section name header

Basics ⬇

Author: KevindeWeber, MD, FAAFP, FACSM, RMSK

Description

A predominantly noninflammatory, slowly progressing, degenerative condition of articular cartilage, sometimes known as “degenerative joint disease”

Epidemiology

Incidence

Exact incidence depends on the definition or technology used to identify. Knee or hip replacement for osteoarthritis (OA) is performed on ~1/3 of Americans.

Prevalence

  • Radiographic prevalence exceeds symptomatic prevalence.
  • Symptomatic prevalence significantly increases with age and varies with affected joint (1):

Etiology and Pathophysiology

  • OA is caused by an imbalance between breakdown and repair of joint tissue:
    • Cartilage matrix (collagen, water, proteoglycans) slowly degrades.
    • Chondrocytes slowly die off; those that remain are unable to maintain adequate repair.
    • Mechanical forces contribute to progressive cartilage loss.
  • Early stages: cartilage fibrillation (fine fraying)
  • Middle and late stages: formation of extra subchondral bone and cysts and osteophytes (usually at joint margins)
  • Predominantly noninflammatory, but occasional mild inflammatory clinical flares

Risk-Factors

ALERT
Systemic risk factors (1) contribute to development of OA by creating an environment where the joint is vulnerable:
  • Age: strongest risk factor—10-fold increase between ages 30 and 65 yr
  • Genetics: comprises 40–65% or risk; stronger for hand/hip than for knee
  • Obesity: 29% of risk; linear increase in risk with rising body mass index (BMI); increases risk in hand, knee, and hip, so metabolic as well as biomechanical factors involved
  • Gender: female sex with higher severity and prevalence
  • Nutritional factors: no conclusive data on vitamins or minerals

Joint biomechanical risk factors (1) cause direct trauma to articular cartilage:

  • Joint injury (fractures, dislocations, ligament and meniscal ruptures, articular surface damage)
  • Occupations involving high physical demands: repetitive use of joints, heavy lifting, frequent squatting
  • Sports: knee OA associated with elite-level impact sports; hip OA associated with elite-level impact sports, especially handball, soccer, and hockey. Competitive running is associated with more knee and hip OA compared to recreational running (2)[A].
  • Abnormal joint biomechanics (dysplasia [hip OA], leg length inequality [knee OA], malalignment, instability, abnormal innervation). Cam-type femoro-acetabular impingement predisposes to hip OA.

Genetics

OA has a genetic component, especially in women. Primary, generalized OA is polygenic and multifactorial; environmental factors play a significant role in gene expression.

General Prevention

  • Avoidance of joint trauma or extremes of joint activity (immobilization or gross overuse)
  • Weight reduction

Commonly Associated Conditions

Diagnosis ⬆ ⬇

  • OA is diagnosed primarily through history and physical examination and confirmed by plain films. It can be classified as primary or secondary.
  • Primary classification (idiopathic): related to systemic risk factors mentioned earlier; may be particular or generalized
  • Secondary classification: Causes include previous trauma/internal derangement and inflammatory or deposition joint diseases (e.g., gout, rheumatoid arthritis [RA], CPPD).
  • Most commonly affected joints include the distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints of the hands; carpometacarpal (CMC) joint of the thumb; and the 1st metatarsophalangeal (MTP), hips, knees, cervical spine, and lumbar spine.

History

  • Insidious onset over months to years is typical.
  • Most common symptoms are pain (especially after excessive activity), crepitus or grinding, and noninflammatory joint swelling.
  • There is typically short-lived (<30 min) stiffness after immobilization (i.e., on awakening), improving with mobilization.
  • Some patients experience muscular weakness in the surrounding soft tissue and pseudoinstability.
  • There may be a personal history of antecedent joint trauma or a family history of OA.

Physical Exam

  • Joint line tenderness is common in hands and knees.
  • Joints may have crepitus, decreased range of motion (ROM), effusion, and atrophy of surrounding muscles.
  • In knees, involved compartments can include medial (most common), patellofemoral, and/or lateral, so accurate palpation is important. Effusion and trace joint warmth are common in acute flares.
  • In hands, may see nodules in the DIP and PIP joints, termed Heberden and Bouchard nodes, respectively
  • In hips, decreased and painful internal rotation are early signs, and tenderness over the anterior joint line is a later finding.
  • Severely affected joints may appear misshapen or deformed due to osteophytes or malalignment.

