Rationale of Endodontic
Treatment
5
 Theories of Spread of Infection
 Culprit of Endodontic Pathology
 Portals for Entr...
59
RationaleofEndodonticTreatment
pulpal and periapical lesions whereas the germ free rats did
not show any development of...
TextbookofEndodontics
to injury to polymorphonuclear cells. This injury causes
release of proteolytic enzymes with resulti...
61
RationaleofEndodonticTreatment
Fig. 5.6: Eosinophil
Fig. 5.7: Macrophage
• Provide antigen to the immunocomplement cell...
TextbookofEndodontics
Fig. 5.10: Cell derived mediators
– Platelet activating factor
– Vasoactive amines
– Prostaglandins
...
63
RationaleofEndodonticTreatment
IL1 β is predominant in cases of periapical pathology.
IL6 – It is secreted by lymphoid ...
64
TextbookofEndodontics
• Metalloenzyme regulated pathway (Matrix Metallo Proteases-
MMPs)
The collagen (proteins) based ...
65
RationaleofEndodonticTreatment
c. Zone of irritation (Histiocytes and osteoclasts)
d. Zone of stimulation (Fibroblasts,...
66
TextbookofEndodontics
RATIONALE OF ENDODONTIC THERAPY
The rationale of root canal treatment relies on the fact that
the...
67
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Rationals of endodontics

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Rationals of endodontics

  1. 1. Rationale of Endodontic Treatment 5  Theories of Spread of Infection  Culprit of Endodontic Pathology  Portals for Entry of Microorganisms  Inflammation  Tissue Changes following Inflammation  Inflammatory Cells  Inflammatory Response to Periapical Lesion  Antibodies (Specific Mediators of Immune Reactions)  Role of Immunity in Endodontics  Endodontic Implications (Pathogenesis of Apical Periodontitis as Explained by FISH)  Kronfeld’s Mountain Pass Theory  Rationale of Endodontic Therapy  Bibliography Endodontic pathology is mainly caused by injury to the tooth which can be physical, chemical or bacterial. Such injury can results in reversible or irreversible changes in the pulp and periradicular tissues. These resultant changes depend on the intensity, duration, pathogenicity of the stimulus and the host defense mechanism. The changes that occur are mediated by a series of inflammatory and immunological reactions (in the vascular, lymphatics and connective tissue). All these reactions take place to eliminate the irritant and repair any damage. However, certain conditions are beyond the reparative ability of the body and need to be treated endodontically to aid the survival of tooth. Rationale of endodontic therapy is complete debridement of root canal system followed by three-dimensional obturation. THEORIES OF SPREAD OF INFECTION Focal Infection Definition: It is localized or general infection caused by the dissemination of microorganisms or toxic products from a focus of infection. Focus of Infection Definition: This refers to a circumscribed area of tissue, which is infected with exogenous pathogenic microorganisms and is usually located near a mucous or cutaneous surface. Theory Related to Focal Infection About a century ago, William Hunter first suggested that oral microorganisms and their products involved in number of systemic diseases, are not always of infectious origin. In year 1940, Reimann and Havens criticized the theory of focal infection with their recent findings. Mechanism of Focal Infection There are generally two most accepted mechanisms considered responsible for initiation of focal infection: 1. Metastasis of microorganisms from infected focus by either hematogenous or lymphogenous spread. 2. Carrying of toxins or toxic byproducts through bloodstream and lymphatic channel to site where they may initiate a hypersensitive reaction in tissues. For example: In scarlet fever, erythrogenic toxin liberated by infected streptococci is responsible for cutaneous features of this disease. Oral Foci of Infection Possible sources of infection in oral cavity which later on may set up distant metastases are: 1. Infected periapical lesions such as: i. Periapical granuloma ii. Periapical abscess iii. Periapical cyst 2. Teeth with infected root canals. 3. Periodontal diseases with special reference to tooth extraction. CULPRIT OF ENDODONTIC PATHOLOGY Many studies have shown that root canal infections are multibacterial in nature. In 1965, Kakehashi found that when dental pulps of conventional and germ free rats were exposed to their own oral microbial flora, the conventional rats showed
  2. 2. 59 RationaleofEndodonticTreatment pulpal and periapical lesions whereas the germ free rats did not show any development of lesion. So he described importance of microorganisms for the development of pulpal and periapical pathologies. PORTALS FOR ENTRY OF MICROORGANISMS (FIGS 5.1 AND 5.2) Though microorganisms may gain entry into pulp through several routes, most common route for entering of micro- organisms to dental pulp is dental caries. They can also gain entry into pulp cavity via mechanical or traumatic injury, through gingival sulcus and via bloodstream. Entry of Microorganisms into Pulp Through Dental caries—Caries is the most common way of entry of microorganisms into the dental pulp. Through open dentinal tubules-Microorganisms can pass into the dentinal tubules and subsequently to the pulp resulting in its necrosis. Through the periodontal ligament or the gingival sulcus, microorganisms can enter into the pulp via accessory and lateral canals which connect pulp and the periodontium. Anachoresis—Anachoresis refers to the attraction of blood borne bacteria in the areas of inflammation. In other words, anachoresis is a process by which microorganisms are transported in the blood to an area of inflammation where they establish an infection. Through defective restorations, faulty restoration with marginal leakage can result in contamination of the pulp by bacteria. INFLAMMATION Inflammation is defined as the local response of living mammalian tissue to injury due to any agent. It is a body defense reaction in order to limit the spread or eliminate it or to remove consequent necrosed cells and tissues. Following agents cause inflammation: a. Physical agents like cold, heat, mechanical trauma or radiation. b. Chemical agents like organic and inorganic poisons. c. Infective agents like bacteria, viruses and their toxins. d. Immunological agents like antigen-antibody cell mediated reactions. Therefore, we can say that inflammation is distinct from infection. Inflammation is the protective response by the body, while infection is invasion into the body by harmful microbes and their resultant ill effects by toxins. Signs of Inflammation The roman writer celsus in 1st century AD gave four cardinal signs of inflammation: 1. Rubor i.e. redness 2. Tumor i.e. swelling 3. Color i.e. heat 4. Dolor i.e. pain Fig. 5.1: Radiograph showing poorly obturated canals Fig. 5.2: Deep carious lesion resulting in pulp necrosis and periapical lesion Virchow later added the fifth sign function lasea, i.e. loss of function. Inflammation is of Two Types • Acute inflammation dominated by PMNLs (Polymorpho- nuclear lymphocytes) and few macrophages • Chronic inflammation dominated by lymphocytes, macrophages and plasma cells. The balance between the host defense and microbial factor determines the formation of lesion. In an infected canal, the microbes are usually confined within the canal. As the blood supply is compromised, the host defense mechanisms do not totally eliminate the bacteria. These bacteria release certain enzymes that stimulate the inflammatory process in the periapical tissue. TISSUE CHANGES FOLLOWING INFLAMMATION As a result of inflammation, tissues exhibit two types of changes viz degenerative changes and proliferative changes. 1. Degenerative changes in the pulp can be: • Fibrous • Resorptive • Calcific. Continuous degeneration of the tissue results in necrosis. Suppuration is another form of degeneration which is due
  3. 3. TextbookofEndodontics to injury to polymorphonuclear cells. This injury causes release of proteolytic enzymes with resulting liquefaction of dead tissues thus leading to formation of pus or suppuration. Three requisites which are necessary for suppuration • Tissue necrosis • Polymorphonuclear leukocytes • Digestion of the necrotic material by proteolytic enzymes released by injured polymorphonuclear cells. Clinical significance: An abscess can result even in absence of microorganisms because of chemical or physical irritation. It results in formation of sterile abscess. 