INTRODUCTION: Dentin matrix protein-1 (DMP-1) is involved in the mineralization of hard dental tissues. DMP-1 is localized in several soft tissues, but its role is unclear. METHODS: Human inflamed dental pulps were collected from the endodontic clinic and human normal pulps from impacted teeth. Dental pulp cells from 8 subjects were explanted to test the effect of DMP-1 on interleukin-6 (IL-6) and IL-8 production by using enzyme-linked immunosorbent assay. RESULTS: DMP-1 was localized in pulp inflammation by using immunohistochemistry but was not present in impacted root pulps. Wherever found, areas of calcification were positively stained against DMP-1, suggesting its possible involvement in pulp inflammation and in pathologic calcification. To test this hypothesis, primary human pulp fibroblasts were cultured. The fibroblasts were identified on the basis of their morphology, immunoreactivity against vimentin and collagen 1a1 by immunofluorescence and negative staining to CD45, CD34, and cytokeratin by flow cytometry. DMP-1 (10 ng/mL) stimulated the production of IL-6 and IL-8 from pulp fibroblasts. DMP-1 showed an additive effect with lipopolysaccharide in IL-6 and IL-8 production. Inhibition of the p38 mitogen-activated protein kinase pathway blocked the proinflammatory effect of DMP-1 on pulp fibroblasts. CONCLUSIONS: Our data indicate that DMP-1 might participate in the development of inflammatory changes in the dental pulp. DMP-1 inhibition might be a new therapeutic strategy to target pulp inflammation and pathologic calcification.
INTRODUCTION:Dentin matrix protein-1 (DMP-1) is involved in the mineralization of hard dental tissues. DMP-1 is localized in several soft tissues, but its role is unclear. METHODS:Human inflamed dental pulps were collected from the endodontic clinic and human normal pulps from impacted teeth. Dental pulp cells from 8 subjects were explanted to test the effect of DMP-1 on interleukin-6 (IL-6) and IL-8 production by using enzyme-linked immunosorbent assay. RESULTS:DMP-1 was localized in pulp inflammation by using immunohistochemistry but was not present in impacted root pulps. Wherever found, areas of calcification were positively stained against DMP-1, suggesting its possible involvement in pulp inflammation and in pathologic calcification. To test this hypothesis, primary human pulp fibroblasts were cultured. The fibroblasts were identified on the basis of their morphology, immunoreactivity against vimentin and collagen 1a1 by immunofluorescence and negative staining to CD45, CD34, and cytokeratin by flow cytometry. DMP-1 (10 ng/mL) stimulated the production of IL-6 and IL-8 from pulp fibroblasts. DMP-1 showed an additive effect with lipopolysaccharide in IL-6 and IL-8 production. Inhibition of the p38 mitogen-activated protein kinase pathway blocked the proinflammatory effect of DMP-1 on pulp fibroblasts. CONCLUSIONS: Our data indicate that DMP-1 might participate in the development of inflammatory changes in the dental pulp. DMP-1 inhibition might be a new therapeutic strategy to target pulp inflammation and pathologic calcification.
Authors: Elisabeth Aurstad Riksen; Maria A Landin; Sjur Reppe; Yukio Nakamura; Ståle Petter Lyngstadaas; Janne E Reseland Journal: Int J Mol Sci Date: 2014-05-05 Impact factor: 5.923
Authors: Carla Renata Sipert; Ana Carolina de Faria Morandini; Karin Cristina da Silva Modena; Thiago José Dionísio; Maria Aparecida Andrade Moreira Machado; Sandra Helena Penha de Oliveira; Ana Paula Campanelli; Carlos Ferreira Santos Journal: J Appl Oral Sci Date: 2013 Mar-Apr Impact factor: 2.698