Differential Diagnosis

Diagnostic Tests & Interpretation

Initial Tests (lab, imaging)

  • Laboratory assessment only used to rule out other disorders, if clinically suspected:
    • Markers of inflammation (erythrocyte sedimentation rate, C-reactive protein) usually are normal but may be slightly elevated during inflammatory flare-ups.
    • Rheumatoid factor and antinuclear antibody titers are negative.
    ALERT
    Plain films are the modality of choice for diagnosis, severity assessment, and monitoring progression (3):
    • Hip: Weight-bearing anteroposterior (AP) films are most sensitive.
    • Knee: Weight-bearing AP in 20 to 45 degrees of flexion (Rosenberg view) is most sensitive and accurate for the medial and lateral compartments. Supine lateral and sunrise or merchant views are best for patellofemoral compartment.
    • Shoulder: true glenohumeral AP (Grashey) view most sensitive
    • Thumb CMC joint: true AP (Robert) view of the thumb, wrist AP, and oblique
    • Hands: AP and lateral
  • X-ray characteristics include osteophytes, joint space narrowing, subchondral sclerosis, and cyst formation.
  • Radiographic severity does not correlate with symptom severity.
    ALERT
    Radiographic severity is quantified using the Kellgren-Lawrence scale; OA is grade 2 or higher:
    • Grade 0: no features of OA
    • Grade 1: equivocal osteophytes
    • Grade 2: definite osteophytes
    • Grade 3: joint space narrowing
    • Grade 4: bone-on-bone appearance
  • Computed tomography (CT) and magnetic resonance imaging (MRI) do not play a significant role in diagnosis of OA but should be considered if other conditions are suspected. MRI is sensitive in detecting OA of the knee, but there is a high rate of false-positive findings that may not correlate with signs and symptoms. However, MRI can help with differentiation of other causes of pain (i.e., insufficiency fracture, interosseous pathology).

Diagnostic Procedures/Other

Arthrocentesis and joint fluid examination are not routinely necessary unless the diagnosis is in question; there is a possibility of septic arthritis/crystal deposition disease, or for treatment of tense effusion.

Treatment ⬆ ⬇

General Measures

  • The “core set” of treatments for all patients should include patient education, weight loss if overweight/obese, and an exercise program (4)[A].
    ALERT
    Patient education is important and effective (5,6,7)[A]:
    • Set reasonable expectations on outcome (pain reduction, increased function, not cure).
    • Modification of activities to minimize pain and risk of joint trauma
    • Importance of nonpharmacologic therapies
  • Weight reduction of 5% or more improves knee and hip pain (4,5,6,7)[A].
  • Exercise and weight reduction of 11.4% is associated with no pain at 18 mo in 38% of patients. Exercise has an immediate beneficial effect.
  • Aquatic and low-impact land-based aerobic exercise, strength training, and ROM exercise are all beneficial; programs involving all types may be most beneficial (4,5,6,7)[A].
  • Walking aids for knee and hip OA (cane, crutch in contralateral hand; walkers for bilateral OA) (5,6,7)[A]
  • Optimal management requires a combination of nonpharmacologic and pharmacologic modalities (7)[A].
ALERT
  • Surgical replacement is best reserved for patients with severe pain that affects quality of life or activities of daily living who have failed multiple conservative measures (7)[C].

Medication

No disease-modifying agents are yet available.

First Line

  • Oral glucosamine sulfate (not hydrochloride [HCl]) 1,500 mg/day and/or chondroitin sulfate 1,200 mg/day modestly reduce pain in hip/knee/hand OA (5,7)[A] but probably have no disease-modifying effect.
  • Topical nonsteroidal anti-inflammatory drugs (NSAIDs) are effective; onset of pain reduction 1 to 2 wk and work as well as oral NSAIDs (4,5,6,7)[A]
  • Older studies show that topical capsaicin is effective for knee OA; high incidence of local irritation (4,5,6,7)[A]

