Oral elastofibromatous lesions: a review and case series.

Elastofibromas of the oral cavity are rare, with only 5 cases reported. In this paper, we present a series of five new cases of oral elastofibromatous lesions, occurring in 4 males and 1 female, with ages ranging from 33 to 76 years. The clinical differential diagnosis includes fibroepithelial polyp or fibroma, among other connective tissue tumours. Elastofibromas probably develop as reactive lesions, for which surgical treatment is definitive.

Juvenile spongiotic gingivitis.

BACKGROUND: This article recognizes the microscopic diagnosis of acute spongiotic mucositis as an analog to acute spongiotic dermatitis of the skin and defines a specific clinicopathological entity "juvenile spongiotic gingivitis" within this microscopic spectrum. METHODS: Twenty-four patients, usually juveniles, with patches of bright red, often slightly thickened, painless, and persistent lesions of the attached gingiva, which may or may not involve the marginal gingiva, were identified by clinical and microscopic features. Immunohistochemical studies for cytokeratins 5/6 and 19, estrogen receptors, and progesterone receptors were completed on 10 of these cases. A comparison to puberty gingivitis, which occurs in the same age group, was done. RESULTS: Microscopically, the epithelium exhibited hyperplasia, significant spongiosis, loss of keratinization, and a neutrophilic infiltrate, sometimes with microabscess formation, whereas the underlying connective tissue exhibited an acute on chronic inflammatory infiltrate. Full-thickness epithelial immunostaining for cytokeratins 5/6 and 19 was found, whereas no reactivity was seen for estrogen receptors or progesterone receptors in the specimens. CONCLUSIONS: Juvenile spongiotic gingivitis differs from puberty gingivitis by not needing to show continuity with plaque-related marginal gingivitis, by a lack of response to hygiene procedures, by an occasional occurrence at ages not related to puberty, and by the absence of sex hormone receptors investigated immunohistochemically in 10 of the cases. We propose juvenile spongiotic gingivitis as a distinct clinicopathological entity.

Immunohistochemical localization of growth factors fibroblast growth factor-1 and fibroblast growth factor-2 and receptors fibroblast growth factor receptor-2 and fibroblast growth factor receptor-3 in normal oral epithelium, epithelial dysplasias, and squamous cell carcinoma.

OBJECTIVES: Fibroblast growth factors (FGFs) and their receptors (FGFRs) have been identified in a variety of carcinomas, but there are few studies concerning their presence in oral cancers. The objective of this study was to determine whether FGF-1, FGF-2, and high affinity receptors FGFR2 and FGFR3 are present in the pathogenesis of oral epithelial dysplasias and oral squamous cell carcinoma. STUDY DESIGN: Sections from formalin-fixed, paraffin-embedded samples of oral normal mucosa (n = 14), epithelial dysplasia (n = 20), carcinoma in situ (n = 10), and squamous cell carcinoma (n = 12) were tested for cytoplasmic staining by standard in situ immunohistochemistry with antibodies for FGF-1, FGF-2, FGFR2, and FGFR3. RESULTS: Staining for FGF-1 is decreased or lost in the development of epithelial dysplasia and carcinoma. Staining for FGF-2 showed increased intensity (although not statistically significant) in oral epithelial dysplasias and squamous cell carcinomas and showed a significant increased expression in the upper layers of dysplasias and stratum spinosum-like cells in squamous cell carcinomas. Staining for FGFR2 showed a statistically significant increase in intensity in all layers of epithelial dysplasias and squamous cell carcinomas. Staining for FGFR3 was found in the upper stratum spinosum cells of normal and dysplastic epithelium and well-differentiated squamous cells in squamous cell carcinomas, with a statistically significant increase in staining intensity in dysplastic and carcinomatous tissues. CONCLUSIONS: The loss of FGF-1 is consistent with loss of differentiation in dysplasias and some squamous cell carcinomas. Changes in the localization of FGF-2 and FGFR2 into upper epithelial layers with increasing dysplasia suggest increased mitotic potential of high level cells. The co-localization of FGF-2 and its high affinity receptors in neoplastic tissues suggests an autocrine mechanism of influence on carcinogenesis.