Pulp Defense Mechanisms

The dental pulp is a highly specialized and complex loose connective tissue encased by mineralized tissues, namely enamel, dentin, and cementum. The dental pulp has close anatomic and functional relationship with the dentin, often referred as dentin-pulp complex ( Fig. 10.1 ). Although the dental pulp is protected by a mineralized case, it is not impervious to irritation. Dental caries, trauma, anatomic defects, and iatrogenic mishaps can lead to inflammation and possibly pulp necrosis. However, the dentin-pulp complex has elaborate defense mechanisms.

Illustration of the dentin-pulp interphase in normal conditions. The fluid-filled dentinal tubules are occupied by odontoblastic processes and free nerve endings that might extend farther than odontoblasts toward the enamel junction. The subodontoblastic complex is composed of a rich capillary bed and innervation network. The pulp capillaries are equipped with arteriole/venule (A/V) shunts that may open upon injury, diverting the circulation to uninjured areas. Dendritic cells are the main antigen presenting cells in the dental pulp that are usually located in the subodontoblastic process in normal conditions of homeostasis.

Invading microorganisms reaching the dentin will encounter an outward flow of dentinal fluid. This positive pressure maintained by the dental pulp acts to “push” out the ingression of microorganisms, and it increases if pulpal inflammation and edema occur. A notable aspect is that this fluid will carry important molecules released from cells of the innate and adaptive immune response such as cytokines, immunoglobulins, and complement proteins. These molecules are able to initiate the pulpal defense before these organisms reach the pulpal cells. In addition, bacteria-mediated demineralization of dentin releases key noncollagenous proteins (NCPs) that mediate reparative responses. Thus dentin is no longer thought to be an inert tissue but instead comprises myriad growth factors, morphogens, and neurotrophins that have shown to be “fossilized” within the dentinal matrix and that can be released upon demineralization and mediate processes of angiogenesis, neurogenesis, and dentinogenesis. These processes are part of an elaborate response of the dentin-pulp complex to increase vascularity, overhauling the immune response and the metabolic demand of an injured area undergoing remodeling, repair, and possibly regeneration. In addition, inflammatory foci within the dental pulp have increased innervation density due to robust neuronal sprouting in the area. These neuronal fibers, mainly nociceptors, play their best recognized role of surveillance by providing nociceptive signals but also participate in the inflammatory process known as neurogenic inflammation by the release of vasoactive peptides such as calcitonin gene–related peptide (CGRP) and substance P, which are responsible for promoting vasodilation and plasma extravasation, respectively, as well as modulation of immune cell function ( Fig. 10.2 ).

Illustration of early events of microbial insult to the dentin-pulp complex. Microbes and their antigens diffuse through dentinal tubules reaching the free nerve endings of the trigeminal ganglia. These neuronal fibers express microbial recognition receptors (i.e., Toll-like receptors) and are activated and sensitized, resulting in the neuronal release of vasoactive peptides (i.e., calcitonin gene–related peptide [CGRP] and substance P [SP]) that, in turn, promote vasodilation and plasma extravasation, also known as neurogenic inflammation. Odontoblasts also express Toll-like receptors that upon recognition of microbial presence, trigger the release of chemokines, attracting dendritic cells to the dentinal tubules. These dendritic cells engulf and digest microbial antigens into epitopes and present these to cells of the adaptive immune cells (i.e., T cells). Subsequent events of pulp inflammation include the exuberant accumulation of polymorphonuclear (PMN) and adaptive immune response cells.

