Osteoarthritis

Allen N. Wilkins, MD, and Edward M. Phillips, MD

Synonym
Degenerative joint disease
ICD-9 Codes
715.0 Osteoarthrosis, generalized
715.1 Osteoarthrosis, localized, primary
715.2 Osteoarthrosis, localized, primary
715.3 Osteoarthrosis, localized, not specified whether primary or secondary
715.9 Osteoarthrosis, unspecified whether generalized or localized
716.1 Traumatic arthropathy
716.9 Arthripathy, unspecified

DEFINITION
Osteoarthritis represents a family of disorders characterized by a relentless
process in which all components of cartilage are destroyed. 1 Osteoarthritis is
steadily becoming the most common cause of disability for the middle-aged and
has become the most common cause of disability for those older than 65 years. 2 It
has been estimated that the total cost for arthritis, inclusing osteoarthritis, is more
than 2% of the United States gross domestic product.3
Osteoarthritis involves all structures in the joint. Subchondral bone, synovial
fluid, and the synovial membrane are major sites of change in the course of the
disease process. In addition to degradation and loss of articular cartilage,
osteoarthritis is characterized by hypertrophic bone changes with osteophyte
formation, subchondral bone remodeling, and, in many cases, chronic
inflammation of the synovial membrane.1
Joint involvement is usually asymmetrical, with a predilection for weight-bearing
joints. Common sites of invovement are the hip, knee, distal and proximal
interphalangeal joints, and facet joints of the spine. Less common sites of
involvement are the ankle, wrist, and shoulder. Inflammation and joint effusion
are present in some cases.
Osteoarthritis is classified into two groups, primary and secondary. Primary
osteoarthritis can be localized or generalized; primary generalized ostoearthritis is
more commonly found in postemenopausal women, with development of
Heberden nodes. Secondary osteoarthritis has an underlying cause (Table 130-1).
Risk factors for osteoarthritis include advanced age, obesity, bone density, and
genetics (Table 130-2). Epidemiologic data suggest increased risk of osteoarthritis
in persons with low levels of vitamins D and C and estrogen deficiency.8
The pathophysiologic mechanism of osteoarthritis involves a combination of
mechanical, cellular, and biochemical processes. The interaction of these

processes leads to changes in the composition and mechanical properties of the

articular cartilage. The normal remodeling process is disrupted in osteoarthritis,
leading to increased degenrative changes and an abnormal repair response.9
The mechanisms of cartilage degenerative, pain, and funtional loss in
osteoarthritis are not completely understood (Fig. 130-1).
Psychosocial
dysfunction
Depression

Decrease activity
Medical
Recreational
comorbidities
Vocational (CAD, CHF, COPD)
Sexual

Pain

Genetic and
biochemical changes
Cytokines
Prostaglandins
Nitric oxide
Collagenase
Free radicals

Inflammation
Effusion

Abnormal loading
and increased
biochemical stress

Disuse of
joint or limb

Cartilage
degeneration

Altered joint
geometry and
biomechanics

Weakness
Atrophy
Loss of motion
Proprioceptive loss

Physiologic impairment
Musculoskeletal
Cardiovascular
Pulmonary

Dissability
Vocational
Becreational
Sexual
Self-care

Altered limb biomechanics

Gait disturbance
Impaired protective responses

SYMPTOMS
Patients usually complain of pain, stiffness, reduced movement, and swelling in

the affected joints that is exacerbated with activity and relieved by rest. Pain at
rest or at night suggests severe disease or another diagnosis. Early morning
stiffness, if it is present, is typically less than 30 minutes. Joint tenderness and
crepitus on movement may also be present. Swelling may be due to bone
deformity, such as osteophyte formation, or an effusion caused by synovial fluid
accumulation. Systemic symptoms are absent.10
In early disease, pain is usually gradual in onset and mild in intensity. Pain is
typically self-limited or intermittent. Patients with advanced disease may describe
a sense of grinding or locking with joint motion and buckling or instability of
joints during demanding tasks. Spasm of periarticular muscles may be prominent
and painful. Patients may complain of fatigue if biomechanical changes lead to
increased energy requirements for activities of daily living. Overuse of alternative
muscle groups can lead to development of pain syndromes in other parts of the
musculoskeletal system.
TABLE 130-1 Causes of Secondary Osteoarthritis
Calcium deposition
Congenital or development disorders
Endrocine disorders
Genetic defects
Infectious diseases
Metabolic disorders
Neuropathic disorders
Trauma
Inflammatory arthritis
Obesity
Paget disease
TABLE 130-2 Risk Factors for Osteoarthritis
Risk Factor Related Studies
Age
Of people older than 65 years, 80% have
some radiographic evidence of
osteoarthritis, but that incidence and
prevalence
of
symptomatic
osteoarthrits leveled off or declined in
men and women at around 80 years of
Obesity
age.4
Increased risk for development of
progressive osteoarthritis seems to be
apparent in over weight people with
Bond density
localized disease.5
There is an inverse relationship between
bone density and osteoarthritis.6
Genetics
There is increased concordance for
osteoarthritis in monozygotic twins

