DENTAL PULP1.pptxDENTAL PULPDENTAL PULP1.pptx1.pptx

DENTAL PULP1.pptxDENTAL PULP1.pptxDENTAL PULP1.pptx

1. DENT A L PULP I BDS CL A SS

2. Contents Introduction Functions Regions and their characteristic features Organisation Composition Fibers Non- Fibrous Matrix Cells Systemic Factors affecting the pulp Arterial blood supply of teeth Venous drainage from the teeth

3. Contents Continued Control of blood from teeth Lymphatic system Clinical correlation of ciculatory system of teeth Nerves of teeth Theories of tooth and pain perception

4. Introduction Responsible for formation of dentin Contained within pulp chamber and root canals of the tooth and at the apical end is continuous with the periodontal ligament Most active during tooth development and eruption but still active throughout life (secondary dentin, respond to applied stimuli)

5. Functions of Dental Pulp Inductive – to induce oral epithelial differentiation into dental lamina and enamel organ formation. The pulp also induces the developing enamel organ to become a particular type of tooth. Formative – the pulp organ cells produce the dentin that surrounds and protects the pulp. The pulpal odontoblasts develop the organic matrix and functions in its calcification. Through the development of the odontoblast processes, dentin is formed along the tubule wall as well as at the pulp – predentin front Nutritive – the pulp nourishes the dentin through the odontoblasts and their processes and by means of the blood vascular system of the pulp.

6. Functions of Dental Pulp contd. Protective – the sensory nerves in the pulp respond with pain to all stimuli such as heat, cold, pressure, operative cutting procedures, and chemical agents. The nerves also initiate reflexes that control circulation in the pulp. This sympathetic function is a reflex, providing stimulation to visceral motor fibers terminating on the muscles of the blood vessals. Defensive or Reparative – pulp responds to irritation by formation of reparative dentin and mineralizing any affected dentinal tubules. The pulp has macrophages, lymphocytes, neutrophils, monocytes, plasma cells and mast cells, all of these help in the repair process.

7. Regions The structure of the dental pulp can be described on a regional basis Supra - Odontoblastic layer Beginning from outside the potential space between the odontoblast layer and the pre-dentin. Sub – Odontoblastic layer Immediately beneath the odontoblast layer (Cell free zone and the cell rich zone)

8. Characteristic features of supra-odontoblastic zone Two important structures found in the supra – odontoblast layer Unsheathed axons, found exclusively in the crowns. These have been described as the predentinal plexus of Bradlaw. This is not a true plexus (network) but an area where a number of axons congregate. These axons are in a position to sense the changes in fluid movement through the dentinal tubules as well as in the extra-cellular fluid composition, which because of the barrier properties of the odontoblast layer, will be delayed in reaching the core of the pulp. Dendritic antigen presenting cells

9. Characteristic features of sub-odontoblastic zone Immediately below the odontoblast layer is a cell free zone of weil – in histological sections no cells are apparent. Electron microscopy reveals that many cell processes of fibroblasts, odontoblasts, axons and capillaries cross this region. This area could also be described as anuclear. The cell free zone is absent from the radicular pulp and usually appears in the pulp once the tooth has erupted. Next to this (below) is the cell rich zone. In this region there is a high concentration of both capillaries (sub-odontoblastic capillary plexus) and axons ( the sub-odontoblastic neural plexus). The Schwann cells, endothelial cell are associated with these plexus and gives the cell rich appearacne.

10. Characteristic features of sub-odontoblastic zone Central to this cell rich zone is the bulk of dental pulp which devoid of its peripheral structures and its central neurovascular core, would be similar to loose connective tissue in other sites except is richer in nerve and blood supply The central core itself is most evident in the root canal. Once it enters the crown repeated branching of both nerves and blood vessels renders the neurovascular bundles less obvious.

11. Organisation of pulp

12. Organization Odontoblasts lie at the periphery of the tissue. Also in this region are two elements capable not only of detecting external stimuli but also of initiating and participating in response to them. These are the nerve terminals of trigeminal afferents and specialized antigen-presenting cells Rest of the pulp acts as a support system Blood vessels and nerves enter and leave the root canals through an apical foramen at the root end Lateral canals most common in the apical third of the root

