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Bone Drug Holds Promise as Therapy for People with OA

Researchers supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) have shown that a medication that triggers new bone formation in people with osteoporosis can restore cartilage in a mouse model of injury-induced osteoarthritis of the knee. Their findings were reported in Science Translational Medicine.

Osteoarthritis (OA) is a painful and often debilitating disease that occurs when cartilage, which normally cushions the bones, breaks down. Currently, there are no medications that treat the cartilage loss in OA. The disease has many causes and, while it can occur in any joint, the knee is commonly affected. Knee OA is often the result of an injury that causes damage to the menisci (cartilage that cushions the knee joint) or ligaments (bands of tissue that support the knee).

Teriparatide, a form of human parathyroid hormone approved to treat osteoporosis, works to restore bone strength by targeting bone-building cells. However, based on the discovery that cartilage in arthritic joints — but in not healthy joints — expresses receptors for parathyroid hormone, combined with the hormone’s known effects on cartilage cells called chondrocytes in the growth plate areas of bone, Randy Rosier, M.D., Ph.D., and his colleagues at the University of Rochester Medical Center, wondered whether teriparatide might also target chondrocytes in arthritic joints. Reports that people with OA who were taking teriparatide for their osteoporosis had less arthritis pain further supported this approach.

In the study, Dr. Rosier and his team used an OA mouse model in which injury to the menisci and ligaments of the knee results in a breakdown of cartilage. In a series of experiments, they demonstrated that mice that received teriparatide daily for one month had nearly a third more cartilage than mice that did not receive the drug.

The researchers made additional observations in the treated mice. Normally, in addition to being present in joint cartilage, chondrocytes are also present in bone. The cells in bone act differently than they do in cartilage—maturing more fully and helping to mineralize (harden) bone tissue. But in OA, chondrocytes in the joint behave as they would in bone, maturing excessively and mineralizing the cartilage, resulting in a gradual destruction of the joint. In the study, Dr. Rosier identified a decrease in the proteins linked to excessive chondrocyte maturation in the mice treated with teriparatide. The scientists also found that, in the treated mice, there was an increase in regenerative chondrocyte activity in cartilage, and a reduction in cartilage breakdown.

Given that teriparatide is already clinically available, the researchers believe that these findings make a case for further investigation of the medication in people with OA. If future studies show that teriparatide has a favorable risk-benefit profile in people with OA, it would be the first disease-modifying drug for this debilitating disease that affects millions of Americans.





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