PDF Diagnosis of salivary gland disorders

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Microscopically, the characteristic feature of necrotizing sialometaplasia is ischemic necrosis or infarction, which is thought to be the primary pathogenetic mechanism of this lesion, with preservation of the lobular architecture. The key histologic features in identifying this lesion are 1 lobular coagulative necrosis of the salivary gland acini Figures and , 2 prominent and proliferative squamous metaplasia of the excretory ducts, 3 pseudoepitheliomatous hyperplasia of the overlying mucosa, and 4 prominent inflammatory infiltrate.

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The most prominent and useful features histologically are the coagulative necrosis and ductal metaplasia Figure The lobules of salivary gland show multiple areas of squamous metaplasia as it replaces the areas of coagulative necrosis. Fibrosis is noted between the lobules. At low power, acinar alteration is noted; however, fibrous septa and ducts define the retained lobular architecture.

At medium power, there is extensive degeneration and necrosis with islands of squamous metaplasia lower. At high power, islands of squamous metaplasia are cytologically bland, not to be confused with malignancy. There is inflammation surrounding the outlines of the acini and ducts.

The diagnosis of necrotizing sialometaplasia can be problematic if the biopsy is not adequate or oriented properly.

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The chief differential diagnoses for this lesion are mucosal squamous cell carcinoma and mucoepidermoid carcinoma. In an adequately oriented biopsy, it is easy to distinguish these lesions based on the maintenance of the salivary gland lobular architecture.

Also, the cytologic features of necrotizing sialometaplasia are bland. In addition, the inflammatory infiltrate characterizing necrotizing sialometaplasia is more prominent than that frequently associated with squamous cell carcinoma and mucoepidermoid carcinoma. Moreover, these two malignancies infiltrate the salivary gland parenchyma.

Salivary gland disease

No specific therapy is required for necrotizing sialometaplasia. These lesions are self-healing. GARY L. Necrotizing sialometaplasia is a reactive lesion characterized by coagulative necrosis of salivary gland lobules, squamous metaplasia of ducts, pseudoepitheliomatous hyperplasia of mucosal epithelium, and inflammation. All age groups are affected. Ischemic necrosis is the pathogenesis. Compression of the greater palatine artery within the greater palatine foramen is likely the cause of palatal lesions. Usually the specific causative factor is unknown, but some lesions have been associated with trauma, local anesthetic injection, dentures, cysts, tumors, surgery, and upper respiratory infection or allergy.

Durations before diagnosis range from a few days to a few weeks. Nodular swelling quickly progresses to a deep ulcer, which is often associated with pain or numbness. The ulcer often persists for several weeks.

Mucosal ulcers range from 0. Lobular coagulative necrosis of acini and ductal squamous metaplasia are hallmark features Fig. Mucosal ulceration is typically conspicuous. Neutrophils and lymphocytes infiltrate surrounding tissues. Squamous epithelium in metaplastic ducts generally lacks significant cytologic atypia.

Pseudoepitheliomatous hyperplasia of mucosal surface epithelium is frequent. Lobular necrosis of the salivary gland A and squamous metaplasia of the ducts B are features of necrotizing sialometaplasia. Features that distinguish necrotizing sialometaplasia from squamous cell carcinoma and mucoepidermoid carcinoma are coagulative necrosis of acini, preservation of lobular architecture, absence of significant cytologic atypia, and a prominent, mixed inflammatory reaction.

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Douglas R. Necrotizing sialometaplasia NSM is a benign, self-healing, necrotizing, ulcerative, inflammatory condition that arises in the minor salivary glands. The oral cavity, typically the palate, is the most common site; less commonly, the major salivary glands, trachea, and larynx may be involved. In the larynx, NSM only rarely produces a visible lesion. It is commonly encountered as an incidental postbiopsy finding within seromucinous glands. In this setting, NSM may cause diagnostic difficulty during evaluation of laryngectomy surgical margins, particularly during intraoperative frozen- section evaluation.

Necrosis as the result of obstructive disease of the salivary glands generally occurs slowly. In necrotizing sialometaplasia, acute necrosis of entire lobules of minor salivary tissue occurs in a short period. It is believed that this process is due to infarction. Although the cause of infarction is unknown and is unrelated to systemic microvascular occlusion or thromboembolic disease, the preservation of cellular outlines, characteristic of the coagulative necrosis seen in infarction, is evident in this disease.

Importantly, this benign, spontaneously healing lesion may be mistaken clinically and microscopically for a malignant salivary gland neoplasm. Usually located at the hard and soft palate junction, necrotizing sialometaplasia is characterized by a deep-seated ulceration that generally lacks a raised or rolled border Figure Instead the ulcer is punched out and within its deep crater are gray, granular lobules that represent necrotic minor salivary glands.

The ulcer often measures 2 to 3 cm in diameter. Although some patients complain of numbness or burning pain, others are completely asymptomatic.


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The palate is the most common site of involvement, and in most cases the ulcer evolves spontaneously without antecedent trauma. However, a few reports have mentioned occurrence after a local palatal anesthetic injection. The lesion rarely occurs in other sites but has been reported in the tongue, retromolar pad, nasal cavity, antrum, and major salivary glands.

In these nonpalatal sites the disease is often traced to a cause such as surgery, trauma, or radiation. Experimental replication of the process in laboratory animals supports the fact that ischemic necrosis accounts for the pathologic features. Ligation of vessels reducing blood supply to the salivary glands recapitulates the same microscopic changes that occur in human tissue.


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    Most cases of necrotizing sialometaplasia occur in adults who have a broad age range and a mean age of about 47 years, although women seem to be affected at a somewhat younger age. Males are afflicted slightly more often than females. The microscopic features are distinctive and specific. In the palate the surface epithelium is lacking in the zone of ulceration and is replaced by fibrin and granulation tissue. Lobules of minor salivary acini that exhibit features of coagulation necrosis underlie this thin granulation tissue covering.

    The cytoplasmic borders of the cells of the acinar bulbs are intact. These acinar cells lack nuclei, are distended, and appear pale and basophilic. Entire lobules are similarly affected, with the result that the lobular architecture of the minor salivary glands is still maintained although the cells are nonvital.

    Scattered neutrophils and foamy histiocytes are often found in the zones of necrosis where mucin has accumulated or leaked from the necrotic acinar cells. Dispersed around the periphery of the necrotic lobules are ductal elements, many of which show squamous metaplasia Figure These metaplastic foci are typically represented by round or oval epithelial islands composed of benign squamous cells. Lumens are no longer evident in most of these islands.

    This represents a reactive process akin to pseudoepitheliomatous hyperplasia. Although some of the squamous islands are surrounded by necrotic ghosts of acinar elements, others show an enveloping fibrous stroma. The histologic features are similar to those encountered in mucoepidermoid carcinoma.


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