13. Composition It’s a loose connective tissue made up of combination of cells embedded in an extracellular matrix of fibres in a semi-fluid gel. 75% by weight is water and 25% is organic material Matrix is more plentiful with cells The extra cellular matrix is made up of a versatile group of polysaccharides and proteins secreted by the cells of the tissue and assembled into a complete framework closely associated with the cells The matrix forms a scaffold that stabilizes the structure of the tissue and controls the activities of the cells within it. It affects their development, migration, division, shape and function. Collagen is the predominant extra cellular matrix component comprising 25 – 32% of dry weight

14. Fibers Chiefly – Type I collagen as is present in bone, cementum, skin, tendon and dentin The collagen is present as fibrils thinly scattered through the pulp in the young tooth Present as 50nm in diameter and several micrometers long that combine into bundles as fibers of varying size

15. Fibers cond. Pulp – arrangement is irregular except at the periphery where they are aligned parallel to the forming predentin surface. About 56% of pulpal collagen is type I and 41% is type III. Small amount of type VI and and type V collagen is also available Overall the collagen forms 3-5% of the wet weight of the pulp. Microfibrils of smaller diameter than collagen have also been detected. These are fibrillin, a large glycoprotein that forms beaded fibrils 10-14nm in diameter.

16. Patterns of Collagen Deposition Two basic patterns Diffuse – in which the collagenous fibers lack definite orientation Bundle Type – in which large, coarse bundles run parallel to nerves or independently Coronal pulp tissue has more bundle collagen than diffuse collagen. In young pulps, few collagen fibers are found. As the pulp gets older, more and more collagen is elaborated and this increase in mostly in type III collagen Regardless of the age, the apical portion of the pulp is usually more fibrous than the coronal portion

17. Non – Fibrous Matrix Fall in two main groups- Glycosaminoglycans and other adhesion molecules GAG’s These are polysaccharide chains composed of repeating disaccharide units, which when covalently linked to proteins form glycoprotein Four GAG’s found in the pulp are –Chondroiten Sulphate, Dermatan Sulphate, Heparan Sulphate and Hyaluron Chondroitin Sulphate predomiates quantitatively and Dermatan Sulphate is present only in small amounts GAG’s are bulky molecules and hydrophillic, hence readily form gels that fill most of the extracellular space

18. GAG’s These molecules swell when hydrated, which may contribute to the high tissue fluid pressure of the pulp This provides mechanical support but also allows easy movement of water soluble molecules and cells Hyaluronan is the only GAG found in quantity unbound to protein. This also facilitates cell migration. Hence most prevalent during development. In mature pulp GAG content is - 60% hyaluron, 20% dermatan sulphate and 12% chondroitin sulphate. In the developing pulp chondroitin sulphate is the major GAG, with hyaluron only a minor component.

19. Proteoglycans – consist of core protein of variable size surrounded by GAG’s and perhaps other sugars

20. Pictures showing presence of Chondroitin Sulphate and Proteoglycans Versican

21. Other Adhesion Molecules Fibronectin is a glycoprotein that plays a role not only in attaching cells to extracellular matrices but also in regulating cell shape, migration and differentiation. Laminin is present in basement membranes binding epithelial cells to the extracellular matrix as well as binding some signaling molecules. In the pulp it is present only around the endothelial cells of blood vessels and schwann cells of nerve fibers

22. Cells - Odontoblasts Is responsible for formation of dentin. The fully differentiated odontoblast is a polarized columnar cells with a single long cell process that extends into the predentin and dentin within a dentinal tubule. Cell body – 50 um long and 5-10um in width, nucleus is usually in the basal (pulpal) half of the cell with the other organelles involved in dentin synthesis – the rER, Golgi complex and mitochondria above it

23. Odontoblasts In a mature tooth the odontoblasts form a layer of single cells attached to the predentin surface with single cell processes extending into the dentinal tubules The odontoblasts in the crown are distinctly columner and in the root they are more cuboidal The nuceli of adjacent cells in the layer lie at different levels and when the layer is sectioned obliquely this gives a false appearance of multiple layers - pseudostratification

24. Odontoblasts The odontoblast layer provides a controlled barrier between the pulp and the dentin The layer also contributes to the protection of the dental pulp from outside irritants. Stimuli that affect the dental pulp to initiate pain do so by causing fluid to move along the dentinal tubules and inducing pressure changes in the pulp The diffusion of molecules pulp wards is opposed by the outward flow of dentinal fluid and by the almost membrane like properties of the odontoblast layer

