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Physiology of a Generalised Inflammatory Response

Briefly describe the physiology of a generalised inflammatory response in the body. How is this modified in the dentine-pulp complex at a cellular and sub-cellular level?

Describe what steps you would take to protect the pulp from damage during crown preparation, and temporisation. How does the pulpal response change from this challenge when compared to a pathological challenge such as dental caries?

Inflammation is the response of living tissue to injury. It involves a well-organized cascade of fluidic and cellular changes. It can be acute or chronic. When an infection occurs in the body, the purpose of the immune system is to control or remove it. (1) The initial response of the immune system to an infection varies, depending on the site that has been invaded and on the nature of the invader. There are many “triggers” that can spur the immune system into action. Examples being:

If the invasion occurs in an area of the body such as the lungs where there are mainly macrophages, then these will be the first immune cells on the scene. They then begin to digest the invading organism, and by presenting antigens which stimulate other cells of the immune system into action. (1)

Some bacteria, for e.g. Staphylococcus Aureus or Salmonella Typhi, produce chemotaxins which when they enter the body, alerts there presence to the immune system, by acting as “breadcrumbs” which reveal the location of the invader. Chemotaxins are chemicals that activate phagocytes, their role is to iconsume and destroy the invading bacteria. (1)

Some bacteria when first present in the body are recognised by the complement system, which produces chemical messengers (cytokines) that warn other cells of the immune system that foreign cells have invaded the body. (1)

The invader may also be recognised by the acquired immune system, i.e. the lymphocytes. These cells directly fight the infection , or control other cells to do so.(1)

In all of these methods, it induces the phagocytes to migrate to the site of invasion, where they are activated and begin to digest and destroy the invading bacteria. They also produce more cytokines e.g. Interleukins, gamma-interferons, tumour necrosis factors, histamines etc. which further activate other cells of the immune system, hence a cascade effect occurs. (1)

Cardinal signs of inflammation are Dolor (pain), Calor (heat), Rubor (Redness), Tumor (swelling) and Functio Laesa (loss of function). Once the inflammatory process has begun, it continues until the infection that caused it has been eliminated and the phagocytes consume and destroy bacteria until so. Once infection has passed, the area should return to normal existence. The process by which it ends is by apoptosis. If the foreign antigen is not eradicated from the body then chronic inflammation occurs. (1)

From this paper are the cellular and molecular mechanisms when bacterial attack the pulp and the pulpal transition between caries-induced inflammations. The different strategies used by odontoblasts and specialized immune cells to combat these dentin-invading bacteria in vivo. (2)

A gram-positive saprophytic symbiotic community of bacteria covers the crowns of human teeth. This bacterial community adheres as a biofilm to the enamel that forms a barrier, which is impermeable to microorganisms and protects the underlying dentine and pulp. (2)

When this barrier is disrupted the gram-positive bacteria degrades the dentine. The proliferation and metabolic activity of these microorganisms release bacterial components into dentinal tubules that can diffuse towards the peripheral pulp. (2)

Recognition of these bacterial components by the host cells at the dentine–pulp interface triggers protective events including immune and inflammatory responses. If these responses do not eliminate the bacterial invasion this can result in irreversible chronic pulp inflammation.(2)

If cessation of the inflammation occurs with subsequent pulp healing, a barrier of reactionary dentine is formed by the surviving odontoblasts.  The quicker the reactionary/reparative dentine is formed the quicker the pulp healing occurs. (2)

In the dentine-pulp interface, the odontoblasts are the first pulpal cells that the dentine invading pathogens face.  Odontoblasts are involved in combatting bacterial invasion by activating innate and adaptive aspects of the dental pulp.  They achieve this by pathogen recognition in the pulp cells by sensing molecular structures, called Pathogen-Associated Molecular Patterns (PAMPs), which are both, essential for microorganism survival.  These PAMPs are sensed by Pattern Recognition Receptors (PRRs). One important class of PRRs for triggering the innate immune response is the Toll-like receptor (TLR) family. (2)

One important consequence of the TLR activation is the up-regulation of innate immunity effectors including antimicrobial agents and pro inflammatory cytokines and chemokines. These recruit and activate resident tissue and blood-borne immune/inflammatory cells. (2)

