10 Dentin-pulp complex development

animation of dentinal hypersensitivity
Figure 10.1: Illustration of dentinal tubules. Order of appearance: odontoblasts, nerve endings, overlying gingiva and enamel.


Dentin and pulp are covered together because of their shared : they are derived from the of the . 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 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 .

One important concept in this chapter involve the cells in (or near) dentin. The of dentin contains long tunnels filled with fluid and cytoplasmic extensions of dentin-producing cells, the . 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.

histology of dentin-pulp interface
Figure 10.2: Important regions during dentinogenesis (developing tooth). Legend: P = pre-dentin, D = mature dentin, arrows = cell bodies of odontoblasts found at the edge of the pulp. Image credit: "Histological section of tooth" by Doc. RNDr. Josef Reischig, CSc. is licensed under CC BY-SA 3.0 / labels added

Dentin formation

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

animation of amelogenesis and dentinogenesis
Figure 10.3: Animated view of amelogenesis and dentinogenesis.

Induction (or initiation)

During the phase, the appear. This happens in the of tooth , as the   grows around the . Cells of the into and secrete , including . The closest of the dental papilla receive BMP morphogens and differentiate into odontoblasts. Odontoblast differentiation involves a change. The neuro-mesenchymal stem cells line up, forming what looks like a , complete with . This sort of polarization is unusual for a connective tissue. Odontoblasts, however,  are not derived from , they are derived from . It is common for neurons and glial cells to be polarized, and odontoblasts share this morphology. Inside odontoblasts, large amounts of and are forming in preparation for the secretion of large amounts of protein.

Figure 10.4: Polarization of odontoblasts, including cell-to-cell junctions that trigger activation of genes for proteins secreted into dentin. Legend: Green = cell-cell junctions help establish cell polarity by triggering intra-cellular signals. Yellow= secretion of collagen-filled vesicles to form pre-dentin (light blue layer) occurs at the apical surface of the cell body. Brown = secretion of enzyme-filled vesicles from the odontoblastic process triggers mineralization of pre-dentin into dentin (darker blue layer). Pink = pulp.


Newly formed begin secreting proteins that act as a . This scaffold guides the mineralization of dentin. The initial protein-rich substance is (lighter blue layer in Fig. 10.4). It is mostly plus a few other dentin-specific proteins. Pre-dentin mineralizes later. Calcium and phosphate react in pre-dentin to form crystals, similar to enamel and (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 , odontoblasts leave behind an 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 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).

and dentin-specific proteins are secreted by the side of the odontoblast cell body facing the enamel (yellow , 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 . and enzymes like are secreted a short distance up the (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.

histology of the dentin-enamel junction

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   extend past the . They become trapped in enamel after begins (which  happens after ). These are known as . Both enamel spindles, and the bushier-looking (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 crystals of are strengthened by the flexible protein . It is also attractive to hypothesize enamel spindles and tufts act similar to the interdigitation of and in the skin and .

histology of DEJ
Figure 10.6: Inter-globular dentin (arrowhead) in an adult tooth. Image credit: "Figure 1a" by Monaogna Vangala is licensed under CC BY-SA 3.0 / labels added

Dentin mineralizes in one of two ways: in globs or in lines. The first dentin produced mineralizes in globs because extra-large fibers are secreted in spheres (there are older theories of what spherical globs are made of).  Around the collagen globs, mineralize into mature dentin. Some regions do not mineralize fully, and are called . The fully mineralized dentin found between inter-globular dentin is . Globular and inter-globular dentin are visible between and (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 . This dentin mineralizes more uniformly, one layer at a time, in a process called . 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 .

The lines that should be clearly visible in the layer of dentin in Fig. 10.6 are , the tubes in which the are found. Notice that they do not run in a straight line. , like , move in a slightly curved direction as they produce . 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 . 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 . In contrast, the bending of enamel rods has no names for bigger or smaller curves.

Histology of dentin pulp
Figure 10.7: Imbrication (incremental) lines of Von Ebner. Image credit “histological section of tooth” by Doc. RNDr. Josef Reischig, CSc. is licensed under CC BY-SA 3.0 /animations added

Similar to the formation of enamel, undergo daily patterns of faster and slower deposition. As a result, light and dark bands are visible in dentin, called the (or the incremental lines of Von Ebner). The Imbrication lines of Von Ebner are comparable to the 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 . 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.