2. Proliferative changes (Fig. 5.3) are produced by irritants which are mild enough to act as stimulants. These irritants may act as both irritant and stimulant, such as calcium hydroxide and its effect on adjacent tissues. In the approximation of the inflamed area, the irritant may be strong enough to produce degeneration or destruction, whereas at the periphery, the irritant may be mild enough to stimulate proliferation. The principal cells of proliferation or repair are the fibroblasts, which lay down cellular fibrous tissues. In some cases collagen fibers may be substituted by a dense acellular tissue. In either case it results in formation of fibrous tissue. In an infected canal, the microbes are usually confined within the canal. As the blood supply is compromised, the host defense mechanisms do not totally eliminate the bacteria. These bacteria release certain enzymes that stimulate the inflammatory process in the periapical tissue. INFLAMMATORY CELLS (FIG. 5.4) 1. Neutrophils (PMNLs) (Fig. 5.5): Along with basophils and eosinophils, polymorphonuclear neutrophils are called granulocytes because of presence of granules in the cytoplasm. Neutrophils are attracted to the site of injury within 24 hours and phagocytose the bacteria and cellular debris releasing lactic acid. Because of its low pH, this lactic acid results in death of the PMNLs and release of proteolytic enzymes (pepsin and cathepsin) prostaglandins and leukotrienes. All these changes result in breaks down of the tissue resulting in the formation of an abscess (dead PMNLs + debris). 2. Eosinophils (Fig. 5.6): They have many functional and structural similarities with neutrophils like their formation in bone marrow, phagocytosis, presence of granules in the cytoplasm, bactericidal and toxic action against many parasites. However, granules of eosinophils lack lysozyme and they are richer in myeloperoxidase than neutrophils. Number of eosinophils increase in following conditions: • Allergic conditions • Skin diseases • Parasitic infestations Macrophages (Fig. 5.7): When the PMNLs fail to remove the bacteria, the circulating monocytes reach the site of 60 Fig. 5.3: Inflammatory cells present at the healing site Fig. 5.4: Inflammatory cells Fig. 5.5: Neutrophil inflammation and change into macrophages. These macrophages are slow moving and remain at the site of inflammation for a longer time (approximately 2 months). This result in development of chronic inflammation. Macrophages perform following functions: • They help in phagocytosis and pinocytosis • Perform immunological function • Secrete lysosomal enzymes • Secrete complement protein and prostaglandins
  4. 4. 61 RationaleofEndodonticTreatment Fig. 5.6: Eosinophil Fig. 5.7: Macrophage • Provide antigen to the immunocomplement cells • They act as scavenger of dead cells, tissues and foreign bodies • They fuse with other macrophages to produce multi- nucleated giant cells like osteoclasts, dentinoclasts and foreign body giant cells. 3. Lymphocytes (Fig. 5.8): They are the most numerous cells (20-45%) after neutrophils. There are two types of lymphocytes seen in apical periodontitis: a. T-lymphocytes – T-helper cells (Th): They are present in the acute phase of lesion expansion. – T-suppressor cells (Ts): They predominate in later stages preventing rapid expansion of the lesion. b. B-lymphocytes – On getting signals from antigens and T-helper cells, they transform into plasma cells and secrete antibodies. Their number increases in following conditions: – hypersensitivity state – prolonged infection with immunological response. 4. Osteoclasts: In the physiologic state, the preosteoclasts remain dormant as monocytes in the periradicular bone. Fig. 5.8: Lymphocyte Fig. 5.9: Inflammatory response to periapical lesion In case of apical periodontitis, they proliferate and fuse on stimulation by cytokines and other mediators to form osteoclasts. These osteoclasts are responsible for deminerali- zation of the bone and enzymatic dissolution of organic matrix at the osteoclast-bone interface. This results in bone resorption. 5. Epithelial cells: Cytokines and other mediators stimulate the dormant cell rests of malassez. These cells undergo division and proliferation which results in inflammatory hyperplasia. INFLAMMATORY RESPONSE TO PERIAPICAL LESION (FIG. 5.9) Nonspecific Mediators of Periradicular Lesions Nonspecific mediators can be classified into following types: 1. Cell derived mediators: – Neuropeptides – Eicosanoids/arachidonic acid derivatives – Cytokines – Lysosomal enzymes
