Osteoarthritis Flashcards
What is Osteoarthritis (OA)?
- Degenerative joint disease
- Painful and often disabling chronic condition
- Can affect any joint
● knee, hip, hand, neck, spine, ankle, feet, shoulder - Multifactorial
● Biomechanical, biochemical, inflammatory, and
immunologic factors - Primary issue: LOSS of articular cartilage
- But, disease of entire joint:
●Cartilage, synovium, capsule, bone & surrounding
ligaments & muscles`
That tends to be more of a chronic nociceptive pain. Although there can be some maladaptive changes that happen in some patients, it can be a bit of an element of dysfunctional pain in there as well depending on what else was going on. But it tends to be more of a tends to be more of a chronic nociceptive.
Pathogenesis of OA
cartilage, synovium
Joint adaptation in response to cartilage injury
Cartilage
* Initial cartilage swelling & matrix synthesis
* Cycle of articular cartilage destruction/repair
* Followed by gradual cartilage loss
The cartilage chondrocytes being the cartilage cells of course, are a vascular and they’re nourished by the cyclic loading and unloading of the joint. The synovial fluid with movement of the joint and loading and unloading allows nutrients and nourishment to flow into the joint. And if you have lots of immobility of the joint, then that is associated with a decreased nutrient supply. So physical activity is very important for joint, joint health.
Synovium
* Synovial inflammation and cytokine release
* Ligament ‘stretching’ and further fibrotic
thickening/encapsulation
Pathogenesis (Continued)
Bone
- Endochondral bony growths (osteophytes)
● “Traction” osteophytes securing ligament
insertions
● Serve to stiffen joint in response to laxity - Early periarticular bone turnover
● Initial trabecular osteopenia - then sclerosis
● Disuse of painful joint - Late subchondral plate sclerosis (thickening)
● Mineralized cartilage ‘tidemark’ duplication
● Cartilage cell death, splitting, full thickness loss
● Necrotic bone cysts
OA Joint Adaptation
This here’s sort of a more three-dimensional depiction of what happens in the difference between the normal anatomy and what you can see in the setting of osteoarthritis, you can see what the osteophytes kinda can look like, as well as some of the cartilage degradation.
. Just kind of an image kinda showing what’s happening more at the cellular level. Looking at the vicious cycle here, right? So you get the tissue damage which results in the release of pro-inflammatory and catabolic factors, which results in more progressive tissue degradation and eventually more release of inflammatory mediators.
What are the causes of OA?
Obesity
* Most important preventable risk factor
* Strong link with knee OA (hip and hand also linked)
* Predictor of prosthetic joint replacement
Occupation, Sports, and Trauma
* Occupations involving excessive mechanical stress and
repetitive motion
* Traumatic injuries (articular cartilage, meniscal damage)
* Quadriceps muscle weakness; ligament injury
● Joint “laxity” (looseness)
Genetic Factors
* Hereditary link
* Heberden’s nodes, Bouchard’s nodes ( > )
Osteoporosis 🡪 “protective” for OA?
Patients who have osteoporosis, gaining weight actually helps because it increases the bone mass, increases the bone thickness, and osteoarthritis, losing weight can be helpful. It’s thought are those two protective for each other? But the studies have shown that not to be the case. And you can actually have both at the same time because osteoarthritis tends to be thickening of the bone kinda closer to the joint. You can still have osteoporosis at other parts of the bone.
Classification
- Primary OA
● More common
● No identifiable cause
● Types: Localized, Generalized, Erosive - Secondary OA
● Known association with underlying cause
● E.g., post-trauma, genetic, obesity
OA Phenotypes
- Post Trauma OA
● Local inflammation (Synovitis) - Metabolic Syndrome OA
● Low grade inflammation - Ageing OA
● Secretory Inflammatory - Genetic OA
● Gene related - Crystal OA
● Innate Immunity
risk factors
knew
hand
hip
Knee
* Age
* Sex (F»M)
* Physical activity
* Obesity
* Intense sport activity
* Quadriceps strength
* Bone density
* Previous injury
* HRT (protective)
* Vitamin D
* Smoking
* Malalignment
* Genetics
hip
* Age
* Physical activity
* Obesity
* Previous injury
* Intense sportbactivity
* Genetics
hand
* Age
* Grip strength
* Occupation
* Intense sport
ctivities
* Genetics
risk factors schematic representation
ok
Clinical Presentation
Progressive development (usually over
years) of:
* Pain*
* Joint stiffness
* Loss of movement/function
Investigations
- History, physical exam, diagnostic imaging, lab
tests all can aid in diagnosis - Need to rule out similar presentations
● Rheumatoid (inflammatory) Arthritis
● OA pain usually confined to affected joints
● RA pain usually multi-joint
● Bursitis, tendinitis, muscle pain
● Suspect infection ? – refer to physician immediately
● Psoriatic arthritis
● Prolonged joint pain – bone tumors ? – refer to
physician
History
* Pain: onset, duration, location, character
● OA tends to be worse after exercise, improves with rest
* Stiffness: AM, inactivity, PM, resolves quickly
(i.e., < 30 min)
* Loss of function: Limited ADL’s
* Distribution: hips, knees, first metatarsophalangeal
joint, distal interphalangeal joints, carpometacarpal
joint, axial skeleton
Physical Exam
* Bony proliferation and/or tenderness
* Crepitus: crepitus or cracking sound from the joint moves,
* Limited range of motion
right now is that osteoarthritis pain is usually confined to the effected joints versus rheumatoid arthritis pain, which usually multi-joint, if you will. I would say that osteoarthritis pain tends to affect only a few joints more commonly, right? So it tends to be more single joint or oligoarticular, if you will, versus rheumatoid arthritis, which tends to affect many joints. Osteoarthritis tends to be asymmetric.
