> Table of Contents > Osteoarthritis
Osteoarthritis
Patrick Wakefield Joyner, MD, MS, LCDR
image BASICS
DESCRIPTION
  • Progressive loss of articular cartilage with reactive changes at joint margins and in subchondral bone
  • Primary
    • Idiopathic: categorized by clinical features (localized, generalized, erosive)
  • Secondary
    • Posttraumatic
    • Childhood anatomic abnormalities (e.g., congenital hip dysplasia, slipped capital femoral epiphysis [SCFE], Legg-Calvé-Perthes disease)
    • Inheritable metabolic disorders (e.g., Wilson disease, alkaptonuria, hemochromatosis)
    • Neuropathic arthropathy (Charcot joints)
    • Hemophilic arthropathy
    • Endocrinopathies: acromegalic arthropathy, hyperparathyroidism, hypothyroidism
    • Paget disease
    • Noninfectious inflammatory arthritis (e.g., rheumatoid arthritis [RA], spondyloarthropathies)
    • Gout, calcium pyrophosphate deposition disease (pseudogout)
    • Septic or tuberculous arthritis
  • System(s) affected: musculoskeletal
  • Synonym(s): osteoarthrosis; degenerative joint disease (DJD)
EPIDEMIOLOGY
  • Symptomatic osteoarthritis (OA) is most common in patients >40 years of age.
  • Leading cause of disability in patients >65 years old
  • Radiographic evidence of OA: 33-90% in those >65 years old
  • Predominant sex: male = female
  • 90% of hip OA is primary. Hip OA is more common in whites.
Prevalence
  • ˜60 million patients
  • Increases with age; radiographic evidence of OA is nearly universally present in patients >65 years old.
  • Moderate to severe hip OA in 3-6% of whites; <1% in East Indians, blacks, Chinese, and Native Americans
ETIOLOGY AND PATHOPHYSIOLOGY
  • Failure of chondrocytes to maintain the balance between degradation and synthesis of extracellular collagen matrix. Collagen loss results in alteration of proteoglycan matrix and increased susceptibility to degenerative change.
  • Biomechanical, biochemical, inflammatory, and immunologic factors contribute to cartilage loss. Attempts at repair most commonly manifest as osteophyte formation.
Genetics
  • Up to 65% of OA may have a genetic link.
  • The heritability of end-stage hip OA has been estimated to be as high as 27%.
  • Twin studies in women show 50% (hip; knee) to 65% (hip) heritability rates of OA.
RISK FACTORS
  • Increasing age: >50 years
  • The effect of age as a risk factor is greatest for hip and knee OA, especially after 70 years of age.
  • Hand OA is most common in postmenopausal women.
  • Obesity (weight-bearing joints)
  • Prolonged occupational or sports stress
  • Injury to a joint from trauma, infection, or preexisting inflammatory arthritis
  • Female gender (knee and hand)
image DIAGNOSIS
PHYSICAL EXAM
  • Joint bony enlargement (Heberden nodes of distal interphalangeal joints; Bouchard nodes of proximal interphalangeal joints)
  • Decreased range of motion of affected joints
  • Tenderness usually absent; may occur along joint margin if synovitis is persistent
  • Crepitation is a late sign.
  • Weakness and wasting of muscles around the joint
  • Local pain and stiffness with OA of spine. Radicular pain (if compression of nerve roots)
  • Changes in joint alignment (genu varum [bow-legs] and genu valgum [knock-knees])
DIFFERENTIAL DIAGNOSIS
  • Crystalline arthropathies (gout; pseudogout): inflammatory arthritides (RA); spondyloarthropathies (reactive arthritis; psoriatic arthritis); septic arthritis
  • Fibromyalgia; avascular necrosis; Lyme disease
DIAGNOSTIC TESTS & INTERPRETATION
Initial Tests (lab, imaging)
  • Routine chemistries are not helpful in diagnosis.
  • X-rays are usually normal early in disease process.
  • As OA progresses, plain films show:
    • Narrowed, asymmetric joint space
    • Osteophyte formation
    • Subchondral bony sclerosis
    • Subchondral cyst formation
  • Erosions may occur on surface of distal and proximal interphalangeal joints (erosive OA).
Follow-Up Tests & Special Considerations
  • May be useful in monitoring treatment with NSAIDs (renal insufficiency and GI bleeding)
  • In secondary OA, underlying disorder may have abnormal lab results (e.g., hemochromatosis [abnormal iron studies]).
