Osteoarthritis

Report
Osteoarthritis
Defenition
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Osteoarthritis (OA) is a common, slowly progressive
disorder affecting primarily the weight-bearing
diarthrodial joints of the peripheral and axial skeleton. It
is characterized by progressive deterioration and loss of
articular cartilage, resulting in osteophyte formation, pain,
limitation of motion, deformity, and progressive disability.
Inflammation may or may not be present in the affected
joints.
Pathophysiology
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Primary (idiopathic) OA, the most common type, has no known
cause. Subclasses of primary OA are localized OA (involving
one or two sites) and generalized OA (affecting three or more
sites).
The term erosive OA indicates the presence of erosion and
marked proliferation in the proximal and distal
interphalangeal (PIP and DIP) hand joints.
Secondary OA is associated with a known cause such as
rheumatoid arthritis or another inflammatory arthritis,
trauma, metabolic or endocrine disorders, and congenital
factors.
Pathophysiology
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OA usually begins with damage to articular cartilage
through injury, excess joint loading from obesity or other
reasons, or joint instability or injury that causes abnormal
loading.
Damage to cartilage increases the metabolic activity of
chondrocytes, leading to increased synthesis of matrix
constituents with cartilage swelling.
This hypertrophic reparative response to damage does
not restore cartilage to normal but instead is the first
step in the process leading to further cartilage loss.
Clinical presentation
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The prevalence and severity of OA increase with age.
Potential risk factors include obesity, repetitive use
through work or leisure activities, joint trauma, and
heredity.
The clinical presentation depends on duration and
severity of disease and the number of joints affected.
The predominant symptom is a localized deep, aching pain
associated with the affected joint.
Early in OA, pain accompanies joint activity and decreases
with rest.
With progression, pain occurs with minimal activity or at
rest.
Clinical presentation
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Joints most commonly affected are the DIP and PIP joints
of the hand, the first carpometacarpal joint, knees, hips,
cervical and lumbar spine, and the first
metatarsophalangeal joint of the toe.
In addition to pain, limitation of motion, stiffness, crepitus,
and deformities may occur.
Patients with lower extremity involvement may report a
sense of weakness or instability.
Clinical presentation
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Upon arising, joint stiffness typically lasts less than 30 minutes
and resolves with motion.
Joint enlargement is related to bony proliferation or to
thickening of the synovium and joint capsule.
The presence of a warm, red, and tender joint may suggest an
inflammatory synovitis.
Joint deformity may be present in the later stages as a resul of
subluxation, collapse of subchondral bone, formation of bone
cysts, or bony overgrowths.
Physical examination of the affected joints reveals tenderness,
crepitus, and possible joint enlargement. Heberden’s and
Bouchard’s nodes are bony enlargements (osteophytes) of the
DIP and PIP joints, respectively.
Diagnosis
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The diagnosis of OA is dependent on patient history, clinical
examination of the affected joint(s), radiologic findings, and
laboratory testing.
Criteria for the classification of OA of the hips, knees, and
hands were developed by the American College of
Rheumatology (ACR). The criteria include the presence of pain,
bony changes on examination, a normal erythrocyte
sedimentation rate (ESR), and radiographs showing
characteristic osteophytes or joint space narrowing.
• For hip OA, a patient must have hip pain and two of the
following: (1) an ESR less than 20 mm/hour, (2) radiographic
femoral or acetabular osteophytes, or (3) radiographic joint
space narrowing.
Diagnosis
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For knee OA, a patient must have knee pain and radiographic osteophytes
in addition to one or more of the following:
(1) age greater than 50 years,
(2) morning stiffness of 30 minutes’ or less duration, or
(3) crepitus on motion,
(4) bony enlargement,
(6) bony tenderness, or
(7) palpable joint warmth.
No specific clinical laboratory abnormalities occur in primary OA.
The ESR may be slightly elevated in patients with generalized or erosive
inflammatory OA.
The rheumatoid factor test is negative.
Analysis of the synovial fluid reveals fluid with high viscosity. This fluid
demonstrates a mild leukocytosis (less than 2,000 white blood cells/mm3)
with predominantly mononuclear cells.
Desired outcome
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The major goals for the management of OA are to:
(1) educate the patient, caregivers, and relatives;
(2) relieve pain and stiffness;
(3) maintain or improve joint mobility;
(4) limit functional impairment; and
(5) maintain or improve quality of life.