25. Electron microscopic findings about odontoblasts Nucleus – ellipsoidal in shape, contains chromatin and nucleoli. The nucleus is surrounded by two thin membranes, each about 50A in thickness. Nucleolus – differentiated odontoblasts contain one to four nucleoli. The nuclei from fully developed teeth are ring shaped, which is typical for the reversibly inhibited, or low, rate of synthesis of RNA. In less developed teeth, compact nucleoli, representative of active RNA production. Cytoplasm – rich in cell organelles

26. Cell Junctions Cell junctions maintain the integrity of the odontoblastic layer and its limited permeability. Three types – The macula adherens juctions (desmosomes) have a clear intercellular component as well as an intracellular system of anchoring fibrils and are largely responsible for mechanical union. Junctions that would completely encircle the cells (zonula type) are not present Tight Junctions (impermeable), which appear almost as a fusion of apposing cell membranes, limit permeability. In the odontoblast layer, these junctions do not encircle the cells, hence they limit the permeability rather than eliminate.

27. Cell Junctions Gap Junction (communicating Junctions) – this allows movement of small molecules directly between adjacent cells. Play a role in cell communication and synchronizing the activity of all the odontoblasts in the layer.

28. General Features Nerve endings are very closely apposed to odontoblast process in the dentinal tubules and many nerve endings occur in and around the odontoblastic layer. It has been suggested that odontoblasts may act as sensory receptors, passing signals from the surface of the dentin to nerve endings via synapses, either chemical or electrical. Odontoblasts may participate in the pulp’s initial response to injury as well as in the later stages of repair. They are first cells to encounter dental pathogens. They are in vitro, able to express interleukin – 8 when challenged with bacterial toxins. (IL-8 is a pro-inflammatory chemokine which can participate in the recruitment of neutrophils)

29. Fibroblasts In pulp they form loose network throughout the tissue linked by adherens type junctions and gap junctions. Morphology variable but mostly stellate shaped with the arms of the stars linking fibroblast to fibroblast or fibroblast to odontoblast. Function is to produce extra cellular fibers and ground substance for the dental pulp Pulpal fibroblasts are able to produce a variety of growth factors and cytokines with roles in controlling development, growth and the response to injury

30. Defence cells T – Lymphocytes are present in small numbers. The number increases enormously when the pulp is injured or subjected to a noxious stimulus Macrophages are also present. In their resting phase called histocytes, they can appear in a variety of form and difficult to distinguish from fibroblasts

31. Defence cells Dendritic antigen presenting cells 50um long and have three or more main dendritic processes which branch Largely distributed around odontoblasts and the central blood vessals These stimulate the division and activity of naïve T-lymphocytes They initiate primary immune response and may migrate, with trapped antigen to regional lymph nodes and induce T-lymphocyte division and differentiation there

32. Undifferentiated Cells It is observed that there is a population of cells in the dental pulp beneath the odontoblast layer, which can in response to a severe challenge, produce tertiary dentin. This led to the suggestion that the mature pulp holds a population of pluripotential, primitive mesenchymal cells capable of differentiating into a variety of cell types

33. Systemic Factors that affect the pulp Certain systemic conditions affect the cells, fibers, and ground substance of the connective tissues of the pulp Vitamin Deficiency – Vit C deficiency affects fibroblasts Ascorbic Acid – Odontoblasts Harmones and Harmone Imbalance – Studies show systemic high doses of steroids inhibit collagen synthesis. Long term systemic steroid therapy delays bone and wound healing and affects the odontoblasts, thereby inhibiting dentinogenesis. The benefits of steroid therapy is highly questionable, since they interference with the process of inflammation permits uninhibited growth of micro-organisms and may lead to pulpal degeneration.

34. Systemic Factors that affect the pulp Diabetes – a rise in plasma glucose levels produces a correlative rise in glucose concentrations in the dentinal pulp fluid. Diabetes produces degenerative and inflammatory changes in the pulp, and dentinogenesis is consequently affected. Thyroid Deficiency – experiments showed a marked reduction in vascularity of the pulp, with a hypermineralization of bone and dentin in case of thyroid deficiency. There was rapid deposition of dentin, which narrowed the lumen of the pulp, and all tissues showed decreased amount of cellular elements. Protein Deficiency – experiments reveal that animals deprived of protein developed larger regions of peri-apical rarefaction around teeth subjected to occlusal interference after pulps were exposed. Osteogenic activity and localized inflammation were also affected. They also showed degeneration of connective tissue fibers of the periodontium, osteoporosis of the alveolar bone, and retardation of cementum deposition.

