SM 225: Osteoarthritis Flashcards
1
Q
What features define Osteoarthritis (OA)?
A
OA is defined by:
Joint failure + pathologic changes in all joints
Loss of Hyaline articular cartilage
Thickening/Sclerosis of the subchondral bony plate
Osteophyte outgrowth at joitn margins
Muscle weakness at effected joints
2
Q
What type of cartilage is affected by OA?
A
OA primarily effects Hyaline cartilage, in areas where joints articulate
3
Q
What is articular cartilage?
A
Hyaline cartilage that is found on the surfaces of bones that interact at a joint, made of collagen and proteoglycans like HA
4
Q
How is the subchondral bony plate effected in OA?
A
The subchondral bony plate thickens and scleroses
5
Q
What are Osteophytes and how do they relate to OA?
A
Osteophytes are outgrowth of bones along the margins of a joint
Osteophytes develop at joints effected by OA
6
Q
How does OA effect the muscles bridging a joint?
A
OA results in weakness of muscle bridging a joint
7
Q
What is Synovitis and how severe is it in OA?
A
Synovitis is inflammation of the Synovial Membrane
The Synovial membrane is a layer of conenctive tissue that lines the inside of a fibrous joint capsule and faces the Synovial fluid in a joint
Mild Synovitis in OA
8
Q
Broadly speaking, what leads to OA?
A
OA Susceptibility caused by Systemic Risk Factors
+
Local Factors
= OA Disease
9
Q
What is the difference between Incident OA and Progressive OA?
A
Incident OA = New OA in healthy joint
Progressive OA = Worsening of pre-existing OA in diseased joint
10
Q
What are the Systemic risk factors for OA?
A
Age (all joint sites)
Gender (all sites, F > M)
Excess Body Weight (especially the knee)
Occupations + Elite Athletic Acitivity
11
Q
Do systemic risk factors for OA predispose OA in a specific joint?
A
No, typically systemic risk factors predispose OA in any joint, but can be worse in a specific joint
Ex: Excess Weight predisposes OA anywhere but especially the Knee
12
Q
What are local risk factors for OA?
A
Local risk factors for OA are risk factors that predipose OA in a specific joint
13
Q
List the local risk factors for incident OA?
A
Incident OA Local Risk Factors:
Major injury (all joints)
Menisectomy (Knee)
Developmental Abnormalities (Hip)
Varus Alignment (Knee)
14
Q
What is a menisectomy and why is it no longer performed?
A
A menisectomy is removal of the meniscus at the Knee joint
No longer performed because it was a strong risk factor for OA, as is any damage to the Meniscus
15
Q
Does OA worsen with age?
A
Yes, OA shows age-related decline as we get older
16
Q
Why does OA worsen with age?
A
OA worsens with age because:
Loss of NMJ protective mechanisms
Chagnes in the cartilage matrix
Reduced regenerative potential of tissue
17
Q
How does the NMJ protect against OA and why does this protection wane with age?
A
NMJ uses muscle/stabilizign ligament function and proprioception to detect dangerous movements and terminate them, to prevent injury that could lead to OA
Older age has less sensitvity to these dangerous movements at the NMJ
18
Q
When do women experience increased risk for OA?
A
Peri and post menopausal women are at increased risk for OA
19
Q
Does excess body weight increase the risk of incident or progressive knee OA
A
Both!
Excess body weight increases the risk of developing knee OA as well as worsening pre-existing OA
Weight reduction reduces risk of incident OA
20
Q
What joints does excess body weight predispose OA in?
A
Incident and Progressive Knee OA
Hip OA (less than Knee)
21
Q
What occupation risk factors increase the risk of Knee OA?
A
Mining and frequent knee bending + heavy lifting
22
Q
What occupational risk factors increase the risk of hip OA?
A
Farming
23
Q
What risk factors increase the risk of elbow OA?
A
Jackhammer operation
24
Q
What occupational risk factors increase the risk of Hand OA?
