Fracture healing and mast cells.

Abstract

We analyzed the morphology and localization of mast cells during the course of fracture repair in control rats and in animals with delayed healing of fractures induced by nonsteroidal antiinflammatory drugs (NSAIDs). In the first 2 weeks of fracture healing in control animals, mast cells were found either in the vicinity of blood vessels or in the vascularized tissue proliferating into the cartilaginous portion of subperiosteal callus. In the later stages (6-8 weeks), mast cells were seen in loose connective tissue in bone marrow surrounded with translucent ground substance. At this stage of healing, a hyperplasia of mast cells and cell degranulation was often seen in close proximity to osteoclasts and areas of bone resorption. Treatment with NSAIDs delayed fracture healing and the appearance of mast cell hyperplasia in bone marrow for approximately 4 weeks, suggesting that mast cells have specifically defined temporal and regional distribution during the process of bone repair. Histochemical studies documented a significant amount of chymase in the mast cells in callus. This enzyme was purified from mast cells by chromatography and was able to digest in vitro proteins extracted from bone. Our data suggest that mast cells in fracture healing are involved in digestion of extracellular matrix in callus tissue that could facilitate (a) angiogenesis in the early stages of healing, and (b) the replacement of provisional tissue with newly formed bone in the later stages of fracture healing.