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 Table of Contents  
REVIEW ARTICLE
Year : 2022  |  Volume : 14  |  Issue : 4  |  Page : 213-217

The why and how of pulpal pain


1 Department of Oral Medicine and Radiology, People's College of Dental Science and Research Centre, Bhopal, Madhya Pradesh, India
2 Private Practitioner, Bhopal, Madhya Pradesh, India

Date of Submission19-Oct-2021
Date of Decision03-Jan-2022
Date of Acceptance28-Jan-2022
Date of Web Publication15-Nov-2022

Correspondence Address:
Priyanka Deepak Deshmukh
Department of Oral Medicine and Radiology, People's College of Dental Science and Research Centre, Opposite Hotel Raja Bhoj, Bhanpur, Bhopal, Madhya Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijds.ijds_137_21

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  Abstract 


A proper understanding of pulpal pain has been an enigma to the scientific community. While neurons and transmitters are active participants, focus on neuropeptides has not been emphatic. A complex array of interaction of inflammatory substances, with assortment of nerve fibers in the presence of these molecules, has shed some light to this mysterious phenomenon of pulp pain. A literature search was made of the standard textbooks, Google Scholars, Pubmed and Scopus database for review, original research, case control studies using key words like “pulpal pain” and 'chemicals responsible for pain mechanism' . This paper is an attempt at highlighting not only the roles of these proteinaceous materials, so that they could be targeted to eliminate pain, but also the neuro anatomy and neurophysiology of the pulp.

Keywords: Nerve fibers, neuropeptide Y, pain, Substance P vasoactive intestinal polypeptide


How to cite this article:
Nair P, Deshmukh PD, Bhavsar S, Shivkumar GC. The why and how of pulpal pain. Indian J Dent Sci 2022;14:213-7

How to cite this URL:
Nair P, Deshmukh PD, Bhavsar S, Shivkumar GC. The why and how of pulpal pain. Indian J Dent Sci [serial online] 2022 [cited 2022 Dec 9];14:213-7. Available from: http://www.ijds.in/text.asp?2022/14/4/213/361196




  Introduction Top


Dental health-care workers are constantly faced with the challenges of diagnosis and successfully managing pulpal and periapical pain. While pain in itself is a complex phenomenon, odontogenic pain poses as a multidimensional experience, involving sensory and emotional responses, motivational and conceptual aspects. The complexity of pain sensation may in part be understood by complexity of not just the neural network, but a strong role of molecules called neuropeptides, notwithstanding a strong role of microcirculation too.

Nociception in the head arises from thermal, mechanical, and polymodal receptors. Damage to tissues results in release of algogenic chemicals, which can either excite or sensitize the nociceptor. The cell bodies of these nociceptor neurons are found in the trigeminal ganglion. These axons project via trigeminal root to synapse in the subnucleuscaudalis. From here, second-order neurons cross the midline and move through the trigeminothalamic tract to the thalamus, namely the venterobasal nuclei. The neurons then project onto the somatosensory cortex.[1]

A literature search was made from standard textbooks, Google Scholar, PubMed, and Scopus Database for articles (review, original research, case–control studies) using


  Review Top


Pulp and its composition

The relation of pulp and dentin is so intricate that they could be considered as married together; the two maintain a close symbiosis. Pulp, which is made of loose connective tissue, lies in the center of the tooth and consists of 2 parts:

  1. Pulp chamber
  2. Root canal.


Histologically the pulp consists of two regions – (1) Peripheral pulp (2) Central pulp.

  1. Peripheral pulp contains 2 zones – (A) Sub odontoblastic layer, i.e., cell-free zone of Weil, which shows ramification of capillary (B) Cell rich zone which consists of fibroblasts and undifferentiated cells
  2. Central pulp zone forms the principal support system for peripheral pulp which includes large vessels and nerves.