35. Systemic Factors that affect the pulp Systemic virus infection – the pulps of mice infected with polyoma virus exhibited degenerative changes that increased severity with the onset of caries (cohen and shklar -1965) Hereditary Diseases – Sickle Cell anemia – Witkop,1983 Leukemia - Stern and Cole, 1973 Disorder of reticulo endothelial cells Certain neurologic diseases

36. THANK YOU

37. Arterial Blood supply to the teeth

38. Venous Drainage from the teeth

39. Control of Blood Flow in pulp The main feeding arterioles enter the root canal through the apical foramina and traversed the central portions to reach the coronal portion of the pulp. The largest of these is 150um in diameter Within the root canals, they send off side branches to periphery The vessels divide and narrow to some degree in the root canal but branch profusely once they are within the coronal pulp

40. Directions of arterioles Pulp chamber arterioles could be separated into two groups – one advanced coronally toward the pulp horn, branching and forming a dense terminal capillary network toward the dentin. The other ran between the floor and the roof of the pulp chamber, also branching into a dense terminal capillary network. The terminal capillary network beneath the dentin i.e. the subodontoblastic capillary plexus, is almost perpendicular to the main trunk vessels.

41. Blood Vessals of Dental Pulp The sub-odontoblastic capillary plexus (network of vessels under the odontoblastic layer) is evident in sectioned histological sections These capillaries are 6-8um in diameter Capillaries are present both within and below the odontoblasts and predentin layer

42. Blood Vessals of Dental Pulp Capillaries do not enter the dentinal tubules. The fluid that is present in the dentine is an ultrafilterate of the pulpal interstitial fluid Approximately 4-5% of capillaries in the sub-odontoblastic zone are fenestrated. Fenestrations are 60-80um in diameter. Only basement membrane is present at the fenestrations, allowing rapid movement of materials out of the capillary Numerous arterio-venous and venous-venous anastomoses are found between peripheral pulpal vessels presumably to allow rapid changes in blood perfusion

43. Control of Blood Flow in pulp The average capillary luminal diameter is less than 10um. The terminal capillaries drain into the venules beneath the dentin, and merge to form the primary venules Arterio-venous and veno-venous anastomoses and U turn loops is the unique feature of the pulpal vessels.

44. Regulation of pulpal hemodynamics Nerves help to regulate the blood supply to the dental pulp (Kim-1980) Sympathetic (adrenergic) nerve fibers liberate nor-epinephrine, which constricts the vessels Parasympathetic (cholinergic) nerves liberate acetylcholine, which dilates the vessels The catecholamines, such as epinephrine or nor epinephrine, exert their physiologic effects on receptors in the blood vessels, called adrenoreceptors. Circulating catecholamines such as adrenaline or nor adrenaline exert less of a vasoconstrictor effect than local sympathetic nerve activation.

45. Vasoconstriction Various studies indicate that the sympathetic adrenergic vasoconstrictor system causes variation in systemic haemodynamics, which in turn influences pulpal haemodynamics. At the resting stage, pulpal vessels are not under the tonic influence of sympathetic nerve discharge. However, electrical stimulation of the cervical sympathetic trunk causes severe reduction of pulp blood flow in dogs owing to activation of # adrenoreceptors. ( Edwall and Kim-1981) Experiments also reveal that reflex excitation of sympathetic nervous system by hypotension or decrease in systemic oxygen transport causes pulpal vasoconstriction and a reduction of pulpal blood flow.

46. Vasodilation Pulpal vessels are apparently equipped with B-receptors by intra-arterial injection of isoproterenol caused a paradoxial reduction of pulpal blood flow in dogs. Tender (1976) proposed that the flow reduction following intra-arterial ISO infusion resulted from stealing of blood flow by the adjacent tissues, which have a much greater vasodilator response.

47. Rates of Pulpal blood flow 40-50ml/min/100g of pulp tissue Blood flow values for various oral and visceral tissues at a hematocrit of 45% were compared, it is seen that blood flow in the pulp is relatively high, compared to that of other oral tissues and skeletal muscles. However, blood flow per unit weight of kidney, spleen and other vital organs was substantially higher. This indicates that blood flow reflects the functional capacity of an organ.

48. Structural and Functional Heterogeneity in Pulpal Circulation The highest capillary density occurs in the peripheral layer of the coronal region. The core of the apical region has lowest density. Blood flow of the coronal half of the pulp is about twice as much as that of the apical half. The average peripheral blood flow in the coronal region is 70ml/min/100g pulp flow, whereas the average flow in the core of the apical region measures 15ml/min/100g The pulp has a high, pulsatile interstitial tissue fluid pressure. This pressure would allow dentinal fluid to move outwards whenever the dentinal tubules were patent peripherally. This may slow the inward movement of irritants during the progression of dental caries.

