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Repaso Board Part 2 Endo

Repaso Board Part 2 Endo

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  • The inherent healing potential of the dental pulp is well recognized.Unlike most tissues, the pulp has essentially no collateral circulation; for this reason, it is theoretically more vulnerable than most other tissues. In the case of severe injury, healing would be impaired in teeth with a limited blood supply. It seems reasonable to assume that the highly cellular pulp of a young tooth, with a wide-open apical foramen and rich blood supply, has a much better healing potential than an older tooth with a narrow foramen and a restricted blood supply.
  • The inherent healing potential of the dental pulp is well recognized.Unlike most tissues, the pulp has essentially no collateral circulation; for this reason, it is theoretically more vulnerable than most other tissues. In the case of severe injury, healing would be impaired in teeth with a limited blood supply. It seems reasonable to assume that the highly cellular pulp of a young tooth, with a wide-open apical foramen and rich blood supply, has a much better healing potential than an older tooth with a narrow foramen and a restricted blood supply.
  •  Tertiary dentin has been suggested to be secreted by original odontoblasts or in case of their death, by newly differentiated replacement odontoblasts originating from nearby mesenchymal stem cells. The function of the tertiary dentin is to protect the pulp from noxious influences. Tertiary dentin is disorganized in structure compared to primary and secondary dentin.The first layer of the primary dentin to be deposited is mantle dentin. It is produced by odontoblasts that are not yet fully differentiated. In the adult tooth, mantle dentin is the oldest dentin and is produced adjacent to the enamel in the crown.Predentin is a 15- to 20-µm unmineralized organic matrix layer of dentin situated between the odontoblast layer and the mineralized dentin.A characteristic of human dentin is the presence of tubules that occupy from 1% (superficial dentin) to 30% (deep dentin) of the volume of intact dentin.[107],[277] The diameter of tubules vary from 1 µ to 2.5 µm and traverse the entire thickness of dentin from the DEJ or CDJ to the pulp. They are slightly tapered, with the wider portion situated toward the pulp.
  • Nos indica el grado de integridad de los tejidos de soporte del diente.
  • Ayuda en la prognosis Diente vital con bolsillos Dinete necrotico con bolsillo
  • La infeccion se puede regar y alojarce en diferentes espacios faciales . La severidad va a depender q haya o no manifestaciones sistemicas de la condicion
  • Therefore its is important in order to achieve predictable results, the clinician must have knowledge of apical anatomy, able to interpret radiographs and be able to correctly use an electronic apex locator
  • Durante el acceso


  • 1. ENDODONTICSReview for the NBDE IIPRET 7326 Endodontic Faculty 2012
  • 2. Endodontic• Branch of dentistry concerned with the morphology, physiology and pathology of the human dental pulp and periradicular tissues.
  • 3. Endodontic• Its study and practice include the biology of the normal pulp tissue.• The etiology, diagnosis, prevention and treatment of diseases and injuries of the pulp and associate periradicular conditions.
  • 4. Dental Pulp• A richly vascularized and innervated specialized connective tissue of ectomesenchymal origin.• Contained in the central space of a tooth, surrounded by the dentin, with inductive, formative, nutritive, se nsory and protective functions.
  • 5. Dental Pulp• The pulp has essentially no collateral circulation.• Its main function is dentin deposition during tooth formation .• Odontoblasts, the dentin- forming cells.
  • 6. Dental Pulp• Theoretically, the pulp is as well equipped to cope with injury as any other organ of the body
  • 7. Causes of Pulpal Injury• Bacterial ▫ Caries  Coronal Ingress  Radicular Ingress• Traumatic• Iatrogenic ▫ Cavity Preparation ▫ Restorations• Idiopathic
  • 8. Causes of Pulpal Disease Bacterial Traumatic Iatrogenic Idiopathic Coronal Radicular Acute Chronic Cavity Restorations Resorption Others Preparation Caries Caries Crown Traumatic Thermal Physical fractures Occlusion Injury properties Internal Defective Perio-Endo Root Attrition Cavity DentalRestorations Fracture Depth Materials External Fractures Anchoress Luxations Abrasion Desiccation Micro- of Dentin leakageAnomalous Avulsion Erosion Pin Tract Insertion Bruxisim
  • 9. Causes of Pulpal Injury • Bacterial ▫ Products of bacterial metabolism are the major cause of pulpal injury.
