ARTHRITIS, OSTEO

ARTHRITIS, OSTEO - Bruce C. Gilliland, MD
BASICS
DESCRIPTION
Most common form of joint disease. Involves progressive loss of articular cartilage and reactive changes at joint margins and in subchondral bone
• Primary
- Idiopathic
- Divided into subsets depending on clinical features
• Secondary
- Childhood anatomic abnormalities (e.g., congenital hip dysplasia, slipped femoral epiphyses)
- Inheritable metabolic disorders (e.g., alkaptonuria, Wilson disease, hemochromatosis)
- Neuropathic arthropathy (Charcot joints)
- Hemophilic arthropathy
- Acromegalic arthropathy
- Paget disease
- Hyperparathyroidism
- Noninfectious inflammatory arthritis (e.g., rheumatoid arthritis, spondyloarthropathies)
- Gout, calcium pyrophosphate deposition disease (pseudogout)
- Septic or tuberculous arthritis
- Post-traumatic
• System(s) Affected: Musculoskeletal
• Synonym(s): Osteoarthrosis; Degenerative joint disease
EPIDEMIOLOGY
• Predominant age
- Symptomatic disease: >40
- Leading cause of disability in those >65
- Radiographic evidence (estimates): 33% to almost 90% in those >65
• Predominant sex: Male = Female
Prevalence
• ~ 60 million patients
• Increases with age
• Almost universal >65 (by x-ray study but not clinically)
RISK FACTORS
• Age >50
• Obesity (weight-bearing joints)
• Prolonged occupational or sports stress
• Injury to a joint from trauma
• Injury to a joint from pre-existing inflammatory arthritis or infectious arthritis
Genetics
Genetic transmission unknown, but a woman with distal interphalangeal joint osteoarthritis is more likely to have a mother or sister with similar joint involvement
ETIOLOGY
Biomechanical, biochemical, inflammatory, and immunologic factors all implicated in pathogenesis


DIAGNOSIS
SIGNS AND SYMPTOMS
• Slowly developing joint pain
• Pain that follows use of a joint
• Stiffness of 15 minutes duration (especially morning and after sitting)
• Joint bony enlargement (e.g., Heberden nodes of distal interphalangeal joints)
• Decreased range of motion
• Tenderness usually absent; may be associated with synovitis and occur along joint margin
• Crepitation as late sign
• Local pain and stiffness with osteoarthritis of spine, with radicular pain (if there is compression of nerve roots)
TESTS
Lab
• Usually not helpful in diagnosis (sedimentation rate not increased)
• May be useful in monitoring treatment with NSAIDs (renal insufficiency and GI bleeding)
• Disorders that may alter lab results: In secondary osteoarthritis, underlying disorder may have abnormal lab results, for example, hemochromatosis (abnormal iron studies).
Imaging
• X-ray films usually normal early
• Later often show
- Narrowed joint space
- Osteophyte formation
- Subchondral bony sclerosis
- Cyst formation
• Erosions may occur on surface of distal and proximal interphalangeal joints when osteoarthritis is associated with inflammation (erosive osteoarthritis).
Diagnostic Procedures/Surgery
• Joint aspiration
- May be helpful in distinguishing between osteoarthritis and chronic inflammatory arthritides
- Osteoarthritis: Cell count usually 500 cells/mm3, predominantly mononuclear
- Inflammatory: Cell count usually >2,000 cells/mm3, predominantly neutrophils
Pathological Findings
• Synovial fluid may have slight leukocytosis, predominantly mononuclear.
• Calcium pyrophosphate dihydrate and/or apatite crystals may occasionally be seen in effusions; require polarized light microscopy or special techniques to see.
• Subchondral bone trabecular microfractures
• Degradation response produced by release of proteolytic enzymes, collagenolytic enzymes, prostaglandins, and immune responses
DIFFERENTIAL DIAGNOSIS
• Distinguish from other types of arthritis by
- Absent systemic findings
- Minimal articular inflammation
- Distribution of involved joints (e.g., distal and proximal interphalangeal joints, not wrist and metacarpophalangeal joints)
• In spine, distinguish from
- Osteoporosis
- Metastatic disease
- Multiple myeloma
- Other bone disease
TREATMENT
GENERAL MEASURES
• Outpatient
• Reassure patient of absence of generalized systemic disease, but recognize potential disability.
• Weight reduction if obese
• General fitness program
• Heat (e.g., local, tub baths)
• Physical therapy to maintain or regain joint motion and muscle strength. Quadriceps-strengthening exercises can relieve knee pain and disability.
• Protect joints from overuse (e.g., cane, crutches, walker, neck collar, elastic knee support)
Diet
No special diet
Activity
As active as tolerated
MEDICATION (DRUGS)
First Line
For management of pain and inflammation
• Acetaminophen 1,000 mg q.i.d. most effective for OA of knee; useful for other sites as 1st line for relief of pain
• If not effective, add nonacetylated salicylates (e.g., salsalate, choline-magnesium salicylate) or low-dose ibuprofen 1,600 mg/day.
