Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2008
Morphometric analysis of the parotid gland affected by alcoholic sialosis.
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Bohl Luciana, Merlo Carolina, Carda Carmen, Gómez de Ferraris María Elsa, Carranza Miriam
Аннотация
BACKGROUND: In alcoholic parotid sialosis, the gland is frequently enlarged due to ductal and/or acinar hypertrophy, ductal hyperplasy and stromal fat infiltration. The aim of this study was to determine acinar and ductal dimensions, the number of striated ducts and the proportion of fat tissue in patients with and without alcoholic parotid sialosis.
METHODS: Twelve parotid biopsy samples from patients with hepatic alcoholic cirrhosis and those from seven controls were used. A morphometrical study with a digital image analyser attached to an optical microscope was carried out. Direct and indirect indicators from acinar and ductal dimensions were recorded. The number of striated ducts and the proportion of fat tissue in stroma were determined. Fifteen records for each variable were taken. Mean values were compared using the Mann-Whitney U-test (P <or= 0.05).
RESULTS: There were no significant differences in acinar and ductal dimensions and the number of striated ducts between alcoholic and control patients. The proportion of fat tissue in alcoholic parotides was significantly lower than that in the controls.
CONCLUSIONS: These results do not corroborate previous qualitative descriptions about acinar and ductal hypertrophy and ductal hyperplasy in alcoholic patients. The main cause of parotid enlargement could not be stromal fat infiltration. The data could be used for differential diagnoses of sialosis.
METHODS: Twelve parotid biopsy samples from patients with hepatic alcoholic cirrhosis and those from seven controls were used. A morphometrical study with a digital image analyser attached to an optical microscope was carried out. Direct and indirect indicators from acinar and ductal dimensions were recorded. The number of striated ducts and the proportion of fat tissue in stroma were determined. Fifteen records for each variable were taken. Mean values were compared using the Mann-Whitney U-test (P <or= 0.05).
RESULTS: There were no significant differences in acinar and ductal dimensions and the number of striated ducts between alcoholic and control patients. The proportion of fat tissue in alcoholic parotides was significantly lower than that in the controls.
CONCLUSIONS: These results do not corroborate previous qualitative descriptions about acinar and ductal hypertrophy and ductal hyperplasy in alcoholic patients. The main cause of parotid enlargement could not be stromal fat infiltration. The data could be used for differential diagnoses of sialosis.