  • 10. Pathways of Pulpal InfectionDental caries• Is the most common pathway for microbes to enter the root canal system.• Most common cause of pulp disease ▫ Bacteria and their by products may have an effect on the pulp before direct exposure
  • 11. Reaction to Caries • Decrease in the permeability of the dentin • The most common response to caries is dentin sclerosis. • Formation of new dentin • Inflammatory reactions.
  • 12. Microorganisms Associated withEndodontic Disease • Primary root canal infections are polymicrobial, typically dominated by obligate anaerobic bacteria. • In infected root canals a selective process takes place over time that allows anaerobic bacteria to predominate. ▫ Apparently tissue fluid, necrotic pulp tissue, low- oxygen tension, and bacteria by products determine which bacteria will predominate. • E. Faecalis has been isolated from cases of failing RCT.
  • 13. Diagnosis Sequence• Systematic approach• Obtain pertinent information ▫ medical history ▫ dental history• Ask about patient’s pain history (subjective) ▫ location ▫ duration ▫ severity ▫ character ▫ eliciting stimuli• Interpret data gathered.• Formulate a differential diagnosis.• Formulate a final diagnosis.
  • 14. PAIN Source  Internally: pulpal  Externally Quality  Sharp  Related to Aδ fibers  Typical of acute tissue injury  Dull, boring or throbbing  Related to severe damage to tissues  C fibers respond
  • 15. PAIN May arise in the periodontal ligament. ▫ Tooth will be sensitive to percussion, chewing, and possibly palpation. ▫ Possible causes:  Pulpal origin - the periodontitis is caused by an extension of pulpal disease  In these cases the pulp is unresponsive to pulp testing, so pulpal vitality testing is key to the diagnosis.  Periodontal origin  Occlusion
  • 16. PAIN• Intensity of the Pain ▫ Described in a scale of 0 to 10 where 0 = no pain and 10 = most painful. ▫ Pulpal pain produced by Aδ fibers can be excruciating and often approaches the upper limits of the scale. ▫ Severe pain is rarely encountered in periodontal disorders. ▫ Mild to moderate pain can be found in either pulpal or periodontal pathosis. ▫ Acute pain is usually a reliable sign that the pain is of pulpal origin.
  • 17. PAIN• The ability of the patient to locate the offending tooth depends if the inflammatory state is limited to the pulp tissue. ▫ Pulp contains no proprioceptive fibers.• If the inflammatory process extends beyond the apical foramen and affects the periodontal ligament it will be easier for the patient to identify the source of the pain.• Dental referred pain ▫ Pain from a diseased pulp could be referred to adjacent teeth or teeth in the opposing quadrant. ▫ Most commonly related to irreversible pulpitis
  • 18. Diagnosis Sequence• Extra oral and Intra oral Examination  Facial swelling  Facial asymmetries  Bimanual palpation  Detection of tender lymph nodes
  • 19. Diagnosis Sequence• Extra oral and Intra oral Examination  Presence of defective restorations  Discolored crowns  Recurrent caries  Fractures
  • 20. Intraoral Examination • Soft Tissues ▫ Any tissue to be examined must be dried. ▫ Unusual alterations of color, texture, consistency or contour of soft tissues.  Examine for sinus tracts, redness or swelling.  Sinus tract = passageway from an enclosed area of infection to an epithelial surface  Fistula = abnormal link between two natural body cavities or two internal organs  Parulis = hyperplasic tissue at gingival opening or sinus tract
  • 21. Intraoral Examination • Hard tissues  Search for signs of caries  Tooth discolorations  Abrasions, attritions and erosions  Fractured teeth  Restorations: appropriate or defective?  Developmental defects  Pulp polyps
  • 22. Intraoral Examination • Hard tissues  Search for signs of caries  Tooth discolorations  Abrasions, attritions and erosions  Fractured teeth  Restorations: appropriate or defective?  Developmental defects  Pulp polyps
  • 23. Intraoral Examination • Hard tissues  Search for signs of caries  Tooth discolorations  Abrasions, attritions and erosions  Fractured teeth  Restorations: appropriate or defective?  Developmental defects  Pulp polyps
  • 24. Diagnosis Sequence• Radiographic examination ▫ Radiographs are helpful but have limitations. ▫ There is a tendency to over-rely on radiographs often with unfortunate consequences. ▫ Periapical ▫ Bite-wings are usually necessary
  • 25. Radiographic Interpretation • Causes of pulpitis • Stage of root development • Calcification of canals • Pulp stones
  • 26. Radiographic Interpretation • Causes of pulpitis • Stage of root development • Calcification of canals • Pulp stones
  • 27. Radiographic Interpretation • Size, shape, number and curvature of roots. • Number, direction, width (M- D) of the canals and pulp chamber ▫ Sudden changes in appearance from dark to light indicate bifurcation. ▫ Presence of extra roots or canals should always be suspected.