Unlike enamel, dentin does not undergo significant changes after it mineralizes. As a result, some textbooks call the mineralization of into dentin as the “maturation” step, while others (including this one) have chosen to use the words apposition and maturation consistently. Why do take an extra step removing some after mineralization occurs, and do not? One possibility is ameloblasts are epithelial cells, and epithelia generally secrete very little . Perhaps they are not very good at it. In contrast, odontoblasts from . It is likely during their they unpack 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 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 .

Classification of dentin

electron micrograph of dentinal tubules
Figure 10.8: Dentinal tubules without odontoblastic processes. Image credit: “Dentinal tubule occlusion of dentine discs after treatment” by Peiyan Yuan is licensed under CC BY-SA 3.0 / cropped and animated labels added

In Fig. 10.8, should be easily visible. In a living tooth, each tubule contains an . 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 , while the rest is . Despite a similarity in names, this is not to and .

animated illustration of type of dentin
Figure 10.9: Types of dentin by location. Image credit: "cross sections of teeth" by Gorak Tek-en is licensed under CC BY 3.0 / animation and text added

Another way to classify types of dentin is on its location relative to the pulp cavity. first. It is a thin layer (15 to 30 μm) next to enamel (therefore, only in the crown). Mantle dentin contains few , they are filled in during the maturation stage. Mantle dentin is where globular mineralization occurs. The mineralizes and fuses together, creating a uniform appearance. Just below mantle dentin is where you find crescents of 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 first begin secreting proteins (near the ), at which time the odontoblasts aren’t fully mature.  The fibers that remain in mantle dentin run perpendicular to the DEJ. The rest of the dentin (in both the crown and roots) is , which mineralizes , 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).

animation of types of dentin
Figure 10.10: Types of dentin by time of production. Original image "cross sections of teeth" by Gorak Tek-en is licensed under CC BY 3.0 / animation and text added

Yet another way to classify dentin is based on when it is formed relative to the apical foramen. If this seems redundant to versus , you are mostly right. is the dentin formed before completion of the apical foramen, therefore it is formed prior to . 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.

scientific image of sclerotic dentin
Figure 10.11: Sclerotic dentin (S). Note how loss of dentinal tubules affects how light pases through sclerotic versus healthy dentin. Image credits "Stereomicroscope image (5X) of tooth with measurement of Sclerotic Dentin Area (S) and Length of Sclerotic Dentin (SL)" by Selvamani M, et al, Journal of International Oral Health is licensed under CC BY-SA 4.0 / cropped

Much later, a tooth may suffer damage and new forms of dentin are produced to repair the injury. can produce and repair small amounts of damage. Tertiary dentin produced by the original odontoblasts (still in the pulp) is called (or sclerotic dentin). Formation of this form of dentin involves secretion of from . These enzymes are also used during the formation of dentin during embryogenesis. Therefore, this is another example of how wound repair embryonic . During embryogenesis, however, dentin is formed . 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).

histology of osteodentin
Figure 10.12: Osteodentin (arrow) inside of the pulp cavity. Image credits "Tooth, Pulp - Osteodentin in a male F344/N rat from a chronic study" by Cora MC, Travlos GS, at the National Toxicology Program is in the Public Domain, CC0

If a large enough injury occurs as to expose the pulp chamber, destroying , a much more robust response is needed. First, new odontoblasts are needed, but how can we get new odontoblasts without from ? The answer is pretty cool: there is a backup system. in the pulp into odontoblasts when they come into contact with a dentin-specific protein (not , 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 to differentiate. The new odontoblasts form a type of tertiary dentin called . Reparative dentin does not form the same way dentin does during . began at the , and layers of dentin were added , towards the pulp chamber.  To form reparative dentin, odontoblasts and start from the pulp chamber, migrate throughout the injured area (after a hematoma forms) and secrete proteins and electrolytes. No are created, these new odontoblasts secrete dentin in all directions. Some of the odontoblasts and fibroblasts become trapped within the . For this reason, reparative dentin is sometimes referred to as , because it resembles under the microscope more than it does tubular dentin. In fact, osteodentin may represent the 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.

