Histology and Physiology of the Dental Pulp PDF

# HISTOLOGIE ET PHYSIOLOGIE PULPAIRE (RAPPELS) You have seen the histopathology of hard tissues (enamel, dentin, cement) in P2 and studied the destructive phenomena caused by the caries process. A good understanding of dental histology and the interactions between these tissues with: * the extern...

# HISTOLOGIE ET PHYSIOLOGIE PULPAIRE (RAPPELS) You have seen the histopathology of hard tissues (enamel, dentin, cement) in P2 and studied the destructive phenomena caused by the caries process. A good understanding of dental histology and the interactions between these tissues with: * the external environment: the oral environment on the one hand, * and the internal environment: the periodontal compartment on the other hand, is the foundation of an enlightened practice of conservative dentistry/endodontics. Knowing the normality and the physiological behavior of these tissues makes it possible to understand the reactions involved in pulp pathologies and their complications, contributes to mastering the diagnosis and the selection of the surgical procedures that are best adapted and the least traumatic to avoid iatrogenic lesions and optimize the chances of preserving teeth with compromised or compromised pulp vitality. ## I TERMINOLOGY: ### 1. The periodontium: A complex tissue comprising: * The cementum, * The periodontal ligament (or periodontal ligament, or alveolo-dental ligament, or dental ligament) that connects, supports and nourishes the tooth (tooth), * The alveolar bone, * The gingiva. ### 2. The endodontium: This is the part of the tooth comprising the pulpo-dentinal complex. It is macroscopically materialized by the canal system (pulp chamber and root canals) ## II TOOTH ENAMEL: It is a tissue of epithelial origin, built during amelogenesis, containing more than 95% of mineral in its mature form. Enamel is the most mineralized tissue in the organism. Its structure is complex, hard and resistant. Enamel, with variable thickness (2.5 mm at the level of the cusps which thins out to disappear at the amelo-cement junction), covers the crowns of teeth, protects the pulpo-dental complex and confers the teeth their appearance in the oral cavity. ### Senescence: Over time, the appearance of enamel changes due to the physiological wear of the surface, but also due to the important and constant exchanges with the oral environment. Physiological wear of enamel causes the disappearance, in whole or in part, of the enamel aprismatic layer. Occlusal morphologies are progressively flattened due to passive eruption. With age, enamel becomes less translucent because its degree of mineralization increases. Intensification and alterations in the enamel hue occur due to incorporation and accumulation of mineral elements and agentscoloring agents, and also due to the modifications of the underlying dentin appearing through a thinner enamel layer. Enamel becomes less soluble and less permeable due to increased fluoride concentration, mainly at the surface, which increases natural resistance to caries. ## III DENTIN: Dentin covered by enamel crown and cement root level, comprises the main mass of the tooth. It is formed by odontoblasts during dentinogenesis and is a mineralized mesenchymal origin tissue that is not vascularized. A fundamental characteristic of dentin is its permeability and its ability to respond to external stimuli of physico-chemical, thermal and tactile nature. Dentin reacts in a concerted manner with the pulp to solicitations and aggressions, hence the name of the pulpo-dentinal complex. It is composed of 70% of mineral (like bone tissue). ### 1. The different types of dentin. Human dentin is an orthodentin, characterized by the fact that only the polarized extensions of odontoblasts cross the calcified tissue, their cell bodies being located outside the dentin in the pulp. #### The peripheral dentin: * At the coronal level, it is made up of the dentin mantle (mantle dentin), resulting from the first odontoblast secretions. It is a layer of hypomineralized dentin located beneath the amelo-dentinal junction, devoid of dentinal tubules and intertwined in the internal enamel. Beneath this dentin mantle lies a band of coronal dentin 250 µm thick in which the tubules have Y-shaped terminal branches. * Interglobular dentin zones (interglobular dentin) are often found in the peripheral zone, at a short distance from the dentin mantle, with poor mineralization (or even non-mineralized islets). * At the root level, the dentin mantle extends to the junction of the inner layer of acellular initial cementum, a layer devoid of dentinal tubules, covered by a