Innervation of Dentin and mechanisms of Pain Sensation
Nerve supply to the coronal pulp is especially rich. It forms a subodontoblastic plexus of nerve (plexus of Raschkow). Unmyelinated nerves from this plexus penetrate between the odontoblasts and enter the predentin. Although most unmyelinated nerves appear to terminate in the predentin, some enter the dentinal tubules.Nerve endings containing many small vesicles and mitochondria have been identified in close association with the odontoblast ceil body and the odontoblast process in dentin. The majority of these nerves are afferent somatosensory pain fibres. Nerves growth factor and its receptor have been localized in relatively high amounts in the odonblastic and subodontoblastic layers of the coronal pulp. The presence of nerve growth factor may be responsible for concentrating nerve ending in the vicinity of the odontoblast. Experimental evidence has shown that nerves grow toward concentration of nerve growth factor. Because the cell process of fibroblasts and odontoblasts can be confused with unmyelinated nervs fibres special staining techniques are needed to accurately distinguish nerve fibres and their terminals. A neuron-specific protein, protein gene product 9.5, has been used to identify pulpal nerve fibres at both the light and electron microscopic level. Fibres containing protein gene product were present in both radicular and cononal predentin. Nerve endings in the predentin have also been identified by immunocy to chemistry for calbindin , a calcium-buiding protein found in high concentrations in nerves cells. Tracer experiments with tritiated proline injected into the brainstem nuclei of the trigeminal nerve have provided convincing proof of a rich supply of sensory nerve terminals in the predentin and dentinal tubules. Vasomotor nerves supply small arteries in the pulp, terminating in close apposition to arteriolar smooth muscle cell. The nerve endings contain many dense-cored adrenergic synaptic vesicles.
Theories of dental pain
Although it is well established that most unmyelinated nerve endings in pulp and dentin are nociceptors, the exact mechanisms whereby noxious conditions are converted into dental pain stimuli have yet to be identified .The most widely held theory centers around fluid flow within dentinal tubules. The hydronamic theory of dental pain is based on the facts that fluid in the dentinal tubules is constrained by the rigid walls of the peritubular dentin and fluxes in temperature or in osmotic pressure produce rapid expansion and contraction of the dentinal fluid. The bulk flow of the dentinal fluid may distort nerve endings, thereby triggering nerve impulses. Experimental support for this theory is provided by the observation that pain occurs when heat or a substance that changes the osmotic pressure of the dentinal fluid is applied to cut dentin surfaces.
However, the hydrodynamic theory does not explain why some chemicals that do not alter osmotic pressure in dentin can still cause dental pain. It is presumed that these chemicals diffuse down their concentration gradients to act directly on nociceptive nerve endings in pre-dentin. The hydrodynamic theory also fails to account for the rapidity of stimulus transduction, especially in relation to mechanoreceptor activity elicited from dentin. Despite the limitation of the hydrodynamic theory, the results of clinical and basic research on dentin sentitivity have shown that patency of dentinal tnbules is a significant factor in controlling the degree of stimulation of dental nerves
Recent investigations have shown that the dentinal tubules are filled with a fibrous hydrogel. Although the hydrogel may limit bulk fluid flow. Its still permit the diffusion of solutes down their concentration gradient. Dentin sensitivity can be reduced by obliteration of the tubules, either by physiologic formation of peritubular dentin and the intratubular deposition of collagen fibrils or by the clinical application of agents that cause mineral precipitation inside the tubules.
It has also been speculated that the odontoblast (and its process) might act as a tranducer to convert noxious stimuli into nerve impulses. This concept is based on the notion that odontoblasts make gap junctions (electronic synapses) with adjacent nerve and that the flow of ions through these junctions, in response to changes in the odontoblast, could lead to depolarization of somatosensory neurons. Patch- clamp recordings made on segments of plasma membrane from isolated odontoblasts have demonstrated potassium and chloride channels and a resting membrane potential of about -40 to -50mV, It has been suggested that mechanosensitive ion channels could lead to changes in ion conductance across the plasma membrane in response to hydrodynamic forces exerted on the odontoblastic process. Although gap junctions between odontoblasts and nerves have been reported, there is still no proof that odontoblasts communicate electrically with nerve endings, A subpopulation of cells cultured from human dental pulp have voltage-gated sodium channels and other properties associated with neuronal satellite cells. Whether these pulp cells originate from the odontoblastic layer and whether or not they have a role in pulpal somatosensation remains to be established. It has also been suggested that dentinal nerves may have an effector functions on odontoblast. Indirect evidence for an effector activity includes the fact that many dentinal nerves contain the neuropetide calcitonin gene-related peptide CGPR. Evidence of protein secretion from dentinal nerves has also been reported. Recent studies of the presence of several exocytosis regulatory proteins (synapsin and synaptogamin) in dentinal nerve endings adds more support that dentinal nerves have an effector function in addition to their somatosensory afferent actions. Many of the nerve endings in odontoblastic layer and predentin contain substance P and CGRP. These neuropeptides may be involved in vascular dilation and neurogenic inflammation. Indirect evidence supports the idea that the release of neuro peptides from dental sensory nerve fibres is important in the recruitment of immuno competent cells to the dental pulp. Experimental studies also suggest that these neuropeptiudes may promote dentinogenesis.
The potential for development of neurogenic inflammation in the pulp is supported by the demonstration that coronal and apical pulp contains CGRP positive nerves in association with blood vessels and within the connective tissues stroma. Some CGRP- positive nerve fibres are found in the subodontoblast layer. Sprouting of CGRP- positive nerve endings occurs following dental injury. The release CGPR increases vascular permeability of pulpal blood vessels. Recent studies have demonstrated excitatory amino acid receptors in bovine dental pulp. Activation of excitatory amino acid receptors leads to release of CGRP in pulp..
