Term
[image]
77 year old man
• Bilateral knee pain
• Began insidiously ten years ago
• Pain worsens as the day goes on and with activity
• Denies any other systemic symptoms. |
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Definition
| so this is a case that would lead you towards thinking that this is more arthritic rather than a systemic inflammatory process |
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Term
[image]
-59 yo woman
• Notesthatherknuckles are changing shape over the past several years
• Difficulty opening jars, typing for prolonged periods of time on the computer because of pain |
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Definition
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Term
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Definition
Disease characterized by
• Loss of articular cartilage
• Increased bone formation
• Mild synovitis
Results in joint pain and dysfunction |
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Term
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Definition
• Disables 10% of persons >60
– 2nd only to ischemic heart disease as cause of work disability in men > 50
• Economic impact >$60 billion (U.S.) |
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Term
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Definition
• Extracellularmatrix
– Collagens (mainly II)
– Hyaluronan
– Proteoglycans (mainly aggrecan)
• Chondrocytes
– Synthesize matrix
– Generate degradative enzymes
• Avascular |
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Term
| Cartilage in Osteoarthritis |
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Definition
• Alteredchondrocyte
phenotype
• Perpetuated by surrounding synoviocytes, osteoblasts
• Imbalance between matrix synthesis/degradation
• Alteration in matrix composition |
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Term
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Definition
So in early stage of disease, like we talked about, you see early degradation of cartilage. You see reactive bone formation. And as the disease progresses, this cartilage damage worsens to the point where the bones can be touching. There's no cartilage in between them. You'll notice that this is asymmetric, meaning that this is happening in the lateral aspect of the knee, whereas the medial aspect of the knee still has normal cartilage and probably, in this patient, would be asymptomatic and painless.
Whereas this area, with bone on bone, maybe may have an infusion. It may be tender. It may be painful. And clearly, you can see at the bottom over here, this bony hypertrophy or bony growth. |
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Term
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Definition
• Classically ,OA has been considered a non- inflammatory, degenerative disorder
• There is increasing evidence that inflammation
may be playing some role
– Histologically: evidence of inflammatory cells,
elevated inflammatory cytokines
– Radiographically: evidence of synovial thickening
– Clinically:
• Local response to injectable steroids
• Clinical subset: inflammatory osteoarthritis
• Source of inflammation unclear – Crystals? |
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Term
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Definition
• Age (75% of persons >70) • Genetics (~50%)
• Biomechanical factors
• Trauma
• Obesity
• Female sex
• Neuromuscular dysfunction
• Metabolic disorders |
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Term
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Definition
| he joints affected increase over time in both men and women as they get older, and that the most common joints affected are the knee, the hip, and the hand, and that you see that the incidence is much greater in women than it is in men, and that this incidence rises uniformly with time and with age, which makes sense. As you get older, your OA gets worse or develops. |
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Term
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Definition
• Pain worse with use
• Pain as day progresses
• Minimal morning stiffness (<30 minutes) and after inactivity (gelling)
• When severe, can have rest and nocturnal pain |
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Term
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Definition
• Pain with movement
• Bony enlargement
• Restricted movement
• Crepitation
• Joint instability
• Joint deformity |
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Term
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Definition
[image]
But you can see here, one of the new joints we haven't talked about when compared to inflammatory arthritis so far is that the Temporal Mandibular Joint, the TMJ joint, is involved. You also have cervical neck involvement.
You have lumbar spine involvement, which is not involved in RA. You have hip involvement, which is involved in RA. When you talk about the hands, you talk about the DIPs, which is not seen in RA. You talk about the PIPs. The DIPs get Hebridean's nodules, which are nodules on the DIP, and the PIPs would get Bouchard's nodules, bumps or nodules on the PIP.
