Hormone could be key to keeping osteoarthritis at bay

WASHINGTON - An osteoporosis drug that prevents cartilage loss in a joint injury may also regenerate some cartilage that has been lost to degenerative osteoarthritis, according to a new study.

While the study was based on mice, the model closely mimics human osteoarthritis that develops following knee injuries, according to the study authors.

Parathyroid hormone (PTH), known as teriparatide in drug form, has emerged as a major player in the maintenance and healing of bone, and the race is on to design new applications for it.

“Right now physicians have no way to bring back cartilage in patients who have lost it to osteoarthritis,” said Randy Rosier, orthopaedics professor at the University of Rochester Medical Centre (URMC).

“Our current results, at least in mice, show that we can inhibit cartilage degeneration and improve the volume of cartilage in diseased joints.”

It’s remarkable enough that this compound delays the loss of cartilage, but these results show it also may be able to restore, at least to some extent, cartilage in already degraded joint surfaces,” Rosier concluded.

Cartilage can become damaged by many kinds of injury and by mechanical stresses that come with age. Over time, damaged cartilage deteriorates to cause osteoarthritis (OA), with its attendant joint inflammation and pain.

Currently available drugs like steroids or non-steroidal anti-inflammatory agents (e.g. Advil, Aleve) reduce pain but do not address the loss of cartilage behind the osteoarthritis, which is projected to afflict more than 50 million in US alone by 2020.

Cartilage forms the sponge-like, shock-absorbing layers that keep the impact of running and jumping and lifting from grinding bones against each other in joints.

The cell type at the heart of osteoarthritis is the chondrocyte, the cartilage-producing cell responsible for maintaining the integrity of joint cartilage.

Study authors observed that chondrocytes within injured and degenerating cartilage have more PTH type 1 receptors on their surfaces, said an URMC release.

This makes them especially sensitive to the PTH signal that prevents harmful chondrocyte maturation into bone in the joint cartilage. Thus, PTH therapy should increase the cartilage supply exactly where cartilage loss is causing disease.

The study was presented at the annual meeting of the American Society for Bone and Mineral Research in Denver.