Unit 2 Joint Cartilage Injury and Osteoarthritis and Rheumatoid Arthritis Flashcards
what is the tidemark line?
where the articular cartilage affixes to the subchondral bone
Is cartilage vascular and neural?
no, and has no perichondrium
what are the 2 main components of articular cartilage composition?
extracellular matrix (fibrous proteins and ground substance) and cells (chondrocytes)
what do the chondrocytes do in cartilage?
responsible for making the extracellular matric components
maintain matrix and break down waste product in the matrix
how do chondrocytes get nutrients and get rid of waste?
through the synovial fluid which is facilitated by the loading and unloading of the tissue
what are the four zones of articular cartilage fibers?
superficial or tangential (highest concentration of fibrils)
middle or transitional (fibers appear disorganized)
deep (fibers perpendicular to surface)
calcified cartilage (fibers perpendicular to surface)
what type of collagen is the articular cartilage mostly made up of?
type 2
what is the function of collagen?
forms a network that can resist tensile load which provided stability to the matric and interacts with the proteoglycans and water to form gel like matrix
what does water do for the articular cartilage?
gives the cartilage the ability to absorb compressive loads
what are the two phases of the biphasic material? describe them.
solid phase: fatigue resistant, sustains high stress and strains of loading
fluid phase: compliant, able to diffuse load over increased surface area
what phase is primarily in use during loading?
fluid phase supports 90% of load
load is being accepted and managed by the movement of fluid within the cartilage
what is the difference between fluid film and boundary?
fluid film: in fast low load movements
boundary: in slow severe load movements
how does cartilage exchange nutrients?
(it is avascular and alymphatic)
uses synovial fluid exchange, passive diffusion, compression-induced convection, and reciprocal loading
what is compression-induced convection?
reciprocal loading and unloading squeezing the fluid in and out like a sponge
what is the main source of metabolism for joint cartilage?
chondrocytes synthesize, repair, and remodel the extracellular matrix
what regulates metabolism activity in cartilage?
chemical factors
mechanotransduction
electrical fields within cartilage
what is the effect of immobilization on cartilage?
cartilage can degrade and sustain damage
there is greater degeneration with rigid immobilizatoin
what are the effects of vigorous exercise after a period of immobilization?
may increase tissue degeneration but moderate exercise may help
what are the effects of aging on cartilage?
chondrocytes slow in production of collagen and PG
chondral cell proliferation ceases, the rate of synthetic activity decreases, and the total number of chondrocytes is reduced
when do aging changes start to appear?
by age 30
what are the mechanical changes to cartilage with osteoarthritis?
decreases tensile stiffness and diminished compressive properties
what does the degree of repair to cartilage depend on?
extent of damage and nature of activity following damage
why is there lack of repair in a cartilage injury?
lack of blood flow, lack of inflammatory process, isolated from sources of stem cells, lack of chondrocyte mobility, ineffective matric formation across lesion
what is arthrocentesis?
the flushing of the joint with saline
what is an arthroscopy?
flushing the joint, clearing debris, and shaving frayed cartilage
what is arthodesis?
fusing a joint (common in arms, toes, and wrist)
how does A/PROM and cyclic motion help a cartilage injury?
active/passive help with PG production
cyclic helps with cell synthesis
Osteoarthritis is the leading cause of ___ amount older adults.
disability
what are the most commonly affected joints with osteoarthritis?
knees, hips, and hands
what is the pathology and disease process of osteoarthritis?
chondrocytes fail to repair damaged articular cartilage causing an unstable matrix
-chondrocytes injured, metabolism decreases, and then decreased proteoglycans
-increased proteases that increase chondrocyte death, decreased ECM production
-decreased water content, become stiff and brittle
what is a type 3 chondral injury?
full thickness
progressive cartilage loss, penetrating to subchondral bone (causes inflammatory response)
what macro changes occur with osteoarthritis?
progressive cartilage loss
subchondral bone reaction/remodeling (sclerosis)
osteophyte formation
synovial inflammation
what are the two types of osteoarthritis?
primary: unknown origin
secondary: due to injury/insult
what is primary osteoarthritis?
localized or generalized forms
localized OA most commonly effects the hands, hips, spine, knees, and feet
-generalized OA affecting three or more joint sites
what is secondary osteoarthritis?
occurs post-traumatic and with congenital or developmental disorders (CPPD)
what is the etiology of osteoarthritis?
multifactoral
-aging
-obesity
-joint injury: trauma or repetitive microtrauma
-chronic low grade joint inflammation
-heredity/genetics
what are the commonly affected joints with osteoarthritis?
cervical and lumbar spine
hand: 1st CMC, PIPs, DIPs
hip
knee
foot: 1st MTP, subtalar joint
what are the risk factors for osteoarthritis?