hypomineralized zone made of poorly fused calcifications (granular layer of Tomes). #### The circumferential dentin: The transformation of predentin contributes at the pre-functional stage to formation of a primary dentin that is completed with the onset of tooth function on the dental arch, at the coronal level and the end of apical edification at the root level. Later, at the functional stage, predentin turns into secondary dentin. Both are physiological canalicular dentins. In the innermost part, close to the metadentin (mineralization front of the predentin-dentin boundary), the least mineralized zone (both inter- and peri-canalicular), is located. This zone (150-200 µm), could represent the dentin formed over the 3-4 years separating the end of coronal morphogenesis and eruption. The ratio of tubules to inter-tubules is high. Dentinal tubules (diameter = 1-2 µm, length = 2.5-3.5 mm) contain the odontoblast extensions and an unmineralized peri-odontoblastic space. Each tubule is bordered by hypermineralized pericanalicular dentin resulting from the secretion of matrix components by the odontoblast extension into the tubule lumen. Between the main tubule trunks lies the intercanalicular dentin, less mineralized and resulting directly from the transformation of predentin. In predentin, the secondary ramifications of the extensions give rise to secondary lateral branches crossing the intercanalicular dentin. The number of tubules depends on the dentin zone considered: * 8,000 / mm² (peripheral: under occlusal fissures) * 58,000 / mm² (central: at the level of the pulp ceiling), * In the middle third of dentin, this number is around 30,000 / mm². Odontoblastic extensions occupy the inner third of the dentin. With aging, empty tubules are gradually obliterated by precipitation and reprecipitation (dentin sclerosis). #### The cicatricial tertiary dentin: Aggressions (caries, trauma, abrasions...) can trigger a cessation of dentinogenesis followed by its resumption in the form of reactionary dentinogenesis (concept of the calcio-traumatic line). This dentin can be elaborated by odontoblasts from the first generation that survived the aggression. The localized mass of dentin will have a structure more or less close to physiological dentin. When formed rapidly, this reactionary dentin is devoid of tubules and may contain cellular inclusions. It is then comparable to osteodentin. When it is deposited slowly, it is a canalicular tertiary dentin that resembles physiological secondary dentin with which it is continuous. When odontoblasts have been destroyed, reparative dentin can be formed by replacement odontoblasts. A layer of atubular dentin (fibrodentin) is synthesized (isolation of the pulp from the external environment) followed by canalicular dentin (orthodentin) which marks the end of pulp healing. ### 2. Senescence: Like ameloblasts, odontoblasts persist and continue to synthesize throughout the life of the tooth. Dentinogenesis is a continuous process, very active during odontogenesis, slowing down after eruption. Dentin apposition is continuous (marked by variations: Von Ebner lines) and leads to a progressive, non-proportional reduction in pulp volume. Gradually, the number of odontoblasts decreases, leaving some tubules empty. Dentin deposition and hypermineralization of pericanalicular dentin narrow dentinal tubules. Finally, intracanalicular mineralizations occur which accentuate sclerosis, a characteristic of senescent dentin. ## IV THE PULP: The pulp is a specialized connective tissue ensuring on the one hand dentinogenesis, physiological and cicatricial, by odontoblasts and on the other hand the detection and signaling of aggressions thanks to neuro-vascular elements. ### 1. General characteristics: The pulp occupies the central part of the tooth, enclosed in an anatomical cavity with rigid walls: the pulp cavity. This pulp cavity is divided into 2 parts, the pulp chamber that contains the coronal pulp or cameral pulp, and root canal that contains the root pulp. At the coronal level, extensions of the pulp ceiling in relation to the occlusal anatomy form the pulp horns. At the root level, the pulp communicates with the periodontal ligament: * through a main foramen which is rarely located at the root apex (works of Kuttler, Vertucci). More than half of them have an eccentric, mesial or distal position (visible on radiographs), buccal or lingual (invisible to radiographs). Several foramina are possible and are located 2 mm from the root apex (works of Uchizono K., Hess J.C.). These anatomical considerations are fundamental when looking for working lengths in endodontics. * Lateral, secondary and