Ultrastructural characterization of craniopharyngioma at the tumor boundary: A structural comparison with an experimental toxic model using “oil machinery” fluid, with emphasis on Rosenthal fibers

• Published in: Acta histochemica 2015-10, Vol.117 (8), p.696-704
• Main Authors: Tena-Suck, Martha Lilia, Morales-del Ángel, Andrea Y., Hernández-Campos, María Elena, Fernández-Valverde, Francisca, Ortíz-Plata, Alma, Hernández, Alma Delia, Santamaría, Abel
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Aged; Animals; Craniopharyngioma; Craniopharyngioma - pathology; Cyst Fluid - physiology; Experimental model; Female; Humans; Male; Middle Aged; Pituitary Neoplasms - pathology; Rats, Wistar; Rosenthal fibers; Tumor invasiveness; “Oil machinery” fluid
• ISSN: 0065-1281; 1618-0372
• DOI: 10.1016/j.acthis.2015.09.006

•Ultrastructure of craniopharyngiomas (CPs) was investigated.•Rosenthal fibers were morphologically characterized.•A toxic model was produced in rats by cortical infusion of oil machinery fluid (OMF).•Enhanced expression of GFAP and vimentin in RFs was found.•The invasive component of CPs is not present in the OMF. Craniopharyngiomas (CPs) are cystic, encapsulated, slow-growing epithelial tumors. CPs can be aggressive forms invading and resorting surrounding structures of adjacent brain tissue, where Rosenthal fibers (RFs) are expressed. The aim of this study was to investigate the ultrastructure of these fibers in human biopsies and compare it with an experimental toxic model produced by the cortical infusion of the oil cyst fluid (“Oil machinery” fluid or OMF) from CPs to rats. For this purpose, the CPs from ten patients were examined by light and electron microscopy. OMF was administered to rats intracortically. Immunohistochemical detection of glial fibrillary acidic protein (GFAP) and vimentin was assessed. In both freshly obtained CPs and rat brain tissue, the presence of abundant cellular debris, lipid-laden macrophages, reactive gliosis, inflammation and extracellular matrix destruction were seen. Ultrastructural results suggest focal pathological disturbances and an altered microenvironment surrounding the tumor–brain junction, with an enhanced presence of RFs in human tumors. In contrast, in the rat brain different degrees of cellular disorganization with aberrant filament–filament interactions and protein aggregation were seen, although RFs were absent. Our immunohistochemical findings in CPs also revealed an enhanced expression of GFAP and vimentin in RFs at the peripheral, but not at the central (body) level. Through these findings we hypothesize that the continuous OMF release at the CPs boundary may cause tissue alterations, including damaging of the extracellular matrix, and possibly contributing to RFs formation, a condition that was not possible to reproduce in the experimental model. The presence of RFs at the CPs boundary might be considered as a major criterion for the degree of CPs invasiveness to normal tissue. The lack of RFs reactivity in the experimental model reveals that the invasive component of CPs is not present in the OMF, although the fluid per se can exert tissue damage.