Diagnostic Procedures/Other
Joint aspiration
  • May help to distinguish OA from chronic inflammatory arthritis
  • OA: cell count usually <500 cells/mm3, predominantly mononuclear
  • Inflammatory: cell count usually >2,000 cells/mm3, predominantly neutrophils
  • Birefringent crystals in gout (-) and pseudogout (+)
Test Interpretation
  • Macroscopic patchy cartilage damage and bony hypertrophy
  • Histologic phases:
    • Extracellular matrix edema and cartilage microfissures
    • Subchondral fissuring and pitting
    • Erosion and formation of osteocartilaginous loose bodies
  • Subchondral bone trabecular microfractures and sclerosis with osteophyte formation
  • Degradation secondary to release of proteolytic and collagenolytic enzymes, prostaglandins, and associated immune response.
image TREATMENT
GENERAL MEASURES
  • Weight management
  • Heat or cold applications for symptomatic relief
  • Physical therapy to maintain or regain joint motion and muscle strength
    • Quadriceps-strengthening exercises relieve knee pain and disability.
  • Muscle strengthening improves pain in general.
  • Aerobic exercise improves long-term functional outcomes.
  • Exercise must be maintained; benefits are lost 6 months after exercise cessation.
  • Protect joints from overuse; ambulatory aides are beneficial (e.g., cane, crutches, walker) as is proper fitting footwear.
  • Assess for bracing, joint supports, or insoles in patients with biomechanical joint pain or instability:
    • Bracing is more beneficial in patients with unicompartmental disease of the knee.
  • For knee OA in particular, nonpharmacologic modalities are strongly recommended: aerobic, aquatic, and/or resistance exercise and weight loss.
  • Nonpharmacologic modalities that are conditionally recommended for knee OA include medial wedge insoles for valgus knee OA, subtalar strapped lateral insoles for varus knee OA, medially directed patellar taping, manual therapy, walking aids, thermal agents, tai chi, self-management programs, and psychosocial intervention.
P.735

MEDICATION
First Line
  • Manage pain and inflammation:
    • Acetaminophen up to 1,000 mg TID-QID: effective for pain relief in OA of knee and hip
    • Topical NSAID gels, creams have short-term (<4 weeks) benefits. Topical NSAIDs should be a core treatment for knee and hand OA.
    • If acetaminophen or topical NSAIDs are insufficient, consider an oral NSAID/COX-2 inhibitor. Use the lowest effective dose for the shortest time possible. Use is associated with renal insufficiency, hypertension, edema, and GI bleeding.
    • May use nonacetylated salicylates (e.g., salsalate, choline-magnesium salicylate) or low-dose ibuprofen ≤1,600 mg/day
    • Topical NSAIDs and capsaicin is effective as adjuncts and alternatives to PO analgesic/anti-inflammatory agents in knee OA.
  • NSAID contraindications:
    • All PO NSAIDs/COX-2 inhibitors have analgesic effects of a similar magnitude but vary in their potential GI and cardiorenal toxicity.
    • NSAIDs should be avoided in patients with renal disease, CHF, HTN, active peptic ulcer disease, and previous hypersensitivity to an NSAID or aspirin (asthma, nasal polyps, hypotension, urticaria/angioedema).
    • Combination of NSAIDs and full strength aspirin (325 mg) is contraindicated due to risk of adverse reactions.
    • In patients at high cardiovascular risk: Combination of a nonselective NSAID and low-dose aspirin (81 mg) is recommended.
    • Oral or parenteral corticosteroids are contraindicated.
  • Precautions:
    • If PO NSAID/COX-2 inhibitor use is necessary for a patient aged >65 years or a patient <65 years with increased GI-bleeding risk factors, protonpump inhibitors are recommended.
    • Significant possible interactions:
      • NSAIDs reduce effectiveness of ACE inhibitors and diuretics.
      • Aspirin and NSAIDs (except COX-2 inhibitors) may increase effects of anticoagulants.
      • Salicylates reduce effectiveness of spironolactone (Aldactone) and uricosurics.
      • Corticosteroids and some antacids increase salicylate excretion, whereas ascorbic acid and ammonium chloride reduce salicylate excretion and may cause toxicity.
Pregnancy Considerations
  • ASA and NSAIDs have reported fetal risk during 1st and 3rd trimesters of pregnancy.
  • Compatible with breastfeeding
Second Line
  • Topical capsaicin is an adjunct therapy for knee and hand OA; may cause local burning
  • Topical NSAIDs (e.g., diclofenac gel) can lower gastric and renal risks associated with oral NSAIDs.
  • Rubefacients (e.g., oil of wintergreen) are not recommended.
  • Physical therapy: Core strengthening for hip OA and knee muscle strengthening for knee OA decrease joint reactive forces on the affected joint and can relieve pain.
  • Bracing; Medial and lateral unloader braces are effective; long leg alignment x-rays can help determine the appropriate brace (1).
