Osteoarthritis (OA) is the most common condition to affect synovial joints and causes significant dysfunction and disability. Because osteoarthritis increases significantly with age, it was long considered to be a degenerative disease that was an inevitable consequence of ageing and trauma. However, it is viewed now as a metabolically dynamic process characterized by an imbalance of joint breakdown in association with a maladaptive and insufficient repair process.
Osteoarthritis is a condition of increasing prevalence characterized by a phasic progression with periods of relative quiescence and flare. An individualized and holistic approach to management is essential as the best means for relieving pain, minimizing disability and improving quality of life.
The aetiology of osteoarthritis is unclear. Mechanical, biochemical, and genetic factors seem to play a role. One theory is that increased levels of cytokines, such as interleukin-1 and tumor necrosis factor prompt chondrocytes to release enzymes that break down the extracellular matrix. Simultaneously, there is a decrease in the substances that usually inhibit this breakdown. The cartilage breakdown products seem to promote further inflammation, continuing this cycle of cartilage breakdown. Osteophyte formation and other alterations in joint architecture are end results. How or why this cycle starts is uncertain?
Osteoarthritis is traditionally separated into two main categories: primary and secondary. Primary osteoarthritis typically involves joints in characteristic locations and is likely to result mainly from genetic predisposition.
Typical symptoms of this include gradual onset of pain and stiffness in and around a joint with decreased function of that joint. Early in the disease process, the pain is typically mild, worsening with use of the affected joint and improving with rest. If present, morning stiffness rarely lasts more than 30 minutes. Stiffness is common after inactivity of the joint, usually resolving after a few minutes. Pain at rest or at night occurs in more severe disease.
Joints affected by osteoarthritis include knees; hips; cervical and lumbar spine; the first metatarsophalangeal joints of the feet; and distal interphalangeal (DIP), proximal interphalangeal (PIP), and first carpometacarpal (CMC) joints of the hand. Patients with knee osteoarthritis may complain of “buckling,” especially while descending stairs. Pain from hip osteoarthritis is usually felt in the groin but can radiate to the anterior thigh or knee. Osteophytes from osteoarthritis of the spine may cause radicular symptoms secondary to nerve root compression.
Multiple Heberden’s nodes (bony enlargement of distal interphalangeal joints of the hand) appear in middle age and are a strong marker for subsequent predisposition to knee osteoarthritis and osteoarthritis at other common target sites (nodal generalized osteoarthritis).
When osteoarthritis occurs in atypical joints, such as the ankle, the presentation alone should trigger consideration of secondary osteoarthritis. Typical aetiologies of secondary osteoarthritis include joint trauma, previous fracture and preceding inflammatory arthropathy such as gout.
Patients with osteoarthritis often have bony enlargement and tenderness of the joint. Periarticular muscle spasm may be present. Range of motion (ROM) is sometimes limited. Locking of a joint during ROM can occur from loose bodies or fragments of cartilage in the joint space. Signs of mild inflammation, such as warmth or swelling, may be present around an affected joint. Evidence of severe inflammation is suspicious for other disorders, such as septic arthritis, gout, or pseudogout.
Crepitus is commonly felt on passive ROM of the knee. It is caused by the irregularity of the opposing cartilage surfaces. A varus deformity of the knee is often seen from medial compartment degeneration, but a valgus deformity is possible with lateral compartment involvement.
Bony enlargements called Heberden’s nodes on the DIP joints and Bouchard’s nodes on the PIP joints are frequently present in osteoarthritis of the hand. These nodes may be painful, especially when they first develop, but are usually nontender after they are formed. Osteoarthritis does not typically involve the metacarpophalangeal joints as rheumatoid arthritis does. Rheumatoid arthritis involves multiple joints in a symmetrical pattern but spares the DIP and first CMC joints commonly affected by osteoarthritis.
Osteoarthritis is a clinical diagnosis. The main investigation that can help confirm osteoarthritis is plain X – ray, with demonstration of characteristic structural abnormalities:
It is important to note that majority of people with radiographic evidence of osteoarthritis have no symptoms of osteoarthritis. Biochemical abnormalities of the joint precede radiographic abnormalities by as much as decades. For this reason, much effort is currently being put into identifying more sensitive imaging modalities, such as magnetic resonance imaging, bone scintigraphy and ultrasound, along with biochemical indicators in blood, urine or synovial fluid, that might identify and quantify osteoarthritis more precisely and earlier than by X-ray.
