10 Dentin-pulp complex development

• Overview
• Dentinogenesis
  • Induction
  • Apposition
  • Maturation
  • Types of dentin
• Clinical considerations of dentinogenesis
• Pulp
  • Anatomy
  • Microscopic features
• Clinical considerations of pulp

Overview

Dentin and pulp are covered together because of their shared lineage: they are derived from the neuro-mesenchyme of the dental papilla. Dentin resembles enamel chemically. But don’t focus too much on chemical composition by weight. Humans are made up of  mostly the same atoms as thalidomide— the morphology of those atoms matters! By the end of this chapter you should see similarities between dentin and pulp. The two are often referred together as the dentin-pulp complex.

One important concept in this chapter involve the cells in (or near) dentin. The ECM of dentin contains long tunnels filled with fluid and cytoplasmic extensions of dentin-producing cells, the odontoblasts. These are significant when it comes to dental hypersensitivity, as well as in the repair of dentin following damage.

Another major concept involves focusing on the ECM of dentin. Like the formation of enamel matrix, studying how dentin matrix is formed teaches us about how it can be repaired. Unlike enamel, dentin can be repaired by cellular activity after eruption. As a result, dentin comes in forms made before birth, shortly after birth, and long after birth. Before you get too comfortable thinking that means there are only 3 types of dentin, be aware there are multiple forms made both before and after birth. Enamel only comes in one form: the stuff made during the embryonic period.

Dentin formation

Dentinogenesis is the process of dentin formation (and should not be confused with the word odontogenesis). Dentinogenesis begins during the bell stage of tooth development. Odontoblasts (arrows in Fig. 10.2) are the cells that produce dentin. The first step is the secretion of proteins, including collagen^←, which act as a scaffold^←. The second step is mineralization around the scaffold. The initial protein-rich material is pre-dentin (P in Fig. 10.2), after it mineralizes it is called dentin (D in Fig. 10.2). Unlike amelogenesis, there is no third step of protein removal (remodeling).

Induction (or initiation)

During the induction phase, the odontoblasts appear. This happens in the bell stage of tooth development, as the enamel organ  grows around the dental papilla. Cells of the IEE differentiate^← into pre-ameloblasts and secrete morphogens^←, including BMP. The closest neuro-mesenchymal stem cells of the dental papilla receive BMP morphogens and differentiate into odontoblasts. Odontoblast differentiation involves a morphological change. The amorphous neuro-mesenchymal stem cells line up, forming what looks like a simple cuboidal epithelium^←, complete with apical-to-basal polarity^←. This sort of polarization is unusual for a connective tissue. Odontoblasts, however,  are not derived from mesoderm, they are derived from neuro-mesenchyme. It is common for neurons and glial cells to be polarized, and odontoblasts share this morphology. Inside odontoblasts, large amounts of rER^← and Golgi apparatus^← are forming in preparation for the secretion of large amounts of protein.

Apposition

Newly formed odontoblasts begin secreting proteins that act as a scaffold^←. This scaffold guides the mineralization of dentin. The initial protein-rich substance is pre-dentin (lighter blue layer in Fig. 10.4). It is mostly collagen^← plus a few other dentin-specific proteins. Pre-dentin mineralizes later. Calcium and phosphate react in pre-dentin to form calcium hydroxyapatite crystals, similar to enamel and bone tissue^← (darker blue layer in Fig 10.4). As layers of dentin mineralize, odontoblasts continue secreting new pre-dentin, pushing the layer of odontoblast cell bodies deeper into the jaw (Fig. 10.3). Unlike ameloblasts, odontoblasts leave behind an odontoblastic process in the dentin they secrete. This arm-like extension contacts nearly every layer of dentin that odontoblast creates. Because dentin mineralizes around the odontoblastic process, a dentinal tubule runs through nearly the entire length of dentin. If you removed the odontoblasts, dentin would be perforated by millions of hollow tubes (Fig. 10.8).

