Editorial Inflammation of the Dental Pulp Sang Hyuk Park, 1 Ling Ye, 2 Robert M. Love, 3 Jean-Christophe Farges, 4 and Hiromichi Yumoto 5 1 Department of Conservative Dentistry, College of Dentistry, Kyung Hee University, Seoul 02447, Republic of Korea 2 e State Key Laboratory of Oral Diseases, West China School of Stomatology, Sichuan University, Sichuan 610042, China 3 Department of Restorative Dentistry, University of Otago, School of Dentistry, Dunedin 9016, New Zealand 4 Department of Oral Biological Sciences, University Lyon 1, Faculty of Odontology and Laboratory of Tissue Biology and erapeutic Engineering, UMR5305 CNRS/University Lyon 1, 69372 Lyon, France 5 Department of General Dentistry, Tokushima University Hospital, Tokushima 770-8503, Japan Correspondence should be addressed to Sang Hyuk Park; shpark94@khu.ac.kr Received 23 November 2015; Accepted 23 November 2015 Copyright © 2015 Sang Hyuk Park et al. is 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. e dental pulp is sensitive to external factors such as micro- bial infection from dental caries and/or mechanical/chemical irritations during dental procedures. Dental tissue behaves differently to the other connective tissues. It is unique in a way that its soſt tissues (pulp and pulp-dentin complex) are enclosed within mineralized hard tissues (enamel, dentin, and cement), and its pulp is supplied by a rich neurovascular network that regulates various inflammatory mediators [1, 2]. Inflammatory signals may progress to rapid degeneration and necrosis, and such events could inflict very serious damage to tissues in the body [3, 4]. Factors that induce inflammation in the dental pulp and the root apex are as follows [1, 2, 5, 6]: the ingression of microorganisms through dental caries, crack or dentinal tubules of the teeth; chemical irritation from etching and/or bonding materials for adhesion of dental materials; mechan- ical irritation during preparation in restorative procedures; trauma from occlusion (TFO) or orthodontic movement of the teeth. Such factors may initiate the inflammatory cascades, which, in turn, further progress to pain and root resorption via neurogenic inflammation and hard tissue remodeling [7–9]. erefore, a thorough understanding of the pulpal inflammatory process is essential in the develop- ment of proper dental procedures and immunotherapeutic agents. is special issue is published with the intent of dissem- inating current knowledge and findings on inflammation in the dental pulp. is issue highlights the molecular mecha- nisms of inflammatory cascades, immunomodulatory effects of various substances, techniques used to study inflammation and regeneration of the dental pulp, and ultimately why an understanding of inflammatory process is important in the field of endodontics. In this issue, J.-H. Jang et al. review pathogen recogni- tion receptors (PRRs) for innate immunity in dental pulp. PRRs recognition of pathogen-associated molecular patterns (PAMPs) on pathogenic structure is important stage of initiating specific adaptive immunity. e paper reviews the various types of PRR families that include the Toll-like receptors (TLRs), the C-type lectin receptors (CLRs), the nucleotide-binding oligomerization domain-like receptors (NLRs), the retinoic acid-inducible gene-I-like receptors (RLRs), and the AIM2-like receptor (ALR). e authors suggest that immunomodulation via PRRs is crucial in the understanding of pathophysiology of pulp inflammation and also in the development of novel therapeutic targets in the pulp injury and/or infection. J.-C. Farges et al. assess responses of the pulp tissues to bacterial infection at cellular and molecular levels. e pulp response is illustrated by mechanisms used by odontoblasts and specialised immune cells to resist pathogenic bacteria. Hindawi Publishing Corporation Mediators of Inflammation Volume 2015, Article ID 980196, 2 pages http://dx.doi.org/10.1155/2015/980196