The progressive ingress of antigen and microorganisms into the dentin first reaches the cells positioned with the dentinal tubules (see Fig. 10.2 ). These cells include nociceptive primary afferent neuronal terminals that have been shown to extend up to 200 μm into the dentinal tubules and odontoblastic processes (see Figs. 10.1 and 10.2 ). Interestingly, pulpal neuronal afferent fibers are mainly nociceptors but have also been shown to have a role in directly detecting microorganisms. This characteristic is particularly interesting because the dentin-pulp complex is one of the most densely innervated tissues in the human body with nociceptors. These neuronal fibers within the dental pulp, regardless their degree of myelination, have been shown to mediate only nociceptive signals. Thus teeth are constantly under surveillance of this neuronal network dedicated to detecting injury or potential injury. These neurons have been shown to express the Toll-like receptor 4 (TLR4) that recognizes liposaccharides or endotoxins from gram-negative bacteria. ^, The activation of TLR4 in neurons results in sensitization of these fibers, lowering their activation threshold and increasing the response magnitude. ^, This increased response, in turn, leads to secretion of vasoactive peptides such as CGRP and substance P (see Fig. 10.2 ). The action of these peptides results in vasodilation and plasma extravasation (i.e., edema) at the site of injury, a process called neurogenic inflammation . The vasodilation and plasma extravasation allow for greater vascularity in the area with increased immune cellular presence and greater outward fluid flow, decelerating the ingress of microorganisms (see Fig. 10.2 ). This unique neuronal–bacterial communication is a sophisticated mechanism for sensory neurons to detect, alert the breach of the biological barrier, and initiate a process of neurogenic inflammation that will be immediately integrated with the immune-driven inflammation. An interesting aspect is that the early symptoms of a carious lesion can be manifested as painful responses to low-intensity stimuli and exaggerated responses to noxious stimuli in reversible pulpitis, matching the previously described neurophysiology.

Odontoblasts are highly specialized cells that serve the primary role of secreting dentin. As with other cell types within the dentin-pulp complex, these cells also have other functions that extend beyond their best-recognized role as secretory cells. Odontoblasts have also been shown to act as “sentinels” because these cells express many subtypes of TLRs and thus can detect the presence of gram-negative and gram-positive viruses and fungi within the dentinal tubules. ^, Activation of these TLRs have been shown to result in upregulation of expression and release of key chemokines and cytokines. ^, These factors are crucial for the recruitment of dendritic cells from the subodontoblastic plexus area to the areas of insult (see Fig. 10.2 ). These cells represent the major form of antigen-presenting cells in the dental pulp and are analogous to Langerhans cells in the skin. They are equipped to engulf, process, and present the antigens to other cells of the immune response system. In addition, dendritic cells will release additional chemokines and cytokines that in conjunction with odontoblast-derived factors and neurogenic inflammation will recruit additional cells of the innate and eventually adaptive immune response, resulting in the amplification of the inflammatory process. It is noteworthy that inflammation is a normal homeostatic response and is essential for containing the invasion of microorganisms. If successful, tertiary dentin is deposited in the area of insult in the form of either reactionary or reparative dentin, providing an additional mineralized barrier. Last, the presence of arteriole/venule (A/V) shunts (see Figs. 10.1 and 10.2 ) that open upon injury allows for the compartmentalization of microabscess regions within the dental pulp that are surrounded by vascularized dental pulp. The careful removal of the infected tissue, allowing the surrounding tissue to promote repair, represents the biologic basis for pulpotomy procedures ( Fig. 10.3 ).

Indirect pulp capping. A 14-year-old female patient consulting with symptoms of reversible pulpitis and symptomatic apical periodontitis on tooth #18 ( A and B ). Extensive decay and infected dentin were removed, exposed, and sealed with WMTA-ketac silver glass ionomer under rubber dam isolation (C) . Final obturation was performed 1 month later with amalgam ( D and E ). At 1-year follow-up, the patient was asymptomatic, and tooth #18 responded normal to clinic tests and radiographic evaluation ( F ). At 5.5-year follow-up, tooth #17 had been extracted and tooth #18 had a received a full-cuspal coverage crown. The patient was asymptomatic, and tooth #18 had normal response to clinicals test ( G , H , and I ).

Courtesy Dr. Tatiana M. Botero, faculty dental practice, University of Michigan, Ann Arbor, MI, USA.

