Rationale of endodontics / /certified fixed orthodontic courses by Indian dental academy


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Rationale of endodontics / /certified fixed orthodontic courses by Indian dental academy

  1. 1. RATIONALE OF ENDODONTICS INDIAN DENTAL ACADEMY Leader in Continuing Dental Education www.indiandentalacademy.com
  2. 2. CONTENTS• Introduction• Inflammation• Causes of pulpal Inflammation• Pathways of pulpal & periapical infection• Responses of the pulp and periradicular tissue Cellular & Vascular Components Chemical mediators.• Syngcuk kim’s hypothetic mechanism of pathophysiology of pulpal disorder• Periradicular tissue changes following inflammation• Endodontic implication Fish theory of zones of inflammation• Sequence of pulpo periapical pathoses• Conclusion
  3. 3. INTRODUCTION• Injury to the calcified structure of teeth and to the supporting tissues by noxious stimuli may cause changes in the pulp and the periradicular tissues.• The inflammatory response of the connective tissue of the dental pulp is modified because of its milieu. Because the pulp is encased in hard tissues with limited portals of entry, it is an organ of terminal and limited circulation with no efficient collateral circulation and with limited space to expand during the inflammatory reaction. A clear concept is necessary for the understanding or the diseases of the pulp and their extension to the periradicular tissues.
  4. 4. INFLAMMATION• Inflammation is a complex reaction to injurious agents such as microbes and damaged, usually necrotic cells that consists of vascular responses, migration and activation of leucocytes, and systemic reactions. Robbins et al 2004
  5. 5. CAUSES OF PULP INFLAMMATION• Bacterial Coronal ingress : caries, fracture,nonfracture tract, anomalous tract. Radicular ingress: caries, retrogenic infection, hematogenic• Traumatic Acute : Coronal #, radicular #, vascular stasis, luxation, avulsion Chronic: adolescent female bruxism,traumatism, attrition
  6. 6. Iatral causes:• Cavity preparation: Heat of preparation, depth of preparation, dehydration, pulp horn extensions, pulp hemorrhage, pulp exposure, pin insertion, impression taking• Restoration: Insertion, Fracture, Force of cementing, Heat of polishing.• Intentional extirpation and root canal filling, Orthodontic movement, Periodontal curettage, Electrosurgery, Laser burn, Periradicular curettage, Rhinoplasty, Osteotomy, Intubation for general anesthesia
  7. 7. Chemical causesRestorative materials: Cements, Plastics,Etching agents, Cavity liners, Dentin bonding agents, Tubule blockage agentsDisinfectants : Silver nitrate, Phenol, Sodium fluorideDesiccants : Alcohol, Ether, Others
  8. 8. Idiopathic causes• Aging• Internal resorption• External resorption• Hereditary hypophosphatemia• Sickle cell anemia• Herpes zoster infection• Human immunodeficiency virus (HIV) and acquired immune deficiency syndrome (AIDS)
  9. 9. PATHWAYS OF PULPAL & PERIAPICAL INFECTIONS• Dentinal tubules• Pulp exposure• Periodontal ligament• Anachoresis
  10. 10. Dentinal tubules• Position, size and number• Dentinal tubules exposed due to loss of enamel and cementum• As per the size and number of the tubules microorganisms enter, multiply and invade exposed tubules• Role of dental caries, dental procedures and periodontal diseases.• Bacterial strains involved
  11. 11. Pulp exposure• Contamination of the pulp – truama, caries, and others• Depending on the virulence of the organism, host resistance, amount of circulation and degree of drianage ranges the pulpal inflammation.• Microbiology involved.
  12. 12. Periodontal ligament• Relation between root canal infection and periradicular lesion ?• Grossman found that periodontal ligament provided pathways for passage of microorganisms into the pulpal tissue.
  13. 13. Anachoresis• Defined as a positive attraction of blood borne microorganisms to inflamed or necrotic tissue during bacteremia.• Csernyei 1939 – demonstrated anachoretic effect of periapical inflammation in dogs.• Dental extractions,toothbrushing can produce bacteremia during which circulating microorganisms can be attracted to the inflamed or necrotic pulp.
  14. 14. • Depending on the level of oxygen tension & the presence or absence of essential nutrients,specific groups of bacteria colonize,multiply,contaminate & establish the flora in the entire root canal system including periradicular tissues.
