UE 4 EC 2 Dental Histology & Physiology PDF

# HISTOLOGIE ET PHYSIOLOGIE PULPAIRE (RAPPELS) You have seen in P2 the histopathology of hard tissues (enamel, dentin, cement) and studied the destructive phenomena due to the carious process. A good knowledge of dental histology and the interactions that these tissues maintain with: - the extern...

# HISTOLOGIE ET PHYSIOLOGIE PULPAIRE (RAPPELS) You have seen in P2 the histopathology of hard tissues (enamel, dentin, cement) and studied the destructive phenomena due to the carious process. A good knowledge of dental histology and the interactions that these tissues maintain 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 informed practice of conservative/endodontic dentistry. Knowing the normality and the physiological behavior of these tissues makes it possible to understand the reactions involved in pulpopathies and their complications, contributes to mastering the diagnosis and to the selection of the best surgical procedures- the least traumatic to avoid iatrogenic lesions and optimize the chances of preserving teeth with compromised pulpal vitality or not. ## I TERMINOLOGY: 1. The periodontium: Complex tissue comprising: - cement, - desmodont (or periodontal ligament, or alveolo-dental ligament, or dental ligament), - alveolar bone, - gingiva. This unit supports and nourishes the dental organ (tooth). 2. The dentin: It is the part of the tooth including the pulpo-dentin complex. It is macroscopically materialized by the canal system (pulp chamber and root canals). ## II ENAMEL DENTAL: 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, of variable thickness (2.5mm at the level of the cusps which thins down to disappear at the amelo-cement junction), covers the tooth crowns, protects the pulpo-dentin complex and gives teeth their appearance in the oral cavity. ## II DENTIN: Dentin, covered by enamel at the coronal level and by cement at the radicular level, constitutes the main mass of the tooth. Formed by odontoblasts during dentinogenesis, it is a tissue of mesenchymal origin mineralized non-vascularized. A fundamental characteristic of dentin is its permeability and its ability to respond to external stimuli of a physico-chemical, thermal and tactile nature. Dentin reacts in a concerted way with the pulp to solicitations and aggressions, hence the name of the pulpo-dentin complex. It is composed of 70% 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 odontoblastic secretions. It is a layer of hypomineralized dentin located beneath the amelo-dentin junction, devoid of dentinal tubules and intermingled with the internal enamel. Beneath this dentin mantle lies a band of coronal dentin of 250µm at the level of which the tubules present terminal branches in Y. Inter-globular zones (inter-globular dentin) poorly mineralized (or even non-mineralized islets) are often found in this peripheral zone at a short distance from the dentin mantle. At the radicular level, the dentin mantle extends to the contact of the internal layer of acellular cement initially by a layer devoid of dentinal tubules (hyaline layer of Hopewell-Smith) covered by a hypomineralized zone made up of poorly fused calcospheres (granular layer of Tomes). - The circum-pulpal dentin: The transformation of predentin contributes in the pre-functional stage to the formation of a primary dentin which is completed with the commencement of tooth function on the dental arch at the coronal level and the completion of the apical build-up at the radicular level. Later, in the functional stage, predentin transforms into secondary dentin. Both are physiological canalicular dentins. In the innermost part, close to the metadentin (front of dentin mineralization of the predentin-dentin border) is the least mineralized zone (both inter- and peri-tubular). This zone (150-200µm) could represent the dentin formed during the 3-4 years separating the end of crown morphogenesis and eruption. The tubule/inter-tubular ratio is high. The dentinal tubules (diameter= 1-2µm, length= 2.5-3.5mm) contain the odontoblast extensions and a non-mineralized peri-odontoblastic space. Each tubule is bordered by the hypermineralized peritubular dentin resulting from the secretion of matrix components by the odontoblast extension in the lumen of the tubule. Between the main trunks of the tubules is the intertubular dentin, less mineralized and resulting directly from the transformation of predentin. In predentin, secondary ramifications of extensions give rise to lateral secondary branches crossing the intertubular dentin. - **The number of tubules depends on the area of dentin considered:** - 8,000/mm² (peripheral: under occlusal fissures) - 58.000 /mm² (central: at the level of the pulp roof), - at the level of the middle third of dentin, this number is around 30,000 /mm². The odontoblast extensions occupy the inner third of dentin. With aging (dentin sclerosis), the empty tubules become blocked by precipitations and reprecipitations (dentin sclerosis). - **The scar dentin**: Aggressions (caries, traumas, abrasions...) can cause an arrest of dentinogenesis