The goals of medical management of osteoarthritis include:
The myth that osteoarthritis is a progressive wearing – out of joints due to old age still persists; this invariably leads to inappropriate reductions in activity. A major contribution to managing osteoarthritis has been the finding that a patient’s psychological status (anxiety, depression and social support) is an important determinant of symptomatic and functional outcome. Good evidence supports the use of educational programmes to help patients understand osteoarthritis and develop self–management strategies.
Local quadriceps – strengthening exercise can reduce pain and disability and improve the physiological accompaniments of knee osteoarthritis (muscle weakness, impaired proprioception and balance, tendency to fall). Aerobic activity also reduces pain and disability from osteoarthritis, improves well – being and sleep quality, and is beneficial for common co-morbidities.
Pool exercise, wherein people weigh just one-eighth what they weigh on land, can mitigate negative effects of excessive joint loading due to obesity and allow freedom of joint movement and aerobic training for individuals with lower extremity osteoarthritis.
Observational studies have demonstrated an increased risk of knee osteoarthritis in obese patients, particularly obese women, when compared with their non-obese counterparts.
TENS machine may help in symptomatic management of joint pain.
A systematic review from 2001 found good evidence from two high-quality RCTs that acupuncture improved pain in knee osteoarthritis when compared with sham acupuncture.
Nutraceuticals provide an alternative in older, high risk patients with co – morbidity because they have no associated renal or gastrointestinal side effects and are very popular with patients. The initiation and use of either glucosamine or chondroitin sulphate requires monitoring of glucose in diabetics, as these agents are associated with mild insulin resistance in animals.
Glucosamine is a natural substance derived from animal products. In vitro studies have concluded that glucosamine stimulates proteoglycan synthesis in articular cartilage, theoretically rebuilding damaged cartilage. This hypothesis might explain why glucosamine seems to take several weeks to demonstrate any therapeutic effect. Animal models have shown a mild anti-inflammatory effect. There is no conclusive evidence of any of these findings in humans. Glucosamine sulfate 1500 mg/d is the most common preparation used. Glucosamine is contraindicated in patients with shellfish allergy.
Chondroitin sulfate is a natural substance derived from animal products. Like glucosamine, it is thought to stimulate proteoglycan synthesis in articular cartilage. There is no evidence from human studies to support this theoretical role in cartilage repair. The most common dosage is 1200 mg/d, although doses have varied in trials.
The national institute of clinical excellence (NICE) does not recommend glucosamine or chondroitin products for the management of osteoarthritis.
Intra articular corticosteroid injection is a valuable treatment that often gives quick effective relief of pain that may last just a few weeks to a few months. It is particularly useful to tide a patient over an important event (e.g. family wedding, holiday) and to improve pain during initiation of other interventions such as an exercise programme.
NICE recommends that intra-articular corticosteroid injections should be considered as an adjunct to core treatments for the relief of moderate to severe pain in people with osteoarthritis.
Hyaluronic acid (HA) is a component of human synovial fluid that increases its viscosity. osteoarthritis is associated with a decrease of hyaluronic acid content in the synovial fluid. It has been theorized that intra-articular viscosupplementation with hyaluronic acid can modify disease progression in knee osteoarthritis. There is insufficient evidence to support this theory.
Two systematic reviews have evaluated the efficacy of intra-articular hyaluronic acid in the treatment of knee osteoarthritis. Both reviews concluded that intra-articular hyaluronic acid has a greater effect on pain and function in the short term than placebo. A series of hyaluronic acid injections were usually performed over several weeks. Generally, it took more than 1 month to demonstrate benefit with hyaluronic acid, but the effects lasted 3 to 6 months. Adverse effects were rare. Higher-molecular-weight preparations, such as Hylan G-F 20 (Synvisc), seem to be more effective than lower-molecular weight preparations.
NICE recommends against the use of intra-articular hyaluronic acid injections for the management of osteoarthritis. Similarly AAOS does not recommend using hyaluronic acid for patients with symptomatic osteoarthritis of the knee due to lack of efficacy, rather than potential harm.
Some small studies have shown platelet rich plasma therapy to be helpful in management of knee osteoarthritis. However, there was a paucity of articles on the use of platelet concentrates in the treatment of osteoarthritis. There is also lack of controlled prospective blinded randomized clinical trials with a placebo control and hence there are no evidence-based recommendations in this regard.
There are no evidence-based criteria regarding indications for the referral of a patient with osteoarthritis for surgical treatment. Most consensus statements recommend that patients who continue to have severe pain and functional limitation from osteoarthritis of the knee or hip, despite maximal conservative therapy, should be referred to an orthopedic surgeon for consideration of surgical treatment.
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