Disease-Modifying Drugs No Help for OA Pain
Disease-modifying antirheumatic drugs (DMARDs)
are not effective treatments for hand or knee osteoarthritis (OA), according to a new meta-analysis. The drugs are commonly used to treat
rheumatoid arthritis (RA)
and other forms of
inflammatory arthritis
, but researchers in the United Kingdom (UK) found they were no better than placebo for OA pain. Their findings appeared in June 2018 in
Rheumatology.
DMARDs aren’t pain medications. They’re meant to slow the disease and prevent further damage to joints and organs by suppressing inflammation. When DMARDs work, pain usually improves as inflammation gets under control.
There are three types of DMARDs. One group includes traditional (also called conventional) drugs like methotrexate ( Rheumatrex, Trexall ) and hydroxychloroquine ( Plaquenil ). These are relatively inexpensive and are often the first medications tried for inflammatory autoimmune diseases such as RA.
The second group includes biologic DMARDS . These target molecules or pathways that trigger or perpetuate inflammation.
The third group is made up of so-called targeted DMARDs (namely, tofacitinib, baricitinib and apremilast), which are too new to have been included in this meta-analysis.
Historically, DMARDs haven’t been used for OA, which was long believed to result from wear and tear on cartilage, not inflammation. But many scientists now agree that OA has an inflammatory component, so researchers have been testing DMARDs for OA in clinical trials. Trial results have been mixed, however, and haven’t settled the question of what role inflammation plays in the disease.
That led researchers at the Arthritis UK Pain Centre at the University of Nottingham to undertake the first meta-analysis on the topic. For it, they analyzed 11 randomized, controlled clinical trials that used conventional or biologic DMARDs to treat OA pain in more than 1,200 patients.
Although there were significant differences in the ways the trials were conducted, the numbers of participants and the quality of the trials, the final outcome showed no difference in pain relief between placebo and either conventional or biologic DMARD.
The authors say this doesn’t necessarily mean that inflammation doesn’t contribute to the development and progression of OA. Inflammation may play a role but isn’t the main driver of the disease. Or DMARDs might not target the right inflammatory pathways.
Another possibility is that the poor quality of some of the trials may have led to biased results. But lead study author Monica Persson, PhD, a researcher, says that’s not the case.
“Five of the 11 trials … may be considered high-quality trials,” she writes, noting that if only those five trials are considered, their conclusions are the same as for all 11.
She also points out that differences among the studies are more likely due to the type of DMARD (conventional vs. biologic), the joint affected and the subtype of OA rather than problems with the trials themselves.
Andrew Laster, MD, a rheumatologist with Arthritis & Osteoporosis Consultants of the Carolinas in Charlotte, North Carolina, isn’t so sure. Although he says the researchers’ conclusions are of interest because of the ongoing debate about the role of inflammation in OA, he cautions not to “put too much weight on this one meta-analysis because of a number of limitations in the analysis that the authors readily acknowledge,” including the varying quality of the studies.
David Pisetsky, MD, a professor of rheumatology and immunology at Duke University in Durham, North Carolina, agrees that it’s natural to want to know if existing therapies like DMARDs are effective for OA. But he points out that the study results are consistent with what doctors have seen with their own patients.
“The question is whether any of the newer [targeted DMARDs] would do better,” he says.
Currently, there are no disease-modifying drugs approved for treating OA. But your own body may be able to help. Many studies have shown that exercise and weight loss not only relieve OA pain, they also have the potential to stop further structural damage to the joint, although it can’t repair or undo it.
One large study found that dropping just 10 percent of body weight can lead to improved mobility and a 50 percent reduction in pain in overweight or obese people with OA. A follow-up study showed that doubling the amount of weight loss cut pain and improved function by another 25 percent – all without drugs or surgery.
Author: Linda Rath
DMARDs aren’t pain medications. They’re meant to slow the disease and prevent further damage to joints and organs by suppressing inflammation. When DMARDs work, pain usually improves as inflammation gets under control.
There are three types of DMARDs. One group includes traditional (also called conventional) drugs like methotrexate ( Rheumatrex, Trexall ) and hydroxychloroquine ( Plaquenil ). These are relatively inexpensive and are often the first medications tried for inflammatory autoimmune diseases such as RA.
The second group includes biologic DMARDS . These target molecules or pathways that trigger or perpetuate inflammation.
The third group is made up of so-called targeted DMARDs (namely, tofacitinib, baricitinib and apremilast), which are too new to have been included in this meta-analysis.
Historically, DMARDs haven’t been used for OA, which was long believed to result from wear and tear on cartilage, not inflammation. But many scientists now agree that OA has an inflammatory component, so researchers have been testing DMARDs for OA in clinical trials. Trial results have been mixed, however, and haven’t settled the question of what role inflammation plays in the disease.
That led researchers at the Arthritis UK Pain Centre at the University of Nottingham to undertake the first meta-analysis on the topic. For it, they analyzed 11 randomized, controlled clinical trials that used conventional or biologic DMARDs to treat OA pain in more than 1,200 patients.
Although there were significant differences in the ways the trials were conducted, the numbers of participants and the quality of the trials, the final outcome showed no difference in pain relief between placebo and either conventional or biologic DMARD.
The authors say this doesn’t necessarily mean that inflammation doesn’t contribute to the development and progression of OA. Inflammation may play a role but isn’t the main driver of the disease. Or DMARDs might not target the right inflammatory pathways.
Another possibility is that the poor quality of some of the trials may have led to biased results. But lead study author Monica Persson, PhD, a researcher, says that’s not the case.
“Five of the 11 trials … may be considered high-quality trials,” she writes, noting that if only those five trials are considered, their conclusions are the same as for all 11.
She also points out that differences among the studies are more likely due to the type of DMARD (conventional vs. biologic), the joint affected and the subtype of OA rather than problems with the trials themselves.
Andrew Laster, MD, a rheumatologist with Arthritis & Osteoporosis Consultants of the Carolinas in Charlotte, North Carolina, isn’t so sure. Although he says the researchers’ conclusions are of interest because of the ongoing debate about the role of inflammation in OA, he cautions not to “put too much weight on this one meta-analysis because of a number of limitations in the analysis that the authors readily acknowledge,” including the varying quality of the studies.
David Pisetsky, MD, a professor of rheumatology and immunology at Duke University in Durham, North Carolina, agrees that it’s natural to want to know if existing therapies like DMARDs are effective for OA. But he points out that the study results are consistent with what doctors have seen with their own patients.
“The question is whether any of the newer [targeted DMARDs] would do better,” he says.
Currently, there are no disease-modifying drugs approved for treating OA. But your own body may be able to help. Many studies have shown that exercise and weight loss not only relieve OA pain, they also have the potential to stop further structural damage to the joint, although it can’t repair or undo it.
One large study found that dropping just 10 percent of body weight can lead to improved mobility and a 50 percent reduction in pain in overweight or obese people with OA. A follow-up study showed that doubling the amount of weight loss cut pain and improved function by another 25 percent – all without drugs or surgery.
Author: Linda Rath
