Absence of beta3 integrin accelerates early skeletal repair

Abstract

Integrins are heterodimeric transmembrane proteins that mediate cell-matrix interactions and modulate cell behavior. Beta3 subunit is a component of αIIβ3 and αVβ3 integrins. In this study, we first determined that β3 transcripts are expressed by cells within fracture calluses at 7 and 10 days after injury in a mouse model. We then analyzed fracture healing in mice deficient of β3 integrin with molecular, histomorphometric, and biomechanical techniques. We found that lack of β3 integrin results in an extended bleeding time and leads to more bone formation and accelerated cartilage maturation at 7 days after injury. However, β3 deficiency does not appear to affect later fracture healing. At days 14 and 21, histological appearance or biomechanical properties of fracture calluses are similar between wild type and mutant mice.Wealso found that altered fracture healing in β3-null mice is not associated with accelerated angiogenesis, because no significant difference of length density and surface density of blood vessels in fracture limbs was detected at 3 days after injury between wild type and β3-null mice. In conclusion, our findings demonstrate that β3 integrin plays an important role during early fracture healing. Further research is required to determine the underlying mechanisms. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc.