Pulpal reactions to caries and dental procedures

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  • Pulpal Reaction to Caries: Def; It is a localized, destructive, and progressive infection of dentin; if left unchecked, caries can result in pulpal necrosis and potential tooth loss. Both bacterial byproducts and products from the dissolution of the organic and inorganic constituents of dentin mediate the effects of dental caries on the pulp. Three basic reactions tend to protect the pulp against caries: a decrease in dentin permeability. A combination of an increased deposition of intratubular dentin and the direct deposition of mineral crystals into the narrowed dentin tubules to decrease dentin permeability is the first defense to caries and is called dentin sclerosis . It occurs by a combination of increased deposition of intratubular dentin and tubule occlusion by precipitated crystals. This results in an effective decrease in dentin permeability that occurs in a relatively short period of time. Classic studies have noted that while sclerosis is observed in the dentin of disease-free and attrition-free teeth, there is a 95% increase in the incidence in carious teeth. In vitro studies with cultured tooth slices implicate TGF-β1 as a central player in the increased deposition of intratubular dentin. The deposition of whitlockite crystals in the tubular lumen most likely results from a similar stimulation of vital associated odontoblasts, possibly in combination with precipitation of mineral released during the demineralization process.
  • a decrease in dentin permeability. A combination of an increased deposition of intratubular dentin and the direct deposition of mineral crystals into the narrowed dentin tubules to decrease dentin permeability is the first defense to caries and is called dentin sclerosis . It occurs by a combination of increased deposition of intratubular dentin and tubule occlusion by precipitated crystals. This results in an effective decrease in dentin permeability that occurs in a relatively short period of time. Classic studies have noted that while sclerosis is observed in the dentin of disease-free and attrition-free teeth, there is a 95% increase in the incidence in carious teeth. In vitro studies with cultured tooth slices implicate TGF-β1 as a central player in the increased deposition of intratubular dentin. The deposition of whitlockite crystals in the tubular lumen most likely results from a similar stimulation of vital associated odontoblasts, possibly in combination with precipitation of mineral released during the demineralization process.
  • (2) tertiary dentin Formation. It is neither the first nor necessarily the most effective pulpally mediated defense. In initial to moderate lesions, current evidence suggests that acidic byproducts of the carious process act indirectly by degrading the dentin matrix, thereby liberating bioactive molecules previously sequestered during dentinogenesis. Once liberated, these molecules once again assume their role in dentin formation, this time stimulatory for tertiary dentinogenesis. This theory is supported by: demineralized dentin matrix implanted at the site of pulpal exposure can induce dentinogenesis. placement of purified dentin matrix proteins on exposed dentin or exposed pulp stimulates tertiary dentin formation, indicating that these molecules can act directly or across intact dentin.
  • (2) tertiary dentin Formation: The resultant dentin character is highly dependent on the stimulus. Mild stimuli activate resident quiescent odontoblasts, whereupon they elaborate the organic matrix of dentin. This type of tertiary dentin is referred to as reactionary dentin and can be observed when initial dentin demineralization occurs beneath the noncavitated enamel lesion. Mediators present during the carious process induce a focal upregulation of matrix production by resident odontoblasts. The resultant dentin is similar in morphology to physiologic dentin and may only be apparent due to a change in the direction of the new dentinal tubules. Sever stimuli , the carious process may prove cytocidal to subjacent odontoblasts and require repopulation of the disrupted odontoblast layer with differentiating progenitors. The appearance of the resultant matrix is a direct reflection of the differentiation state of the secretory cells. This accounts for the heterogeneity of reparative dentin , where the morphology can range from organized tubular dentin to more disorganized irregular fibrodentin . Fibrodentin, owing to its irregular configuration and tissue inclusions, is more permeable than Physiologic dentin.
  • Sever stimuli , the carious process may prove cytocidal to subjacent odontoblasts and require repopulation of the disrupted odontoblast layer with differentiating progenitors. The appearance of the resultant matrix is a direct reflection of the differentiation state of the secretory cells. This accounts for the heterogeneity of reparative dentin , where the morphology can range from organized tubular dentin to more disorganized irregular fibrodentin . Fibrodentin, owing to its irregular configuration and tissue inclusions, is more permeable than Physiologic dentin.
  • (3) inflammatory and immune reactions. When relatively unhindered access to pulpal tissue is present, both bacterial metabolites and cell wall components induce inflammation. In the advancing infection front of the carious lesion, multiple intrinsic and extrinsic factors are released that are stimulatory to subjacent pulpal parenchyma. Bacterial metabolites such as acids have been thought to be initiators of pulpal reactions, yet the buffering capacity of dentin fluid likely attenuates the pH before it can directly effect a deleterious response, except when the remaining dentin thickness is minimal . Although dentin can provide a physical barrier against noxious stimuli, the pulpal immune response provides humoral and cellular challenges to invading pathogens. Recent evidence offers several candidate molecules that are stimulatory for reparative dentinogenesis. Heparin-binding growth factor, transforming growth factor (TGF)-β1, TGF-β3, insulin-like growth factors (IGF)-1 and -2, platelet-derived growth factor, and angiogenic growth factors have been shown to be stimulatory for dentinogenesis in vitro. The TGF-β superfamily in particular seems to be important in the signaling process for odontoblast differentiation as well as primary and tertiary dentinogenesis. As the predominant isoform, TGF-β1 is equally distributed in the soluble and insoluble fractions of dentin matrix. During the carious dissolution of dentin, it is intact dentin while the insoluble pool is immobilized on insoluble dentin matrix and serves to stimulate odontoblasts, much like membrane-bound TGF-βs during odontogenesis.
  • (3) inflammatory and immune reactions. In the progressing carious lesion, the host immune response increases in intensity as the infection advances. It has been shown that titers of T helper cells , B-lineage cells , neutrophils , and macrophages are directly proportional to lesion depth in human teeth. The disintegration of large amounts of dentin, however, is not necessary to elicit a pulpal immune response. This is supported by the observation that a pulpal inflammatory response can be seen beneath noncavitated lesions and noncoalesced pits and fissures . The early inflammatory response is characterized by the focal accumulation of chronic inflammatory cell s. This is mediated initially by odontoblasts and later by dendritic cells . (Why?) As the most peripheral cell in the pulp, the odontoblast is positioned to encounter foreign antigens first and initiate the innate immune response. Pathogen detection in general is accomplished via specific receptors called pattern recognition receptors (PRRs). These receptors recognize pathogen-associated molecular patterns (PAMPs) on invading organisms and initiate a host defense through the activation of the nuclear factor (NF)-κB pathway. One class of the PAMP recognition molecules is the toll-like receptor family (TLRs). Odontoblasts have been shown to have increased expression of certain TLRs in response to bacterial products. Under experimental conditions, odontoblast expression of TLR3, 5, and was increased in response to lipoteichoic acid, whereas lipopolysaccharide increased TLR2 expression. Once the odontoblast TLR is stimulated by a pathogen, proinflammatory cytokines, chemokines, and antimicrobial peptides are elaborated by the odontoblast, resulting in recruitment and stimulation of immune effector cells as well as direct bacterial killing. Many cells constitutively produce chemokines at low levels. Unstimulated odontoblasts express genes coding for CCl2, CXCL12, and CXCL14, three genes known to code for factors chemotactic for immature dendritic cells. They also produce CCL26, a natural antagonist for CCR1, CCR2, and CCR5, which are chemokines normally produced by monocytes and dendritic cells. Stimulation with bacterial cell wall constituents has been shown to upregulate the production of several chemokines, suggesting that odontoblasts sense pathogens and express factors that recruit immune effector cells. These data suggest a scenario whereby stimulated odontoblasts express high levels of chemokines such as interleukin (IL)-8 (CXCL8) that act in concert with the release of formerly sequestered TGF-β1 from carious dentin, the result of which is a focal increase in dendritic cell numbers, with additional release of chemotactic mediators.68 The subsequent influx of immune effector cells is composed of lymphocytes, macrophages, and plasma cells. This cellular infiltrate is accompanied by localized capillary sprouting in response to angiogenic factors, as well as coaggregation of nerve fibers and HLA-DR-positive dendritic cells. As the carious lesion progresses, the density of the chronic inflammatory infiltrate, as well as that of dendritic cells in the odontoblast region, increases. Pulpal dendritic cells are responsible for antigen presentation and stimulation of T lymphocytes . In the uninflamed pulp, they are scattered throughout the pulp. With caries progression, they aggregate initially in the pulp and subodontoblastic regions, then extend into the odontoblast layer, and eventually migrate into the entrance to tubules beside the odontoblast process. There are two distinct populations of dendritic cells that have been identified in the dental pulp. CD11c+ are found in the pulp/dentin border and subjacent to pits and fissures. F4/80+ dendritic cells are concentrated in the perivascular spaces in the subodontoblastic zone and inner pulp. CD11c+ dendritic cells express toll-like receptors 2 and 4 and are CD205 positive. F4/80+ dendritic cells have migratory ability. As they migrate from the central pulp, they increase in size and become CD86 positive. The close spatial relationship between odontoblasts and dendritic cells under the carious lesion have led to speculation that dendritic cells may play a role in odontoblast differentiation and/or secretory activity in the immune defense and dentinogenesis. Pulpal Schwann cells have also been shown to produce molecules in response to caries, which is indicative of the acquisition of the ability for antigen presentation. Evidence suggests that odontoblasts also play a role in the humoral immune response to caries. Immunoglobulin (Ig)G, IgM, and IgA have been localized in the cytoplasm and cell processes of odontoblasts in human carious dentin, suggesting that these cells actively transport antibodies to the infection front. In the incipient lesion, antibodies accumulate in the odontoblast layer and with lesion progression can be seen in the dentinal tubules. Eventually this leads to a focal concentration of antibodies beneath the advancing lesion. In the most advanced phase of carious destruction, the immune response is accompanied by immunopathologic destruction of pulpal tissue, as antigenantibody complex formation, in addition to various products of the inflammatory cascade, gives rise to a nonspecific response that, while designed to rid the body of pathogens, effects destruction of parenchymal tissues as well.