49. Blood Vessals of Dental Pulp The presence of lymphatics in the pulp has been established by tracing particulate material kept within the pulp from the pulp to regional lymph nodes Nerve endings are associated with the smooth muscles of the arteriole walls. These are mainly vasoconstrictor. The extensive innervation of the peripheral pulp is also very significantly involved in control of blood flow. The most common neuropeptide in these nerves is calcitonin gene related peptide, peripheral action of which is vasodilatation. Substrate P, neuropeptide Y and nitric oxide synthetase are also present.

50. Lymphatics The lymphatic system is a second circulatory system whose primary function is to recirculate the interstitial fluid to the blood stream. The lymphatic system also serves as a transport system for the products of the cells into the blood circulation In the tissues, the lymphatic system arises from a fine mesh of small, thin walled lymph capillaries. Interstitial fluid diffuses through the walls of these capillaries to become lymph, a colorless or pale yellow liquid. The composition of lymph is similar to that of the interstitial fluid and to that of blood plasma. The lymphatic capillaries converge to form larger vessels that resemble veins.

51. Scheme of lymphatics and lymph drainage of the oral structures

52. Lymphatics in the dental pulp The presence to lymphatic vessels in the dental pulp has been under lot of controversy, because of the close morphologic resemblance of lymphatic vessels and veins or capillaries (sulzmann -1965) Observation with the light (Ruben 1971) and electron microscope ( Kukletove 1970) point to the probability that the pulp does contain lymphatics. Brown et al ( 1969) have claimed that a recording of osmotic pressure in the pulp is indirect evidence that the pulpal lymphatics do exist. The presence of lymphatic vessels in the dental pulp is still subject of lot of controversy.

53. Clinical Correlations - Local Anesthetics Vasoconstrictors are added to LA agent for the purpose of prolonging the anesthetic state and for obtaining a deeper anesthesia by confining the anesthetic to the injection site. Epinephrine most commonly used Blood flow in the pulp is reduced following infiltration of LA with epinephrine. (Olgart and Gazelius 1977) When dogs teeth were infilterated with lignocaine and 5ug to 20ug of epinephrine, the blood flow to the pulps was reduced by 30% (Meyer 1964)

54. Clinical Correlations – Temperature Changes A 10 to 15 C increase in the pulp pressure induced by heating wire wrapped around the tooth, caused arteriolar dilation and a linear increase in intrapulpal pressure of 2.5 mm of Hg per degree centigrade. The pressure gradually returned to normal as the tooth cooled. Irreversible changes occurred when vasodilatation was sustained by heating the pulp to 45 C for prolonged periods, resulting in persistent increased pulp pressure (Van Hassel -1969) Experiments show tooth preparation without water spray caused considerable reduction in pulpal blood flow. This reduction remained low even 1 hour after the preparation, indicating permanent damage to the circulatory system ( Kim -1983)

55. Clinical Correlations – Temperature Changes There was an increase in flow through the apically positioned arteriovenous anastomoses and a redistribution of flow from the drilled side to the opposite side. The initiation of pulpal damage probably resulted from alteration of micro-vasculature. Histopathologic changes in response to tooth preparation indicated that a burn lesion developed in the pulp when tooth was prepared within 1mm of the remaining dentin layer. At temperatures lower than -2 C, the pulp tissues exhibit immediate pulpal pathology, such as vascular engorgement and necrosis ( Frank -1972)

56. Clinical Correlations – Endodontic Therapy During endodontic therapy, if only part of the pulp is extirpated, profuse hemorrhage occurs, because of the increased diameters of vessels in the central part of the pulp. From clinical point of view, there would be less hemorrhage if the pulp were extirpated closer to the apex of the tooth. Excessive bleeding during instrumentation of the canal may indicate that some pulp tissue is still remaining in the apical third of the root canal. After eruption, the sub-odontoblastic capillary plexus is larger than during tooth development. In the floor of the pulp chamber, there is a rich blood supply.