Collagen^← and dentin-specific proteins are secreted by the side of the odontoblast cell body facing the enamel (yellow vesicles, Fig 10.4). This ensures the cell body does not get cemented in place by hard dentin, and instead always touches a thin layer of gelatinous pre-dentin. Glycoproteins and enzymes like matrix metalloproteinase are secreted a short distance up the odontoblastic process (less than 1 mm, brown vesicles in Fig. 10.4) which trigger mineralization of dentin. This traps the odontoblastic process within mineralized dentin, but leaves the cell body free to move.

Figure 10.5: Histology of the dentin-enamel junction, with an enamel tuft indicated (pink arrow). Image credit: "Histologic cross-section of tooth showing enamel, labeled A, and dentin, labeled B." by Dozenist is licensed under CC BY-SA 3.0 / cropped and arrow added

A few odontoblastic processes  extend past the DEJ. They become trapped in enamel after amelogenesis begins (which  happens after dentinogenesis). These are known as enamel spindles. Both enamel spindles, and the bushier-looking enamel tufts (Fig. 10.5) are referred to as hypo-mineralized regions or defects in enamel. There is something important missing in those descriptions, however. Teeth that exert more force have more enamel tufts (such as human molars, or the teeth of animals who eat nuts), suggesting enamel tufts strengthen enamel. It is not impossible for enamel spindles and tufts to both be less mineralized and increase the strength of enamel. Recall how hard but brittle calcium hydroxyapatite crystals of bone tissue^← are strengthened by the flexible protein collagen^←. It is also attractive to hypothesize enamel spindles and tufts act similar to the interdigitation of rete pegs^← and dermal papillae^← in the skin and oral mucosa.

Dentin mineralizes in one of two ways: in globs or in lines. The first dentin produced mineralizes in globs because extra-large collagen^← fibers are secreted in spheres (there are older theories of what spherical globs are made of).  Around the collagen globs, pre-dentin mineralize into mature dentin. Some regions do not mineralize fully, and are called inter-globular dentin. The fully mineralized dentin found between inter-globular dentin is globular dentin. Globular and inter-globular dentin are visible between mantle dentin and circum-pulpal dentin (see below). Low levels of phosphate during the first trimester can increase the amount of inter-globular dentin.

After the first collagen fibers are secreted in globs, fibers are lengthened by odontoblasts. This dentin mineralizes more uniformly, one layer at a time, in a process called linear mineralization. In regions that mineralize linearly, collagen fibers run parallel to each other, but perpendicular to the dentinal tubules. Only after linear mineralization begins do odontoblasts leave behind an odontoblastic process.

The lines that should be clearly visible in the layer of dentin in Fig. 10.6 are dentinal tubules, the tubes in which the odontoblastic process are found. Notice that they do not run in a straight line. Odontoblasts, like ameloblasts, move in a slightly curved direction as they produce ECM. Like the curves you see on most bridges, this curvature is no accident. Curves increase the strength of dentin. The large curves are called the primary curvature. If you zoomed out you would see the primary curvature has a sinusoidal (S) shape. The curvature is more pronounced in the crown than the root. If you zoomed in on a single odontoblastic process, you might see areas where it briefly curves opposite of the primary curvature. That is called a secondary curvature. In contrast, the bending of enamel rods has no names for bigger or smaller curves.

Similar to the formation of enamel, odontoblasts undergo daily patterns of faster and slower pre-dentin deposition. As a result, light and dark bands are visible in dentin, called the Imbrication lines of Von Ebner (or the incremental lines of Von Ebner). The Imbrication lines of Von Ebner are comparable to the Lines of Retzius in enamel. Don’t ask how Retzius discovered lines in enamel but missed the same pattern in dentin a few millimeters away, leaving it to Von Ebner to name a hundred years later. People get credited for re-discovering things all the time. These should both be renamed incremental lines in enamel and the incremental lines in dentin, anyway. Furthermore, prominent imbrication lines can be called contour lines of Owen. This includes the neonatal line, similar to the one found in enamel. These represent big changes in nutrition that lead to changes in the density of dentin produced that day. You can read part of Owen’s treatise on the comparative anatomy of the tooth, someone scanned 30 pages if you are curious about what it was like to learn histology without pictures.