Table 10.1: Summary of the types of dentin.
Type of dentin Location Features
Peri-tubular Walls of tubules Found in circum-pulpal dentin
Inter-tubular Between walls Found in circum-pulpal dentin
Mantle Thin border next to DEJ

No tubules

Collagen perpendicular to DEJ

Circum-pulpal Rest of tooth


Collagen parallel to DEJ

Primary Formed before apical foramen

Made by original odontoblasts

Contains tubules

Secondary Formed after apical foramen



Formed after injury

Made by original odontoblasts

Tubules filled in

Reparative Formed after large injury

Made by new odontoblasts and fibroblasts

Cell trapped in calcified tissue (osteodentin)

No tubules form

histology of Tomes' granular layer
Figure 10.13: Tomes’  granular layer (arrow) found in root dentin (D), just deep to cementum (C). image credit “Tomes granular layer" by Shaik Mohamed Shamsudeen is licensed under CC BY-SA 3.0 / letters and arrow added

Root dentin

Roots do not contain , but they do contain a superficial layer of dentin that is visually distinct from the . Close to the border with cementum, spots are visible in a band of dentin known as . 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 fibers. This suggests they are similar to . 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

elctronc micrograph of MTA and dentin
Figure 10.14: Electron micrograph of the interface between dentin and a mineral aggregate (MTA) used in the a root canal therapy to boost replacement of resorbed root dentin. Image credit: “Scanning electron microscopic images that are representative of the root canal dentin and mineral trioxide aggregate (MTA) interface by Yoo, Yeon Gee et al is licensed under CC BY 3.0

Mineral aggregates

If there is a large amount of damage to dentin, the production of may be too slow. When treating root resorption, or for root end filling during , artificial can be used. Unlike some of the artificial tissues discussed in gingival healing, solid crystals do not make good . The goal is to mimic something more gelatinous like , not crystalline dentin, whose dense matrix would inhibit migration of . Mineral aggregates provide the necessary materials required by without inhibiting their movement during . 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.

photo of teeth
Figure 10.15: The appearance of dentin should be glistening and moist. Image credit: "Dentin appearance" by Pinkmanggis is licensed under CC BY-SA 4.0

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 contains crystals, 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 and . There is not enough of a difference between and , 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. is secreted from the body, but it is similar to in human connective tissues, especially . 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 (a major component of ground substance).

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


illustration of Wnt morphogens
Figure 10.16: Wnt morphogens induce the differentiation of different cell types in different environments.

The formation of requires to the of into new . 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 . In the brain, Wnts induce the differentiation of into specific types of neurons and glia. But when neural crest cells migrate to the face and become parts of the , the same Wnt induces them to into odontoblasts. The difference arises because of a second morphogen. This second signal comes from the , and ECM is very different in the developing brain than it is in developing 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 , however, makes new avenues of treatment more obvious.]

Attrition and erosion

photo of tooth erosion
Figure 10.17: Erosion of enamel and dentin. Image credit: “Own work” By Klaus Limpert, Scuba-limp is licensed under CC BY-SA 3.0

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

animated illustration of dental caries
Figure 10.18: Caries in enamel versus dentin. Image credit “Tooth “By ADuran is licensed CC BY-SA 3.0

Dentin caries

Once spread through enamel and reaches the , it spreads at an increased rate. The triangle pattern of enamel loss is quickly repeated in a new triangle of . 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 is harder to detect than one at the surface of a tooth.

animation of dentinal hypersensitivity
Figure 10.19: Dentinal hypersensitivity is caused by exposed dentinal tubules.

Dentin hypersensitivity

The loss of enamel or cementum covering dentin may expose . In the crown, the few millimeters of at the outer surface contain few open dentinal tubules. But if enamel and mantle dentin are lost,  tubules in the 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 . There is a small amount of ECF between the and peritubular dentin (). 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 . 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, add layers of 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, 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. 

radiograph of root resorption
Figure 10.21: Dentin resorption (arrow), also known as internal resorption. Image credit: "An irregular radiolucency in the coronal third to middle third of the root" by Fang-Chi Li is licensed under CC BY-SA 3.0

Dentin resorption

During of primary teeth, (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 are related to . Osteoclasts have baseline activity throughout life maintaining bone tissue as part of a . Odontoclasts, on the other hand, are not always present, their differentiation from as well as their activity is  regulated by different . Dentin resorption occurring at any time other than the shedding of primary teeth is (of unknown cause). We do understand that the 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 or side.

photo of dentinogenesis imperfecta
Fig 10.22: Photographs of a patient with dentinogenesis imperfecta. Image credit: "Oral photographs from the affected individual" by unknown is licensed under CC BY 2.0

Dentinogenesis Imperfecta

A mutation in the gene for one of the dentin-specific proteins (dentin sialophosphoprotein) leads to a genetic condition known as (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 has a different color from healthy dentin because it lacks dentinal tubules). Unlike , the teeth of people with dentinogenesis imperfecta do not have a higher susceptibility to . The teeth are weaker than normal, and are more prone to fracture and loss. The lack of one protein leads to reduced dentin mineralization. Reduced mineralization leads to higher levels of inter-globular dentin.