  15. 15. SIGNS OF INFLAMMATIONDescribed in a Egyptian papyrus-in 3000BC by Celsus as: Rubor [redness] Tumor [swelling] Calor [heat] Dolor [pain] Functio laesa [virchow in 1793]
  16. 16. Components Of Inflammation Cellular Vascular
  17. 17. Cellular Components of Inflammation• Polymorphonuclear neutrophils• Eosinophils• Basophils• Mast cells• Monocytes & Macrophages• Lymphocytes• Osteoclasts• Epithelial cells
  18. 18. Polymorphonuclear Neutrophils
  19. 19. Eosinophils,Basophils & Mast cells
  20. 20. Monocytes & Macrophages
  21. 21. Lymphocytes
  22. 22. Osteoclasts &Epithelial Cells
  23. 23. CHEMICAL MEDIATORSDEFINITION Inflammatory mediators are chemical substances present in plasma or produced by certain cells which mediate the inflammatory reactions.
  25. 25. Plasma derived mediatorsComplement System The complement system consists of 20 component proteins and their cleavage products found in greatest concentration in plasma. The complement system is activated by two pathways. 1.Classic pathway. 2.Alternate pathway.
  26. 26. Complement Cascade
  27. 27. Actions1. vascular phenomenon: -C3a, C5a- increases vascular permeability, vasodilation -C5a- activates lipoxygenase pathway in neutrophil and monocyte2. Leukocyte adhesion and chemotaxis: -C5a- powerful chemotactic agent for neutrophils, monocytes, eosinophils, basophils -Increased adhesion of leukocytes to endothelium -Increases avidity of surface integrins to endothelial ligand
  28. 28. Hageman factor activatedkinin and coagulation system
  29. 29. Kinin system• Bradykinin:is shortlived due to the activity of kinase enzyme• KallikrienActions:• Kallikrien converts High Molecular Weight Kininogen (HMWK) into bradykinin, which in turn converts plasminogen into plasmin• Plasmin splits C3 into C3a• Kallikrien also directly converts C5 into C5a and has chemotactic activity
  30. 30. Clotting System:Two components of activated coagulation system links coagulation inflammation1. Fibrinopeptides- increase vascular permeability, chemotactic for leukocytes2. Thrombin- increase leukocyte adhesion, fibroblast proliferation
  31. 31. Cell derived mediatorsHistamineHistamine is released by mast cell degranulation in response to variety of stimuli like:• Physical injury - trauma, heat, cold.• Immune reactions involving binding of antibody to mast cell.• Fragments of complement called anaphylatoxins - C3a, C5a.• Histamine releasing proteins derived from leucocytes.• Neuropeptides e.g. substance P.• Cytokines - IL1, IL8.
  32. 32. ACTIONS: Acts on microcirculation mainly via H1 receptors. Histamine causes1 Dilatation of arterioles, constriction of large arteries.2 Increased vascular permeability of venules.
  33. 33. SEROTONIN:(5 - hydroxytryptamine. )• Present in platelets and enterochromaffin cells.• Their release is stimulated by when platelets aggregate after contact with collagen, thrombin, ADP, antigen-antibody complexes.• Platelet aggregation and release stimulated by platelet activation factor(PAF)• PAF derived from mast cells during IgE mediated reactionsACTIONS:• Platelet aggregation.• Increases vascular permeability.
  34. 34. Lysosomal enzymes• Neutral proteases – elastase, collagenase, cathepsin can mediate tissue injury by degrading elastin collagen and other tissue proteins• Proteases – cleave C3 and C5 directly to generate anaphylotoxins.• Kallikerin released from the lysosomes promotes the generation of bradykinin• Cationic proteins
  35. 35. Phospholipid metabolism & Arachidonic acid metabolism
  36. 36. Neuropeptides• Several neuropeptides have been detected in the dental pulp of humans• These include substance P (SP), calcitonin gene-related peptide(CGRP), neurokinin A (NKA), neuropeptide K, neuropeptide Y, somatostatin and vasoactive intestinal peptide (VIP)• Increased production and release of neuropeptides play an important role in initiating and propagating pulpal inflammation.• SP, CGRP and VIP are potent vasodilators• Neuropeptide Y is a vasoconstrictor
  37. 37. Cytokines• Cytokines are polypeptides produced by many cell types that modulate the function of other cell types• Cytokines that appear to be important mediators of inflammation are IL-1 and TNF and IL-8• IL-1 and TNF are produced by activated macrophages, they induce the synthesis and surface expression of the endothelial achesion molecules that mediate leucocyte sticking and increase surface thrombogenicity of the endothelium TNF also causes aggregation and activation of neutrophils.• IL-8 is a small polypeptide, produced by activated macrophages and other cell types, that is a powerful chemoattractant and activator of neutrophils