Odontoblasts also produce several antibacterial agents, such as beta-defensins and nitric oxide (NO). Beta-defensins (BDs) are broad-spectrum antimicrobial peptides that kill the microorganisms by forming channel-like micro pores that disrupt membrane integrity and induce leakage of the cell content. (2)

BD-1 is constitutively expressed, whereas microorganisms that come into contact with host cells induce BD-2, BD-3, and BD-4. BD-2 possesses antibacterial activity against S. mutans and L. casei and BD-3 exhibits antibacterial activity against mature biofilms containing Actinomyces naeslundiiLactobacillus salivariusStreptococcus mutans, and Enterococcus faecalis. (2)

A pro-inflammatory role was also proposed for BD- 2, which up regulates interleukin (IL-) 6 and as Chemokine [C-X-C Motif] Ligand 8 (CXCL8, also known as IL-8) in odontoblast-like cells in vitro (2)

The pro inflammatory effect of BD-2 chemo attracts immature antigen-presenting dendritic cells (DCs), macrophages, CD4+ memory T cells, and natural killer (NK) cells by binding to cell surface chemokine receptors (2)

NO is another potent antibacterial agent, which is a free radical, produced from L-arginine through oxidation by NO synthases (NOS). There are 3 isoforms of NOS, NOS1 (neuronal NOS) and NOS3 (endothelial NOS), which are expressed in most healthy tissues, and NOS2 (inducible NOS) which is induced inflamed pulp.(2)

NOS2 activation promotes neutrophils and macrophages in inflamed rat incisor pulps. (2)

NO produced was also found to inhibit the growth of Streptococcus mutans, thus limiting the progression of caries-related microorganisms. (2)

In vitro studies have also shown when by PAMPs from Gram-positive bacteria attack the odontoblasts, it produces inflammatory cytokines and chemokines when. Odontoblasts differentiated andwere responsive to lipoteichoic acid (LTA), which is a Gram-positive bacteria wall component recognized at the cell surface through TLR2. (2)

When the odontoblast TLR2 engaged to LTA this up regulates TLR2 and NOD2, a cytosolic PRR, which led to the activation of nuclear factor- B (NF- B) and p38 mitogen-activated protein kinase (MAPK) signalling, inhibition of dentinogenesis, and production of the pro-inflammatory chemokines Chemokine [C-C Motif] Ligand 2 (CCL2), CXCL1, CXCL2, CXCL8, and CXCL10. Chemokine produced by odontoblasts following bacterial challenge attracts immune cells into the odontoblasts layer beneath the carious lesion.  When dentin is being demineralised by caries, immature DCs accumulate at the dentin-pulp interface to catch the foreign antigens. A accumulation of T cells (= T lymphocytes), macrophages, neutrophils, and B cells (= B lymphocytes) occurs in the pulp. This increases the bacterial insult, and the development of the pulpal inflammatory process.(2)

CCL2 are expressed in odontoblasts beneath dentin carious lesions. Odontoblast- derived CXCL1, CXCL2, and CXCL8, attract neutrophils, and CXCL10, attracts T cells, and it accumulates other types of populations of immune cells at the dentin-pulp interface. (2)

Numerous studies show that odontoblasts detect oral microorganisms that invade mineralized dental tissues from the oral cavity. They position themselves against the foreign invaders by building their own antibacterial kit such as defensins, nitric oxide and by sending molecular messengers such as chemokines, cytokines to the neighbouring pulp, so to alert the immune cells so that they can mount a response to the invading microorganisms as well.(2)

But the majority of the studies done have been performed in vitro and so little or no  information is available about the role of antibacterial and immune effectors in caries-affected teeth in vivo.

So additional experiments are needed to further investigate the molecular effectors and regulators of human dental pulp immunity and determine their ability  to promote the recovery of the dental pulp. (2)

When carrying out crown preparation and temporisation in vital teeth damage can because to the pulp-dentine complex thus steps have to be taken in order to prevent and protect the pulp from such damage.

The pulp is a viscous connective tissue of collagen fibers and ground substance supporting the vital cellular, vascular and nerve structures of the tooth.