57. Clinical Correlations – Aging, Periodontal Disease Aging – in older pulps, circulation is decreased. Atherosclerotic changes take place in the blood vessels, which narrow and become increasingly calcified. Finally, circulation becomes impaired; consequently, cells atrophy and die and fibrosis inreases. Periodontal Diseases – also cause reduction of the cias a consequence of degenerative pulp changes may take place

58. Clinical Correlations – changes due to inflammation In acute inflammation, chemical mediators released from injured cells excite sensory nerve fibers, which then act on the muscular elements of the blood vessels and cause dilation of the vessels. The permeability of the capillaries, which do not have muscle cells is increased by the action of similar substances in the ground substance of the capillary walls. The increased permeability of the vessels permits the escape of plasma proteins and leucocytes from the capillaries into the inflamed area to carry out neutralization, dilution and phagocytosis of the irritant. In chronic inflammation the pulp tissue pressure is elevated, although is less than that in acute inflammation.( Van Hassel – 1973)

59. Clinical Correlations – changes due to inflammation The muscular elements in the microcirculation re-establish control over capillary pressure. Capillary permeability is gradually decreased as repairs occurs. During inflammation, the effects of infilteration anesthesia are diluted which results in a diminution of anesthesia. In severe inflammation, the lymphatic vessels are closed, resulting in persistently increased fluid and pulp pressure. The end result may be pulp necrosis (Bernick- 1977)

60. Innervation of the teeth

61. Innervation of the teeth Pulpal pain excites all nuclei in the trigeminal spinal tract nucleus. Pulp afferent inputs project to the subnucleus caudalis, which is specifically involved in pain and temperature transmission. Afferents also project to other nuclei at more rostral levels, including the subnucleus oralis, which has been associated with tactile sensation Thus, dental nerves may contain receptors associated with other sensory modalities, such as temperature and touch. (Mumford-1969)

62. Innervation of the teeth Both the medullated and the nonmedullated nerve fibers leave the alveolar nerve as a common dental nerve. This nerve divides into multiple branches as it traverses the bone. At the apical alveolar plate, the branches, probable A$ and C axons enter the periodontal ligament in each of the four tooth surfaces. The nerves enter the apical foramina and unite to form a common pulpal nerve. The nerve trunks enter the root with the afferent blood vessels either as accompanying individual units or as intimately associated nerve sheaths (neuroadventitia; Provenza 1969)

63. Nerves of the Dental Pulp Pulp is heavily innervated – app. 2500 axons enter the apical foramen of a mature pre-molar. 25% of these are myelinated afferents whose cell bodies lie in the trigeminal ganglion. Of these 90% are narrow A$ fibers (1-6um in diameter) with the rest belonging to the wider A# group (6-12um in diameter). The unmyelinated C fibers are either afferent or autonomic. Although the nerve fibers enter the dental pulp in bundles, there is only a scant perineurium or epineurium. The nerve bundles run centrally in the pulp of the root in close association with the blood vessels. A few fibers leave the central bundles in the root and travel to the periphery. Most continue to the coronal pulp where they spread apart and branch profusely.

64. Nerves of the Dental Pulp Most of the branches end in the odontoblastic or sub-odontoblastic regions. In the crown there is a pronounced plexus of nerves beneath the odontoblasts, known as the plexus of Raschkow. This plexus is not evident until after the tooth has erupted. Branches from the plexus pass into the odontoblast layer and form the marginal plexus between the odontoblast layer and the pre-dentin, others continue into the dentin to accompany odontoblast processes in the dentinal tubules

65. Nerves of the Dental Pulp This sub-odontoblastic plexus may be one of the sites of sensory activation in the pulp. Many of the axons are devoid of a Schwann Cell covering, either completely or partially, rendering them susceptible to changes in the extra-cellular environment. The axons branch profusely, providing a broad surface area for activation. Within the Schwann cell, there are often many axons in a single pocket and the spread of signals from axon to axon is possible

66. Nerve fiber types It has been suggested that some pulpal nerves may have direct trophic effects, perhaps controlling in part the activity of odontoblasts. Some of the C fibers are sympathetic efferents and supply arteriolar smooth muscle. As there are only a few arterioles within the pulp sympathetic fibers are scarce. They seem to mediate their vaso-constrictive effect by the release of nor-adrenaline and neuropeptide Y.

67. Nerve fiber types Acetylcholine, the principal mediator for the parasympathetic system, is rarely detected in the dental pulp Vasodilatation seem to be effected by axons reflexes involving afferent nerves as well as by build up of metabolites locally. Nitric oxide produced following hypoxia and tissue injury in the dental pulp is the signaling molecule most likely to induce vasodilatation under these conditions.