then its resumption in the form of reactive dentinogenesis (notion of calcified-traumatic line). This dentin may be formed by odontoblasts which have survived the aggression. The localized mass of dentin will have a more or less similar structure to physiological dentin. When built up quickly, this reactive dentin is devoid of tubules and may contain cellular inclusions. It is then comparable to osteodentin. When deposited slowly, it is a canalicular tertiary dentin which resembles the physiological secondary dentin with which it is continuous. When odontoblasts have been destroyed, a reparative dentin may be formed by replacement odontoblasts. A layer of tubular dentin (fibrodentin) is synthesized (isolation of the pulp from the external environment) then a canalicular dentin (orthodentin) which marks the end of pulpal scar formation. ## IV THE PULP: Pulp is a specialized connective tissue that ensures on the one hand dentinogenesis, physiological and scar formation by odontoblasts and on the other hand detection and signaling of aggressions, thanks to neuro-vascular elements. 1. General characteristics: 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 which contains the coronal or chamber pulp and the root canal which contains the radicular pulp. At the coronal level, extensions of the pulp roof in relation to occlusal anatomy form the pulp horns. At the radicular level, the pulp communicates with the periodontal ligament by: - a main foramen which is rarely located at the apex of the root (works of Kuttler, Vertucci). More than half of them have an eccentric, mesial or distal position (visible on radiography), vestibular or lingual (invisible on radiography). Several foramina are possible and are located 2 mm from the apex of the root (works of Uchizono K., Hess J.C.). These anatomical considerations are fundamental when looking for working length in endodontics: - lateral, secondary and accessory canals (works of De Deus) generally located at the apical third of the root. Lateral canals may exist at the middle third of the root. On multirooted teeth, accessory canals have been observed leaving from the pulp floor and reaching the inter-radicular periodontium (pulpo-periodontal canals). Periodontal lesions of the furcation may have a periodontal cause and transmit the infection to the pulp or have a pulpal cause (necrosis) (endo-periodontal relationships). Their frequency is ≈ 50% (works of Vertucci and Lowmann). The pulp is a loose connective tissue containing 75% water and 25% of organic material consisting of different types of cells within an extra-cellular matrix. 2. Structural organization: - The peripheral pulp cells: They constitute the dentinogenic region, traditionally divided into 3 zones, from the peripheral pulp 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 radicular level. This layer is stratified from 3 to 5 rows of cells, which narrows down as the pulp volume decreases during ageing. The odontoblast is a polarized cell, at the apex of its differentiation. Each functional odontoblast emits at least one extension towards dentin which can have lateral branches. The extension into the tubule varies according to different authors, from the inner third of dentin for some, to the dentin-enamel junction for others. - **The acellular layer of Weill:** This layer, adjacent to the odontoblastic palisade, is poor in cells and contains the sub-odontoblastic 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, in mesenchymal cells (daughter cells of pre-odontoblasts, not odontoblasts, resulting from the last mitosis of pre-odontoblasts) and dendritic cells that constitute a reservoir of immune surveillance cells and waiting cells. These cells in "stand-by" can differentiate into replacement odontoblasts when primary odontoblasts have been destroyed by an aggression. - **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 extra-cellular pulp matrix. They are in high density and very active in young pulps, they evolve in older pulps into fibrocytes, cells with reduced metabolic activities. - **Undifferentiated cells**: They are most often located near blood vessels and can differentiate into fibroblasts or new odontoblasts. Their number decreases in older pulps, this decrease affecting the pulp's repair potential. - **Immunocompetent cells** They are present in healthy pulp and are solicited during inflammatory responses to aggressions. They are dendritic cells, macrophages and lymphocytes T. Dendritic cells (named after their cytoplasmic extensions, dendrites, that connect them to each other) form a continuous network throughout the pulp and constitute the pulp's immune surveillance system. They capture antigens, bind them to their membrane, internalize them by endocytosis, break them down 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 bacterial and antigenic elements. - **Extra-cellular matrix:** It originates from the cells it contains, one of its most important roles being inter-cellular communication. - **Collagens**: They represent 34% of all pulp proteins (types III, IV, V, VI). The large amount of type III collagen is characteristic of pulp connective tissue. Collagen fibers have a structural support role. Their density is highest in the apical area of the root, and increases with the age of the pulp. - **Glycoproteins::** fibronectin, laminin, tenascin... - **Elastin fibers**: They are mainly confined to the walls of arterioles. - **Glycosaminoglycans**: chondroitin, dermatan and keratan sulfates (polymers of disaccharidic units) and proteoglycans represent over 50% of the pulp matrix proteins and their main role is to retain water in the pulp. - **Lipids**. - **Metalloproteinases**: They play a key role in pulp remodeling during normal conditions and during inflammatory and scarring phenomena (collagenases, stromolysins...). 