When interesting-- we know RA effects the wrist, but when we talk about OA, it typically spares the carpal bones, but effects the carpal metacarpal bone and junction. And patients can get crepitus here, and you can do multiple therapies for this, which include corticosteroid injection or conservative therapy with splinting or a systemic NSAID therapy. Knees, obviously, we know are a sign of-- a place for getting OA. And when it comes to the foot, the ankle and feet and tarsal bones are typically spared. Typically, OA of the foot manifests in the first metatarsal or the great toe. |
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Term
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Definition
• No specific tests
• No associated laboratory abnormalities; eg, sedimentation rate
• Investigational: Cartilage degradation products in serum and joint fluid |
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Term
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Definition
| Clear/yellow, transparent, High, Firm, <2,000, <25% PMNs, Negative |
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Term
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Definition
• Joint space narrowing
• Marginal osteophytes
• Subchondral cysts
• Bony sclerosis
• Malalignment
[image] |
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Term
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Definition
• Diagnosis is made clinically; xrays are supplementary/confirmatory
– Early OA can be painful but without xray changes
– Radiographic OA can be present but without pain, or not the source of patient’s pain |
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Definition
| thumb pinch and grip, affected in OA |
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Definition
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Definition
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Term
| What if the patient has OA in the “wrong” joint? |
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Definition
• Then you must consider secondary causes of OA
– Ask about previous trauma and/or overuse
– Consider neuromuscular disease, especially diabetic or other neuropathies (lower extremity bias)
– Consider metabolic disorders, especially CPPD (calcium pyrophosphate deposition disease) (upper extremity bias) |
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Term
| Secondary OA: Diabetic Neuropathy |
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Definition
• MTPs 2 to 5 involved in addition to the 1st bilaterally
• Destructive changes on x-ray far in excess of those seen in primary OA
• Midfoot involvement also common |
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Term
| Differential Diagnosis for OA |
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Definition
• Non-joint pain
– Hip pain: ex. bursitis, iliopsoas tendinitis – Knee pain: ex. bursitis, patellar tendinitis
• Inflammatory arthritis |
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Term
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Definition
• Goals
– Patient education about disease and management – Pain control
– Improving function and decrease disability
– Altering the disease process and its consequences*
• Treatmentmodalities – Nonpharmacologic
– Pharmacologic
– Surgical |
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Term
| non-pharmacologic treatment for OA |
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Definition
• Patienteducation
– Heat/cold application – Weight loss
• Physicaltherapy:progressive exercise to
– Increasefunction
– Increaseenduranceandstrength – Reducefallrisk
• Orthotics
– Neoprene sleeves
– Braces (unicompartmental knee OA)
– Shoe inserts |
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Term
| Pharmacologic: Analgesia for OA |
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Definition
• Acetaminophen: first line
– Maximum dose 4 g/day
– Hepatic toxicity
– Caution with multiple acetaminophen containing compounds
• NSAIDs: if acetaminophen ineffective/signs of inflammation
– Possibly more effective than acetaminophen but more toxicity (GI, renal, cardiovascular)
– Lowest effective dose
– COX-2 inhibitors
– Topical NSAIDs (1% diclofenac gel) |
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Term
| Pharmacologic therapy for OA |
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Definition
• Tramadol
– Affects opioid and serotonin pathways
– Nonulcerogenic
– May be added to NSAIDs, acetaminophen
– Side effects: nausea, vomiting, lowered seizure threshold, rash, constipation, drowsiness, dizziness
• Opioids
• Topicalagents – Capsaicin
– NSAIDs |
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Term
| OA: Intra-articular Therapy |
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Definition
• Intra-articular steroids
– Good pain relief
– Most often used in knees, up to q 3 mo
– With frequent injections, risk infection, worsening diabetes, or CHF
• Hyaluronate injections
– Symptomatic relief
– Improved function
– Expensive
– Require series of injections
– Predominantly used in knees |
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Term
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Definition
• Arthroscopic irrigation: – No benefit
• Osteotomy:
– May delay need for TKR for 2 to 3 years
• Total joint replacement:
– When pain severe and function significantly limited |
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