Osteoarthritis

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Osteoarthritis (OA) is the breakdown of the cartilage cushion in one or more joints of the body leading to pain, to limitation in movement, and in many cases to joint replacement. More than twenty million adults in the United States currently have some form of OA, with the number expected to double over the next fifty years. Therapy for OA patients involves mostly pain management, and no drugs are currently available to limit the cartilage and bone destruction.

Some patients have OA in one joint that may have resulted from a prior injury, but many OA patients have a more generalized form of the disease affecting multiple joints. The generalized form of OA is often the most challenging in terms of patient management.

Osteoarthritis is the most common adult joint disease, increasing in frequency and severity in all aging populations. The estimated U.S. prevalence is 20-40 million patients or 5 times that of rheumatoid arthritis. OA involvement of the hand, knee, hip and spine is common, with total knee replacements numbering over 250,000/yr and total hip replacements numbering over 150,000 per year in the U.S. alone. OA may involve a single joint or multiple joints in the same individual, with current therapy focused on pain relief as there is no FDA-approved therapy that arrests or reverses the joint deterioration. The etiology of OA is multifactorial involving both mechanical and biochemical factors. OA progression is associated with accelerated cartilage degradation leading to joint space narrowing, painful joint disruption, and functional compromise. The pattern of expression for OA in many ways mimics that of osteoporosis in that it is more common in women than in men, and it appears to be related to postmenopausal changes with hormone replacement therapy suppressing cartilage degradation. OA disease progression is characterized by a proinflammatory gene expression pattern in cartilage and in joint synovium, with a reactive increase in bone density in the subchondral bone. Substantial data provide support for a central role of interleukin-1 in the pathogenesis of OA including animal susceptibility models and models of IL-1-targeted therapy.

On August 16, 2007, Interleukin Genetics announced that it has initiated a study on the genetics of osteoarthritis in collaboration with Dr. Steven Abramson, Director of the Division of Rheumatology at the Hospital for Joint Diseases of New York University Medical Center.