Odontogenic and Non-odontogenic Pain

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Department of Endodontics, New York University College of Dentistry, New York, NY, USA
 
Abstract
It is important for the clinician to recognize basic terminology associated with the peripheral nervous system and the biology of pain. This chapter describes the significance of allodynia, hyperalgesia, and central and peripheral sensitization. These terms are important because clinicians rely on clinical tests to evaluate the status of the pulp and periapical tissues. Hyperalgesia, allodynia, and central and peripheral sensitization are important findings during the diagnostic process.
This chapter also discusses the differential diagnosis of heterotopic (referred pain) sinusitis and headache disorders all of which can mimic endodontic pain. Herpes zoster can also pose a diagnostic challenge especially prior to the presence of intraoral or skin lesions. A classic case of herpes zoster that seemed initially to be an endodontic problem is described.
The deep, dull ache commonly caused by myofascial pain is reviewed, and the muscles most often involved are described. Differential diagnosis of myofascial pain from endodontic pain is a common problem, and this chapter reviews important diagnostic procedures that can be helpful. Headache disorders may pose another complicated diagnosis. Migraine, tension headache, and cluster headaches are reviewed since their symptoms may mislead a clinician into thinking that the patient’s pain is odontogenic in nature.

2.1 Terminology: Basic Pain Biology

2.1.1 Peripheral Nervous System

Most often pain is caused by tissue damage, or the potential for tissue damage, and is transmitted via terminal nerve fibers known as primary afferent nerve fibers to higher centers.
Two major classes of nociceptive (or pain-sensing) primary afferent nerve fibers can detect potentially damaging noxious stimuli: the A-delta and C fibers. Both fiber types have a wide distribution throughout the body including the dental pulp. In addition, separate classes of nerve fibers exist that are involved in detecting non-noxious stimuli such as vibration and proprioception. Such fibers can be found in the periodontal ligament, skin, and oral mucosa and include the A-beta fibers [13].

2.1.2 Primary Afferent Neurons

In the peripheral nervous system, neurons or nerves are referred to as primary afferent (i.e., sensory) fibers. The primary afferent fibers can be divided broadly into A-beta fibers, which transmit light touch or proprioceptive information, and A-delta and C fibers, which encode pain. The tooth is richly innervated by afferent nerve fibers, which are believed to primarily transmit pain in response to thermal, mechanical, or chemical stimuli. The vast majority of dental nerves are C fibers that innervate the central pulp, most of which terminate beneath the odontoblasts [6].

2.1.3 A-Beta Fibers

Rapidly conducting myelinated neurons that respond to light touch are called A-beta fibers. Under normal conditions, activation of the A-beta fibers by high-intensity stimulation results in low-frequency output in the central nervous system. Activation of A-beta fibers normally is interpreted as non-painful mechanical stimulation [15] or “pre-pain” [6]. A-beta fibers have been shown to undergo phenotypic changes that allow them to encode painful stimuli under inflammatory conditions [19].

2.1.4 A-Delta Fibers

A-delta fibers are lightly myelinated, have a faster conduction velocity than C fibers, and are believed to transmit a sharp or pricking sensation. A-delta fibers respond primarily to noxious mechanical stimuli rather than to chemical or thermal stimuli. Other A-delta fibers may be polymodal (responding to mechanical, chemical, and thermal stimuli) [3] or respond only to cold/mechanical [15] or hot/mechanical noxious stimuli [10].
In the dental pulp, A-delta fibers cross the odontoblastic layer and terminate in the dentinal tubules [13]. Due to their location and their sensitivity to mechanical stimulation, A-delta fibers are believed to respond to stimuli that result in movement of fluid within the dentinal tubules (e.g., osmotic, mechanical probing, or thermal stimuli applied to the external surface of the tooth) [13]. Consistent with that theory of dentinal pain is the fact that the stimuli causing dentinal fluid movement result in sharp pain associated with A-delta fiber activation. When intense noxious stimuli activate the A-delta fibers, the input to the central nervous system consists of high-frequency action potentials.