Maturation

Unlike enamel, dentin does not undergo significant changes after it mineralizes. As a result, some textbooks call the mineralization of pre-dentin into dentin as the “maturation” step, while others (including this one) have chosen to use the words apposition and maturation consistently. Why do ameloblasts take an extra step removing some scaffolding^← after mineralization occurs, and odontoblasts do not? One possibility is ameloblasts are epithelial cells, and epithelia generally secrete very little ECM. Perhaps they are not very good at it. In contrast, odontoblasts differentiate^← from neuro-mesenchymal stem cells. It is likely during their epithelial-to-mesenchymal transition^← they unpack genes that make them efficient at creating ECM. A second possibility is that the high percentage of minerals in mature enamel (96%) can only occur after protein scaffolding is removed. Remember, calcium and phosphate react to form crystals on their own, but to get these crystals to adopt the morphology of a tooth requires scaffolds. The reason is not as important as the illustration of another difference between enamel and dentin due to their different cell lineages.

Classification of dentin

In Fig. 10.8, dentinal tubules should be easily visible. In a living tooth, each tubule contains an odontoblastic process. Not all regions of dentin are the same, and there are several ways of classifying different types of dentin. One way to classify different types of dentin is based on how close the dentin is to a dentinal tubule. The thin white area of dentin immediately surrounding each dentinal tubule is called peri-tubular dentin, while the rest is inter-tubular dentin. Despite a similarity in names, this is not homologous to rod enamel and inter-rod enamel.

Another way to classify types of dentin is on its location relative to the pulp cavity. Mantle dentin develops first. It is a thin layer (15 to 30 μm) next to enamel (therefore, only in the crown). Mantle dentin contains few dentinal tubules, they are filled in during the maturation stage. Mantle dentin is where globular mineralization occurs. The globular dentin mineralizes and fuses together, creating a uniform appearance. Just below mantle dentin is where you find crescents of inter-globular dentin between globular dentin. Got that? If not, see Fig. 10.6. Mantle dentin is thought to be different from other dentin because it is here that odontoblasts first begin secreting proteins (near the DEJ), at which time the odontoblasts aren’t fully mature.  The collagen^← fibers that remain in mantle dentin run perpendicular to the DEJ. The rest of the dentin (in both the crown and roots) is circum-pulpal dentin, which mineralizes linearly, leaving dentinal tubules intact. Collagen fibers run parallel to the DEJ in circum-pulpal dentin. Mantle and circum-pulpal dentin have slightly different levels of mineralization and protein content. Mantle dentin is more elastic, which provides a cushioning effect for the enamel above (like a yoga mat).

Yet another way to classify dentin is based on when it is formed relative to the apical foramen. If this seems redundant to mantle dentin versus circum-pulpal dentin, you are mostly right. Primary dentin is the dentin formed before completion of the apical foramen, therefore it is formed prior to tooth eruption^←. Secondary dentin is formed after the completion of the apical foramen (after tooth eruption). Unlike mantle versus circum-pulpal dentin, there are no major histological differences between primary and secondary dentin.

Much later, a tooth may suffer damage and new forms of dentin are produced to repair the injury. Odontoblasts can produce tertiary dentin and repair small amounts of damage. Tertiary dentin produced by the original odontoblasts (still in the pulp) is called reactionary dentin (or sclerotic dentin). Formation of this form of dentin involves secretion of matrix metalloproteinases from dentinal tubules. These enzymes are also used during the formation of dentin during embryogenesis. Therefore, this is another example of how wound repair recapitulates embryonic development. During embryogenesis, however, dentin is formed appositionally. Reactionary dentin mineralization occurs within dentinal tubules, causing the tubules to become occluded (to become blocked). Therefore, fewer dentinal tubules are found in reactionary dentin. Furthermore, it is the parallel dentinal tubules that give primary and secondary dentin their yellow-ish hue. With reduced or no tubules, reactionary dentin becomes more translucent (see Fig 10.11).

If a large enough injury occurs as to expose the pulp chamber, destroying odontoblasts, a much more robust response is needed. First, new odontoblasts are needed, but how can we get new odontoblasts without morphogens from pre-ameloblasts? The answer is pretty cool: there is a backup system. Mesenchymal stem cells in the pulp differentiate into odontoblasts when they come into contact with a dentin-specific protein (not collagen^←, but a molecule called dentin sialoprotein 2). This does not happen in a healthy tooth because odontoblast cell bodies are a barrier between dentin sialoprotein 2 and  pulp mesenchymal stem cells. When those odontoblasts die (as long as there is some pulp left), new odontoblasts are induced to differentiate. The new odontoblasts form a type of tertiary dentin called reparative dentin. Reparative dentin does not form the same way dentin does during development. Dentinogenesis began at the DEJ, and layers of dentin were added appositionally, towards the pulp chamber.  To form reparative dentin, odontoblasts and fibroblasts start from the pulp chamber, migrate throughout the injured area (after a hematoma forms) and secrete proteins and electrolytes. No dentinal tubules are created, these new odontoblasts secrete dentin in all directions. Some of the odontoblasts and fibroblasts become trapped within the ECM. For this reason, reparative dentin is sometimes referred to as osteodentin, because it resembles bone tissue^← under the microscope more than it does tubular dentin. In fact, osteodentin may represent the phylogeny of dentin. The teeth of some species (such as eels) and the fossils of our ancient ancestors' teeth is made of osteodentin, not mantle or peri-tubular dentin.

Root dentin

Roots do not contain mantle dentin, but they do contain a superficial layer of dentin that is visually distinct from the circum-pulpal dentin. Close to the border with cementum, spots are visible in a band of dentin known as Tomes’ granular layer. This layer has no known clinical significance. It is useful for orienting yourself when looking at histological sections of teeth. Those grain are not the nucleuses of cells. Older data suggested the grains are loops of dentinal tubules, but re-analysis using more advanced microscopes suggests the grains are loops of collagen^← fibers. This suggests they are similar to globular dentin. Whatever the cause of the granulations is, the important concept to remember is the order of events in root formation. Odontoblasts are less mature (newer) when they are secreting dentin in Tome’s granular layer than when they are closer to the root canal, similar to globular dentin formation in the mantle region of the crown.

Clinical considerations of dentinogenesis

Mineral aggregates

If there is a large amount of damage to dentin, the production of tertiary dentin may be too slow. When treating root resorption, or for root end filling during endodontic therapy, artificial ECM can be used. Unlike some of the artificial tissues discussed in gingival healing, solid crystals do not make good scaffolds^←. The goal is to mimic something more gelatinous like pre-dentin, not crystalline dentin, whose dense matrix would inhibit migration of stem cells. Mineral aggregates provide the necessary materials required by odontoblasts without inhibiting their movement during dentinogenesis. One such compound, Mineral Trioxide Aggregate (MTA), was developed in California by Dr. Mahmoud Torabinejad. MTA contains a purified version of Portland cement plus calcium-containing minerals. The addition of mineral aggregates speeds up the formation of tertiary dentin. MTA slowly releases calcium hydroxide, which provides a raw material for mineralization of tertiary dentin, as well as attracting phosphate from the blood or ECF. Author’s note: Portland cement was invented in Portland, England. Do not apply Portland cement from your hardware store to teeth, it is caustic and may contain arsenic or other heavy metals. The Portland cement used in dentistry is highly purified.

In one type of dental restoration (a tooth filling), a wet resin is bonded (glued) to dentin and hardened using a special light. To bond a resin to dentin, one should take into account the chemical structure of dentin. Dentin ECM contains calcium hydroxyapatite crystals, collagen^← and other proteins, plus water molecules. The water molecules, along with collagen, allow dentin to bend and compress in response to stress, as opposed to harder enamel which resists stress (summarized in Table 8.3). Water molecules  give dentin a moist appearance. Many bonding agents do not adhere well to a wet surface, and require dentin to be dried first. This is usually done with a volatile solvent such as ethanol. Mineral acids may be used to remove an amount of the mineral ECM of dentin, leaving behind the more porous collagen framework. This can improve bonding, somewhat similar to acid-etching of enamel. However, acid etching took advantage of the mineral differences between rod and inter-rod enamel. There is not enough of a difference between peri-tubular and inter-tubular dentin, both lose minerals when mineral acids are applied.

