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Morphologische Untersuchungen zur formalen Pathogenese der Sialadenose menschlicher Speicheldrüsen
Morphologische Untersuchungen zur formalen Pathogenese der Sialadenose menschlicher Speicheldrüsen
Besides of dental erosions, sialadenosis manifesting as bilateral swelling of parotid glands, is a typical manifestation of bulimia. Objective: The mechanism of acinar enlargement in sialadenosis is obscure, although peripheral polyneuropathy secondary to systemic disorders is assumed to be significant. This study aimed to find new aspects of pathogenesis of sialadenosis. Methods: Based on a fortuitous observation of diminished alpha-actin-positive myofilaments in myoepithelial cells in sialadenosis, 11 cases each of control and sialadenosis parotid glands were morphometrically analysed assisted by immunohistochemistry for alpha-actin, p63, cytokeratin 14 and Ki67 including double staining. Results: In sialadenosis: the acini were significantly (p<0,001) larger (1991,5 mm2 versus 1017.5 µm²); the number of myoepithelial cells as % per acinus was moderately (p= 0,005) reduced (77.2% versus 93.8%); the amount of alpha-actin-positive myofilaments as % per total circumference was significantly (p<0,001) reduced (7.2% versus 47.2%); and the proliferation rate of acinar cells was moderately (p=0,02) reduced (0.8% versus 2.0%). Conclusion: Taking into account previous ultrastructural observations of degenerative changes in peripheral nerves and in myoepithelial cells of sialadenosis our observations indicate new aspects of the pathogenesis: The loss of myofilaments of myoepithelial cells is compatible with myoepithelial insufficiency that is secondary to peripheral polyneuropathy. Possibly the resulting loss of support for the acini allows acinar secretory cells to expand. Secretory granules accumulate and produce the massive enlargement of acinar secretory cells characteristic of sialadenosis. These results might lead the ancient understanding of the pathogenesis of sialadenosis towards a new comprehension of the development of this prevalent painful disease causing „hamster cheeks“. They also promise to support the therapeutic management of complications of bulimia.
Sialadenose, Myoepithelzellen, Bulimie, Immunhistologie
Rath, Christian
2007
Deutsch
Universitätsbibliothek der Ludwig-Maximilians-Universität München
Rath, Christian (2007): Morphologische Untersuchungen zur formalen Pathogenese der Sialadenose menschlicher Speicheldrüsen. Dissertation, LMU München: Medizinische Fakultät
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Abstract

Besides of dental erosions, sialadenosis manifesting as bilateral swelling of parotid glands, is a typical manifestation of bulimia. Objective: The mechanism of acinar enlargement in sialadenosis is obscure, although peripheral polyneuropathy secondary to systemic disorders is assumed to be significant. This study aimed to find new aspects of pathogenesis of sialadenosis. Methods: Based on a fortuitous observation of diminished alpha-actin-positive myofilaments in myoepithelial cells in sialadenosis, 11 cases each of control and sialadenosis parotid glands were morphometrically analysed assisted by immunohistochemistry for alpha-actin, p63, cytokeratin 14 and Ki67 including double staining. Results: In sialadenosis: the acini were significantly (p<0,001) larger (1991,5 mm2 versus 1017.5 µm²); the number of myoepithelial cells as % per acinus was moderately (p= 0,005) reduced (77.2% versus 93.8%); the amount of alpha-actin-positive myofilaments as % per total circumference was significantly (p<0,001) reduced (7.2% versus 47.2%); and the proliferation rate of acinar cells was moderately (p=0,02) reduced (0.8% versus 2.0%). Conclusion: Taking into account previous ultrastructural observations of degenerative changes in peripheral nerves and in myoepithelial cells of sialadenosis our observations indicate new aspects of the pathogenesis: The loss of myofilaments of myoepithelial cells is compatible with myoepithelial insufficiency that is secondary to peripheral polyneuropathy. Possibly the resulting loss of support for the acini allows acinar secretory cells to expand. Secretory granules accumulate and produce the massive enlargement of acinar secretory cells characteristic of sialadenosis. These results might lead the ancient understanding of the pathogenesis of sialadenosis towards a new comprehension of the development of this prevalent painful disease causing „hamster cheeks“. They also promise to support the therapeutic management of complications of bulimia.