Humans have dealt with the pain, stiffness and swelling of osteoarthritis, or OA, for ages. Yet researchers still study the disease vigorously with the goals of finding more about what causes OA, what steps may help people prevent OA and what new treatments may alleviate its symptoms and halt joint damage. In recent months, news on OA treatment developments and insight into the disease’s possible causes, and what may prevent it, have emerged.

Most important, researchers now have a deeper understanding of OA, a concept called patho-mechanics, and this knowledge affects OA treatment development. At the American College of Rheumatology’s (ACR) State-of-the-Art Symposium held in April 2010 in Chicago, lecturers noted OA must be viewed as a combination of how your body’s mechanics work, how your genes may have set you up to develop OA, and outside factors that can affect your bone, cartilage and various tissues and lead to the disease.

The November 2010 Annual Meeting of the American College of Rheumatology (ACR) in Atlanta featured reports from a number of researchers who are digging deeper in OA’s mysteries and its possible treatment.

 Revealing Research About the Causes of Osteoarthritis

• Speakers at the ACR Basic Science Symposium session on new OA findings suggested that OA should be viewed as an inflammatory disease, almost like rheumatoid arthritis, not just a “wear-and-tear” disease of structural breakdown from overuse. Inflammation-causing chemicals and their effects on joints must be the focus of research, they said.

• One study suggested a link between the Unfolded Protein Response (UPR), typically the basic way cells resolve stress due to aging, and OA development. The study found UPR is impaired in older adults, and that impairment provides a foundation for the development of osteoarthritis affecting the connective tissues.

• Other studies focused on OA’s potential genetic triggers. One finding springing from the Johnston County Osteoarthritis Project, a University of North Carolina study focusing on a group of around 5,000 adults age 45 or older, revealed that six genes in particular showed significant signs of rendering a person susceptible to developing knee OA: ABCG2, GDF5, IL1RN, IL6 and VDR.

• Some types of hand OA – particularly erosive interphalangeal disease affecting the fingers – may predict faster progression of OA in the knees, another study suggested.

• Researchers showed that a gene called FAAH, previously linked to increased pain sensitivity, was shown to be higher in people with knee OA than in other patients in the control group.

• A protein in the body called Complement C5 might also play a key role in OA, one study suggested.

New Details on Osteoarthritis Treatments

• Vitamin D is touted as having many almost miraculous benefits for treating and preventing disease, including OA pain and structural damage. Yet a two-year clinical trial funded by the National Institutes of Health (NIH) found no benefit of Vitamin D therapy in reducing pain or modifying structure in knee OA.

• One ACR study looked at possible therapeutic angles to activating particular gene pathways – LKB1-AMPK and CaMKKb-AMPK – to reduce the progression of osteoarthritis.

• Another study showed that OA patients taking a combination of naproxen sodium and esomeprazole magnesium (Vimovo) had similar efficacy and tolerability to those taking celecoxib (Celebrex), a COX-2 specific inhibitor, and had more heartburn-free days than those taking celecoxib.

New Osteoarthritis Medicines on the Horizon?

One new treatment in development for OA pain, tanezumab, showed great promise in Phase II and III clinical trials for inhibiting nerve growth factor, a chemical which may be linked to OA pain in injured or inflamed tissues. Yet one key trial was halted last summer when patients’ OA damage worsened although their pain was lessened by the drug. Some trial participants had to get hip replacement surgery.

Stem-cell therapy, a dynamic field of study for cancer and other serious diseases, may also hold promise for OA, one researcher revealed at November’s ACR meeting. Rocky S. Tuan, PhD, director of the Center for Cellular and Molecular Engineering at the University of Pittsburgh, suggested stem cells might be used to rebuild damaged tissues in people with OA, helping them boost their affected joints’ function.

New Scrutiny for Longtime Treatment

On Jan. 13, 2011, the Food and Drug Administration announced new restrictions on the drug acetaminophen (Tylenol), widely used for treating the OA pain. Acetaminophen often is sold in products that combine it with other drugs, such as the narcotic analgesics hydrocodone (Vicodin) and oxycodone (Percocet). The FDA’s announcement on the matter noted that the agency had received reports of cases of severe liver injury associated with acetaminophen use.

Due to acetaminophen’s possible risk of liver damage when taken in higher doses, the FDA announced that prescription products containing acetaminophen, including in combination with other drugs such as narcotic pain relievers, must have no more than 325 milligrams of acetaminophen per tablet or capsule. Such products must also carry a boxed warning of the risk of severe liver injury associated with taking too much acetaminophen.