Approach to the patient with Monoarthritis
Diseases that commonly present with 1 joint:
Approach to the pt w/ Monoarticular sx:Diseases that commonly p/w monoarthritis
Septic: bacterial, mycobacterial, lyme, fungal Traumatic: fx, internal derangemt, hemarthrosis
(sickle) Crystal deposition: gout, CPPD, hydroxyapatite
deposition disease, calcium oxalate Other: OA, JA, coagulopathy, AVN bone, foreign-
body synovitis, tumor
Polyarticular diseases occasionally p/w one joint of onset
RA JA Viral Sarcoid ReA PsA IBD-arthritis Whipples OA
Important questions? What should you ask the patient? What’s critical to determine ASAP? What’s the most useful test to determine
etiology? What other labs/studies should be obtained?
The patient with polyarticular symptoms Diseases that present with acute polyarticular sx:
Chronic polyarticular sx?
Acute polyarticular Infection: GC, Meningococcal, lyme, ARF, BE,
viral (hepatitis B/C, parvovirus, EBV, HIV)
Other inflammatory: RA, systemic JA, SLE, ReA, PsA, polyarticular gout, sarcoid
Chronic polyarticular
Chronic Polyarthritis Inflammatory: RA, JA, SLE, SSc, polymyositis,
ReA, PsA, gout, IBD, CPPD, sarcoid, vasculitis,
PMR Non-inflammatory: OA, FM, hypermobility
syndrome, hemochromatosis
Migratory, Additive, Intermittent
Evaluation and Management of Osteoarthritis
Osteoarthritis: Case 1
• A 65-year-old man comes to your office complaining of knee pain that began insidiously about a year ago. He has no other rheumatic symptoms• What further questions should you ask?• What are the pertinent physical findings?• Which diagnostic studies are appropriate?
OA: Symptoms and Signs Pain is related to use Pain gets worse
during the day Minimal morning
stiffness (<20 min) and after inactivity (gelling)
Range of motion decreases
Joint instability Bony enlargement Restricted movement Crepitus Variable swelling
and/or instability
OA Case 1: Radiographic Features Joint space narrowing Marginal osteophytes Subchondral cysts Bony sclerosis Malalignment MAKE THE
DIAGNOSIS
OA: Laboratory Tests No specific tests No associated laboratory abnormalities;
eg, sedimentation rate Investigational: Cartilage degradation products in
serum and joint fluid
Understanding Disease Mechanisms OA is mechanically driven, but chemically
mediated…
Immunostain of OA Cartilage
Melchiorri, et. al. 1998
TN Fa
IL -1 B
IL -6
IL -8
MC P-1
N O
PGE2
IL -1 8
0 2 0 4 0 6 0 8 0 1 0 0
IL-18
PGE2
NO
MCP-1
IL-8
IL-1
TNF
IL-6
0 20 40 60 80 100
EL
ISA
Units
Spontaneous Production of Inflammatory Mediators by Normal and OA-affected Cartilage
Attur et al. Osteoarthritis and Cartilage 2002
Candidate Biomarkers in OA
• CRP (obesity??)• COMP, Keratan sulfate, HA, YPL-70• Type II collagen fragments• Type II C-propeptide (synthesis)• Proteoglycan/aggrecan fragments• Markers of bone turnover
(osteocalcin,NTx)• Imaging (x-ray, MRI, ultrasound)
OA: Risk Factors Why did this patient develop osteoarthritis?
OA: Risk Factors (cont’d) Age: 75% of persons over age 70 have OA Female sex Obesity Hereditary Trauma Neuromuscular dysfunction Metabolic disorders
Case 1: Cause of Knee OA On further questioning, patient recalls fairly
serious knee injury during sport event many years ago
Therefore, posttraumatic OA is most likely diagnosis
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Case 1: Prognosis Natural history of OA: Progressive cartilage loss,
subchondral thickening, marginal osteophytes
OA: Case 2 A 75-year-old woman presents to your office with
complaints of pain and stiffness in both knees, hips, and thumbs. She also has occasional back pain
Family history reveals that her mother had similar problems
On exam she has bony enlargement of both knees, restricted ROM of both hips, squaring at base of both thumbs, and multiple Heberden’s and Bouchard’s nodes
Distribution of Primary OA Primary OA typically
involves variable number of joints in characteristic locations, as shown
Exceptions may occur, but should trigger consideration of secondary causes of OA
0
20
40
60
80
20 40 60 80
Men
Age (years)
Pre
vale
nce
of O
A (
%)
0
20
40
60
80
20 40 60 80
Women
Age (years)
Pre
vale
nce
of O
A (
%)
Age-Related Prevalence of OA: Changes on X-Ray
DIP
Knee
Hip
DIP
Knee
Hip
Case 2: Distal and Proximal Interphalangeal Joints
Radiograph shows severe changes
Most common location in hand
May cause significant loss of function
Case 2: Carpometacarpal Joint
X-ray shows osteophytes, subchondral sclerosis, and complete loss of joint space
Patients often present with deep groin pain that radiates into the medial thigh
Case 2: Hip Joint
What If Case 2 Had OA in the “Wrong” Joint, eg, the Ankle?