A
Cotton Mill Work
25
How does non-occupational physical activity alter the risk of OA?
Non-occupational = Rec or non-Elite or Elite
Rec = no increase in risk
Non-Elite Activity = risk only if injured
Elite Athletic = increase in risk
26
Does recreational activity increase the risk of OA?
Nope
27
Does elite physical activity increase the risk of OA?
Yup
28
How does physical activity in general alter the risk of OA?
Both extremes of physical activity incease OA risk
Immobilzation = increased OA Risk
Elite Physical Activity = increased OA Risk
29
Why do developmental abnormalities increase the risk of OA?
Developmental abnormalities can alter the joint surface fit, increasing risk of OA especially at the hip
Ex. Acetabular Dysplasia
30
What is this showing and how does it lead to OA?
This is an Xray comparing a normal hip to a hip with Acetabular Dysplasia
Hip because you can see the Ischium and the Femur's greater Trochanter
Left = normal (rounded socket and head)
Right = abnomral (flattened head/socket and less joint space)
31
What factors in a joint are protective?
Joint capsule and ligaments
Muscle and tendon reactive motion
Synovial fluid
32
How do the joint capsule and ligaments protect against OA?
Soft tissue in the joint restrains excessive motion
Mechanoreceptors give feedback to the spinal cord about dangerous activity via sensory nerves
33
How do muscles and tendons protect against OA?
In a joint, muscles and tendons can distribute load and decelerate/adapt to an impact to minimize injury, lowering chance of OA
34
How does synovial fluid protect against OA?
Synovial fluid reduces friction between the articular cartilage surfaces, helping to preserve cartilage and the bone underneath
35
Is the cartilage in OA the same as healthy aged cartilage?
Nope, OA is a metabolically active damage/repair process that differs from normal aging
36
Is OA a passive process?
No, OA is a metabolically active process that involves a cycle of destruction and repair, with all joint components attempting to produce new tissue
37
Which components of a joint can contribute to repair efforts in OA?
All of them:
New bone = Osteophytes
Synovial hyperplasia
Capsular thickening
Increase in Chondrocyte number/activity
38
Which site of the joint is typically the initial insult in OA?
Any site in the joint can trigger OA:
Bone
Cartilage
Synovium
Capsule
Ligament
Muscle
39
Do all joints with OA experience disease progression, and do they all experience symptom worsening?
Not all joints with OA experience disease progression or symptom worsening
Natural history of compensated and decompensated phases
Disease progression and symptom worsening are indpendent
40
How does disease progression correlate with symptom worsening in OA?
They don't - a joint can look really bad (serious progression) but have mild symptoms, or vice versa
Lots of variation, between and within patients
41
What is compensated OA?
Compensated OA:
Joint Remodeling = Tissue loss
Increased Chondrocyte activity + New bone formation + capsular thickening
42
What cellular/structural changes occur in compensated OA and why?
In compensated OA:
More Chondrocytes
New Bone formation
Capsular thickening
Results in redistribution of forces across a compromised joint
43
What is decompensated OA?
Decompensated OA:
Tissue Loss \> Repair response = Disease + Symptoms
44
Which form of OA results in symptoms, Compensated or Decompensated OA?
Decompensated OA causes symptoms because the repair response can't keep up with tissue loss, leading to disease progression + symptoms
45
Why does healthy Hyaline cartilage have an impact-absorbing activity?
Healthy cartilage has impact-absorbing activity as a result of Compressible Stiffness due to it's makeup:
Type II Collagen + Aggrecan + ECM + Chondrocytes
46
What are the components of healthy Hyaline cartilage?
Type II Collagen
Aggrecan
ECM Proteins
Chondrocytes
47
How does Type II collagen support healthy Hyaline cartilage?
Type II Collagen forms a tight weave that constrains Aggrecan and provides tensile strength
48
What is Aggrecan?