Tertiary Dentinogenesis

The process of dentin mineralization occurs prenatally for most teeth and throughout the life of a tooth as long as the pulp is vital. The primary dentin is formed during tooth development, whereas secondary dentin is deposited at a slower rate, after tooth maturation, resulting in the gradual deposition of dentin throughout the entire extent of the pulp canal spaces and pulp chamber. The most superficial layer of dentin in contact with the dental pulp is the predentin that is formed by the unmineralized matrix secreted by the odontoblasts. It is the mineralization of the predentin that forms the mature primary and secondary dentin that are composed roughly by 70% hydroxyapatite crystals, 20% organic matrix, and 10% water. Thus primary dentin and secondary dentin are deposited in response to normal physiologic conditions. Tertiary dentin, on the other hand, is secreted in response to any injury to the dentin-pulp complex.

A mild injury to the pulp that can provide sufficient inflammatory stimuli for odontoblasts, increasing the secretion of tertiary dentin at a higher rate, promotes “reactionary” dentinogenesis ( Fig. 10.4 ). This reaction of the surviving odontoblasts results in localized increased thickness of the dentinal layer as it maintains the overall architecture of the dentin odontoblast interphase. Odontoblast death could occur with more intense stimuli for a period of time sufficient to lead to the loss of odontoblasts in the area of injury. If the surrounding pulp remains vital and there is a favorable balance between inflammation and repair, progenitor cells are recruited to the site of injury, possibly by chemotactic factors released from the demineralized dentin matrix and neighboring cells. These progenitor cells differentiate into mineralizing cells often referred as “odontoblast-like cells.” Although these cells differ in morphology from native odontoblasts, they also secrete a matrix that upon mineralization forms a “mineralized bridge” over the area of injury called reparative dentin ( Fig. 10.5 ). This dentin is typically atubular and, due to its rapid secretion, often traps the mineralizing cells within its matrix resembling osteocytes; it is often referred to as “osteodentin.” This nontubular dentin bridge, if formed uniformly without tubular defects, can provide a biological barrier with fluid permeability seen with tubular dentin. This inherent reparative and regenerative capacity of the dental pulp forms the basis for contemporary vital pulp therapies.

Reactionary dentin formation as result of an indirect pulp capping procedure. Upon the removal of infected dentin, the cavity is layered with a biomaterial that stimulates surviving odontoblasts to secrete dentin at a faster rate, creating a localized accumulation of dentin, distancing the pulp from the area of mild injury.

Reparative dentin formation as result of a direct pulp capping or partial pulpotomy. Upon the removal of infected dentin and part of the injured pulp, the cavity is layered with a biomaterial that stimulates migration of pulp progenitor cells (such as a tricalcium silicate material) and the differentiation into mineralizing cells in the area of injury. These cells secrete a mineralized bridge called reparative dentin in the attempt to create a biologic seal between the injured area and the underlying dental pulp.

Pulp Necrosis and Root Development

Despite the advanced defense and reparative mechanisms already described in this chapter and in Chapter 1 , the dental pulp may succumb to infections. The progressive process of liquefaction pulp necrosis results in complete loss of homeostatic functions. An important factor is that the loss of odontoblasts in the radicular pulp results in arrested tooth development in teeth still undergoing development. Indeed, root development is known to continue 2 to 3 years after the eruption of a permanent tooth in the oral cavity. ^, This process of root formation and maturation requires the complex interaction of the epithelial root sheath and mesenchymal cells located in the dental apical papilla. Pulp necrosis and/or trauma can severely disrupt this interaction, resulting in interruption of normal development in addition to the development and maintenance of apical periodontitis. Thus all efforts must be directed toward avoiding complete pulp necrosis through vital pulp therapies. Nonetheless, vital pulp therapy as a treatment alternative depends on the initial clinical presentation and the often-challenging assessment of the degree of inflammation.