  38. 38. Nitric oxideIn macrophages nitric oxide acts as free radicals- cytotoxic to certain microbes and tumor cellsOxygen derived free radicals:Released from leukocytes after exposure to chemotactic agents, immune complexes or phagocytes.Produce effects by:• Generation of super –oxide• Combining with nitric oxide to form toxic derivativesActions:• Endothelial cell damage- vascular permeability increases• Inactivation of anti-proteases• Injury to other cells e.g. tumor cells, red cells
  39. 39. Vascular changes Changes in vascular flow and calibera] Vasodialation induced by histamine and nitrous oxide follows a trasient constriction of arteriolesincreased blood flow cause of heat & rednessb] Increased permeability of the microvasculature increased outflow of protein rich tissues into the extra vascular tissues increase in concentration of red cells in small vessels increase in viscosity of blood with slower blood flowc] Leucocyte accumulation and migration accumulate along the vascular endothelium
  40. 40. Increased vascular permeability loss of protein from plasma Decrease in intra vascularosmoticpressure Increase in the osmotic pressure of the interstitial Fluid&increased hydrostatic pressure Accumulation in the Interstitial Fluid net increase of extra vascular fluid Edema
  41. 41. Cellular Events Leukocyte extravasations and Phagocytosis• Leukocyte extravasations:• Delivery of leukocytes to the site of injury and activate them to perform normal functions.• The events are:• Margination• Rolling and adhesion• Transmigration(diapedesis)• Migration towards chemotaxic stimulus• Opsonization
  42. 42. Margination• In venules- erythrocytes occupy central column with leukocytes displaced towards vessel wall. In inflammation- stasis occurs with more leukocytes assuming a peripheral position.Rolling• Rows of leukocytes adhere transiently to endotheliumPavementing• After adhesion leukocytes insert pseudopods between endothelial cells and basement membrane.• Traverse the basement membrane and escapes to tissue space.
  43. 43. Leucocyte exudation & Phagocytosis
  44. 44. Chemotaxis
  45. 45. Opsonization & Phagocytosis
  46. 46. To summarizeVasodilatation:• Prostaglandins• Nitric oxideIncrease in vascular permeability• Vasoactive amines• C3a, C5a• Bradykinin• Leucotrienes C4,D4, E4• Platelet activation factor
  47. 47. Chemotaxis• C5a• Leucotrienes B4• IL8• Bacterial productsTissue damage• Lysosomal enzymes• Oxygen derived free radicals• Nitric oxide
  48. 48. Syngcuk kim’s hypothetic mechanism of pathophysiology of pulpal disorder
  49. 49. Periradicular tissue changes following inflammation Degenerative changes• May be fibrotic, resorptive, or calcific.• If degenerative changes continues necrosis will result.• Another form – PMN are injured releasing proteolytic enzymes & causing liquefaction of dead tissue - suppuration / formation of pus. 3 requisites are necessary for pus : – Necrosis of tissue cells – Sufficient number of PMNs – Digestion of dead material by proteolytic enzymes
  50. 50. • If the reaction is not great enough , when the irritant is weak, an exudate consisting of serum, lymph, & fibrin will result.• PMN liberate proteolytic enzymes which digest not only leukocytes but also the adjacent dead tissue leading to abscess formation.• Microorganism are not necessary for development of an abscess. eg : A sterile abscess may result from chemical or physical irritation in the absence of microorganism.
  51. 51. Proliferative changes • Irritant must be mild enough to act as stimulant to produce proliferative changes. • Within the same inflammatory area , a substance can be both an irritant & a stimulant such as calcium hydroxide. • When it is strong in the center it may produce degeneration or destruction whereas at the periphery it may be mild enough to stimulate proliferation.
  52. 52. • When the tissue is in apposition fibroblastic repair will take place & when a gap is present repair is made with granulation tissue which is resistant to infection.• Fibroblasts are the principle cells of repair which lay down cellular fibrous tissue.• In some cases when collagen fibres are laid down dence acellular tissue is formed.• Destroyed bone is not always replaced by new bone but it may be replaced by fibrous tissue.
  53. 53. Endodontic implication Fish theory of zones of inflammation• The reaction of the periradicular tissues to noxious products of tissue necrosis, bacterial products, & antigenic agents from the root canal has been described by Fish
  54. 54. Four well defined zones of reaction were found• Zone of infection Exudative(acute)zones• Zone of contamination Transitional area• Zone of irritation Proliferative(chronic) zones• Zone of stimulation
  55. 55. Zone of necrosis ( zone of infection)Necrotic or infected root canal contents are1. Pus fluid contains dead cells, destructive components released from phagocytes, end products of protein decomposition ( proteolysis)2. PMN3. Microorganism, exotoxins, endotoxins, antigens , bacterial enzymes, chemotactic factors.