Third Line
  • Intra-articular corticosteroid injections can be used for acute flares and for patients failing firstand second-line treatments. Minimize injections (<2/joint/year).
  • Current recommendations do not support the use of viscosupplementation injections for OA.
  • Platelet-rich plasma (PRP) is more effective than HA injections for early stage knee OA (2).
  • PRP injections appear to be more effective for early OA when done in a series of three (3).
  • Glenohumeral joint OA managed with HA injections and corticosteroid injection have similar outcomes (4).
  • TENS is effective for pain relief in large joint OA.
  • Ultrasound improves injection accuracy.
ADDITIONAL THERAPIES
Address psychosocial factors (i.e., self-efficacy, coping skills). Screen for and appropriately treat anxiety and depression. Improve social support.
SURGERY/OTHER PROCEDURES
Surgery (e.g., osteotomy, débridement, removal of loose bodies, joint replacement, fusion) may be indicated in advanced disease.
COMPLEMENTARY & ALTERNATIVE MEDICINE
  • Nutritional supplements (glucosamine and chondroitin sulfate) may benefit some patients and have low toxicity. There is lack of standardized outcome assessments.Trial results using glucosamine and chondroitin have been mixed. If no response is apparent within 6 months, treatment should be discontinued.
  • TENS units and acupuncture have shown benefit.
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
  • Regularly assess joint range of motion and functional status.
  • Monitor for GI blood loss, cardiac, renal, and mental status in older patients on NSAIDs or aspirin.
  • Periodic CBC, renal function tests, stool for occult blood in patients on chronic NSAID therapy
PATIENT EDUCATION
  • American College of Rheumatology: http://www.rheumatology.org/public/factsheets/index.asp?aud=pat
  • Arthritis Foundation: http://www.arthritis.org
PROGNOSIS
  • Progressive disease: early in course, pain relieved by rest; later, pain may persist at rest and at night.
  • Joint effusions and enlargement may occur (especially in knees), as disease progresses.
  • Osteophyte (spur) formation, especially at joint margins
  • Advanced stage with full-thickness loss of cartilage at which point joint replacement is a consideration
REFERENCES
1. Dessery Y, Belzile EL, Turmel S, et al. Comparison of three knee braces in the treatment of medial knee osteoarthritis. Knee. 2014;21(6):1107-1114.
2. Guler O, Mutlu S, Isyar M, et al. Comparison of short-term results of intraarticular platelet-rich plasma (PRP) and hyaluronic acid treatments in early-stage gonarthosis patients. Eur J Orthop Surg Traumatol. 2015;25(3):509-513.
3. Görmeli G, Görmeli CA, Ataoglu B, et al. Multiple PRP injections are more effective than single injections and hyaluronic acid in knees with early osteoarthritis: a randomized, double-blind, placebo-controlled trial [published online ahead of print August 2, 2015]. Knee Surg Sports Traumatol Arthrosc.
4. Colen S, Geervliet P, Haverkamp D, et al. Intraarticular infiltration therapy for patients with glenohumeral osteoarthritis: a systematic review of the literature. Int J Shoulder Surg. 2014;8(4):114-121.
Additional Reading
&NA;
  • Chen WL, Hsu WC, Lin YJ, et al. Comparison of intraarticular hyaluronic acid injections with transcutaneous electric nerve stimulation for the management of knee osteoarthritis: a randomized controlled trial. Arch Phys Med Rehabil. 2013;94(8):1482-1489.
  • Jiang L, Tian W, Wang Y, et al. Body mass index and susceptibility to knee osteoarthritis: a systematic review and meta-analysis. Joint Bone Spine. 2012;79(3):291-297.
  • Shimizu M, Higuchi H, Takagishi K, et al. Clinical and biochemical characteristics after intra-articular injection for the treatment of osteoarthritis of the knee: prospective randomized study of sodium hyaluronate and corticosteroid. J Orthop Sci. 2010;15(1):51-56.
Codes
&NA;
ICD10
  • M19.90 Unspecified osteoarthritis, unspecified site
  • M19.91 Primary osteoarthritis, unspecified site
  • M19.93 Secondary osteoarthritis, unspecified site
Clinical Pearls
&NA;
  • Patients with OA typically have morning stiffness lasting for <15 minutes.
  • OA most commonly affects the hips, knees, and hands (PIP and DIP joints).
  • Intra-articular steroid injections should be limited to no more than 2 per joint per year (if used at all).
  • Consider PRP for early stage knee OA.
  • American Academy of Orthopaedic Surgeons (AAOS) recommends against the use of HA injections for OA.
  • Long-term therapy should be based on individual patient goals and expectations, particularly regarding pain management and activity level.