NNN

Osteoarthritis

Oct 03, 20244 min read

Osteoarthritis (OA) is a noninflammatory degenerative disorder of the joints. It is the most common form of joint disease, sometimes also called degenerative joint disease. It may be primary, occuring without known causative event, disease, or injury (idiopathic) or secondary, occuring as a result of previous joint injury or inflammatory disease, similar to rheumatoid arthritis (RA). Primary OA is not autoimmune or inflammatory, and is limited to the affected joints, with no associated systemic symptoms.

  • OA begins in the third decade of life, becoming more common with age and peaking between the fifth and sixth decades. By 40 years of age, 90% of the population exhibit degenerative joint changes in their weight-bearing joints, but most are asymptomatic. 85% of the population over 65 years of age will show radiographic changes indicating OA.
  • Women, especially Hispanics or African Americans, are more susceptible to OA.

Pathophysiology

  • All joints compose of bone, particularly of subchondral bone or the bony plate to which the articular cartilage is attached. It is lubricated, smooth tissue that protects the bone from damage with physical activity. Between the bones of a joint is the joint space, containing synovial fluid for lubrication and facilitation of movement.
  • With OA, the articular cartilage breaks down, leading to progressive damage to the underlying bone and eventual formation of osteophytes (bone spurs) that protrude into the joint space.
  • The joint space narrows, decreasing joint movement and increasing the potential for more damage. This leads to the joint progressively degenerating.

Risk Factors

  • Older age
  • Female Gender
  • Obesity (the most prominent modifiable risk factor)
  • Certain occupation e.g. those requiring laborious tasks
  • Engagement in sports
  • History of previous injuries
  • Muscle weakness
  • Genetic predisposition
  • Certain diseases that place patients at risk for joint destruction.

Clinical Manifestations

The main clinical manifestations of OA are pain, stiffness, and functional impairment. The onset is routinely insidious, progressing over multiple years. There are no systemic manifestations. Areas susceptible to OA are weight-bearing joints (hips, knees, cervical and lumbar spine), and both proximal and distal interphalangeal (PIP, DIP) joints.

  • The joint pain is usually aggravated by movement or exercise, and relieved by rest.
  • If morning stiffness is present, it is usually brief, lasting less than 30 minutes.
  • Upon physical examination, the joint may be enlarged with a decreased range of motion. Crepitus may be palpated, especially over the knee.
  • Joint effusion, a sign of inflammation, is usually mild.

Diagnostic Examination

Blood tests and examinations of the joint fluid are not useful, but may be used to rule out autoimmune causes of joint pain (e.g. RA).

  • X-rays can display the narrowing of joint space, osteophyte formation, and thickened and dense subchondral bone.

Management

  1. Medical: decrease pain, stiffness, and preserve or improve joint mobility.
    • Exercise, especially in the form of cardiovascular aerobic exercise and lower extremity strength training, has been found to prevent OA progression and decrease the symptoms of OA. This may also help with weight loss, which reduces the load on joints, which can also be extremely beneficial.
    • Occupational and physical therapy can also help with self-management strategies.
    • Orthotics can help reduce pain and the force on the affected joints, or potentially (currently under study) correct biomechanical abnormalities related to OA.
  2. Pharmacologic: symptomatic management and pain control. Prescription is based on patient needs, disease staging, and side effect risks. These are used in conjunction with nonpharmacologic strategies.
    • Most patients start analgesia with acetaminophen. Some patients respond to NSAIDs and COX-2 enzyme blockers. The use of COX-2 medications is associated with cardiovascular disease and little to no decreasessss in GI upset, and therefore is used with caution.
    • Nonopioids such as tramadol and Intraarticular Corticosteroids may also be considered. Opioid analgesics are used for severe cases.
    • Topical analgesia such as capsaicin and methylsalicylate are also used.
  3. Nursing: pain management and optimal functional ability are the major goals of nursing interventions.
    • Education: the patient’s understanding of the disease and treatment processes is crucial.
    • Weight loss (when appropriate, as many patients are also overweight) and exercise (progressive) are important approaches to lessen pain and disability. Assistive devices should be considered. Exercise should coincide with the time of least pain or with the use of analgesia to manage pain.
    • Open discussion for complementary, alternative, and integrative health therapies is encouraged to ensure safe and effective practices for patients.

Backlinks

Graph View