Structural (cellular) elements of pulp

Fibroblasts

Most common cells of pulp. Baume referred fibroblasts as mesenchymal cells, pulpoblasts, or pulpocytes because of their ability to form calcified tissues that cannot be accomplished by regular connective tissue fibroblasts.[2]

Odontoblasts

Principal cells of dentin-forming layer arise from peripheral mesenchymal cells of dental papilla during tooth development and differentiate by acquiring glycoprotein synthesis and secretion.

Defense cells

The defensive cells of pulp include histiocytes, macrophages, polymorphonuclear neutrophils, lymphocytes, dendritic cells, and plasma cells. Extracellular elements composed of collagen fibers and ground substance, i.e., glycoprotiens and glycosaminoglycans, play a major role in integrity of pulp organ.

Supportive elements of pulp

Blood supply of dental pulp

Pulp blood vessels have thinner muscular walls as compared to other parts of the body. One or more arterioles, which are present at the apex and extending through central pulp, branch off into metaarterioles in border of the coronal pulp. Loops of the capillaries pass between odontoblasts in the subodontoblastic region.[3] U– Looping of pulpal arterioles is related to regulation of pulpal blood flow. Diameter of capillaries in subodontoblastic area is 4–8 μm and main portion of capillary bed is situated just below the odontoblasts.[4] Arteriovenous anastomoses have the same size as that of arterioles, with endothelium composed of cuboid cells that project toward the lumen.

Innervation of dentin-pulp complex

Nerves enter the tooth through the apical foramen with afferent vessels and lead to the formation of neurovascular bundle. In the cell-free zone, behind the cell bodies of odontoblasts in the crown part, one nerve fiber develops eight terminal branches that form an enormous plexus of nerves. This group of nerves is called “subodontoblastic plexus of Rashkow.”[5] Nerve bundle of pulp consists of – (1) Sensory afferent nerves from trigeminal nerve; (2) Sympathetic branches from superior cervical ganglion. The latter is associated with innervation of smooth muscle of the arterioles. Though a nerve bundle consists of myelinated and unmyelinated nerves, the majority are unmyelinated.[6] From the “plexus of Raschkow,” many fibers start losing myelin sheath as they pass the cell-free zone and terminate as receptors near the odontoblasts for short distance up the dentinal tubules adjacent to the odontoblastic process.[5]

Sympathetic nerve activity regulates tooth eruption rate and secondarily affects tooth eruptive pressure by influencing local blood flow and tissue pressure by opening or closure of arterio-venous shunts. Very few nerves are observed in human pulp before tooth eruption. After tooth is erupted, maximum number of nerves are found in pulp horns (about 40% of tubules are innervated).[7]

Coronal pulp is more painful to stimuli than the radicular pulp. Bernick,[8] on observing how caries and restoration affect the nerves of pulp, found degeneration of subodontoblastic plexus associated with production of irritation dentin.


  Pulpal Response to Inflammation Top


Injury in the pulp affects pulp structure and its function, resulting in inflammation. In response, neutrophils get chemotactically attracted to the site. Due to phagocytosis of bacteria and dead cells, lysosomal enzymes are produced which destroy surrounding normal tissue and cause additional damage. By-products of hydrolysis of collagen and fibers act as kinins, which result in vasodilation and increased vascular permeability. Escaping fluid enter the pulp interstitial space, increasing the pressure, that has deleterious effects on its local microcirculation. When local tissue pressure exceeds the local venous pressure, the local veins collapse and their resistance increases. Hence, blood flows from high to low tissue pressure area. Persistent pressure results in compromised circulation which allows irritants such as injurious enzymes and bacterial toxins to accumulate in the inflamed pulp tissue.[9] This event may lead to the formation of “compartment syndrome.”[10] This results in increased pressure in the space of pulp chamber, with cell death and resultant inflammation. These in turn lead to release of vasoactive neuropeptides, i.e., substance P (SP), calcitonin gene-related peptide (CGRP), found in pulp nerve fibers. These peptides promote and maintain inflammation in pulp; hence this is referred to as neurogenic inflammation.


