Background and purpose
A recently developed animal model of posttraumatic contractures reflects the chronic stages of the human condition. To understand the initiation of the process, we evaluated the cellular, matrix, and growth factor changes in the joint capsule in the early stages of the animal model, which would not be possible in humans.
18 skeletally mature rabbits had intraarticular cortical windows removed from the medial and lateral femoral condyles, and the knee joint was immobilized. The contralateral unoperated limb served as a control. Equal numbers of rabbits were killed 2, 4, and 6 weeks after surgery. Myofibroblast, mRNA, and protein determinations were done with immunohistochemistry, RT-PCR, and western blot, respectively.
Myofibroblast numbers were statistically significantly elevated in the joint capsules of the experimental knees as compared to control knees. The mRNA and protein levels for collagen types I and III, matrix metalloproteinases 1 and 13, and transforming growth factor β1 were statistically significantly greater, and for tissue inhibitor of matrix metalloproteinases 1 significantly less, in the experimental capsules than in the control capsules.
The experimental joint capsule changes in the acute stages of posttraumatic contractures are similar to those in the chronic stages of the process in this model. Thus, it appears that the mechanisms that attenuate the acute stages of the response to injury are circumvented, contributing to a prolonged modulation of myofibroblast numbers, matrix molecules and growth factors, and leading to joint contractures. Thus, in clinical practice, new approaches to prevention of posttraumatic contractures should be implemented as soon as possible.