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Step 2 CK · Internal Medicine · Rheumatology

Osteoarthritis: Diagnosis & Stepwise Management

Diagnose at the bedside, then climb the ladder: move, lose weight, rub on an NSAID, replace the joint

Rheumatology·Crystal, Degenerative & Soft-Tissue Disorders·6 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy
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Overview and pathophysiology

Definition. Osteoarthritis is the most common arthritis and a leading cause of disability in older adults. It is a failure of the whole joint: articular cartilage is progressively lost, subchondral bone remodels and scleroses, osteophytes form at the joint margins, and the synovium shows only low-grade inflammation. Synovial fluid therefore stays noninflammatory, with fewer than 2000 WBC/µL.

Risk factors. Age, female sex, obesity, prior joint injury such as ACL or meniscal tears, malalignment, repetitive occupational loading and genetic predisposition all raise risk.

Clinical features and joint pattern

Symptoms and signs. Pain is worse with use and eased by rest; advanced disease adds rest and night pain. Morning stiffness lasts less than 30 minutes, with brief gelling after inactivity. The exam shows crepitus, hard bony enlargement, reduced range of motion and sometimes a cool effusion. Fever, weight loss and other systemic features are absent.

Hands. Heberden nodes (DIP) and Bouchard nodes (PIP) are bony osteophytes. First carpometacarpal disease squares the base of the thumb and hurts with pinch and grip.

Knees, hips and spine. Knee OA usually begins in the medial compartment and produces a varus (bow-legged) deformity. Hip OA causes groin or anterior thigh pain, sometimes felt only in the knee, and the earliest and most painful lost motion is internal rotation; a patient with knee pain, a normal knee exam and painful hip rotation needs hip imaging. Facet and disc degeneration in the cervical and lumbar spine cause axial pain and can narrow the canal or foramina.

Primary OA rarely involves the MCPs, wrists, elbows or ankles. Degenerative change at the second and third MCPs, especially with hook-like osteophytes or chondrocalcinosis, points to hemochromatosis or CPPD: check transferrin saturation and ferritin. Phlebotomy treats iron overload but rarely reverses established arthropathy.

Osteoarthritis versus rheumatoid arthritis
FeatureOsteoarthritisRheumatoid arthritis
Morning stiffness<30 minutes>1 hour
Effect of activityWorsens painEases stiffness
Hand jointsDIP, PIP, first CMCMCP, PIP, wrist; DIPs spared
SwellingHard, bonySoft, boggy synovitis
LaboratoryNormal ESR and CRP; serology unnecessary↑ESR and CRP; RF and anti-CCP
RadiographAsymmetric narrowing, osteophytes, subchondral sclerosis and cystsUniform narrowing, marginal erosions, periarticular osteopenia

Diagnosis and imaging

Clinical diagnosis. A patient aged 45 or older with activity-related joint pain and morning stiffness of 30 minutes or less can be diagnosed without laboratory tests or imaging. ESR and CRP are normal. RF and anti-CCP are not needed; low-titer RF is common in older adults and misleads.

Radiographs. Films are reserved for atypical features, diagnostic doubt or surgical planning. The findings spell LOSS: loss of joint space (asymmetric and nonuniform), osteophytes, subchondral sclerosis and subchondral cysts, without erosions or periarticular osteopenia. Radiographic severity correlates poorly with pain, and MRI is rarely needed.

Erosive hand OA. This inflammatory subset typically affects postmenopausal women, with abrupt, painful and sometimes red flares of the DIPs and PIPs. Radiographs show central erosions with a gull-wing contour, sometimes progressing to ankylosis, and serologies are negative. Psoriatic arthritis differs by marginal pencil-in-cup erosions, dactylitis and nail pitting.