68. Nerve Endings Autonomic nerves end on the smooth muscles of the arterioles and special neuromuscular junctions are present. Some of the afferent fibers (portion of A$ fibers) enter the tubules largely in the coronal dentine and pre dentine. Others may end at the pulp – predentine junction (marginal plexus) Many axons end in close proximity to the odontoblasts – studies describe the proteins synapsin and synaptotagmin, characteristic of neural junctions, in the dentinal tubules. The nerves in the dentinal tubules, at the pulp-predentin border and among the odontoblast cell body have all lost their ensheathing Schwann cells and their axolemmas are exposed directly to the extracellular environment

69. Nerve Endings Changes in the composition of, or movement within, the extracellular fluid could readily affect the membrane properties of these terminals. Calcitonin Gene Related Peptide is a potent vasodilator and quite possibly the principal agent controlling the blood flow locally in the periphery of the dental pulp. CGRP is synthesized in the cell bodies of the nerves in the trigeminal ganglion and moved peripherally by axonal transport. CGRP may also participate in initiating or controlling hard tissue production.

70. Nerve Endings Nerve growth factor and NGF receptors have been detected in the peripheral dental pulp. NGF are not produced by odontoblasts but are donated by neighboring fibroblasts. The expression of NGF and its receptors increases in the injured pulp. NGF acts as a chemo-attractant for leukocytes in the damaged pulp. In short the major role of the trigeminal afferents in the dental pulp is in controlling the local environment rather than in carrying sensory information centrally. Some neuropeptides may function to control the flow of sensory activity centrally.

71. Theories of tooth and pain perception There is no clear cut explanation of how a stimulus applied to dentin can influence nerve fibers that apparently do not penetrate all of the dentinal tubules or even the bulk of the dentin. Several hypothesis have been suggested, the three most prevalent theories are Dentinal nerve stimulation Dentinal receptor theory Hydrodynamic theory

72. Dentinal Nerve Stimulation theory Whether dentin is actually innervated is a subject of controversy. Silver salts have been used to disclose the distribution of nerve fibers because nerve tissue has an affinity for silver. However, the demonstration of nerves by staining with silver salts may be an artifact in as much as other structures, such as reticular fibers and collagen fibers. Thus blackened collagen fibers may be mistaken for nerves. At light microscopic level, variable penetration of dentin by a limited number of nerve fibers has been demonstrated (Bermick 1968, Yagi 1972)

73. Dentinal Nerve Stimulation theory Several electron microscopic studies have differed with respect to finding on dentin innervation. It is difficult to identify unmyelinated nerve fibers in dentin because cellular extensions of the odontoblasts have similar ultrastructural components. A scanning electron microscope study by Tidmarsh (1981) revealed beaded structures, possibly nerves, in the dentin as far as halfway between the pulp and the dentinoenamel junction. Frank (1966) demonstrated that in the predentin and inner dentin - the nerve fiber followed a straight course along the odontoblast process and was in close contact with it.

74. Dentinal Receptor Theory The odontoblasts and their processes are perceived to act as dentinal receptor mechanisms whereby they participate in the initiation and transmission of sensory stimuli in dentin. Numerous investigations have provided structural evidence for presence of nerve fiber like structures adjacent to the odontoblastic processes in the dentinal tubules close to the pulp dentin junction. Because of their proximity, it is tempting to hypothesize a close functional relationship between these associated cells and the odontoblastic process. However synaptic junctions, which are essential for nerve conduction between associated cells and odotoblastic process, have not been definitely found.

75. Recording of Electrical Activity from Dental Nerve Fibers Mathew (1970) conducted experiments on the canine teeth of cats, and reported that the response to thermal stimulation recorded directly from an intact pulp was similar to that recorded from the overlying dentin. Furthermore, impulses could be recorded with an electrode placed on the floor of a cavity from electrically stimulated radial nerve fibers placed in the pulp chambers after the original pulps had been removed. Such findings indicated that recordings of electrical activity from the dentin do not necessarily originate from nerves in the dentin but probably originate from nerves in the pulp.

