OSTEOARTHRITIS

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					                                                                            RHEUMATOLOGY—1
                                                            X-rays are confirmatory and not useful for following pts
                                                                because there is a poor relationship between X-ray
        OSTEOARTHRITIS                                          findings and symptoms.
Acquired, noninflammatory, MS disorder that results
    from slow progressive loss of articular cartilage       Management:
    without adequate regeneration.                          Prevention: ID and modification of risk factors for
Prevalence: 90% of the U.S. population > 65 yo has               occupational and athletic joint injury, such as
    radiographic evidence of dz.                                 repetitive, unsupported motion, poor conditioning,
                                                                 and poor technique.
Etiology and pathophysiology                                Cognitive and Behavioral Control of Arthritis Pain:
Risk factors                                                Highly motivated pts and those w/favorable rational
1) Age: predominant risk factor for all sites of OA              thinking indices have significantly  levels of pain
2) Obesity: for weight-bearing joints, such as the knee          and psychological distress, and better overall health.
    and hip. Added mechanical stress on the joints.         Psycho-educational interventions are effective in  pain,
3) Previous joint damage from trauma/infection: esp.             disability, and medication and health resource
    at the DIP and PIP joints of the hand and, to a lesser       utilization.
    extent, at the knee. Causes stiffness of the            Biomechanical Factors
    subchondral bone  excessive wear of overlying
                                                             joint loading on weight-bearing joints: weight loss or
    cartilage. Also involving the articular surface, or s/p      the use of aids, such as a cane in the contralateral
    knee meniscectomy.
                                                                 hand, crutches, or appliances such as heel or insole
4) Congenital defective joints: mechanical incongruity           wedges, as indicated.
    of joints.
                                                            Weight loss: modest loss can dramatically  joint-
5) Family History: Particularly in PIP’s/DIP’s and hip.
                                                                 loading forces.
Normal: Cartilage remodeling  equilibrium between
    cartilage matrix degradation & chondrocyte-
                                                            Exercise:
    mediated synthesis of type II collagen and
                                                            Exercise regimens in patients with OA have discernible
    glycosaminoglycans.
                                                                 benefits.
OA:
Cartilage degradation exceeds its regeneration             Fitness walking  pain and disability over the short term
    progressive erosion and fissuring of cartilaginous      Continued exercise in people with mild to moderate OA
    joint surfaces.                                              does not damage cartilage and may in fact slow the
Insult  release of enzymes from chondrocytes                   progression of disease.
    degrade collagen and proteoglycans  repartive          Acute MS pain  cold applied to the joint may 
                                                                 symptoms.
    process w/ bone formation.
                                                            Subacute pain  heat applied superficially or deeply, is
Clinical Features:                                               preferable to  pain threshold  muscle relaxation.
AM stiffness generally short in duration < 30 min.
Pain: Progressive. “Deep ache.” Made worse by                          Medical Management:
    movement, especially movement and weight
    bearing. Made better with rest. Prolonged AM            Analgesics
    stiffness.                                              Acetaminophen: First-line therapy. Up to 4 gm/day for
No systemic symptoms                                             OA of the hip and knee. Same efficacy as NSAIDs
Crepitus                                                         w/ SE. Acts centrally   pain threshold. It has
Deformity: Joint enlargement. Also varus or valgus               no anti-inflammatory properties at therapeutic
    bowing of knee.                                              doses.
Limited ROM                                                 Opioids: can be added to analgesic regimens in OA for
Joint contraction                                                short periods.
Common Joints/Spine:
                                                            NSAIDS, Including Cox-2 Inhibitors
Need to distinguish between OA (involving facet joints)
    and degenerative disk disease with disk space           Exert their anti-inflammatory and SE through
    narrowing and osteophytes on vertebrae.                      cyclooxygenase (COX) inhibition.
Hips: Earliest abnormality  restricted ROM, w/limited Similar efficacy among the different agents in this class.
    internal rotation (<35*) and abduction (<45*) Pain.
    Symptoms are aggravated by excessive weight             Toxicity
    bearing and prolonged immobility.                       Gastropathy: most common complication. Dyspepsia,
Knees: Pain on weight bearing, descending stairs more            ulceration, or perforation of GI tract. Elderly are
    so than by climbing stairs, rising from a sitting            more prone to NSAID-induced GI ulceration, and
    position.                                                    endoscopic evidence of this complication is seen in
Spine: Lower C and L spine. Pain is often poorly                 up to 20% of users.
    localized. Muscle spasm and stiffness often             Aspirin: more ulcerogenic than other NSAIDs.
    accompany it, and restricted ROM develops with          Platelet dysfunction: All NSAIDs inhibit platelet
    progression of dz. .                                         adhesion  potentiate GI bleeding and perforation.
Neck: Limited extension and lateral bending and                  Misoprostol w/NSAIDs may  GI bleeding, but
    rotation are the first motions.                              may not reduce other GI symptoms.
Hand: Small joints. Pain  aching and stiffness of          Acute renal insufficiency: more commonly seen in the
    fingers, worsened by repetitive finger use                   elderly
   Heberden Nodes: DIP                                     CNS: Indomethacin  mental confusion, HA.
   Bouchard’s Nodes: PIP                                   Hepatotoxicity: diclofenac.
Wrist, elbow, shoulder and ankle are usually spared.        Aseptic meningitis: Very rare toxicity of all NSAID’s.
                                                            Others: Skin reactions, CNS disturbances, and
Diagnosis                                                        interference with diuretics and antihypertensive..
Clinical findings confirmed by x-ray changes w/typical
    features of localized narrowing of the joint space.     COX-2:  GI ulceration vs. conventional NSAID.
X-ray features that must all be present for diagnosis:
                                                            Chondroprotective Agents
Early unequal joint space narrowing (<4 mm in the hip)
Osteophytes                                                 Documented symptomatic benefit for knees. Benefit to
Juxta-articular sclerosis ("eburnation")                         other joints unknown.
Subchondral bone cysts.                                     Glucosamine: may provide pain relief, reduce
                                                                 tenderness, and improve mobilityimprovement is
2—RHEUMATOLOGY
    generally delayed compared vs. conventional OA
    meds.