Pulpal responses to crown preparations depend on many factors such as thermal injury, injury to odontoblastic processes, desiccation of dentin, vibration and remaining dentin thickness.(3)

Thermal injury

Tooth preparation with a diamond rotating bur produces a fair amount of frictional heat. The degree to which how much intrapulpal heat is generated, is determined by many factors, such as the rotation speed of the drill, type, size and shape of cutting instrument, length of time the instrument is in contact with dentine, the amount of pressure exerted on the handpiece, the cutting technique used and the use of water coolants.

Studies have shown that high-speed cutting with copious water coolant and intermittent force use while preparing results in a reduced histological alteration of the pulp.(4)

Stanley showed in 1976 that given the same conditions with respect to the remaining dentine thickness (RDT), cutting instruments used and use of water-cooling, the pulpal responses would be less with high speed rather than lower speed cutting. This is because of the lower application of force required by the high-speed handpiece.(5)

Also during the preparation close to the pulp you may generate frictional heat causing a significant and detrimental increase in the pulp temperature. The repair will usually occur but the formation of reparative dentine can be vast and the pulp vulnerability to repeated injury increases. Clinical follow-ups of teeth restored with cast restorations such full crowns and teeth included as abutments in bridge framework have shown that pulpal necrosis occurs with a frequency of 10-15% over a 5-10 year period.(6)

Another complication in crown preparation is internal bleeding. In rare cases, it may be that pulpal necrosis occurs almost instantaneously. The tooth structure of such teeth can turn red and later a grey colour.(3)

Injury to odontoblasts processes

Odontoblasts are exposed to a variety of insults, such frictional heat, amputation of it the odontoblastic processes, displacement of its cell body, vibration and exposure to bacterial toxins and other chemical irritants.

The odontoblastic cells are very closely packed together with junctions between the cellular membranes. The spacing of the odontoblastic layer allows the passage of molecules and tissue fluids between the pulp and dentine. During crown preparation this can temporarily disrupt the odontoblastic layer and may sometimes inflict permanent cellular damage.(7)

Desiccation of the dentine

The use of compressed air to dry a preparation for a prolonged period can result in a delayed healing response. Drying surface dentinal fluids causes a strong capillary force, which results in a rapid outflow of fluid in the dentinal tubules. This rapid outflow stimulates mechanoreceptors, which not only causes post- operative pain, but also can even cause the displacement of the odontoblast from the odontoblastic layer up the tubule. The displaced cells undergo autolysis and disappear. These can be replaced with cells from the uninjured underlying pulp. Tertiary or reparative dentine is then laid down in about 1 to 3 months by the odontoblasts to wall off the pulp from the site of injury.(3)


The effects of the vibratory movement from the diamond cutting burrs on the pulp have not been thoroughly researched into. According to Holden under the point of application of the bur, the shock waves generated can move towards the pulp.(8) They appear to be more pronounced when the bur is stalled by digital pressure. Stalling of the bur not only reduces cutting efficiency by clogging up, it also leads to an increase in temperature.(4)

Remaining Dentine Thickness

The severity of the immediate pulp reactions depends on the remaining dentine thickness  (RDT) as well as the depth of the preparation.(9) Stanley suggested that a RDT of 2mm is needed to protect the pulp from most restorative procedures.(5) Whereas Pameijer, Stanely and ecker reported that a RDT of 1mm or more would protect the pulp tissue from pulp injury and so will reduce the need for pulpal responses thereby decreasing the probability of any complications that could occur.(10) Murray suggested that deeper cavities carefully cut down to 0.5mm appeared to have only a limited effect on underlying odontoblast survival.(11)

Provisional crowns help us evaluate the entire range of requirements, which a person desires from definitive prosthesis with the exception of longevity and shade selection.(12)

Though, their fabrication should be done with care, since, the materials and methods used may have a detrimental effect on the vitality of the pulp. The fabrication of the provisional restorations chair side are made using the direct technique, presents two major problems 1) the free residual monomers, may cause soft tissue lesions and allergic stomatitis. 2), exothermic heat is released during polymerization of the material.  This exothermic heat released is a major threat to the pulp because a study by Zach and Cohen stated a thermal rise of 10°F is sufficient to cause irreversible damage to pulpal tissues. So having a material with less or no exothermic heat released should be used to preserve the vitality of the pulp.(12)

Also we must take into account that this particular study did not consider the clinical conditions within which provisional is fabricated, where the temperature can be reduced via pulpal circulation, the periodontal ligaments fibers and extensions within the dentinal tubules.

