BACKGROUND: Among the agents that cause parotid sialosis, diabetes mellitus type 2 and chronic alcoholism are included. In this study, the morphometrical modifications in the diabetic parotid sialosis were determined to compare them with the histopathological characteristics of alcoholic parotid sialosis. METHODS: Five parotid biopsy samples obtained from patients with diabetic sialosis, 12 samples from patients with alcoholic sialosis and seven from individuals without these pathologies (control group) were analyzed. A morphometrical study of parotid parenchyme and stroma, using a digital image analyzer attached to an optical microscope, was carried out. Dimensions of serous acini and striated ducts, the area occupied by the fatty tissue, and the number of ducts were recorded. Mean values were compared using the Mann-Whitney U-test (P <or= 0.05). RESULTS: The variables analyzed in diabetic patients did not show significant differences with respect to the control group. However, when diabetics were compared with alcoholics, the alcoholics exhibited a noticeable reduction in the proportion of fatty tissue of stroma and a significant development of ductal epithelium that contributed to increase the caliber of the striated ducts. CONCLUSIONS: These results indicate that the glandular hypertrophy in the diabetic parotid sialosis is not directly associated with the ductal and acinar size, amount of fatty tissue and ductal hyperplasy. Nevertheless, these findings show that the ductal dimensions and the proportion of adipose tissue are variables that allow us to establish histopathological differences between diabetic and alcoholic sialosis.
BACKGROUND: Among the agents that cause parotid sialosis, diabetes mellitus type 2 and chronic alcoholism are included. In this study, the morphometrical modifications in the diabetic parotid sialosis were determined to compare them with the histopathological characteristics of alcoholic parotid sialosis. METHODS: Five parotid biopsy samples obtained from patients with diabetic sialosis, 12 samples from patients with alcoholic sialosis and seven from individuals without these pathologies (control group) were analyzed. A morphometrical study of parotid parenchyme and stroma, using a digital image analyzer attached to an optical microscope, was carried out. Dimensions of serous acini and striated ducts, the area occupied by the fatty tissue, and the number of ducts were recorded. Mean values were compared using the Mann-Whitney U-test (P <or= 0.05). RESULTS: The variables analyzed in diabeticpatients did not show significant differences with respect to the control group. However, when diabetics were compared with alcoholics, the alcoholics exhibited a noticeable reduction in the proportion of fatty tissue of stroma and a significant development of ductal epithelium that contributed to increase the caliber of the striated ducts. CONCLUSIONS: These results indicate that the glandular hypertrophy in the diabetic parotid sialosis is not directly associated with the ductal and acinar size, amount of fatty tissue and ductal hyperplasy. Nevertheless, these findings show that the ductal dimensions and the proportion of adipose tissue are variables that allow us to establish histopathological differences between diabetic and alcoholic sialosis.