  • (3) inflammatory and immune reactions. In the progressing carious lesion, the host immune response increases in intensity as the infection advances. It has been shown that titers of T helper cells , B-lineage cells , neutrophils , and macrophages are directly proportional to lesion depth in human teeth. The disintegration of large amounts of dentin, however, is not necessary to elicit a pulpal immune response. This is supported by the observation that a pulpal inflammatory response can be seen beneath noncavitated lesions and noncoalesced pits and fissures . The early inflammatory response is characterized by the focal accumulation of chronic inflammatory cell s. This is mediated initially by odontoblasts and later by dendritic cells . (Why?) As the most peripheral cell in the pulp, the odontoblast is positioned to encounter foreign antigens first and initiate the innate immune response. Pathogen detection in general is accomplished via specific receptors called pattern recognition receptors (PRRs). These receptors recognize pathogen-associated molecular patterns (PAMPs) on invading organisms and initiate a host defense through the activation of the nuclear factor (NF)-κB pathway. One class of the PAMP recognition molecules is the toll-like receptor family (TLRs). Odontoblasts have been shown to have increased expression of certain TLRs in response to bacterial products. Under experimental conditions, odontoblast expression of TLR3, 5, and was increased in response to lipoteichoic acid, whereas lipopolysaccharide increased TLR2 expression. Once the odontoblast TLR is stimulated by a pathogen, proinflammatory cytokines, chemokines, and antimicrobial peptides are elaborated by the odontoblast, resulting in recruitment and stimulation of immune effector cells as well as direct bacterial killing. Many cells constitutively produce chemokines at low levels. Unstimulated odontoblasts express genes coding for CCl2, CXCL12, and CXCL14, three genes known to code for factors chemotactic for immature dendritic cells. They also produce CCL26, a natural antagonist for CCR1, CCR2, and CCR5, which are chemokines normally produced by monocytes and dendritic cells. Stimulation with bacterial cell wall constituents has been shown to upregulate the production of several chemokines, suggesting that odontoblasts sense pathogens and express factors that recruit immune effector cells. These data suggest a scenario whereby stimulated odontoblasts express high levels of chemokines such as interleukin (IL)-8 (CXCL8) that act in concert with the release of formerly sequestered TGF-β1 from carious dentin, the result of which is a focal increase in dendritic cell numbers, with additional release of chemotactic mediators.68 The subsequent influx of immune effector cells is composed of lymphocytes, macrophages, and plasma cells. This cellular infiltrate is accompanied by localized capillary sprouting in response to angiogenic factors, as well as coaggregation of nerve fibers and HLA-DR-positive dendritic cells. As the carious lesion progresses, the density of the chronic inflammatory infiltrate, as well as that of dendritic cells in the odontoblast region, increases. Pulpal dendritic cells are responsible for antigen presentation and stimulation of T lymphocytes . In the uninflamed pulp, they are scattered throughout the pulp. With caries progression, they aggregate initially in the pulp and subodontoblastic regions, then extend into the odontoblast layer, and eventually migrate into the entrance to tubules beside the odontoblast process . There are two distinct populations of dendritic cells that have been identified in the dental pulp. CD11c+ are found in the pulp/dentin border and subjacent to pits and fissures. F4/80+ dendritic cells are concentrated in the perivascular spaces in the subodontoblastic zone and inner pulp. CD11c+ dendritic cells express toll-like receptors 2 and 4 and are CD205 positive. F4/80+ dendritic cells have migratory ability. As they migrate from the central pulp, they increase in size and become CD86 positive. The close spatial relationship between odontoblasts and dendritic cells under the carious lesion have led to speculation that dendritic cells may play a role in odontoblast differentiation and/or secretory activity in the immune defense and dentinogenesis. Pulpal Schwann cells have also been shown to produce molecules in response to caries, which is indicative of the acquisition of the ability for antigen presentation. Evidence suggests that odontoblasts also play a role in the humoral immune response to caries. Immunoglobulin (Ig)G, IgM, and IgA have been localized in the cytoplasm and cell processes of odontoblasts in human carious dentin, suggesting that these cells actively transport antibodies to the infection front. In the incipient lesion, antibodies accumulate in the odontoblast layer and with lesion progression can be seen in the dentinal tubules. Eventually this leads to a focal concentration of antibodies beneath the advancing lesion. In the most advanced phase of carious destruction, the immune response is accompanied by immunopathologic destruction of pulpal tissue, as antigenantibody complex formation, in addition to various products of the inflammatory cascade, gives rise to a nonspecific response that, while designed to rid the body of pathogens, effects destruction of parenchymal tissues as well.
  • (3) inflammatory and immune reactions. There are two distinct populations of dendritic cells that have been identified in the dental pulp. CD11c+ are found in the pulp/dentin border and subjacent to pits and fissures. F4/80+ dendritic cells are concentrated in the perivascular spaces in the subodontoblastic zone and inner pulp. CD11c+ dendritic cells express toll-like receptors 2 and 4 and are CD205 positive. F4/80+ dendritic cells have migratory ability. As they migrate from the central pulp, they increase in size and become CD86 positive. The close spatial relationship between odontoblasts and dendritic cells under the carious lesion have led to speculation that dendritic cells may play a role in odontoblast differentiation and/or secretory activity in the immune defense and dentinogenesis. Pulpal Schwann cells have also been shown to produce molecules in response to caries, which is indicative of the acquisition of the ability for antigen presentation. Evidence suggests that odontoblasts also play a role in the humoral immune response to caries. Immunoglobulin (Ig)G, IgM, and IgA have been localized in the cytoplasm and cell processes of odontoblasts in human carious dentin, suggesting that these cells actively transport antibodies to the infection front. In the incipient lesion, antibodies accumulate in the odontoblast layer and with lesion progression can be seen in the dentinal tubules. Eventually this leads to a focal concentration of antibodies beneath the advancing lesion. In the most advanced phase of carious destruction, the immune response is accompanied by immunopathologic destruction of pulpal tissue, as antigenantibody complex formation, in addition to various products of the inflammatory cascade, gives rise to a nonspecific response that, while designed to rid the body of pathogens, effects destruction of parenchymal tissues as well.
  • (3) inflammatory and immune reactions. Evidence suggests that odontoblasts also play a role in the humoral immune response to caries. Immunoglobulin (Ig)G, IgM, and IgA have been localized in the cytoplasm and cell processes of odontoblasts in human carious dentin, suggesting that these cells actively transport antibodies to the infection front. In the incipient lesion, antibodies accumulate in the odontoblast layer and with lesion progression can be seen in the dentinal tubules. Eventually this leads to a focal concentration of antibodies beneath the advancing lesion. In the most advanced phase of carious destruction, the immune response is accompanied by immunopathologic destruction of pulpal tissue, as antigenantibody complex formation, in addition to various products of the inflammatory cascade, gives rise to a nonspecific response that, while designed to rid the body of pathogens, effects destruction of parenchymal tissues as well.
  • (3) inflammatory and immune reactions. In the most advanced phase of carious destruction, the immune response is accompanied by immunopathologic destruction of pulpal tissue, as antigenantibody complex formation, in addition to various products of the inflammatory cascade, gives rise to a nonspecific response that, while designed to rid the body of pathogens, effects destruction of parenchymal tissues as well .
  • Dentin Hypersensitivity and Its Management: It is represented as a special chronic, short, sharp pulpal pain arises from exposed dentin in response to different stimuli (thermal, evaporative, tactile, osmotic, or chemical), it does not seem to be associated with irreversible pulpal pathosis in the majority of cases. The degree of inflammation in the pulp in cases of dentin hypersensitivity is not well characterized because the condition is usually not severe enough to warrant tooth extraction or endodontic therapy. Common site: Facial root surfaces in canines, premolars, and molars are particularly affected, especially in areas of periodontal attachment loss. Dentin hypersensitivity may be related to: excessive abrasion during tooth brushing, periodontal disease, erosion from dietary or gastric acids Performance of scaling and root planning.
  • Mechanism: The dentin is hypersensitive most likely due to the lack of protective layer (cementum, smear layer), and the hydrodynamic movement of fluid in patent dentinal tubules that are present in areas of hypersensitivity. Increase of irritation may cause reversible inflammation of the pulp at the sites involved. Treatment: The application of neural modulating agents (potassium nitrate) or tubule blocking agents (strontium chloride, oxalates, or dentin bonding agents) usually alleviates the condition, at least temporarily. For a more lasting solution (several weeks), there has been a need to provide biocompatible . One such material was a calcium sodium phosphosilicate bioactive glass, or a combination of a calcium oxalate and an acid-etched bonding material to seal the dentinal tubules. N.B: A concern has been raised that the acidic pH during etching may cause dissolution of the oxalate crystals, thus interfering with the effectiveness of the material. In the long term, the development of smear layer, such as from tooth brushing, dentin sclerosis, reactionary dentin, and the blockage of tubules with large endogenous macromolecules are all thought to reduce the problem.
  • A, Scanning electron microscope (SEM) image of an exposed dentin surface of a hypersensitive area. A large proportion of dentinal tubules (arrows) are seen to be open. B, SEM image of a fractured dentinal tubule of a hypersensitive area. The lumen of the dentinal tubule is partitioned by membranous structures (arrow) . C, SEM image of exposed dentin surface of a naturally desensitized area. The lumens of dentinal tubules (arrows) are mostly occluded, and the surface is extremely smooth. D, SEM image of a fractured dentinal tubule of a naturally desensitized area. Rhombohedral platelike crystals of 0.1 to 0.3 μm (arrow) are present.
  • Pulpal Reactions to Local Anesthetics: An intact pulpal blood flow is critical for maintaining the health of the dental pulp. (Why?) Because the dental pulp is enclosed in a rigid chamber and supplied by few arterioles through the apical foramina, it cannot benefit from collateral circulation or volumetric changes that compensate for changes in blood flow in other soft tissues. So, any reduction in blood flow has the compounding effect of reducing the clearance of large molecular-weight toxins or waste products, thus causing irreversib pulpal pathosis. Vasoconstrictors (such as lidocaine and 1:100,000 or 1:80,000 epinephrine) are added to local anesthetics to enhance the duration of anesthesia. However, it could negatively impact the health of the pulp by reducing the blood flow, particularly if the pulp is inflamed preoperatively (How?) compromising the inflamed pulp’s ability to recover from inflammation. The supplemental anesthetic techniques (periodontal ligament or intraosseous injections) cause more severe reduction or even transient cessation of pulpal blood flow. N.B: The pulpal blood flow was measured by laser Doppler flowmetry, which has some limitation ………………………
  • N.B: Intrapulpal anesthesia is often used as a last resort when pulpal anesthesia is insufficient during root canal therapy. The effect of intrapulpal anesthesia on the pulp in these cases is not considered, since the pulp will be removed. However, occasionally a pulpotomy is performed to maintain pulpal vitality in tooth with immature apex, with no detected differences on follow-up of over 24 weeks after administration of intrapulpal anesthesia that contain epinephrine.