76. Experiments Conducted on Humans show – Edwall and Olgart (1977) Thermal changes implicate alteration in the response of nerves in or near the dentin. However, they have not been found to alter the reaction time of dentin uniformly. Naylor (1963) found the threshold temperature to cold stimulation of human dentin to be approximately 30 C. He later reported that the reaction time to thermal stimulation of dentin was lengthened by cutting the dentin with an uncooled bur. Such cutting caused damage to the odontoblasts. Drugs, pressure and osmotic changes also alter dentinal pain responses. Topical application of aspirin to the dentin promptly inhibited both steady state discharge and response to a brief heat stimulus (Scott 1968). however damaging drugs, such as silver nitrate, zinc chloride did not reduce dentin sensitivity (Anderson-1963)

77. Transducer Mechanism Dentinal receptor mechanism carries the implication that the odontoblast has a special sensory function and that the odontoblastic process-nerve ending junctional complex in or near the odontoblastic layer functions as an excitatory synapse. Furthermore, it implies that a mechanism similar to the inhibitory synapse found in other nerve cells must be present. Frank (1969) estimated that a cavity preparation of 1mm 2 would involve about 60,000 dentinal tubules. Should there be one nerve fiber for each 2000 dentinal tubules, at least 30 nerve endings would be stimulated; if there were one nerve fiber for each 200 tubules, 300 nerve endings would be irritated in a cavity preparation of 1mm 2 .

78. Transducer Mechanism The number of innervated dentinal tubules in human teeth may actually be much greater. Beyers – 1983 found frequent clusters of coronal dentin with innervation in three to ten adjacent tubules. Frank concluded that the intradentinal receptor presents a unique type of neurosensitive complex in which intimate connections exist between the odontoblast process and a sensory fiber.

79. Cholinergic Nerves in Dentin On stimulation of the nerves, Ach is released from an inactive, bound form and is rapidly converted to less active free choline and acetate by the enzyme AchE. AchE terminates the passage of nerve impulses by its inactivation of Ach. Thus the localization of AchE in tissues indicates the presence of ACh. The presence of AchE has been demonstrated in the dentin and pulp of human teeth by histochemical studies (Avery and Rapp – 1967) Although dentin innervation is almost entirely sensory, some adrenergic nerve endings have been found in the walls of the pulpal blood vessels and in the odontoblastic layer and predentin (Avery - 1975).

80. Hydrodynamic Theory Brannstrom (1963) hypothesized that dentin pain and odontoblastic displacement were related. Injury to the odontoblasts caused displacement of the contents of the dentinal tubules.The intimate relationship of the odontoblasts with nerve fibers at the pulpodentinal border would result in mechanical stimulation of those fibers. He (Brannstrom – 1975) postulated a hydrodynamic mechanism underlying dentinal sensitivity. The dentinal pulp fluid expands and contracts in response to the application of stimuli. As the fluids have a coefficient of expansion greater than that of solid dentin, the contents of dentinal tubules move pulpward or externally in response to a given stimulus.

81. Hydrodynamic Theory A rapid outward flow of dentinal pulp fluid by capillary attraction occurs through exposed dentinal tubule apertures. Thus, thermal stimuli, scraping, drilling, and sugar application all cause outward movement of dentinal fluid. The fluid movement stimulates the nerves in the pulp. Pain on probing on dentin can be explained by the fact that the force exerted on the dentin by light pressure from an explorer may be high. Thus, compression of fluid or mechanical distortion of tubule orifices by a probe tip can cause fluid displacement and pulpal sensory nerve excitation. Acid etching of dentin, which opens dentinal tubules, is also capable of increasing fluid flow resulting in increased dentin sensitivity (Brannstrom -1979)

82. Fluid or Hydrodynamic Theory Brannstrom pointed out that, displacement of tubule content (either inwards or outwards), if produces movement which is rapid enough, may produce deformation of nerve fiber in the predentin or pulp which is capable of producing pain. These endings may act as mechanoreceptors as they are affected by mechanical displacement of tubular fluid

83. Fluid or Hydrodynamic Theory – Damage by blowing air A short air blast evaporates 0.1 to 0.3 mm of fluid from the dentinal tubule This results in immediate capillary fluid replacement from the pulp’s blood supply, sucking the odontoblasts and nerve fibers up into the tubules. On continued exposure to the air blast , a plug of fluid protein builds up in the tubule preventing fluid outflow. The plug closes the pump and leads to dentin insensitivity. When water is applied to the dentin surface, the plug melts and sensitivity returns

84. Possible mechanisms of reduction of dentin sensitivity Pashley (1982), the fluid flow in the dentinal tubules may be reduced, consequently lessening dentinal sensitivity, by several possible mechanisms Occlusion of tubules by large number of bacteria from plaque or saliva Mineralized deposits within the dentinal tubules from exposure of dentin to saliva Adsorption of salivary or plasma proteins on to dentinal tubules. Heating of the tooth and pulpitis cause tissue pressure to increase significantly. Cold causes the intrapulpal pressure to drop (Beveridge - 1965)

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