Nickel - Induced Oral Pemphigus Vulgaris -Like Lesions

U literaturi je zabilježen samo jedan slučaj oralnog pemfigusa za koji se kao uzrok navodi nikal. U ovom prikazu opisali smo deskvamativni gingivitis kod 49-godišnjeg muškarca. Lezija se nalazila u prednjoj regiji mandibule koja je bila u kontaktu s keramičkim krunicama i mostovima. Osim tog oštećenja pronađene su i opsežne ulceracije u području lijeve i desne obrazne sluznice. Nakon godine dana liječenja lezije se nisu povukle. Uklanjanjem krunica i mostova te jakim topikalnim kortikosteroidima postignut je zadovoljavajući rezultat. Dentalna legura ispitivala se nakon toga metalurgijskim tehnikama. Rezultati su pokazali da je njezin glavni sastojak nikal. Patohistološki test i test imunofluorescencije potvrdili su dijagnozu pemphigus vulgaris. To nas je navelo na zaključak da pacijent boluje od lezija nalik na pemphigus vulgaris izazvanih niklom.So far, only a single case of nickel-induced pemphigus has been reported in the literature. We present a case of a 49-year-old male who had experienced a desquamative gingivitis on the anterior mandibular region which was in contact with porcelain crowns and bridges and severe ulcerations on the right and left buccal mucosa. The lesions did not respond to any medications for a year. After removal of those crowns and bridges with the treatment of potent topical steroids, the lesions responded dramatically. The dental alloy used as the core of crowns and bridges was further investigated using metallurgy techniques. The results showed that the dental alloy mainly contained nickel. Histopathologic and direct immunofluorescence evaluations confirmed a diagnosis of pemphigus vulgaris. We concluded that the patient had experienced nickel-induced pemphigus vulgaris-like lesions on the oral mucosa

Rac1 modulates TGF-beta 1-mediated epithelial cell plasticity and MMP9 production in transformed keratinocytes

Transforming growth factor-beta 1 (TGF-beta 1) activates Rac1 GTPase in mouse transformed keratinocytes. Expression of a constitutively active Q61LRac1 mutant induced an epithelial to mesenchymal transition (EMT) linked to stimulation of cell migration and invasion. On the contrary, expression of a dominant-negative N17TRac1 abolished TGF-beta 1-induced cell scattering, migration and invasion. Moreover, Q61LRac1 enhanced metalloproteinase-9 (MMP9) production to levels comparable to those induced by TGF-beta 1, while N17TRac1 was inhibitory. TGF-beta 1-mediated EMT involves the expression of the E-cadherin repressor Snail1, regulated by the Rac1 and mitogen-activated protein kinase (MAPK) pathways. Furthermore, MMP9 production was MAPK-dependent, as the MEK inhibitor PD98059 decreased TGF-beta 1-induced MMP9 expression and secretion in Q61LRac1 expressing cells. We propose that regulation of TGF-beta 1-mediated plasticity of transformed keratinocytes requires the cooperation between the Rac1 and MAPK signalling pathways

TGF‐β1 regulates the invasive and metastatic potential of mucoepidermoid carcinoma cells

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/86879/1/j.1600-0714.2011.01051.x.pd