• Other NSAIDs have similar efficacy; prolonged use associated with renal insufficiency, hypertension, leg edema, and GI bleeding. Because pain in osteoarthritis varies from day to day, brief courses of an NSAID are preferable.
• Cyclo-oxygenase-2 specific inhibitors are less likely to cause GI ulcers and work as well as NSAIDs in reducing arthritis inflammation and pain; are much more expensive than conventional NSAIDs and should be reserved for patients who are at higher risk for stomach ulcers and bleeding.
• Opioid analgesics (e.g., codeine, oxycodone, propoxyphene) should be restricted for treatment of acute episodes of pain.
Contraindications
• NSAIDs contraindicated in patients with
- Renal disease
- Congestive heart failure
- Hypertension
- Active peptic ulcer disease
- Previous hypersensitivity to an NSAID or aspirin (asthma, nasal polyps, urticaria/angioedema, hypotension)
• Combinations of NSAIDs are contraindicated due to risk of adverse reactions without concomitant improved efficacy.
• Oral or parenteral adrenal corticosteroids are contraindicated.
Precautions
• In patients with history of peptic ulcer disease or risk factors for upper GI bleeding, acetaminophen is recommended.
• If NSAID is necessary because of inadequate response to acetaminophen, it should be given with misoprostol or with proton pump inhibitor.
• Risk factors for upper GI bleeding: Previous history of bleeding or peptic ulcer, 65 years of age, and concomitant use of oral corticosteroids or anticoagulants. In these patients, risk of stomach ulcers can be reduced by such drugs as misoprostol (Cytotec) and the proton pump inhibitors. Be cautious in patients at high risk of coronary artery disease or stroke, given possible increased risk with COX2 inhibitors.
Significant possible interactions
• NSAIDs reduce effectiveness of ACE inhibitors and diuretics; may induce renal insufficency.
• Aspirin and NSAIDs (except COX2 inhibitors) may increase effects of anticoagulants.
• Increased hypoglycemic effects of oral hypoglycemics with aspirin
• Avoid concomitant use of aspirin with NSAIDs.
• 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.
Second Line
• Judiciously use intra-articular injections of corticosteroids for selected acute flare-ups of joints (no more than 3 per year up to a maximum of 12 injections per joint). If used excessively, can accelerate joint deterioration
• Series of injections of hyaluronic acid preparation into painful knee may provide relief of pain and improve function.
• Local application of capsaicin cream for pain relief; most effective in small joints of hand; may cause local burning
ALERT
Pregnancy Considerations
• Acetylsalicylic acid (ASA) and NSAIDs: Some risk to fetus during 1st and 3rd trimester of pregnancy
• Compatible with breast feeding
SURGERY
May be indicated in advanced disease (e.g., osteotomy, debridement, removal of loose bodies, joint replacement, fusion)
FOLLOW-UP
PROGNOSIS
• Tends to be progressive
• Early in course, pain relieved by rest; later, pain may occur at rest and at night.
• Joint effusions may occur, especially in knees.
• Joint enlargement occurs later in course owing to bony enlargement.
• Osteophyte (spur) formation, especially at joint margins, as disease progresses
• Advanced stage with full-thickness loss of cartilage down to bone
COMPLICATIONS
• Decompensated CHF, GI bleeding, decreased renal function on NSAIDs or ASA
• Hypoglycemic reactions (rare) in diabetic patients taking oral hypoglycemic agents
• Infection or accelerated cartilage loss with intra-articular corticosteroids
PATIENT MONITORING
• Follow range of motion and functional status at regular intervals.
• Watch for GI blood loss and follow cardiac, renal, and mental status in older patients on NSAIDs or ASA.
• Periodic CBC, renal function tests, stool for occult blood
REFERENCES
1. Brandt KD. Management of osteoarthritis. In: Ruddy S, Harris ED, Sledge CB, eds. Kelley's Textbook of Rheumatology. 5th ed. Philadelphia: WB Saunders; 2001:1419-1432.
2. Golden BD, Abramson SB. Selective cyclooxygenase-2 inhibitors. Rheumatic Dis Clin N Am. 1999;25:359-378.
3. Hochberg MC, Altman RD, Brandt KD. Guidelines for the medical management of osteoarthritis. Part I. Osteoarthritis of the hip. Arthritis Rheum. 1995;38:1535-1540.
4. Hochberg MC, Altman RD, Brandt KD. Guidelines for the medical management of osteoarthritis. Part II. Osteoarthritis of the knee. Arthritis Rheum. 1995;38:1541-1546.
5. Mankin HJ, Brandt KD. Pathogenesis of osteoarthritis. In: Ruddy S, Harris ED, Sledge CB, eds. Kelley's Textbook of Rheumatology. 5th ed. Philadelphia: WB Saunders; 2001:1391-1407.
6. Solomon L. Clinical features of osteoarthritis. In: Ruddy S, Harris ED, Sledge CB, eds. Kelley's Textbook of Rheumatology. 5th ed. Philadelphia: WB Saunders; 2001:1409-1417.