Early temporary porosis of bone induced by internal fixation implants. A reaction to necrosis, not to stress protection?

Abstract

Stabilization of the fracture using implants requires contact surfaces between implant and bone. Such contact has been observed to induce bone porosis first seen at one month after surgery. Bone loss in the vicinity of implants has hitherto been explained as being induced by mechanical unloading of the bone (stress protection). Experiments in sheep, dogs, and rabbits combining intravital staining of blood circulation and polychrome fluorescent labeling of bone remodeling leads to the conclusion that early bone porosis in the vicinity of the implants is the result of internal remodeling of cortical bone and is induced by necrosis rather than by unloading. This theory is favored by the evidence that (1) the bone porosis is of a temporary nature, an intermediate stage in internal bone remodeling; (2) the pattern of the remodeling zone is closely related to that of the disturbed circulation, and not to that of unloading; (3) plastic plates may produce more porosis than steel plates; and (4) improved blood circulation using modified plates resulted in reduced porosis. The clinical relevance of these findings is related first to the temporary weakening of the bone, and second to the possibility of sequestration. Sequestration may be the result of intensified remodeling activity in the presence of inflammation or infection.