Mutation to the gene for type I 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.

histology of pulp
Figure 10.23: Histology of pulp. Arrow indicates odontoblastic layer. Image credit "Tooth, Odontoblast necrosis" by Cesta MF, Herbert RA, Brix A, Malarkey DE, Sills RC (Eds.), National Toxicology Program Nonneoplastic Lesion Atlas is in the Public Domain, CC0

Pulp overview

The dentin and pulp both develop from of the . make a specialized tissue, containing just one cell type. The rest of the neuro-mesenchymal cells make  , which contains numerous cell types, including . It is here that blood vessels, nerve fibers and lymphatic vessels have space and structural support.

Histology of pulp

photo of a stained tooth in cross section
Figure 10.24: Coronal and radicular pulp. Image credit: "Longituinal tooth 5" by Natdental is licensed under CC BY-SA 4.0

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

photo of a steined tooth in cross section
Figure 10.25: Layers of the pulp. Legend: 1) odontoblast layer 2) cell-free layer 3) cell-rich layer 4) pulp core. Image credit: Pulp Histology” by Dododopamine at the School of Dentistry, University of Dundee is licensed under CC BY-SA 4.0

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 , 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 . This zone contains cells, but they are not visible under a traditional stain. Deep to that is a , composed primarily of , , white blood cells and other connective tissue cells. Lastly is the , which contains the same types of cells, but more spaces them apart. The pulp core is where most of the larger blood and lymphatic vessels are located.

Clinical considerations of pulp

photo of a gumboil
Figure 10.26: Gum boil caused by an underlying periapical abscess. Image credit "abcès parulique" by Damdent is licensed under CC BY-SA 3.0

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 . Death of pulp tissue can lead to accumulation of pus around the roots, which is called a . The release of inflammatory molecules from damaged tissue can lead to swelling of the overlying gingival tissue, often referred to as a . 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 . 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 and the high mitotic potential of .

radiograph of endodontic therapy
Figure 10.27: Endodontic therapy (root canal). Image credit: “Tooth #30” By DRosenbach at English Wikipedia is in the Public Domain CC0

Endodontic therapy

A likely requires the removal of the infected pulp tissue and replacement by a material that is similar in density and elasticity. This  procedure is known as . 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.

Photo of a non-vital tooth
Figure 10.28: Discoloration of a non-vital tooth after endodontic therapy. Image credit Discolored maxillary left central incisor tooth" by Anandkumar Patil is licensed under CC BY-SA 4.0

Removal of living pulp tissue removes all cells from the tooth, including . This tooth is referred to as . 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 , or molecules from pulp necrosis may invade dentin by traveling up dentinal tubules.

photo of pulp vitality testing
Figure 10.29: Pulp vitality testing. Image credit: “Own work” By Coronation Dental Specialty Group is licensed CC BY-SA 3.0

Pulp vitality testing

Painful stimuli at the surface of the teeth are detected by nerve endings located within the pulp. (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 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.

photo of tooth pulse oximetry
Figure 10.30: A pulse oximeter (A) and dental adapter (B used instead of pulp vitality testing). Image credit: "Pulse oximeter and sensor with specially manufactured adapter" by Lorena Ferreira Lima, et al is licensed under CC BY 4.0

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 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 , dentin becomes gradually thicker with age. This is most noticeable in the fine , which recede with age. Couteracting this, as with many cells, the ability of within the pulp decreases with age. As a result, older pulp tends to contain more (cross-linked fibers) and has decreased regenerative capability and diminished sensitivity.

radiograph of pulp stones
Fig 10.31: Radiograph of multiple pulp stones. Image credit: “OPG revealing pulp stones and taurodontism in all primary molars” by Mohita Marwaha et al, Case Reports in Dentistry is licensed under CC BY 4.0 / cropped

Pulp stones

Elsewhere in the body, damage to connective tissue may lead to the formation of . In the pulp, however, the presence of 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 (or denticles). These occur in both and . The major clincal significance of pulp stones is they may  complicate . Pulp stones can not only be found in pulp (free), they also appear on dentin (adherent) and within dentin (embedded).

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Histology and Embryology for Dental Hygiene Copyright © 2020 by Laird C Sheldahl is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License, except where otherwise noted.

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