  5. 5. TextbookofEndodontics Fig. 5.10: Cell derived mediators – Platelet activating factor – Vasoactive amines – Prostaglandins 2. Plasma derived mediators – The fibrinolytic system – The complement system – The kinin system 3. Extracellular matrix derived mediators – Effector molecules Cell Derived Mediators (Fig. 5.10) 1. Neuropeptides: These are generated following tissue injury by the somatosensory and autonomic nerve fibers. Neuropeptides include: – Substance P (SP): Causes vasodilation, increased vascular permeability and increased blood flow. – Calcitonin-gene related peptide (CGRP): results in vasodilation. 2. Eicosanoids: The injury to cells results in release membrane phospholipid, arachidonic acid which is metabolized by either cyclooxygenase pathway or lipoxygenase pathway to form prostaglandins (PGs) or leukotrienes (LTs) respectively, which are involved in inflammatory process. a. Prostaglandins are of various types: – PGE2, – PGD2, – PGF2a, – PGI2 In cases of acute apical periodontitis and areas of bone resorption, PGE2 and PGI2 are commonly observed. Action of PGs can be inhibited by administration of indomethacin which inhibits the enzyme cyclooxygenase thus inhibiting formation of prostaglandins. b. Leukotrienes: These are produced by activation of lipoxygenase pathway of arachidonic acid metabolism. Studies have shown the presence of LTB4, LTC4, LTD4 and LTE4 in periradicular lesions which cause different effects on the tissues as shown in (Fig. 5.11). 3. Cytokines – These are low molecular weight polypeptides secreted by activated structural and hematopoietic cells. 62 Different cytokines such as interleukins and tumor necrosis Fig. 5.11: Leukotrienes factor (TNF) cause development and perpetuation of periradicular lesions. They are of two types: a. Proinflammatory cytokines – IL1 α and β, (Interleukins) – IL6 α and β, – IL8 α and β. b. Chemotactic cytokines – TNFα (macrophage derived) (Tumor necrosis factor) – TNFβ (T-lymphocyte derived) – TNFγ. a. Proinflammatory cytokines IL1 – The local effects of IL1 are – – Enhanced leukocyte adhesion to endothelial walls. – Stimulate PMNLs and lymphocytes. – Activates production of prostaglandins and proteolytic enzymes. – Enhances bone resorption. – Inhibits bone formation.
  6. 6. 63 RationaleofEndodonticTreatment IL1 β is predominant in cases of periapical pathology. IL6 – It is secreted by lymphoid and non-lymphoid cells and causes inflammation under the influence of IL1, TNF α and interferon γ (IFN). It is seen in periapical lesions. IL8 – It is produced by macrophages and fibroblasts under the influence of IL1 β and TNF α and is associated with acute apical periodontitis. b. Chemotactic cytokines TNF – They are seen in chronic lesions associated with cytotoxic and debilitating effect. TNF α is seen in chronic apical lesions and root canal exudates. 1. Colony stimulating factor (CSF) – They are produced by osteoblasts and regulate the proliferation of PMNLs and preosteoclasts. 2. Growth factors (GF) – They are the proteins produced by normal and neoplastic that regulate the growth and differentiation of non- hematopoietic cells. They can transform a normal cells to neoplastic cells and are known as transforming growth factors (TGF). They are of two types - a. TGF α (produced by malignant cells) – not seen in periapical lesions. b. TGF β (produced by normal cells and platelets). They counter the adverse effects of inflammatory host response by: – Activating macrophages. – Proliferation of fibroblasts. – Synthesis of connective tissue fibers and matrices. Lysosomal Enzymes Lysosomal enzymes such as alkaline phosphatase, lysozyme, peroxidases, collagenase cause increase in vascular permeability, leukocytic chemotaxis, bradykinin formation and activation of complement system. Platelet Activating Factor It is released from IgE—sensitized basophils or mast cells. Its action include increase in vascular permeability, chemotaxis, adhesion of leukocytes to endothelium and broncho- constriction. Vasoactive Amines Vasoactive amines such as histamine, serotonin are present in mast cells, basophils and platelets. Their release cause increase in tissue permeability, vasodilation used vascular permeability (Fig. 5.9). Prostaglandins These are produced by activation of cyclooxygenase pathway of arachidonic acid metabolism. Studies have shown high levels of PGE2 in periradicular lesions. Torbinejad et al found that periradicular bone resorption can be inhibited by administration of indomethacin, an antagonist of PGs. This indicates that prostaglandins are also involved in the pathogenesis of periradicular lesions. Plasma Derived Mediators (Fig. 5.12) 1. The fibrinolytic system: The fibrinolytic system is activated by Hageman factor which causes activation of plasminogen. This results in release of fibrinopeptides and fibrin degradation products which cause increase in vascular permeability and leukocytic chemotaxis. 