  • Pulpal Reactions to Restorative Procedures: Restorative procedures are performed primarily to treat an infectious disease, restore missing teeth, correct developmental anomalies, fractures, cracks, or failures of previous restorations. One key requirement of a successful restorative procedure maintaining the pulp vitality is to cause minimal additional irritation of the pulp so as not to interfere with normal pulpal healing. So, diagnosis should be performed perfectly, because sometimes irreversible pulpitis may be asymptomatic. In such cases any restorative procedure leads to the quiet demise of the pulp. The cumulative effect of pulp insults, diminish its capacity to remain vital. The effects of dental procedures on the pulp depend on several key factors, such as:
  • Degree of Pretreatment Pulp Inflammation: As stated previously, the dental pulp is compromised in its ability to respond to external irritants because (1) it is enclosed in a noncompliant environment. (2) it lacks sufficient collateral circulation. Thus the more severely the pulp is inflamed, the less will be its ability to respond to further irritation, such as in the form of restorative procedures. Most research studies designed to evaluate the effects of restorative procedures (or materials) on the pulp are conducted on human or experimental animal teeth with normal pulp. Classic experiments have documented that different levels of irritation induce different degrees of inflammation in the pulp, and more severe inflammation may take longer to heal. In a study that evaluated the response of the pulp to capping procedures as a function of duration of exposure, it was shown that the pulp responds favorably to exposures of up to 24 hours after exposure, but not as favorably after longer periods of exposure to oral environment. It may be that the longer exposure periods lead to the formation of a bacterial biofilm that is difficult for the pulpal immune responses to eliminate. This is relevant in cases of aseptic mechanical exposures or teeth where the pulp is exposed by traumatic injuries for a brief duration. In these cases, the pulp usually responds favorably to vital pulp therapy procedures. Models of standardized pulpal inflammation with chronic caries are not commonly used in determining the effects of dental procedures. Older clinical studies show an unfavorable long-term outcome of capping cases with carious pulp exposures, but newer studies in which MTA was used show more favorable results in these cases. In the absence of severe spontaneous symptoms or pulp exposure, the clinician currently cannot accurately determine the degree of preoperative pulpal inflammation. Thus, every effort should be made to minimize added irritation during restorative procedures, because it is possible that excessive irritation could convert the inflammatory status of the pulp from a reversible to an irreversible condition.
  • Degree of Physical Irritation Caused by Procedure: Heat: Any restorative procedures such as cavity preparation, crown preparation, or curing of resins during direct fabrication of provisional restorations may cause significant increases in pulpal temperatures. In case of 10° C rise → irreversible pulp pathosis is expected & 15%, and a 20° C rise → pulp abscess formation. However, a study, in which gradual controlled heat application over a large area of the intact occlusal surface of human unanesthetized teeth was employed, failed to corroborate these earlier findings. If the cavity floor ≤ 0.5 mm from the pulp, areas of coagulation necrosis could be seen. The heat transmission is depends on the proximity of the heat source to the pulp. The measurement of heat in the tooth being prepared - in areas other than the site of tooth preparation - occasionally shows reduction in temperature (Why?) presumably because of the poor conductive properties of dentin and the cooling effect of compressed air from the high-speed. Furthermore, cavity and crown preparations include a number of other irritating stimuli, such as desiccation, severance of odontoblastic processes, vibration, and smearing of bacterial irritants onto the surface of dentin.
  • Desiccation: It is the aspiration of odontoblastic nuclei into dentinal tubules. 30 seconds of continuous air drying can cause significant displacement of odontoblastic nuclei → pulp inflammation → areas of necrosis related to the areas that were dried. transient, in that within 7 to 30 days there is autolysis of the aspirated cells and formation of reactionary dentin. The pulp in cases with aspirated odontoblasts, following desiccation for 1 minute, was not sensitive to clinical scraping with an explorer. The sensitivity was restored with rehydration of the cavities and was increased in other cases where pulp inflammation was induced by microbial contamination.
  • Biologic and Chemical Irritation: Dental caries is clearly an infectious disease in which microorganisms and their virulence determinants constantly irritate the pulp, even at the early stages long before pulp exposure. However, despite the elimination of visible caries during cavity preparation, the cavity floor is undoubtedly left with some contamination by caries bacteria. Whereas the rubber dam should be used with any cavity preparation to prevent cavity contamination with salivary microorganisms , the use of water coolants allows the cavity to be contaminated with bacteria from water lines. Concerns about residual cavity contamination prompted some to use cavity disinfection with caustic chemicals. Chemicals such as hydrogen peroxide, sodium hypochlorite, or calcium hydroxide solutions have been proposed for this purpose, although they may exert a toxic effect. Once dentin is exposed, there is constant outward flow of dentinal fluid that minimizes the inward flow of any noxious agents . This may aid in the reduction of irritation from residual microbial factors in dentinal tubules. In contemporary practice, most chemical irritation during restorative procedures results from the application of etching agents, especially strong acids in the form of total dentin etch, particularly if capping of exposed pulp is performed. Etching is performed to remove the smear layer, promote physical adhesion of bonding agents to dentin by forming resin tags in the dentinal tubules, and promote permeation of the newer unfilled resin primers into the unmineralized surface layer of collagen to form the so-called hybrid layer. If the cavity is relatively superficial and is adequately sealed with a restorative resin, then etching of dentin is probably not detrimental to the pulp, because of the narrow diameter of dentinal tubules and their low density in peripheral dentin. In recent years, self-etching formulations have become popular because they eliminate the separate etching step involved in total-etch procedures. Some have speculated that the bonding of self-etching systems may be poorer than total-etch systems because of the weaker acidity of the acidic primers of self-etching systems compared to total-etch systems.  self-etching formulations have become popular Other factors that may contribute to pulpal irritation during resin placement from chemical/biologic irritants include unpolymerized monomer and polymerization shrinkage. Higher concentrations of monomeric resin components were shown to exert an inhibitory effect on T-lymphocytes and spleen cell and monocytes/macrophages in vitro. These components may leach directly into the pulp in deep cavities and cause chemical irritation. Shrinkage during polymerization of composites may induce internal stresses on dentin and create voids that allow microleakage. Shrinkage of resins is estimated to range from 0.6% to 1.4% and should be minimized during placement by incremental curing and possibly starting the restoration with flowable resins. In summary, the available evidence indicates that chemicals involved in modern restorative procedures may irritate the pulp if placed directly on an exposure or if there is microbial leakage along the tooth/restoration interface.
  • Proximity of Restorative Procedures to Dental Pulp and Surface Area of Dentin Exposed: In other terms: depth and/or width of a tooth preparation there is an increasingly severe pulpal reaction, with a greater likelihood of the pulp undergoing irreversible pathosis, as the carious lesion progresses towards the pulp, particularly when the remaining dentin thickness (RDT) is less than 0.5 mm. The diameter and density of dentinal tubules increase closer to the pulp, it was estimated that the area occupied by tubule lumina at the DEJ was 1% of the total surface area at the DEJ and 22% at the pulp. Clinically, postoperative sensitivity following resin composite restorations was related to the depth of the cavity but not to the presence or absence of liners or bases. N.B: With the passage of time following cavity preparation, there is reduction in the permeability of RDT, due to rapid deposition of reactionary dentin, the migration of large proteins into the tubules, and/or the diminution of tubule diameter as dentin becomes more sclerotic.
  • Proximity of Restorative Procedures to Dental Pulp and Surface Area of Dentin Exposed: In other terms: depth and/or width of a tooth preparation there is an increasingly severe pulpal reaction, with a greater likelihood of the pulp undergoing irreversible pathosis, as the carious lesion progresses towards the pulp, particularly when the remaining dentin thickness (RDT) is less than 0.5 mm. The diameter and density of dentinal tubules increase closer to the pulp, it was estimated that the area occupied by tubule lumina at the DEJ was 1% of the total surface area at the DEJ and 22% at the pulp. Clinically, postoperative sensitivity following resin composite restorations was related to the depth of the cavity but not to the presence or absence of liners or bases. N.B: With the passage of time following cavity preparation, there is reduction in the permeability of RDT, due to rapid deposition of reactionary dentin, the migration of large proteins into the tubules, and/or the diminution of tubule diameter as dentin becomes more sclerotic.
