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Impaired wound healing in factor XIII deficient patient was reported by Duckert et al, since then aroused great interest in the role of this factor in tissue repair. Many investigators have been described on the property of factor XIII, and recent studies revealed its deficiency interfers fibrin net work deposition which plays an important role in the formation of connective tissue repair. Kim, reported delayed skin wound healing of experimentally induced factor XIII deficiency in the rabbit. On the other hand, Biel reported increased tensile strength of wound in guinea pigs injected with factor XIII than in untreated controls. This experiment was designed to observe the effect of factor XIII on healing process of bone fracture, Experimental animals were divided into four groups: control group, factor XIII deficiency group, factor XIII deficiency with administration of factor XIII group, and factor XIII injected group. Lightmicroscopic and ultrastructural studies were carried out on the, specimen of fracture site. Obtained results were as follows. Fibrin mesh formation, fibroblast proliferation and chondrocyte formation were delayed at the fracture site in experimentally induced factor XIII deficiency rabbits than in controls. With injection of factor XIII in rabbits, fibrin mesh formation, fibroblast proliferation were enhanced and chondrocyte formation appears earlier than controls or factor XIII deficiency group. Consequently accelerated and enhanced callus formation were observed with the injection of factor XIII in rabbits than controls or factor XIII deficiency group. The above results indicated that formation of cross-linked fibrin by activated factor XIII is involved in callus formation.
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