There is interest in the research community for developing bonding agents that adhere to wet surfaces (all living human tissues are wet). One promising area is the study of mollusk mucus. Mucus is secreted from the body, but it is similar to ground substance^← in human connective tissues, especially mesenchyme^←. Mucus secreted by limpets adheres to wet surfaces with great strength, and it stimulates tertiary dentin formation (link to pdf download). One of the most abundant molecules in mucus is hyaluronic acid (a major component of ground substance).

Lastly, bonding agents typically adhere to primary and secondary dentin more readily, because of the higher degree of surface area from dentinal tubules. In contrast, bonding agents do not adhere as well to tertiary dentin, where tubules are filled in or never form.

Morphogens

The formation of tertiary dentin requires morphogens^← to induce the differentiation^← of mesenchymal stem cells into new odontoblasts. As more is learned about these morphogens, it opens up the possibility to administer  morphogens to speed up natural healing processes, potentially reducing the need for inorganic cements or caps. One such morphogen is a Wnt. In the brain, Wnts induce the differentiation of neural crest cells^← into specific types of neurons and glia. But when neural crest cells migrate to the face and become parts of the pharyngeal arches^←, the same Wnt induces them to differentiate^← into odontoblasts. The difference arises because of a second morphogen. This second signal comes from the ECM, and ECM is very different in the developing brain than it is in developing neuro-mesenchyme of the pharyngeal arches. The significance of this is that a drug used to treat Alzheimer’s Disease (AD) [Tideglusib is used off-label in dentistry to boost tooth repair. We suspect it is very rare to randomly test psychoactive drugs for their use in dentistry. Prior knowledge of shared lineages, however, makes new avenues of treatment more obvious.]

Attrition and erosion

Because dentin has a lower mineral content than enamel, dentin erodes more quickly than enamel. If mantle dentin is lost, this exposes dentinal tubules in the underlying circum-pulpal dentin. Exposed tubules increases the surface area for acids to dissolve calcium hydroxyapatite crystals, speeding up dentin erosion. Surface exposure of dentinal tubules also leads to increased sensitivity of the teeth (see below).

Dentin caries

Once dental caries spread through enamel and reaches the DEJ, it spreads at an increased rate. The triangle pattern of enamel loss is quickly repeated in a new triangle of dentin caries. It is possible, but not agreed upon, that a small enough enamel caries might spread to the DEJ without causing changes visible at the surface, and upon reaching the DEJ the rate of tooth loss accelerates. Whatever the exact cause, caries can start below enamel and spread through dentin. This hidden caries is harder to detect than one at the surface of a tooth.

Dentin hypersensitivity

The loss of enamel or cementum covering dentin may expose dentinal tubules. In the crown, the few millimeters of mantle dentin at the outer surface contain few open dentinal tubules. But if enamel and mantle dentin are lost,  tubules in the circum-pulpal dentin are exposed. These tubules extend to the root pulp, where nerve endings are located. Changes in the environment of the oral cavity, including the temperature, pH, alcohol level or osmotic concentration, now affect the temperature, pH, alcohol level or osmotic concentration of the pulp ECF. There is a small amount of ECF between the odontoblastic process and peritubular dentin (dentinal fluid). Changes to the chemical composition of this ECF can be detected by nerve endings, which in turn relay painful stimuli to the brain. This can be called tooth, root, cervical or cemental  hypersensitivity, but it is more accurate to call it dentin hypersensitivity . Treatments for dentinal hypersensitivity include special toothpastes, mouthwashes or chewing gums that deposit minerals into exposed dentinal tubules and occlude them. Such products likely contain salts and fluoride. Alternately, varnish mineral aggregates such as Portland cement might be applied to the affected area. Conversely, with age, odontoblasts add layers of peri-tubular dentin inside dentinal tubules, causing the tubules to become narrower. As this happens, teeth become less sensitive. This may not sound so bad until you take into consideration the role that proprioception has in preventing excessive occlusal forces. Cranial nerve V is one of the larger cranial nerve, it transmits a lot of important sensory information to the brain from the teeth. With diminished sensitivity comes an increased risk of occlusal trauma.