Trauma

When patients present with traumatic dental emergencies, management is crucial for the prognosis of the tooth. It is important to perform an extensive evaluation and diagnosis of the case as well as schedule adequate follow-up visits to detect possible complications such as pulp necrosis and resorptions. The incidence of dental trauma is higher among boys than among girls, and the anterior maxillary teeth are the most commonly affected teeth, ^, particularly in patients with increased overjet and active participation in sports. The incidence of dental trauma has overall (all ages) a frequency of 5%, but in 0- to 6-year-old patients it is 17%. Traumatic injuries are more common in permanent (58%) than in primary teeth (36%). ^, The maxillary central incisor is more frequently affected (66%) than is the lateral incisor (17%). Uncomplicated crown fractures (without pulp exposure) are the most common traumatic lesions (41% to 68%). ^{, ,} Pulpitis and necrosis can also occur as a result of dentinal exposure to bacteria and bacterial byproducts in uncomplicated (nonpulp-exposed) or complicated (pulp-exposed) crown or crown-root fractures. The incidence of pulp necrosis after uncomplicated crown fractures is low (2% to 5%), but when there is a concomitant injury such as a luxation the chances of necrosis increases, especially in cases with a close apex (55% to 65%) compared with open apex teeth (3.5% to 11%). The traumatized dental pulp in immature or open apex teeth will have greater chances to heal and survive.

Trauma to the periradicular tissues can disrupt the neurovascular supply of the dental pulp, leading to necrosis. Severe traumatic incidents such as intrusions, lateral luxations, and avulsions result in greater incidence of pulp necrosis and resorptions. Indeed, depending on the type of luxation injury, an immature permanent tooth would become necrotic 14% to 67% of the time. If an immature permanent tooth is avulsed and replanted, the risk of pulp necrosis is as high as 77%. Therefore dental trauma is a major cause of interruption of tooth development because the dental pulp is readily infected and becomes necrotic in immature permanent teeth.

Caries

Dental caries is one of the most common infectious diseases in children and young adults, with high prevalence in the United States. ^, The National Health and Nutrition Examination Survey (NHANES) showed a decrease in its overall incidence, although 21% of children (6 to 11 years old) continue to have dental caries on permanent teeth, with 8% of children having untreated decay. Approximately 59% of adolescents (12 to 19 years old) and 92% of adults (20 to 64 years old) have dental caries in their permanent teeth. Untreated decay affects 20% of adolescents and 26% of adults. The incidence and rate of progression of dental caries are multifactorial, depending on genetics, diet, and oral hygiene habits. The lack of prompt treatment for carious lesions and/or the resulting microleakage from defective restorations leads to pulpitis, which can eventually progress to pulp necrosis, periapical lesions, infection dissemination, and systemic involvement, with eventual tooth loss. Therefore early treatment is crucial to maintain the vitality of the pulp, especially in young patients with immature teeth undergoing development. In active caries lesions, it is important to differentiate the infected from affected dentin. As discusses previously, indirect or direct pulp capping procedures can be employed after adequate caries excavation, allowing for remineralization of affected dentin or formation of a new mineralized bridge.

Dental Anomalies

Dental anomalies such as dens evaginatus, dens invaginatus , or radicular lingual or palato-gingival groove are less frequent etiologic factors but can also cause pulpal necrosis. In these conditions, bacteria will have a direct access to the pulp through the malformations. Dens evaginatus, which is an occlusal tubercle formed during development by folding of inner enamel epithelium into the stellate reticulum, is most commonly found in mandibular secondary premolars. Dens evaginatus has been reported to be prevalent in 1% to 4% of Asian populations and up to 15% in Alaskan Yupik and Inupiat people and North American Indian population. Dens invaginatus, on the other hand, is formed from in-folding of the inner enamel epithelium and odontoblast layer into the pulp. The highest incidence of dens invaginatus is observed in maxillary lateral incisors, and the overall prevalence has been reported as 1% to 10%. ^{, ,} Oehlers has classified this anomaly by the degree of invagination affecting either the periodontium, pulp canal space, or both. The pulp is exposed, in the most severe cases, when the communication passes directly to the apical papilla, communicating with the apical third of the canal and giving a direct entrance for bacteria. The radicular lingual grooves, similarly to dens invaginatus, are mostly found in lateral incisors and less common in central incisors. ^,