2. The complement system: Trauma to periapex can result in activation of kinin system which in turn activates complement system. Several studies have shown elevated levels of kinins and C3 complement component in periradicular lesions. Products released from activated complement system cause swelling, pain and tissue destruction. 3. The kinin system: These are produced by proteolytic cleavage of kininogen. Release of kinins cause smooth muscle contraction, vasodilation and increase in vascular permeability (Fig. 5.13). Effector Molecules The inflammatory process causes not only the destruction of the cells but also the extracellular matrix in the periapical pathosis. The extracellular matrix is degraded by enzymatic effector molecules by various pathways like • Osteoclast regulated pathway, • Phagocyte regulated pathway, • Plasminogen regulated pathway and Fig. 5.12: Plasma derived mediators Fig. 5.13: Kinin system
  7. 7. 64 TextbookofEndodontics • Metalloenzyme regulated pathway (Matrix Metallo Proteases- MMPs) The collagen (proteins) based matrices are degraded by MMPs. ANTIBODIES (SPECIFIC MEDIATORS OF IMMUNE REACTIONS) These are produced by plasma cells and are of two types: • Polyclonal antibodies – are nonspecific like IgE mediated reactions which interact with antigen resulting in release of certain chemical mediators like histamine or serotonin. • Monoclonal antibodies – like IgG and IgM, interact with the bacteria and its by-products to form antigen-antibody complexes that bind to the platelets resulting in release vasoactive amines thus increasing the vascular permeability and chemotaxis of PMNs. The monoclonal antibodies exhibit antimicrobial effect. • In acute abscess, the complex enters the systemic circulation. The concentration of these complexes return to normal levels after endodontic treatment. • In chronic lesions, the Ag-Ab complexes are confined within the lesion and do not enter into the systemic circulation. The response of periapical/host tissue is controlled by: • Cells • Molecular mediators (Nonspecific mediators of inflammation), and • Antibodies (Specific mediators of inflammation) ROLE OF IMMUNITY IN ENDODONTICS The immune system of human being is a complex system consisting of cells, tissues, organs as well as molecular mediators that act together to maintain the health and well-being of the individual. The cells and microbial irritants interact with each other via a number of molecular mediators and cell surface receptors to result in various defense reactions. Immunity is of two types: • Innate immunity • Acquired/adaptive immunity Innate immunity: It consists of cells and molecular elements which act as barriers to prevent dissemination of bacteria and bacterial products into the underlying connective tissue. The innate immunity is responsible for the initial nonspecific reactions. Cells providing innate immunity are neutrophils, monocytes, eosinophils, basophils, NK cells, dendritic cells, and odonto- blasts. Acquired/Adaptive immunity: It involves release of specific receptor molecules by lymphocytes which recognize and bind to foreign antigens. Adaptive immunity is provided by: • T-Lymphocytes that release T-cell antigen receptors • B-Lymphocytes that release B-cell antigen receptors or Histopathology of Periapical Tissue Response to Various Irritants Root canal of teeth contains numerous irritants because of some pathologic changes in pulp. Penetration of these irritants from infected root canals into periapical area can lead to formation and perpetuation of periradicular lesions. In contrast to pulp, periradicular tissue have unlimited source of undifferentiated cells which can participate in inflammation and repair in inflammation and repair. Also these tissues have rich collateral blood supply and lymph drainage. Depending upon severity of irritation, duration and host, response to periradicular pathosis may range from slight inflammation to extensive tissue destruction. Reactions involved are highly complex and are usually mediated by nonspecific and specific mediators of inflammation. ENDODONTIC IMPLICATIONS (PATHOGENESIS OF APICAL PERIODONTITIS AS EXPLAINED BY FISH) (FIG. 5.14) FISH described the reaction of the periradicular tissues to bacterial products, noxious products of tissue necrosis, and antigenic agents from the root canal. He established an experimental foci of infection in the guinea pigs by drilling openings in the jaw bone and packing it with wool fibers saturated with a broth culture of microorganisms. FISH in 1939 theorised that the zones of infection are not an infection by themselves but the reaction of the body to infection. Thus he concluded that the removal of this nidus of infection will result in resolution of infection. Four well defined zones of reaction were found during the experiment: a. Zone of infection or necrosis (PMNLs) b. Zone of contamination (Round cell infiltrate – lymphocytes) immunoglobulins. Fig. 5.14: FISH zones
