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Background: Dermal fillers such as hyaluronic acid (HA) have been widely used in recent years as a less surgically invasive cosmetic treatment. Although delayed foreign body granuloma may occur as a rare adverse reaction after the procedure, detailed histological reports are still limited. When occurring on the buccal mucosa of the oral cavity, the histopathology may resemble some lesions of minor salivary gland origin due to the material properties of HA. Here we report a delayed foreign body granuloma associated with HA showing eosinophilic infiltration of the buccal mucosa, with characteristic histological and immunohistological features. Case Presentation: A 61‐year‐old woman presented with swelling and a burning sensation in the right buccal mucosa. On initial examination, a 25 × 20‐mm mass was palpated on the anterior margin of the right masseter muscle. Examination of a biopsy specimen revealed multiple pseudoduct‐like structures containing mucoid substance within the mucosal lamina propria. The mucoid substance was positively stained with Alcian blue (AB) and surrounded by CD68‐positive epithelioid cells and multinucleated giant cells. Many histiocytes had infiltrated into the surrounding area, and numerous eosinophilic infiltrates were also evident. After a review of the patient's history, a diagnosis of delayed foreign body granuloma associated with HA injection was made. Conclusion: We have reported a case of delayed foreign body granuloma with eosinophilic and histiocytic infiltration following injection of HA. It was suggested that the marked eosinophilic infiltration around macrophages was due to not only an allergic reaction, but also in part to increased macrophage aggregation. [ABSTRACT FROM AUTHOR]

Congenital deformities in the oral and maxillofacial region mostly affect the lower lip, particularly the vermilion border, and lower lip fistulas are generally associated with various syndromes or deformities, mostly inherited as an autosomal dominant trait with variable penetrance. However, congenital fistulas on the lower lip unassociated with any syndrome or deformity may occur as extremely rare developmental malformations, females being affected more often than males. Here, we report a case of non-syndromic congenital fistula of the lower lip. [ABSTRACT FROM AUTHOR]

Abstract Background Cimetidine, a histamine type-2 receptor antagonist, has been reported to inhibit the growth of glandular tumors such as colorectal cancer, however the mechanism of action underlying this effect is unknown. Adenoid cystic carcinoma is well known as a malignant salivary gland tumor which preferentially invades neural tissues. We demonstrated previously that human salivary gland tumor (HSG) cells spontaneously express neural cell adhesion molecule (NCAM), that HSG cell proliferation may be controlled via a homophilic (NCAM-NCAM) binding mechanism and that NCAM may be associated with perineural invasion by malignant salivary gland tumors. We further demonstrated that cimetidine inhibited NCAM expression and induced apoptosis in HSG cells. Here, we investigated the effects of cimetidine on growth and perineural/neural invasion of salivary gland tumor cells. Methods In this study, we have examined the effect of cimetidine on cancer cell adhesion to neural cells in vitro, one of the critical steps of cancer invasion and metastasis. We have also used an in vivo carcinogenesis model to confirm the effect of cimetidine. Results We have demonstrated for the first time that cimetidine can block the adhesion of HSG cells to neural cell monolayers and that it can also induce significant apoptosis in the tumor mass in a nude mouse model. We also demonstrated that these apoptotic effects of cimetidine might occur through down-regulation of the cell surface expression of NCAM on HSG cells. Cimetidine-mediated down-regulation of NCAM involved suppression of the nuclear translocation of NF-κB, a transcriptional activator of NCAM gene expression. Conclusion These findings suggest that growth and perineural/neural invasion of salivary gland tumors can be blocked by administration of cimetidine via induction of apoptosis and in which NCAM plays a role.