Second Line

  • Oral NSAIDs effective but have higher risks; reserved for short-term therapy (4,5,6,7)[A]:
    • Cyclooxygenase-2 (COX-2) inhibitors are not more effective; less gastrointestinal (GI) toxicity but not without risks
    • Discourage chronic use of NSAIDs; if necessary, add gastroprotection with a proton pump inhibitor or misoprostol.
  • Viscosupplementation with intra-articular injection of hyaluronate derivatives may be modestly effective in pain reduction (4,5,6,7)[A]:
    • 2 to 5 weekly injections
    • 2- to 5-wk delay in effects
    • 1- to 6-mo duration of effects
  • Intra-articular injections with corticosteroids are effective for 2 to 4 wk (4,5,6,7)[A]:
    • Reserve for patients not responding to oral medications or for inflammatory flare-ups
    • Limit to 3 to 4 injections per year per joint.
    • No long-term adverse effect on diabetic control

Third Line

  • Duloxetine (a pain-modulating serotonin and norepinephrine reuptake inhibitor [SNRI]) reduces chronic pain in knee or multijoint OA, especially in those who catastrophize (4,5)[A].
  • Weak opioids (e.g., tramadol, codeine) can be considered for short-term refractory pain; those requiring long-term use may benefit from maximization of nonpharmacologic therapies and/or surgery (4,5,6,7)[A]. Long-term use and stronger opioids should be avoided because research now shows no improved pain scores at 1 yr compared to acetaminophen or NSAIDs and greater risks. Opioids if given within 2 yr of total knee arthroplasty (TKA) worsen long-term outcomes after surgery.
  • Intra-articular injection of platelet-rich plasma (PRP) improves pain and function in knee OA up to 12 mo after single injection, with greater efficacy than hyaluronate (8)[A].
  • Intra-articular stem cell injection may improve pain and function in knee OA for 24 to 48 mo and may have disease-modifying activity, but results are limited by high risk of bias (9)[B].

Issues for Referral

  • A multidisciplinary approach may help patients make the most of available therapies: physical therapy, personal exercise training, health care education, nutrition, complementary and alternative medicine, and so on.
  • Surgical referral when cartilage has thinned to “bone-on-bone” status and pain/dysfunction are marked despite conservative therapies.

Additional Therapies

  • Valgus bracing for isolated medial knee OA with varus malalignment improves stability and reduces pain in some patients (4,5,6,7)[A]. Ideal patients are not obese and are younger and more physically active.
  • Soft braces for knee OA can improve pain and function (4,5,6)[A].
  • Wedge insoles for isolated medial or lateral knee OA may be effective; evidence is conflicting (4,5)[A].
  • Thermal therapies (heat, cold) may be effective (5)[A].
  • Transcutaneous electrical nerve stimulation (TENS) can provide only short-term relief for knee OA (4)[A].
  • Walking aids (e.g., cane) reduce pain in hip/knee OA (4,5,6,7)[A].

COMPLEMENTARY & ALTERNATIVE MEDICINE

  • Acupuncture reduces pain briefly and slightly in knee OA (7)[A].
  • Massage therapy may improve pain and function (7)[A].
  • Balneotherapy (spa, mineral baths; common in Europe) may improve pain and function in knee OA (6)[A].
  • Traditional Chinese medications are likely effective in improving pain in knee OA (10)[A].
  • Therapies with no proof of efficacy include static magnets and electrotherapy/neuromuscular electric stimulation.

Surgery/Other Procedures

  • Indicated in patients with recalcitrant pain and interference with activities of daily living despite maximizing conservative management (5)[B]
  • Arthroscopic débridement for mechanical symptoms (catching, giving out) not effective, even for partial meniscal tears (5)[A]
  • Medial or compartment knee OA:
    • Wedge osteotomy may be effective (5)[B].
    • Unicompartmental arthroplasty (replacement) effective (5)[B]
    • Interposition arthroplasty (joint spacer insertion); no data on safety/efficacy
  • TKA: very effective (4)[C]:
    • Hardware durable 10 to 15 yr
    • Try to delay TKA until after 55 yr by maximizing other treatments.
    • Rate of hardware failure <10 yr is 3 times in <55 versus >70 yr of age.
  • Patellofemoral joint (PFJ) OA in isolation (rare):
    • Elevation of tibial tubercle may be effective.
    • PFJ arthroplasty sometimes used
  • Total hip arthroplasty or joint resurfacing is effective in hip OA (5)[B].
  • Glenohumeral OA: total shoulder replacement more effective/durable than humeral head replacement
  • Cartilage replacement techniques for severe focal defects are gaining in popularity and evidence:
    • Autologous cartilage implantation: Arthroscopy harvests patient’s cartilage, chondrocytes are replicated in culture, and second arthroscopy fills cartilage defect with cells.
    • Osteoarticular cartilage transplant: Cartilage from patient’s non–weight-bearing surface in knee joint is placed into defect.
    • Cadaver cartilage allografts to fill large defects

