[Type 1 allergy to formaldehyde in root canal sealant after dental treatment: two case reports and review of the literature].

Two cases of generalized urticaria after the dental treatment were reported. These cases had clearly positive RAST to formaldehyde, whereas skin prick testings were negative. We diagnosed them as type I allergy due to formaldehyde. Immediate type formaldehyde allergy is not widely recognized as a major allergic complication of dental treatment. Previous reports of immediate allergy to formaldehyde in dental treatment were reviewed. The characteristics are the followings, first, it tends to represent severe symptom like anaphylaxis, second, the symptom often appears a few hours later than usual cases of anaphylaxis. Allergen tests show highly positive ratio to formaldehyde RAST, whereas skin prick test often shows false negative. Assessment of specific IgE to formaldehyde is a useful and a diagnostic measurement, and is recommended in patients at risk.

In vivo cooperation between Bcl-xL and the phosphoinositide 3-kinase-Akt signaling pathway for the protection of epidermal keratinocytes from apoptosis.

To investigate the function of Bcl-xL in the skin, we established keratinocyte-specific Bcl-x gene-targeted mice under the keratin 5 promoter (K5). K5.Bcl-xL-/- mice were viable, devoid of alteration in the development of skin or appendages. However, they harbored spontaneous apoptotic keratinocytes in the epidermis. Bcl-xL-deficient keratinocytes cultured in vitro readily underwent apoptosis in the absence of growth factors, but the addition of HGF or EGF resulted in restoration of cell survival, which was reversed by treatment with wortmannin, an inhibitor of phosphoinositide-3 kinase (PI3K). Topical treatment of K5.Bcl-xL-/- mice with wortmannin sensitized the skin for apoptosis induced by UV (UV) B, although wild-type epidermis was only marginally affected by this treatment, suggesting that the resistance to UVB largely depended on PI3K-Akt signaling in Bcl-xL-deficient mice but not in wild-type mice. Furthermore, UVB irradiation resulted in redistribution of phosphorylated Akt from the basal layer to the suprabasal layer, indicating that Akt could spatially cooperate with Bcl-xL upon UVB exposure in the upper epidermis where Bcl-xL is normally localized. These results suggest that Bcl-xL and the PI3K-Akt pathway form a cooperative, intercompensatory axis for the protection of epidermal keratinocytes from apoptosis in vivo.