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Rational of endodontic treatment/ rotary endodontic courses by indian dental academy


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Indian Dental Academy: will be one of the most relevant and exciting training center with best faculty and flexible training programs for dental professionals who wish to advance in their dental practice,Offers certified courses in Dental implants,Orthodontics,Endodontics,Cosmetic Dentistry, Prosthetic Dentistry, Periodontics and General Dentistry.

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  • 1. RATIONALE OF ENDODONTIC TREATMENT INTRODUCTION INFLAMMATION - Definition - Causes - Signs and Symptoms - Cells of inflammation - Inflammatory process - Tissue change - Periradicular manifestation - Repair ENDODONTIC IMPLICATION 1
  • 2. INTRODUCTION: The term “Rationale” can be defined as the fundamental reason or the rational basis for a procedure. The rationale for endodontic therapy is based on the belief that a natural tooth function more efficiently and comfortably than a bridge, partial denture or an implant tooth. Endodontic therapy allows the removal of vital or necrotic pulp from the canal system of an infected tooth and replaced by an inert filling material. This is mainly done to prevent extension of the disease from the pulp into the periapical tissues. INFLAMMATION: Definition: Can be defined as a local physiologic response of a living tissue to injury. The main objective of inflammation is to destroy the irritant causing tissue changes and bring back the tissue to a normal form and function. Mediators of inflammation: The agents that cause the changes in inflammation, the alterations in the blood vessels, the escape of proteins and cells into the tissues, and the change in the tissue – are called the mediators of inflammation. The initiated, transient vasoconstriction in due to the direct stimulation of the blood vessels and the flare is caused by an/ or on reflex. “Nerves are not necessary for the inflammatory process.” Inflammation develops normally in derivated tissue, except that the flow is absent. Nerves may play some part in modifying the severity of the vascular change, but in most circumstances their effect is slight. 2
  • 3. Agents causing inflammation: a. Physical agents: Heat, cold, mechanical trauma as in sports injuries, bruxism, accidental exposure during cavity preparation, rapid tooth movement during orthodontic treatment. b. Chemical agents: ZnPO4, Silicate, acid etching agents etc. c. Infection agents: Bacterial, Virus, Parasites. d. Immunological agents: Cell mediated reaction antigen – antibody, reaction. Factors modifying the inflammatory respond 1) Host resistance 2) Intensity 3) Duration 4) Virulence of irritant / microorganism (pathogenicity of stimulus). Based on these premises we can generalize that mild or moderate noxious stimuli to the pulp may produce sclerosis of dentinal tubules, formation of reparative dentine, or reversible inflammation. Irreversible inflammatory changes caused by severe injury can lead to necrosis of pulp and subsequent pathologic changes in periradicular tissues. The inflammatory process allows: 1. The arrival of phagocytic cells to digest bacteria or cellular debris. 2. Antibodies to recognize attack and destroy foreign material. 3. Edema or fluid to distribute and neutralize the irritant. 4. Fibrin formation to limit the spread of inflammation. 3
  • 4. Symptoms of inflammation: According to Roman hunter Celcus in 1st century A.D. typical signs of inflammation can be witnessed. 1. Dolar (Pain): Caused by the action of cytotoxic agents released from humoral, cellular and microbial elements of the nerve endings. 2. Tumor (Swelling): Produced by infiltration of macromoleculars and fluids into the affected tissues. 3. Rubor + Color (Redness + Heat): Produced by vasodilatation of the vessels and the rushing of blood to the affected tissues. 4. Loss of function: was later added by Verchow resulting of from changes in the affected tissues. As in any other inflamed organ of the body these symptoms also occur in inflamed pulp but only pain and loss of function can be clinically appreciated because of the encasement of pulp with in dentin does not permit swelling. But in case of inflammation including the periapical tissues all the symptoms of inflammation may be clinically recognized. Cells of inflammation: Glanulocytes Agranulocytes - Neutrophils - Lymphocytes - Eosinophils - monocytes - Basophils The main cells of acute inflammation are poly morphonuclear neutrophil (PMN’s). 4