  • 28. Radiographic Interpretation • Root Resorption Internal External
  • 29. Radiographic Interpretation • Condensing Osteitis • Osseous Dysplasia (Cementoma)
  • 30. Radiographic Interpretation• Apical Radiolucencies ▫ Significant medullar bone destruction may occur before any radiographic signs begin to appear. ▫ To be able to see radiographic changes, the inflammatory process should have begun to demineralize the cortical plate.
  • 31. Radiographic Interpretation A change in the x-ray beam angle can show missing roots/ canals A bitewing shows decay not shown in the periapical x-ray
  • 32. Diagnosis Sequence• The best test is to repeat the stimulus that reportedly causes the pain to identify the offending tooth.• Thermal tests• Percussion and palpation sensitivity tests to determine periapical status  Palpation over the apex  Digital pressure on tooth if severed pain upon mastication is reported  Light percussion with the mirror’s handle  Selective biting on an object• Periodontal examination  Always necessary
  • 33. Palpation • Digital pressure to check tenderness in the oral tissue underlying suspected teeth • Indicates how far the inflammatory process has extended periapically. • May detect incipient swelling. • A positive response indicates that the underlying tissues are inflamed.
  • 34. Percussion • Indicates some degree of inflammation in the periodontal ligament. • It is not a test of pulp vitality. ▫ Occlusion ▫ Trauma ▫ Sinusitis ▫ Periodontal Disease ▫ Crack tooth ▫ Extension of pulpal disease into the PDL
  • 35. Mobility • Provides an indication of the integrity of the attachment apparatus.
  • 36. Mobility • Causes: ▫ Periodontal disease ▫ Root fracture ▫ Recent trauma ▫ Chronic bruxism ▫ Orthodontic tooth movement ▫ Pressure by purulent exudates by an acute periradicular abscess.  Resolves once drainage for the exudates is established.
  • 37. Thermal Pulp Tests • Cold Test ▫ Dichlorodifluoromethane- Endo Ice ▫ False negative  Calcified canals  Trauma
  • 38. Thermal Pulp Tests • Cold Test
  • 39. Thermal Pulp Tests• Heat Test ▫ GP Dental Stopping
  • 40. Electric Pulp Test • Stimulate the alpha δ sensory fibers within the pulp. • Indicates that there are vital sensory fibers present in at least in part of the pulp. • It fails to provide information about the vascular supply to the pulp. • Unreliable on immature teeth
  • 41. Electric Pulp Test • The presence of a response usually indicates vital tissue whereas the absence of such a response usually indicates pulpal necrosis. • May produce false positives or false negative • Interpretation, comparison and correlation with other findings and tests must be done.
  • 42. Periodontal Probing • Bone and periodontal soft tissue destruction are induced by both periodontal disease and periradicular lesions and may not be easily detected or differentiated radiographically.
  • 43. Periodontal Probing • Probing is a diagnostic aid that has prognostic value. ▫ Prognosis of a tooth with a necrotic pulp that induces cervical extending periapical inflammation is good after adequate root canal treatment. ▫ Outcome of root canal treatment on a tooth with severe periodontal disease usually depends on the success of periodontal treatment.
  • 44. Diagnosis• Pulpal • Periapical ▫ Normal ▫ Normal ▫ Pulpitis ▫ Apical Periodontitis  Reversible  Irreversible  Symptomatic-Acute  Symptomatic  Asymptomatic-Chronic  Asymptomatic ▫ Apical Abscess ▫ Necrosis  Acute  Chronic ▫ Condensing Osteitis
  • 45. Additional Diagnosis• Previously treated• Previously initiated treatment• Pulp Calcification
  • 46. Diagnosis
  • 47. Normal Pulp • Asymptomatic • Mild to moderate transient response to thermal and electrical stimuli that subsides almost immediately after stimulus is removed. • No painful response to percussion or palpation. • No evidence of root resorption, • Lamina dura is intact. • In the absence of other signs and symptoms, teeth with canal calcifications are considered within normal limits.
