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rationale of endodontics
- 2. RATIONALE OF ENDODONTICS BY:Dr. Akshita Mahajan
- 3. CONTENTS • INTRODUCTION • DEFINITION •SCOPE OF ENDODONTICS • PATHOGENESIS OF ENDODONTIC DISEASE • THEORIES OF SPREAD OF INFECTION • CULPRIT OF ENDODONTIC PATHOLOGY • PORTALS FOR ENTRY OF MICROORGANISMS • ROUTS OF ROOT CANAL INFECTION • INFLAMMATION • PERIRADICULAR DISEASES • VASCULAR CHANGES
- 4. CONTENTS • TISSUE CHANGESFOLLOWING INFLAMMATION • INFLAMMATORY CELLS • HISTROPATHOLOGY OF PERIRADICULAR DISEASES • ENDODONTIC IMPLICATIONS (PATHOGENESIS OF APICAL PERIODONTITIS AS EXPLAINED BY FISH) • KRONFELD’S MOUNTAIN PASS THEORY • RATIONALE OF ENDODONTIC THERAPY • CONCLUSION
- 5. rationale ˌ/raʃəˈnɑːl/ Noun: A set ofreasons or a logical basis for a course of action or belief. The term Rationale INTRODUCTION
- 6. Rationale of endodontictherapy iscomplete debridement of root canal system followed by three-dimensional obturation The word “Endodontics” is combination of two Greek words: endo which means inside and odont which means tooth. Rationale of endodontic therapy is based on the belief that a natural tooth functions more efficiently and comfortably than a bridge, partial denture or a metal implant.
- 7. DEFINITION OF ENDODONTICS: Itis that branch of dentistry that is concerned with the morphology, physiology and pathology of the human dental pulp and peri- radicular tissues. Acc. to American Association of Endodontics (1987)
- 8. SCOPE OF ENDODONTICS: •Differential diagnosis and treatment of oral pain of pulpal or periradicular origin. • Vital pulp therapy, such as pulp capping and pulpotomy. • Non surgical treatment of root canal systems with or without periradicular pathosis of pulpal origin and the obturation of these root canal system.
- 9. • Selective surgicalremoval of pathological tissues. • Intentional replantation of avulsed teeth. • Surgical removal of tooth structure, such as root end resection and root end filling. • Hemisection, bicuspidization and root resection • Endodontic implants • Bleaching of discoloured dentin and enamel • Retreatment of teeth previously treated endodontically • Treatment procedure related to coronal restoration by means of post and core involving the root canal space. • Diagnosis of extra-oral referred pain • Management of traumatic injuries of the teeth. Can also cover: • Biopsy of pathological tissue • Recognition of pathological conditions between the maxillary posterior teeth and the maxillary sinus.
- 10. PATHOGENESIS OF ENDODONTIC DISEASE: •Physical agents: ex. heat generated during cavity preparation • Chemical agents: ex. Dental cements with acidic pH • Microbial agents: micro-organisms. • In 1894, W D Miller identified bacteria in the diseased pulp.
- 11. Endodontic pathology iscausedby Physicalinjury Chemicalinjury Bacterial injury Thesecausereversible or irreversible changes in thepulp & periradiculartissues.
- 13. Focal Infection Definition: It islocalized or general infection caused by the dissemination of microorganisms or toxic products from a focus of infection.
- 14. Focus of Infection Definition: Thisrefers to a circumscribed area of tissue, which is infected with exogenous pathogenic microorganisms and is usually located near a mucous or cutaneous surface.
- 15. Theory Related toFocal Infection 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.
- 16. PORTALS OF ENTRYOF MICROORGANISMS • Microorganisms may gain access through several routes. • Eg; Dental caries, mechanical or traumatic injury, gingival sulcus, periodontium and via blood stream.
- 17. • Under normalconditions, the pulpodentin complex is sterile and isolated from oral microbiota by overlying enamel and cementum. • When the integrity of these natural layers is breached, the pulpodentin complex is exposed to the oral environment and then challenged by micro-organisms present in caries lesions, in saliva bathing the exposed area, or in dental plaque formed onto the exposed area.