Aggrecan is a proteoglycan made of negatively charged GAG's that is linked to HA
Constrained by Type II Collagen
Repulsion of it's charges and water retion
= Cartilage's compressive stiffness
49
How do Aggrecan and Type II Collagen give Hyaline Cartilage compressive stiffness?
Aggrecan = Proteoglycan made of negatively charged GAG's + Hyaluronic Acid
Type II Collagen constrains Aggrecan in Cartilage
Repulsion of Aggrecan's negative charges and water retention provide Cartilage compressive stiffness, since Collagen holds the Aggrecan in place
50
What is the structure-function relationship in Cartilage?
Cartilage gains structure from Collagen holding Aggrecan in place, allowing water to provide compressive stiffness
51
How does the compressive stiffness of Collagen and Aggrecan benefit chondrocytes?
The compressive stiffness of Collagen and Aggrecan in the ECM protect Chondrocytes from high/repetitive loading
52
Does Aggrecan make cartilage hydrophilic or hydrophobic?
Aggrecan makes Articular Cartilage hydrophilic, allowing for water retention that generates a Hydrostatic pressure that resist compression
53
Besides the ECM, what else do Chondrocytes produce?
Chondrocytes maintain dynamic equilibrium in the Cartilage, producing:
Cytokines + Growth Factors + Enzymes
54
How does OA effect the composition of Cartilage?
Aggrecan is lost and the Collagen-Aggrecan matrix unfurls, leading to loss of Type II Collagen
55
How does the water content of Cartilage change in OA?
Water content initially increases due to more room in the Collagen-Aggrecan matrix as it loses fibers
However, compressive stiffness is lost
Over time, water content in Cartilage decreases
56
How does OA effect the compressive stiffness of Cartilage?
OA results in the loss of Aggrecans and then Type II Collagen, decreasing the compressive-stiffness of Cartilage
Cartilage and underlying bone at a joint becomes vulnerable
57
What factors mediate the Cartialge self-repair effort?
Growth factors:
PDGF + IGF-1 + TGF-B
58
How do Synovial cells alter Articular cartilage equilibrium?
Synovial cells phagocytize Cartialge fragments, causing inflammation and releasing MMP's and Cytokines which further alter the ECM and activate Chondrocytes
59
What enzymes are the major mediators of Cartilage degredation in OA?
Matrix Metalloproteinases (MMPs)
Main protienases = MMP13 and ADAMTS4
Normally regulated by Tissue Inhibitors of MMPs (TIMPs)
60
Describe the pathology of Cartilage over the course of OA?
Initial surface irregularity
Full-thickness defect extending to bone
= Larger Area of Cartilage lost exposing bare bone
61
Describe the pathology of Bone over the course of OA?
After Cartilage is lost exposing Bone:
Thickening and stiffness of Subchondral plae
Osteophytes form at joint margins
62
How is the Synovium altered by OA?
Synovium can become edamtous and inflamed
63
How is the Capusle altered by OA?
Capsule becomes edematous and later fibrosed
64
How many phases of OA are there?
3: Phases 1, 2, 3
65
What occurs during Phase 1 OA?
Phase 1 OA:
Microcracks on Cartilage surface
Edema of ECM
Focal loss of Chondrocytes alternating with areas of Chondrocyte proliferation
66
Which phase of OA presents with focal loss of chondrocytes as well as focal areas of proliferation?
Phase 1:
Early OA shows loss of Chondrocytes in some areas where Cartilage cracks while others proliferate to compensate
67
What occurs during Phase 2 of OA?
Cartilage microcracks deepen
Vertical clefts form in Cartilage
Clusters of Chondrocytes appear around these clefts and at the surface
68
Which phase of OA has vertical clefts form in the Cartilage?
Phase 2 OA, as the microcracks from Phase 1 OA worsen
69
What occurs during Phase 3 OA?
Fissures form in Cartilage causing fragments known as osteocartilaginous loose bodies ot break off
Subchondral bone uncovered
Subchondral cysts form
Subcholdral bone sclerosis
Mild Synovitis
70
What are osteocartilaginous loose bodies?