  • 48. Reversible Pulpitis • Thermal stimuli cause a quick, sharp, hypersensitive response that subsides as soon as the stimuli is removed. • Responsive to electrical stimulation. • No painful response to percussion or palpation. • Asymptomatic • It is not a disease, it is a symptom. • Resolves if the cause is removed • Does not involve a complaint of spontaneous (unprovoked) pain.
  • 49. Reversible Pulpitis: Treatment• The irritant should be removed and further insult should be prevented by sealing the dentinal tubules.• If caries is diagnosed, the tooth should be properly restored.• Treatment ▫ Pulp Capping  Indirect  Direct ▫ Pulpotomy
  • 50. Irreversible Pulpitis • Pulp is damage beyond repair. • Severe inflammation in the pulp tissue. • Will not resolve if the cause is removed. • Pulp incapable to heal. • Progress to necrosis if untreated. • Symptomatic. • Asymptomatic. ▫ Hyperplasic pulpitis (pulp polyp) ▫ Internal Resorption
  • 51. Symptomatic Irreversible Pulpitis • Pain ▫ Spontaneous ▫ Intermittent or continuous ▫ Moderate to Severe ▫ Referred Pain ▫ Provoked • Occasionally patients may report that a postural change induces pain. ▫ For example: Patient wakes up at night with pain • The pain may be relieved by application of cold. ▫ Indicates that is becoming increasingly necrotic.
  • 52. Symptomatic Irreversible Pulpitis • Thermal tests ▫ Lingering painful response • Vitality test ▫ Pulp is still responsive to electrical stimulation. • Radiographic ▫ No periapical changes ▫ Thickening of PDL • Normal/ Positive to percussion and palpation • Treatment: Root Canal Treatment
  • 53. Asymptomatic Irreversible Pulpitis • Deep caries or restorations • Trauma • Slight or no pain • Hyperplasic pulpitis (pulp polyp) • Internal Resorption • Treatment: Root Canal Therapy
  • 54. Internal Resorption▫ Resorption initiated within the pulp cavity.▫ Accidental blow or traumatic cavity preparation have been indicated as possible causes.▫ It is often symmetric and exhibits distortion of the canal wall.
  • 55. Internal Resorption• Pathologic state of the pulp• Asymptomatic• Vitality tests ▫ Normal ▫ Irreversible pulpitis• Radiographic Evidence• Once diagnosed endodontic treatment must be performed.
  • 56. External Resorption▫ Resorption initiated in the periodontium and affecting the external or lateral surface of a tooth.▫ Pulp inflammation begins when it reaches the pulp.
  • 57. External Resorption• Lesion changes position on angled radiographs.
  • 58. Necrosis • Death of the Dental Pulp • Variable Symptoms • Vitality Tests ▫ Non-responsive ▫ False positive- due to partial necrosis • Radiographic ▫ Thickening PDL ▫ Apical lesion • Bacterial Invasion • Treatment: Root Canal Therapy
  • 59. Pulpal Diagnosis SummaryQuick Sharp response Response with Nonresponse No lingering Lingering sensation responsiveNo pain No spontaneous Spontaneous pain Pain/No Pain pain IrreversibleNormal Reversible PulpitisPulp Pulpitis Symptomatic Necrotic Asymptomatic
  • 60. Symptomatic (Acute) ApicalPeriodontitis • Pain ▫ Moderate to severe ▫ Biting • Vitality test ▫ Pulpitis: sensitive to cold, + to EPT ▫ Necrosis: non-responsive to cold and EPT • Positive to percussion and palpation. • Radiographic: ▫ Thickening of the PDL
  • 61. Symptomatic (Acute) ApicalPeriodontitis • Treatment: ▫ Normal/ Reversible Pulpitis  Occlusal adjustment ▫ Irreversibly inflamed or necrotic pulp  Root canal treatment ▫ Other causes  Remove irritants if possible. ▫ Adjustment of occlusion and prescription of anti-inflammatory agent (if patient is not allergic to aspirin) must be necessary.