  • Permeability of Dentin and Odontoblastic Layer Between Area Being Restored and Pulp: It plays an important role in the ingress of potential irritants to the pulp. The dentin is not uniformly permeable, and that permeability depends on factors such as; the location within the same tooth, The tubular diameter increases from about 0.6 to 0.8 μm close to the DEJ to about 3 μm at the pulp. Given that bacterial cells are about 0.5 to 1 μm in diameter, it is evident that in deep cavity preparations, particularly when total-etch procedures are employed, bacteria can migrate through the remaining dentin into the pulp. the age of the patient, the width of peritubular dentin increases with age, causing reduction in tubular lumen or sclerosis. The presence of pathologic conditions such as dental caries. Fundamentally, the permeability of dentin depends on the collective sum of permeability of individual tubules at a particular site in the tooth. in superficial dentin, which is associated with remineralization and the formation of caries crystals within the tubules of inner undemineralized dentin → decrease in permeability in dentin subjacent to the carious lesion → delaying its progress (protective mechanism). Related odontoblasts, it was shown that irritation from cavity preparation increased the odontoblastic permeability only at the site of the cavity preparation. N.B: In addition to the physical barrier to permeability and the production of reactionary or reparative dentin, the odontoblastic layer may in fact contribute to the host response of the dental pulp by expressing important inflammatory mediators or recognize bacteria through toll-like receptor
  • Permeability of Dentin and Odontoblastic Layer Between Area Being Restored and Pulp: It plays an important role in the ingress of potential irritants to the pulp. The dentin is not uniformly permeable, and that permeability depends on factors such as; the location within the same tooth, The tubular diameter increases from about 0.6 to 0.8 μm close to the DEJ to about 3 μm at the pulp. Given that bacterial cells are about 0.5 to 1 μm in diameter, it is evident that in deep cavity preparations, particularly when total-etch procedures are employed, bacteria can migrate through the remaining dentin into the pulp. the age of the patient, the width of peritubular dentin increases with age, causing reduction in tubular lumen or sclerosis. The presence of pathologic conditions such as dental caries. in superficial dentin, which is associated with remineralization and the formation of caries crystals within the tubules of inner undemineralized dentin → decrease in permeability in dentin subjacent to the carious lesion → delaying its progress (protective mechanism). Related odontoblasts, it was shown that irritation from cavity preparation increased the odontoblastic permeability only at the site of the cavity preparation. N.B: In addition to the physical barrier to permeability and the production of reactionary or reparative dentin, the odontoblastic layer may in fact contribute to the host response of the dental pulp by expressing important inflammatory mediators or recognize bacteria through toll-like receptor
  • Permeability of Dentin and Odontoblastic Layer Between Area Being Restored and Pulp: It plays an important role in the ingress of potential irritants to the pulp. The dentin is not uniformly permeable, and that permeability depends on factors such as; the location within the same tooth, The tubular diameter increases from about 0.6 to 0.8 μm close to the DEJ to about 3 μm at the pulp. Given that bacterial cells are about 0.5 to 1 μm in diameter, it is evident that in deep cavity preparations, particularly when total-etch procedures are employed, bacteria can migrate through the remaining dentin into the pulp. the age of the patient, the width of peritubular dentin increases with age, causing reduction in tubular lumen or sclerosis. The presence of pathologic conditions such as dental caries. in superficial dentin, which is associated with remineralization and the formation of caries crystals within the tubules of inner undemineralized dentin → decrease in permeability in dentin subjacent to the carious lesion → delaying its progress (protective mechanism). Related odontoblasts, it was shown that irritation from cavity preparation increased the odontoblastic permeability only at the site of the cavity preparation. N.B: In addition to the physical barrier to permeability and the production of reactionary or reparative dentin, the odontoblastic layer may in fact contribute to the host response of the dental pulp by expressing important inflammatory mediators or recognize bacteria through toll-like receptor
  • Permeability of Dentin and Odontoblastic Layer Between Area Being Restored and Pulp: It plays an important role in the ingress of potential irritants to the pulp. The dentin is not uniformly permeable, and that permeability depends on factors such as; the location within the same tooth, The tubular diameter increases from about 0.6 to 0.8 μm close to the DEJ to about 3 μm at the pulp. Given that bacterial cells are about 0.5 to 1 μm in diameter, it is evident that in deep cavity preparations, particularly when total-etch procedures are employed, bacteria can migrate through the remaining dentin into the pulp. the age of the patient, the width of peritubular dentin increases with age, causing reduction in tubular lumen or sclerosis. The presence of pathologic conditions such as dental caries. in superficial dentin, which is associated with remineralization and the formation of caries crystals within the tubules of inner undemineralized dentin → decrease in permeability in dentin subjacent to the carious lesion → delaying its progress (protective mechanism). Related odontoblasts, it was shown that irritation from cavity preparation increased the odontoblastic permeability only at the site of the cavity preparation. N.B: In addition to the physical barrier to permeability and the production of reactionary or reparative dentin, the odontoblastic layer may in fact contribute to the host response of the dental pulp by expressing important inflammatory mediators or recognize bacteria through toll-like receptor
  • Permeability of Dentin and Odontoblastic Layer Between Area Being Restored and Pulp: It plays an important role in the ingress of potential irritants to the pulp. The dentin is not uniformly permeable, and that permeability depends on factors such as; the location within the same tooth, The tubular diameter increases from about 0.6 to 0.8 μm close to the DEJ to about 3 μm at the pulp. Given that bacterial cells are about 0.5 to 1 μm in diameter, it is evident that in deep cavity preparations, particularly when total-etch procedures are employed, bacteria can migrate through the remaining dentin into the pulp. the age of the patient, the width of peritubular dentin increases with age, causing reduction in tubular lumen or sclerosis. The presence of pathologic conditions such as dental caries. in superficial dentin, which is associated with remineralization and the formation of caries crystals within the tubules of inner undemineralized dentin → decrease in permeability in dentin subjacent to the carious lesion → delaying its progress (protective mechanism). A, Stained TEM of undemineralized specimens following the application of the self-etch ABF system to caries-affected dentin. The hybrid layer (H, between arrows) was about 3 μm thick, and the underlying undemineralized dentin (U) was highly porous (arrowhead) . The dentinal tubule was covered with a smear plug (SP) and was partially obliterated with large caries crystals (pointer) . (A), filled adhesive. Related odontoblasts, it was shown that irritation from cavity preparation increased the odontoblastic permeability only at the site of the cavity preparation. N.B: In addition to the physical barrier to permeability and the production of reactionary or reparative dentin, the odontoblastic layer may in fact contribute to the host response of the dental pulp by expressing important inflammatory mediators or recognize bacteria through toll-like receptor.
  • Permeability of Dentin and Odontoblastic Layer Between Area Being Restored and Pulp: It plays an important role in the ingress of potential irritants to the pulp. The dentin is not uniformly permeable, and that permeability depends on factors such as; the location within the same tooth, The tubular diameter increases from about 0.6 to 0.8 μm close to the DEJ to about 3 μm at the pulp. Given that bacterial cells are about 0.5 to 1 μm in diameter, it is evident that in deep cavity preparations, particularly when total-etch procedures are employed, bacteria can migrate through the remaining dentin into the pulp. the age of the patient, the width of peritubular dentin increases with age, causing reduction in tubular lumen or sclerosis. The presence of pathologic conditions such as dental caries. in superficial dentin, which is associated with remineralization and the formation of caries crystals within the tubules of inner undemineralized dentin → decrease in permeability in dentin subjacent to the carious lesion → delaying its progress (protective mechanism). Related odontoblasts, it was shown that irritation from cavity preparation increased the odontoblastic permeability only at the site of the cavity preparation. N.B: In addition to the physical barrier to permeability and the production of reactionary or reparative dentin, the odontoblastic layer may in fact contribute to the host response of the dental pulp by expressing important inflammatory mediators or recognize bacteria through toll-like receptor
  • Permeability of Dentin and Odontoblastic Layer Between Area Being Restored and Pulp: It plays an important role in the ingress of potential irritants to the pulp. The dentin is not uniformly permeable, and that permeability depends on factors such as; the location within the same tooth, The tubular diameter increases from about 0.6 to 0.8 μm close to the DEJ to about 3 μm at the pulp. Given that bacterial cells are about 0.5 to 1 μm in diameter, it is evident that in deep cavity preparations, particularly when total-etch procedures are employed, bacteria can migrate through the remaining dentin into the pulp. the age of the patient, the width of peritubular dentin increases with age, causing reduction in tubular lumen or sclerosis. The presence of pathologic conditions such as dental caries. in superficial dentin, which is associated with remineralization and the formation of caries crystals within the tubules of inner undemineralized dentin → decrease in permeability in dentin subjacent to the carious lesion → delaying its progress (protective mechanism). Related odontoblasts, it was shown that irritation from cavity preparation increased the odontoblastic permeability only at the site of the cavity preparation. N.B: In addition to the physical barrier to permeability and the production of reactionary or reparative dentin, the odontoblastic layer may in fact contribute to the host response of the dental pulp by expressing important inflammatory mediators or recognize bacteria through toll-like receptor
  • Patient Age: resting pulpal blood flow (PBF), response to cold application, decrease with age. reduction in pulpal neuropeptides. Thus in humans with advancing age, the net result of the ability of the pulp to cope with external stimulation or irritation is not clear.
  • Pulpal Reactions to Restorative Materials: these chemicals have an effect on the pulp, but the effect seems to be short lived and, in the absence of bacteria, reversible. leading to chronic stimulation and a resultant prolonged inflammatory response. In some instances, prolonged cytotoxicity, stimulation of hypersensitivity reactions, or impairment of the host immune response to bacteria. N.B: subtoxic concentrations of certain agents are capable of eliciting allergic reactions in humans. Primates hyperimmunized with BSA showed significant pulpal damage with repeated antigenic challenge in class V cavity preparations, suggesting a role for antigen-antibody complex–mediated hypersensitivity in tissue destruction.
  • Pulpal Reactions to Restorative Materials: The technique sensitivity of certain materials predisposes them to faulty bonds to tooth structure that can translate to dentin hypersensitivity, recurrent disease, and pulpal inflammation or necrosis.
  • During the etching process: The more highly mineralized peritubular dentin is preferentially dissolved, leaving free collagen fibrils and opening lateral tubular branches. Applied resin infiltrates the exposed collagen mesh, creating a layer 5 to 10 μm thick referred to as the hybrid layer . This layer, along with the resin permeating exposed tubules, forms the bond between the resin and dentin. If the preparation is too dry, the collagen fibrils collapse, and the resin cannot effectively permeate the mesh, which results in a defective bond. The optimal degree of hydration of the preparation surface can vary from material to material, so resin restoration placement is technique sensitive.
  • During the etching process: This same principle is applicable to the practice of bonding fractured tooth fragments where the segment has become dehydrated while outside of the mouth. Current protocols recommend rehydration of the segment prior to bonding, thus increasing the mechanical and presumably the microbial seal. This is particularly important with a complicated crown fracture where the pulpal protection by intact dentin is absent.
  • Pulpal Reactions to Restorative Materials: N.B: pulpal irritation is not considered a negative sequela all the time, the irritant potential of certain restorative materials has a useful motivated effect on odontoblasts, initiating the protective mechanism. In generally, the carious pulp exposures offer poor therapeutic opportunities for continued pulp vitality with direct capping techniques
  • Pulpal Reactions to Restorative Materials: N.B: pulpal irritation is not considered a negative sequela all the time, the irritant potential of certain restorative materials has a useful motivated effect on odontoblasts, initiating the protective mechanism.