Non-pharmacological therapy
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educate the patient about the extent of the disease, prognosis, and
management approach.
Dietary counseling and a structured weight-loss for overweight.
Physical therapy—with heat or cold treatments to maintain and
restore joint range of motion and reduce pain and muscle spasms.
Exercise programs to strengthen muscles, improve joint function and
motion, and decrease disability, pain, and the need for analgesic use.
Assistive and orthotic devices such as canes, walkers, braces, heel
cups, and insoles can be used during exercise or daily activities.
Surgical procedures (e.g., osteotomy, partial or total arthroplasty,
joint fusion) are indicated for patients with functional disability
and/or severe pain unresponsive to conservative therapy.
Pharmacological therapy
General approch
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Drug therapy in OA is targeted at relief of pain. Because
OA often occurs in older individuals who have other
medical conditions, a conservative approach to drug
treatment is warranted.
An individualized approach to treatment is necessary. For
mild or moderate pain, topical analgesics or
acetaminophen can be used. If these measures fail or if
there is inflammation, nonsteroidal antiinflammatory
drugs (NSAIDs) may be useful. Appropriate non-drug
therapies should be continued when drug therapy is
initiated.
Acetaminophen
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Acetaminophen is recommended by the ACR as
first-line drug therapy for pain management of OA.
The dose is 325 to 650 mg every 4 to 6 hours on a
scheduled basis (maximum dose 4 g/day; maximum 2 g/day
if chronic alcohol intake or underlying liver disease).
However, some patients respond better to NSAIDs.
Acetaminophen is usually well tolerated, but potentially
fatal hepatotoxicity with overdose is well documented. It
should be used with caution in patients with liver disease
and those who chronically abuse alcohol. Renal toxicity
occurs less frequently than with NSAIDs.
NSAIDs
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NSAIDs at prescription strength are often prescribed for OA
patients after treatment with acetaminophen proves
ineffective, or for patients with inflammatory OA. Analgesic
effects begin within 1 to 2 hours, whereas anti-inflammatory
benefits may require 2 to 3 weeks of continuous therapy.
All NSAIDs have similar efficacy in reducing pain and
inflammation in OA, although individual patient response
differs among NSAIDs.
Selection of an NSAID depends on prescriber experience,
medication cost, patient preference, toxicities, and adherence
issues. An individual patient should be given a trial of one drug
that is adequate in time (2 to 3 weeks) and dose. If the first
NSAID fails, another agent in the same or another chemical
class can be tried. Combining two NSAIDs increases adverse
effects without providing additional benefit.
NSAIDs
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Cyclooxygenase-2 (COX-2) selective inhibitors (e.g.,
celecoxib) demonstrate analgesic benefits that are similar
to traditional nonselective NSAIDs.
NSAIDs
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NSAIDs should be avoided in late pregnancy because of
the risk of premature closure of the ductus arteriosus.
The most potentially serious drug interactions include the
concomitant use of NSAIDs with lithium, warfarin, oral
hypoglycemics, high-dose methotrexate, antihypertensives,
ACEI, β-blockers, and diuretics.
Topical therapy
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Capsaicin, an extract of red peppers that causes release and
ultimately depletion of substance P from nerve fibers, has been beneficial
in providing pain relief in OA when applied topically over affected joints. It
may be used alone or in combination with oral analgesics or NSAIDs.
To be effective, capsaicin must be used regularly, and it may take up to 2
weeks to work. It is well tolerated, but some patients experience
temporary burning or stinging at the site of application. Patients should be
warned not to get the cream in their eyes or mouth and to wash their
hands after application.
Application of the cream, gel, or lotion is recommended four times daily,
but tapering to twice-daily application may enhance long-term adherence
with adequate pain relief.
Topical diclofenac in a dimethyl sulfoxide carrier (Pennsaid) is a
safe and effective treatment for OA pain. It is thought to act primarily by
local inhibition of COX-2 enzymes.
Topical rubefacients containing methyl salicylate, trolamine salicylate,
and other salicylates may have modest, short-term efficacy for treating
acute pain associated with OA.
Glucosamine & chondroitin
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are dietary supplements that were shown to stimulate
proteoglycan synthesis from articular cartilage in vitro.