Until now iatrogenic challenges have been talked about with respect to crown preparation and pulp vitality, comparing this against dental caries which is a more pathological challenge and the pulp responses depends on the extent of the caries lesion. Nowadays the introduction of minimally invasive dentistry and now the use of better restorative materials decreases the chances of pulp preservation and decrease the need of more invasive treatment such as root canal treatment.

According to this study (13) of following guidelines are used to avoid pulp exposures and optimize restorative outcomes, such as monitor tooth lesions and distinguish between active and arrested caries. No need to remove caries affected dentine from the cavity floor. Prior to removal of whole fillings clinicians should consider repair instead.

From this assignment from the numerous papers and articles read, I have gained a greater appreciation and knowledge when what can possibly occur during a crown preparation.

When it comes to the type of crown needed, the crown must be in the patient’s best interest and depends on the functional requirements, strength, the aesthetic demands, also taking into account the thickness of enamel and dentin layers.(14)

For example, when constructing full metal crowns it requires a relatively minimal tooth preparation, compared to ceramic and metal-ceramic that require a deeper preparations and thus are more destructive for the tooth structures.(14)

The dental pulp shows structural changes, in the odontoblastic zone, when being correlated with the depth and the technique of preparation.

Despite the technical advances in modern dentistry, there is no harmless, completely non- traumatic technique for crown preparation. Histological changes in the underlying pulp occur anyway and are difficult to avoid as long as the crown preparation is performed at high speed, even if an adequate water-cooling system is used.

Pulpal complications such as inflammation, degradation and necrosis are the result iatrogenic errors of the clinician. So, care has to be taken by the dentist to minimize the trauma to dentin and pulp during crown preparation and temporisation.


1.  The Inflammatory Response [Internet]. [cited 2018 Nov 4]. Available from:

2.  Farges J-C, Alliot-Licht B, Renard E, Ducret M, Gaudin A, Smith AJ, et al. Dental Pulp Defence and Repair Mechanisms in Dental Caries. Mediators Inflamm. 2015;2015:1–16.

3.  Seeburrun R. How might Operative Dentistry be a Threat to the Pulp? :5.

4.  Morrant GA. Dental instrumentation and pulpal injury II – Clinical considerations. J Br Endo Soc. 1977; 10(2):55-63.

5.  Stanley HR. Pulpal responses. In: Burns and Cohen S, editors. Pathways of the pulp. 3rd ed. St Louis Mosby; 1984. p. 465-489.

6.  Bergenhotlz G. Evidence for bacterial causation of adverse pulpal responses in resin-based dental restorations. Crit Rev Oral Biology Med. 2000; 11: 467- 80.

7.  Brannström M. Communication between the oral cavity and the dental pulp associated with restorative treatment. Oper Dent. 1984; 9:57-68.

8.  Holden GP. Some observations on the vibratory phenomena associated with high-speed air turbines and their transmission to living tissue. Br Dent J. 1962; 7113:265.

9.  MJOR I.A., Pulp-dentin biology in restorative dentistry. Part 2: Initial reactions to preparation of teeth for restorative procedures, Quintessence Int, 2001, 32:537-551.

10.  Pameijer CH, Stanley HR, Ecker G. Biocompatibility of a glass-ionomer luting agent, crown cementation. Am J Dent. 1991; 4:134-141.

11.  Murray PE, About I, Lumley PJ, Smith AJ, et al. Human odontoblast numbers after dental injury. J Dent. 2000; 28:277-285.

12.  Khajuria R, Madan R, Agarwal S, Gupta R, Vadavadgi S, Sharma V. Comparison of temperature rise in pulp chamber during polymerization of materials used for direct fabrication of provisional restorations: An in-vitro study. Eur J Dent. 2015;9(2):194.

13.  Murray PE, Windsor LJ, Smyth TW, Hafez AA, Cox CF. A nalysis of P ulpal R eactions to R estorative P rocedures, M aterials, P ulp C apping, and F uture T herapies. Crit Rev Oral Biol Med. 2002 Nov;13(6):509–20.

14.  Morphological changes in dental pulp after the teeth preparation procedure [Internet].Available from:

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