Osteoarthritis and 
Rheumatoid ­Arthritis 2012: Pathophysiology, Diagnosis, 
and Treatment

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Osteoarthritis and 
Rheumatoid ­Arthritis 2012: Pathophysiology, Diagnosis, 
and Treatment
Osteoarthritis and 
Rheumatoid ­Arthritis 2012: Pathophysiology, Diagnosis, 
and Treatment
This article is provided by the Nurse Practitioner Healthcare Foundation.


Introduction

Osteoarthritis (OA) and rheumatoid arthritis (RA) are two of the most common musculoskeletal conditions affecting individuals across the United States. Distinguished by cartilage degeneration and bony overgrowth, OA affects approximately 13.9% of adults who are ≥25 years of age.1

The incidence of OA rises with age with estimates that OA affects 12.4 million adults ≥65 years of age.1 OA occurs more frequently in women, particularly after reaching 
50 years of age; women are also at greater risk for developing OA in the knee or hip.1

RA, unlike OA, is an autoimmune condition characterized by inflammation, usually in bilateral joints, and systemic features, such as fatigue or fever.2 RA is estimated to affect 1.5 million adults.2 RA sufferers are typically younger than those who develop OA, with RA occurring between 20 to 30 years of age, and the incidence peaking at 35 to 50 years of age.2,3 The incidence of RA is higher in women2 with a higher lifetime risk (3.6%) compared to men (1.7%).4

While there is no cure for OA or RA, treatments that slow or halt the progression of RA are available. Unfortunately, the same is not true for OA, where current pharmacologic treatment focuses on symptomatic relief. This article not only highlights the differences in the pathophysiology and diagnostic criteria for OA and RA, but also describes current and potentially new treatment options for these conditions.


Pathophysiology 


Although the primary manifestations of OA and RA involve the joints, the underlying pathophysiology of each condition is distinct. 


Osteoarthritis and cartilage degeneration


Normally, cartilage undergoes a remodeling process, stimulated by joint movement or use.5 In OA, this process is altered by a combination of mechanical, cellular, and biochemical processes, resulting in abnormal reparation of cartilage and an increase in cartilage degradation.5 (Figure 1)

OA is primarily characterized by progressive cartilage loss, accompanied by an increased thickness of the subchondral plate, osteophytes (new bone at joint margins) and subchondral bone cysts.6 With disease progression, vascular invasion and further calcification of nearby articular cartilage may occur, leading to decreased thickness of articular cartilage and, over time, bone remodeling and enhanced cartilage deterioration.6 The inflammation that occurs typically involves the periarticular tissues and is generally milder in severity compared to RA.5

Osteoarthritis is associated with specific risk factors or causes including age, joint trauma, injury, or obesity.7 Individuals who are >50 years of age are at a higher risk of developing OA.5 The aging process has an impact on the cartilage extracellular matrix structure and components6; it is also associated with declining chondrocyte function and response rate to stimuli.5

Joint injury and trauma, prolonged stress on the joint from sports activities or strenuous occupations, and joint overactivity, can increase an individual's risk over time.5 Obesity increases the risk of OA, particularly in the weight-bearing joints.1,5 With the growing number of both overweight and obese individuals, the incidence of OA and the number of hip and knee replacements is rising.8-10 Genetics may also contribute to an increased risk.6

Joint damage in rheumatoid arthritis


Unlike the pathophysiology of OA, which is largely mechanical, RA is an autoimmune disease. The initial triggers of 
RA are unclear; hormones, genetics and environmental factors may all play a role.2

Once the initial immune response is triggered, cells of the immune system produce autoantibodies and inflammatory cytokines, creating a cascade of inflammation resulting in the formation of pannus; the pannus invades and destroys cartilage and bone. Additional joint damage and systemic complications ensue, resulting from a complex process of inflammatory mediators being released in the affected joint.11 (Figure 1)


Figure 1. Joint impact of osteoarthritis and rheumatoid arthritis
© Adapted from MedicineNet, Inc.

