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].

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].

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].

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.

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].

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.

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].

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].

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).

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].

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].

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.