  8. 8. 65 RationaleofEndodonticTreatment c. Zone of irritation (Histiocytes and osteoclasts) d. Zone of stimulation (Fibroblasts, capillary buds and Osteoblasts). Zone of Infection In FISH study, infection was confined to the center of the lesion. This zone is characterized by polymorphonuclear leukocytes and microorganisms along with the necrotic cells and detructive components released from phagocytes. Zone of Contamination Around the central zone, FISH observed the area of cellular destruction. This zone was not invaded by bacteria, but the destruction was from toxins discharged from the micro- organisms in the central zone. This zone is characterized by round cell infiltration, osteocyte necrosis and empty lacunae. Lymphocytes were prevalent everywhere. Zone of Irritation FISH observed evidence of irritation further away from the central lesion as the toxins became more diluted. This is characterized by macrophages, histocytes and osteoclasts. The degradation of collagen framework by phagocytic cells and macrophages was observed while osteoclasts attack the bone tissue. The histologic picture is much like preparatory to repair. Zone of Stimulation FISH noted that, at the periphery, the toxin was mild enough to act as stimulant. This zone is characterized by fibroblasts and osteoblasts. In response to this stimulatory irritant, fibroblasts result in secretion of collagen fibers, which acted both as wall of defense around the zone of irritation and as a scaffolding on which the osteoblasts synthesize new bone. So the knowledge gained in FISH study can be applied for better understanding of reaction of periradicular tissues to a nonvital tooth. The root canal is the main source of infection. The microorganisms present in root canal are rarely motile. Though they do not move from the root canal to the periapical tissues; but they can proliferate sufficiently to grow out of the root canal. The metabolic byproducts of these microorganisms or the toxic products of tissue necrosis may also get diffused to the periradicular tissues. As the microorganisms enter in the periradicular area, they are destroyed by the polymorphonuclear leukocytes. But if microorganisms are highly virulent, they overpower the defensive mechanism and result in development of periradicular lesion. The toxic byproducts of the microorganisms and the necrotic pulp in the root canal are irritating and destructive to the periradicular tissues. These irritants along with proteolytic enzymes (released by the dead polymorphonuclear leukocytes) result in the formation of pus. This results in development of chronic abscess. At the periphery of the destroyed area of osseous tissue, toxic bacterial products get diluted sufficiently to act as stimulant. This results in formation of a granuloma. After this fibroblasts come in the play and build fibrous tissue and osteoblasts restrict the area by formation of sclerotic bone. Along with these if epithelial rests of Malassez are also stimulated, it results in formation of a cyst. KRONFELD’S MOUNTAIN PASS THEORY (FIG. 5.15) Kronfeld explained that the granuloma does not provide a favorable environment for the survival of the bacteria. He employed the FISH concept so as to explain the tissue reaction in and around the granulomatous area. Zone A: He compared the bacteria in the infected root canal with the invaders entrenched behind high and inaccessible “mountains”, the foramina serving as mountain passes. Zone B: The exudative and granulomatous (proliferative) tissue of the granuloma represents a mobilized army defending the plains (periapex) from the invaders (bacteria). When a few invaders enter the plain through the mountain pass, they are destroyed by the defenders (leukocytes). A mass attack of invaders results in a major battle, analogous to acute inflam- mation. Zone C: Only complete elimination of the invaders from their mountainous entrenchment will eliminate the need for a defense forces in the “plains”. Once this is accomplished, the defending army of leukocytes withdraws, the local destruction created by the battle is repaired (granulation tissue) and the environment returns to its normal pattern. This explains the rationale for the non-surgical endodontic treatment for teeth with periapical infection. The complete elimination of pathogenic irritants from the canal followed by the three-dimensional fluid impervious obturation will result in complete healing of periapical area. Fig. 5.15: Kronfeld’s mountain pass theory
