are shown on radiographs for OA

osteophyte formation, subchondral sclerosis, bony cyst formation, joint space narrowing, periarticular sclerosis

subchondral sclerosis

new bone formed in areas of stress

bony cyst formation

fluid filled sac within subchondral bone

Hand in OA

heberden's nodes at distal PIP

symptoms of OA

dull aching pain, relieved by rest

signs of OA

stiffness lasting 30 min or less, crepitus, joint deformity, loss of function

medical tests for OA

radiographs, class 1 synovial fluid analysis

Kellgren and Lawerence Grade 1 (KL)

softening of cartilage, doubtful narrowing of space, possible osteophyte formation

KL grade 2

fragmentation and fissuring cartilage, area is .5 inch or less in diameter, definite osteophyte and possible narrowing

KL grade 3

area of involvement more than .5 inch in diameter, moderate multiple osteophytes, definite narrowing, some sclerosis, possible deformity on bone ends

KL grade 4

full thickness injury with exposed bone, large osteophytes, marked narrowing, severe sclerosis, definite deformity of bone ends

Eburnation

degeneration process of bones, changes the subchondral bone into dense substance with smooth surface (like ivory)