CHAPTER 44

Osteoarthritis

Maureen F. Cooney, DNP, FNP-BC

Osteoarthritis (OA) is a clinical condition of diarthroidal joints characterized by pain, stiffness, and structural alteration. Underlying this condition are destruction and abnormal repair of articular cartilage, followed by deposition of new bone and cartilage at the margins of the joint. The process may lead to joint deformity, decreased range of motion (ROM), and in later stages severe functional impairment. Although all diarthroidal joints may be affected, OA is most commonly seen in hand, hip, and knee joints.

Primary care providers are at the front line of diagnosing and treating OA. The national ambulatory medical care survey reveals that problems of the musculoskeletal system are one of the most frequent reasons for office visits. With proper attention to details of diagnosis, treatment, and outcomes, the primary care provider is best suited to care for patients with OA and to coordinate the use of other specialists.

The pain of OA is characteristically worsened with activity and relieved by rest. Conversely, the stiffness associated with OA is worse after rest of the affected joint and better with motion. The bony structural alteration of joints associated with OA seen in radiographic studies may or may not be associated with pain or stiffness. Hence, the diagnosis of OA is clinically based on more than just the radiological features of a joint.

OA is classified as either primary/idiopathic (without a discernible explanatory event such as joint trauma) or secondary (to a specific insult to the joint). OA may affect one or more joints simultaneously. Although OA is not characterized as a systemic inflammatory illness, it is widely accepted that synovial inflammation is a characteristic of OA, although the role of immune cells and their cytokines is mostly unknown (de Lange-Brokaar et al., 2012).

ANATOMY, PHYSIOLOGY, AND PATHOLOGY

Three types of joints exist within the body: diarthroidal or synovium-lined joints, which are involved in the movement of limbs; synarthrosis or pseudojoints; and amphiarthroses or cartilaginous joints. OA is a disease strictly of diarthrodial joints. Examples of diarthrodial joints are the knee, hip, and joints of the hands. The bony articular prominences of diarthrodial joints are lined by articular cartilage, which facilitates motion at the joint. The biochemical composition of adult cartilage is roughly 70% water and 30% solids. Current understanding of the pathophysiology of OA suggests that articular cartilage trauma, possibly complicated by normal aging, results in alteration of the water/solid ratio. An inflammatory process involving a variety of biochemically initiated cellular events leads to cartilage breakdown. Further joint response leads to changes in bone, resulting in osteophyte formation and bone reconstruction. The exact role that aging plays in OA is uncertain.

Joint remodeling occurs initially at the edge of the affected joint. Osteophyte formation (new bone at the edge of joints) is thought to be the result of endochondral ossification of existing and new cartilage. The relationship between osteophyte formation and the development of clinical symptoms is not known. Osteophytes are often present in radiological studies of asymptomatic persons and may represent a normal response to a variety of joint stressors. Osteophyte formation and other bone remodeling, however, are generally present in advanced OA.

EPIDEMIOLOGY

OA is thought to result from a complex interplay between a variety of host-specific characteristics, such as immunologic, biomechanical, or bioinflammatory variables, and functional characteristics, such as joint use, environmental trauma, or stresses. OA is the most prevalent joint disease in the United States and one of the most common diagnoses in primary care practice.

OA generally develops over several years, although symptoms may be stable for an extended period of time. The prevalence of OA is thought to have increased in recent years, with an estimated 27 million adults having clinical OA of a hand, hip, or knee joint in 2005, an increase from 21 million in 1995 (Neogi & Zhang, 2013). The increase is thought to be related to the aging of the population and the rising prevalence of obesity. The risk factors for OA are age and gender; prevalence increases with age, and after the age of 50 years, more women than men are affected. The diagnosis of OA is both clinical and radiological; however, there is no universal definition of OA. Organizations such as the American College of Rheumatology have developed criteria for the classification of OA of the knee, hip, and hand. Although these criteria have proven helpful, the lack of a uniform definition for the diagnosis hampers the determination of prevalence and incidence of OA in this country and worldwide.