  • 5. Chronic inflammation: lymphocytes, plasma cells, monocytes and macrophages. Poly morphonuclear neutrophils (PMN’s) (Neutrophils or Polymorphs). 1. Their cells constitute 40-75% of Leucocytes. 2. Seen in acute inflammation. 3. They contain a. Nucleus having 2-4 lobes, which is connected. b. Cytoplasm containing characteristic violet pink granules. These granules are said to contain enzymes i. Lysosomes ii. Alkaline phosphatase iii. Collagenase iv. Lactoferrin 1. These cells get attached to the area of inflammation by chemotactic factors produced by bacteria or the complement system. 2. They then allow the binding of opsonised bacteria onto this surface. 3. In the binding sites the bacteria are encapsulated into the neutrophils where lysosomal enzymes are released that kill the bacteria. 4. These PMNs have a narrow range of life. They are destroyed in the inflammatory site when the pH of the tissues falls to 6.5. 5
  • 6. 5. This change in pH is brought about due to the release and production of lactic acid by the neutrophil during phagocytosis. 6. Destruction of the PMN’s also cause the release of 2 proteolytic enzymes. a. Pepsin b. Cathepsin These enzymes result in tissue lysis. 1. The PMN’s with the products of cellular lysis and debris are principal constituents of pairs. Eosinophils: 1. They are fewer in number, constitute, 1-6% of leukocytes. 2. They consist of; a. Nucleus usually has 2 lobes. b. Cytoplasm made up of cause deep red staining granules. 3. They are most predominant in allergic reactions and parasitic infection. 4. During the immune response, they are involved in phagocytosis of Ag-Ab complexes and in detoxicate on of histamine. Basophils: 1. These cells are least in number contain 1% of all incubating leukocytes. 2. They resembles all other leukocytes but can be distinguished by their coarse intensity basophilic granules which usually fill the cytoplasm. 6
  • 7. 3. These granules contain Heparin, Histamine and Hydroxy tryptamine and when these granules are stimulated by tissue injury or antigen they degranulate and release these substances, which can initiate an inflammatory or a allergic response. 4. Basophils and masts cells are considered similar cells except that Basophils are found in hemopoetic system and mast cells in tissues. Functions of both these cells are same. Macrophages: 1. These cells are derived from circulating monocytes. Immature monocytes in extravascular areas of inflammation differentiate into macrophages. a. Macrophages are phagocyte cells that ingest - Cellular debris - Microorganisms - Particulate matter b. They release mediation of inflammation such as lysosomal enzymes, complement proteins and prostaglandins. c. They enhance the immunological reaction by ingesting processing and degrading the antigen before presenting it to the lymphocytes. d. Then capacity to remove debris from area facilitates repair. e. Macrophages are mononucleated cells that, in periods of great activity, may fuse into other macrophages to produce a multinucleated giant cell. 7
  • 8. They release enzymes like 1. Acid hydrolases. 2. Neutral proteases, these enzymes result in digestion of dead cells. 3. Collagenase. 4. Elastase. Lymphocyte: 1. These cells appear in the chronic stage of inflammation. They are intimately related to the immunological system of the organism. 2. It is seen that immune system also fights infection along with the inflammatory process. 3. If the normal inflammatory process fails to sum up with the infection then the body mounts up a more massive highly efficient response that is capable of memory as well as specificity – viz., the immune system. The immune system is comprised of two basic. 1) B cells 2) T cells Both derived from the haemopoitic system. These cells have a large spherical or slightly indented nucleus surrounded by a thin band of cytoplasm containing small granules. The stem cells are carried by the blood to the thymus where they differentiate as T - Cells B - Cells 1. In thymus they become 1. Become immuno 8
  • 9. immuno comp. T cells. competent in bone manner 2. Most common cells of lymphocytes 2. Lesser in number than T cells. 3. Responsible for cell mediated immunity + immuno surveillance of the human organisms 3. Responsible for humoral immunity. 4. Circulate through the lymphoid tissues and other organs of body except thymus. 4. 5. Found in para cortical area of lymph nodes. 5. Found in cortical areas of lymph nodes. 6. When stimulated by foreign body they form sensitized T. lymphocytes 6. When stimulated by foreign body they become large cells called plasma blasts. Plasma blasts divide into c. Plasma cells d. Memory B Cells 7. Types a) Memory T-cells – Speed up immunological reaction when in contact with same antigen. b) Helper or suppressor cells– which stimulate or suppress the development of effects T or B cells. 7. Types a) Plasma cells – Large oral round cells with chromatic nucleus, which contains chromatic network in cartwheel form. These cells produce immunologlobulin or antibodies. c) Effector T cells – Produce cell mediated immune reaction such as delayed hypersensitivity b) Memory B cells – speed up the immunologic reaction in subsequent encounters with same antigen. 8) Cells release chemical mediations known as lymphokines 8) 9) Lymphokines- may activate 9) Immunoglobulin or antibodies of which have 9
