Osteoarthritis (OA) is a common, slowly progressive
joints of the peripheral and
is characterized by progressive deterioration and loss
cartilage, resulting in
, deformity, and progressive disability.
Inflammation may or
be present in the affected
Primary (idiopathic) OA, the most common type, has no known
Subclasses of primary OA are
localized OA (involving
one or two sites) and generalized OA (affecting three or more
The term erosive OA
indicates the presence of erosion and
marked proliferation in the proximal and distal
(PIP and DIP) hand joints.
Secondary OA is associated with a known cause such as
arthritis or another inflammatory arthritis,
trauma, metabolic or endocrine
disorders, and congenital
OA usually begins with damage to
through injury, excess joint loading from obesity or other
reasons, or joint instability or injury that causes abnormal
Damage to cartilage increases the metabolic activity of
, leading to increased synthesis of matrix
constituents with cartilage swelling.
reparative response to damage does
not restore cartilage to normal but instead is the first
step in the process leading to further cartilage loss.
The prevalence and severity of OA increase with age.
Potential risk factors include obesity, repetitive use
through work or leisure activities, joint
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 progression, pain occurs with minimal activity or at
Joints most commonly affected are the DIP and PIP joints
of the hand, the first
joint, knees, hips,
cervical and lumbar spine, and the first
joint of the toe.
In addition to pain, limitation of motion, stiffness,
and deformities may occur.
Patients with lower extremity involvement may report a
sense of weakness or instability.
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
and joint capsule.
The presence of a warm, red, and tender joint may suggest an
Joint deformity may be present in the later stages as a
, collapse of
bone, formation of bone
cysts, or bony overgrowths.
Physical examination of the affected joints reveals tenderness,
possible joint enlargement.
Bouchard’s nodes are bony
) of the
DIP and PIP joints, respectively.
The diagnosis of OA is dependent on patient history, clinical
examination of the affected joint(s),
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
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
, or (3) radiographic joint
For knee OA, a patient must have knee pain and radiographic
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
(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
The rheumatoid factor test is negative.
Analysis of the
fluid reveals fluid with high viscosity. This fluid
demonstrates a mild
(less than 2,000 white blood cells/mm3)
with predominantly mononuclear cells.
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.
educate the patient about the extent of the disease, prognosis, and
and a structured weight
loss for overweight.
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.
devices such as canes, walkers, braces, heel
cups, and insoles can be used during exercise or daily activities.
Surgical procedures (e.g.,
, partial or total
joint fusion) are indicated for patients with functional disability
and/or severe pain unresponsive to conservative therapy.
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,
) may be useful. Appropriate non
therapies should be continued when drug therapy is
Acetaminophen is recommended by the ACR as
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
with overdose is well documented. It
should be used with caution in patients with liver disease
and those who chronically abuse alcohol. Renal toxicity
frequently than with 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
benefits may require 2 to 3 weeks of continuous therapy.
have similar efficacy in reducing pain and
inflammation in OA, although individual patient response
Selection of an NSAID depends on
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
providing additional benefit.
2) selective inhibitors (e.g.,
analgesic benefits that are similar
should be avoided in late pregnancy because of
the risk of premature closure of the
The most potentially serious drug interactions include the
concomitant use of
blockers, and diuretics.
Capsaicin, an extract of red peppers that causes release and
depletion of substance P from nerve
, 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
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
with adequate pain relief.
) is a
effective treatment for OA pain. It is thought to act primarily by
local inhibition of COX
may have modest, short
term efficacy for treating
acute pain associated with OA.
are dietary supplements that were shown
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
combination therapy when compared to placebo.
1,500 mg/day and
mg/day in divided doses.
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
Systemic corticosteroid therapy is not recommended in OA,
given the lack of proven benefit and the well
effects with long
corticosteroid injections can provide relief,
particularly when a joint effusion is present. Average doses for
injection of large joints in adults are
acetate 20 to 40 mg or
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
response to therapy.
acid is a constituent of normal
cartilage that provides lubrication with motion and shock
absorbency during rapid movements.
acid injections temporarily and modestly increase
fluid viscosity and were reported to decrease pain, but
many studies were short term and poorly controlled with high
placebo response rates.
acid preparations are available for treating
pain associated with OA of the knee:
Injections are well tolerated, but acute joint swelling and local skin
reactions (e.g., rash,
) 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.
) may be
useful for patients
who experience no relief with
They are particularly useful in patients who cannot take
because of renal failure, or for patients in whom
all other treatment options have failed and who are at
high surgical risk, precluding joint
should be used initially, usually in
combination with acetaminophen. Sustained
compounds usually offer better pain con
with or without acetaminophen has modest
analgesic effects in patients with OA. It may also be effective as
on therapy in patients taking concomitant
2 selective inhibitors. As with
helpful for patients who cannot take
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
like adverse effects such as nausea, vomiting, dizziness,
constipation, headache, and somnolence are common.
Evaluation of therapeutic outcome
To monitor efficacy, the patient’s baseline pain can be assessed with a visual
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
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
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
effects, such as skin rash, headaches, drowsiness, weight gain, or
, hematology profiles, and serum
with repeat levels at 6
month intervals are useful in identifying
specific toxicities to the kidney, liver, GI tract, or bone marrow.