Download Assessing for Risk and Progression of Osteoarthritis: The Nurse`s Role

State of the Science
By Mary Carol Antonelli, RN, CRNP, and Terence W. Starz, MD
Assessing for Risk and Progression of
Osteoarthritis: The Nurse’s Role
Understanding pathophysiology, epidemiology, and risk
will aid nurses who are seeking to expand their role in
management.
Overview: The authors review the primary and secondary risk factors for osteoarthritis (OA), its pathophysiology and epidemiology, the evidence-based approaches to slowing progression, and the role of nurses
encountering OA in primary care and other settings.
Keywords: management, osteoarthritis, risk factors
T
he most common type of arthritis in the
United States,1, 2 osteoarthritis (OA) is a complex disease involving biomechanical, genetic, and environmental processes. Of the many
risk factors for OA, genetics and aging are the most
significant contributors to the primary form of the
disease, while obesity and injury are the most common secondary factors. Its manifestations range
from asymptomatic joint changes seen on X-ray
to severe disability. While the most common problems with OA are joint pain and functional impairment, the risk factors, clinical manifestations,
and radiographic findings vary for different joints.
The course of OA is extremely variable, and its outcome is difficult to predict.
Although no approved disease-modifying drugs
or other curative interventions are available, certain
measures can have a positive impact on pain, function,
and quality of life in people with OA. We’ll ­review
the factors involved in the development of OA and
the evidence-based measures that can slow its progression and consider the roles of nurses encountering OA in primary care and specialty settings.
PATHOPHYSIOLOGY, EPIDEMIOLOGY, AND RISK OF OA
An understanding of the pathophysiology and epidemiology of OA is required to assess and manage risk
factors and implement preventive measures (see
­Table 1).3, 4 The pathologic processes behind OA result in cartilage loss and bony changes in diarthrodial
joints (also called synovial joints), the freely movable
unions between bones that have hyaline cartilage on
their articulating surfaces.2 The joint is surrounded
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Nurse Marie Callari, total joint replacement coordinator at
­Winthrop-University Hospital in Mineola, New York, visits
patient Saundra Viviani after her total knee replacement.
Photo courtesy of Winthrop-University Hospital.
by a capsule and lined with a synovial membrane,
which produces synovial fluid.
Hyaline cartilage consists of a matrix that includes
protein and sugar compounds (proteoglycans and glycosaminoglycans such as chondroitin sulfate, keratin
sulfate, and hyaluronic acid) synthesized by chondrocytes (cartilage-forming cells); it’s composed of the
collagen fibers that give the cartilage structure. The
glycosaminoglycan matrix of cartilage regenerates
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Preventing and Managing OA
every one to three months, while the collagen structural elements are replaced even more slowly.
Synovial fluid nourishes the chondrocytes and lubricates the joint. Hyaline cartilage has no blood supply, significantly limiting its reparative, restorative
capacity. OA affects the degradation–synthesis cycle of
the chondrocytes, as well as of the extracellular matrix
and the subchondral bone, which in turn leads to softening, fibrillation, ulceration, and loss of cartilage.
OA bony changes include fractures of subchondral
trabecular (spongy) bone, marginal osteophytes (bone
spurs), and subchondral cysts. Hyaline cartilage has no
nerves, and the pain that accompanies OA arises from
the subchondral trabecular bone, the joint capsule, and
the periarticular tissues. Synovial inflammation may be
present, in part because of cartilage debris, which may
result in joint effusion (swelling). Periarticular structures, especially the muscles, are also affected.2
While any diarthrodial joint can be involved in OA,
the distal and proximal interphalangeal joints of the
hands are the most commonly affected, followed by
the knees and the hips.3, 5 A diagnosis of OA is determined by joint symptoms, including pain and functional impairment or joint pathoanatomic changes,
or both. A significant problem in addressing risk and
progression of OA is the wide spectrum of clinical
features that depend in part on demographic factors and the joint affected. Although epidemiologically OA is often described by a single joint region,
in reality patients often have OA in multiple joints.
The American College of Rheumatology6 and
other groups have developed criteria for diagnosing
OA in the knee, hip, and hand; however, diagnosis
is challenged by the limitations of X-ray findings in
the early stages of OA and the fact that such findings
do not correlate well with clinical symptoms. For
example, estimates of the prevalence of knee OA
vary widely according to whether clinical or radiographic criteria are used and the characteristics of
the cohort studied.3, 5 Computed tomography and
magnetic resonance imaging can more readily detect
cartilage and bony changes, but criteria for defining
OA using them have not yet been established.