3. Vascularisation: Pulp is a very well-vascularized tissue where drainage would be efficient if it were not confined between rigid, inextensible walls and if it had a collateral circulation. 5% of the pulp volume is occupied by blood vessels, which are distributed in a ratio of 3/1 between venous exit axes and arterial entry axes. Arterioles enter the pulp, venules and lymphatics leave through the apical foramen. Apical lateral canals as well as those of the pulp floor are supplementary routes of pulp vascularization. Vessels end up in a dense sub-odontoblastic capillary network. Pulp vessels have thin walls with a discontinuous presence of endothelial cells and fenestrations. This configuration is adapted to transcapillary flows (governed by Starling's equation) and facilitates exchanges between plasma components and interstitial fluid according to hydrostatic and osmotic pressures. It improves the diffusion of nutrients to odontoblasts which make dentin and intervene in the regulation of inflammation. Lymphatic vessels drain fluids away from the pulp and participate in maintaining a balanced equilibrium of pulpal fluids . In the event of a lesion, the presence of this rich vasculo-lymphatic network, allows for an immediate increase in blood flow and results in localized or generalized hyperemia, without the need for new capillary formation. The sub-odontoblastic capillary network has a peculiar configuration with loops, arteriovenous anastomoses and capillary shunts. This allows, in cases of aggression, to divert blood flow, isolate the damaged area and contain initial inflammation (edema and increase in pulpal tissue pressure) in the peripheral area of the pulp without causing pulpal ischemia. Due to the efficiency of the sub-odontoblastic capillary network, any substance entering the pulp is captured by the immune surveillance system, neutralized, then absorbed and carried away in the circulation (blood clearance). This is a protective system that reduces the concentration of irritants in the pulp compartment. 4. The pulpal intra-pressure: Pulp, confined in an incompressible space, cannot expand or contract. This results in a permanent increase in pulpal interstitial pressure, relatively high and with a low compliance (increase in volume in mL/ increase in pressure in cm H2O, and reflects the resistance to expansion of the system considered) of the pulpal space. In this case, compliance of the interstitial space represents the ratio between interstitial volume variations and interstitial hydrostatic pressure. Pulp has the particularity of having a strong capacity of capillary reabsorption of extravasated fluids. In most tissues, compliance is high and any increase in filtering forces or any decrease in reabsorption forces causes an accumulation of fluids in the interstitial space, which results in edema, accumulated fluids being secondarily reabsorbed then evacuated by lymphatics. In pulp, any volume variation, even small, induces a significant variation in pressure, which tends to bring back fluids that leave the capillaries (filtration) to their starting point, that is to say inside the capillary (reabsorption), limiting the formation of edema. Pulpal pressure plays a role in hydrodynamic movements and painful manifestations that accompany cavity preparation (Brännström's hydrodynamic theory). 5. The Innervation: Pulp has rich innervation composed of sensory and sympathetic nerve fibers that enter and leave the pulp through the same pathways as blood vessels. Inside the pulp, these fibers accompany blood vessels in the central area and at the periphery where they end in arborizations: - subodontoblastic - odontoblastic - peri-odontoblastic intradentin. The following two usual categories of nerve fibers are found in pulp: - **Sensory fibers** responsible for pain perception: - **Myelinated fibers Aδ:** - low pain threshold - fast conduction (13m/s) - thermosensitive - responsible for acute, sharp pain (early, intense, localized, short duration) such as that experienced during cutting. - **Non-myelinated fibers C:** - higher pain threshold - slower conduction (1 m/s) - responsible for protopathic pain (late, lasting, radiating) - mainly involved in pulpitis. - **Autonomic fibers** that regulate blood flow and ensure pulpal vascular tone: - the walls of pulpal vessels are equipped with α- and β-adrenergic receptors