Lumps are a common manifestation of pathology involving the palatal tissues. These range from salivary gland tumours such as pleomorphic adenoma, basal cell adenoma, mucoepidermoid carcinoma or adenoid cystic carcinoma to locally aggressive vascular neoplasms such as Kaposi sarcoma, and haematolymphoid malignancies of either lymphoid, plasma cell, histiocytic/dendritic or myeloid origin. Clinical differential diagnosis is complicated by overlapping clinical presentations which include raised soft tissue lumps, often taking on a blue/ purple appearance, with variability in symptoms and clinical onset.
A lesser-known lesion with a similar clinical presentation previously described as a “sheep in wolf’s clothing” is adenomatoid hyperplasia. Adenomatoid hyperplasia of the oral minor salivary glands is an uncommon lesion which is mostly encountered in the palate (Fig 1), although cases have also been reported in other oral sites including the buccal mucosa, retromolar pad and lip. Its importance lies in its clinical resemblance of more sinister pathology, often mimicking salivary gland tumours. About 50 cases of adenomatoid hyperplasia have been reported in the literature, but it is likely that more cases exist, but have been misdiagnosed as salivary gland lesions such as monomorphic or pleomorphic adenomas, or salivary gland malignancies.
Adenomatoid hyperplasia is composed of hyperplastic glandular tissue with acinar morphology (Fig 2), with acini appearing hypertrophic and filled with excessive mucous, with the nuclei being pushed to the basal aspect of cells (Fig 3). The hypertrophic mucous acini are superficially located, often separated from the overlying epithelium by a thin layer of collagenous connective tissue. Additional staining beyond routine hematoxylin and eosin (Figs 2 & 3), shows abundant positivity with Periodic Acid-Schiff (Fig 4) and Alcian Blue (Fig 5) revealing mucin laden acini, and normal positive staining with CK7 (low molecular weight cytokeratin), CK14 (high molecular weight cytokeratin), and p63 and calponin (myoepithelial cells).
The exact etiology of adenomatoid hyperplasia is not known, but commonly thought to occur as a consequence of trauma to the minor salivary gland tissues in affected areas. Chromosomal aberrations seen in other malignant neoplasms such as leukaemia have been reported in adenomatoid hyperplasia, although at different breakpoint locations.
Management of such lesions includes local excision which limits recurrence, although one case of purported malignant transformation to mucoepidermoid carcinoma has been reported.
Adenomatoid hyperplasia was first reported by Giansanti in 1971, and can affect patients of any age and gender, although the greater majority have been described in Caucasian cohorts. Inclusion of adenomatoid hyperplasia in the clinical differential diagnosis of oral lumps is important to limit invasive and inappropriate surgical management reserved for other more sinister tumours and neoplasms. More importantly, expert histopathological assessment is required to differentiate this local nonneoplastic salivary gland enlargement from other lesions such pleomorphic adenoma, mucoepidermoid carcinoma or adenoid cystic carcinoma.
More detailed information can be found in Contemporary Oral Medicine
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