This article is more than 5 years old. Information may no longer be current.
Superhealing mice may offer clues to preventing post-traumatic arthritis
Click Here to Manage Email Alerts
New research indicates that a specific strain of laboratory mice found to be resistant to inflammation after knee fracture may also avoid developing arthritis at the injury site.
“After a patient’s traumatic injury, orthopedic surgeons realign the joint surface as anatomically as possible and then hope for the best,” Steven A. Olson, MD, FACS, principal investigator of the post-traumatic arthritis project and chief of the orthopedic trauma section at Duke University, said in a press release.
“They haven’t been thinking about why patients with injuries are subsequently getting arthritis. Our research examines how we could possibly prevent arthritis development with growth factors and anti-inflammatory therapies after a fracture, either before or at the time of the surgery to fix it.”
Olson and colleagues presented their findings at the Orthopaedic Research Society meeting in Las Vegas.
Previous research on the MRL/MpJ strain of mouse known as “superhealers” has shown that the mice can regenerate tissue over holes made in their ears for laboratory purposes. Additional work comparing healthy to healed knees after fracture in the mice revealed no significant differences between the joints.
“The superhealer can almost regenerate tissue,” Bridgette Furman, a research analyst and lead scientist in the study, said in a press release. “We thought, ‘If they can regenerate cartilage in the ear, what about cartilage in the knee?’ This happened in our pilot study, and we now have taken these results further and learned what happens in terms of inflammation. If you can figure out why the animal is a superhealer and apply that to people, then you may help prevent the development of arthritis,” she said in the release.
In their latest experiment, the investigators examined the inflammatory response of superhealer mice compared to control mice (C57BL/6) after fracture. They discovered that the control mice exhibited more than a 700-fold increase in Interleukin 1-beta (IL-1ß) within the first 4 hours after fracture. The group also showed a 37-fold increase in IL-1ß 7 days postfracture.
In comparison, the superhealer mice showed a 70-fold increase in the cytokine at day 0 and a 3.5-fold increase by day 7.
The control mice showed a 13-fold increase in tumor necrosis factor-alpha (TNF-alpha) just after fracture and a 5-fold increase at 7 days, but the investigators found no change in TNF-alpha in the superhealer mice over time, according to the release.
Farshid Guilak, PhD, a study scientist and director of the Orthopaedic Bioengineering Laboratory in the Duke University Department of Surgery, said future studies will use rheumatoid arthritis medications after fracture to inhibit the inflammatory cytokines in normal mice.
“If a reduced inflammatory response is what helps the superhealers, we would like to know whether controlling inflammation in fracture patients can prevent arthritis,” he said in the press release.