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CHRONIC SIALADENITIS

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The etiology of chronic inflammatory states of the salivary glands varies by the specific gland in question. Chronic inflammatory changes in the parotid gland tend to be related to autoimmune disease (Sjögren syndrome), recurrent suppurative parotitis, or radiation injury. Other etiologies include granulomatous infections such as tuberculosis or sarcoidosis. Chronic inflammation of the submandibular gland and, to a lesser degree, the sublingual gland is more commonly due to obstructive disease, particularly sialolithiasis. In the chronically inflamed state, the glands are enlarged but over longer periods of time progressively reduced in size, and heterogenous density may be seen on CT with extensive fibrosis and small focal (punctate) calcification. The density on CT is often increased due to cellular infiltration and edema during acute phases of exacerbation. The surrounding subcutaneous fat may not show signs of edema as is seen with acute sialadenitis. MRI demonstrates similar changes with heterogenous signal on both T1 and T2. The duct or ducts may be dilated, strictured, or both. Both may be visible by contrast CT and MRI (Sumi et al. 1999b; Shah 2002; Bialek et al. 2006; Madani and Beale 2006a). Chronic sclerosing sialadenitis (aka Kuttner tumor, or IgG4‐related disease [see Chapter 6]) can mimic a mass of the salivary (most commonly submandibular) glands (Huang et al. 2002). It presents with a firm, enlarged gland mimicking a tumor. The most common etiology is sialolithiasis (50–83%) but other etiologies include chronic inflammation from autoimmune disease (Sjögren syndrome), congenital ductal dilatation and stasis, disorders of secretion (Huang et al. 2002). It is best diagnosed by gland removal and pathologic examination as fine needle aspiration biopsy may be misleading (Huang et al. 2002). Chronic sialadenitis can also be caused by chronic radiation injury. US studies have demonstrated a difference in imaging characteristics between submandibular sialadenitis caused by acalculus versus calculus disease. The acalculus sialadenitis submandibular gland US demonstrates multiple hypoechoic lesions, mimicking cysts, with diffuse distribution throughout a heterogenous hypoechoic gland. They did not, however, demonstrate increased thru transmission, which is typically seen with cysts and some soft‐tissue tumors. Sialadenitis caused by calculus disease demonstrates hyperechoic glands relative to the adjacent digastric muscle, but some are iso‐ or hypoechoic relative to the contralateral gland (Ching et al. 2001).


Figure 2.53. Axial contrast‐enhanced fat saturated T1 MRI demonstrating heterogenous enhancement consistent with abscess of the left accessory parotid gland.


Figure 2.54. Reformatted coronal CT demonstrating enlargement and enhancement of the submandibular glands consistent with viral sialadenitis.

Salivary Gland Pathology

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