Objective/Hypothesis: To determine if angiogenic growth factors including vascular endothelial growth factor (VEGF) and platelet‐derived endothelial cell growth factor (PD‐ECGF) are expressed in human paragangliomas. Study Design: A histopathologic and molecular examination of paraganglioma specimens obtained from surgical cases or retrieved from the Pathology Department of the Massachusetts Eye and Ear Infirmary. Methods: Fresh tumor or archival, paraffin‐embedded paraganglioma specimens were analyzed by immunohistochemistry, Western blotting, and ELISA. Results: Positive immunohistochemical staining for VEGF was observed in five of nine surgical specimens and in six of eight archival specimens (11/17, or 65%). PD‐ECGF immunoreactivity was detected in four of five surgical specimens and six of eight archival specimens (10/13, or 77%). The presence of PD‐ECGF was confirmed by Western blot assay and ELISA confirmed the presence of VEGF in tumor extract. Conclusions: Both VEGF and PD‐ECGF are expressed in paragangliomas and may contribute to the extreme vascularity of these tumors.
Jaffe 1 coined the term "giant cell reparative granuloma" (GCRG) in 1953 to describe lesions of the maxilla and mandible. Subsequently, numerous other sites have been reported including the orbit, cranial vault, sphenoid, ethmoid, facial bones, the small bones of the hands and feet, and the long bones of the axial skeleton. [2][3][4][5][6] The first account of GCRG in the temporal bone was recorded by Hirschl and Katz 7,8 in 1974. Since then, because of the rare nature of this tumor in the temporal bone, only a handful of cases have been described. 3,5,6,9,10 Although regarded as a benign process, GCRG may be locally aggressive, and surgical excision is recommended whenever possible. Recurrence rates are thought to be low, ranging between 10% and 15% in most studies. 5,7,[11][12][13] However, some smaller series have reported recurrence rates as high as 69% to 75%. 13,14 We report a case of recurrent GCRG of the temporal bone that involved the glenoid fossa, necessitating reconstruction.
Significant challenges remain in generating tissue-engineered cartilage in immunocompetent animals. Scaffold materials such as polyglycolic acid lead to significant inflammatory reactions, inhibiting homogeneous matrix synthesis. This study examined the generation of tissue-engineered cartilage, using a polyglycolic acid-polylactic acid copolymer (Ethisorb; Ethicon, Norderstedt, Germany) in an autologous immunocompetent pig model. The goals of this study were to determine the role of interleukin 1alpha (IL-1alpha) in this system and to assess the effect of serum treatment on tissue generation. Porcine auricular chondrocytes were seeded onto Ethisorb disks cultured for 1 week in medium supplemented with either fetal bovine serum or serum-free insulin-transferrin-selenium supplement. Specimens were implanted autogenously in pigs with unseeded scaffolds as controls. After 1, 4, or 8 weeks, six specimens from each group were explanted and analyzed histologically (hematoxylin and eosin, safranin O, trichrome, and Verhoeff's staining) and biochemically (glycosaminoglycan content). The presence and distribution of IL-1alpha were assessed by immunohistochemistry. Histology revealed acute inflammation surrounding degrading scaffold. Cartilage formation was observed as early as 1 week after implantation and continued to increase with time; however, homogeneous matrix synthesis was not present in any of the specimens. Strong IL-1alpha expression was detected in chondrocytes at the implant periphery and in cells in the vicinity of degrading polymer. Histologically there was no significant difference between the experimental groups with respect to the amount of matrix synthesis or inflammatory infiltration. The glycosaminoglycan content was significantly higher in the serum-free group. These results suggest that inflammatory reactions against scaffold materials and serum components lead to the production of cytokines such as IL-1alpha that may inhibit cartilage tissue formation in autologous transplant models.
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