  • Pulpal Reactions to Restorative Materials: Calcium hydroxide: It is one of the oldest and most widely used medicaments for stimulation of dentinal bridge formation. In direct pulp capping subsequent to microscopic or gross pulpal exposure : It induces a low grade pulpal irritation that stimulate the formation of dentinal bridge in exposures site. The degree of inflammation is dependent on the preparation of calcium hydroxide used. Aqueous suspensions of calcium hydroxide applied to exposed pulps causes superficial necrosis of pulpal tissue followed by tissue displaying low-grade inflammation. Within 30 days, the tissue subjacent to the necrotic zone has reorganized and resumed normal architecture. Hard-setting calcium hydroxide preparations are effective in eliciting dentinal bridge formation with a much smaller to nonexistent necrotic zone. This is preferable in vital pulp therapies, where maintenance of the maximum amount of vital pulp tissue is desirable, and the extent of pulpal inflammation is minimal.
  • Pulpal Reactions to Restorative Materials: Calcium hydroxide: In indirect pulp capping: The irritation potential is dependent on the remaining dentin thickness and permeability. Application of calcium hydroxide to intact dentin appears to induce sclerosis by promoting crystal precipitation within the tubules, accompanied by reductions in permeability.
  • Materials containing zinc oxide and eugenol (ZOE): It falls into the category of materials has medicinal properties & ability to seal a cavity preparation. ZOE is used for a variety of purposes in dentistry, largely because of its anesthetic and antiseptic properties. It has been shown to block transmission of action potentials in nerve fibers and to suppress nerve excitability in the pulp when applied to deep excavations. In addition, ZOE has good adaptation to dentin and inhibits bacterial growth on cavity walls. These properties have made this a favored material for temporary fillings but not long-term restorations; (Why ?) It has been shown to leak after only a few weeks in situ.
  • Direct Pulp Caping with Mineral Trioxide Aggregate: Direct capping of pulp exposures is indicated in pulps that were previously healthy and exposed by trauma or dental restorative procedures. the use of mineral trioxide aggregate (MTA) has recently been proposed, even on carious pulp exposures, due to its ability for allowing the formation of a reparative dentin bridge and maintain continued pulp vitality. one concern is tooth discoloration if the gray MTA formulation is used on anterior teeth. At 1 week, none of the capped pulps showed necrosis close to the exposure site, and odontoblast-like cells were observed at the periphery with the deposition of calcified bridge. At 2 weeks, almost all of the specimens from both types of MTA showed complete calcified bridge formation just below the exposure site. Success was determined radiographically, with subjective symptoms, pulp testing with cold, and continued root formation on immature teeth. Outcomes were measured over a period of up to 9 years postoperatively and showed an overall success of 97%, with all the teeth in the immature root group showing success. Within the parameters of these studies, it seems that white MTA is a suitable capping agent for pulp exposures of healthy or reversibly inflamed pulps. It must be emphasized, however, that not only must the pulp capping agent be biocompatible and hopefully stimulate the formation of reparative dentin, but the prevention of bacterial ingress by the placement of a well-sealed restoration must also be provided.
  • Direct Pulp Caping with Mineral Trioxide Aggregate: Success was determined radiographically, with subjective symptoms, pulp testing with cold, and continued root formation on immature teeth. Outcomes were measured over a period of up to 9 years postoperatively and showed an overall success of 97%, with all the teeth in the immature root group showing success. Within the parameters of these studies, it seems that white MTA is a suitable capping agent for pulp exposures of healthy or reversibly inflamed pulps. It must be emphasized, however, that not only must the pulp capping agent be biocompatible and hopefully stimulate the formation of reparative dentin, but the prevention of bacterial ingress by the placement of a well-sealed restoration must also be provided.
  • Use of Hemostatic Agents and Disinfectants on Direct Pulp Exposures: the ideal hemostatic agent also would have the ability to kill bacteria. 2% chlorhexidine , or 5.25% sodium hypochlorite . Although the 7-day saline specimens showed slightly less inflammatory response, there were no statistically significant differences between the groups with respect to all dependent measures over the course of the study. Complete healing was seen in 88% of all specimens at 90 days. The pulps in these teeth were previously uninjured, and the exposures were made in a clean environment. Therefore, it seems that a mechanical exposure of a healthy pulp created during cavity preparation could be disinfected with either 2% chlorhexidine or 5.25% sodium hypochlorite (full concentration is now 6.0%), capped with a hard-setting calcium hydroxide formulation, and expected to have a favorable prognosis for healing.
  • Pulpal Reactions to Laser Procedures: Laser use on soft / hard tissues has potential benefits of efficiency, reduced sensitivity, disinfection, and precision. There are several different types of laser technologies available that depend on the wavelength, active medium, emission mode, delivery system, power output, and duration of application. The main types available in dentistry today are: The CO2 laser is the oldest type used on soft tissues. It has the longest wavelength 10,600 nm. It cannot be delivered in an optic fiber, thus must be used in a hollow-tubelike wave guide in continuous gated-pulse mode. This means that the operator does not feel a solid resistance when using this laser. Er:YAG has a wavelength of 2940 nm, delivered using a solid optic fiber. It has a high affinity for water and hydroxyapatite, thus can be used for removal of caries and cutting dentin with coolant. It can also be used on soft tissue. Ho:YAG laser has a wavelength of 2120 nm and has high affinity to water but not to tooth structure, thus is used primarily for soft-tissue surgery. Nd:YAG laser is also delivered fibroptically, has a wavelength of 1064 nm, it has high affinity for water and pigmented tissues and offers good hemostasis, thus is used extensively in surgery. All have an active medium of a solid crystal of yttrium-aluminum-garnet, which is impregnated in erbium, neodymium, or holmium, respectively . HeNe, or helium neon (632 nm), and GaAlAs, or galliumaluminum- arsenide (diode; semiconductor) (720-904 nm) lasers, which have been used in laser Doppler flowmetry and in treating dentin hypersensitivity.
  • CO2 laser is the oldest type, used on soft tissues . It has the longest wavelength (10,600 nm) . It cannot be delivered in an optic fiber , thus must be used in a hollow-tubelike wave guide in continuous gated-pulse mode. This means that the operator does not feel a solid resistance when using this laser. Er:YAG laser has an active medium of a solid crystal of yttrium-aluminum-garnet which is impregnated in erbium It has a wavelength of 2940 nm, delivered using a solid optic fiber. It has a high affinity for water and hydroxyapatite, thus can be used for removal of caries and cutting dentin with coolant. It can also be used on soft tissue. Nd:YAG laser has an active medium of a solid crystal of yttrium-aluminum-garnet which is impregnated in neodymium It has a wavelength of 1064 nm, also delivered fibroptically. It has a high affinity for water and pigmented tissues and offers good hemostasis, thus is used extensively in surgery. Ho:YAG laser has an active medium of a solid crystal of yttrium-aluminum-garnet which is impregnated in holmium. It has a wavelength of 2120 nm and has high affinity to water but not to tooth structure, thus is used primarily for soft-tissue surgery. I lasers with low power output, such as HeNe, or helium neon (632 nm), and GaAlAs, or galliumaluminum- arsenide (diode; semiconductor) (720-904 nm) lasers, which have been used in laser Doppler flowmetry and in treating dentin hypersensitivity.
  • Pulpal Reactions to Cavity Preparation Using Air Abrasion Techniques: Air abrasion is another modality that has been adopted for conservative, non-painful cavity preparations. Aluminum oxide particles are forced in a rapid stream onto the tooth structure and simultaneously evacuated from the field. An earlier study evaluated the effects of air abrasion using two different particle sizes (25 and 50 μm) with two different forces (80 and 160 psi), The findings showed that histologically, higher pressures and smaller particles yielded significantly fewer pulpal effects than the high-speed treated teeth, whereas lower pressures and larger particles were not significantly different. Air abrasion cavity preparations were more recently shown to be equivalent to high-speed bur preparations in microleakage studies if both techniques are followed by acid etching.(Why?) Because of the lack of tactile control. The use of air abrasion is limited to specific situations such as shallow caries or pediatric applications
  • Pulpal Reactions to Vital Bleaching Techniques: Vital bleaching techniques employ the use of strong oxidizing agents, namely 10% carbamide peroxide and hydrogen peroxide, to bleach enamel of teeth with vital pulp. There have been concerns about the potential for pulpal irritation during these procedures because of the long duration that the chemicals are in contact with the teeth, particularly if dentin with open tubules or cracks are present. An earlier study identified the toxicity of these chemicals showed minor inflammatory changes up to 2 weeks in the pulp of the bleached teeth that were reversible, that could be prevented by treating the teeth with fluorides and by correcting restorative pretreatment deficiencies. One clinical report documented that if 16% carbamide peroxide was used, gingival irritation was evident; however, no changes in pulp vitality or in symptoms were noted. Even in patients who develop post-treatment symptoms, these tend to be reversible and Clinical symptoms are likely to be due to increases in neuropeptides in the pulp. Peptides expressed by selective populations of neurons, they act as specific signals between one population of neurons and another, affecting the excitability of other neurons, by depolarising them or by hyperpolarising them. A recent report showed that light- and laser-activated bleaching systems increase substance P expression in the pulp to significant levels. An earlier clinical trial showed that vital bleaching using 10% carbamide peroxide in a custom tray for 6 weeks was safe for the pulp health for up to 10 years post treatment, although the bleaching effectiveness may decline with time
  • Clinical symptoms are likely to be due to increases in neuropeptides in the pulp. Peptides expressed by selective populations of neurons, they act as specific signals between one population of neurons and another, affecting the excitability of other neurons, by depolarising them or by hyperpolarising them. A recent report showed that light- and laser-activated bleaching systems increase substance P expression in the pulp to significant levels. An earlier clinical trial showed that vital bleaching using 10% carbamide peroxide in a custom tray for 6 weeks was safe for the pulp health for up to 10 years post treatment, although the bleaching effectiveness may decline with time
  • Pulpal Reactions to Periodontal Procedures: in the oral cavity. Periodontal disease causes attachment loss, which exposes the root surface to the oral cavity, allowing a chance for microbial irritation of the pulp due to infiltration through dentinal tubules. Occasionally, pulpal inflammation secondary to severe periodontitis is observed. It is much more common for pulp necrosis or failed healing of periradicular lesions to present clinically with signs of periodontal disease than for periodontal disease to cause pulpal pathosis. Primary endodontic, secondary periodontal pathosis is particularly evident if a perforation occurs in the pulp chamber or coronal third of the root during endodontic treatment and is not promptly treated, as happens in cases of vertical root fractures or congenital tooth defects such as palatal groove defect. Periodontal scaling and root planing may result in removal of cementum and exposure of dentin to the oral cavity. Frequently this treatment results in dentin hypersensitivity, as discussed previously. (Why?) it is more likely for microbial irritants to move outward from a necrotic pulp to cause periodontal breakdown than for them to move inward from a periodontal pocket to cause irreversible pathosis in the pulp. (How?) If the assumption is that bacteria may migrate through patent dentinal tubules in these situations, then it may be that the outward dentinal fluid flow in teeth with vital pulp contributes to the resistance to ingress of bacteria in sufficient amounts to cause a clinically significant disease process. Once the pulp degenerates, dentinal fluid flow no longer exists. Thus microbial irritants from the pulp may promote pocket formation and periodontal bone loss, and the prognosis of endodontic and periodontal treatment may be related, since the microbial factors may pass across dentin more readily. In theory, periodontal disease and its treatment should be associated with increased incidence of pulpal pathosis. In an older study, in teeth that received scaling, a similar percentage of 32% developed the same mild inflammation, but none developed pulp necrosis. In a later clinical study, The results showed a significantly higher chance of pulpal complications in teeth that were bridge abutments than teeth that were not abutments. Considering that both types of teeth had similar degrees of periodontal disease, the authors concluded that prosthodontic treatment is associated with pulpal involvement more frequently than periodontal disease and its treatment. Another histologic analysis of 46 teeth with varying degrees of periodontal disease and coronal restorations reached a similar conclusion. Furthermore, two comprehensive reviews of the topic concluded that although the potential exists for periodontal disease and its treatment to cause pulpal pathosis, particularly if large lateral or accessory canals are exposed, this occurrence is rare.