  • 10. a) Macrophages b) PMNS c) Non-sensitized T cells or d) Produce interferron which inhibits viral replication five classes IgM, IgG, IgA, IqD & IgE. Antibodies in humoral immunity IgM: In the first antibody to be produced when host is stimulated by an antigen. Plasma cells then produce IgG. IgG + Igm: are the circulatory antibodies and one the most important of the serum antibodies. IgG + IgM base the capacity to bind to the antigen on specific receptor sites. This process is termed as Opsonization and the antibodies are called opsonins. IgA: Is found in saliva, tears etc. IgE: In conjunction with eosinophil serves a function of protection against parasitic infection. IgD: Function is not yet known but is considered to be a surface on B-lymphocytes hence triggering antigen related lymphocytes differentiation. These antibodies combine with specific antigen to form a complex that activates the compliment system. The complement system then release chromatic factors that attract phagocytic cells to the area that eugenol the antigen and destroy it. Inflammatory Process Acute inflammation: This process can be studied as a. Vascular changes b. Escape of cells from blood vessels into tissues c. Tissue changes 10
  • 11. Vascular Changes: In any kind of injury 2 types of vascular changes can be appreciated a. Vasodilatation. b. Increase in vascular permeability Immediate response to injury results in transient vaso constriction of blood vessels, which lasts for few seconds. This is followed by vasodilatation of blood vessels that persists for day to weeks that is as long as the inflammation persists. This vasodilatation of arterioles is caused by the relaxation of anterior and capillary sphincters. As a result of vasodilatation there is increased rate of blood flow, which also results in opening of dormant capillary beds that increases the blood supply to the affected area. This causes rise in intra vascular pressure leading to redness and heat. Simultaneously because of release of proteolytic enzymes from injured cells, bacterial toxins and traumatic mechanical forces, histamine is triggered off from the mast cells. This histamine contracts the endothelial cells and increases the intracellular gaps between them. These gaps along with the intra vascular pressure results in some plasma fluid to leave the vessels. This fluid is less in protein and is termed as inflammatory transudate. This transudate is soon over shadowed by the blood plasma which contains rich plasma proteins such as albumin, fibrinogen, immunoglobulin, which is called as inflammatory exudates. 1. This blood plasma helps in bringing the chemical mediation and cells of inflammation to start the inflammatory reaction. 2. It also dilutes bacterial toxins. 11
  • 12. 3. It helps to form fibrin to contain the inflammatory reaction. This exudate accumulates in the tissue producing edema. As the increased blood flow through the vessels fills up the capillary beds, the volume of capillary bed increases so there is slowing down of blood flow. This alteration in the caliber of blood flow results in structural changes in the micro vasculature i.e., 1. The RBCs come in the center 2. Leukocytes move towards the vessel wall. This process is called margination of leukocytes. After margination the leukocytes adhere to the vessel wall, which is termed as pavementation. After the procedure the next step is Emigration of Leukocytes. At the site of inflammation these leukocytes are attracted by - Compliment system - Prostaglandins - Kallikrein Which acts a chemotactic agent. This is called as ‘chemotoxis’ where the leukocytes migrate through the vessel wall by amoeboid movements. The PMN’s migrate 1st followed by monocytes and lymphocytes. Simultaneously ‘Heggman factor’ or factor XII is also released into the tissue in the inflammatory exudates. This factor is activated by collagen; damaged blood vessels; Ag-Ab complexes. Reacts with PreKallikrien – Kinin. Kinin produced 1) Helps in dilatation of blood vessels, 12