  • 62. Asymptomatic (Chronic) ApicalPeriodontitis • Pulpal origin: necrotic pulp • Pain ▫ Asymptomatic • Clinically ▫ None to slight sensitivity to percussion and palpation • Vitality test ▫ Non-responsive: Necrotic • Radiographic ▫ Radiolucent lesion • Treatment: Root Canal Therapy
  • 63. Acute Apical Abscess(Acute Periradicular Abscess) • Clinically ▫ Rapid onset of slight to severe swelling ▫ Moderate to severe pain ▫ Pain to percussion and palpation ▫ Slight increase in tooth mobility • Vitality test ▫ No response to EPT or thermal stimulation: Necrosis • Systemic manifestations such as fever and general malaise. • Radiographically: ▫ Thickening of PDL ▫ Apical lesion
  • 64. Acute Apical Abscess(Acute Periradicular Abscess) • Treatment ▫ Removal of irritants by canal debridement. ▫ Drainage through soft tissue. ▫ Teeth should not be left open to drain. ▫ Systemic antibiotic  Generally, the use of antibiotics alone (without concurrent attempts to establish drainage and clean the pulpal space) is not considered an appropriate treatment. ▫ After the swelling subsides, root canal treatment or extraction is indicated.
  • 65. Chronic Apical Abscess(Chronic Periradicular Abscess) • Pain ▫ Asymptomatic ▫ Slight percussion and palpation • Vitality test ▫ No response to EPT or thermal stimulation: Necrosis • Radiographically: ▫ Thickening of PDL ▫ Apical lesion • Sinus tract • Isolated probing to the apex
  • 66. Periapical Diagnosis SummaryPain No Pain Pain +++ No/Slight PainPerc/Palp +++ Perc/Palp - - Swelling PercussionThermal/EPT Thermal/EPT - - Perc/Palp +++ Thermal - -+/- Radiolucent lesion Thermal - - Radiolucent lesionThickening PDL Thickened PDL Sinus Tract Mobility Symptomatic Asymptomatic Acute Apical Chronic Apical (Acute) (Chronic) Abscess Abscess Apical Apical (Phoenix) Periodontitis Periodontitis
  • 67. Condensing Osteitis• Increase in trabecular bone in response to persistent irritation• Variety of Signs and Symptoms• Vitality Tests ▫ Normal to non-responsive• Percussion and palpation ▫ May or may not be sensitive• Radiographic ▫ Radiopacity at the apex Condensing osteitis
  • 68. Differential Diagnosis forPeriapical RadiolucenciesAnatomical landmarks Vitality tests should be done and teeth involved should test vital. NO treatment needed. Maxillary sinus Mental Foramen
  • 69. Differential Diagnosis for PeriapicalRadiolucencies: Cysts Teeth tested vital. Cases referred to maxillofacial and oral surgeon for treatment.
  • 70. Differential Diagnosis for PeriapicalRadiolucenciesCementoma or Cemental Dysplasia Osteolytic stage Mature lesion (radiolucent) (radiopaque) Vitality tests should be done. Teeth involved should test vital. NO treatment needed.
  • 71. Endodontic Emergencies: Definitions• An emergency is a severe problem requiring an unscheduled appointment with diagnosis and treatment now.• An urgency is a less severe problem that can be attended during a scheduled appointment.• A rule of the true emergency is: one tooth is the offender, i.e. the source of pain.
  • 72. Management of PainfulIrreversible Pulpitis• Pain is the result of inflammation primarily in the coronal pulp.• Removal of the inflamed tissue will usually reduce pain.  Complete cleaning and shaping  With limited time:  pulpal tissue should be extirpated  pulpotomy is usually effective in molars  Mild analgesics may be prescribed  Antibiotics are not indicated. with sodium hypochlorite. Always irrigate
  • 73. Management of Pulpal Necrosis• Pain is related to periradicular inflammation which results from potent irritants in the necrotic tissue in the pulp space.• Treatment is directed to remove or reduce pulp irritants and the relieve of apical fluid pressure.• With pain and pulp necrosis there may be:  No swelling  Localized swelling  Diffuse swelling
  • 74. Management of Pulpal Necrosis• Pulpal Necrosis without swelling ▫ The aim is to reduce canal irritants and to try to encourage some drainage through the tooth.  Complete canal debridement after working length determination.  If time is limited, partial debridement at the estimated working length.  Fill canal with calcium hydroxide paste if possible; seal with cotton pellet and temporary filling.  Prescribe analgesics  Antibiotics are not indicated. Always irrigate with sodium hypochlorite.
  • 75. Fascias Space Infections• If the reaction to the infection occurs very quickly, the involved tooth may or may not show radiographic evidence.• In most cases, treatment involves incision and root canal treatment of the involved tooth to remove the source of infection.• Antibiotic therapy may be indicated.• Fascias space infections of odontogenic origin are infections that have spread into the fascial spaces from the periapical area of the tooth and may become life threatening.
