Oral ulcers in HIV-positive Peruvian patients: an immunohistochemical and in situ hybridization study.

BACKGROUND: This study describes the histopathological, immunohistochemical (IHC) and in situ hybridization (ISH) data of 25 cases of oral ulcers in HIV-positive patients, with clinical and microscopical features similar to ulcers not otherwise specified (NOS)/necrotizing ulcerative stomatitis (NUS). METHODS: Sex, age and clinical history were obtained from the clinical records. Histological analysis for H&E, Gomori-Grocott and Ziehl-Neelsen stains, IHC analysis to detect infectious agents and to characterize inflammatory cellular infiltrate, and ISH for cytomegalovirus (CMV) and EBER1/2 were performed. RESULTS: Twenty-one patients were men and four were women (mean age of 34.6 years). The tongue was preferentially affected. Microscopically, the lesions showed extensive necrosis, leukocytoclasia, vasculitis with luminal fibrin clots and an intense inflammatory cellular infiltrate predominated by CD68(+) atypical large cells, normal-sized and crescent-shaped nuclei macrophages, interspersed by CD8(+) T lymphocytes. Mast cells were also observed in all samples studied. CD4(+) T lymphocytes, CD20(+) B lymphocytes and VS38c(+) plasma cells were practically absent. CMV and EBER1/2 were identified in scarce cells of 3 and 16 of 25 cases respectively. CONCLUSION: These results show that CD68(+) macrophages, followed by CD8(+) T lymphocytes, were the predominant inflammatory cells, indicating they are relevant to the pathogenesis of the ulcers, possibly reflecting an abnormal immune response in the oral mucosa. The clinicopathological and immunoprofile features of the present cases are similar to NOS ulcers/NUS in HIV-positive patients.

Amyloid deposits in labial salivary glands identified by electron microscopy.

Abnormal proteinaceous deposits identified by light microscopy as amyloid in labial salivary gland biopsies were studied by transmission electron microscopy in order to establish their ultrastructural characteristics. Results showed fine fibrils approximately 10 nm in diameter located in close relation to the basal lamina of the secretory end-pieces and ducts as well as in the interstitial connective tissue stroma of labial salivary glands; these are the typical features of amyloid. Thus, the present study confirms the light microscopy diagnosis of amyloid deposits in labial salivary gland biopsies, supporting the use of lip biopsy as a readily accessible method for the diagnosis of secondary amyloidosis.

A highly sensitive method for diagnosis of secondary amyloidosis by labial salivary gland biopsy.

Both labial salivary gland and gingival biopsies were taken from 19 patients with clinical findings suggestive of secondary amyloidosis. Amyloid deposits were present in all salivary gland biopsies (19/19) while amyloid deposits in gingiva were observed only in three cases (16%). No amyloid was found in similar biopsies from 11 control patients. Periductal amyloid involvement was found along the basement membrane in all salivary gland samples; additionally, 16 cases had periacinar infiltration (84%), 13 had perivascular (68%) and 7 (37%) showed interstitial deposits. Amyloid in gingiva was seen along the epithelial basement membrane, as in salivary glands, although in isolated areas and scattered at the top of some dermal papillae and small blood vessels. In secondary amyloidosis it therefore appears that amyloid is deposited along the epithelial basement membrane before perivascular deposition occurs. This study presents a new highly sensitive and reliable method for the diagnosis of secondary amyloidosis, a method which is technically simple, free from complications and well-accepted by the patients.