Data on the prevalence of OA are based primarily
on X-ray surveys and self-report questionnaires.3, 5 It’s
estimated that 27 million people over the age of 25 in
the United States have OA.1 The Centers for Disease
Control and Prevention predicted in 2006 that 67
million people, or one-quarter of the U.S. adult population, will be diagnosed with some form of arthritis
by 2030.7 Although uncommon under the age of 40,
the prevalence of radiographic OA in all joints increases with age.5 People—including the aging baby
boom population—are living longer now, so the burden of OA is rising sharply. Radiographic screening
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Table 1. Risk Factors for Osteoarthritis
Primary (systemic) factors
Secondary (biomechanical) factors
Genetics
Obesity
Ethnicity
Joint injury
Age
Occupation
Gender
Physical activity
Hormonal status
Muscle weakness
studies have demonstrated that more than 80% of
people over the age of 55 have OA X-ray changes in
some joint.3 Between 1993 and 2006, the prevalence
of OA increased by 76%, with a 167% increase in
the 45-to-64-year-old age group.8
With aging, changes in the hyaline cartilage matrix
and decreases in its water content influence its biomechanical properties and reduce its shock-absorbing
capacity.2 Pathologic abnormalities found in the cartilage in OA patients significantly differ from the
changes in the matrix and collagen composition seen
with aging. In addition, degradative enzymes and
cytokines are produced by chondrocytes and the
synovium of OA patients, which can further damage the cartilage. Although the cartilage and subchondral bone make attempts at repair, the body is
not able to reverse the OA disease process.
Current evidence suggests that the
influence of heredity on OA development
is greater in women than in men.
Genetic factors play a major role in the expression
of OA; however, the influence of heredity varies in
different joints.9 Susceptibility to OA has been investigated by genome-wide linkage of families with OA
and candidate gene association studies in unrelated
individuals.9 No specific genes for predicting OA have
been identified yet, but those that regulate the synthesis of the various components of cartilage rather
than coding for specific structural proteins offer the
greatest promise. Current evidence suggests that the
influence of heredity on OA development is greater
in women than in men—as high as 60% for hand
and hip OA, but considerably lower for knee OA
(estimates range from 10% to 39%).9 In several epidemiologic studies, the influence of inheritance in
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State of the Science
knee OA was too low for linkage information to be
determined.10
SECONDARY RISK FACTORS
In addition to age, sex, and genetics, a variety of
secondary factors can influence load distribution
across a joint.5, 11
Obesity. The relationship among obesity, joint
pain, functional impairment, and physical activity
levels is complex. Obesity, which now affects 33.8%
of adults ages 20 years and older in the United States,
is a significant risk factor for the development and
progression of OA, especially in the knee but also in
other joints.12 The increased load that obesity places
on joints can exacerbate the pain and functional limitations of OA.4, 13 Because of the physics of knee movement, activity magnifies the load across the knee from
upper-body weight by three to seven times. Therefore,
weight loss in obese patients, especially if accompanied by increased physical activity, can improve physical function and quality of life.14
overhead sports activities, while OA of the elbow is
associated with weight lifting and sports involving
throwing. Other joints can also be affected by OA,
and significant trauma or injury to those joints is
frequently a major factor. Examples include the ankle and foot in ballet dancers, the shoulder after rotator cuff injury, and the metacarpophalangeal joints
in workers using jackhammers.17, 20, 21
A knee injury that prevents unaided walking for
more than a week is a strong predictor of knee OA.
Such injuries often involve rupture of the anterior
cruciate ligament (ACL), which may be associated
with a tearing of the meniscus or the medial collateral ligament. Both ACL damage and meniscus tears
are strongly linked to early OA development.22, 23
Because the incidence of ACL injury is two to eight
times higher among female compared with male
athletes, the rising number of women participating
in sports can be expected to result in higher rates of
knee OA in women.22, 23 Early ACL reconstruction
with meniscal preservation may help to protect
Female runners and tennis players are three times
more likely to develop tibiofemoral and patellofemoral
knee OA than are age-matched controls.
Thirty percent of women with body mass indexes
(BMIs) of less than 25 will have knee OA during
their lives, compared with 60% with BMIs of 30 or
higher.15 Weight change can have a significant modifying effect: women who lost just two points in BMI
in 10 years had a 35% reduction in risk of developing symptomatic knee OA.15
Being overweight may also play a role in OA in
other joints, including the hips, hands, and shoulders,
although in those cases the role is not well defined.