Figure 10.20: The importance of proper dental hygiene procedures. Image credit: “Dental details” by Senior Airman Kristi Emler, US Air Force is in the Public Domain, CC0

Dentin may become exposed due to loss of cementum or enamel, or if the edge of enamel does not meet/overlap cementum. Furthermore, gingival recession exposes the thin layer of cementum to environments it is not designed to handle, making dentin exposure along the neck of the tooth the most likely area for dentinal hypersensitivity. Improper technique on the part of dental hygienists or dentists may inadvertently remove protective layers of cementum as well. 

Dentin resorption

During exfoliation of primary teeth, dentin resorption (the loss of dentin due to cell-mediated demineralization) assists in the loss of attachment between the tooth root and alveolar bone. This is mediated by odontoclasts. Odontoclasts are related to osteoclasts. Osteoclasts have baseline activity throughout life maintaining bone tissue as part of a remodeling unit^←. Odontoclasts, on the other hand, are not always present, their differentiation from mesenchymal stem cells as well as their activity is  regulated by different morphogens^←. Dentin resorption occurring at any time other than the shedding of primary teeth is idiopathic (of unknown cause). We do understand that the dentinal tubules found throughout dentin create a large amount of surface area for odontoclasts to adhere to and trigger demineralizion. This is similar to what we observe in spongy bone: spongy bone is lost at a faster rate than compact bone because it has a higher amount of surface area (thus symptoms of osteoporosis appear first in bones with higher amounts of spongy bone, like the mandible).

Dentin resorption  triggered from the pulp-cavity side is referred to as internal resorption. Conversely, external resorption occurs from the DEJ or CEJ side.

Dentinogenesis Imperfecta

A mutation in the gene for one of the dentin-specific proteins (dentin sialophosphoprotein) leads to a genetic condition known as dentinogenesis imperfecta (types II and III). In this condition, the dentinal tubules are wider than normal. This in turn alters the color of dentin, causing teeth to appear more grey or bluish (similar to how reactionary dentin has a different color from healthy dentin because it lacks dentinal tubules). Unlike amelogenesis imperfecta, the teeth of people with dentinogenesis imperfecta do not have a higher susceptibility to dental caries. The teeth are weaker than normal, and are more prone to fracture and loss. The lack of one scaffold^← protein leads to reduced dentin mineralization. Reduced mineralization leads to higher levels of inter-globular dentin.

Mutation to the gene for type I collagen^← leads to a condition called osteogenesis imperfecta, or brittle bone disease. About 50% of people with osteogenesis imperfecta have dentinogeneis imperfecta (type I). These individuals have the dentin sialophosphoprotein, but the defect in collagen leads to brittle dentin.

Pulp overview

The dentin and pulp both develop from neuro-mesenchymal stem cells of the dental papilla. Odontoblasts make a specialized tissue, containing just one terminally differentiated cell type. The rest of the neuro-mesenchymal cells make  areolar connective tissue^←, which contains numerous cell types, including adult stem cells. It is here that blood vessels, nerve fibers and lymphatic vessels have space and structural support.

Histology of pulp

Pulp can be divided into coronal pulp and radicular pulp. The coronal pulp is in the crown of the tooth and contains smaller pulp horns beneath the cusps. Radicular pulp is in the roots, and may extend into accessory canals. Accessory canals connect the pulp to connective tissue external to the tooth, traveling laterally rather than out the apical foramen. Accessory canals form when HERS runs into a blood vessel and is forced to grow around it. Otherwise, radicular pulp terminates at the apical foramen.

Pulp layers

Pulp is a single tissue, but there are four layers that look different from one another under a microscope. The first is the odontoblast layer, which is closest to the dentin. Odontoblasts initially form a single layer of cells along the broad region of the DEJ. But as they add dentin, the pulp cavity becomes smaller. As the pulp cavity becomes smaller, odontoblast cell bodies crowd together, ultimately forming a thicker layer of cell bodies at the edge of the pulp cavity. Deep to the odontoblasts is what is called the cell-free zone. This zone contains cells, but they are not visible under a traditional H&E stain. Deep to that is a cell-rich zone, composed primarily of fibroblasts, mesenchymal stem cells, white blood cells and other connective tissue cells. Lastly is the pulp core, which contains the same types of cells, but more ground substance^← spaces them apart. The pulp core is where most of the larger blood and lymphatic vessels are located.