  9. 9. 66 TextbookofEndodontics RATIONALE OF ENDODONTIC THERAPY The rationale of root canal treatment relies on the fact that the nonvital pulp, being avascular, has no defense mechanisms. The damaged tissue within the root canal undergoes autolysis and the resulting breakdown products will diffuse into the surrounding tissues and cause periapical irritation associated with the portals of exit even in the absence of bacterial contamination. It is essential therefore, that endodontic therapy must seal the root canal system three-dimensionally so as to prevent tissue fluids from percolating in the root canal and toxic byproducts from both necrotic tissue and microorganisms regressing into the periradicular tissues. Endodontic therapy includes: • Non-surgical endodontic treatment • Surgical endodontic treatment Non-surgical endodontic treatment includes three phases: • Access preparation: The rationale for this is to create a straight line path for the canal orifice and the apex. • Shaping and cleaning: The rationale for this is the complete elimination of vital or necrotic pulp tissue, microorganisms and their byproducts. • Obturation: Main objective of obturation is to have a three dimensional well fitted root canal with fluid tight seal so as to prevent percolation and microleakage of periapical exudate into the root canal space and also to prevent infection by completely obliterating the apical foramen and other portals of communication. Surgical Endodontic Treatment The rationale of surgical endodontics is to remove the diseased tissue present in the canal and around the apex, and retrofil the root canal space with biologically inert material so as to achieve a fluid tight seal. QUESTION Q. What is rationale of endodontics? Explain in detail about fish zones. BIBLIOGRAPHY 1. Abou-Rass, Bogen G. Microorganisms in closed periapical lesions. Int Endod J 1998;31:39. 2. Alavi AM, Gulabivala K, Speight PM. Quantitative analysis of lymphocytes and their subsets in periapical lesions. Int Endod J 1998;31:233. 3. Baumgartner JC, Falkler (Ir) WA. Detection of immunoglobulin from explant cultures of periapical lesions. J Endod 1991;17:105. 4. Brännström M, Astrom A. The hydrodynamics of the dentin; its possible relationship to dentinal pain. Int Dent J 1972;22:219. 5. Dippel HW, et al. Morphology and permeability of the dentinal smear layer. J Prosthet Dent 1984;52:657. 6. FISH EW. Bone infection. J Am Dent Assoc 1939;26:691. 7. Goldman LB, Goldman M, Kronnman JH, Lin PS. The efficacy of several irrigating solutions for endodontics:a scanning electron micriscopic stody. Oral Surg 1981;52:197. 8. Jontell M, Bergenholtz G, Scheynius K, Ambrose W. Dendritic cells and macrophages expressing class I antigens in normal rat incisor pulp. J Dent Res 1988;67:1263. 9. Kuo M, Lamster I, Hasselgren G. Host mediators in endodontic exudates. J Endod 1998;24:598. 10. Lukic A, Arsenijevic N, Vujanic G, Ramic Z. Quantitative analysis of immunocompetent cells in periapical granuloma: Correlation with the histological characteristics of the lesions. J Endod 1990;16:119. 11. Michelich VJ, Schuster GS, Pashley DH. Bacterial penetration of human dentin, in vitro. J Dent Res 1980;59:1398. 12. Ogilvie RW, et al. Physiologic evidence for the presence of vasoconstrictor fibers in the dental pulp. J Dent Res 1966;45:980. 13. Pashley DH, Michelich V, Kehl T. Dentin permeability: Effect of smear layer removal. J Prosthet Dent 1981;46:531. 14. Robinson HB, Boling LR. The anachoretic effect in pulpitis. J Am Dent Assoc 1949;28:268. 15. Stern MH, Driezen S, Mackler BF, Selbst AG, Levy BM. Quantitative analysis of cellular composition of human periapical granuloma. J Endod 1981;7:117. 16. Torabinejad M, Kigar RD. Histological evaluation of a patient with periodontal disease. Oral Surg 1985;59:198. 17. Trope M, Rosenberg E, Tronsdat L. Dark field microscope spirochete count in the differentiation of endodontic and periodontal abscesses. J Endod 1992;18:82. 18. Wayman BE, Murata SM, almeida RJ, Fowler CB. A bacteriological and histological evaluation of 58 periapical lesions. J Endod 1992;18:152.
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