- 21. ANACHORESIS • It isa Greek word which means refuge and also convocation. • It is a process by which microbes may be transported in the blood or lymph to an area of inflammation such as a tooth with pulpitis, where they may establish an infection. ANACHORESIS
- 22. • Microbes fromsubgingival biofilms associated with periodontal disease have access to the pulp via dentinal tubules at the cervical region of the tooth and lateral and apical foramens. • Most of the bacteria in the carious process are non-motile; they invade dentin by repeated cell division which pushes cells into tubules. • Bacterial cells may also be forced into tubules by hydrostatic pressure developed on dentin during mastication.
- 23. • Schuller in1880 was one of the first to study the attraction of circulating bacteria to areas of tissue injury. • Later , Richert cited clinical cases in which bacteria from extra oral site were localized in the pulps of filled teeth. • In 1941, Robinson & Boiling cited the movement of systemic bacteria into inflammed pulps.
- 24. • Circumscript chronicperiapical inflammation & dental granuloma have been considered as foci for various disease.
- 25. • Once thedental pulp becomes necrotic the root canal system becomes a “privileged sanctuary” for clusters of bacteria, bacterial by-products and degradation products of both the microbes and the pulpal tissues. • The occurance of anachoresis explains clinical situations in which there would be no possibility of bacterial contamination of the pulp or periapical region, yet establishment of inflammatory process with significant post operative symptoms is seen.
- 26. • It isthe mechanism through which traumatized teeth with intact crowns become infected. • It is also implied to certain cases of post operative idiopathic pulpitis known as “anachorectic pulpitis” • E C rosenow has also introduced the concepts of “elective localization” where by bacteria would have affinity for specific body organs.
- 27. INFLAMMATION • Inflammation isthe local physiologic reaction of the body to noxious stimuli or irritants. • • Traumatic • • Chemical • • Bacterial • The objective of inflammation is to remove or destroy the irritant and to repair damaged tissue.
- 30. • The inflammatoryresponse of connective tissue of dental pulp is modified because of its surroundings • Because the pulp is enclosed in hard tissues with limited portals of entry, it is an organ of terminal and limited circulation with no efficient colateral circulation and with limited space to expand during the inflammatory reaction. • In inflammed pulp only pain and disturbance of function are recognized clinically.
- 32.
- 33. PERIAPICALLESIONSare produced byan inflammatory responseat the root apices of teeth with non vital pulp. Apical granuloma Apical cyst Apical abcess
- 34. The root canalis the main source of infection microorganisms present in root canal are rarely motile they can proliferate sufficiently to grow out of the root canal the microorganisms enter in the periradicular area, they are destroyed by the polymorphonuclear leukocytes.
- 35. As But ifmicroorganisms are highly virulent, they overpowerthe defensive mechanism and result in development of periradicular lesion At the periphery of the destroyed area of osseoustissue toxic bacterial products get diluted sufficiently to act as stimulant. form a granuloma
- 36. Toxic byproducts +necrotic pulp Irritate and destroy the periradicular tissues. Irritants + proteolytic enzymes CHRONICABSCESS
- 38. fibroblasts come intoplay build fibrous tissue osteoblasts restrict the area by formation of sclerotic bon e these if epithelial rests of Malassez are also stimulated formation of a cyst.
- 41. • 2 fundamentalvascular changes: • A. Vasodilatation • B. Increased capillary permeability, which in turn leads to a series of interrelated physiologic and morphologic changes characteristic of the inflammatory response
- 43. • Proteolytic enzymesreleased from injured cells, bacterial toxins, and traumatic mechanical forces may release HISTAMINE from mast cells
- 45. TISSUE CHANGES FOLLOWING INFLAMMATION •2 TYPES DEGENERATIVE PROLIFERATIVE a)Degenrative changes in pulp can be Fibrous Resorptive Calcific Suppuration
- 46. b)Proliferative • Irritants aremild and act as stimulant • In the inflame area the irritant may be strong enough to produce degeneration or destruction • The principal cells of proliferation or repair are the fibroblast
- 47. INFLAMMATORY CELLS • NEUTROPHILS-PMNLs, basophils, eosinophils, also called as granulocytes • Reach site of injury within 24 hrs • Phagocytose bacteria and cellular debris • In low Ph, neutrophils die and release proteolytic enzymes, prostaglandins and leukotrienes • This breaks down tissue leading to abscess abcess formation
- 48. • Macrophages –circulation monocytes reaches site of inflammation and change to macrophages • Remain at site for longer time – 2 months • Function- phagocytosis, pinocytosis, secrete lysosomal enzymes, complement protein and prostaglandin secretion • Provide antigen to immunocomplement cells • Scavenger of dead cells • Produce multinucleated giant cells
- 49. • Lymphocyte- seenin apical periodontits. Two types T-lymphocytes B- lymphocytes • Osteoclast – in case of apical periodontitis, they proliferate and fuse on stimulation by cytokines and other mediators to form osteoclasts. • Causes demineralization, dissolution of organic matrix • Results in bone resorption
- 50. • Epithelial cells-cytokines and other mediators stimulate the dormant cell rests of malassez. • Results in inflammatory hyperplasia
- 51.
