Volume 1 Issue S1 - 2016
Pannexins In Dentistry: Hype, Hope or Both?
Paula Ibarra1,2, Javier Campos1,2, Constanza Jiménez1,3 and Ziyad S Haidar1-3*
1BioMAT’X, Facultad de Odontología, Universidad de los Andes, Santiago de Chile
2Plan de Mejoramiento Institucional (PMI) en Innovación I+D+i, Universidad de los Andes, Santiago de Chile
3Centro de Investigación Biomédica, Facultad de Medicina, Universidad de los Andes, Santiago de Chile
*Corresponding Author: Prof. Dr. Ziyad S. Haidar, DDS, Cert. Implantology, MSc Oral and Maxillofacial Surgery, MBA, PhD; Professor and Scientific Director, Facultad de Odontología, Universidad de los Andes, Mons. Álvaro del Portillo 12.455 - Las Condes, Santiago, Chile. Founder and Head of BioMAT’X (Biomaterials, Pharmaceutical Delivery and Cranio-Maxillo-Facial Tissue Engineering Laboratory and Research Group), Biomedical Research Center/Centro de InvestigaciónBiomédica (CIB), PMI I+D+i, Department for Research, Development and Innovation/Dirección de Innovación, Universidad de los Andes, Mons. Álvaro del Portillo 12.455 - Las Condes, Santiago, Chile.
Received: December 23, 2015; Published: January 07, 2016
Citation: Ziyad S. Haidar., et al. “Pannexins In Dentistry: Hype, Hope or Both?” EC Dental Science 1.S1 (2016): S8-S9.
Sensation of inflammatory tooth pain or dentinal hypersensitivityoccurs in response to a variety of innocuous stimuli and is therefore initiated via distinct mechanisms (thermo-, hydro- and/or mechanico-dynamic).With the increased consumption of acids in our diet (i.e. carbonated drinks), for example, approximately one out of four adults will experience/suffer from dentinal hypersensitivityduring the course of their life, causing discomfort; one of the main reasons for patients to consult the dental office. Furthermore, oro-dental pathologies that also result in dentin hypersensitivity can alter both the dentin structure and the function of the intra-dental nerves. This often complicates preventive oral hygiene procedures thereby jeopardizing periodontal therapy. If left untreated, dentinal hypersensitivity can lead to chronic inflammation of the dentin-pulp complex and/or surrounding periodontal and oral tissues, which could eventually lead to therapy failure and more complex perio-/endo-donticconditions.
On the other hand, the known healing processes whether within the tooth and/or post-application or use of de-sensitizing therapies can target both dentinal as well as nerve function - in order to alleviate or reduce the stimulus and its sequelae. Indeed, current non-invasive treatments are mainly based eitheron (a) ion saturation of the buccal cavity and saliva (strategy which impedes pain signal conduction through the pulp nerve) or (b) physical blocking of the exposed dental tubule with hydroxyapatite and/or arginine; yet, with major limitations in clinical self-reported efficacy, where no definitive solution to pain and inflammation is provided.
Hence, it has been suggested to approach this dilemma from the anatomic, physiological, and more importantly, perhaps, the molecular perspective; in order to facilitate the developmentof novel preventive and therapeutic strategies, effective in cases of dentinal hypersensitivity; an alternate offer topatients in need. 
Several molecular mechanisms have been attributed in relation to pain conduction. However, to date, the physiological mechanisms responsible for these pain sensations are not fully understood. It is well-known today that extracellular ATP signaling as a neurotransmitter is involved in one of the pathways that could lead to the transmission of the nociceptive electrical stimuli. Actually, ATP signaling seems to participate in dentin hypersensitivity and dental pain. Taking this into consideration, Pannexin (Panx), a hemi-channel glycoprotein- discovered in the year 2000 as the second family of gap junction proteins, in vertebrates – has been shown to form mechano-sensitive ATP-permeable channels, in human dental pulp.
Briefly, the Panx family has 3 members - Panx1, Panx 2 and Panx3; which are involved in the (1) signaling of pain through ATP and calcium homeostasis; and (2) initiation of inflammation via enhancement of the production of inflammatory cytokines by neutrophils and other cells of the immune system. It has been recently reported that Panx channels play a role in external dentin stimulation-induced ATP release. On the other hand, Panx expression has been demonstrated in tissues including the brain, heart/coronary arteries, skeletal muscle, skin, lung, liver, etc …
Thus, the blocking of Panx, a logical strategy, has been pre-clinically explored as a therapeutic approachto decreasepain in neuropathic diseases of the central nervous system, with promising results. Recently, Panx has been found to be expressed in the oral cavity, mainly via epithelial and fibroblast cells, in gingival soft tissue (in vivo) and odontoblasts (in vitro). This opens the door wide for investigating the potential of blocking Panx as a novel therapeutic target and strategy in the management of oral disease-associated acute and chronic pain and inflammation. In fact, Panx blockers, such as Probenecid or Probalan - a Panx1 channel inhibitor used to treat gout and hyperuricemia, have already been developed targeting different diseases. However, no application in oral diseases, to the best of our knowledge, exists. This, in our opinion, will definitively not be the case soon, with the accumulating evidence-based knowledge (expression characterization and efficacy testing/evaluation) becoming available to the scientific community; regarding potential application in the management of oral pain and inflammation. Without doubt, Panx carries hype and hope to the future of dentistry.
This work was supported by generous funding/operating grants provided to the BioMAT’X (Biomaterials, Pharmaceutical Delivery and Cranio-Maxillo-Facial Tissue Engineering Laboratory and Research Group), part of CIB (Centro de InvestigaciónBiomédica), through the Faculty of Dentistry and PMI (Plan de Mejoramiento Institucionalen Innovación I+D+i), Dirección de Innovación, Universidad delos Andes, Santiago, Chile.
Copyright: © 2016 Ziyad S. Haidar., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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