Many factors impact the risk of developing RA. The risk of developing RA doubles with a first degree relative who has RA. There is also a hormonal relationship; RA is more common in females, and there are high rates of disease onset associated with pregnancy.2,11,12

The impact of environmental stressors, especially smoking and chemical exposure (e.g., silicate), on genes is thought to drive the processes that induce autoimmune reactions leading up to the inflammation seen in RA.11,12 Research estimates that a history of smoking can increase the relative risk of RA onset more than 2-fold, especially in individuals who are positive for anti-citrullinated protein antibodies (ACPA) or anti-cyclic citrullinated protein antibodies (anti-CCP); smoking is the strongest risk factor associated with RA.2

Assessment of osteoarthritis and 
rheumatoid arthritis


Diagnosing osteoarthritis


The diagnosis of OA is based on patient history as well as the physical exam (Table 1). In advanced disease, radiologic signs of OA include asymmetrical narrowing of the joint space indicating loss of cartilage and/or the presence of osteophytes or bony overgrowth. The lack of radiologic evidence does not, however, rule out the presence of OA.5

Joint aspiration is an invasive procedure and not required for diagnosis. However, if done, synovial fluid analysis may help confirm OA is non-inflammatory, with a white blood cell count <2000/mm3; it may also help rule in or out other conditions, such as gout or inflammatory arthritis.13 Unlike RA, biologic markers are typically absent in OA patients.13 OA symptoms tend to start on one side of the body initially and may include one or more joints.5 The distal joints of the hands are most commonly affected as are the weight-bearing joints (e.g., knees, hips, cervical and lumbar spine).1

Morning stiffness is generally short-lived, usually lasting 
30 minutes or less and may also occur with moderate 
activity5,13; pain is usually relieved by rest.13 Other signs associated with OA typically involve joint tenderness, limited mobility, and local inflammation; systemic symptoms are usually absent.13 Crepitus, a grating sensation between the joints, may also be present in later stages of the disease.13

Diagnosing rheumatoid arthritis


To diagnose RA, patient history is important. However, the physical exam, laboratory tests, radiographs, and other assessments (ie, functional status, disease activity) are frequently helpful in confirming a diagnosis (Table 1).

Table 1. Summary of diagnostic criteria for osteoarthritis and rheumatoid arthritis

RA usually affects multiple joints, although it may only affect a few sites during its initial presentation.11 Contrary to OA, joint involvement in RA is typically symmetric and commonly affects small distal joints (ie, wrists, proximal interphalangeal joints, metacarpophalangeal joints).11 Affected joints are usually tender, warm, and erythematous, with a "puffy" appearance, due to increased blood flow and synovial infiltration or synovitis from pannus formation.11 This inflammation or pannus is generally palpable on physical exam as a "bogginess" or fullness over the joints. 


Morning stiffness lasting >30 minutes is also a common sign of RA; the stiffness typically improves with movement.11 Early symptoms of pain and stiffness in the joints, which may be accompanied by systemic features (e.g., anorexia, weakness, low-grade fever, fatigue), are recognized as the prodromal phase.11 Assessment of the patient's prognosis can impact treatment decisions. The American College of Rheumatology (ACR) recommendations for RA finds a poor prognosis can be inferred by one or more of the following features: functional limitations, presence of extra-articular manifestations (e.g., Felty's syndrome, rheumatoid nodules, RA vasculitis), positive rheumatoid factor or anti-CCP antibodies; or radiographic evidence of bony erosions.14

Treatment and management strategies


Numerous treatment strategies are available to help improve patient functionality and mobility in both RA and OA. Treatment for OA is mostly symptomatic whereas treatment for RA can slow down or prevent disease progression and joint destruction.


Nonpharmacologic treatment options


Nonpharmacologic therapy plays an important role in the successful treatment of OA and RA.17,18 Exercise, a key component of nonpharmacologic management, helps patients maintain mobility and function.18,19 Both OA and RA guidelines recommend regular aerobic exercise18,19; RA patients, in particular, are urged to participate in strengthening exercises to maintain joint function, while non-weight bearing exercises (e.g., water aerobics) are highly recommended for OA patients.18,19

Weight loss may also be suggested for patients with OA as a means to alleviate stress on weight-bearing joints.17,19-21 Self management, including patient education and cognitive and behavioral therapy, can also help manage OA and RA symptoms and improve both social and self-care capabilities.19,21

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