  • 13. 2) permeability of blood vessels. The Heggman factor also activates the fibrinolytic and blood co-aggulating systems. Fibrinogen XII---- Fibrin ---– confines the inflammatory reaction to a limited area. Plasminogen XII----- plasmin --- activates the complement system - --- digests fibrin to remove blood clots. - ---Activates kinin system. This complement system in turn releases the chemotactic factors, which aid in chemotoxis. The vascular response continues with the aggregating of RBC in the vessel causing resistance of blood flow. This resistance along with the increase in blood viscosity produced by the loss of plasma causes metabolic changes such as 1. Decrease in oxygen concentration. 2. Increase in carbon dioxide. 3. Low pH. Relating these changes to pulpal tissues as elsewhere in the body are detrimental as they prevent the removal of waste products. The spread of inflammation is faster in pulp tissue as it is in a closed chamber, which may lead to total necrosis of the pulp. Also the migration of monocytes and lymphocytes at the inflammatory sites start a immunologic reaction. The macrophages, plasma cells derived by B- lymphocytes and lymphocytes mediators of the immune response are also found at the site. 13
  • 14. Extra vascular immunoglobulins found are predominantly IgG apart from IgE, IgA, IgM. The recovery of pulp can be explained by some unique vascular responses. Anterior venous anastamoses and U turn loops open in the pulpal vasculature to reduce the flow to the area of inflammation there by decrease in the vascular pressure. The increased tissue pressure plays an important role in the recovery of pulp by allowing return of macromolecules and fluids to the venules. Therefore these 2 changes return the vascular pressure and tissue pressure to normal and stimulate the repair. Phagocytosis: This is defined as process of engulfment of solid particulate material by the cells. This is carried out by cells called as Phagocytes mainly 1. PMN’s; 2. Circulating monocytes or Macrophages. Phagocytosis takes place in 3 stages 1. Attachment stage: The serum at the injury site contains naturally occurring opsonins. These opsonins get coated on the microorganisms. Main opsonins are: 1) IgG opsonin 2) C3B opsonin 2. Engulfment stage: The phagocyte gets attracted to this opsonised microorganism and sends out cytoplasmic pseudopods that envelop and encloses the organism forming a vacuole. The plasma membrane enclosing the phagocytic vacuole breaks. The lysosomes fuse to the phagocytic vacuole to form a phagolysosome. 14
  • 15. 3. Degranulation stage: Degranulation takes place releasing antibacterial substances, which kills the microorganisms. The enzyme released help in digestion and liquefying of the dead cells and damaged tissues. Tissue changes following inflammation: Can be either 1. Degenerative 2. Proliferative 1. Degenerative changes: Degenerative changes in the pulp may be i. Fibrous ii. Resorptive iii. Calcific iv. Necrosis v. Supportive Suppuration occurs due to release of proteolytic enzymes from the PMN resulting in liquifaction of dead tissue resulting in to pus formation. Accumulation of this pus forms an abscess. Requirements for pus formation a. Necrosis of tissue cells b. Sufficient number of PMN’s and Leukocytes c. Digestion of the dead material by protolytic enzymes. 2. Proliferative changes: These are produced by irritants mild enough to act as a stimulatant. Within an area, a substance may be both irritant and a stimulant. For e.g. Ca(OH)2 in the center of inflammatory area may act as an irritant strong enough the produce regeneration or 15
  • 16. distruction where as at the periphery it may be mild enough to stimulate proliferation. When a gap is present between tissue parts, repair is made by granulation tissue. Periradicular manifestations: If the inflammatory response over whelms the pulp there is partial or total necrosis of the pulp in the root canal, this serves as a pathway to the periradicular area for the noxious products of tissues necrosis and antigenic agents. The inflammatory and immunologic reaction continue in the periradicular area as in pulp In the periradicular area the noxious products cause. Bone resorption and resorbed bone is replaced by granulation tissue. The affected tissue contains neutrophils, lymphocyte, plasma cells, macrophages, mast cells along with immunoglobulins IgG, IgA, IgM, IgE and complement. Some recent reports indicate that some endodontic flare -ups are mediated by IgE reactions and that have bone resorption is mediated by lymphokine called ostoelastic activating factor. These findings tells us the important role that immunology plays in the physiology, and pathology of the periradicular tissue. Repair: Repair is the return of tissue to normal structure and function and it begins as the tissue becomes involved in the inflammatory process. Repair of the tissue depends on 1. Severity of injury 2. Host resistance Reversible damage  Repair 16
