Histopathological findings in the peritumoral edema area of human glioma

Abstract

Peritumoral brain edema (PTBE) is considered to be one of the main biological behaviors of brain glioma. However, the histopathological features of PTBE remain imprecisely defined. We analyzed the histopathological characteristics in the PTBE area of 22 cases of glioma. Microscopically, the pre-existing basic structure in the edema area was still preserved but there were varying degrees of loose tissue. The main components of the edema tissue were scattered invasive tumor cells, reactive cells, and various blood vessel patterns. Invasive tumor cell density was significantly higher in high-grade glioma than in low-grade glioma, and the density was significantly higher in the area near compared to the area far from the glioma. The Ki-67 proliferative index of the invasive tumor cells was higher in high-grade glioma than in low-grade glioma, but the index was not different in the area near compared to the area far from the glioma. The microvessel pattern in PTBE was primarily branching capillary. The microvessel densities (MVDs) of CD34+ and CD105+ were higher in high-grade glioma and the area near the glioma than in low-grade glioma and the area far from the glioma. Compared to CD34+, the MVD of CD105+ exhibited a more significant downward trend in terms of distance from the glioma. The most obvious types of reactive cells were reactive astrocytes and activated microglia. The reactive astrocytes were positive for nestin. The activated microglia emerged in the area near the glioma in most cases and in the area far from the glioma in more than half of the cases. In addition, several cases displayed focal collections of small lymphocytes around small blood vessels and tumor cells arranged around a neuronal cell, and a limited number of cases displayed giant dysmorphic neurons in an edematous cortex. Our data indicate that PTBE is a consequence of tissue reconstruction resulting from tumor cell invasion and is an appropriate niche for the growth and spread of glioma cells.