Death associated with OA is most often a direct result of functional impairment of the joint with resulting injury or immobility. Given the aging of the population in the United States, and the resultant increase in the prevalence of OA, the financial impact of this illness can be expected to rise in the next 20 to 30 years. There is a significant earning loss from work disruption in patients with OA <65 years old.

Risk Factors for OA

Because OA has a multifactorial etiology, risk factors may also be multifactorial. For example, an individual with a genetic tendency to develop OA may only develop symptoms if subjected to repetitive mild joint injury. Risk factors vary for different joints, different disease stages, and for radiological OA versus development of clinical OA. Specific risk factors associated with OA include:

Age: Prevalence is directly related to advancing age.

Gender and hormones: Women are more likely to have OA than men, and their symptoms tend to be more severe. The rise in OA around the time of menopause suggests a hormonal influence on the development of this disease process.

Race/ethnicity: Prevalence and patterns of joint involvement with OA varies among racial and ethnic groups. Both hip and hand OA were found to be more common among White women in the Framingham Study than Chinese women in the Beijing Osteoarthritis Study, but Chinese women had higher prevalence of knee OA. Studies have demonstrated differences in the radiological features of OA in the joints of African Americans compared to their White counterparts (Zhang & Jordan, 2010). African Americans generally report more hip and knee symptoms than Whites.

Obesity: Although the exact mechanism has yet to be described, there appears to be a relationship between obesity and OA. The effects may be both mechanical and systemic (metabolic or inflammatory). Adipose tissue is known to be metabolically active, but the role of adipokines is unclear. The relationship between obesity and OA varies according to the involved site. Studies have demonstrated a strong relationship between obesity and OA of the knee, but the relationship between obesity and OA of the hip is not clear. Although the association of obesity and OA in the joints of the lower extremities may make biomechanical sense in terms of the increased stress that is placed on these joints, what is less well understood is the increased association between obesity and hand OA, further raising the question of a systemic process in OA development. It is suspected but not clinically proven that weight loss may be an opportunity for clinical prevention of OA in later ages.

Exercise: Studies have suggested a link between specific forms of exercise and sports and OA, but none have been conclusive. In the Framingham Study, elderly subjects who engaged in higher levels of activity, such as walking and gardening, had a threefold greater risk of developing OA radiological changes than sedentary subjects. Repetitive joint use may predispose to the development of OA. For example, correlation has been shown between occupational lifting and prolonged standing and the development of OA of the hip. However, it is thought that physical activity in OA may be beneficial, as strengthening of periarticular muscles may result in joint stabilization. More recent studies suggest just the opposite—that exercise in moderate forms may be beneficial in primary prevention.

Genetics: The results of several studies have shown a 50% to 60% heritable component of OA and the data are even stronger for hip and hand OA than for knee (Neogi & Zhang, 2013). Familial tendencies in the development of joint deformities such as Heberden’s nodes have been described. Although genetic factors are most likely polygenic, specific gene mutations resulting in changes of joint components that may lead to the development of OA also have been described. For example, a variety of collagen disorders linked to gene defects are thought to be involved in the development of certain forms of OA. As the molecular genetic revolution progresses, more genes will be elucidated as playing a role in this disease. In the interim, more research on the complex interaction between genetics and family history and environment has to be performed.

Occupation: Occupation is a risk factor for OA (Zhang & Jordan, 2010). Work-related activity has been linked to the development of OA of the knee and other joints. This is thought to be the result of repeated minor trauma, exacerbating an already increased risk at a joint predisposed from underlying mechanical factors such as joint deformity or malalignment.

Trauma: A history of major trauma to the knees is strongly associated with the development of OA. The same is true for injuries to other joints. In general, any injured joint is at risk for the later development of OA.

Diet: There is great interest in OA and the role of dietary factors. Although studies have yielded conflicting results, the relationships between vitamins C, D, and selenium deficiencies on OA development and progression have been examined. Additionally, the protectant value of vitamins E and K is under consideration.

