Histology and histopathology Vol.30, nº9 (2015)

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Browsing Histology and histopathology Vol.30, nº9 (2015) by Subject "Histopathology"

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    Functional histopathology of keloid disease
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Jumper, N.; Paus, R.; Bayat, A.
    Keloid disease is a benign, yet locally aggressive and recurrent cutaneous fibroproliferative condition characterised by excessive scarring. Unique to humans, keloids represent the end-point of a spectrum of abnormal wound healing, are aesthetically disfiguring and can cause major functional impairment. Its heterogeneous phenotype can confound clinical diagnosis leading to mismanagement. This review examines the histological morphology of keloid disease relative to the underlying pathobiology, places it in the context of other cutaneous fibroses and highlights gaps within the literature that hinder differential diagnosis. The pathological similarity to hypertrophic scarring, dermatofibrosarcoma protuberans, dermatofibroma and scleroderma emphasise the importance of detailing the architectural and cellular components of this unique entity. In the papillary dermis keloid tumours show a tongue-like advancing edge that resembles invasive tumour growth. A thickened but flattened epidermis, hyalinised haphazardly arranged collagen bundles that dominate the dermis with subsequent obliteration of the papillary-reticular boundary along with displacement and eventually destruction of skin appendages, exemplify additional hallmark findings associated with keloid disease. Compared to healthy skin, keloid scars show an increased type I/III collagen ratio, decreased fibrillin-1 and decorin expression, increased dermal cellularity and increased expression of fibronectin, versican, elastin and tenascin in the reticular dermis and hyaluronan and osteopontin in the epidermis. We illustrate these “pathognomonic” features of keloid disease by representative micrographs and discuss them in the context of inflammation, hypoxia and tension - as key elements of keloid disease. Finally, we highlight deficits within the keloid research literature as well as discuss important areas for future research in keloid histology.
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    Histopathological findings in the peritumoral edema area of human glioma
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Wang, Xingfu; Liu, Xueyong; Chen, Yupeng; Lin, Guoshi; Mei, Wenzhong; Chen, Jianwu; Liu, Ying; Lin, Zhixiong; Zhang, Sheng
    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.