It tends to affect joints on one side of the body. Rheumatoid arthritis tends to be symmetric. It tends to affect the same joints on both sides of the body
Gout would be the presence of uric acid crystals in the joint and pseudo go to be in the presence of calcium pyrophosphate crystals in the joint that would be identified via fluid analysis, of course, some findings relating to history.
You tend to get joint stiffness, particularly in the morning, I would say. Or after long periods of inactivity. Asking about does it tend to be do you tend to have joint stiffness in the morning or other times of the day
usually in osteoarthritis it takes less than 30 min for that joint stiffness to go away with usage of the joint. Another key change or key difference with compared to rheumatoid arthritis where it tends to be that joint stiffness takes longer than 30 min to resolve.
getting a sense of what particular activities tend to tend to elicit the pain
jelly phenomenon is just where after periods of inactivity where the joint becomes really stiff again then actually can sometimes even lock up for a little bit. That’s called the jelly phenomenon and that usually resolves with movement of the joint and such
Investigations
Imaging
Lab Tests
Imaging
● X-ray is gold standard
● Joint space narrowing, osteophyte formation,
subchondral cysts, and bony sclerosis are
hallmarks of OA
● Useful to confirm clinical suspicion of OA and
rule out other causes
Lab Tests
* Not typically indicated for diagnosis
● Moreso to rule out other causes
ESR CRP to try to rule out that there might be some other more significant inflammatory state going on. So I mentioned that the inflammation that happens in osteoarthritis tends to be very minor and usually not enough to create a big raging CRP or something like that,
There’s not really currently any clinically used serum markers of osteoarthritis,
American College of Rheumatology (ACR)
Diagnostic Criteria
Knee OA
(Clinical & radiographic criteria)
* Pain in the knee most days
* Osteophytes on X-ray
* Plus one of the following:
● Age > 50 yrs
● morning stiffness no more than 30min
● crepitus on motion
So they have for knee criteria using both clinical and radiographic findings. So if the patient has pain in the knee most days, as well as osteophytes on x-ray plus one of these down here, then that would be considered meeting the criteria for a diagnosis of knee osteoarthritis
half of patients with radiographic factors or radiographic evidence of osteoarthritis don’t have any symptoms of osteoarthritis, which is pain and et cetera, and vice versa. That about half of patients with pain related to osteoarthritis will not have any radiographic evidence of it.
Hip OA
(Clinical & radiographic criteria)
* Pain in the hip most days and at least 2 of the following:
● ESR < 20 mm/h
● Femoral or acetabular osteophytes
on X-ray
● Joint space narrowing on X-ray
Knee OA (Clinical criteria only):
⚫ Pain in the knee most days and at least 3 of the following:
◦ Age > 50 yrs
◦ morning stiffness no more than 30min
◦ crepitus on motion
◦ bony enlargement
◦ bony tenderness
◦ no palpable warmth
Pharmacist Role in OA?
PHIT OA – Pharmacist Initiated Intervention for OA
* Cluster RCT, 32 pharmacies, n=139 patients
* Intervention: Questionnaire, education, pain med
management, physio guided exercise, communication with GP
* Usual care: Education Pamphlet
* Results
● OA Quality Indicator Pass Rate: 45% higher (34 – 56%)
● Improved WOMAC global, pain & function scores (at 3&6 m)
* Authors’ Conclusion: Pharmacists can launch a
multidisciplinary intervention to screen for OA, improve
utilization of treatments, and improve function, pain, & QOL
Goals of Therapy
- Modification of disease progression
● Disease Modifying OA Drugs (DMOADs) ? There is no D modes we have do not have any drugs that actually modify the disease progress, at least not that are actively routinely use, that modify the disease progression, the drugs that we use or more so for symptomatic management. - Pain and symptom relief
● Joint stiffness, swelling - Maintain or improve mobility
● Joint function - Maintain or improve Quality of Life
