An Insight Into Neurophysiology of Pulpal Pain: Facts and Hypotheses

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Abstract

Pain and pain control are important to the dental profession because the general perception of the public is that dental treatment and pain go hand in hand. Successful dental treatment requires that the source of pain be detected. If the origin of pain is not found, inappropriate dental care and, ultimately, extraction may result. Pain experienced before, during, or after endodontic therapy is a serious concern to both patients and endodontists, and the variability of discomfort presents a challenge in terms of diagnostic methods, endodontic therapy, and endodontic knowledge. This review will help clinicians understand the basic neurophysiology of pulpal pain and other painful conditions of the dental pulp that are not well understood.

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Most cited references 63

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Dental injury models: experimental tools for understanding neuroinflammatory interactions and polymodal nociceptor functions.

V Närhi, Patricia Byers (1998)

Recent research has shown that peripheral mechanisms of pain are much more complex than previously thought, and they differ for acutely injured normal tissues compared with chronic inflammation or neuropathic (nerve injury) pain. The purpose of the present review is to describe uses of dental injury models as experimental tools for understanding the normal functions of polymodal nociceptive nerves in healthy tissues, their neuroinflammatory interactions, and their roles in healing. A brief review of normal dental innervation and its interactions with healthy pulp tissue will be presented first, as a framework for understanding the changes that occur after injury. Then, the different types of dental injury that allow gradation of the extent of tissue damage will be described, along with the degree and duration of inflammation, the types of reactions in the trigeminal ganglion and brainstem, and the type of healing. The dental injury models have some unique features compared with neuroinflammation paradigms that affect other peripheral tissues such as skin, viscera, and joints. Peripheral inflammation models can all be contrasted to nerve injury studies that produce a different kind of neuroplasticity and neuropathic pain. Each of these models provides different insights about the normal and pathologic functions of peripheral nerve fibers and their effects on tissue homeostasis, inflammation, and wound healing. The physical confinement of dental pulp and its innervation within the tooth, the high incidence of polymodal A-delta and C-fibers in pulp and dentin, and the somatotopic organization of the trigeminal ganglion provide some special advantages for experimental design when dental injury models are used for the study of neuroinflammatory interactions.

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Estimated prevalence and distribution of reported orofacial pain in the United States.

Allan Lipton, J Ship, D C Larach (1993)

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Pulpal pain diagnosis--a review.

I B Bender (2000)

Evidence gathered from our studies and the work of others appears to support the presence of two distinct nerve pain pathways in the dental pulp, represented by fast conducting A-delta and slow conducting C-fibers. Each of these types of fibers has different pain characteristics: A-delta fibers evoke a rapid, sharp, lancinating pain reaction, and C-fibers cause a slow, dull, crawling pain. Pain response thresholds vary in different regions of the tooth, and thermal, osmotic, ionic, and electric stimuli involve different mechanisms to provoke nerve excitation of the dental pulp. Evidence also points to the fact that the incidence of pain increases as the histopathosis worsens. On interrogation, patients who manifest severe or referred pain almost always give a previous history of pain in the tooth with the ache. Eighty percent of patients who give a previous history of pain manifest histopathologic evidence of chronic partial pulpitis with partial necrosis, the untreatable category, for which endodontics or extraction is indicated. The other 20% exhibit histopathosis of the pulp with slight inflammation to chronic partial pulpitis without necrosis, a treatable category. Clinically, one can determine the degree of pulp histopathosis by asking the patient about a previous history of pain in the involved tooth. This history of previous pain adds another dimension in diagnosis for the clinician as to whether the painful pulpitis is reversible. This information also aids in referred pain localization.

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Author and article information

Journal

Journal ID (nlm-ta): Korean J Pain

Journal ID (iso-abbrev): Korean J Pain

Journal ID (publisher-id): KJP

Title: The Korean Journal of Pain

Publisher: The Korean Pain Society

ISSN (Print): 2005-9159

ISSN (Electronic): 2093-0569

Publication date (Print): October 2013

Publication date (Electronic): 02 October 2013

Volume: 26

Issue: 4

Pages: 347-355

Affiliations

Department of Conservative Dentistry & Endodontics, Hitkarni Dental College & Hospital, Jabalpur, India.

[* ]Department of Orthodontics & Dentofacial Othopaedics, Hitkarni Dental College & Hospital, Jabalpur, India.

[† ]Department of Conservative Dentistry & Endodontics, V.S Dental College & Hospital, Bangalore, India.

Author notes

Correspondence to: Niharika Jain, MDS. Department of Conservative Dentistry & Endodontics, Hitkarini Dental College & Hospital, Dumna Hills, Jabalpur 482004, Madhya Pradesh, India. Tel: +91-9424392599, Fax: +91-0761-2620261, niharika.dr@ 123456gmail.com

Article

DOI: 10.3344/kjp.2013.26.4.347

PMC ID: 3800706

PubMed ID: 24156000

SO-VID: 73887d8b-0f18-4430-8c89-1545ba8dcb1d

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This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

An Insight Into Neurophysiology of Pulpal Pain: Facts and Hypotheses

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Cardiovascular Innovations and Applications

Most cited references 63

Dental injury models: experimental tools for understanding neuroinflammatory interactions and polymodal nociceptor functions.

Estimated prevalence and distribution of reported orofacial pain in the United States.

Pulpal pain diagnosis--a review.

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