Although their excellent safety profile makes them appealing
for patients at high risk of adverse drug events, enthusiasm
waned after results of clinical trial demonstrated no significant
clinical response to glucosamine alone, chondroitin alone, or
combination therapy when compared to placebo.
glucosamine sulfate 1,500 mg/day and chondroitin sulfate 1,200
mg/day in divided doses.
Glucosamine adverse effects are mild and include GI gas,
bloating, and cramps; it should not be used in patients with
shellfish allergies. The most common adverse effect of
chondroitin is nausea.
Corticosteriods
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Systemic corticosteroid therapy is not recommended in OA,
given the lack of proven benefit and the well-known adverse
effects with long-term use.
Intraarticular corticosteroid injections can provide relief,
particularly when a joint effusion is present. Average doses for
injection of large joints in adults are methylprednisolone
acetate 20 to 40 mg or triamcinolone hexacetonide 10
to 20 mg. After aseptic aspiration of the effusion and
corticosteroid injection, initial pain relief may occur within 24
to 72 hours, with peak relief occurring in about 1 week and
lasting for 4 to 8 weeks. The patient should minimize joint
activity and stress on the joint for several days after the
injection. Therapy is generally limited to three or four
injections per year because of the potential systemic effects of
the drugs and because the need for more frequent injections
indicates poor response to therapy.
Hyaluronate injection
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High-molecular-weight hyaluronic acid is a constituent of normal
cartilage that provides lubrication with motion and shock
absorbency during rapid movements.
Hyaluronic acid injections temporarily and modestly increase
synovial fluid viscosity and were reported to decrease pain, but
many studies were short term and poorly controlled with high
placebo response rates.
4 intraarticular hyaluronic acid preparations are available for treating
pain associated with OA of the knee: sodium hyaluronate.
Injections are well tolerated, but acute joint swelling and local skin
reactions (e.g., rash, ecchymoses, or pruritus) have been reported.
These products may be beneficial for OA of the knee that is
unresponsive to other therapy, but they are expensive because
treatment includes both drug and administration costs.
Opioid analgesics
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Low-dose opioid analgesics (e.g., oxycodone) may be
useful for patients who experience no relief with
acetaminophen, NSAIDs, intraarticular injections, or
topical therapy.
They are particularly useful in patients who cannot take
NSAIDs because of renal failure, or for patients in whom
all other treatment options have failed and who are at
high surgical risk, precluding joint arthroplasty.
Low-dose opioids should be used initially, usually in
combination with acetaminophen. Sustained-release
compounds usually offer better pain con
Tramadol
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Tramadol with or without acetaminophen has modest
analgesic effects in patients with OA. It may also be effective as
add-on therapy in patients taking concomitant NSAIDs or
COX-2 selective inhibitors. As with opioids, tramadol may be
helpful for patients who cannot take NSAIDs or COX-2
selective inhibitors.
Tramadol should be initiated at a lower dose (100 mg/day in
divided doses) and may be titrated as needed for pain control
to a dose of 200 mg/day. It is available in a combination tablet
with acetaminophen and as a sustained-release tablet.
Opioid-like adverse effects such as nausea, vomiting, dizziness,
constipation, headache, and somnolence are common.
Evaluation of therapeutic outcome
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To monitor efficacy, the patient’s baseline pain can be assessed with a visual
analog scale, and range of motion for affected joints can be assessed with
flexion, extension, abduction, or adduction.
Depending on the joint affected, measurement of grip strength and 50-feet
walking time can help assess hand and hip/knee OA, respectively.
Baseline radiographs can document the extent of joint involvement and
follow disease progression with therapy.
Other measures include the clinician’s global assessment based on the
patient’s history of activities and limitations caused by OA, the Western
Ontario and McMaster Universities Arthrosis Index, Stanford Health
Assessment Questionnaire, and documentation of analgesic or NSAID use.
Patients should be asked if they are having adverse effects from their
medications. They should also be monitored for any signs of drug-related
effects, such as skin rash, headaches, drowsiness, weight gain, or
hypertension from NSAIDs.
Baseline serum creatinine, hematology profiles, and serum transaminases
with repeat levels at 6- to 12-month intervals are useful in identifying
specific toxicities to the kidney, liver, GI tract, or bone marrow.

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