Gender

compared with dizygotic twins,

indicating that there is a genetic
susceptibility to the disease.
The defective genes are often coding for
structural proteins of the extracellular
matrix of the joint and collagen
proteins.
Children of parents with early onset
osteoarhritis are at higher risk.7
Before the age of 50 years, men have a
higher prevalence and incidence than
women do. However, once older than
50 years women have a higher overall
prevalence and incidence than men
do.5

PHYSICAL EXAMINATION
Joint Examination
Diagnosis of osteoarthritis involves assessment of the affected joints range of
clinical features. Table 130-3 outlines the pertinent features of an ostearthritis
joint. These features include tenderness, bone enlargement, and malalignment. In
many cases, the patient presents with a warm, swollen joint. Osteophytes, joint
surface irregularly, periarticular muscle spasm, or chronic disuse may also results
in decreased range of motion, pain, and crepitus. Locking during range of motion
suggests loose bodies or floating cartilage fragments in the joint. Joint contracture
can result from from holding a joint in slight flexion, which is less painful for
inflamed or swollen jonts. There may be secondary abnormalities in joints above
or below the primarily involved joint.

Neuromuscular Examination
Pariarticular muscle atrophy and wekaness may also be present in chronic
osteoarthritis. It is notable that manual muscle testing is typically unrealibe in the
lower extremities because of the high baseline strength of these muscle groups. A
careful neurologic examination should be performed to ensure that pain is not a
result of nerve impingement or neuropathic process.
In addition, gait should be observed. There may be antalgia (a limp secondary to
pain) and a slow gait pattern because of pain in a specific joint. If the patient uses
a cane, appropriate use of the cane should be assessed during gait.
Flexibility in both the affected and unaffected joints should also be evaluated.
Messier and colleagus11 suggested that patients with symptomatic osteoarthritis of
the knee have poorer flexibility in the both affected and unaffected legs and
demonstrate significantly less knee angular velocity and knee range of motion

during gait. They have an increased loading rate in the unaffected leg after heel
strike, exert less peak verticcal force during push-off, and are significantly weaker
in both the dominant and nondominant legs compared with adults with no lower
extremity disease.
Because obesity has been identified as a risk factor for osteoarthritis, assessment
of the patients body mass index may also be useful.

FUNCTIONAL LIMITATIONS
Functional limitations depend on the joints involved. Patients with disease in the
hips and knees can suffer from reduced walking speed and efficiency, difficulty in
climbing stairs, trouble with transfer (in and out of cars, chairs, or toilet facilities),
and problems with lower body dressing and grooming. Degenaration in the
shoulders or hands can limit vocational and recreational activities, grooming,
eating, and other activities of daily living. Spinal degeneration can results in
limitations with all mobility.

DIAGNOSTIC STUDIES
Plain radiographs are important in confirming the diagnosis of osteoarthritis. The
classic findings include asymmetric joint space narrowing, osteophytes at joint
margins, cortical sclerosis, and subchondral cyst formation. There is a welldemonstrated discordance between radiographic findings and symptoms in
osteoarthritis. Asymptomatic individuals may have significant radiographic
disease, and severe pain and dysfunction can occur in the setting of limited
radiologic changes. Magnetic resonance imaging is typically not needed for
diagnosis of osteoarthritis but can be helpful in ruling out early ostoenecrosis if
osteoarthritis is not evident on plain radiographs of painful joints.
Because osteoarthritis is a noninflammatory arthritis, routine laboratory test
results are usually normal. Because of the high prevalence of laboratory
abnormalities in elderly people, such as raised erythrocyte sedimentation rate and
anemia, however, these will commonly be detected and may prompt an
unnecessary investigation.
Joint fluid analysis can be helpful in ruling out crystal deposition disease (gout,
pseudogout), inflammatory arthritis, or infectious arthritis and should be persued
in patients with significant joint inflammation. In osteoarthritis, synovial fluid
leukocyte counts are typically less than 2000 cells/mm3.
TABLE 130-3 Clinical Features of an Osteoarthritic Joint
Tenderness to palpation
Bone enlargement
Malalignment
Warmth
Joint effusion or swelling

Crepitus
Periarticular muscle spasm, athropy, or weakness
Decreased, painful range of motion
Differential Diagnosis
Neoplasm
Deep venous thrombosis
Osteomyelitis
Occult fracture
Aseptic necrosis
Chondromalacia
Soft tissue infection
Bursitis
Tendinitis
Ligamentous injury
Overuse injury
Radiculopathy
Neuropathy
Polymyalgia rheumatica
Inflammatory arthritis
Crystal arthritis (gout, pseudogout)