2.1.5 C Fibers

C fibers are unmyelinated, have slower conduction velocity, and are associated with a dull, aching, or burning sensation. Most C fibers respond to mechanical, thermal, and chemical stimuli. Because of the difference in conduction velocities, A-delta fibers are believed to transmit early shooting pain, while C fibers transmit late, dull pain.
Noxious stimuli that exceed the receptor threshold of these nociceptive primary afferent terminals result in action potentials that travel centrally, signaling tissue damage. In the pulp tissue, the more centrally located C fibers respond to thermal, mechanical, and chemical stimuli and are believed to be sensitized by inflammation [10]. All visceral structures are innervated primarily by afferent fibers conducting nociceptive information such as that carried by A-delta and C fibers [13].

2.1.6 Allodynia and Hyperalgesia

Allodynia and hyperalgesia are two different pain entities characterized by an increased patient response to painful stimuli. In some situations they can occur shortly after pain stimuli or take some time to develop.

2.1.7 Allodynia

Allodynia is defined as a reduction in pain threshold so that previously non-noxious stimuli are perceived as painful.
A classic example is an experience with sunburn. Following sunburn simply wearing a shirt can cause pain. This is an example of a reduced pain threshold (allodynia), resulting in pain from a stimulus that would not normally be painful. If someone gently touches the burned skin, the result may be sudden severe pain.
During irreversible pulpitis simply touching a tooth or exerting pressure on it may be enough to provoke pain. Allodynia focuses on a reduced pain threshold. This is an example of increased pain perception (hyperalgesia) caused by a stimulus that would not normally be painful [13].

2.1.8 Hyperalgesia

Hyperalgesia may be defined as an increase in the perceived magnitude of a painful stimulus. The focus in this condition is on the disproportionate reaction to a stimulus. If a patient has pulp/periapical pathosis, they may experience severe pain from gentle tapping a tooth with pericementitis. This is an example of both a reduced pain threshold (allodynia) and an increased pain perception (hyperalgesia.)
Clinicians often rely on clinical testing and the patient’s symptoms to detect the presence of hyperalgesia and allodynia. These are important symptoms associated with irreversible pulpitis [13].
Hyperalgesia can be partially accounted for by sensitization of nociceptors (primary hyperalgesia) and by central nervous system mechanisms (secondary hyperalgesia).
In the absence of tissue damage, activation of C or A-delta fibers produces transient pain. This pain is believed to serve as a physiological warning. When there is tissue injury, afferent fibers may be activated by lower-intensity stimuli than usual, and the quality of pain may be more persistent and intense. This phenomenon is due, in part, to sensitization of nociceptors, including an increase in spontaneous activity.
At the site of tissue injury, there are a number of inflammatory mediators that can directly or indirectly sensitize primary afferent nociceptors. These inflammatory mediators may be released from the local tissue cells, circulating and resident immune cells, vasculature and endothelial smooth muscle cells, and peripheral nervous system cells [13].

2.1.9 Central Sensitization

After peripheral tissue injury there is an afferent barrage from C fibers resulting from peripheral tissue inflammation, decreased afferent thresholds, and spontaneous firing of afferent fibers. When a second-order neuron receives a prolonged barrage of nociceptive input, the second-order neuron may also become sensitized. This results in a phenomenon referred to as central sensitization. The result of central sensitization is enhanced processing (i.e., amplification) of neural impulses that are being transmitted to higher brain centers. Two effects of central sensitization are secondary hyperalgesia and referred pain [13].
Secondary hyperalgesia is an increased response to painful stimulation at the site of pain resulting from central nervous system changes. This is in contrast to primary hyperalgesia, which is a lowered pain threshold resulting from sensitization of peripheral neurons. Secondary hyperalgesia might be felt in superficial (e.g., gingiva or skin) or deep structures (e.g., muscles or teeth).

2.1.10 Peripheral Sensitization

After tissue insult there is an inflammatory reaction that often causes pain. The severity of pain that follows is related to several aspects of the injury. Important are the type, extent, and location of the injury; the innervation of the tissue; and the phase of the inflammation. In the nociceptive system, tissue injury can manifest itself as increased responsiveness and/or reduced thresholds to a noxious stimulus, referred to as hyperalgesia [13].

