Diagnosis of Osteoarthritis

Osteoarthritis (OA) is typically caught during annual physical exams. During the exam, physicians inspect the joints for swelling, sensitivity, and range of motion. If OA is expected, additional medical tests will be performed.

• X-ray or magnetic resonance imaging (MRI) may be performed to visualize changes in the joints. While an X-ray cannot image cartilage it can reveal narrow spaces between joint bones and bone spurs. MRIs can directly image cartilage. MRI is not typically used for diagnosis of OA, but may be used for more intricate cases.
• Blood tests can be used to rule out other possible forms of arthritis such as rheumatoid arthritis. Joint fluid can also be examined for elevated levels of inflammation and to rule out other causes of pain such as infections.

Treatment of Osteoarthritis

Most treatments for OA aim at relieving symptoms rather than reversing the disease. Painkillers such as acetaminophen are prescribed to reduce the pain. In mild to moderate cases nonsteroidal anti-inflammatory drugs (NSAIDs) are prescribed to treat inflammation and pain. While effective at reducing pain, long-term use is associated with severe side effects such as liver and kidney damage, gastric bleeding and cardiovascular complications. In more severe cases, opioids and narcotics are used to relieve the pain. However, these treatments are not ideal due to the risk of development of dependence, and side effects including constipation, nausea, and fatigue.

Future therapies are aiming to treat the disease rather than the symptoms. One therapy of interest is Calcitonin. Calcitonin is a hormone that hinders osteoclast bone-resorbing activity while enhancing the bone-forming activity of osteoblasts in order to preserve bone density. This hormone is currently being used to treat related diseases such as osteoporosis, osteogenesis imperfecta, and bone metastases.

Another type of therapy in development is antibodies that target specific pro-inflammatory proteins. Because inflammation plays a significant role in the progression of OA, several researchers have looked to treatments that inhibit specific cytokines that support its progression.

Other targets that have been suggested include nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) and its targets. The pro-inflammatory cytokines elevated in OA activate NF- kB. This protein, in turn, regulates several pro-inflammatory mediators and proteins that support OA inflammation. Infliximab and etanercept target pro-inflammatory cytokine TNFα and are approved in the US and Europe to treat rheumatoid arthritis.

Because growth factors and blood vessel formation in the subchondral bone have also been implicated in advanced cases of OA, therapies that target specific growth factors and mechanisms that support vessel formation are in development.