  • 17. Irreversible damage  Necrosis Stages of Repair: 1. After organization of the blood clot there is formation of granulation tissue. During this stage the endothelial loops become canalized by the pressure of the blood allowing new channels for circulation of blood. Anastomasis of these loops occur forming a rich network of small blood vessels. 2. In the soft tissues, development of scar tissue begins fibroblasts grow along fibrin strands and help to form the protein matrix by laying down collagen fibres. After this both the fibroblast and the capillaries become fewer in number and an avascular fibrous tissue i.e. scar tissue is formed. 3. In bone the process is more complex as soft tissue, has to get converted into hard matrix. Bone is composed of protein matrix infiltrated by calcium salts like calcium phosphate Ca(PO4)2 and calcium carbonate Ca(CO3)3. This protein matrix is formed by osteoblasts. Surrounding the matrix is a fluid subsaturated with calcium salts. The osteoblasts produce alkaline phosphatase which help in forming Ca(PO4)2 which gets precipitated as matrix. There areas or islands in which the Ca(PO4)2 is precipitated unite to form spongy trabecular. Repair always proceeds from periphery towards the center Therefore to summarise. Granulation tissue------- fibrous connective tissue ----- bone. 17
  • 18. Endodontic Implications: Fish described the reaction of periradicular tissues to noxious products of tissue necrosis, bacterial products, and antigenic agents from the root canal and established an experimental focci of injection, which he described as 4 zones. Four zones of reaction are 1. Zone of infection 2. Zone of contamination 3. Zone of irritation 4. Zone of stimulation Zone of infection: 1. Infection is present in the center of the lesion. 2. Micro-organisms are also present only in that area. 3. It contains pus fluid, which contains i. Dead cells. ii. Destructive components released from phagocyts. iii. Intermediate and end products of protein decomposition (Proteolysis). 4. Main cells are polymorphoneuclear leukocytes 5. Micro-organisms are attacked by these leukocytes. 6. The microorganisms not attacked by leukocytes are found in the Haversian canals or in the fissures of bone matrix made by bur. Zone of contamination: 1. The principal difference cells are the round cells mainly ‘lymphocytes’. 2. Macrophages are less in number. These appear later because they are less motile and survive longer than neutrophils or lymphocytes. 3. Dilution of toxic elements takes place. 18
  • 19. 4. Fish observed cellular distortion around the central zone, not from bacteria themselves but from toxins discharged from the central zone. 5. Bone cells die and undergo Autolysis. Therefore the lacunae appear empty as opposed to that of the central zone. Zone of irritation: Toxicity diminishes as distance increases from central zone. 1. Principal cells a. Macrophages. b. Osteoclass. 2. Undifferentiated cells join to form osteoclast which resorb the contaminated bone. 3. Phagocytosis takes place of collagen network by macrophages and cells. 4. The activity of osteoclasts on bone open up gap in the bone all around the center of lesion. This space gets filled with leukocytes Because in this; -Healing starts to take place -Repair. 5. Capillary proliferation. 6. Cells like plasma cells, lymphocytes, macrophages etc., starts developing more from undifferentiated cells. Zone of stimulation: Toxicity reduced to mild stimulatant 1) Cells a. Fibroblasts b. Osteoblasts 19
  • 20. This zone takes care of periphery i.e. peripheral orientation takes place. 2) Collagen fibres are laid down by fibroblast which act as a. Wall of difference around zone of irritation. b. Scaffolding on which osteoblasts lays new bone. New bone is irregular in pattern. By this experiment fish concluded that root canal is a seat of infection. The microorganisms from the root canal are rarely motile. However they can multiply sufficiently enough to grow out of the root canal or the metabolic products of microorganisms or toxic products of tissue necrosis may diffuse into the periradicular tissue. As the microorganisms gain entry into the periradicular area they are destroyed by the leukocytes. If the number of microorganisms is less a stalemate occurs. If it is more, chronic abcess occurs. The toxic products of microorganisms and the necrotic pulp in the root canal acts as irritants and destroy the periradicular tissues along with proteolytic enzymes resulting in pus formation. At the periphery of the lesion there is stimulation of fibroblasts to build the fibrous tissues and osteoblasts to limit the area with a wall of sclerotic bone. This happens because of dilution of toxic products, which acts as a stimulant. If in addition the epithelial cell rests of mallesez are stimulated a cyst develops. Once the root canal has been treated and the reservoir of bacteria or noxious products has been eliminated and the root canal thoroughly obturated the destroyed periapical bone undergoes repair. 20
  • 21. REFERENCES:  Grossman – Endodontic Practice.  Robbins – Basic Pathology. 21