accessory canals (works of De Deus) are generally located in the apical third of the root. Lateral canals can exist at the middle third level of the root. In multi-rooted teeth, accessory canals have been found in the pulpal floor, extending from the pulpal floor to the inter-radicular periodontium (pulpo-periodontal canals). Periodontal involvement can be the cause of pulpal infection or pulp involvement can have a periodontal cause (endo-periodontal relationships). Their frequency is ≈ 50% (works of Vertucci and Lowmann). The pulp is a loose connective tissue containing 75% water and 25% organic material consisting of different types of cells within an extracellular matrix. ### 2. Structural organization: #### Peripheral pulp cells: They constitute the dentinogenic region which is classically divided into 3 zones, from the pulp periphery to the center: * **The odontoblast layer:** This layer forms a continuous palisade of highly differentiated cells responsible for dentin formation and repair. These cells are more numerous at the coronal level than at the root level. This stratified layer of 3 to 5 rows of cells becomes thinner as pulp volume decreases with aging. The odontoblast is a polarized cell with an apex directed towards the dentin. Each functional odontoblast emits at least one extension towards the dentin, which can have lateral branches. The extension of the extension in the tubule is variable depending on the different authors, from 1/3 of the dentin for some to the dentin-enamel junction for others. * **The acellular layer of Weil:** This layer, contiguous with the odontoblastic palisade, is poor in cells and contains the subodontoblastic capillary plexus as well as unmyelinated sensory and autonomic nerve fibers (Raschkow's plexus). * **The cellular layer of Höhl:** This layer is rich in fibroblasts, mesenchymal cells (daughter cells not odontoblasts resulting from the last mitosis of pre-odontoblasts) and dendritic cells, constituting a reservoir of immune surveillance cells and cells in waiting. These cells on "stand-by" can differentiate into replacement odontoblasts when the primary odontoblasts have been destroyed by an attack. #### The central pulp mass: The cells of the central pulp include fibroblasts, mesenchymal and immune cells. * **Fibroblasts:** They are involved in the elaboration and remodeling of the extracellular pulpal matrix. In high density and very active in young pulps, they develop in older pulps into fibrocytes, cells with reduced metabolic activities. * **Undifferentiated cells:** Most often located near blood vessels, they can differentiate into fibroblasts or neoodontoblasts. Their number decreases in older pulps, this decrease affecting the pulp's repair potential. * **Immunocompetent cells:** These cells are present in healthy pulp and are recruited during immune responses to attacks. These are dendritic cells, macrophages and lymphocytes T. Dendritic cells (named for their cytoplasmic extensions, dendrites, which connect them to each other), form a continuous network in the entire pulp and constitute the pulp's immune surveillance system. They capture antigens, fix them on their membrane, internalize them by endocytosis, degrade them into peptide fragments in their lysosomes, then present them to T4 lymphocytes patrolling in pulp vessels or those present in regional lymph nodes (after lymphatic migration). They thus activate phagocytic and antibody-producing cells, macrophages and B lymphocytes, which ensure the destruction of extra-cellular bacteria and antigens. ### The extracellular matrix: Its origin comes from the cells it surrounds, one of its most important roles being intercellular communication. * **Collagens (types III, IV, V, VI):** représentent 34% of the total pulp proteins. The high amount of type III collagen is characteristic of connective pulp tissue. Collagen fibers have a structural support role. Their density is maximum in the apical region of the root and increases with the age of the pulp. * **Glycoproteins:** fibronectin, laminin, tenascin... * **Elastin fibers:** mainly confined to the walls of arterioles. * **Glycosaminoglycans (chondroitin, dermatan and keratan sulfates):** (polymers of disaccharide units) and proteoglycans represent more than 50% of the pulpal matrix proteins and their main role is to maintain water in the pulp. * **Lipids.** * **Metalloproteinases:** Play a critical role in pulp remodelling in normal conditions and during inflammatory and cicatricial phenomena (collagenases, stromelysins...). ### 3. Vascularization: The pulp is a highly vascularized tissue where drainage would be efficient if it were not enclosed between rigid, inextensible walls and if it had a collateral circulation. 