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.