Nerve supply to the coronal pulp is especially rich. It forms a subodontoblastic plexus of nerve (plexus of Raschkow). Unmyelinated nerves from this plexus penetrate between the odontoblasts and enter the predentin. Although most unmyelinated nerves appear to terminate in the predentin, some enter the dentinal tubules.Nerve endings containing many small vesicles and mitochondria have been identified in close association with the odontoblast ceil body and the odontoblast process in dentin. The majority of these nerves are afferent somatosensory pain fibres. Nerves growth factor and its receptor have been localized in relatively high amounts in the odonblastic and subodontoblastic layers of the coronal pulp. The presence of nerve growth factor may be responsible for concentrating nerve ending in the vicinity of the odontoblast. Experimental evidence has shown that nerves grow toward concentration of nerve growth factor. Because the cell process of fibroblasts and odontoblasts can be confused with unmyelinated nervs fibres special staining techniques are needed to accurately distinguish nerve fibres and their terminals. A neuron-specific protein, protein gene product 9.5, has been used to identify pulpal nerve fibres at both the light and electron microscopic level. Fibres containing protein gene product were present in both radicular and cononal predentin. Nerve endings in the predentin have also been identified by immunocy to chemistry for calbindin , a calcium-buiding protein found in high concentrations in nerves cells. Tracer experiments with tritiated proline injected into the brainstem nuclei of the trigeminal nerve have provided convincing proof of a rich supply of sensory nerve terminals in the predentin and dentinal tubules. Vasomotor nerves supply small arteries in the pulp, terminating in close apposition to arteriolar smooth muscle cell. The nerve endings contain many dense-cored adrenergic synaptic vesicles.
Theories of dental pain
Although it is well established that most unmyelinated nerve endings in pulp and dentin are nociceptors, the exact mechanisms whereby noxious conditions are converted into dental pain stimuli have yet to be identified .The most widely held theory centers around fluid flow within dentinal tubules. The hydronamic theory of dental pain is based on the facts that fluid in the dentinal tubules is constrained by the rigid walls of the peritubular dentin and fluxes in temperature or in osmotic pressure produce rapid expansion and contraction of the dentinal fluid. The bulk flow of the dentinal fluid may distort nerve endings, thereby triggering nerve impulses. Experimental support for this theory is provided by the observation that pain occurs when heat or a substance that changes the osmotic pressure of the dentinal fluid is applied to cut dentin surfaces.
However, the hydrodynamic theory does not explain why some chemicals that do not alter osmotic pressure in dentin can still cause dental pain. It is presumed that these chemicals diffuse down their concentration gradients to act directly on nociceptive nerve endings in pre-dentin. The hydrodynamic theory also fails to account for the rapidity of stimulus transduction, especially in relation to mechanoreceptor activity elicited from dentin. Despite the limitation of the hydrodynamic theory, the results of clinical and basic research on dentin sentitivity have shown that patency of dentinal tnbules is a significant factor in controlling the degree of stimulation of dental nerves
Recent investigations have shown that the dentinal tubules are filled with a fibrous hydrogel. Although the hydrogel may limit bulk fluid flow. Its still permit the diffusion of solutes down their concentration gradient. Dentin sensitivity can be reduced by obliteration of the tubules, either by physiologic formation of peritubular dentin and the intratubular deposition of collagen fibrils or by the clinical application of agents that cause mineral precipitation inside the tubules.
It has also been speculated that the odontoblast (and its process) might act as a tranducer to convert noxious stimuli into nerve impulses. This concept is based on the notion that odontoblasts make gap junctions (electronic synapses) with adjacent nerve and that the flow of ions through these junctions, in response to changes in the odontoblast, could lead to depolarization of somatosensory neurons. Patch- clamp recordings made on segments of plasma membrane from isolated odontoblasts have demonstrated potassium and chloride channels and a resting membrane potential of about -40 to -50mV, It has been suggested that mechanosensitive ion channels could lead to changes in ion conductance across the plasma membrane in response to hydrodynamic forces exerted on the odontoblastic process. Although gap junctions between odontoblasts and nerves have been reported, there is still no proof that odontoblasts communicate electrically with nerve endings, A subpopulation of cells cultured from human dental pulp have voltage-gated sodium channels and other properties associated with neuronal satellite cells. Whether these pulp cells originate from the odontoblastic layer and whether or not they have a role in pulpal somatosensation remains to be established. It has also been suggested that dentinal nerves may have an effector functions on odontoblast. Indirect evidence for an effector activity includes the fact that many dentinal nerves contain the neuropetide calcitonin gene-related peptide CGPR. Evidence of protein secretion from dentinal nerves has also been reported. Recent studies of the presence of several exocytosis regulatory proteins (synapsin and synaptogamin) in dentinal nerve endings adds more support that dentinal nerves have an effector function in addition to their somatosensory afferent actions. Many of the nerve endings in odontoblastic layer and predentin contain substance P and CGRP. These neuropeptides may be involved in vascular dilation and neurogenic inflammation. Indirect evidence supports the idea that the release of neuro peptides from dental sensory nerve fibres is important in the recruitment of immuno competent cells to the dental pulp. Experimental studies also suggest that these neuropeptiudes may promote dentinogenesis.
The potential for development of neurogenic inflammation in the pulp is supported by the demonstration that coronal and apical pulp contains CGRP positive nerves in association with blood vessels and within the connective tissues stroma. Some CGRP- positive nerve fibres are found in the subodontoblast layer. Sprouting of CGRP- positive nerve endings occurs following dental injury. The release CGPR increases vascular permeability of pulpal blood vessels. Recent studies have demonstrated excitatory amino acid receptors in bovine dental pulp. Activation of excitatory amino acid receptors leads to release of CGRP in pulp..
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