• Then you must consider secondary causes of OA• Ask about previous trauma and/or overuse• Consider neuromuscular disease, especially
diabetic or other neuropathies• Consider metabolic disorders, especially
CPPD (calcium pyrophosphate deposition disease—aka pseudogout)
Secondary OA: Diabetic Neuropathy 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
Underlying Disease Associations of OA and CPPD Disease (pseudogout)
Hemochromatosis Hyperparathyroidism Hypothyroidism Hypophosphatasia Hypomagnesemia Neuropathic joints Trauma Aging, hereditary
Management of OA
• Establish the diagnosis of OA on the basis of history and physical and x-ray examinations
• Decrease pain to increase function• Prescribe progressive exercise to
• Increase function• Increase endurance and strength• Reduce fall risk
• Patient education: Self-Help Course• Weight loss• Heat/cold modalities
Pharmacologic Management of OA Nonopioid analgesics Topical agents Intra-articular agents Opioid analgesics NSAIDs Unconventional therapies
Strengthening Exercise for OA
• Decreases pain and increases function• Physical training rather than passive therapy• General program for muscle strengthening
• Warm-up with ROM stretching• Step 1: Lift the body part against gravity,
begin with 6 to 10 repetitions
• Step 2: Progressively increase resistance with
free weights or elastic bands• Cool-down with ROM stretchingRogind, et al. Arch Phys Med Rehabil. 1998;79:1421–1427.
Jette, et al. Am J Public Health. 1999;89:66–72.
Reconditioning Exercise Program for OA
• Low-impact, continuous movement exercise for 15 to 30 minutes 3 times per week• Fitness walking: Increases endurance, gait
speed, balance, and safety• Aquatics exercise programs—group support• Exercycle with minimal or no tension• Treadmill with minimal or no elevation
Nonopioid Analgesic Therapy
• First-line—Acetaminophen• Pain relief comparable to NSAIDs, less toxicity• Beware of toxicity from use of multiple
acetaminophen-containing products• Maximum safe dose = 4 grams/day
Nonopioid Analgesic Therapy (cont’d)
• NSAIDs• Use generic NSAIDs first• If no response to one may respond to another• Lower doses may be effective• Do not retard disease progression• Gastroprotection increases expense• Side effects: GI, renal, worsening CHF, edema• Antiplatelet effects may be hazardous
Nonopioid Analgesics in OA
• Cyclooxygenase-2 (COX-2) inhibitors• Pain relief equivalent to older NSAIDs• Probably less GI toxicity• No effect on platelet aggregation or bleeding
time• Side effects: Renal, edema• Older populations with multiple medical
problems not tested• Cost similar to generic NSAIDs plus proton
pump inhibitor or misoprostol
Medical Letter. 1999;41:11–12.
Medical Letter. 1999;41:11–12.
Nonopioid Analgesics in OA (cont’d)
• Tramadol • Affects opioid and serotonin pathways• Nonulcerogenic• May be added to NSAIDs, acetaminophen• Side effects: Nausea, vomiting, lowered
seizure threshold, rash, constipation, drowsiness, dizziness
Opioid Analgesics for OA
• Codeine, oxycodone• Anticipate and prevent constipation• Long-acting oxycodone may have fewer CNS
side effects• Propoxyphene• Morphine and fentanyl patches for severe pain
interfering with daily activity and sleep
Topical Agents for Analgesia in OA
• Local cold or heat: Hot packs, hydrotherapy• Capsaicin-containing topicals
• Use moderately supported by evidence • Use daily for up to 2 weeks before benefit• Compliance poor without full instruction• Avoid contact with eyes
OA: Intra-articular Therapy• 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
• Joint lavage• Significant
symptomatic benefit demonstrated
• Hyaluronate injections*• Symptomatic relief • Improved function• Expensive• Require series of
injections• No evidence of long-
term benefit• Limited to knees
* Altman, et al. J Rheumatol. 1998;25:2203.
OA: Unconventional Therapies
• Polysulfated glycosaminoglycans—nutriceuticals • Glucosamine +/- chondroitin sulfate:
Symptomatic benefit, no known side effects
• Doxycycline as protease/cytokine inhibitors• Under study• Have disease-modifying potential
OA: Unconventional Therapies (cont’d)
• Keep in touch with current information.
• ACR Website (http://www.rheumatology.org)
• Arthritis Foundation Website (www.arthritis.org)
Referral and Imaging If pain out of proportion to XRAY findings, can
refer to rheum or ortho, and get MRI Also, for unstable joints, need MR Primary or secondary failure of treatment regimen
should prompt further imaging and referral Please obtain imaging BEFORE THE PATIENT
GETS TO THE CONSULTANT If there is any question of systemic inflammatory
disease, check labs including CBC, ESR, CRP, rheumatoid factor, anti-CCP, (ANA), IgGs as well
Surgical Therapy for OA
• Arthroscopy• May reveal unsuspected focal abnormalities• Results in tidal lavage• Expensive, complications possible
• Osteotomy: May delay need for TKR for 2 to 3 years
• Total joint replacement: When pain severe and function significantly limited
OA: Management Summary
• First: Be sure the pain is joint related (not a tendonitis or bursitis adjacent to joint)
• Initial treatment• Muscle strengthening exercises and
reconditioning walking program• Weight loss• Acetaminophen first• Local heat/cold and topical agents
OA: Management Summary (cont’d)
• Second-line approach• NSAIDs if acetaminophen fails• Intra-articular agents or lavage• Opioids
• Third-line • Arthroscopy• Osteotomy• Total joint replacement