Chondroitin sulfate:OTC med. Preparations have
   variable amounts of Chondroitin. May slow or
   prevent tissue damage in the joint in addition to
   alleviating symptoms.
Intra-articular Therapy
Intra-articular steroid injection:
Short term relief of symptoms.
   Synovitis
   inflamed Heberden's nodes.
   large, painful, inflammatory effusions of
     osteoarthritic knees  arthrocentesis  steroid
     injection and topical anesthetic agents effective in 
     symptoms
Pt should minimize joint loading for some period after
     injection  longer period of improvement
Should not be repeated > 3 to 4 x/yr in any given joint
     because of the possibility of steroids potentiating
     rapidly progressive joint failure.
Hyaluronic acid: prototype glycosaminoglycan that is
normally produced by chondrocytes and synoviocytes.
Sustained pain relief, comparable w/naproxen, w/ SE
     but  cost
Onset of pain relief less rapid than intra-articular steroid
     injection
Duration of pain relief may be much longer.
Used in pts who fail non-drug management and
     NSAIDS
Surgery:
Arthroscopy: Surgical removal of loose bodies and
    fragments
Osteotomy: Tibial osteotomy  symptomatic relief in
    pts w/varus angulation < 10* and good ligamentous
    support.
Joint replacement:
   Considered with severe pain and end-stage
    structural dz.
   Better results if profound muscle weakness has not
    set in so that postop rehab is possible.
   Pain relief is achieved in > 90% who undergo total
    joint replacement of the knee or hip.

				
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posted:2/8/2013
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