DIAGNOSTIC CRITERIA

The American College of Rheumatology developed classification criteria for OA of the hip, knee, and hand in the early 1990s, which continue to be a popular method of classifying OA in clinical studies and in primary care practice. However, a criticism of the use of these criteria is that they may reflect later signs of the disease process in advanced disease (Peat et al., 2006). The diagnosis of OA is based on clinical and radiological features. However, nearly half the people with osteoarthritic radiological features are asymptomatic, while a similar proportion of those with clinical features lack radiological findings (Bijlsma, Berenbaum, & Lafeber, 2011). The diagnostic criteria developed by the American College of Radiology appear in Table 44.1.

HISTORY AND PHYSICAL EXAMINATION

Pain, stiffness, and locomotor restriction are the main symptoms of OA. Pain is the most common presenting complaint in OA. The pain is usually localized to the involved joint, but it may be referred. An example of referred pain is cervical OA presenting as pain in the shoulder, or lumbar facet joint OA causing pain in the buttock or hip regions. Early in the course of OA, pain may be intermittent and it may have a nagging or aching quality that varies in intensity according to the level of activity. Pain usually occurs with activity or motion and is relieved by rest. In early disease, the pain is not severe, but as the disease progresses pain may be present with minimal motion or even at rest. Inflammatory flares may develop during the course of the disease.

Stiffness is very common. Early in the disease, it is felt when the patient resumes activity after a period of rest, and later it may become a permanent complaint. Bony swelling and joint deformity, especially of affected knees and interphalangeal joints, are common later in the disease. Muscle wasting, bowing of the legs, and knock knees are also late manifestations. Bony swelling of the interphalangeal joints may make it difficult to perform activities requiring fine motor skills, such as writing, as well as gross motor skills, such as opening jars or grasping objects. Patients complain of loss of function according to the site involved.

The cause of pain in OA is not completely understood but may arise from nociceptive fibers and mechanoreceptors in the synovium, subchondral bone, periosteum, capsule, tendons, or ligaments (Abhishek & Doherty, 2013). Pain may be related to muscle spasm and fatigue, joint contracture, capsular fibrosis, and in some cases mild to moderate synovitis. Acute inflammatory flares can be related to trauma or crystal-induced synovitis. Temporal and seasonal changes in OA pain have been reported. For many, it is worst upon arising, then diminishes, but worsens again in the early evening after a period of activity and diminished with rest and sleep. Stiffness follows a similar pattern. However, stiffness worsens with periods of inactivity, whereas pain may be reduced with rest.

The degree of locomotor restriction is related to the location of involved joints. OA of the hand may result in difficulties with grasp and pincer function, whereas OA of the hip and knee may impair ability to move from a lying or sitting position to a standing position, and may interfere with gait.

On the physical examination, multiple joints may be involved. The patient’s gait should be evaluated for disturbances related to OA of the hip and knees. A limp or stiff-knee gait may be present. Bony swelling and deformity are usually easily recognized, especially at the interphalangeal joints of the hand and the knees. In the later stages of the disease, muscle wasting may become obvious. During acute flares, there may be signs of inflammation, including erythema, warmth, and swelling. Passive joint motion is restricted and painful, and there may be crepitus or a feeling of crackling as the joint is moved through its ROM. Crepitus of the joint may be more pronounced on active than passive ROM. Reduced ROM may be present in any affected joint, and may ultimately result in fixed flexion deformities. On palpation, joint tenderness, intra-articular effusions, synovial thickening, and marginal osteophytes may be present. In most cases, there is no joint instability.

Hand

The most commonly affected joints of the hand are the first carpometacarpal joint and the distal and proximal interphalangeal joints. Hand OA is usually bilaterally symmetric. Heberden’s nodes are spurs formed at the distal interphalangeal joints (Figure 44.1). Bouchard’s nodes are present at the proximal interphalangeal joints. Deformity or loss of motion tends to be gradual. There is a lateral deviation of the joints involved. Hand OA may progress or remain stable over time. The progression is usually fastest in the distal interphalangeal joints. When the first carpal metacarpal joint is involved, there is tenderness at the site and later a squared appearance of the hand. The trapezioscaphoid joint is also commonly involved. Metacarpophalangeal involvement is rare. Despite the development of bony deformities, function of the hands remains relatively good.