  • 76. Fascias Space Infections• Some fascias space infections may become life threatening cellulitis.• If the submental, sublingual, and submandibular spaces are involved at the same time, a diagnosis of Ludwig´s Angina is made ▫ This cellulitis can advance into the pharyngeal and cervical spaces resulting in an airway obstruction.
  • 77. Fascias Space Infections• Spread of infections from the maxillary canine or buccal spaces can be very dangerous because they can result in Cavernous Sinus Thrombosis. ▫ Life threatening infections in which a thrombus form in the cavernous sinus breaks free, resulting in a blockage of an artery or Canine space abscess spread of infection. spreading into the periorbital spaces
  • 78. Fascias Space Infections• These are infections that have spread into the fascias spaces from the periapical area of the tooth.• Swelling may be localized to the vestibule or extend into a fascial space.• Mild to severe pain may be present and the patient may exhibit systemic manifestations.
  • 79. Management of Pulpal Necrosis• Pulp necrosis with localized swelling ▫ Abscess has now invaded regional soft tissues and, at times, there is purulence in the canal.  Complete debridement of root canal  Fill canal with calcium hydroxide paste  Seal with cotton pellet and temporary filling.  Tissue drainage  relieve of pressure and pain  removal of a very potent irritant (purulence).  Prescribe analgesics.  Patient seldom has elevated temperature or other systemic signs so antibiotics may not be necessary. Always irrigate with sodium hypochlorite.
  • 80. Management of Pulpal Necrosis• Pulp necrosis with diffuse swelling ▫ These rapidly progressive and spreading swellings are not localized and may have dissected into the fasciae spaces. ▫ These patients occasionally have systemic signs.  Most important is the removal of the irritant by canal debridement or by extraction.  Fill canal with calcium hydroxide paste  Seal with cotton pellet and temporary filling.  Incision of swelling  Rubber dam drain inserted in incision may be necessary.  Diffuse swelling decreases slowly over a period of three or four days.  Prescribe analgesics and antibiotics. Always irrigate with sodium hypochlorite.
  • 81. Management of Abscesses andCellulitis• Biomechanical debridement root canals• Incision for drainage• Prescription of antibiotics• Endodontic treatment should be completed as soon as possible.
  • 82. Antibiotics for Endodontic Infections • Typical regiment to treat an endodontic infections is from 6 to 10 days on and around the clock schedule. ▫ Improvement should be seen in 24 to 48 hours after initial treatment and initiation of the prescription. • Penicillin VK ▫ Antibiotic of choice for treatment of endodontic infections. ▫ High efficacy and low toxicity ▫ Spectrum includes many of the bacteria most often identified from endodontic infections (facultative and anaerobic bacteria). ▫ Loading dose of 1,000 mg followed by 500 mg every six hours for 6 to 10 days.
  • 83. Antibiotics for Endodontic Infections• Amoxicillin ▫ Broader spectrum of activity than Penicillin VK. ▫ Absorb more rapidly and gives a higher and more sustained serum level. ▫ Selects for more resistant organisms. ▫ Loading dose of 1,000 mg followed by 500 mg every 8 hours for 6 to 10 days.
  • 84. Antibiotics for Endodontic Infections • Clindamycin ▫ Recommended for patients with a serious infection and an allergy to penicillin. ▫ Effective against both facultative and strict anaerobes. ▫ Although antibiotic-associated colitis has been linked to clindamycin, it only rarely occurs in the doses recommended for endodontic infections. ▫ 300 mg loading dose followed by 150 to 300 mg every 6 hours for 6 to 10 days.
  • 85. Access Preparation • The objective of the entry is to give direct access to the apical foramina. • Study thoroughly diagnostic radiographs. • The likely interior anatomy of the tooth under treatment must be determined. • Endodontic entries are prepared through the occlusal in posterior teeth or the lingual in anterior teeth – never through the proximal or gingival surface. • Caries, defective restorations and weak structure should be removed before starting the access preparation.
  • 86. Anterior Teeth• Preparation relates to internal anatomy• Lingual surface in the middle third of the crown.• Centrals and laterals: triangular shaped with base towards incisal . ▫ Max. Laterals: curvature in about 70% ▫ Mand. Incisors: two canals: 41.4%• Canines: ovoid ▫ Max. Canines:  Longest tooth in the dental arch  Apex often curves in the last 2-3 mm: 60%
  • 87. Premolars • Access shape is ovoid extended more bucco- lingually than mesio- distally. • First maxillary premolars ▫ Two canals: 85% ▫ Three canals : 6% • Mandibular premolars ▫ One canal: 75% ▫ As a group can be the most difficult cases to treat endodontically.
