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1.
Int J Comput Dent ; 25(1): 57-70, 2022 Mar 24.
Artículo en Inglés | MEDLINE | ID: mdl-35322653

RESUMEN

AIM: The aim of the present study was to review the current development status of additive manufacturing (AM) technology for fabricating frameworks for removable partial dentures (RPDs) considering fit accuracy, surface condition, and mechanical strength. METHODS: A search of the databases of MEDLINE, Cochrane Library, and Science Direct was conducted using definite keywords ("removable partial denture" or "framework" or "dental prosthesis design") and ("additive manufacturing technology" or "rapid prototyping" or "3D-printing"). RESULT: A total of 23 articles were selected according to certain inclusion criteria. The direct AM techniques were applied to manufacture metal RPD frameworks consisting of selective laser melting (SLM), selective laser sintering (SLS), and metal binder jetting (MBJ). The SLM technique showed a good surface and mechanical strength, but low accuracy. The SLS technique showed higher accuracy than indirect AM, but further studies are required. The MBJ technique showed lower accuracy and a rougher surface than the conventional method. CONCLUSION: AM techniques can produce RPD frameworks within the acceptable range for clinical practice; however, more clinical studies are needed.


Asunto(s)
Dentadura Parcial Removible , Humanos , Rayos Láser , Impresión Tridimensional
2.
J Clin Med ; 11(3)2022 Jan 20.
Artículo en Inglés | MEDLINE | ID: mdl-35159975

RESUMEN

Metal allergy is a T-cell-mediated delayed type of hypersensitive reaction. The pathogenetic mechanisms underlying the allergy are unclear, although the condition has been reported to be related to oral lichen planus (OLP), despite an absence of immunological studies to support this relationship. In this study, histopathological samples of OLP patients were examined to compare the metal allergy-positive and -negative groups, with a focus on the network of epidermal keratinocytes and T cells induced by thymic stromal lymphopoietin (TSLP) and its receptor, TSLPR. Infiltration of T cells into the epithelium was revealed to be higher in the OLP lesions of metal allergy-positive patients than in those of metal allergy-negative patients. Moreover, TSLP-TSLPR signaling and TNF-α production were higher in the epithelial tissue samples of the metal allergy-positive patients than in the metal allergy-negative patients. Metal allergy is associated with both increased expressions of TSLP in keratinocytes and increased TNF-α levels in the epithelium. We propose that this would promote the accumulation of T cells at the lesion site, contributing to the formation of the disease. These results suggest that metal allergy may be an aggravating factor in the pathogenesis of OLP.

3.
Commun Biol ; 5(1): 671, 2022 07 07.
Artículo en Inglés | MEDLINE | ID: mdl-35798870

RESUMEN

Metal allergy is one of the typical immune disorders encountered during the application of dental/medical materials and has a highly complex pathogenic mechanism. Semaphorin 3A (Sema3A), a member of the semaphorin family, is reported to be involved in various immune disorders. However, its role in metal allergy has not been clarified yet. Herein, we show that Sema3A expression was upregulated in nickel (Ni) allergy-induced mouse ear tissue and in NiCl2-stimulated mouse keratinocytes. Moreover, Sema3A regulated tumor necrosis factor-alpha production and mitogen-activated protein kinase activation in keratinocytes. The specific deletion of Sema3A in keratinocytes did not affect immune cell infiltration but reduced edema and ear swelling; it also impeded Th1 responses to cause a slight alleviation in Ni allergy in mice. Our results demonstrate that Sema3A promotes the development of metal allergy and should be explored as a potential target for the prevention and treatment of metal allergy.


Asunto(s)
Hipersensibilidad , Níquel , Semaforina-3A , Animales , Hipersensibilidad/prevención & control , Queratinocitos/metabolismo , Ratones , Níquel/toxicidad , Semaforina-3A/genética , Semaforina-3A/metabolismo
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