TREATMENT
Initial
The management of osteoarthritis involves attenton to four important principles:
avoid drug toxicity, limit physical disability, relieve pain and others symptoms,
and maximize physical function and psychosocial adjustment.
No intervention has been shownn conclusively to alter disease progression in
osteoarthritis. A number of interventions have been demonstrated to reduce pain
and stiffness and to improve functional status.
Acetaminophen and nonsteroidal anti-inflammatory drugs (NSAIDs) are typically
first-line and useful in reducing pain. Head-to-head randomized trials showed that
NSAIDs are more efficacious than acetaminophen. 12,13 However, the superiority of
NSAIDs over acetaminophen (at doses of 4 g/day) is modest. 12 The literature is
not as clear about the role of NSAIDs in both acute and chronic soft tissue
injury.14
A quantitative systematic review of 86 trials evaluating the efficacy of topical
NSAIDs in osteoarthritis and tendinitis found them significantly more effective
than placebo.15 However, no one topical NSAID seemd to be better than others. 16
Topical capsaicin cream has also been shown to reduce pain in joints affected by
osteoarthritis. This derivative of cayenne pepper causes exuberant release and
depletion of substance P, which is involved in pain transmission. Limited data

from controlled trials have shown improvements in pain with capsaicin. 17 It is

worthwhile to caution patients that they may experience increased pain while
beginning therapy with capsaicin.
Topical capsaicin or NSAIDs may also help reduce the use of systemic NSAIDs.
The American Pain Society guidelines recommend a tramadol-acetaminophen
combination for treatment of osteoarthritis pain when NSAIDs alone cannot
provide adequate relief. It is considered to be safe and effective in a subset of
elderly patients.18 Oxycodone has been shown to be useful in the treatment of
ostearthritis pain. Patients with moderate to severe pain from osteoarthritis can
achieve effective pain relief when opioids are included as part of a comprehensive
pain management program. Studies have also indicated that relief with low-dose
opioids can be achieved without deterioration in function.19
Recent attention has focused on the use of chondroitin or glucosamine.
Chondroitin and glucosamine are naturally occuring substrates for the synthesis of
articular cartilage. To date, there have been no large-scale randomized controlled
trials of these compounds in humans with osteoarthritis. Small controlled studies
have shown that glucosamine affords pain relief that is similar in magnitude to
that of NSAIDs.20 Meta-analyses of both chondroitin and glucosamine found
moderate to large reduction in symptoms of pain and immobility.21 Studies that
have evaluated the time course of improvement have shown a delay of up to 1
month in onset of pain relief after treatment begins. The benefit has persisted for
several weeks or months after glucosamine is discontinued. Patients considering
the use of glucosamine or chondroitin should be cautioned that no long-term trials
have evaluated their safety and that these products are not subject to regulation of
purity or accuracy of labeling.
Patients with osteoarthritis should be screened for depression and treated
appropriately with nonpharmocologic and pharmacologic interventions.
Nonpharmacologic intervensions are also important and effective in promoting
wellness and reducing disability. Multifactorial self-management programs
improve self-efficacy by providing experiential skills in disease management.,
physiologic self-regulation, emotional hygiene, and interpersonal communication.
Studies have demonstrated reduced pain, improvements in health behavior, and
reduction in use of health care resources in patients with chronic pain and
arthritis.22-25 Group-based self-management programs are often available through a
local chapter of the Arthritis Foudation and may overlap significantly in content
with typical hospital-based behavioral medicine programs.

Rehabilitaion
A comprehensive rehabilitative approach addresses prevention and treatment of
pain and disability through counseling, education and encouragement of weight
loss, exercise, adaptive equipment, and superficial modalities such as heat and
cold.

A physical therapist can guide and encourage a stretching program that can ease
the stiffness associated with sleep or prolonged immobility and prevent or reduce
impairment in range of motion. Patients should be educated in appropriate
positioning during extended inactivity or sleep. Appropriate use of heat before
stretching can help loosen tight periarticular muscles, and application of ice packs
after excercise can reduce the need for analgesic medications. Treatment time with
the therapist should focus on education in the use of these interventions, rather
than passive treatment. Gait and transfer training can improve functional mobility
in patients with limitations in range of motion or strength. Finally, a program of
aerobic and resistance exercise can safely decrease pain, prevent disability, and
promote general conditioning.
Occupational therapy can provide training in energy conservation techniques to
reduce fatigue in patients with reduced activity tolerance. In the setting of
significant functional impairments, the therapist can provide assistive devices that
help with feeding, grooming, dressing, and other activities of daily living.
As there is currently no cure for osteoarthritis, most research continues to evaluate
the use of exercise as a treatment to alleviate symptoms of the disease and to
enhance funcional capacity. Two meta-analyses published in 2004 focus
specifically on the efficacy of strengthening 26 and aerobic exercise27 for
osteoarthritis.
With muscle strengthening, improvememts in strength, pain, function, and quality
of life were noted. However,