Objective: To determine whether the periosteal response to skeletal trauma
is impaired when muscle is also injured, thereby providing a possible expla
nation for why fractures with extensive soft-tissue damage may take longer
to heal,
Methods: A bone defect was made in the tibia of male Fisher rats, and the p
roliferative response, osteoblast concentration, and callus formation that
occurred within 7 days were measured in the presence and absence of simulta
neously administered model soft-tissue injury (removal of 10% of the anteri
or tibialis muscle from a region within 2 to 3 mm of the bone defect), Meas
urements were made by using autoradiography, quantitative histology, and mo
rphometry.
Results: Addition of the muscle injury increased proliferation in the cambi
um and in the fibrous periosteum on day 1, but had no effect thereafter; pr
oliferation of fibroblasts in the loose connective tissue above the periost
eum was not affected. Addition of the muscle injury resulted in increased o
steoblast levels 2 to 5 days after injury but had no effect on the amount o
f callus produced.
Conclusion: The inflammatory milieu created by the muscle injury unexpected
ly resulted in an increased periosteal response to skeletal trauma, suggest
ing that inflammatory mediators generated in response to wounding of soft t
issues are unlikely to account for delayed fracture healing. These findings
may indicate that surgical trauma associated with internal fixation by usi
ng plates and screws may not be as deleterious to the fracture-healing resp
onse as previously thought.