This document provides guidance on evaluating and managing patients presenting with monoarthritis or polyarthritis. It discusses common causes of monoarthritis including septic, traumatic, and crystal deposition diseases. It also reviews key questions to ask patients and appropriate diagnostic tests. For polyarthritis, it distinguishes between acute and chronic presentations and lists associated diseases. The document then focuses on osteoarthritis, outlining risk factors, symptoms, diagnostic criteria, and pharmacological and non-pharmacological treatment approaches including exercise, weight loss, analgesics, and surgery.

1. Approach to the patient with Monoarthritis
 Diseases that commonly present with 1 joint:

2. 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

3. Polyarticular diseases occasionally p/w one
joint of onset
 RA
 JA
 Viral
 Sarcoid
 ReA
 PsA
 IBD-arthritis
 Whipples
 OA

4. 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?

5. The patient with polyarticular symptoms
 Diseases that present with acute polyarticular sx:
 Chronic polyarticular sx?

6. 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

7. Chronic polyarticular

8. 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

9. Evaluation and Management
of Osteoarthritis

10. 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?

11. 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

12. OA Case 1: Radiographic Features
 Joint space narrowing
 Marginal osteophytes
 Subchondral cysts
 Bony sclerosis
 Malalignment
 MAKE THE
DIAGNOSIS

13. OA: Laboratory Tests
 No specific tests
 No associated laboratory abnormalities;
eg, sedimentation rate
 Investigational: Cartilage degradation products in
serum and joint fluid

14. Understanding Disease Mechanisms
 OA is mechanically driven, but chemically
mediated…

16. Immunostain of OA Cartilage
Melchiorri, et. al. 1998

17. TNFa
IL-1B
IL-6
IL-8
MCP-1
NO
PGE2
IL-18
0 20 40 60 80 100
IL-18
PGE2
NO
MCP-1
IL-8
IL-1b
TNFa
IL-6
0 20 40 60 80 100
ELISA
Units
Spontaneous Production of Inflammatory Mediators
by Normal and OA-affected Cartilage
Attur et al. Osteoarthritis and Cartilage 2002

18. 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)

19. OA: Risk Factors
 Why did this patient develop osteoarthritis?

20. OA: Risk Factors (cont’d)
 Age: 75% of persons over age 70 have OA
 Female sex
 Obesity
 Hereditary
 Trauma
 Neuromuscular dysfunction
 Metabolic disorders

21. 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

22. QuickTime™ and a
Photo CD Decompressor
are needed to use this picture
Case 1: Prognosis
 Natural history of OA: Progressive cartilage loss,
subchondral thickening, marginal osteophytes

23. 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

24. 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

25. 0
20
40
60
80
20 40 60 80
Men
Age (years)
Prevalence
of
OA
(%)
0
20
40
60
80
20 40 60 80
Women
Age (years)
Prevalence
of
OA
(%)
Age-Related Prevalence of OA:
Changes on X-Ray
DIP
Knee
Hip
DIP
Knee
Hip

26. Case 2: Distal and Proximal
Interphalangeal Joints

27.  Radiograph shows
severe changes
 Most common
location in hand
 May cause significant
loss of function
Case 2: Carpometacarpal Joint

28.  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

29. 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)

30. 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

31. Underlying Disease Associations of
OA and CPPD Disease (pseudogout)
 Hemochromatosis
 Hyperparathyroidism
 Hypothyroidism
 Hypophosphatasia
 Hypomagnesemia
 Neuropathic joints
 Trauma
 Aging, hereditary

32. 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

33. Pharmacologic Management of OA
 Nonopioid analgesics
 Topical agents
 Intra-articular agents
 Opioid analgesics
 NSAIDs
 Unconventional therapies

34. 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 stretching
Rogind, et al. Arch Phys Med Rehabil. 1998;79:1421–1427.
Jette, et al. Am J Public Health. 1999;89:66–72.

35. 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

36. 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

37. 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

38. 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.

39. 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

40. 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

41. 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

42. 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.

43. 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

44. OA: Unconventional Therapies (cont’d)
• Keep in touch with current information.
• ACR Website
(http://www.rheumatology.org)
• Arthritis Foundation Website (www.arthritis.org)

45. 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

46. 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

47. 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

48. 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