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BioMed Research International
Volume 2017, Article ID 8724503, 9 pages
https://doi.org/10.1155/2017/8724503
Research Article

Decreased Expression of Semaphorin3A/Neuropilin-1 Signaling Axis in Apical Periodontitis

1Department of Operative Dentistry and Endodontics, Guanghua School and Hospital of Stomatology & Institute of Stomatological Research, Sun Yat-sen University, Guangzhou, China
2Department of Stomatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China
3Zhujiang New Town Dental Clinic, Guanghua School and Hospital of Stomatology & Institute of Stomatological Research, Sun Yat-sen University, Guangzhou, China
4Biomaterials and Tissue Engineering Division, Department of Endodontics, Periodontics and Prosthodontics, University of Maryland Dental School, Baltimore, MD, USA
5Key Laboratory of Oral Medicine, Guangzhou Institute of Oral Disease, Stomatology Hospital of Guangzhou Medical University, Guangzhou, China
6Department of Pathology, Guanghua School and Hospital of Stomatology & Institute of Stomatological Research, Sun Yat-sen University, Guangzhou, China
7Center for Stem Cell Biology & Regenerative Medicine, University of Maryland School of Medicine, Baltimore, MD, USA
8Department of Mechanical Engineering, University of Maryland Baltimore County, Baltimore County, MD, USA

Correspondence should be addressed to Wei Qin; nc.ude.usys.liam@2iewniq and Zhengmei Lin; nc.ude.usys.liam@mhznil

Received 27 April 2017; Revised 23 September 2017; Accepted 10 October 2017; Published 31 December 2017

Academic Editor: Fabrizio Montecucco

Copyright © 2017 Ying Lin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Apical periodontitis (AP) is a chronic infection of endodontic origin accompanied with bone destruction around the apical region. Semaphorin3A (Sema3A) and neuropilin-1 (Nrp1) are regarded as a pair of immune regulators in bone metabolism. In this study, we firstly investigated the expression pattern of Sema3A/Nrp1 in apical periodontitis and its correlation with bone destruction. Using rat animal model, we analysed the level of mandibular bone destruction and the expression of Sema3A/Nrp1 on days 0, 7, 14, 21, 28, and 35 after pulp exposure. In addition, clinical samples from apical periodontitis patients were obtained to analyse the expression of Sema3A/Nrp1. These results indicated that the bone destruction level expanded from days 7 to 35. The number of positive cells and level of mRNA expression of Sema3A/Nrp1 were significantly decreased from days 7 to 35, with a negative correlation with bone destruction. Moreover, expression of Sema3A/Nrp1 in the AP group was reduced compared to the control group of clinical samples. In conclusion, decreased expression of Sema3A/Nrp1 was observed in periapical lesions and is potentially involved in the bone resorption of the periapical area, suggesting that Sema3A/Nrp1 may contribute to the pathological development of apical periodontitis.