  56. 56. Zone of contamination ( exudative inflammatory zone) Immediate response to toxic elements coming out of root canal are1. Principal exudative defense response – vasodilatation, fluid exudation, cellular infiltration2. Dilution of toxic elements plus antibacterial action of inflammatory fluid.3. Principal defense cells – PMN’s, macrophages
  57. 57. Zone of irritation ( granulomatous zone, proliferative inflammatory zone) Toxicity diminishing as distance from canal foramina increases1. Function – defense, healing , repair.2. Principal proliferative response – granulation tissue ( capillary proliferation & fibroblastic activity)3. Granulomatous – granulation tissue plus chronic defense cell4. Principal Chronic defense cell – lymphocytes, plasma cells, blood derived macrophages,tissue macrophages
  58. 58. Conti..5. Cell derived mediators of inflammation – antibodies from plasma cells, lymphokines from sesitized T cells, histamine & serotonin from basophils.6. Russel bodies- enlarged plasma cells with numerous antibody inclusion.7. Eosinophils – attracted by mast cell ECF- A & lymphokine ECF – A.. They modulate inflammation & allergy by destroying certain vasoactive substances like PAF & SRS – A8. Foam cells , cholesterol crystals , epithelial clusters & strands.9. Favorable environment for osteoclast
  59. 59. Zone of stimulation ( zone of encapsulation / productive fibrosis) Toxicity reduced to a mild stimulant1. Peripheral orientation of collagen ( fibroblastic activity )2. Favorable environment for osteoblastic activity3. Bone apposition & reversal lines evident4. Reactive hyperostosis when lesion encroaches on the cortical plate.
  60. 60.
  61. 61. Sequence of pulp pathoses related to inflammation
  62. 62. CLINICAL CORRELATIONHyperemia• It is an initial & potentially reversible response that sets the stage for inflammatory cycle.• Caused by Pulpal reaction to external stimuli such as caries , restorative procedures.• Pain does not occur spontaneously & requires an external stimulus, ceases when the irritant is removed.• H/P: Increased blood volume, prolonged vasodilatation, increased intrapulpal pressure , edema, with minimal amount of WBC infiltration.Treatment• Preventive measures such as controlled operative procedures and in deep cavities pulp capping procedures may be performed.
  63. 63. Painful pulpitis• Clinically detectable inflammatory response of the pulpal connective tissue to an irritant.• The exudative (acute) forces are hyperactive• Acute pulpalgia ( acute pulpitis): – Severely painful , irreversible acute inflammatory response.• Chronic pulpalgia( subacute pulpitis) : – Mild exacerbation of a chronic pulpitis. sometime described as “smouldering inflammatory response”
  64. 64. • C/F : pain varies from mild discomfort to severe, even excruciating throbbing.• Spontaneous because of the presence of necrotic tissue & lingers even after the primary irritant has been removed.• H/P:• Prolonged vasodilation, increased vascular permeability, edema & increased intrapulpal pressure, congestion & blood stasis producing small zones of necrosis.• PMN is the characteristic principal cell & macrophages also appear.
  65. 65. • The disintegration of leukocytes release proteases & liquefy the injured cells & tissue, resulting in pus formation.• The suppurative core (zone I ) may be referred to as Zone of Necrosis or Infection.• The inflamed connective tissue surrounding zone I is termed as Zone of Contamination( zone II ) where the exudative activity has its greatest effect.• As the inflammation persists chronic pulpitis ensues.• Treatment – Root canal treatment is the definitive treatment procedure.
  66. 66. Non painful pulpitisChronic pulpitis:• Here the proliferative zones become hyperactive and attempts to heal & repair.• Pain is absent due to diminished exudative activity & coresponding decrease in intra pulpal pressure.
  67. 67. H/P :• characterized by PMNs infiltration , inflammatory edema leading to formation of abscess surrounded by granulomatous tissue termed as pulpal chronic abscess/ pulpal granuloma.• Young fibroblast & new capillaries develop & form granulation tissue in attempt to replace the exudate in zone II.• This zone of repair & healing tissue is the Zone of Proliferation ( zone III).• Lymphocytes , Plasma cell & macrophages are prominently present.Treatment• Root canal treatment is the definitive treatment procedure.
  68. 68. • If the conditions is not treated the persistant chronic pulpitits may lead to the formation of dentinoclasts by activating undifferentiated reserve connective tissue cells of the pulp and may lead to internal resorption.• When the inflammatory process or the toxic components of pulpal necrosis approach the connective tissue of the pulpoperiapical junction, an apical periodontitis ensues.
