Osteoarthritis is the most prevalent rheumatic disease. There is an enormous disability and loss of productivity associated with this condition; osteoarthritis is second only to cardiovascular diseases. The prevalence and severity of osteoarthritis increases with age. The degree of osteoarthritis is almost universal after 75 years of age; if someone lives long enough, they will have some form of osteoarthritis. Women are more affected than men in osteoarthritis, especially in nodal osteoarthritis.
Osteoarthritis is primarily a disease of the joint cartilage. The cartilage is the low-friction surface covering bone ends which functions in lubrication during movement, shock absorbency, load support and joint stability. Th cartilage is mainly composed of water, chondrocytes (controls synthesis and degradation of cartilage), collagen (proteins involved in tensile strength and maintenance of shape) and proteoglycans (provides the “stuffing material” for the cartilage). The failure of the chondrocytes to maintain the balance between cartilage formation and destruction exposes the underlying bone, leading to microfractures and osteophytes.
The major symptoms of osteoarthritis are pain, and to a lesser extent stiffness. Loss of mobility and function ensue. Instability of the weight-bearing joints and limited motion can also present as symptoms of osteoarthritis. As there are no proven cure for osteoarthritis, the underlying goals of treatment are to reduce pain, improve function, and prevent associated disability.
The pain experienced during osteoarthritis is usually a deep, aching pain. The pain worsens on motion and weight-bearing, but improves with rest. On the other hand, the other symptom of osteoarthritis, stiffness, resolves with motion but recurs with rest. This stiffness usually lasts for about 30 minutes or less in duration.
The sources of pain in osteoarthritis are multiple, and includes structures within and around the joint as well as psychosocial factors. The focus in osteoarthritis research has been on articular cartilage, and clinically this is monitored by joint-space narrowing on X-ray. However, the articular cartilage contains no neural or vascular structures.
Intra-articular sources of pain include periosteum and osteophyte formation, subchondral bone engorgement and microfractures, intra-articular ligament degeneration, capsular distension with effusions, and synovitis. Periarticular sources can include inflammation of tendon, fascia or bursa, muscle spasm, and nerve pressure. Psychosocial aspects can contribute, with lower education levels and depression both being associated with greater pain and disability in patients with osteoarthritis.