  • 88. Maxillary First Molar• Largest tooth in volume and the most complex in root and canal anatomy.• Is the posterior tooth with  Second MB the highest rate in failures in canal RCT.• Access opening shape is triangular with the apex towards the lingual leaving the transversal ridge intact.• Usually has three roots: mesio-buccal, disto-buccal and lingual.
  • 89. Maxillary First Molar• Mesio-buccal root: ▫ Most difficult root ▫ Should always be assumed  that has two canals until Second MB canal proven there is only one ▫ The second canal is usually localized lingual to the mesio-buccal canal
  • 90. Mandibular First Molar • Access is triangular to rhomboid in shape with the apex to the distal and the base to the mesial. • Three or four canals in 93% of cases: two mesial canals and one or two canals in distal.
  • 91. Second and Third Molars• Access preparation similar to first molars.• Maxillary molars: ▫ Access opening shape is triangular with the apex towards the lingual leaving the transversal ridge intact.• Mandibular molars: ▫ Access is triangular to rhomboid in shape with the apex to the distal and the base to the mesial.• Third molars: ▫ Access preparation dictated by internal anatomy.
  • 92. Instrumentation• Main Objectives ▫ Biologic ▫ Mechanic  To free the root canal system from  To remove pulp, bacteria and restrictive dentin their endotoxins. and shape the canal for obturation in three dimensions.
  • 93. Mechanical Objectives• Continuously tapering preparation• Original anatomy maintained ▫ Retained pre-operative shape ▫ Over instrumentation, failure to pre- curve instruments and disregarding the pass of the guide file produce a preparation that does not follow the original canal anatomy.
  • 94. National and International Standardsfor Instrumentation• The cross section at the first rake angle is term D0.• D16 is the area of the largest diameter 16 mm coronally to D0.• Standardized instruments have a taper of 0.32 mm from D0 to D16, e.g. file #10 has a D16 of 0.42 mm.
  • 95. National and International Standardsfor Instrumentation• Files #10 through #60 have diameters of D0 that increases by 0.05 mm.• From file #60 to #140 the D0 increases by 0.10 mm.• D0 corresponds to the number of the file in tenths of mm, e.g. file #10 is 0.10 mm in diameter at its D0.
  • 96. Sodium Hypochlorite (NaOCl) • Is an excellent antimicrobial agent. • Is a powerful and inexpensive irrigant • Dissolve pulp tissue. • Lubricates canal facilitating instrumentation. • Used clinically in concentrations of 3 to 5%.
  • 97. Chelating Agents • The purposes of the chelator are: ▫ lubrication ▫ emulsification ▫ holding debris in suspension • Chelating agents may be used clinically to facilitate cleaning and shaping. • In calcified canals EDTA (ethylene- diaminetetracitic acid) soften dentin and minimize blockages. • RC-Prep or ProLube are chelators in a viscous suspension.
  • 98. Calcium Hydroxide • Intra-canal medicament most recommended and used. • Powerful alkaline (pH approximately 12.5) • It is a slowly working antiseptic. • Kills bacteria in the root canal space • Controlled laboratory studies support the use of calcium hydroxide as an antimicrobial agent before obturation of teeth with pulp necrosis.
  • 99. Obturation Objective • To create a complete seal along the length of the root canal system from the coronal opening to the apical termination. Pre-treatment Post-treatment
  • 100. Obturation Objective • Eliminate all avenues of leakage from the oral cavity or the periradicular tissues into the root canal system. Pre-treatment Post-treatment
  • 101. Obturation Objective • Seal within the system any irritants that can not be fully removed during canal instrumentation. Pre-treatment Post-treatment
  • 102. Coronal Restoration• After canal obturation, coronal seal (with a proper Recurrent caries restoration) is of due to poor marginal seal ultimate importance.• Coronal leakage due to improper coronal restoration is the most common cause Leaking of failure in root canal temporary treatment. restoration
  • 103. Procedural Accidents• Perforations during access preparation• Accidents during cleaning and shaping• Accidents during Obturation• Accidents during pos space preparation
  • 104. Perforations • During access preparation • Lateral root perforation at or above the height of the crestal bone • Lateral root perforation below crestal bone • Furcation perforation
  • 105. PerforationsLateral▫ Prognosis for perforation repair is favorable.▫ These defects can be easily repaired with standard restorative materials such as amalgam, glass ionomer or composite.  In some cases the best repair is placement of a full crown with the margin extended apically to cover the defect.
