Pulpo-dentinal Changes due to Caries

What is the pulpo-dentinal complex?

  • The pulpo-dentinal complex is a single functional entity.
  • It consists of an outer layer of dentin which is made up of mineralised connective tissue and odontoblasts.
  • The inner layer consists of pulp tissue is made up of extracellular matrix like type I and II collagens, glycosaminoglycan, glycoprotein and water. It is embed with capillaries, venules, lymphatic vessel and nerve fibers.
  • The majority of the cell types in this compartment are fibroblasts, undifferentiated mesenchymal cells, macrophages and other immunocompetent cells (e.g. B & T lymphocytes). These cells are involved in the defense against caries.
  • Mesenchymal stem cells are able to differentiate into either odontoblast-like cells or fibroblasts (Torneck 1994).
  • Odontoblast-like cells are responsible for the synthesis and secretion of reparative dentin under the circumstances where original odontoblasts are destroyed due to severe dental injury (D’Souza et al. 1995).
  • Macrophages are involved in the elimination of dead cells and bacteria, and also interact with other inflammatory cells to protect the pulp (Torneck 1994).
  • We will describe the exact mechanisms in the following sections.

Responses and mechanisms

1. Odontoblasts

  • Odontoblasts encounter oral pathogens that invade the dentine via the dentinal processes of the odontoblasts.
  • Odontoblasts undergo clustering of chromatin, irregularities in nuclear membrane and swollen mitochondria due to vasculature being cut off due to pulp inflammation, leading to hypoxic conditions.

Pulpo-dentinal Changes due to Caries - Cariology

Fig. 1: Odontoblasts at the pulpo-dentinal junction.
(SC - subodontoblastic capillaries, TA - terminal arterioles, PC- precapillary sphincters, PCV - postcapillary venules, AVA - ateriovenous anastomosis, LC - lymphatic channels)
(University of Texas, 2001)

  • Odontoblasts send a mechanical signal to the pulp, often causing pain (Yu & Abbott, 2007).
    • In the hydrodynamic theory (most widely accepted), pain impulse is elicited by the rapid variations in pressure and fluid movement in the tubular dentin affecting the sensitive free nerve endings at the pulpo-dentinal junction (Matthews B & Hughes SH., 1988).
    • Cold/compressed air draws dentinal fluid; heat/chewing pressure pushes dentinal fluid in towards the pulp. Responses due to heat are slightly slower and duller compared to those due to cold (Matthews B, 1994).
    • This fluid movement exerts an uninterrupted mechanical warp on the tubular fibers and the pulp tissue below (Matthews B, 1994).
    • Odontoblasts move together with the fluid, pressing on nerves and deforming them.
    • Nerves experience an increase in NA+ permeability, rapidly depolarizing, eliciting pain impulse.

Pulpo-dentinal Changes due to Caries - Cariology

Fig 2 : Hydrodynamic Theory indicating movement of the fluid within the dentin tubuli
(Brännström et al. 1967)

2. Immune response by defence cells in the pulp

  • Nerve endings receive stimulus from odontoblasts.
  • Neurons send signals to dendritic antigen-presenting cells that trap the attacking antigen and migrate with the trapped antigen to nearby lymph nodes.
  • At lymph nodes, T cells and macrophages that exist in the dental pulp (mainly around blood vessels and the odontoblastic area) are activated and increase in number.
  • T cells and macrophages carry out immune or inflammatory response.
3. Change in the morphology of the pulp
  • Shunt vessels (that bypass capillaries and join the arterioles and venules directly) open when pressure of pulp chamber rises during inflammation so as to reduce pressure in the pulp and maintain normal blood flow (Kim S, et al, 1992).

Recovery, transient pulpitis and irreversible pulpitis

The severity of the caries determines the fate of the pulp. (Smith, 2002)
If the pathogen insult is mild, it will result transient pulpitis and follow by pulp recovery.

An environment free of bacteria, severe haemodynamic changes and inflammation favours repair of the pulp. In healing, new generation of odontoblast-like cells generate tertiary dentin to repair border of the pulp and dentin.

If the protective mechanism that elicit by the pulp is not able to eliminate the pathogens insult, the pulp will proceed to irreversible pulpitis and lead to a total necrosis of the pulp.

Varying extents of injury

1. Mild injury such as slowly progressing caries in the dentin, mild abrasion and erosion, fracture of the enamel and dentin, chemical irritation. (D. Tziafas, 2004)

  • Odontoblasts survive.
  • Up regulation of biosynthetic activity of primary odontoblasts to form tertiary dentin beneath injury site and peritubular dentin in affected dentin tubules.
  • Pulp protected by opposing external stimuli.
2. Severe dentinal injury with no exposure of pulp such as rapidly progressive caries, cavity preparation, cytotoxic injury in pulpal cells during restoration. (D. Tziafas, 2004)

  • Odontoblasts under injury site are destroyed (forming dead tracts).
  • Inflammatory-healing cascade occurs.
  • Proliferation of pulpal cells into the dentin surrounding the pulp.
  • Fibroblast cells laid down as fibrodentin on dentin-pulp border.
  • If cariogenic environment is removed, new generation odontoblast-like cells (dentin forming cells) differentiate from pulp to form tubular tertiary dentin.
3. Severe dentinal injury with pulpal exposure; with low potential for recovery especially for caries-caused pulpal exposure as pulp has infected with bacteria. (D. Tziafas, 2004)

Pulpo-dentinal Changes due to Caries - Cariology
(Taylor P. Cotton , 2009)


Pulpitis refers to the inflammation of the pulp within the tooth.