- 52. Apical Granuloma Dominatedby- Macrophage ,lymphocyte and plasma cells Abundant capillaries + fibroblast +connective tissue fibers. Often encapsulated in collagenous connective tissue. lymphocytes (green arrow) and macrophages (yellow arrow), with abundant fibroblasts (blue arrow).
- 53. Epithelial cell proliferation. Formed from the epithelial cell rest of malasez. Under the influence of cytokines and growth factors generated in the granuloma. They are the source of the epithelial lining of cysts that may develop in apical granulomas.
- 54. Apical abcess • PUSpresent + an area with liquefied tissue. • From a pre-existing granuloma • Represent a shift in cellular dynamics. • The influx of PMNs is dramatically increased. • Thus tissue macrophages are no longer able to effectively cope with the tissue damage caused by hydrolytic enzymes from a vast number of dying PMNs.
- 55. Apical cyst • Anepithelium lined cavity • With fluid / semisolid material • Surrounded by dense connective tissue. • Associated with necrotic pulp • Develop within the granuloma. • Cyst cavity- stratified squamous epithelium. • From Epithelial cell rest of malasez. • The epithelial lining can be continuous or disrupted or completely missing.
- 56. Apical cyst. A partialview of the wall of a space that was filled with liquid and lined with stratified cuboidal epithelium (yellow arrow and enlargement), originating from the epithelial rests of Malassez.
- 57. • An apicalinflammatory cyst • Sac-like • Epithelium lined cavity. • Open to and continuous with the root canal space. • Within the periapical granuloma with no connection between their cavity and the rootcanal space. >half of the apical cysts are true apical cyst Remaining are pocket cyst variety. Periapical cyst is divided into PERIAPICAL POCKET CYST TRUE CYST (BAY CYST)
- 58. The mechanism ofcyst formation in periapical inflammatory lesions ‘‘Nutritional deficiency theory’’ epithelial proliferation results in an epithelial mass that is too large for nutrients to reach its core results in necrosis and liquefaction of the cells in its center, Forms the cystic cavity.
- 59. The ‘ Abscesstheory’’assumes that, Tissue liquefaction occurred first, at the central part of an abscess Due to the inherent nature of epithelial cells to cover the exposed connective tissue surfaces Gets lined by locally proliferating epithelium.
- 60. ENDODONTIC IMPLICATIONS (PATHOGENESIS OFAPICAL PERIODONTITIS AS EXPLAINED BY FISH) • Fish, in 1939, described the reaction of periradicular tissues to bacterial products, noxious products of tissue necrosis and antigenic agents from root canals. • Theorized that the zones of infection are not an infection by themselves but the reaction of the body to infection.
- 62. • Around thecentral zone, there is an area of cellular destruction. • not invaded by bacteria, • the destruction was from toxins discharged organisms in the centralfrom the micro- zone. • characterized by round cell infiltration, osteocyte necrosis and empty lacunae. Lymphocytes were prevalent everywhere. Zone of Infection • Infection was confined to the center of thelesion. • characterized by polymorphonuclear leukocytes and components microorganisms. • along with the necrotic cells and destructive released from phagocytes. Zone of Contamination
- 63. 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. • degradation phagocytic while of collagen framework by cells and macrophages was osteoclasts attack the boneobserved tissues.
- 64. 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 aroundthe zone of irritation and as a scaffolding on which the osteoblasts synthesize new bone.