For example, one study showed a moderate relationship between obesity and the development of hip OA,
but only limited evidence of an association between
obesity and bilateral hip OA.16 OA in these joints may
be related to mechanical factors, abnormalities in intermediary metabolism in adipose tissue, or the production of cytokines.17
Physical activity. Light or moderate physical activity and exercise that do not cause pain or injury
do not increase the risk of OA.18 Female runners and
tennis players are three times more likely to develop
tibiofemoral and patellofemoral knee OA than are
age-matched controls.19 The risk of developing OA
of the shoulder is increased by participation in
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against knee OA. The poorest postoperative outcomes have been seen following meniscectomy.3, 5
Occupation. The influence of occupation on the
development of OA is unclear and seems quite variable.24, 25 Occupations that require repetitive overuse
of joints, especially with impact loading, cause high
biomechanical stresses and may predispose to OA.
Repeated crouching, kneeling, squatting, stair climbing, and heavy lifting can result in abnormal loading
across the joint and articular damage. Few occupational studies have included women, but the evidence
suggests that the risk factors are similar in both sexes.24
Mechanical environment. Knee alignment has
a strong impact on joint load distribution.11 Varus
alignment is associated with progressive medial compartment OA (wearing of the medial meniscus) and
valgus alignment with lateral compartment OA (wearing of the lateral meniscus); the degree of alignment
correlates with the magnitude of the joint-space narrowing. People with varus knee alignment have a
greater loss of function when walking than those
with valgus alignment do.
A decrease in proprioception, which helps to establish and maintain joint stability, is present in both
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Preventing and Managing OA
the involved and the uninvolved knees of patients
with unilateral knee OA and may precede overt
pathologic changes in the joints.5, 26 Laxity of the
knee ligaments is another contributing factor. With
aging, varus–valgus laxity increases more often in
women than in men, and it may also precede knee
OA. Patients with unilateral knee OA have greater
varus–valgus laxity in both the involved and the
contralateral knee. Forefoot varus alignment may
increase the likelihood of hip OA.1, 3, 5
Muscle strength. Muscles are the major supporting structures for joints and are critical for joint
movement and stability.26 Studies have shown that
quadriceps weakness commonly accompanies knee
OA.27 This finding was attributed to disuse atrophy
secondary to knee pain and abnormal biomechanics,
but extensor weakness is also present with asymp­
tomatic tibiofemoral OA, suggesting that quadriceps
weakness is a risk factor for knee OA development.
Individuals who developed knee OA during followup had 18% less quadriceps strength at baseline than
those who did not. The influences of muscle strength
and afferent sensory dysfunction on the progression
of knee OA are uncertain.27
Other factors may also influence the risk and
progression of OA.4 Estrogen has a physiologic effect on cartilage and bone metabolism: while both
estrogen deficiency and OA occur with advancing
age, observational studies on the influence of estrogen, including with hormone replacement therapy,
have been inconclusive.5 It has been suggested that
vitamin D and K deficiencies contribute to the development of OA.4 Inflammatory arthritides such
as rheumatoid arthritis and systemic lupus erythematosus can injure cartilage and bone and result in
secondary OA changes.17, 28
EVIDENCE-BASED MANAGEMENT
While there is no cure for OA, the American College of Rheumatology (ACR), the European League
Against Rheumatism, and others have established
nonpharmacologic and pharmacologic management
guidelines.29, 30 Therapy is primarily directed at controlling pain and maintaining functional activity.
The Osteoarthritis Research Society International
(OARSI) has published evidence-based recommendations for the management of knee, hip, and hand
OA.29, 30 Of the nonpharmacologic therapies, relief
has been demonstrated for self-management, education, exercise, acupuncture, and weight loss. Inclu­ded
in these measures are instruction on disease pathophy­
siology; use of self-management techniques such as
thermal modalities and activity modification; reg­ular
telephone contact; referral to physical therapy; walking aids; knee braces; aerobic, muscle-strengthening,
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and water-based exercises; and footwear and insoles.
Pharmacologic therapies for OA also focus on pain
management since no medications can significantly
influence the disease’s course. The 2008 OARSI pharmacologic recommendations29 included acetaminophen, cyclooxygenase-2 nonselective and selective
nonsteroidal antiinflammatory drugs (NSAIDs), topical NSAIDs and capsaicin, glucosamine sulphate,
chondroitin sulfate, intraarticular injections of corticosteroids and hyaluronates, and the use of opioid
analgesics for refractory pain. The ACR guidelines
recommend acetaminophen and NSAIDs as primary
agents for OA. Studies have suggested that for analgesic efficacy in OA, NSAIDS have a therapeutic advantage over acetaminophen,29, 30 but NSAIDs can cause
adverse gastrointestinal and cardiovascular effects.
