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Accelerated fracture healing reported in mice lacking functioning T and B cells
Researcher cites an unrelated genetic aberration as one factor possibly affecting the repair.
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SAN DIEGO — Mice with a specific immunodeficiency may experience more rapid healing of closed tibial fractures than normal mice without such a deficiency, according to a new study presented here.
Researchers from the University of Edinburgh, Scotland, discovered that severe combined immunodeficient (SCID) mice without mature T and B lymphocyte cells had significantly more callus at 1 and 2 weeks postfracture compared to normal mice.
"Histological analysis of the callus in the SCID [animals] showed that the cartilage progressed through the stages of fracture repair at a faster rate," said Mark S. Gaston, MRCSEd, during the Orthopaedic Research Society annual meeting.
The immunodeficient mice also showed significantly more regenerated bone at 2 and 3 weeks postinjury and had a significantly higher stress yield and Young's modulus at 3 weeks compared to controls.
To examine the effect of a specific immune system on fracture repair, the researchers created closed tibia fractures in SCID as well as normal mice, and treated both groups with casting. The investigators noted greater callus formation in the SCID mice at 7 and 14 days postinjury, but recorded no significant differences between groups at 21 days follow-up.
They also reported that immunodeficient mice had significantly more bone mineral content than normal mice at up to 21 days postfracture (P<.01).
"We demonstrated that a lack of a specific immune system accelerates the fracture repair process in an animal model," Gaston said, noting several potential factors could have influenced the finding, including indirect effects on the immune system that may have accelerated the repair process.
"Of course, it's important to remember that an unrelated genetic aberration in the SCID animal, which has been described, may be actually affecting fracture repair," Gaston said.
For more information:
- Gaston MS, Noble BS, Simpson AHRW. Enhanced fracture repair in-vivo in the absence of the specific immune system. #357. Presented at the Orthopaedic Research Society 53rd Annual Meeting. Feb. 11-14. 2007. San Diego.