  Pathophysiology of Pulpal Pain Top


Neurological response

Pain is the single sensory response of the dental pulp. Sensory afferent nerve fibers of trigeminal nerve reach the root canal through apical foramen and enter root pulp in lumps. These lumps, along with blood vessels in collagen sheath, forms neurovascular bundle. On the basis of diameter, conduction velocity, and function, the nerve fibers that act as nociceptors are divided in 2 groups - (1) A-delta and beta (Myelinated) fibers and (2) C (unmyelinated) fibers.[11]

A-fibers

These fibers are superficial (located in the pulp and dentin junction), having fast conduction speed and low stimulation threshold. They help in direct transmission of pain to the thalamus. A-delta - fibers are activated by hydrodynamic stimuli such as – drilling, cold air, sweet foods, hypertonic solutions which result in rapid fluid movement within the tubules.[12] This activates the mechanosensitive nerve endings and results in short, sharp initial pain. A-β fibers have different response toward vibration and stimulates at lower electrical threshold. A-fibers are sensitized by serotonin.[12]

C fibers

The unmyelinated fibers have low conduction velocity, smaller diameter, and higher excitation threshold. Located deeper than A-delta fibers, they are activated by heat. Pain produced is slow, diffuse, and dull in intensity. C fibers are located in the central core of the pulp and cause diffuse pain called referred pain, from a specific tooth. This referred pain occurs because these C-fibers innervate multiple teeth with multiple pulps. When hypoxia occurs in tissues, C-fibers have the ability to maintain functional integrity because oxygen consumption of thick A-fibers is higher. Thus when injury occurs in tooth, interrupting the pulp microcirculation, the C-fibers function remains unaffected for longer time in comparison to A-fibers because the latter have been inactivated.[13] As a result, dull vague pain occurs on intake of hot food. Due to high threshold of C-fibers, they do not respond electric pulp testing.[14] With continuous application of heat, the C-fibers get affected due to temporary increase in vasodilatation and results in intense pain. C-fibers are activated by bradykinin and histamine.


  Molecular Basis of Pulp Nociception Top


Rutz et al.[15] stated an interesting relationship between dental pulp and endocrine system. Release of CRF from hypothalamus is enhanced by physical and psychological stresses. When CRF binds to its receptor in anterior hypophysis, it results in release of ACTH and endorphins into the bloodstream. ACTH act on suprarenal gland cortex to stimulate cortisol secretion and endorphins cause decrease in nociception. Endogenous opioid peptides or endorphins are naturally occurring, pain-suppressing neurotransmitters and neuromodulators and are present in large quantities in the brain. They cause decrease in pain transmission by prevention of release of excitatory neurotransmitter SP from the primary afferent nerve terminal.

Wakisaka et al.[16] showed that before and after cavity preparation, the distribution of feline dental pulp adrenergic nerve fibers occurs. Nor-adrenaline, adrenaline, and dopamine are present in high concentrations in inflamed pulps.


  Molecular Origin of Pulpal Inflammation Top


Pulpal inflammation has two key components – microcirculation and activity of nerve fibers. The stimulation of A-delta fibers has no effect on pulpal blood flow, whereas the stimulation of C-fibers causes augmentation, which is caused by SP. In injured tissue, some proteins are obtained from somatosensory and autonomic nerve fibers referred as Neuropeptides.[17] Due to interaction between exogenous irritants and defensive host cells, different neuropeptides such as SP, CGRP, vasoactive intestinal peptide, neurokinin A, neuropeptide Y are released.