Iatrogenic Factors

Cavity Preparation Aspects and Remaining Dentin

The blood flow to the pulp is reduced to less than half its normal rate when local anesthetics containing vasoconstrictors are used in restorative dentistry. In procedures on teeth with pulps that are already compromised, this reduction may be an additional stressor. A healthy pulp may survive episodes of ischemia lasting for 1 hour or longer. An already ischemic pulp subjected to severe injury may hemorrhage (blush) when subjected to trauma such as that associated with full crown preparation without the use of coolant. Any intervention that extends to the dentin during cavity preparation may result in some degree of injury to the odontoblasts and their processes. However, dentin matrix demineralization during the carious process of cutting and etching of the dentin during cavity preparation can lead to release of important bioactive molecules, with the consequent stimulation of reparative cellular responses in the pulp. ^, Dentin is an effective insulator; for this reason, careful cutting with adequate cooling is less likely to damage the pulp unless the thickness of the dentin between preparation and pulp is less than 1 mm. Even then, the inflammatory response may be mild ( Fig. 10.6 ). The greatest amount of frictional heat is generated during crown preparations when the pulp is particularly at risk of injury. The heat generated may also have a desiccating effect by “boiling” away dentinal tubule fluid at the dentin surface. The “blushing” of dentin during cavity or crown preparation is thought to be due to frictional heat, resulting in vascular injury (hemorrhage) in the pulp. Dentin may take on an underlying pinkish hue soon after a operative procedure, reflecting significant vascular changes that could result in the development of pulpitis. Thus crown preparation must be performed with adequate use of profuse water spray with new sharp burs and minimizing the pressure of the instrument on the tooth and the time of contact. In addition, it is imperative to establish the preoperative and postoperative pulp status through vitality testing.

Mild inflammation beneath a deep cavity preparation with adequate coolant.

Courtesy Dr. H.O. Trowbridge.

Dentin permeability increases exponentially with increasing cavity depth, because both the diameter and density of dentinal tubules also increase with cavity depth ( Fig. 10.7 ). ^, Thus the deeper the cavity, the greater the tubular surface area into which potentially toxic substances can penetrate and diffuse to the pulp. The length of the dentinal tubules beneath the cavity is also important. The farther substances diffuse, the more they are diluted and buffered by the dentinal fluid. Deeper cavity preparations sever the odontoblast processes in their region of greater length. This severing negatively affects the cell’s attempts to restore its membrane integrity and increases the risk of a cell leaking its contents.

Difference in size and number of tubules in the dentinal floor of a shallow (A) , deep (B) and cervical (C) cavity preparations.

From Trowbridge HO: Dentistry today, Dentistry 82:22, 1982.

Dental Materials

The most important characteristic of any restorative material on its effect on the pulp is its ability to form a seal that prevents the leakage of bacteria and their products onto dentin and the pulp. Cytotoxicity is another important factor to evaluate in the restorative materials, because they are composed of chemicals that have the potential to irritate the pulp. However, when these materials are placed in a cavity, the intervening dentin usually neutralizes or prevents leachable ingredients from reaching the pulp in a high enough concentration to cause injury. Materials are more toxic when they are placed directly on an exposed pulp. Cytotoxicity tests carried out on materials in vitro or in soft tissues may not predict the effect of these materials on the dental pulp. The toxicity of the individual components of a material may vary. ^, A set material may differ in toxicity from an unset material. The immediate pulpal response to a material is much less significant than the long-term response. A few days after placement, the pulp may show a strong inflammatory response. A few months later, the inflammatory response may subside, and repair occurs. A good measure of long-term response is the thickness of tertiary dentin laid down by the affected pulp ( Fig. 10.8 ). As discussed previously in this chapter, new bioactive silicate materials have been found by numerous studies to promote healing of the injured pulp by reparative and regenerative processes.

Tertiary dentin (TD) formed under a deep preparation and irritating material.

Courtesy Dr. H.O. Trowbridge.