Pharmacologic therapies for OA focus on
pain management since no medications can
significantly influence the disease’s course.
The response to different NSAIDs is variable and
clinically unpredictable. Lower NSAID doses are
primarily analgesic, while larger doses are required
for antiinflammatory effects. A therapeutic trial of
two weeks or longer is recommended to assess the
effect of a particular agent. Tolerance can develop
to NSAIDs, and switching agents periodically can be
beneficial. Because of the frequent need for continuous, long-term use of NSAIDs in OA, compliance
is better with once- or twice-daily dosing than with
more frequent doses. When medical treatment fails
to alleviate OA symptoms, especially in the knee
and hip, arthroplasty is often a consideration.31
THE NURSE’S ROLE IN MANAGING OA RISK AND
PROGRESSION
The role of the nurse in managing OA risk and
­progression has been evolving, for example, in primary care, teaching, research, and other tasks and
settings.32-35 (See Table 2.) With the projected increase
in OA prevalence forewarning of a much larger patient population, it will be essential for facilities to
have coordinated OA teams staffed with trained professionals. But there is a critical shortage of these practitioners: there are roughly 500 nurse members of the
Association of Rheumatology Health Professionals,
a division of the ACR, and 415 physicians were in
rheumatology training in 2009. Furthermore, there
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State of the Science
Table 2. The Nurse’s Role in Assessing for Risk and Managing Progression of OA
•• Evaluation, including a targeted history and physical examination along with laboratory and joint imaging
studies to establish diagnosis
•• Education of the patient on the manifestations of OA and its management
•• Risk management for medications and other management activities
•• Care coordination among the patient and health care professionals
•• Compliance strategies, including proper medication use, weight reduction, and exercise
are limited data on specific nursing interventions for
OA and their effectiveness in primary care, rheumatology, and orthopedic surgery practice settings.35, 36
Nurses assist in diagnosing and assessing the disease’s
functional and psychosocial impacts, provide medication and pain management,37 monitor disease progress,38 educate patients, and coordinate care with other
providers (physical, occupational, and psychosocial
therapists39). Understanding the clinical manifestations
of and the diagnostic criteria for OA provide the foundation for these activities.
Patient evaluation for OA should begin with taking
a targeted history of the problem. The circumstances
surrounding the onset of the joint problem, including
precipitating factors such as trauma, and the problem’s duration are first determined, along with the
impact it has on activities of daily living such as walking, bending, performing fine motor activities, and
climbing stairs. Additional information, as stipulated
by the diagnostic OA criteria being used, such as those
of the ACR, should also be obtained.
After a diagnosis of OA, education will help patients compensate for and manage its effects by adapting their usual activities; using assistive devices; and
complying with medication, exercise, and weight
management programs.40-43 Nurses can impart this
information to patients in formal discussions or educational materials and by giving them advice on using electronic resources to find more information. An
accurate assessment of the patient’s educational level
must be made before an effective program can begin.
According to the 2003 National Assessment of Adult
Literacy, 14% of the population in the United States
has “below basic” health literacy, which limits their
ability to understand health information and make
informed health-related decisions.44
Studies in primary care settings demonstrate that
nurses are key assessors of and coordinators in managing their OA patients’ care.37, 39, 45 There are programs and protocols designed specifically for OA that
define screening tools for uniformly collecting patient
data,46 provide models for treatment, and promote
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the integration of interventions among various health
care providers.45, 47 Self-report instruments such as the
Western Ontario and McMaster Universities Osteoarthritis Index, the Health Assessment Questionnaire,
and the Medical Outcomes Study Short Form 36Item Health Survey are validated tools that can provide important information for assessing outcomes in
OA.46 Helping patients accept their disease and encouraging them to actively participate in the care
process are essential. It is also important to identify
patients who are hiding their symptoms from health
care professionals and trying to self-manage their
problems. In addition to all of these responsibilities,
orthopedic nurses must also actively engage in preand postoperative care.48-50 ▼
Mary Carol Antonelli is a CRNP at Arthritis and Internal
Medicine Associates–UPMC, University of Pittsburgh Medical Center, and Terence W. Starz is a clinical professor of medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Contact author: Mary Carol Antonelli, antonellicarol@yahoo.
com. The authors have disclosed no potential conflicts of interest, financial or otherwise.
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Preventing and Managing OA
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