Critical-size bone defects are defined as bone defects where spontaneous regeneration is not expected without treatment1. The characteristics of bone defects (etiology, location, size, presence of infection, and soft-tissue conditions) vary greatly and, to be effective, the treatment method should address this variability. The induced-membrane technique, or Masquelet technique, is a method for treating critical-size bone defects2,3 of various sizes and anatomic locations. It has been used to treat infected and noninfected bone defects and may be performed with a variety of fixation methods2,3.

The induced-membrane technique is a 2-stage procedure. The first stage consists of debridement followed by insertion of a polymethylmethacrylate (PMMA) spacer in the bone defect. The presence of the PMMA leads to a foreign-body reaction with the development of a thick pseudosynovial membrane that is extremely vascularized and rich in growth factors. The filling of the bone defect with the cement spacer prevents fibrous tissue invasion and allows the development of an optimal vascularized gap for bone-grafting. After 6 to 8 weeks, the membrane around the spacer is carefully opened for the removal of the spacer, which is then replaced by bone graft2,3, which can be expanded with allograft or biomaterials.

Alternatives include vascularized or nonvascularized autologous bone graft, allograft, bone transport methods, titanium cages, megaprostheses, shortening, and amputation.

Posttraumatic bone defects frequently are associated with soft-tissue injury and infection that impair the local vascularization and the healing potential. The highly vascularized induced membrane may play a role in restoring the local regenerative capacity. Numerous studies have demonstrated its successful use in the treatment of posttraumatic bone defects in the hand, forearm, humerus, femur, tibia, and foot. The induced-membrane technique is especially advantageous in the treatment of infected bone defects because the presence of the spacer helps in the treatment of the infection by reducing dead space, acting as a local antibiotic carrier, and promoting some degree of bone stability3-5.

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