Ongoing Care ⬆ ⬇

Follow-up Recommendations

  • Follow-up to monitor efficacy of treatments and to try additional treatments if needed may improve outcomes by building a trusting patient-provider relationship.
  • Reassessment of radiographic joint space worsening in patients not responding to conservative measures can be considered every 2 to 4 yr to assist in planning surgical referral.

Diet

  • Supplements that may produce large, clinically important short-term pain reduction in OA include collagen hydrolysate, passion fruit peel extract, Curcuma longa extract, Boswellia serrata extract, curcumin, pycnogenol, and L-carnitine (11)[A].
  • Supplements that may produce clinically important medium-term pain reduction are green-lipped mussel extract and undenatured type II collagen (11)[A].
  • Supplements that may produce statistically significant pain reduction of unclear clinical importance include undenatured type II collagen, avocado soybean unsaponifiables, methylsulfonylmethane (MSM), and diacerein (11)[A].

Patient Education

See “Treatment”/“General Measures”:

Prognosis

OA is a progressive arthropathy with highly variable course.

References ⬆ ⬇

American College of Radiology. ACR Appropriateness Criteria. See Nontraumatic Knee Pain, Chronic Hip Pain, Chronic Ankle Pain, Chronic Wrist Pain. https://acsearch.acr.org/list. Accessed August 29, 2018.

  1. Neogi T, Zhang Y. Epidemiology of osteoarthritis. Rheum Dis Clin North Am. 2013;39(1):1–19.
  2. Alentorn-Geli E, Samuelsson K, Musahl V, et al. The association of recreational and competitive running with hip and knee osteoarthritis: a systematic review and meta-analysis. J Orthop Sports Phys Ther. 2017;47(6):373–390.
  3. Bruyère O, Cooper C, Pelletier JP, et al. An algorithm recommendation for the management of knee osteoarthritis in Europe and internationally: a report from a task force of the European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO). Semin Arthritis Rheum. 2014;44(3):253–263.
  4. Rillo O, Riera H, Acosta C, et al. PANLAR consensus recommendations for the management in osteoarthritis of hand, hip, and knee. J Clin Rheumatol. 2016;22(7):345–354.
  5. McAlindon TE, Bannuru RR, Sullivan MC, et al. OARSI guidelines for the non-surgical management of knee osteoarthritis. Osteoarthritis Cartilage. 2014;22(3):363–388.
  6. Zhang W, Nuki G, Moskowitz RW, et al. OARSI recommendations for the management of hip and knee osteoarthritis: part III: changes in evidence following systematic cumulative update of research published through January 2009. Osteoarthritis Cartilage. 2010;18(4):476–499.
  7. Dai WL, Zhou AG, Zhang H, et al. Efficacy of platelet-rich plasma in the treatment of knee osteoarthritis: a meta-analysis of randomized controlled trials. Arthroscopy. 2017;33(3):659.e1–670.e1.
  8. PasHI, Winters M, Haisma HJ, et al. Stem cell injections in knee osteoarthritis: a systematic review of the literature. Br J Sports Med. 2017;51(15):1125–1133.
  9. Chen B, Zhan H, Marszalek J, et al. Traditional Chinese medications for knee osteoarthritis pain: a meta-analysis of randomized controlled trials. Am J Chin Med. 2016;44(4):677–703.
  10. Liu X, Machado GC, Eyles JP, et al. Dietary supplements for treating osteoarthritis: a systematic review and meta-analysis. Br J Sports Med. 2018;52(3):167–175.

Clinical Pearls ⬆

  • OA is a degenerative disorder of joints and is predominantly noninflammatory but can have inflammatory flares.
  • Core treatments for all types include patient education on goals and self-management, multimodal exercise, and weight reduction for those overweight.
  • Multidisciplinary treatment—providers, physical therapists, nutritionists, fitness trainers, nurse educators, complementary/alternative therapists—can optimize outcomes.
  • Topical NSAIDs, exercise, and weight loss are first-line therapies.
  • Opioids should be avoided.