FRACTURE-HEALING AND MAST-CELLS

We analyzed the morphology and localization of mast cells during the c ourse of fracture repair in control rats and in animals with delayed h ealing of fractures induced by nonsteroidal antiinflammatory drugs (NS AIDs). In the first 2 weeks of fracture healing in control animals, ma st cells were found either in the vicinity of blood vessels or in the vascularized tissue proliferating into the cartilaginous portion of su bperiosteal callus. In the later stages (6-8 weeks), mast cells were s een in loose connective tissue in bone marrow surrounded with transluc ent ground substance. At this stage of healing, a hyperplasia of mast cells and cell degranulation was often seen in close proximity to oste oclasts and areas of bone resorption. Treatment with NSAIDs delayed fr acture healing and the appearance of mast cell hyperplasia in bone mar row for similar to 4 weeks, suggesting that mast cells have specifical ly defined temporal and regional distribution during the process of bo ne repair. Histochemical studies documented a significant amount of ch ymase in the mast cells in callus. This enzyme was purified from mast cells by chromatography and was able to digest in vitro proteins extra cted from bone. Our data suggest that mast cells in fracture healing a re 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 t he later stages of fracture healing.