The relief of oral pain is important for urgent care and emergency physicians. Dental pain is multifactorial, which involves factors like sensory, conceptual, emotional and motivational aspects.

Pulpal pain and periapical pains are two important aspects of dental care. Identification of the right source of pain is important for developing therapeutic strategies, and understanding the neurophysiology of pulpal pain makes the treatment easy.

The dental pulp contains vascularized tissue, which gives a response called pain upon stimulation. Neural tissue consists of sensory trigeminal efferent axons. Sensory fibers are the ends of the trigeminal crainial nerve. These fibers reach the root canal in lumps and are often associated with blood vessels forming a vascular bundle.

When these fibers reach the coronal pulp, the nerve endings divide and distribute the branches to dentin. The fibers form a network in subodontoblastic region called "plexus of Raschkow." After this region, the myelinated fibers emerge as free nerve endings by losing their myelin sheath.

The sensory nerves are of two types, including delta fibers (myelinated) and C fibers (unmyelinated). The myelinated axons have low stimulation threshold. These axons conduct the stimulus at a faster rate and transmit the pain to the thalamus and thus generate sharper pain. The unmyelinated axons conduct the stimulus with a low velocity, and they have higher excitation threshold. The presence of “C fibers” in the core region of the pulp explains the diffuse pain, also known as referred pain from the specific tooth.

Rutz et al. explained the relation between endocrine system and dental pain. He commented that the dental pain is due to the binding of corticotrophin-releasing factor (CRF) to its membrane receptor. This binding of CRF is followed by release of adrenocorticotropic hormone (ACTH) and endorphins. Endorphins interact with opioid receptors of the peripheral afferent nerves and thus increase the antinociception.

Opioid peptides give relief from pain by preventing the release of neurotransmitter substance P from the primary afferent end of nerve. Recently, it was observed that opioid receptors regulate the balance of potassium ions. However, their role in pulpal pain should be further discovered.

Catecholamines (epinephrine and norepinephrine) have physiological effects on adrenoreceptors in blood vessels. Change in the morphology and biochemical content of the nerve fibers has been observed during inflammation of dental pulp. Noradrenaline, adrenaline and dopamine were observed at higher levels during the inflammation of dental pulp.

The activation of C fibers increases the intensity of pain due to the action of a neurokinin, the substance P. The neuropeptide SP is released from the nerve fibers, which causes inflammation and leads to vasodilation and contraction of the endothelial cells. This is followed by mastocyte degranulation and plasma extravasation.

The neuropeptide SP is a major mediator of inflammation, and it is the prime target for dental therapy. The cells such as lymphocytes, granulocytes and macrophages possess receptors for SP. After stimulation, these cells produce cytokines. Stimulated macrophages produce inflammatory mediators like PGE2, thromboxane and also the proinflammatory cytokines IL-1, IL-6 and TNF.

Such molecular events release new SP and increase the pain intensity. These effects are mediated by G proteins and NK-1 receptors. Higher concentrations of SP can also activate NK2 and NK3 receptors.

Many chemical mediators such as histamine, bradykinin, 5-hydroxytryptamine and prostaglandins are also related to pain and inflammation. Bradykinin causes vasodilatation, plasma extravasation and movement of inflammatory cells. The concentration of bradykinin is significantly increased during irreversible pulpitis, and is responsible for pain and inflammation.

PGE2 possesses hyperalgesic qualities and sensitizes the nociceptive nerve endings. It can also increase the pain response to other mediators like histamine and 5-hydroxytryptamine. Fibroblasts are also involved in the development of pulpitis through the production of IL-6 and COX-2.

Recent data indicate that co-expression of COX-2 and vascular endothelial growth factor (VEGF) in the inflamed pulps suggested the release of VEGF in inflamed pulp through COX-2 dependent pathway.

The role of sodium and potassium channels in pulp inflammation was also investigated. The painful pulp inflammation was associated with an increase in the sodium channels, i.e. NaV1.8 channels. Whereas the potassium channels, i.e. Kv1.4, might have been responsible for hyperalgesia and allodynia pulp generation.

In summary, pain represents as an urgent care or emergency situation for dental treatment. Information regarding the characteristics and neurophysiology during dental pain is important for the development of preventive steps or therapeutic strategies. Future studies in this direction would be helpful to determine the correct methods and for pain management.