in contact with the nerve endings of the sympathetic nervous system with vasoconstrictor and vasodilator properties, participating in the regulation of pulpal blood flow. - pulpal nerve endings contain neurotransmitters: - noradrenaline - neuropeptides: substance P, CGRP (calcitonin-gene-related peptide) - neurokinins Released when nerve endings are excited, they are mainly vasodilators and increase blood flow and vascular permeability of the damaged areas during the initial neurovascular phase of pulpal inflammation. - **The neuropeptide Y** has a vasoconstrictor effect. During aggressions, pulpal nerve fibers are responsible for tooth pain by direct stimulation of nociceptive nerve endings or indirectly due to modifications in their immediate environment (Brännström's hydrodynamic theory of dentin-pulpal sensitivity: rapid movements of dentinal fluids and activity of Aδ fibers). ## V DENTAL PHYSIOLOGY: 1. The function of formation: The main task of pulpal tissue is to produce dentin. The internal framework of the crown and the root being completed, dentin deposition continues over time, despite the absence of chemical or bacterial irritants. The forces of mastication or wear are sufficient. 2. The function of nutrition: Through vascularization, during all stages of tooth development, pulp provides nutrients and the tissue fluids necessary for the construction of mineralized tissues. The odontoblast extension, which lengthens along with the centripetal deposition of dentin, is the pathway for the transport of all these elements. Despite the narrowing of the pulp chamber due to age or pathology, pulp remains vital and continues this function. 3. The function of sensitivity: By reacting to aggression through pain, the pulp acts in such a way that it tends to preserve the integrity of the tooth. 4. The function of defense: In addition to the formation of reactive dentin, the last function of pulp is to defend the tooth against any aggression. In this respect, like any connective tissue, it only has one response: inflammation. The outcome of a pulpal inflammation can be: - scar formation - chronicity which can lead to pulpal necrosis (loss of vitality). ## VI DENTAL SENESCENCE: With age, changes occur within the pulpal parenchyma and affect almost all components of pulp: 1. Reduction of size and volume of the pulp: This reduction in space, while reducing the space where pathological processes can occur, also decreases the possibilities for metabolic exchanges and therefore the means of defense. 2. Decrease in cellular components: In general, in humans, the number of cellular elements decreases by 50% between 20 and 70 years: - odontoblasts decrease in number and volume. The presence of cytoplasmic vacuoles indicates metabolic deficiencies (Zach et al.) - fibroblasts also decrease in number and present a reduced number of organelles. 3. Fibrosis: The number and thickness of collagen fibers increase. Aged fibroblasts produce more collagen, this creates areas of fibrosis in the pulp: Von Korff fibers (collagen fibers emerging from predentin to enter the pulp). 4. Vascularisation and nervous system: With age, there is a decrease in blood vessels, lymphatic vessels and nerves associated. - **Heller et coll** studied vascularisation in relation to age: - from age 40, the number of vessels decreases. There are only two arterioles which enter the apical foramen. Collateral vessels decrease in number. At the periphery of the pulp, capillaries are less numerous. Venous structures evolve in parallel fashion - at age 70, the reduction is more significant. In general, there is only one arteriole that enters the foramen and one venule that leaves. Collateral vessels, fewer in number, have looser walls. Many capillaries have disappeared. 5. Dystrophic apposition: Bernick, observed the effects of age on vascular walls. From age 40, signs of arteriosclerosis appear in arterioles. The intima (inner layer of blood vessels) thickens with hyperplasia of elastic fibers. The onset of calcification occurs in the adventice (outer layer) and progresses towards the lumen of capillaries. These calcifications erode the intima and sometimes protrude into the capillary lumens. - **There is a constant production of secondary dentin which narrows the pulp chamber and the tissue volume. Along with this, there are other types of mineralization which develop at the core of the pulp and which are distinguished as follows: - **False pulpolithes:** They are located on sites of necrosis or on a vascular thrombosis. It is a calcific deposit that forms by concentric deposition around a central nucleus of nucleation (onion bulb image). - **True pulpolithes:** They present in the form of rounded masses of dentin that contain radiating tubules, with odontoblasts at the periphery (wheel image). Senescence is not a pathologic phenomenon in itself. These changes reduce the considerable potential defense and scarring of the pulpal tissue. The mineralization which occurs in the pulp chamber, and sometimes in the canals, is mainly pathological or traumatic (dental instruments, bad habits, etc.)