The Complement System in Neuropathic and Postoperative Pain
David C. Fritzinger, Daniel E. Benjamin*
Identifiers and Pagination:Year: 2016
First Page: 26
Last Page: 37
Publisher Id: TOPAINJ-9-26
Article History:Received Date: 07/06/2016
Revision Received Date: 02/08/2016
Acceptance Date: 11/08/2016
Electronic publication date: 30/09/2016
Collection year: 2016
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
Certain types of pain are major unmet medical needs that affect more than 8 percent of the population. Neuropathic pain can be caused by many pathogenic processes including injury, autoimmune disease, neurological disease, endocrine dysfunction, infection, toxin exposure, and substance abuse and is frequently resistant to available pain therapies. The same can be said of post-surgical pain, which can arise from uncontrolled inflammation around the wound site. The complement system is part of the innate immune system and can both initiate and sustain acute and chronic inflammatory pain. Here we review the complement system and original investigations that identify potential drug targets within this system. Drugs that act to inhibit the complement system could fill major gaps in our current standard of care for neuropathic pain states.