- 65. Zone of infectionor necrosis (PMNLs) Zoneof infection Zone of contamination(Round cell infiltrate – lymphocytes) Zone of irritation (Histiocytes and osteoclasts) Zone of stimulation(Fibroblasts, capillary buds and Osteoblasts).
- 66. • • Responseto this stimulation, collagen fibres get laid down by fibroblasts, which acts both as a wall of defence around the zone of irritation and as a scaffolding on which the osteoblasts built new bone. • According to his concept, periapical lesion is not an infection by itself but the reaction of body to infection in the canal.
- 68. KRONFELD’S MOUNTAIN PASSTHEORY 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. Micro organisms Body’s defence
- 69. Micro-organisms inrootcanal is the army in the mountain Enters the PLAINSthrough the foramina / MOUNTAINPASS Smaller group of bacteria entered –gets destroyedby the ARMYof leucocyte which stands in the front to counter the attacks. Thorough cleaning and shaping will bring down the army allowing the environment to return to normality
- 71. Zone A: Bacteria/ invaders entrenched behind high and inaccessible “mountains”, the foramina serving as mountain passes. Cameup with 4zones
- 72. Zone B: Theexudative 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 inflammation.
- 73. Zone C: Onlycomplete 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.
- 74. This explains therationale for the non-surgical treatment for teeth with periapicalendodontic 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.
- 75. Indications for RCTbased on rationale • All teeth with irreversible damage to pulp from physical,chemical or bacteria attack • Intentional RCT- for restorative / prosthetic restorations • Elective endodontics : -is done with crack or heavily restored tooth, -to prevent premature loss of cusp during its restoration(crown preparation)
- 76. • Inadequate restorations: -cracked or carious teeth having crowns repair of the crown margins. -use of pre-existing crowns even after another restoration • Devitalization of tooth : -severe attrited/ rampant caries / smooth surface defects -so that patient do not feel discomfort to cold or sweet. • Endodontic emergency : acute dental pain
- 77. THE HEALING Healing ofthe lesions may take many months .It may be argued that if a given lesion eventually heals in 12, 24, or even 36months, there is no benefit in rushing the process. Immune response • It neutralizes and removes any foreign material • allows and probably initiates the second part, recovery, repair, and regeneration
- 78. Macrophages areknown to persist in tissues for many months and if their state of activation persists, they may maintain osteoclastic activity, inhibit the fibroblasts inhibit osteogenesis, thus preventing both soft connective tissue and bone repair from taking place.
- 79. Early surgical removalof the tissue containing activated macrophages, allowed its replacement with fresh granulation tissue that contains a fresh set of cells that will not delay repair.
- 80. RATIONALE OF ENDODONTICTHERAPY • Rationale of endodontic therapy relies on the fact that non-vital pulp being avascular has no defence mechanisms. • Breakdown products from damaged tissue diffuses into surrounding tissue leading to periapical irritation. • Endodontic therapy seals the root canal system 3-dimensionally and prevents percolation of toxic byproducts into periapex.
- 81. CONCLUSION • When theroot canal has been treated, the reservoir of bacteria or noxious products gets eliminated; when the root canal is cleaned and obturated, the destroyed periapical bone will undergo repair. • The ultimate goal of endodontic treatment is either to prevent the development of endodontic lesions or in cases where it is present, to create adequate conditions for tissue healing.
- 82. FactorsAffecting theLong-term Results ofEndodonticTreatment UIf Sjbgren,DDS, Bjorn H,'igglund, DSS, Goran Sundqvist, DDS, PhD, and Kenneth Wing, DMD, PhD. JOURNALOFENDODONTICS,Printed in U.S.A. VOL.16, NO.10, OCTOBER1990 A multivariate analysis of the influence of various factors upon healing after endodontic surgery JORGEN RUD, J. O. ANDREASEN AND J. E. Mt3LLER JENSEN. Int. J.oral Surg. 1972: 1:258-271 Ingle’sIngle’s ENDODONTICS6 Textbook of endodontics –NishaGargh Grossman’sendodontics https://www.dentalcetoday.com/courses/175%2FPDF%2FDT_Aug_14_NPR_Germai n_fn l1.pdf www.googlescholars.com www.pubmed.com