Conference Coverage

‘Bright future’ for growth factor therapy in osteoarthritis



With many active phase 3 trials of promising agents, the “future looks bright for growth factors and disease modification” in osteoarthritis (OA), according to David Hunter, MBBS, PhD.

Dr. Hunter, who is the Florance and Cope Chair of Rheumatology and professor of medicine at the University of Sydney and the Royal North Shore Hospital, Sydney, Australia, outlined some of the recent research with these agents in OA.

Dr. David Hunter of the University of Sydney and Royal North Shore Hospital, Australia Sara Freeman/MDedge News

Dr. David Hunter

There has been declining mortality from all causes over the years, thanks to improvements in cardiovascular and other fields of medicine, with subsequent increasing life expectancy, Dr. Hunter pointed out. This is important if you consider that OA remains one of the most prevailing forms of joint disease, and data suggest people are developing OA at younger ages than in the past.

In 2013, a U.S. study (Arthritis Care Res. 2013;65[5]:703-11) showed that the 2007-2008 incidence of symptomatic knee OA was highest between the ages of 54 and 64 years, with the estimated median age at diagnosis of 55.8 years. Patients were substantially younger than were those who had been diagnosed at a median age of 68.5 years more than a decade earlier in 1991-1992.

“So, we’re developing [OA] at a much earlier age, but we’re obviously living longer and living with that morbidity for a substantial period of time,” Dr. Hunter said at the World Congress on Osteoarthritis, sponsored by the Osteoarthritis Research Society International.

“It’s within that context that we really need to think about both the individual and societal burden of osteoarthritis, and why we’re developing agents such as growth factors to help retard symptoms related to disease,” continued Dr. Hunter, chair of the Institute of Bone and Joint Research, deputy dean of the Northern Clinical School, and consultant rheumatologist at North Sydney Orthopaedic and Sports Medicine Centre, Sydney.

OA is characterized by articular cartilage damage, low-grade synovial inflammation, and hypertrophic bone changes that lead to pain and functional deterioration (Expert Opin Emerg Drugs. 2015;20[3]:361-78). Attempts to modify the disease process have thus focused on these three areas, aiming to regulate cartilage catabolism and anabolism, control inflammation, and remodel subchondral bone (Rheumatology [Oxford]. 2018;57[suppl. 4]:iv108-iv123).


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