Comparative Study of Cytokeratin Immunostaining of Parotid Gland Parenchyma in Normal, Diabetic, and Excretory Duct Ligation of Mongrel Dogs

Abstract

Objectives: The present study aimed to give a glimpse of the normal distribution of intermediate filaments within the parotid gland parenchyma of mongrel dogs and to reveal the pathological changes that may occur as a result of the effects of diabetes mellitus or atrophy of the gland caused by the ligation of the excretory duct to discover whether there is a similarity in these pathological behaviors.

Materials and methods: Twelve healthy mongrel dogs were used in the experiment and were divided into three groups: group I (the control group), group II (dogs with alloxan-induced diabetes), and group III (dogs with the right-side duct-ligated parotid gland). The dogs were sacrificed 45 days after the parotid excretory duct were tied. The right parotid gland of all groups was dissected and prepared for histological and immunohistochemical expression of cytokeratin 17 assay.

Results: Histological findings confirmed that the parotid gland parenchyma of the diabetic group had glandular atrophy characterized by the loss of gland structure, degenerated acini, and dilatation of the duct system. Moreover, there is a predominance of the fibrous component with the presence of fat cells within the gland compartments. On the contrary, the excretory duct-ligated group undergoes severe glandular atrophy of the previous character with the presence of duct-like structure as well as extravasation and vasodilatation. Immunohistochemical expression of cytokeratin 17 in control parotid using an immunoperoxidase technique showed that cytokeratin expression varies from negative to mild in all ducts and some serous acinar cells. The gland parenchyma of the diabetic group showed mild to strong cytokeratin expression of duct cells more concentrated in the apical part with moderate to strong expression of diffuse type in some serous acini. The intensity of cytokeratin 17 in gland compartments of the excretory duct-ligated group revealed a variation in expression that ranged from negative to strong diffuse staining throughout the gland.

Conclusion: The severity and prevalence of cytokeratin 17 in our results are predictive of the pathological influence of both diabetes mellitus and duct ligation on the cytokeratin intracellular filaments of the salivary gland parenchyma in a different way that interferes with saliva production and/or secretion leading to xerostomia.

Fig. 1

Parotid gland of control group showing definite gland lobules ( A ) contain spherical serous acini ( B ), intralobular duct ( C ) (H&E X 100).

Fig. 2

Parotid gland of diabetic dogs showing the atrophy of serous acini ( A ), fibrosis ( B ), dilated interlobular ducts ( C ) (H&E X 100).

Fig. 3

Parotid gland of duct-ligated dogs showing the atrophy of serous acini ( A ), dilated duct ( B ), duct-like structure ( C ), extravasated blood ( D ) (H&E X 200).

Fig. 4

Parotid gland of control dogs showing the negative expression of CK17 in most of serous acini ( A ), mild in little of them ( B ), and weak of striated duct ( C ) (X 200).

Fig. 5

Parotid gland of diabetic dogs showing the strong expression of CK17 in ducts ( A ) and serous acini ( B ), and moderate in other serous acini ( C ) (X 200).

Fig. 6

Parotid gland of excretory duct-ligated dogs showing the strong expression of CK17 in both striated duct ( A ), some serous acini ( B ), negative in other ( C ), and moderate in islands of mucous acini ( D ) (X 200).

Fig. 7

Expression of CK17 in both acinar and duct cells of all groups.