  • Pulpal Reactions to Periodontal Procedures: in the oral cavity. Periodontal disease causes attachment loss, which exposes the root surface to the oral cavity, allowing a chance for microbial irritation of the pulp due to infiltration through dentinal tubules. Occasionally, pulpal inflammation secondary to severe periodontitis is observed. It is much more common for pulp necrosis or failed healing of periradicular lesions to present clinically with signs of periodontal disease than for periodontal disease to cause pulpal pathosis. Primary endodontic, secondary periodontal pathosis is particularly evident if a perforation occurs in the pulp chamber or coronal third of the root during endodontic treatment and is not promptly treated, as happens in cases of vertical root fractures or congenital tooth defects such as palatal groove defect. Periodontal scaling and root planing may result in removal of cementum and exposure of dentin to the oral cavity. Frequently this treatment results in dentin hypersensitivity, as discussed previously. (Why?) it is more likely for microbial irritants to move outward from a necrotic pulp to cause periodontal breakdown than for them to move inward from a periodontal pocket to cause irreversible pathosis in the pulp. (How?) If the assumption is that bacteria may migrate through patent dentinal tubules in these situations, then it may be that the outward dentinal fluid flow in teeth with vital pulp contributes to the resistance to ingress of bacteria in sufficient amounts to cause a clinically significant disease process. Once the pulp degenerates, dentinal fluid flow no longer exists. Thus microbial irritants from the pulp may promote pocket formation and periodontal bone loss, and the prognosis of endodontic and periodontal treatment may be related, since the microbial factors may pass across dentin more readily. In theory, periodontal disease and its treatment should be associated with increased incidence of pulpal pathosis. In an older study, in teeth that received scaling, a similar percentage of 32% developed the same mild inflammation, but none developed pulp necrosis. In a later clinical study, The results showed a significantly higher chance of pulpal complications in teeth that were bridge abutments than teeth that were not abutments. Considering that both types of teeth had similar degrees of periodontal disease, the authors concluded that prosthodontic treatment is associated with pulpal involvement more frequently than periodontal disease and its treatment. Another histologic analysis of 46 teeth with varying degrees of periodontal disease and coronal restorations reached a similar conclusion. Furthermore, two comprehensive reviews of the topic concluded that although the potential exists for periodontal disease and its treatment to cause pulpal pathosis, particularly if large lateral or accessory canals are exposed, this occurrence is rare.
  • Pulpal Reactions to Orthodontic Surgery: It has been known for decades that osteotomies in the maxilla or mandible may cause disruption in the blood supply to teeth in the area of the surgery, with resultant inflammation and/or necrosis. Occasionally the teeth affected show postoperative manifestations common with traumatic injuries, such as pulp canal obliteration. Studies have shown that if a safe distance of 5 to 10 mm is maintained between the site of the surgery and the teeth, minimal disruption occurs. In most cases, the blood flow is regained within months of the surgery. Recently a modification of the Le Fort I osteotomy technique was described in which the Le Fort I sectioning was combined with a horseshoe palatal osteotomy to spare any disruption to the descending palatine artery. An examination of PBF of maxillary teeth using laser Doppler flowmetry, as well as the responsiveness to electric pulp testing, showed significant differences between the two surgical techniques in the postoperative recovery values. In cases where the surgery did not disrupt the palatine artery, the PBF in the anterior teeth consistently increased without disruption in the postoperative period. It should also be noted that occasionally teeth are traumatized during endotracheal intubation for surgery that requires general anesthesia, when the surgery itself is not related to the jaws or teeth. Osteotomy of the jaw This is performed to realign the mandible (lower jaw) or maxilla (upper jaw) with the rest of the skull and/or teeth. This is usually performed to correct skeletal malocclusions, that is discrepancies in tooth position that cannot be corrected by simple orthodontic movement, and realignment of the TMJ , or to correct facial deformities such as mandibular retrognathia . There is little scarring, and all of the surgery takes places inside of the mouth. Orthodontic braces may have to be worn pre- and post- operation to realign the teeth to match the newly realigned jaw.
  • Pulpal Reactions to Implant Placement and Function: Osseointegrated implants are now a common option for the replacement of missing teeth. The placement of implants requires multifaceted preoperative radiographic techniques, including intraoral, tomographic, cephalometric, and panoramic imaging. (Why?) to assure that implant placement fully rests in bone and does not compromise neighboring structures, including teeth. The lack of attention to (1) the threedimensional anatomy of the site of implant placement & (2) the orientation of neighboring teeth may lead to the implant perforating the root and devitalizing the pulp. It is usually recommended that implants not be placed directly at a site where a periradicular lesion, particularly one with signs of purulence, exists; microbial irritants may interfere with osseointegration. Case reports have also claimed that teeth with periradicular lesions may reduce the success of neighboring implants, even if adequate endodontic treatment is performed. However, recent data suggest that immediate implant placement in sites that have been adequately débrided is successful. Furthermore, implants that are not mobile but have apical periimplant lesions have been successfully treated with local débridement and “implant-apex resection” procedures.13
  • Pulpal Reactions to Implant Placement and Function: Osseointegrated implants are now a common option for the replacement of missing teeth. The placement of implants requires multifaceted preoperative radiographic techniques, including intraoral, tomographic, cephalometric, and panoramic imaging. (Why?) to assure that implant placement fully rests in bone and does not compromise neighboring structures, including teeth. The lack of attention to (1) the threedimensional anatomy of the site of implant placement & (2) the orientation of neighboring teeth may lead to the implant perforating the root and devitalizing the pulp. It is usually recommended that implants not be placed directly at a site where a periradicular lesion, particularly one with signs of purulence, exists; microbial irritants may interfere with osseointegration. Case reports have also claimed that teeth with periradicular lesions may reduce the success of neighboring implants, even if adequate endodontic treatment is performed. However, recent data suggest that immediate implant placement in sites that have been adequately débrided is successful. Furthermore, implants that are not mobile but have apical periimplant lesions have been successfully treated with local débridement and “implant-apex resection” procedures.
  • Regenerative Potential of the Dental Pulp: Recent studies and case reports suggest that the dental pulp has great regenerative potential, particularly in the immature permanent tooth. This has been attributed to the store of Mesenchymal stem cells (MSCs) found in a variety of tissues and have proven to be pluripotential. Stem cells from the apical papilla (SCAP) of immature teeth have likewise been identified and have been shown to develop into dentinogenic cells, given the proper stimulation. The results of these studies, coupled with case reports of continued root development subsequent to apical periodontitis in young teeth, suggest the potential for bioroot engineering in the future.
  • Pulpal reactions to caries and dental procedures

    1. 1. Pulpal Reactionsto Caries and Dental Procedures
    2. 2. Topic outline:• Pulpal Reactions to Caries.• Pulpal Reactions to Local Anesthetics.• Pulpal Reactions to Restorative Procedures.• Pulpal Reactions to Restorative Materials.• Pulpal Reactions to Laser Procedures.• Pulpal Reactions to Cavity Preparation Using Air Abrasion Techniques.• Pulpal Reactions to Vital Bleaching Techniques.• Pulpal Reactions to Periodontal Procedures.• Pulpal Reactions to Orthodontic Surgery.• Pulpal Reactions to Implant Placement And Function.
    3. 3. I. Pulpal Reaction to CariesProtective Pulpal Reactions includes;1)Decrease in dentin permeability.2)Tertiary dentin formation.3)Inflammatory and immune reactions.
    4. 4. I. Pulpal Reaction to CariesProtective Pulpal Reactions includes;1)Decrease in dentin permeability:It is the first & fastest defense to caries and iscalled Dentin Sclerosis.Increase the deposition of mineral crystals inintratubular dentin → narrowing the dentinaltubules → decreasing dentin permeability
    5. 5. I. Pulpal Reaction to CariesProtective Pulpal Reactions includes;2)Tertiary dentin formation:It is not the most effective pulpally mediateddefense.Mechanism; acidic byproducts of the cariousprocess → degrade the dentin matrix →liberate bioactive molecules sequesteredduring dentinogenesis → reassume their role indentin formation.