50+
male <45, female >45
family history
occupation
past injuries, congenital/developmental conditions
obesity
what clinical signs would we see in our physical examination that would point towards an osteoarthritis diagnosis?
crepitus
bony enlargement
decreased ROM
malalignment or deformity
tenderness to palpation
mild, localized joint effusion + ^ temp
impaired muscle performance
impaired balance
impaired gait and transfers
what is crepitus?
can be palpated when the joint is in motion
feels like crackle, grindy, crunchy (lack of smoothness)
if the patient is not fitting the pattern for OA what other diagnoses could be affecting the patient (similar to presentation of OA)?
rheumatoid arthritis
gout
CPPD
septic joint
polymyalgia rheumatica
what would you see in a radiographic evaluation of osteoarthritis?
reduced joint space
osteophyte formation
subchondral sclerosis
subchondral cysts
what is sclerosis?
a response of bone to change in load.
cartilage is not there to absorb some of the load so the increased pressure causes thickening of the bone
what are osteophytes?
spurs that grow off bone as bone responds to change in load
what are the differences between RA and OA?
RA: systemic autoimmune, symmetrical, can occur at any age, morning pain/stiffness > 30 min, constitutional symptoms, small joints of hand (MCPs and PIPs)
OA: local joint disease, unilateral/asymmetrical, more common as older, morning pain/stiffness <30 min, no constitutional symptoms, PIPs and DIPs, thumb CMC
what are constitutional symptoms?
fatigue, low grade fever, appetite changes
when homeostasis is disrupted
what would you see in a radiographic evaluation of RA?
periarticular osteoporosis
joint space narrowing
juxta articular erosions
large cystic erosions of bone
bony proliferation
marked deformities
when ambulation or joint stability is significantly impacted what assistive device can a patient with osteoarthritis use?
cane (strong)
tibiofemoral brace (strong)
patella (conditional)
what are some joint protection and energy conservation strategies that a patient with OA can use?
monitor activities and stop when discomfort or fatigue developed
alternate activities, balance work and rest
maintain ROM and strength
avoid deforming positions
use stronger and larger muscles when possible
The best exercise is ___.
the exercise that the pt will actually do.
what is the benefit of retraining proprioception in the LE in patients with OA?
could decrease fall risk and even out some of the loads that may be antagonizing the condition
how long does a joint replacement usually last?
10-15 years or more
what is rheumatoid arthristis?
a progressive, systemic, autoimmune inflammation
often aggressive, devastating consequences
what is RA characterized by?
symmetric synovitis - chronic polyarthritis
joint erosions, cartilage and bone destruction
multisystem - extra-articular manifestations
onset usually slow and insidious over months
With RA there is an imbalance between ___ and ___. What does this cause?
proinflammatory and anti-inflammatory markers.
causes a constant and chronic inflammatory reaction
what is the time line of function loss in RA?
2 years from onset of symptoms = moderate loss of function
5 years from onset = severe loss of function
10 years from onset = very severe loss of function
I order to diagnose RA 4 or more of these criteria must be present”
morning stiffness > 1 hour
arthritis of > 3 joint area of the possible 28
arthritis of hand joints
symmetric swelling
(first 4 must be present for 6 weeks or more)
serum rheumatoid factor
rheumatoid nodules
radiographic changes
With RA what is typical involved?
Wrist joints and MCP joints - very commonly involved
Index and middle Metacarpophalangeal joints
Proximal interphalangeal joints (PIP)
Metacarpophalangeal joint (MCP)
Metatarsophalangeal joints (MTP)
Elbows, Shoulders
Knees, Ankles, Hips. Lumbosacral area is not involved
Spine: only Atlanto-axial joint (C1– C2), subluxation
Terminal interphalangeal (TIPS) joints are not involved
In the spine why do you think only the atlanto-axial joint (C1-C2) is involved or affected in RA?
it is the only purely synovial joint in the cervical spine
synovial inflammation leads to joint erosion and erosion of soft tissue
does not have a lot of inert/boney stability and requires soft tissue integrity for stability