2.2 Recognizing “What the Pain Is Not”

Often, a dentist feels under pressure to develop a precise diagnosis for the cause of pain, but that may not always be possible. It is critical that the dentist recognizes the significance of clues provided in the history and by clinical examination. While the dentist may not be able to synthesize the information and diagnose the precise cause of pain, it is possible that pulp/periapical can be ruled out. This is a critical point in the diagnostic process and leads the inquiry in a different direction.
Recognizing that the cause of pain is non-odontogenic is a crucial finding. The patient’s complaint of tooth-based pain may be misleading. When it becomes clear that the cause is non-odontogenic, a different path of inquiry is required. In diagnostically challenging cases, the astute diagnostician recognizes when it is wise to reach out to others for assistance. For example, referral to an endodontist, an orofacial pain specialist, or neurologist can be helpful in establishing the precise cause of pain. Failure to reach an evidence-based diagnosis increases the possibility of unnecessary treatment.
When the diagnosis is unclear, and the patient is not in severe pain, the clinician may have the option of delaying the definitive diagnosis and treatment plan. Often, symptoms will localize in the days or weeks following an initial visit and that transition facilitate the diagnostic process. In contrast, if the patient is in severe pain and diagnostic tests do not provide a clear diagnosis, the dentist should describe the situation to the patient and provide reasonable options including the possibility of referral. The patient must be brought into the decision making process in order to avoid potential unpleasantness if the treatment provided turns out to be in error.

Wise Advice
“You can see a lot just by listening.”
Yogi Berra
American baseball player and humorist

2.2.1 Odontogenic Toothache

Pulpal pain is mediated by C fibers and may be described as dull, aching, or throbbing in nature. This is in contrast to the quick short sharp sensation produced by A-delta fibers that mediate dentinal pain. When pulp testing, it is important to note not only whether the patient perceived the stimulus but also the nature of the stimulus perceived.
Pulp inflammation can result in sensitization of nerve fibers. When peripheral nociceptors (e.g., pulpal C fibers) are sensitized, the threshold of firing in response to a given stimulus (e.g., temperature and pressure) is lowered. In states of sensitization these nociceptors can be provoked with a less intense stimulus. The threshold for excitation is still “all or nothing,” but the required level of stimulation has decreased. These factors are involved in development of what is termed a “hot tooth,” and its management is discussed in Chap. 6 [13].
Unlike pulpal pain, pain of periradicular origin is easier to localize. Mechanoreceptors are numerous in the periodontal ligament (PDL) and are most densely concentrated in the apical third [17]. When inflammation from pulpal disease extends into the periodontal ligament, patients are more able to locate the source of the pain [13].
Clinical Tips
  • Gently tapping a suspect tooth with a mirror handle (or even just finger pressure against a highly sensitive tooth) is an excellent means of confirming a patient’s complaint.
  • A painful response to percussion is an indication of inflammation of the periodontal ligament and is termed pericementitis.
  • In the absence of a new restoration in hyper-occlusion or acute periodontal disease, pericementitis is an indication of pulpitis extending into the periapical tissue.
  • In the presence of sensitivity to percussion, treatment often involves endodontic therapy including occlusal reduction.
The degree of discomfort that a patient feels in relation to their periradicular pain is dependent on the degree of peripheral sensitization and the amount of provocation to this structure. A sensitized PDL will be uncomfortable to a patient if percussed lightly but more uncomfortable if percussed heavily. This is known as a graded response [13].
It is helpful to record the results of periradicular testing such as percussion and palpation in terms of degrees of tenderness (vs. “all or nothing”). Even using simple numerical values such as +1, +2, +3 provides useful information if a patient must return for a second diagnostic visit. See pain scale Fig. 1.​1. As with pulpal pain, pain of periradicular origin should also have an identifiable etiology.

Heterotopic Pain (Referred Pain)

Most patients reporting dental pain have symptoms that are odontogenic. However, the site the patient feels pain may not be the actual source of pain. Although patients may perceive that pain originates in a specific tooth, the pain may actually be referred from non-dental structures. Similarly, dental pain may be referred to non-dental structures.
The dentist must start the diagnostic process recognizing that a significant percentage of patient’s reports concerning the origin of pain are erroneous. Initiating endodontic treatment without confirmatory tests can lead to unnecessary treatment and continued pain. See Chaps. 1

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Sep 7, 2015 | Posted by in Endodontics | Comments Off on Odontogenic and Non-odontogenic Pain
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