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Comparative Study
. 2004 Jan-Feb;9(1):24-32.

Alcoholic parotid sialosis: a structural and ultrastructural study

[Article in English, Spanish]
Affiliations
  • PMID: 14704614
Free article
Comparative Study

Alcoholic parotid sialosis: a structural and ultrastructural study

[Article in English, Spanish]
Carmen Carda et al. Med Oral. 2004 Jan-Feb.
Free article

Abstract

Objectives: The purpose of this study is to demonstrate the histopathological differences between the initial and advanced stages of Alcoholic Sialosis, a pathology that generally involves parotid hypertrophy and structurally affects, to diverse degrees, the other salivary glands.

Study design: An analysis and comparison was carried out of the structural and ultrastructural modifications of the parotid glands from the hepatic biopsies of chronic alcoholics with clinical diagnosis of cirrhosis and from autopsies on individuals who had died from alcoholic hepatic cirrhosis. Various samples of normal gland obtained from surgical material were used as a control.

Results: The alterations found in the biopsies corresponded to the modifications discovered in the autopsies of alcoholics. Notable in both cases was the massive accumulation of secretory granules of different size, shape and electrodensity, which occupied the cytoplasm of the acinar cells. In both sample types the excretory ducts were enlarged and the epithelium of the striate ducts presented cells with nuclei and cytoplasm of irregular appearance and arrangement. A moderate adipose infiltration in the stroma and slight periacinal edema was also observed. The biopsies revealed, both at optical and electron microscopical levels, lipid inclusions in the acinar cells and the glandular parenchymal ducts.

Conclusions: The structural and ultrastructural findings of the parotid biopsies and autopsies, clearly show that alterations are already present in the salivary glands of chronic alcoholics before the terminal phase of hepatic cirrhosis. The enlargement of the ductal system lumens could be the principal cause of glandular hypertrophy.

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