Early Histologic and Ultrastructural Changes in Microvessels of Periosteal Callus

医学 超微结构 病理 老茧 解剖 遗传学 生物
作者
Carl T. Brighton,Robert M. Hunt
出处
期刊:Journal of Orthopaedic Trauma [Lippincott Williams & Wilkins]
卷期号:11 (4): 244-253 被引量:109
标识
DOI:10.1097/00005131-199705000-00002
摘要

Objective: To document early histological and ultrastructural changes in periosteal fracture callus blood vessels. Design: Rabbit control and fractured ribs, after healing for three, six, and twelve hours and daily for seven days, were evaluated by light and electron microscopy. Results: Control periosteal microvessels were formed mainly by endothelial cells and occasionally by pericytes. Only these cells displayed basal lamina within the periosteum. Three to twelve hours postfracture, periosteal microvessels were little changed. By two days postfracture, dramatic increases in size and population of microvessel cells resulted in a smaller lumen and thicker wall. Microvessel cells, while retaining their basal lamina, had transformed to mesenchymal cells. Transformed pericytes, as evidenced by their basal lamina, had extravasated. Three to four days postfracture, additional transformed pericytes had extravasated. Within the distal periosteal callus, a close spatial relationship among transformed microvessels, extravascular mesenchymal cells (some with basal lamina), and osteoblasts was present. Four to five days postfracture, within the proximal periosteal callus, a close spatial relationship among transformed microvessels (rapidly disappearing because of continued extravasation), extravascular mesenchymal cells (some with basal lamina), and chondroblasts (some with basal lamina) was present. Conclusions: New evidence showed that after fracture, periosteal microvessel endothelial cells and pericytes increased in population and transformed to mesenchymal cells. These changes, their subsequent extravasation as mesenchymal cells, and their development into chondroblasts were verified by basal lamina evidence. New evidence also suggested that continued extravasation of transformed microvessel cells rendered the fracture callus cartilage avascular.

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