  69. 69. Sequence of pulpoperiapical pathoses related to inflammation
  70. 70. Painful pulpoperiapical pathosis• They are inflammatory response of the periapical connective tissues to pulpal irritants in which exudative ( acute) forces become hyperactive.• Acute apical periodontitis: – Is an incipient exudative reaction – Caused by contaminants from the pulp canal which produce vasodilation, fluid exudation, WBC infiltration in the periapex.
  71. 71. • Acute periapical abscess – It is an advanced exudative reaction – Caused by contaminant from pulp canal that produce increasing inflammatory exudate, edema, WBC infiltration & suppuration.• Recrudesscent abscess ( phoenix abscess) – It is an acute excerbation of chronic apical periodontitis
  72. 72. • H/P: vasodilation, edema & increased intrapriapical pressure will activate osteoclast formation to resorb the bone. This increase pdl space.• PMN s causes proteolysis & suppuration occurs.• Thus acute exudative zones (I & II ) develop identical with those described for pulpal inflammation.
  73. 73. NON PAINFUL PULPOPERIAPICAL PATHOSIS• Here the proliferative components are hyperactive.• Pain is absent because of diminished intraperiapical pressure.Incipient Chronic apical periodontitis: – Widened PDL space , with dilated blood vessel , edema& accumulation of chronic inflammatory cells.Periapical Granuloma: – This advanced form of chronic apical periodontitis is characterized by growth of granulation tissue & presence of chronic inflammatory cells.
  74. 74. • Chronic periapical abscess: – Develops from chronic apical periodontitis• Periapical cyst: – Develops from chronic lesion with preexisting granulomatous tissue . – Characterized by a central fluid filled epithelium lined cavity surrounded by granulomatous tissue & peripheral fibrous encapsulation.
  75. 75. • H/P:• Similar to histopathological features of non painful pulpal pathosis.• The zone of necrosis( zone I) is then ecrotic tissue in the root canal.• There is capilary dilation, PMNs infiltration closest to the zone, surrounded by lymphocytes and plasma cells.• As the necrotic products diffuse into the periapex they enter the zone of contamination (Zone II), Where the toxicity is reduced by fluid and cellular exudative activity.
  76. 76. • This stimulates the osteoclasts to resorb the contaminated periapical bone.• The gap surrounding the lesions is filled with the granulomatous tissue to form the zone of irritation (Zone III).• It is important to note that viable microorganisms are absent in this zone III.• Here the periapical granuloma may be compared to the pulpal granuloma.• Unlike the chronic pulpal response here the zone of stimulation (Zone IV) becomes well developed.
  77. 77. • In this zone the fibroblasts lay down a wall of collagen fibres to encapsulate the entire inflammatory complex and osteoblasts lay down additional bone matrix over the surface of the older resorbed bone.• Treatment: – Pulpectomy followed by adequate apical seal for healing and repair to take place – But if the periapical lesion does not resolve for prolonged periods and patient is symptomatic then surgical management may be considered where periapical curettage is performed to completely remove the granulation tissue and root resection done.
  78. 78. Kronfeld’s Mountain Pass Concept• Kronfeld has pointed out that the granuloma is not an environment in which bacteria live but one in which they are destroyed.• He compared the bacteria in the root canal (Zone I) with an army entrenched “behind high and inaccessible mountains” the foramina serving as mountain passes.• The exudative and granulomatous tissues of the granuloma represents a mobilized army defending the plains (periapex) from the invaders.• If only a few invaders enter the plain through the mountain pass they are destroyed be the defenders (leukocytes)
  79. 79. • Only complete elimination of the invaders form their mountainous entrenchment will eliminate the need for a defense force in the “plains”.• Once this is accomplished the defending army of leukocytes withdraws the local destruction created is repaired (granulation tissue of zone III) and the environment returns to with normal pattern.• Therefore the objective in non-surgical root canal therapy of teeth with periapical pathoses is elimination of the irritant from the canal and keeping it out by a “Three- dimensional” filling of the canal. If the contents of the zone of necrosis are eliminated the granuloma can complete its function of healing and repair.
  80. 80. Conclusion Removal of the irritants and their source bydebridement and proper obturation permits thehealing of periradicular tissues and is oftenassociated with formation and organization of afibrin clot, granulation tissue formation andmaturation, subsidence of inflammation andfinally restoration of normal architecture of theperiodontal ligament. Since the inflammatoryreactions are usually accompanied by microscopicand macroscopic resorption of hard tissues boneand cementum repair occur as well.