5% of the pulp volume is occupied by vessels, which are distributed in a 3/1 ratio between the venous axes of exit and the arterial axes of entry. Arterioles enter the pulp, venules and lymphatics exit through the apical foramen. Apical lateral canals and those of the pulp floor are supplementary routes of pulp vascularization. The vessels end in a dense subodontoblastic capillary network. The pulpal vessels have thin walls with a discontinuous presence of endothelial cells and fenestrations. This configuration is adapted to transcapillary flows (governed by the Starling equation) and facilitates exchanges between plasma elements and the interstitial fluid according to hydrostatic and osmotic pressures. It improves the diffusion of nutrients to the odontoblasts which make dentin and it intervenes in the regulation of inflammation. Lymphatic vessels drain fluids outside the pulp and participate in maintaining a balanced pulpal fluid levels. In the event of injury, the presence of this rich vasculo-lymphatic network allows an immediate increase in blood flow resulting in localized or generalized hyperemia without the need for capillary neoformation . The subodontoblastic capillary network has a particular configuration with loop circulations, arterio-venous anastomoses and capillary shunts. This allows, in case of aggression, to divert circulation, isolate the injured area and confine initial inflammation (edema and increase of pulpal tissue pressure) in the peripheral zone of the pulp without causing a pulp ischemia. Thanks to the efficiency of the subodontoblastic capillary network, any substance that penetrates into the pulp is captured by the immune surveillance system, neutralized, then absorbed and transported into the circulation (blood clearance). This is a protective system that reduces irritant concentration in the pulp compartment. ### 4. Intra-pulpal pressure: The pulp, contained in a non-collapsible space, can neither expand nor shrink. This is reflected by the permanent pressure of pulpal interstitial fluids, which is relatively high, and by a low compliance (increase in volume in mL/increase in pressure in cm H2O, and indicates the resistance to the expansion of the system considered) of the pulpal tissue. In this case, interstitial compliance represents the ratio between the variations in interstitial volume and tissue hydrostatic pressure. The pulp has a unique capacity to reabsorb extravasated fluids. In most tissues, compliance is high and any increase in filtration forces or any decrease in reabsorption forces causes an accumulation of fluids in the interstitial medium, resulting in edema, the accumulated fluids being subsequently reabsorbed and then drained by the lymphatic system. . In the pulp, any variation, even of small volume, induces a significant variation in pressure, which has the effect of tending to bring the fluids coming out of the capillaries (filtration) to their starting point, i.e., inside the capillary (reabsorption), limiting the formation of edema. The high pulpal pressure also plays a role in hydrodynamic movements and painful manifestations associated with cavity preparation (Brännström's hydrodynamic theory). ### 5. Innervation: The pulp has a rich innervation composed of afferent and efferent fibers from the sensory and sympathetic systems that enter and exit the pulp through the same pathways as the blood vessels. Within the pulp, these fibers accompany the vessels in the central zone and at the periphery where they end in arborescent structures: * Subodontoblastic * Odontotoblastic * Intradental peri-odontoblastic. There are two usual categories of nerve fibers in the pulp : * **Sensory fibers** responsible for pain perception: * **Myelinated Aδ fibers:** * Have a low excitation threshold * Conduct rapidly (13 m/s) * Are thermosensitive * Are responsible for acute type pain (early, intense, localized, short-duration) such as pain from drilling. * **Unmyelinated C fibers:** * Have a higher excitation threshold * Conduct more slowly (1 m/s) * Are responsible for protopathic pain of a lancinating type (delayed, long-lasting, radiating) * are particularly involved in pulpitis. * **Autonomic fibers** that regulate blood flow and maintain pulpal vasomotor tone: * The walls of the pulpal blood vessels are equipped with alpha and beta-adrenergic receptors in contact with the nerve endings of the sympathetic system, having vasodilating and vasoconstricting properties, participating in regulating pulp blood flow. * Pulpar nerve endings contain neuromodulators: * Noradrenaline * Neuropeptides: Substance