“For every copy of the risk allele carried, individuals are 17 percent more likely to develop OA compared to those who do not carry the risk allele,” lead author Eleftheria Zeggini PhD, of the Wellcome Trust Sanger Institute in the UK, says.

Before any genetic test could be developed to detect individual risk, researchers need to figure out how MCF2L works to increase OA risk. In their next series of studies, Zeggini and her team will conduct these functional studies as well as continue to investigate the genetic causes of OA and related traits.

“This particular study was very elegantly performed to a very high standard, which gave them the ability to find links on a finer level that would have been in prior days not able to be seen,” says Dr. Jordan.

The fact that some participants in the study’s control group may have had very early OA reinforces the importance of the result, Dr. Jordan adds, because if so, it should be harder for researchers to find a genetic signal for OA and the signal was indeed present. One limitation of the study is the fact that the subjects all came from European populations; the results may or may not hold for people elsewhere.

The MCF2L gene is the third in which researchers have found an allele that raises the risk of arthritis.

Because MCF2L directs nerve growth factor, it may be related to pain and OA, says Dr. Jordan. A clinical trial that tested a drug that targeted nerve growth factor helped with pain, but some people quickly progressed to OA and the trial was stopped early.

 “If there’s a certain genotype that we can bring to the clinic one day that would identify these individuals, then we can help with prevention and early intervention, once we have that information,” says Dr. Jordan. “The day will come.”