Indirect Pulp Capping

A clinician must always first identify the etiology of the insult and reach an accurate diagnosis. In the case of caries or uncomplicated crown fractures (without pulp exposure), excavation of infected dentin and cavity disinfection must be first achieved. If possible, the pulp tissue should not be violated. This goal can be achieved by progressive removal, using caries indicator to detect contaminated dentinal tissue. It has been shown that cavity preparations with residual dentin thickness of at least 0.5 mm from the pulp could be successfully capped with a bioactive material, resulting in the desirable formation of reactionary dentin, particularly in young patients. This capping approach is called indirect pulp capping because the bioactive material does not directly contact the pulp tissue. Yet its bioactive components and high pH can neutralize bacteria ^, and their antigens and directly stimulate odontoblasts to produce reactionary tertiary dentin in the site of injury. Ideally, the bioactive materials are placed over residual healthy, uninfected dentin. However, there is evidence that residual softened dentin can be capped, still resulting in tertiary dentin and arrested progression of the disease with the use of these materials. This partial caries removal approach can be accomplished in one visit or may be followed by additional visits for excavation followed by capping, called step-wise caries excavation . ^, These conservative approaches strongly rely on the remineralization of the residual dentin and further formation of tertiary dentin by a healthy pulp. Therefore clinicians need to maintain a close follow-up to ensure that these biological goals are being achieved and that the pulp remains vital and the patient asymptomatic ( Fig. 10.9 ).

An 18-year-old male patient with asymptomatic deep caries lesions on #14 and #15 and diagnosed with reversible pulpitis and normal periapical tissues diagnosed ( A , B , and C ). Caries were removed and indirect pulp capping performed on both teeth under rubber dam isolation with Biodentine™ (Septodont, Saint-Maur-des-Fossés, France) and coronal seal with Fuji IILC (GC America), followed by an amalgam final coronal restoration ( D ). At 1-year follow-up, tooth was asymptomatic and was diagnosed with normal pulp and normal periradicular tissues ( E and F ).

Case courtesy Dr. Tatiana M. Botero, private practice, Alsip, Illinois, USA.

Direct Pulp Capping

The exposure of the pulp tissue without major contamination can happen upon mechanical exposure of the dental pulp by trauma or during cavity preparation. In this instance the pulp may be protected and its vitality maintained by immediately covering it (pulp capping) with a bioactive material and placing a restoration, thereby avoiding root canal treatment. This approach has been shown to have an excellent prognosis in incompletely formed teeth but has also been shown successful in permanent teeth with fully formed roots. However, in cases of long-standing carious exposure of the pulp, lower success rates are expected when a direct pulp-capping procedure is performed. Recently, new data on the regenerative potential of the dental pulp and the development of newer bioactive materials have broadened the effectiveness of direct pulp-capping procedures.

Pulpotomies

If the exposure is large or seriously contaminated, it may require the removal of the superficial layer of the diseased pulp (partial pulpotomy) or the entire coronal pulp to the level of the root canal orifice (pulp chamber pulpotomy). As with direct pulp capping, close follow-up is recommended to ensure that, if needed, appropriate further treatment is provided in a timely fashion ( Fig. 10.10 ).

A 16-year-old female presents to clinic with a chief complaint of pain in the upper right tooth. Tooth #3 was restored 4 months before with an occlusal composite restoration. Patient reported pain triggered by hot, cold, and chewing but she was not experiencing spontaneous pain or pain that woke her up at night ( A and B ). Vital pulp therapy was completed under rubber dam isolation. The pulp chamber was accessed, coronal pulp tissue removed, and hemostasis achieved with less than 5 minutes of a sodium hypochlorite (NaOCl)-soaked cotton pellet pressure. Biodentine™ was placed in the pulp chamber, and restoration completed with Fuji II LC and composite core build-up material (C) . Patient returned 4 weeks later with throbbing pain triggered by hot and chewing, which had started 2 weeks earlier. Nonsurgical root canal treatment was completed under rubber dam isolation, obturation completed with gutta-perch and Roth’s sealer. Tooth was restored with glass ionomer and core build-up material (D) . Patient was asymptomatic 2 months post-non-surgical root canal therapy (NSRCT).

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1. Protecting the pulp and promoting tooth maturation
2. Retreatment
3. Endodontic-periodontic interrelationship
4. Pathogenesis of Pulp and Periapical Diseases
5. Endodontic Armamentarium
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