Fragments of Cartilage that break off during Phase 3 of OA as microcracks form clefts that worsen into fissures
71
Which phase of OA exposes subchondral bone?
Phase 3, as Cartilage is literally falling apart and forming Osteocartilaginous loose bodies
72
Which phase of OA involves synovitis?
Phase 3
73
How can Synovitis in OA be differentiated from RA?
OA Synovitis is mild and focal
RA synovitis is intense and diffuse
74
What joints are effected by OA?
Distal and Proximal Intrapharyngeal Joints of Hands
Cervical and Lumber Spine
First Metatrasopharyngeal Joint of Feet (Big Toe)
Knees
Hips
75
Does Primary OA effect the Tibiofemoral or Patellofemoral joint of the Knee?
Either, or Both
76
Which compartment of the knee is effected by OA, the medial or lateral tibiofemoral compartment?
Either or, but not both, because OA is an asymmetric disease
77
Which joints suggest Primary OA?
Hand
Cervical and Lumbar Spine
Feet
Knees
Hips
Can be one, a few, or many
78
Which joints suggest Generalized OA?
Hands + at least 1 large joint
79
Which joints suggest Secondary OA?
OA in atypical joints, such as:
```
Metacarpopharyngeal Joint (Finger and Hand base)
Wrist
```
Elbow
Shoulder
Ankle
80
Which type of OA has a familial predisposition?
Generalized OA, more common in middle-aged women
81
What are Heberden's nodes?
Enlargements at the Distal Intrapharyngeal Joints
![]()
82
How do Heberdens Node appear in generalized OA?
Multiple Heberden's nodes ![]()
83
How do symptoms vary in Generalized OA?
Symptoms persist for years, but settle down even as disease progresses
Physical Exam may look bad but symptoms may be mild late in disease
84
When should Secondary OA be considered?
Secondary OA if:
Early onset
Atypical site: MCP, Wrist, Elbow, Shoulder, Ankle
85
What conditions can cause secondary OA?
A lot:
Other arthritis, since Secondary is a final common pathway
Injury
Developmental Abnormality
86
Which form of OA represents a final common pathway for arthritis?
Secondary OA, which can be caused by other arthritis like RA and gout
87
Describe the onset of OA?
OA tends to develop slowly, both structurally and for symptoms, and only effect one/few joints at a time
Strong age association
88
How do symptoms change over the course of OA?
Aching is consistent
Early OA - Pain increases with age and is releived by rest
Advanced OA - Pain at rest and use, night pain not relieved easily, sleep interference worsens pain
89
Which form of OA, Early or Advanced, involves constant pain that can extend into the night?
Advanced OA
90
Which form of OA, Early or Advanced, is worsened by sleep interference?
Advanced OA
91
Describe the stiffness in OA and compare it to RA?
Morning stiffness that lasts less than 30 min, shorter duration than RA
Stiffness after inactivity = Gelling
92
Which involves gelling, RA or OA?
Gelling = stiffness after inactivity = OA
93
How does swelling in OA compare to RA?
RA has more pronounced and more persistent swelling than OA
94
What symptoms suggest OA at the Knee?
Knee Pain
Difficulty Walking Up Stairs
Difficulty Standing after Sitting
95
What suggests OA in the Hip?
Pain in groin/buttock
Pain getting in/out of car, shoes, and socks
96
What suggests OA in the spine?
Pain in the region of involvement
Radicular symptoms if Osteophytes compress nerve roots
97
What physical exam findings suggest OA?
Bony enlargement = limit range of motion
Creptius = Crackling sounds
Malalignment
Mild Inflammation
98
What is Crepitus?
A crackling sensation that suggests OA
99
Does moderate/severe inflammation suggest OA?
No, consider joint infection or crystal process
100
What are Bouchards nodes?