P, CGRP (Calcitonin-Gene-Related Peptide) * Neurokinins. When nerve endings are excited, they release vasoconstrictors and increase blood flow and vascular permeability of the injured areas during the initial neurovascular phase of pulp inflammation. * The neuropeptide Y has a vasoconstrictor effect. In aggressions, pulp nerve fibers are responsible for dental pain by stimulation of nociceptive nerve endings directly or indirectly through modifications in their local environment (theory of Brännström's dentin-pulp sensitivity: rapid movement of dentin fluids and activity of Aδ fibers) ## V PULP PHYSIOLOGY: ### 1. Formation Function: The main function of pulpal tissue is to produce dentin. The internal framework of the crown and root having been completed, dentin apposition continues over time, in the absence of chemical or bacterial irritants. The actions of chewing or attrition are sufficient. ### 2. Nutrient Function: Through vascularization, during all stages of tooth development, the pulp provides nutrients and tissue fluids necessary for construction of mineralized tissues. The odontoblastic extension, which elongates with centripetal dentin deposition, is the pathway for transportation of all these elements. Despite the narrowing of the pulp cavity due to age or pathology, the pulp remains vital and continues this function. ### 3. Sensitivity Function: By reacting to aggression through pain, the pulp acts in such a way that it tends to protect the integrity of the tooth. ### 4. Defense Function: In addition to the formation of reactionary dentin , the pulp's last function is to defend the tooth against any aggression. Like any connective tissue, it only has one response: inflammation. The outcome of pulp inflammation can be:: * Healing. * Chronicity which can lead to pulp necrosis (loss of vitality). ## VI PULP SENESCENCE: With age, changes occur in the pulp parenchyma and affect almost all of the pulp components . ### 1. Reduction in pulp size and volume: This spatial decrease, while it reduces the space where the pathological processes can occur, it also limits the opportunity for metabolic exchanges and therefore the means of defense. ### 2. Decrease in cellular components In general in humans, cell count decreases by 50% between 20 and 70 years: * Odontoblasts decrease in both number and volume. The presence of cytoplasmic vacuoles indicates metabolic deficiencies (Zach et al.) * Fibroblasts also see their number decreased and have fewer organelles. ### 3. Fibrosis: The thickness and number of collagen fibers increase. Although aging fibroblasts secrete more collagen, they create areas of fibrosis within the pulp: Von Korff fibers (collagen fibers emerging from predentin to enter the pulp). ### 4. Vascularization and decrease in the nervous system There is a decrease in blood vessels, lymphatic vessels and nerves. * **Blood Vessels:** * **From 40 years of age:** The number of blood vessels decreases. Only 2 arterioles enter the apical foramen. Collaterals decrease in number. The peripheral pulp capillaries are less numerous. Venous structures evolve in parallel. * From 70 years of age:** The reduction is more significant. In general, there is only one arteriole that enters the foramen and one venule that exits. The collaterals are less numerous and have looser walls. Many capillaries have disappeared. ### 5. Dystrophic apposition: Bernick noted the effects of age on vascular walls. * **From 40 years of age:** Arteriosclerotic changes appeared in the arterioles. The intima ( inner layer of blood vessels) thickens with hyperplasia of elastic fibers. Calcifications begin in the adventitia (outer layer) and progress towards the lumen of the capillaries. These calcifications erode the intima and sometimes protrude into the capillary lumen. There is a constant formation of secondary dentin which narrows the pulp chamber and the volume of the tissue. In addition, there are other types of mineralization that occur at the heart of the pulp and that can be divided into two distinct forms: * **False pulpolithes:** They are located on sites of necrosis or on a vascular thrombosis. It is a calcified deposit that forms by concentric deposition around a central nucleation core (onion bulb image). * **True pulpolithes:** They appear as rounded masses of dentin containing radiated tubules, with odontoblasts at the periphery (spoke-wheel image). Senescence is not a pathological phenomenon in itself. These changes reduce the pulp's defense and tissue healing potential. Mineralization, which occurs in the pulp chamber and sometimes in the canals, is mainly pathological or traumatic (dental instruments, tics...).