  Central Sensitization Top


Hyperexcitation of dorsal neurons at the level of spinal cord is known as central sensitization which is enhanced by release of SP and CGRP; this result in hyperalgesia. A number of central neural changes occur when inflammation takes place in the periphery demonstrating that it produces a reaction to pain impulses. These include–

  1. Augmented CGRP-positive cells within L4 dorsal ganglion
  2. SP and CGRP levels rise in the spinal cord
  3. Enhanced spontaneous firing
  4. Discharge response gets increased
  5. Expansion of receptive fields occurs in dorsal horn neurons.[18]


Substance P

In a subset of capsaicin-sensitive peripheral neuron cell bodies located in dorsal root and trigeminal ganglia, the neuropeptide SP is produced that helps in the transmission of noxious stimuli to spinal cord.[19] This is released from afferent fibers, produces neurogenic inflammation of pulp, causing vasodilatation and endothelial cell contraction. As a result, plasma extravasation and mastocyte degranulation occur.[20]

Mechanism of Substance P

SP stimulates lymphocytes, granulocytes, and macrophages to produce cytokines. Macrophage stimulation by SP produces inflammatory mediators prostaglandin E-2 (PGE-2) and thromboxane as well as proinflammatory cytokines, i.e., interleukin-1 (IL-1), IL-6, tumor necrosis factor (TNF). All these events maintain synthesis and secretion of new SP and further vicious cycle of pulp inflammation continues. These effects are mediated by Natural killer type-1 (NK-1) receptors but SP, at high concentration, activates NK-2 and NK-3 receptors. The 3 tachykinin receptors – NK-1, NK-2, NK-3 – have preferences for SP, neurokinin A, and neurokinin B, respectively.[21] Vanilloid receptor 1 is activated by chemicals (capsaicin) and heat resulting in SP being produced from sensory neurons.[22] SP increases the production of PGE-2 and cyclo oxygenase-2 (COX-2) expression. It is metabolized by various enzymes like Neutral endopeptidase and angiotensin-converting enzyme.

Key effects of substance P in dental pulp

In healthy tissues, SP maintains homeostasis of tissues whereas in inflamed tissues, it results in vasodilation followed by increase in blood flow. It causes chemotaxis of inflammatory cells to the pulp tissue. Inflammatory and nociceptive mediators sensitize nociceptors to stimulate more release of SP in both spinal cord and dental pulp tissue.[23] Histamine release causes increased vascular permeability and increase in blood pressure.

Substance P in dental care procedures and pathological conditions

  • Increased extracellular levels of SP (>8-fold) was observed in irreversible pulpitis and in granuloma tissues as compared to normal dental pulp. SP concentration is 3.4 times more than CGRP concentration in normal pulp and 22.3 times greater than CGRP, in inflamed pulp. In symptomatic pulpitis, greater amount of SP is produced via fibroblasts of carious teeth. On stimulation of monocyte-macrophage by SP, an important inflammatory cytokine TNF-alpha is produced and hence SP has a key role in pulpal inflammation[24]
  • High level of SP expression is observed when inflammation occurs in the periapical region of RCT treated tooth and also after light and laser-activated tooth bleaching.


Calcitonin gene-related peptide

CGRP receptors commonly occur in both nociceptive and pain pathways of peripheral and central nervous system. Increased CGRP receptor expression is usually detected in acute irreversible pulpitis. It has been observed that induced pulpal inflammation occurs in pulp tissue of tooth that has been indicated for extraction for orthodontic purpose. CGRP receptor is expressed in greater amount in acute irreversible pulpitis than the number of CGRP receptors in induced pulpal inflammation and the number of CGRP receptors which occur in this induced inflammation is comparatively more than the healthy pulp.[25]

Peripheral nerve sprouting

CGRP containing nerve fibers is predominantly found in dental pulp. Most of CGRP fibers survive the injuries such as cavity preparation, pulpal exposure, occlusal trauma, etc., and continue to innervate dentin and are located only in tubules that have viable odontoblasts. Dentinal cavities result in depletion of CGRP and SP in rat molars. However, after 1–2 days, extensive sprouting reaction and greater neuropeptide immunoreactivity than normal are seen in these fibers. When inflammation reduces, the sprouting reaction subsides. Byers noticed that after tooth injury, synthesis of nerve growth factors exceeds the increased CGRP and SP nerve sprouting. He observed that nerve sprouting is responsible to bring more neuropeptides to the inflamed tissues. Nerve sprouting and increased levels of CGRP were found following trauma, orthodontic tooth movement.[19]

