Inflammation of Salivary Glands - pediagenosis
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Monday, November 25, 2019

Inflammation of Salivary Glands


Inflammation of Salivary Glands
The major salivary glands and the accessory mucous glands are subject to functional abnormalities as well as inflammation. Amylasemia (ptyalism), or excessive salivation, is associated with the use of several drugs, specifically, clozapine, pilocarpine, and risperidone. Toxins such as mercury, copper, and organophosphates have also been reported to cause excessive salivation. Most often, however, excessive salivation is caused by a form of gastroesophageal reflux known as water brash. On the other hand, xerostomia, or dryness of the mouth, most often results from frequently used medications such as anticholinergic agents, radiation to the head and neck, chemotherapeutic treatment, obstructive sleep apnea, and, less often, Sjögren syndrome, vitamin deficiencies, and other systemic conditions. Inflammation of the major glands is usually shown by swelling and may be a feature of a generalized syndrome. Epidemic parotitis or Hodgkin or leukemic infiltration should be considered diagnostically whenever more than one gland is involved or when a local cause is not obvious.

Inflammation of Salivary Glands

The submandibular gland may be the site of an acute or subacute infection, causing pain on palpation. The swelling differs from that of an alveolar abscess by being deeply seated, not complicated by trismus, and presenting as subepithelial nonadherent swelling beneath the mandible with distinct borders. The orifice of the Wharton duct is reddened, and its course is tender and edematous. Pus may sometimes be expressed by milking the duct. Swelling of the submandibular gland is most often due to obstruction in the form of a salivary calculus. Precipitation of calcium salts is probably initiated by irritation of the duct and stasis of saliva, aided by the presence of a matrix of filamentous colonies of sapro- phytic Actinomyces or other organisms.
The parotid gland is  subject to  similar  acute  and chronic swellings superimposed on recurrent obstruction of its duct. It may also become infected by an ascending pyogenic infection of the Stensen duct in debilitated or postoperative patients. In this “terminal parotitis,” the onset is sudden, with severe pain, fever, and swelling of the parotid gland. Obstructive parotitis, in contrast to submandibular adenitis, is usually not associated with calculus formation. An inflammatory disturbance in the duct or catarrhal constriction causes characteristic recurrent swelling. Complete obstruction predisposes to abscess formation, with reddening of the skin and a tense, fluctuant swelling of the parotid space. Repeated parotitis may lead to stenosis of the interlobar ducts or main excretory duct.
Mumps, a highly contagious viral infection causing parotid gland swelling, usually affects both glands, which have a doughy or elastic consistency. The frequency of this infection had diminished after immunization became available for young children, but now that parents are becoming more resistant to immunizations, the frequency is again increasing. The glands enlarge to the maximum size within 24 to 48 hours and remain enlarged for 7 to 10 days. Microscopically, the glands are heavily infiltrated by lymphocytes and show destruction of acinar cells in varying degrees. The danger of mumps lies in the complications, which include epididymoorchitis, oophoritis, meningoencephalitis, deafness, ocular lesions, and neuritis of the facial and trigeminal nerves.

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