AT THE TIME of fracture, the trauma which interrupts the continuity of a bone also ruptures the walls of numerous blood vessels in the periosteum, haversian canals and marrow. There results a more or less extensive hemorrhage at the site of fracture which, because of tissue juices from injured cells, clots rapidly. The fibrinous network of this clot is soon invaded by fibroblasts which come from the periosteum, endosteum, vessels, fasciae, stroma of muscle tissue and areolar tissue and the haversian canals. The hematopoietic cells of the marrow quickly disappear and are replaced by undifferentiated connective tissue, this change being much more rapid in the red marrow of young bones than in fatty marrow. Young blood vessels invade the clot as granulation tissue, these vascular buds consisting of capillaries surrounded by a thin layer of accompanying fibroblasts.1 In the gap intervening between the bone ends the vessels are at
GEORGE EM. PHOSPHATASE ACTIVITY IN BLOOD SERUM, BONE AND SOFT TISSUES FOLLOWING FRACTURE IN THE CAT. Arch Surg. 1948;57(1):113–136. doi:10.1001/archsurg.1948.01240020116010
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