Vasoactive intestinal polypeptide

This neuropeptide which is found primarily in parasympathetic neurons continues to exist in pulp even after any injury to the nerve or after sympathectomy.[26] Apart from neurons, mast cells and neutrophils also produce VIP which has both physiological actions (cause smooth muscle cell relaxation and salivary secretion) and Immunomodulatory actions (regulates pro and anti-inflammatory mediators' synthesis) VIP causes shedding of CD-14 receptors located on the macrophages, thus results in deactivation of macrophages as it prevents the binding of complex (Lipopolysaccharide – lipopolysaccharide-binding protein complex) to CD-14 receptors. Hence, VIP has an important role in neuroimmunomodulation. It helps in the production of an important anti-inflammatory cytokine–IL-10 and also prevents T-cell proliferation.[27]

Neuropeptide Y

Neuropeptide Y (NPY) in normal dental pulp is primarily presented in the sympathetic neurons and not in the sensory neurons. Increased amount of NPY is commonly observed in sensory neurons, in pulp of carious teeth. NPY levels are increased in trigeminal ganglion after extraction, pulp exposure, and nerve transection. NPY works through activation of 4 G-protein coupled receptors, namely – Y1, Y2, Y4, Y5; among these receptors the 2 most commonly involved receptors are - Y1and Y2 which amend the sensory and nociceptive processes. CGRP release from capsaicin-sensitive neurons is prevented in peripheral tissue, i.e., dental pulp on the stimulation of Y1 receptor by Y1 agonist. NPY Y1 receptor occurs along with TRPV1 receptor in the cell body of trigeminal sensory neurons. NPY Y1 receptor stimulation results in activation of intracellular signaling pathway that prevents the release of CGRP and SP from pulpal afferent terminals.[28]

Sundqvist et al.[29] pointed out that PGE-2 secreted from pulp cells cause tissue destruction in pulpal disease. PGE-2 produces pulp pain in two different ways, i.e., (1) it has hyperalgesic qualities which sensitizes nociceptive nerves. (2) Increases pain response to bradykinin, 5-hydroxytryptamine, and histamine.

Human dental pulp cells are regulated by matrix metalloproteinases and tissue plasminogen activator by proinflammatory cytokines such as IL-1 and TNF-alpha. As a result, they play a crucial role in pulp injury. Inflammation of the pulp produces a large amount of IL-1.[30]

Lin et al.[31] showed that fibroblasts are involved in pulpitis through production of IL-6 and COX-2 since in many inflammatory disease pathogenesis, excessive amounts of IL-6 and prostaglandins are produced.

Two important enzymes involved in inflammatory and pain processes are – (1) Aspartate aminotransferase (AST) (2) Alkaline phosphatase (ALP). Spoto et al.[32] observed increased levels of AST enzyme in early stages of inflammatory process which occurs because of early necrosis of pulp cells. He also observed that in irreversible pulpitis, ALP activity diminishes due to excessive release of inflammatory mediators which cause inhibition of ALP production.


  Summary Top


Appropriately targeting the neuropeptides and neurotransmitters of pain and inflammation, with pharmacological agents should be the main goal of pain management. To achieve this, a profound understanding of the neurophysiology of head and neck pain would be meaningful, so that the cause could be treated. The prevalence of patients with pain arising from pulp seeking medical advice should be adequate impetus to the dentists to unfold their minds around the enigmatic experience. Evidence-based evaluation of drugs targeted to alleviate pain with emphasis on the main culprits should become the forerunner in the field of research of tooth pain.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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