SALIVARY GLANDS - ENDOCRINE ISSUES JUNE 1999

Diabetic sialosis is a persistent non-inflammatory bilateral painless soft symmetric hypertrophy of the parotid glands, with infrequent involvement of the submandibular salivary glands. A diabetic autonomic neuropathy leads to impairment of salivary gland protein secretion and synthesis. Intracellular zymogen (an amylase precursor) granule engorgement results and causes the acinar hypertrophy that leads to parotid enlargement. Parotid hypertrophy can also originate from an increased fatty deposition secondary to diabetic disturbances in lipid metabolism and hyperlipidemia.

The thyroid is often implicated in Sjogren's syndrome (SS), a chronic autoimmune exocrinopathy of the lacrimal and salivary glands. With the onset of xerophthalmia and xerostomia, a diagnosis of primary SS is made. Secondary SS occurs when another connective tissue disease (rheumatoid arthritis, lupus erythematosus etc) is present. Besides a clinical history, diagnosis is based upon serologic evidence, histologic examination of labial salivary glands, volumetric and chemical evaluation of tears and saliva, and sialography. Serum studies testify to the presence of characteristic antibodies - RF, ANA, anti-SSA, anti-SSB. Labial salivary glands demonstrate a significant lymphocytic infiltration. Decreased tear and salivary volumes (both measurable) are accompanied by changes in their chemistry. Sialographically, the abnormal pattern (sialectasis) is pathognomonic. Approximately 45-50% of patients with SS have subclinical evidence of hypothyroidism while 24% of patients with some form of autoimmune thyroid disease have a subclinical SS. Hashimoto's thyroiditis represents the usual thyroid entity associated with SS. Not uncommonly, both SS and Hashimoto's are prey to the development of a MALT lymphoma.

Following surgery, therapeutic management of most thyroid cancers includes radioactive iodine 131I, a radioisotope with an affinity for thyroid tissue. After diagnostic scanning and thyroid ablation with 131I, eradication of residual carcinoma in the thyroid bed or in metastatic locations is accomplished with elevated doses of 131I. Unfortunately, normal salivary glands (particularly the parotid) also selectively concentrate the 131I and thereby suffer the sequelae of radiation. Immediate transient parotid gland swelling and pain are to be expected. However, permanent injury and a clinically persistent sialadenitis is not an unexpected result.

Propylthiouracil therapy for hyperthyroidism prevents the organification of iodine for thyroid hormone synthesis. The resulting elevated serum iodide is actively secreted by the salivary glands. A work hypertrophy with enlarged parotids can develop.

An increase in circulating progesterone and estrogen (pregnancy) can be associated with sialorrhea. These hormones decrease lower esophageal sphincter contractility. Gastric reflux occurs. The acids cause esophageal irritation (heartburn). Effective clearance of the acids is a protective function of the esophagosalivary reflex mediated thru the vague. Sialorrhea results and serves to neutralize the acids, ravage the esophageal wall and discourage esophageal disease.


The Salivary Gland Center (SGC) was developed because a void existed in the diagnostic and comprehensive care of patients with salivary gland problems and/or secretory dysfunction. Since the diversity of these salivary conditions presents challenges to the clinician, the SGC is available for referrals.

Louis Mandel, DDS

Director, Salivary Gland Center

(212) 305-9982