Knee

FIGURE 44.1
Nodules on the dorsolateral aspects of the distal interphalangeal joints (Heberden’s nodes) are due to the bony overgrowth of osteoarthritis. Usually hard and painless, they affect the middle-aged or elderly and often, though not always, are associated with arthritic changes in other joints. Flexion and deviation deformities may develop. Similar nodules on the proximal interphalangeal joints (Bouchard’s nodes) are less common. The metacarpopha-langeal joints are spared.

OA of the knee is the most common cause of lower-limb disability in older people. Development of pain and impairment in function tend to be gradual in onset. Both knees are usually involved, although symptoms on one side may be worse. Knee joint pain is usually felt anteriorly, and is worsened by prolonged sitting, standing up from a low chair, and climbing stairs or inclines. Descending stairs tends to cause more pain than ascending. Generalized knee pain and radiation suggest moderate to severe OA. There may be a stiff-knee gait. Visual inspection may reveal bony swelling or genu varus or genu valgus deformity. Any of the three compartments (medial, lateral, tibiofemoral) of the patellofemoral joints may be involved; most commonly, the medial compartment is affected. Medial compartment OA involves joint line tenderness and a loss of articulator cartilage, leading to joint space narrowing and a varus deformity of the knee. With progression of disease, there is a loss of active and passive motion in both flexion and extension. Crepitus may be present, especially at the patellofemoral joint. In more advanced cases, a flexion contracture, quadriceps atrophy, and joint effusion may be present. Knee OA does not progress in all persons, and in some joint symptoms may improve with time.

Hip

OA of the hip usually begins with a gradual onset of pain, often followed by a limp. The pain typically occurs in the groin or anterior thigh, but occasionally it is in the buttock or even in the knees because of pain referred along contiguous nerves. It may be difficult to differentiate hip OA pain from referred spinal pain or concomitant knee OA. Unlike knee OA, hip OA is often unilateral. ROM in the hip, especially internal rotation, becomes limited. In chronic OA, weak abductor muscles may result in a positive Trendelenburg sign and an ataxic gait. Some patients with OA of the hip experience radiological and symptomatic improvement.

Spine

The intervertebral disc, intervertebral osseous bodies, and posterior apophyseal articulations are involved in OA of the spine. Lumbar facet joint OA is thought to lead to localized lumbar pain, which may radiate unilaterally or bilaterally to the buttocks, groin, and thighs, usually ending above the knees. Physical findings include restricted ROM and localized paraspinal muscle tenderness and spasm. Nerve root compression from osteophyte impingement can lead to radicular pain and other signs such as muscle weakness and atrophy, reflex changes, and positive tension signs including positive straight leg raising tests. There is restricted motion because of pain, stiffness, and bony changes.

Foot

The first metatarsophalangeal joint is the most commonly involved joint of the foot and usually occurs bilaterally. Joint tenderness, bony swelling, bony enlargement (bunion), irregular joint contours, and restricted motion, especially in dorsiflexion, may occur.

Disease Course

The course of OA is variable. Although it is a slowly progressive disease, some patients can improve, especially over the short term. Those with multiple affected joints appear to have a more rapid progression. This increased risk of progression is especially seen in the knee. Crystal deposition (calcium pyrophosphate, hydroxide apatite, or a mixture) in the joints of patients with OA is associated with an increased risk of progressive disease. Age is also a risk factor for progression of OA. Elderly persons are more likely to have rapid deterioration of their joints than younger persons with the same degree of OA. Other risk factors associated with progression and poor prognosis include obesity, knee malalignment, lower-limb length inequality, excess or no joint use, muscle wasting and weakness, joint laxity and instability, peripheral neuropathy, poor mental health, lack of self-efficacy, and poor social support (Abhishek & Doherty, 2013).

DIAGNOSTIC STUDIES