    6. 6. I. Pulpal Reaction to CariesProtective Pulpal Reactions includes;2)Tertiary dentin formation:The resultant dentin character is highlydependent on the stimulus.In Mild Carious Lesion, odontoblasts areactivate to elaborate the organic matrix ofdentin (reactionary dentin), which is similar inmorphology to physiologic dentin and mayonly be apparent due to a change in thedirection of the new dentinal tubules.
    7. 7. I. Pulpal Reaction to CariesProtective Pulpal Reactions includes;2)Tertiary dentin formation:The resultant dentin character is highlydependent on the stimulus.In Aggressive Carious Lesion, repopulation ofthe disrupted odontoblast layer withdifferentiating progenitors, forming reparativedentin, its morphology can range fromorganized tubular dentin to more disorganizedirregular fibrodentin.
    8. 8. I. Pulpal Reaction to CariesThree basic reactions tend to protect the pulp:3)Inflammatory and immune reactions:In the advancing infection front of the cariouslesion, multiple extrinsic and intrinsic factorsthat stimulate inflammatory reactions,provides cellular and humoral challenges toinvading pathogens.N.B: The buffering capacity of dentin fluidlikely attenuates the pH before it can directlyeffect a deleterious response, except whenthe remaining dentin thickness is minimal
    9. 9. I. Pulpal Reaction to CariesThree basic reactions tend to protect the pulp:3)Inflammatory and immune reactions:The early inflammatory response can be seenbeneath noncavitated lesions andnoncoalesced pits and fissures.It is characterized by the focal accumulationof chronic inflammatory cells.
    10. 10. I. Pulpal Reaction to CariesThree basic reactions tend to protect the pulp:3)Inflammatory and immune reactions:It is mediated;Initially by odontoblasts; the most peripheralcell in the pulp, and encounter foreignantigens first.& later by dendritic cells, which areresponsible for antigen presentation andstimulation of T lymphocytes.
    11. 11. I. Pulpal Reaction to CariesThree basic reactions tend to protect the pulp:3)Inflammatory and immune reactions:Two distinct populations of dendritic cells:•CD11c+ found in the pulp/dentin border andsubjacent to pits and fissures.•F4/80+ concentrated in the perivascularspaces in the subodontoblastic zone and innerpulp.
    12. 12. I. Pulpal Reaction to CariesThree basic reactions tend to protect the pulp:3)Inflammatory and immune reactions:Odontoblasts play a role in the humoralimmune response to caries. Immunoglobulin(Ig)G, IgM, and IgA have been localized in thecytoplasm and cell processes of odontoblastsin human carious dentin, suggesting that thesecells actively transport antibodies to theinfection front.
    13. 13. I. Pulpal Reaction to CariesThree basic reactions tend to protect the pulp:3)Inflammatory and immune reactions:N.B: In the most advanced phase of cariousdestruction, the immune response isaccompanied by immuno-pathologicdestruction of pulpal tissue.
    14. 14. Dentin Hypersensitivity and Its ManagementDefinition:It is represented as a special chronic, short,sharp pulpal pain arises from exposed dentinin response to different stimuli.Dentin hypersensitivity may be related to:•Excessive abrasion during tooth brushing.•Periodontal disease.•Erosion from dietary or gastric acids•Performance of scaling and root planning.
    15. 15. Dentin Hypersensitivity and Its ManagementMechanism:the lack of protective layer allows thehydrodynamic movement of fluid in patentdentinal tubules that are present in areas ofhypersensitivity.Treatment:The application of neural modulating agentsor tubule blocking agents or materials thatbond to the tooth surface.
    16. 16. Dentin Hypersensitivity and Its Management
    17. 17. Dentin Hypersensitivity and Its ManagementN.B:•A concern has been raised that the acidicpH during etching may cause dissolution ofthe oxalate crystals, thus interfering with theeffectiveness of the material.•In the long term, the development of smearlayer, such as from tooth brushing, dentinsclerosis, reactionary dentin, and theblockage of tubules with large endogenousmacromolecules are all thought to reduce theproblem.
    18. 18. II. Pulpal Reactions to Local Anesthetics:Vasoconstrictors:•such as: lidocaine and 1:100,000 or 1:80,000epinephrine.•Benefits: enhance the duration of anesthesia.•Side effect: reduce the blood flow of thepulp.N.B: The supplemental anesthetic techniquescause more severe reduction or even transientcessation of pulpal blood flow.
    19. 19. II. Pulpal Reactions to Local Anesthetics:N.B: The effect of intrapulpal anesthesia on thepulp is not considered, since it is used duringroot canal therapy when other anestheticadministrations are insufficient.•However, during pulpotomy in tooth withimmature apex, no difference was detectedon follow-up of over 24 weeks afteradministration of intrapulpal anesthesia thatcontain epinephrine.
    20. 20. III. Pulpal Reactions to Restorative Procedures:One key requirement of a successfulrestorative procedure maintaining the pulpvitality is to cause minimal additional irritationof the pulp so as not to interfere with normalpulpal healing.Pulp reaction to restorative procedure iscontrolled by:1.Degree of Pretreatment Pulp Inflammation.2.Degree of Physical Irritation3.Biologic and Chemical Irritation:4.Proximity of Restorative Procedures to Pulp
    21. 21. III. Pulpal Reactions to Restorative Procedures:1) Degree of Pretreatment Pulp Inflammation:In the absence of severe spontaneous symptoms or pulp exposure, the clinician cannot accurately determine the degree of preoperative pulpal inflammation. Thus, every effort should be made to minimize added irritation during restorative procedures.In cases of aseptic mechanical exposures, exposure longer than 24 hours associated with the formation of a bacterial biofilm that is difficult for the pulpal immune responses to eliminate.
    22. 22. III. Pulpal Reactions to Restorative Procedures:2) Degree of Procedure Physical Irritation:• Heat:Any restorative procedures leads to increase in pulpal temperatures;In case of 10° C rise → In case of 20° C rise →irreversible pulp pathosis pulp abscess formationGradual controlled heat application over a largearea may not cause adverse reactions in the pulp.If the cavity floor ≤ 0.5 mm from the pulp, areas ofcoagulation necrosis could be detected.
    23. 23. III. Pulpal Reactions to Restorative Procedures:2) Degree of Procedure Physical Irritation:• Desiccation:It is the aspiration of odontoblastic nuclei into dentinal tubules.It is transient, within 7 to 30 days there is autolysis of the aspirated cells and formation of reactionary dentin.The pulp in cases with aspirated odontoblasts, following desiccation for 1 minute, was not sensitive to clinical scraping with an explorer.
    24. 24. III. Pulpal Reactions to Restorative Procedures:3) Biologic and Chemical Irritation:The sources of microbial irritaion: cariogenic microorganisms remaining on cavity floor. contamination with salivary microorganisms. contamination with bacteria from water lines.prompting the use of cavity disinfection (chemicals irritation), and so the most common irritant is etching agents.
    25. 25. III. Pulpal Reactions to Restorative Procedures:N.B:Once dentin is exposed, there is constant outward flow of dentinal fluid that minimizes the inward flow of any noxious agents. This may aid in the reduction of irritation from residual microbial factors in dentinal tubules.
    26. 26. III. Pulpal Reactions to Restorative Procedures:4) Proximity of Restorative Procedures to Dental Pulp & Surface Area of Dentin Exposed:= Depth and/or Width of a Tooth Preparation:There is an increasingly severe pulpal reaction, with a greater likelihood of the pulp undergoing irreversible pathosis, as the carious lesion progresses towards the pulp, particularly when the remaining dentin thickness (RDT) is less than 0.5 mm.
    27. 27. III. Pulpal Reactions to Restorative Procedures:4) Proximity of Restorative Procedures to Dental Pulp & Surface Area of Dentin Exposed:= Depth and/or Width of a Tooth Preparation:N.B:With the passage of time following cavity preparation, there is reduction in the permeability of RDT, due to rapid deposition of reactionary dentin, the migration of large proteins into the tubules, and/or the diminution of tubule diameter as dentin becomes more sclerotic.
    28. 28. III. Pulpal Reactions to Restorative Procedures:5) Permeability of remaining dentin & related odontoblastic :The dentin is not uniformly permeable, and that permeability depends on factors such as;a) The location within the same tooth the pulp.b) The age of the patient.c) The presence of pathologic conditions.
    29. 29. III. Pulpal Reactions to Restorative Procedures:5) Permeability of remaining dentin and related odontoblastic :a) The location within the same tooth:The tubular diameter increases from about 0.6 to 0.8 μm close to the DEJ to about 3 μm at the pulp. Given that bacterial cells are about 0.5 to 1 μm in diameter, it is evident that in deep cavity preparations, particularly when total-etch procedures are employed, bacteria can migrate through the remaining dentin into the pulp.
    30. 30. III. Pulpal Reactions to Restorative Procedures:5) Permeability of remaining dentin and related odontoblastic :b) The age of the patient,:The width of peritubular dentin increases with age, causing reduction in tubular lumen or sclerosis.
    31. 31. III. Pulpal Reactions to Restorative Procedures:5) Permeability of Remaining Dentin and Related Odontoblastic :c) The presence of pathologic conditions such as dental caries.• In superficial dentin, formation of caries crystals within the tubules of inner undemineralized dentin → decrease in permeability in dentin.
    32. 32. III. Pulpal Reactions to Restorative Procedures:5) Permeability of Remaining Dentin and Related Odontoblastic :c) The presence of pathologic conditions such as dental caries.• In superficial dentin,
    33. 33. III. Pulpal Reactions to Restorative Procedures:5) Permeability of Remaining Dentin and Related Odontoblastic :c) The presence of pathologic conditions such as dental caries.• In superficial dentin, formation of caries crystals within the tubules of inner undemineralized dentin → decrease in permeability in dentin.• Related odontoblasts, it was shown that irritation from cavity preparation increased the odontoblastic permeability only at the site of the cavity preparation.
    34. 34. III. Pulpal Reactions to Restorative Procedures:5) Permeability of Remaining Dentin and Related Odontoblastic :N.B:In addition to the physical barrier to permeability and the production of reactionary or reparative dentin, the odontoblastic layer may in fact contribute to the host response of the dental pulp by expressing important inflammatory mediators or recognize bacteria through toll-like receptor
    35. 35. III. Pulpal Reactions to Restorative Procedures:6) Patient Age:• Resting pulpal blood flow (PBF),• Response to cold application, decrease with age.• Reduction in pulpal neuropeptides.
