Osteoarthritis and Crystalline Arthritis

Question 1

Describe the clinical signs and symptoms of osteoarthritis (OA)

Answer 1

Pain related to use
Pain worsens throughout day
Minimal morning stiffness

Question 2

Describe the risk factors for OA

Answer 2

Age (75% of persons over 70 have OA)
Female sex
Obesity
Hereditary
Trauma
Neuromuscular dysfunction (can't feel pain, don't stop stressing joint)
Metabolic disorders

Question 3

Upon investigation, what would you find in OA if you were to sample the serum of the pt and synovial fluid of an affected joint?

Answer 3

Cartilage degradation products in serum and joint fluid

Question 4

In which joints do you typically find OA?

Answer 4

Hips
Knees
Feet (big toe joint) 
Hands
Spine (lumbosacral and cervical)
*NOT ANKLE*

Question 5

What are Heberden’s and Bouchard’s nodes?

Answer 5

Bony outgrowths from joints of DIP (Heberden’s) and PIP (Bouchard’s)

Question 6

Generally, how do we treat OA?

Answer 6

decrease pain to increase function

• nonopioid analgesics
• topical agents
• intraarticular agents
• opioid analgesics
• NSAIDS

prescribe progressive exercise
weight loss
hot/cold modalities

Question 7

Describe the changes in normal cartilage seen histologically?

Answer 7

Pits and fissuring of the cartilage surface. Smooth surface converted to jagged surface with crevasses and subsurface microcysts. No major lymphocytic infiltration.

Question 8

Gout - pathophysiology

Answer 8

• hyperuricemia results from either overproduction or underexcretion (more common) of uric acid, which is produced in the course of purine turnover
• long-term hyperuricemia (>6.8mg/dl) results in the precipitation of monosodium urate (MSU) crystals (not uric acid crystals) and deposition into the joints, where inflammatory cells (esp. NTs) are activated, attracting additional inflammatory cells/mediators
• most commonly affected joints are the distal lower extremities (lower blood supply, lower temp, more acidic - easier to precipitate) as well as the skin over extensor surfaces of UE and LE joints, and chronic gout can lead to tophi, or MSU deposits in the skin
• contributing factors include red meat, beer, hereditary deficiency of HGPRT, and renal insufficiency (failure to excrete as much uric acid as it should)

Question 9

Gout - clinical presentation and treatments

Answer 9

• begins as acute monoarticular arthritis, typically reaching maximal inflammation within a day and resolving in 5-7days
• will present with hyperuricemia, MSU crystals in synovial fluid and/or tophi samples (needle shaped crystals are negatively birefringent), and radiologic findings
• cholchicine, indomethacine, allopurinol, febuxostat, probenecid, pegloticase (reserved for refractory tophaceous gout)

Question 10

Calcium Pyrophosphate Dihydrate (CPPD) Crystal Deposition Disease - pathophys and etiological associations

Answer 10

aka, pseudogout (positive birefringence)

• deposition of CPPD crystals (rhomboid) can cause spectrum of conditions ranging from asymptomatic to arthritis that mimics other arthritides
• crystals deposit in cartilage (chondrocalcinosis), synovium, periarticular ligaments, and tendons
• pathologic calcification related to dysregulated chondrocyte response to GF, and dysregulated chondrocyte differentiation
• etiology unknown, most is idiopathic onset, but some early onset assoc. with ANKH mutation (chr 5)
• high assoc. with age, primary OA, and prior joint trauma; also moderately assoc. with hereditary, systemic metabolic disease, and other conditions

Question 11

Calcium Pyrophosphate Dihydrate (CPPD) Crystal Deposition Disease - clinical syndromes

Answer 11

• may resemble gout, septic arthritis, OA*, neuropathic arthritis, RA, PMR, may also cause carpal tunnel syndrome, hemarthrosis, tophi deposits, and CNS disease
• chronic degenerative arthropathy in CPPD disease commonly affects some joints that are typically spared in primary OA like the MCP joints, wrists, elbows, and glenohumeral joints

Question 12

Calcium Hydroxyapatite Deposition Disease (HADD)

Answer 12

• an abnormal accumulation of HA
• can cause acute synovitis (unusual); bursitis from periarticular HA deposition; and/or joint destruction from attenuation or rupture of supporting structures (leads to instability/deformity)
• assoc. with chronic renal failure and hypophosphatemia which enhances HA deposition in and around joints