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Osteoarthritis Powered By Docstoc
Hoveda Mufti M.D.
• Also known as
    degenerative joint
    disease or “wear and
    tear arthritis”.
•   Progressive loss of
    cartilage with
    remodeling of
    subchondral bone and
    progressive deformity
    of the joint (s).
•   Cartilage destruction
    may be a result of a
    variety of etiologies
Prevalence and epidemiology
• Over 20 million affected in U.S.
• About 60-90% of people over age 65
• Under 45 yrs it is equally common in men
  and women
• Over 55 yrs its more common in women
• Nodal OA involving DIP and PIP joints is
  more common in women and their first
  degree female relatives
• Premature OA associated with gene mutations
    that encode collagen types 2, 9, 10
•   OA of knee is more common in African American
•   Commonest cause of long-term disability
•   Large economic impact as a result of medical
•   OA cost the U.S. economy nearly $125 billion
    per year in direct expenses and lost wages and
• It is not an inevitable part of aging, some
  people are more susceptible than others
• A combination of different factors are
• Both mechanical and biologic destructive
  processes play a role in OA.
Risk factors
• Metabolic (hemachromatosis)
• Inflammatory (RA, infection)
• age
• gender
• genetic factors
• trauma
• weight
• Primary                     • Secondary
• Idopathic                   • Post-traumataic
• Localized or                • Congenital or
    generalized                   developmental
•   Local: knee, hip,
    spine, hands              •   Localized or
•   Generalized: large
    joints and spine          •   Calcium deposition
•   Small peripheral joints       disease
    and spine                 •   Other:
•   Mixed and spine           •   Inflammatory
                              •   Avascular necrosis
Inflammatory OA
• OA is generally a non-inflammtory arthritis.
• Increasing evidence for inflammatory type:
    caused by cytokines, metalloproteinase release.
•   This erosive inflammatory type may have flares
    but later acts like typical OA.
•   Primarily in women
•   May be suspected from evidence of active
    synovitis, chondrocalcinosis on x-rays, morning
    stiffness greater than 30 mins, history of
    swelling and night pain.
Overview of the process

• Articular cartilage
   gets disrupted

• Damage progresses
   deeper to
   subchondral bone
• Fragments of
    cartilage released into
•   Matrix degenerates
•   Eventually there is
    complete loss of
•   Bone is exposed
Normal knee anatomy
• left: Normal x-ray
• Right: worn away cartilage reflected by
  decreased joint space
The process –            at a cellular level
•    Cartilage matrix has increased water content and
    decreased proteoglycan
•   This is different from the changes that occur with aging
     cartilage dries up.
•   Increased activity of proteinases compared to inhibitors
    of proteinases.
•   Breakdown products of cartilage cause inflammatory
    reaction of synovium
•   Cytokines cause matrix degeneration. Where do they
    come from?
•    chondrocytes
•   Cycle of destruction starts
•   Compensatory bone overgrowth occurs - subchondral
    bone increases in density
Left: View of normal elbow cartilage through an
  arthroscope - white, glistening, smooth
Right: severe elbow osteoarthritis - cartilage is lost
  and the bone underneath is exposed
The process cont’d
• Bony proliferations at joint margins form,
  what are they called?
•  osteophytes
• Thought to be new bone formation in
  response to degenerating cartilage
• They cause joint motion restriction
What to look for in an x-ray
• Radiographic changes visible relatively late
  in the disease
• Subchondral sclerosis
• Joint space narrowing esp where there is
• Subchondral cysts
• Osteophytes
• Bone mineralization should be normal
• Joint space narrowing
    where there is more
•   Subchondral bone has
•   bony overgrowth
significant joint space narrowing as well as proliferative
   bone formation around the femoral neck (arrows)
Left: normal hip
Right: There is some joint space medially but the superior portion is
   completely destroyed. Supralateral aspects affected most because
   the weight is transfered through the roof of the acetabulum.
Note the sclerosis and oseophyte formation (arrow).
painful bone on bone contact at the CMC joint and the large bone
   spurs -- osteophytes.
X-ray shows lateral osteophytes, varus deformity, narrow joint space in
   a 70 yr old female with OA
• Are crystals found in osteoarthritic joints?
• Yes
• Calcium pyrophosphate dihydrate and
• Are of unknown significance and
Clinical features and diagnosis
• Pain
    –   Joint effusion and stretching of the joint capsule
    –   Torn menisci
    –   Inflammation of periarticular bursae
    –   Periarticular muscle spasm
    –   Psychological factors

•   Deep, aching localized to the joint
•   Slow in onset
•   Worsened with activity in initial stages
•   Occurs at rest with advanced disease
• May be referred eg hip pain referred to
  the thigh, groin, knee.
• Pain may be aggravated with weather

• Joint line tenderness
• Bony enlargement of
•   +/- effusion
•   Crepitus
•   Decreased range of
Joint exam
• Joint line pain can
  indicate tear of the
  lining of the capsule
  or the meniscus.