Stepwise management

  1. Foundationexercise, weight loss, tai chi, education, cane, brace or thumb splint
  2. Topical NSAIDfirst drug for knee and hand OA; preferred at age 75 or older
  3. Oral NSAID or duloxetinelowest effective dose with GI, renal and cardiovascular precautions
  4. Intra-articular corticosteroidshort-term relief of knee or hip flares
  5. Total joint arthroplastyrefractory pain and disability with radiographic disease

Nonpharmacologic care. Every patient should get strengthening and aerobic exercise, often through physical therapy, plus weight loss if overweight; losing 5% or more of body weight improves pain and function. Tai chi and self-management programs help. A cane is held in the hand opposite the painful hip or knee, and knee braces and a first CMC orthosis for thumb-base OA are useful.

4 lbless knee load per step for each pound of weight lost
≥5%weight loss that meaningfully improves knee pain and function

NSAIDs. Topical NSAIDs such as diclofenac gel are the first drug for knee and hand OA, particularly in older or comorbid patients, because systemic exposure is minimal. Oral NSAIDs are used at the lowest dose for the shortest time. When GI risk is high (age over 65, prior ulcer, anticoagulant or glucocorticoid use), add a PPI or choose celecoxib; after a prior ulcer bleed, celecoxib plus a PPI carries the lowest risk. Avoid oral NSAIDs in advanced CKD, heart failure and recent myocardial infarction, and monitor blood pressure.

An NSAID added to an ACE inhibitor or ARB plus a diuretic (the triple whammy) can precipitate acute kidney injury.

Other drugs. Duloxetine, an SNRI, is an alternative or add-on, especially with depression or widespread pain. Acetaminophen gives only modest benefit and is hepatotoxic at high doses. Tramadol is reserved for patients in whom other options have failed or are contraindicated.

Injections. Intra-articular corticosteroid, for example triamcinolone, relieves knee or hip flares for several weeks. Injections are spaced at least about 3 months apart because frequent injections may accelerate cartilage loss, and the hip needs image guidance.

Surgery and therapies to avoid

Arthroplasty. Total knee or hip replacement is indicated for severe pain and functional limitation that persist despite adequate conservative therapy, with radiographic disease; it reliably relieves pain and restores function. Complications include venous thromboembolism (routine prophylaxis is given), prosthetic joint infection, dislocation after hip replacement and aseptic loosening. Younger patients with unicompartmental knee disease may be offered osteotomy or partial replacement.

What not to offer. Opioids other than tramadol are avoided because of falls, dependence and poor long-term benefit. Glucosamine and chondroitin perform no better than placebo. Intra-articular hyaluronic acid, platelet-rich plasma and stem cell injections lack convincing benefit. Arthroscopic lavage or debridement, including partial meniscectomy for degenerative meniscal tears, adds nothing to physical therapy. DMARDs such as hydroxychloroquine and methotrexate, and biologics, have no role, even in erosive hand OA.

Secondary osteoarthritis

Clues. Onset before about 45, joints that primary OA spares (MCP, wrist, shoulder, elbow, ankle), rapid progression or florid disease should prompt a search for an underlying cause.

Causes of secondary osteoarthritis
CauseClues
Prior traumaSingle joint; old fracture, ligament or meniscal injury
Hip dysplasia, SCFE, Perthes diseaseHip OA in a young adult
Hemochromatosis2nd–3rd MCP hook osteophytes, chondrocalcinosis, diabetes, bronze skin, hypogonadism
CPPDChondrocalcinosis, wrist and MCP disease, pseudogout attacks
AcromegalyLarge-joint OA, enlarged hands and jaw, coarse features
Ochronosis (alkaptonuria)Urine darkens on standing, blue-black ear cartilage and sclera, calcified discs
Wilson diseaseYoung patient with liver disease or Kayser–Fleischer rings
Neuropathic (Charcot) jointDiabetes or tabes dorsalis; painless, rapidly destroyed joint
HemophiliaRecurrent hemarthroses since childhood
Alkaptonuria is an autosomal recessive deficiency of homogentisate dioxygenase.