Nodes at the PIP Joints
![]()
101
What should laboratory studies show in OA?
Synovial fluid is non-inflammatory:
Low turbidity
Low WBC's ( \< 2000)
102
What role do blood and urine tests have in OA?
None
103
What could be seen on radiography in OA?
Focal joint space narrowing
Osteophytes
Subchondral sclerosis and cysts
104
What is the role of X-Ray in OA?
Confirm Dx and r/o other conditions
Assess OA severity to develop a plan to treat symtpoms
Predict prognosis and course
105
Which predicts course and prognosis in OA, X ray or symptoms?
X ray
106
What is the Role of MRI in OA?
Limited
Shows lots of lesions due to Arthritis but doesn't alter management
Useful if considering arthroscopy or unusually rapid progression of OA
107
When should an MRI be used in OA?
Only if considering an Arthroscopy or investigating rapidly progressing OA
108
What are the key outcomes of OA?
Disease progression = structural changes at joint
Symptoms = pain, stiffness
Function = ability to perform discrete actions
Disability = limition of socially required tasks
109
What is the difference between function and disability?
Function refers to a specific task like getting up or climbing stairs
Disability refers to a socially defined task like cooking or shopping
110
How does the outcome of OA vary?
Outcome varies between each patient and within the joints effected in each patient
111
Can OA worsen without worsening symptoms, limitation, or disability?
Yes, and vice versa: OA can be normal structurally with worse symptoms, limitation, or disability
112
What factors are associated with progression of Knee OA?
Excess body weight
Varus and Valgus alignment
Meniscal damage (ie meniscusectomy)
![]()
113
What factors are associated with function decline in Knee OA?
Excess body weight
Pain severity
Inactivity
Low self-efficacy + Depression + Poor social support
114
What factor is associated with progression of Knee OA and function decline in Knee OA?
Excess body weight
115
Does worsened mental health effect Knee OA structural progression or functional decline?
Worse mental health from low self-efficacy, depression, and low social support predicts function decline in Knee OA
116
What are the treatment goals in OA?
Relieve symptoms
Maintain or improve function
Limit disability
Avoid drug toxicity
117
What drug can modify the course of OA?
None
118
What encompasses non-pharmacologic treatment in OA?
Patient education = self-management programs and social support
Physical and occupation therapy = exercise to preserve ROM's/strength and ADL's
Weight Loss if overweight
119
How does patient education benefit OA?
Increased self-efficacy and coping strategies from self-management programs
120
How do PT and OT benefit OA?
Exercises in PT/OT preserve Range of Motion (ROM) and strength, also improve capacity of Activities of Daily Living (ADL)
121
Does exercise offer physical or cognitive benefits to the prognosis of OA?
Both!
122
What are the systemic pharmacologic treatments for OA?
Non-narcotic analgesics (Acetaminophen)
Anti-inflammatory (NSAIDS)
Narcotics (Advanced OA)
123
What are the local pharmacologic treatments for OA?
Corticosteroids (sparingly) and Hyularonic Acid supplementation
124
Are pharmacologic treatments recommended over non-pharmacologic treatmetns for OA?
No, they're less effective and have an increased risk of side effects and toxicities
125
With NSAIDS, are selective COX-2 inhibitors better than non-selective inhibitors?
Slightly better GI risk, but not more effective and greatly increase CV risk (Vioxx)
126
Does intra-articular Hyularonic Acid supplementation benefit patients with OA?
No clear evidence of benefit
127
What OTC's are available for OA, and do they work?
Glucosamine and Chondroitin, no actual benefit
128
Why are there no disease-modifying agents for OA?
OA progression (structurally) is measured with Xray and that takes years to show change, so no drug trials by companies because it's expensive to track for so long
129
What is the surgical therapy for advanced OA?
Total Joint Replacement
Mild/Moderate OA is less clear
130
What is the surgical treatment for Mild/Moderate OA and when is it used?
Arthroscopy, but only if mechanical symptoms like locking are present