• Where is the patella?
Joint exam
• In the evaluation of joint
    line pain, perform a varus
    or valgus stress test.
•   Apply stress across the
    joint, place fingers
    directly over the joint line
    to assess for pain, a clunk
    may indicate a meniscal
    tear, or crepitus may
    indicate cartilage
• Have the patient to lie supine on the exam
  table with leg muscles relaxed
• Press the patella downward and quickly
  release it.
• the patella visibly rebounds.
• What does this mean?
• a large knee effusion
• Ballotable patella
• Have the patient lie supine
    with leg muscles relaxed
•    Compress the suprapatellar
    pouch with your thumb, palm,
    and index finger.
•   "Milk" downward and laterally
    so that any excess fluid
    collects on the medial side.
•   Tap gently over the collected
    fluid and observe the effect on
    the lateral side
•   A fullness on the lateral side
    indicates the presence small
    knee effusion
Involved joints

•   DIP, PIP
•   1st carpometacarpal
•   cervical/lumbar facet joints
•   1st metatarsophalangeal
•   Hips
•   Knees

• Uncommon
• Wrist, elbows, shoulders,
• 1st metatarso-phalangeal most commonly
  affected in OA of the foot.
Typical findings

• Heberden’s nodes

• Bouchard’s nodes
Rt: varus deformity of the knee
• Non-pharmacokinetic
• No proven medication-based disease modifying
    intervention exists.
•   Analgesics (acetominophen)
    Help pain symptoms but controversial for long
    term use in non-inflammatory OA because of
    risks vs benefits
•   Narcotics
•   Intra-articular steroids
•   Chondroprotective agents
•   Anti-depressants
Non-pharmacokinetic rx
• Reasonable evidence for
• Exercise – prevent disuse
  atrophy of muscles
• Physical therapy:
  paraffin baths
• Weight loss
• Education
• Wedges shoe
• Refer to physiatrist for
  management plan.
• Acetominophen at doses of upto 4g per
• 2004 meta analysis of 10 trials showed
  that acetominophen superior to placebo
  but less efficacious in relieving pain than
• Do you worry about hepatotoxicity?
• Only seen in pts who are taking excessive
  amounts of alcohol, underlying disease.
Opioid analgesics
• Generally should be avoided for long term
• For short term rx they may be effective. A
  study showed oxycodone to be synergistic
  with NSAIDS.
• In older pts use caution because of side
  effects such as confusion, constipation,
• Can use tramadol with acetominophen, in
  addition to NSAID/COX-2 inhibitor
• A controlled study showed codeine and
 acetominophen combination to be
 equivalent to to tramadol and

• Consider opiates if pt is not a candidate
 for surgery, or is at high risk for side
 effects from NSAIDS
• Useful in non-inflammatory OA when pain
 is moderate to severe

• Topical preparations available

• PGE2 may contribute to local inflammation
 and so there is a role for NSAIDS in
 inflammatory OA
• There is variability amongst patients in
  terms of side effects and efficacy of
• Non-acetylated salicylates have less renal
Sulindac, salsalate

• Indomethacin has been associated with
 accelerated joint destruction, so avoid it
 for long term use in pts with hip OA
Selective COX-2 inhibitors
• They have 200-300 times selectivity for
  COX-2 over COX-1.
• Less gastroduodenal toxicity
• But if used with ASA pts may be at
  increased risk for GI bleeding.
• Use GI prophylaxis
• Avoid in pts with atherosclerotic CAD - use
  traditional NSAIDS with a
Side effects
• Rash/hypersensitivity
• GI bleeding
• CNS dysfunction in elderly
• Impairment of renal/hepatic/platelet
  function. How can NSAIDS lead to renal
• By interfering with vasodilator renal PG
  and causing renal ischemia.
Intra-articular corticosteroids
• May be used if NSAIDS are contraindicated,
    persistent pain despite use of other medications.
•   (not > 4 injections per year per joint)
•   2004 meta-analysis of controlled trials (w/
    placebo) showed short term improvement in
    knee pain, but efficacy in other joints is
•   saline vs steroid injection?
•    A study comparing the two in knee OA showed
    no effect on joint space narrowing or significant
    difference in pain at the end of the study, but
    over a 2 yr period saline injections has less pain
Intra-articular hyaluronans
• Evidence shows they have a small
  advantage in terms of pain control,
  compared to intra-articular placebos or
• No evidence for improvement in function
• Two studies comparing intra-articular
  steroids to hyaluronans have come to
  opposite conclusions-more trials are
Surgical: arthroscopy
• arthroscopy is not recommended for
  nonspecific "cleaning of the knee“.
• Used to fix specific structural damage on
  imaging (repairing meniscal tears,
  removing fragments of torn menisci that
  are producing symptoms).
Joint replacement
• If all other rx
  ineffective, and pain
  is severe

• Loss of joint function

• Joints last 8-15 years
  without complications
The end

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