Clinical considerations of pulp

Periapical abscess

If damage to dentin exposes pulp to oral bacteria, an infection of the pulp may occur. This usually triggers inflammation of pulp tissue, known as pulpitis. Death of pulp tissue can lead to accumulation of pus around the roots, which is called a periapical abscess. The release of inflammatory molecules from damaged tissue can lead to swelling of the overlying gingival tissue, often referred to as a gum  boil. Less commonly, a gum boil may also form due to an infection of periodontal tissues, in which case it is not a periapical abscess, it is a periodontal abscess. It is possible to remove necrotic pulp surgically. If some healthy pulp remains, regeneration of the pulp may occur. This is because of the high degree of vascularization of areolar connective tissue^← and the high mitotic potential of mesenchymal stem cells.

Endodontic therapy

A periapical abscess likely requires the removal of the infected pulp tissue and replacement by a bio-compatible material that is similar in density and elasticity. This  procedure is known as endodontic therapy. The preferred material used is gutta-percha, a naturally-occurring latex polymer from the sap of trees in Malaysia. It was once widely used as an insulator for electronics, but has been replaced by synthetic polymers, except in endodontic therapy. It is radiopaque because of an additive, barium sulfate. Otherwise, latex does not show on radiographs, which would make it difficult to confirm gutta percha had completely filled the pulp cavity.

Removal of living pulp tissue removes all cells from the tooth, including odontoblasts. This tooth is referred to as non-vital. A non-vital tooth cannot make repairs to dentin, which leads to increased brittleness and the accumulation of stains over time. Stain molecules may invade from the enamel side down dentinal tubules, or molecules from pulp necrosis may invade dentin by traveling up dentinal tubules.

Pulp vitality testing

Painful stimuli at the surface of the teeth are detected by nerve endings located within the pulp. Pulp vitality testing (or pulp sensitivity testing) takes advantage of this to estimate the health of the tooth pulp. An electrical stimulus is applied at the surface of teeth followed by self-reporting of the discomfort level experienced by the patient. Loss of nerve endings reduces tooth sensitivity, and indicates pulp tissue has undergone fibrosis or necrosis. However, a reduction in the diameter of dentinal tubules also reduces the ability of electrical signals at the surface to be detected within the pulp. Conversely, loss of enamel and exposure of dentinal tubules may increase sensitivity without any changes to pulp vitality.

Because different patients report pain differently, and because factors besides the health of the pulp affect the degree of discomfort reported, false-positive and false-negative results are possible with pulp vitality testing. Other less-invasive tests exist, including pulse oximetry and laser doppler flowmetry. These measure the vascular supply to each tooth, which correlates with the vitality of the tooth. Pulse oximetry takes advantage of the color change hemoglobin undergoes as it picks up oxygen. Laser doppler flowmetry takes advantage of the doppler shift waves exhibit when they bounces off moving objects (such as flowing red blood cells) but not stationary ones– similar to the way the sound of a motorcycle changes pitch when it is rapidly travelling toward you or away from you.

Age-related changes

Because a vital tooth contains a layer of living odontoblasts, dentin becomes gradually thicker with age. This is most noticeable in the fine pulp horns, which recede with age. Couteracting this, as with many cells, the mitotic ability of mesenchymal stem cells within the pulp decreases with age. As a result, older pulp tends to contain more scar tissue (cross-linked collagen^← fibers) and has decreased regenerative capability and diminished sensitivity.

Pulp stones

Elsewhere in the body, damage to connective tissue may lead to the formation of scar tissue. In the pulp, however, the presence of odontoblasts causes scar tissue to mineralize. The formation of calcified scar tissue is a rare condition known as Dystrophic calcification elsewhere in the body, but is common in pulp. Localized regions of calcification in pulp are called pulp stones (or denticles). These occur in both radicular pulp and coronal pulp. The major clincal significance of pulp stones is they may  complicate endodontic therapy. Pulp stones can not only be found in pulp (free), they also appear on dentin (adherent) and within dentin (embedded).

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