When the pulp becomes inflamed, there is build-up of pressure in the pulp chamber. This exerts pressure on the nerve of the tooth, causing the pain associated with pulpitis. Pain due to this pressure is hard to dissipate as the pulp chamber is enclosed within relatively hard dentin before pulpal necrosis (death of dental pulp).

There are two ways to categorize pulpitis: Acute or Chronic; Reversible or Irreversible. (Dentalfind.com, 2008)

Acute pulpitis Chronic pulpitis
Usually found in teeth of children and adolescents Found in adults
More noticeable pain; constant throbbing pain often made worse by lying down, swelling of gum and/or face Less noticeable pain
Acute sensitivity to hot/cold
Change in colour of the tooth
Purulent acute pulpitis: complete inflammation of tooth;
Gangrenous acute pulpitis: pulp dies in less painful manner leading to formation of abscess at the tip of the tooth root.

Table 1: Comparison between Acute Pulpitis and Chronic Pulpitis

Reversible pulpitis Irreversible pulpitis
Caused by caries encroaching on pulp Caused by progression of reversible pulpitis
Mild inflammation Severe inflammation
Does not have to be treated; heals over time Treated via root canal treatment or tooth extraction
Table 2: Comparison between Reversible Pulpitis and Irreversible Pulpitis

Vital Pulp Therapy

Vital pulp therapy aims to treat reversible pulpitis and maintain pulp health and activity. (D. Tziafas, 2004)

1. Transdentinal stimulation of reactionary dentinogenesis

  • For mild dentinal injuries.
  • Increase biosynthetic activity of leftover odontoblasts, stimulating formation of peritubular dentin.
  • Results in primary dentin sclerosis and affected pulpo-dentin border.
  • "Transdentinal stimulation": demineralized dentin releases bioactive substances (eg. growth factor TGF-ßs) that stimulate dentinogenesis.
2. Transdentinal stimulation of reparative dentinogenesis

  • For severe dentinal injury without pulp exposure.
  • Increase differentiation of odontoblast-like cells to replace the destroyed odontoblasts.
  • Tertiary dentin forms at affected site.
  • "Transdentinal stimulation": demineralised dentin releases bioactive substances, and induces the pulp to deposit fibrodentinal matrices before reparative dentinogenesis - odontoblast-like cells differentiate on the matrices.
3. Direct induction of reparative dentinogenesis
  • Direct pulp capping/ pulpotomy for severe injury dentinal injury with pulp exposure.
  • Induce differentiation of odontoblast-like cells at the capping material surface, stimulating biosynthetic activity of primary odontoblasts there.
  • Continuum of reparative dentin and reactionary dentin around the pulp-dentin border should be formed.
  • Requires mechanical support (eg. fibrodentinal matrix)

Post-arrest of lesion

Once the lesion is arrested, no further enamel or dentin demineralization takes place within the lesion unless the lesion becomes active again due to poor oral hygiene. Tissue may be scarred after the lesion has been arrested, however, as the enamel and dentin have limited uptake of minerals from the saliva after the disease has been arrested.


The Dental Root System - how it works and how it reacts to external influences.

Videos taken from youtube.

Further research areas

Currently, not much is known about the possible chemical or electrical transmission mechanisms between odontoblasts and the nerve endings - can the odontoblasts send chemicals or electric signals to the nerve endings to initiate immune response? This is a highly exciting area to explore as discovery of such mechanisms may call for a re-look into the role of odontoblasts in eliciting pulpal response. Furthermore, the time taken for the pulp to respond to an attack on the tooth by caries might have a new regulatory pathway - by regulating chemical or electrical signalling of the odontoblasts to the pulp.


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D.J. Smith (2002).Dental caries vaccines: prospects and concerns.Crit Rev Oral Biol Med;13(4), 335-349

D'Souza RN, Bachman T, Baumgardner KR, Butler WT & Litz M (1995) Characterization of cellularresponses involved in reparative dentinogenesis in rat molars. J Dent Res 74: 702–9.

D. Tziafas (2004).The Future Role of a Molecular Approach to Pulp-Dentinal Regeneration.Caries Res;38(3):314-20

Kim S, Dorscher-Kim JE, Liu M, Grayson. (1992). Functional alterations in pulpal microcirculation in response to various dental procedures and materials. Proc Finn Dent Soc 1992;88 Suppl 1:65-71.

Matthews B, Hughes SH. (1988).The ultrastructure and receptor transduction mechanisms of dentine.Prog Brain Res;74:69-76.

Matthews B, Vongsavan N. (1994). Interactions between neural and hydrodynamic mechanisms in dentine and pulp. Arch Oral Biol;39 Suppl:S87-S95.

Taylor P. Cotton (2009). What is Endodontics? Retrieved October 22, 2009 from http://www.advancedcareendo.com/endodontics.asp

Torneck CD (1994) Dentin-pulp complex. In: Ten Cate AR (ed) Oral Histology. Development,Structure and Function. 4th edition. Mosby, St. Louis, pp. 169–217

University of Texas. (2001). Microvasculature of dental pulp. Retrieved October 22, 2009 from http://www.uth.tmc.edu/courses/dental/pulpalmicro/fig_1.htm

Yu C, Abbott PV. (2007). An overview of the dental pulp: its functions and responses to injury.Aust Dent J;52(1 Suppl):S4-16.

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