    36. 36. IV. Pulpal Reactions to Restorative Materials: 1)Direct Effect 2)Indirect Effect1) Direct effect of restorative materials:• Certain cytotoxic components of resin monomers (Triethylene glycol dimethacrylate & 2-hydroxyethyl methacrylate).• Some of the components of resin restorations are released at cytotoxic levels after polymerization is completed.
    37. 37. IV. Pulpal Reactions to Restorative Materials:These chemicals have either:A short lived and in the absence of bacteria,is reversible OrIrreversible prolonged cytotoxicity,stimulation of hypersensitivity reactions, orimpairment of the host immune response tobacteria.N.B:•Subtoxic concentrations of certain agentsare capable of eliciting allergic reactions inhumans.
    38. 38. IV. Pulpal Reactions to Restorative Materials: 1)Direct Effect 2)Indirect Effect2) Indirect effect of restorative materials:The technique sensitivity of certain materials predisposes them to faulty bonds to tooth structure that can translate to dentin hypersensitivity, recurrent disease, and pulpal inflammation or necrosis.
    39. 39. IV. Pulpal Reactions to Restorative Materials:During the etching process:The more highly mineralized peritubular dentin ispreferentially dissolved, leaving free collagen fibrilsand opening lateral tubular branches. Applied resininfiltrates the exposed collagen mesh, creating a layer5 to 10 μm thick referred to as the hybrid layer.•If the preparation is too dry, the collagen fibrilscollapse.N.B:The optimal degree of hydration of the preparationsurface can vary from material to material.
    40. 40. IV. Pulpal Reactions to Restorative Materials:N.B:•It is recommend to rehydrate the fragmentsegment of the tooth prior to bonding, toincrease the mechanical and the microbialseal.•This is particularly important with acomplicated crown fracture where the pulpalprotection by intact dentin is absent
    41. 41. IV. Pulpal Reactions to Restorative Materials:Pulpal irritation is not considered a negativesequela all the time, the irritant potential ofcertain restorative materials has a usefulmotivated effect on odontoblasts in case ofdirect & indirect pulp capping.The outcome of such treatments depends on:•The biocompatibility of used medicaments.•The ability to seal the cavity.•A combination of the above.•Ability to control hemorrhage at theexposure site.
    42. 42. IV. Pulpal Reactions to Restorative Materials:For example: Calcium Hydroxide Zinc Oxide Eugenol Mineral Trioxide Aggregate Hemostatic Agents 2% chlorhexidine or 5.25% sodium hypochlorite
    43. 43. IV. Pulpal Reactions to Restorative Materials:Calcium hydroxideIn direct pulp capping: It induces theformation of dentinal bridge•Aqueous suspensions preparation: causessuperficial necrosis of pulpal tissue followed bytissue displaying low-grade inflammation.Within 30 days, the tissue subjacent to thenecrotic zone has reorganized and resumednormal architecture.•Hard-setting preparation: is effective ineliciting dentinal bridge formation with amuch smaller to nonexistent necrotic zone.
    44. 44. IV. Pulpal Reactions to Restorative Materials:Calcium hydroxide:In indirect pulp capping:•The Application of calcium hydroxide tointact dentin appears to induce sclerosis bypromoting crystal precipitation within thetubules, accompanied by reductions inpermeability.•The irritation potential is dependent on theremaining dentin thickness and permeability.
    45. 45. IV. Pulpal Reactions to Restorative Materials:Materials containing zinc oxide and eugenol:ZOE is used for;•Anesthetic properties:It has been shown to block transmission ofaction potentials in nerve fibers & suppressnerve excitability in the pulp when applied todeep excavations.•Antiseptic properties:It inhibits bacterial growth on cavity walls.•Sealing ability:It has good adaptation to dentin.
    46. 46. IV. Pulpal Reactions to Restorative Materials:Direct Pulp Caping with Mineral Trioxide Aggregate(MTA):Indication: in pulps with traumatic or carious exposure,for allowing the formation of a reparative dentinbridge and maintain continued pulp vitality.•At 1st week, no sign of necrosis close to the exposuresite, and odontoblast-like cells are observed at theperiphery with the deposition of calcified bridge.•At 2nd weeks, complete calcified bridge formation justbelow the exposure site.
    47. 47. IV. Pulpal Reactions to Restorative Materials:Direct Pulp Caping with Mineral TrioxideAggregate (MTA):Success was determined:•Radiographically.•Disappearance of subjective symptoms.•Normal pulp testing with cold.•continued root formation on immature teeth.Success depends on the prevention ofbacterial ingress by the placement of a well-sealed restoration must also be provided.
    48. 48. IV. Pulpal Reactions to Restorative Materials:Use of Hemostatic Agents and Disinfectants onDirect Pulp Exposures:The mechanical exposure of a healthy pulpcreated during cavity preparation could bedisinfected with either 2% chlorhexidine or5.25% sodium hypochlorite.
    49. 49. V. Pulpal Reactions to Laser Procedures:• Laser use on soft / hard tissues has potential benefits of efficiency, reduced sensitivity, disinfection, and precision.• There are several different types of laser available that depend on the wavelength, active medium, emission mode, delivery system, power output, and duration of application.
    50. 50. V. Pulpal Reactions to Laser Procedures:The main types available in dentistry today are:•The CO2 laser (10,600 nm).•Er:YAG laser (2940 nm), has a high affinity for waterand hydroxyapatite.•Ho:YAG laser (2120 nm), has high affinity to waterbut not to tooth structure.•Nd:YAG laser (1064 nm), has high affinity for waterand pigmented tissues and offers good hemostasis.•HeNe laser (632 nm). laser Doppler•GaAlAs laser (720-904 nm). flowmetry and in treating dentin hypersensitivity.
    51. 51. VI. Pulpal Reactions to Cavity Preparation Using Air Abrasion Techniques: Effect on pulp:During cavity After restoration:preparation:Higher pressures & It producessmaller particles (160 psi microleakage in a- 25 μm) has less pulpal equivalent degree toeffects than the high- high-speed burspeed and lower preparations, (Why?)pressures &larger Because of the lack ofparticles (80 psi - 50 μm) tactile control.treated teeth.
    52. 52. VII. Pulpal Reactions to Vital Bleaching Techniques: Using of strong oxidizing agents(such as: carbamide peroxide & hydrogen peroxide) pulpal irritationMinor inflammation up to Sever inflammation2 weeks → reversible → irreversiblepulpitis, prevented by pulpitis → pulpaltreating the teeth with necrosis.fluorides & by correctingdefective restorative.
    53. 53. VII. Pulpal Reactions to Vital Bleaching Techniques:Clinical symptoms are likely to be due toincreases in neuropeptides in the pulp.N.B: A recent studies showed that 10%carbamide peroxide in a custom tray for 6weeks was safe for the pulp health, while light-& laser-activated bleaching systems, due toincrease neuropeptides expression in the pulpto significant levels.
    54. 54. VIII. Pulpal Reactions to Periodontal Procedures: It is much more common for pulp necrosis or failed healing of periradicular lesions to present clinically with signs of periodontal disease than for periodontal disease to cause pulpal pathosis.1ry pulpal, 2ry periodontal 1ry periodontal , 2ry pulpalpathosis:. pathosis:is particularly evident with is rare to occur. Butpulp chamber / coronal third periodontal scaling and rootperforation, vertical root planning results in dentinfractures or congenital tooth hypersensitivity.defects.
    55. 55. VIII.Pulpal Reactions to Periodontal Procedures: (Why?)It is more likely for microbial irritants to moveoutward from a vital / necrotic pulp to causeperiodontal breakdown than for them tomove inward from a periodontal pocket to avital pulp causing irreversible pathosis.
    56. 56. VIII.Pulpal Reactions to Periodontal Procedures: (How?)The outward dentinal fluid flow in teeth withvital pulp contributes to the resistance toingress of bacteria in sufficient amounts tocause a clinically significant disease process.Once the pulp degenerates, dentinal fluidflow no longer exists.
    57. 57. IX. Pulpal Reactions to Orthodontic Surgery: Osteotomy of the jaw Disruption in the blood supply• Postoperative • Inflammation manifestations common and/or with traumatic injuries necrosis.
    58. 58. IX. Pulpal Reactions to Orthodontic Surgery:N.B: Studies have shown that if a safe distanceof 5 to 10 mm is maintained between the siteof the surgery and the teeth, minimaldisruption occurs. In most cases, the bloodflow is regained within months of the surgery.
    59. 59. IX. Pulpal Reactions to Orthodontic Surgery:N.B: Studies have shown that if a safe distanceof 5 to 10 mm is maintained between the siteof the surgery and the teeth, minimaldisruption occurs.N.B: In most cases, the blood flow is regainedwithin months of the surgery.
    60. 60. X. Pulpal Reactions to Implant Placement and Function:• The placement of implants requires multifaceted preoperative radiographic techniques. (Why?)The lack of attention to:(1)3-dimensional anatomy of the site of implant placement.(2) the orientation of neighboring teeth.  perforating the root and devitalizing the pulp.
    61. 61. X. Pulpal Reactions to Implant Placement and Function:It is usually recommended to place theimplants at a site free of periradicular lesion. (Why?)microbial irritants may interfere withosseointegration.•Some studies claimed that teeth withperiradicular lesions may reduce the successof neighboring implants, even if adequateendodontic treatment is performed.
    62. 62. X. Pulpal Reactions to Implant Placement and Function:However, recent data suggest that immediateimplant placement in sites that have beenadequately débrided is successful.Furthermore, implants that are not mobile buthave apical periimplant lesions have beensuccessfully treated with local débridementand “implant-apex resection” procedures.
    63. 63. Regenerative Potential of the Dental Pulp:Recent studies and case reports suggest thatthe dental pulp has great regenerativepotential, particularly in the immaturepermanent tooth. (How?)Stem cells from the apical papilla (SCAP) ofimmature teeth have likewise been identifiedand have been shown to develop intodentinogenic cells, given the properstimulation.

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