Cinnamon spice and everything not nice: many features of intraoral allergy to cinnamic aldehyde.

Intraoral allergic contact dermatitis (ACD) is an uncommonly reported entity. The most commonly implicated allergens are metals that are incorporated into dental appliances. Intraoral ACD to nonmetal allergens is even less frequently described. Cinnamic aldehyde is widely used as a flavoring agent in foods and dentifrices. However, intraoral ACD to cinnamon flavoring agents has only been sporadically reported. In these cases, a variety of sources have been implicated, including candy, chewing gum, mouthwash, lip sunscreen, cinnamon toast, volatile oils, and toothpaste. The clinical presentation of intraoral ACD reactions varies greatly, and as a result, clinicians often do not recognize the diagnosis. Furthermore, because patients are typically unable to provide a list of putative allergens, a high degree of clinical suspicion is required to make the correct diagnosis. We describe several patients with intraoral ACD caused by cinnamon and review the literature associated with this condition.

Lichen planopilaris and pseudopelade of Brocq involve distinct disease associated gene expression patterns by microarray.

BACKGROUND: Lichen planopilaris (LPP) and pseudopelade of Brocq (PPB) are two scarring alopecia diagnoses that exhibit similar clinical features. Some suggest LPP and PPB are not distinct diseases, but rather different clinical presentations in a spectrum derived from the same underlying pathogenic mechanism. OBJECTIVE: We explored the degree of similarity between LPP and PPB gene expression patterns and the potential for common and unique gene pathway and gene activity in LPP and PPB using microarrays. METHODS: Microarray analysis, using a 21K cDNA set, was performed on pairs of biopsies obtained from affected and unaffected scalp of untreated patients. Diagnosis was confirmed by histopathology. Significantly differentially expressed genes were identified by analysis of microarray results in various datasets and screened for signaling pathway involvement. Selected genes were validated by quantitative PCR and immunohistology. RESULTS: The global gene expression profiles in LPP and PPB versus comparative intra-control scalp tissue were distinguishable by significance analysis of microarrays (SAM). There was limited commonality in the gene expression profiles between LPP and PPB. Specific genes, such as MMP11, TNFSF13B, and APOL2, were identified with significantly differential expression in association with LPP versus PPB. CONCLUSIONS: Our findings may have important implications for understanding the pathogenesis of LPP and PPB at the molecular level. Results suggest LPP and PPB involve different mechanisms of disease development and should be regarded as biologically distinct cicatricial alopecia diagnoses. Genes that we have identified may be useful as markers of the respective diagnoses and may be potential therapeutic targets.