  • 106. Lateral root perforation below crestalbone • These perforations generally have the poorest prognosis. ▫ Attachment often recedes and a periodontal pocket forms. • Treatment goal is to position the apical portion of the defect above the crestal bone. ▫ Orthodontic root extrusion is the procedure of choice ▫ Crown lengthening may be considered • Internal repair of these perforations by mineral trioxide aggregate (MTA) has been shown to provide an excellent seal as compared to other materials.
  • 107. Furcation Perforation▫ A direct perforation usually occurs during a search for a canal orifice.▫ Should be immediately repaired with MTA or, if proper condition exists (dryness), glass ionomer or composite in an attempt to seal the defect.  Prognosis is usually good if the defect is sealed immediately.
  • 108. Furcation Perforation • Surgical Treatment ▫ Surgery requires more complex restorative procedures and more demanding oral hygiene from the patient. ▫ Surgical alternatives are hemisection, bicuspidization, root amputation and intentional replantation.
  • 109. Ledge or Block FormationPrognosis • Depends on the amount of debris left in the uninstrumented and unfilled portion of the canal. • Patient must be informed about the prognosis, the importance of the recall examination and which signs indicate failure. • Appearance of clinical symptoms or radiographic evidence of failure may require referral for apical surgery or retreatment
  • 110. Root Perforations • Roots may be perforated at different levels during cleaning and shaping. • Location of the perforation affects the prognosis. ▫ Repair of stripping perforation in the coronal third of the root have the poorest long term prognosis. • The periodontal response to the injury is affected by the level and size of the perforation. • Perforations in the early stages of cleaning and shaping that leave undebrided portions of the canal(s) have a poorer prognosis that those where the canal(s) are thoroughly clean.
  • 111. Separated Instruments • Imperative to inform the patient • Attempt to remove the instrument • Attempt to by-pass the separated instrument using a small file. • If the instrument cannot be by-passed, preparation and obturation should be done up to the fragment. • If symptoms appear, a periapical surgery or extraction are the options. • A separated instrument, per se, does not lead to a failure of endodontic therapy. However, may lead to a treatment failure if it obstructed proper debridement of the root canal space.
  • 112. Traumatic Injuries• Coronal Injuries• Luxation Injuries ▫ Concussion ▫ Subluxation ▫ Extrusive Luxation ▫ Lateral Luxation ▫ Intrusive Luxation• Avulsion Injuries• Horizontal Root Fractures• Alveolar Fractures
  • 113. Cracked Tooth Syndrome• Hairline, incomplete fracture of a vital tooth.• The fracture involves enamel and dentin and sometimes involves the dental pulp.• Most cracks run mesio-distally and are rarely detected radiographically when are incomplete.
  • 114. Cracked Tooth Syndrome• Chief complaint: ▫ Sporadic sharp pain ▫ Pain on chewing, ▫ Occasional pain from cold.• Unable to locate the source of pain.• Asymptomatic.
  • 115. Diagnosis Tooth Slooth Transillumination Methylene Blue
  • 116. Treatment• Immediate reduction of the occlusal contacts• Reversible pulpitis ▫ Preserve pulp vitality ▫ Full occlusal coverage ▫ Cusp protection• Irreversible pulpitis ▫ Root canal treatment ▫ Questionable prognosis
  • 117. Prognosis• The apical extension and future migration of the defect down onto the root will decide the outcome.• The prognosis for a vertical root fracture extending apically from the alveolar crest is poor, and tooth extraction is often indicated.
  • 118. Vertical Root Fracture• Indicators ▫ Narrow periodontal pocket ▫ Sinus tract ▫ Lateral radiolucency extending to the apical portion of the vertical fracture. ▫ The fracture is rarely visible on radiographs• Prognosis and Treatment ▫ Poorest prognosis of all procedural accidents ▫ Treatment is removal of the involved root in multirooted teeth or extraction.
  • 119. Vertical Root FractureEtiology• Excessive instrumentation• Excess force during compaction of root filling material• Widening of canal during post space preparation• Unfavorable post length
  • 120. Endodontic Failures • Can be attributable to inadequacies in: ▫ Cleaning ▫ Shaping ▫ Obturation ▫ Iatrogenic events ▫ Re-infection of the root canal system when the coronal seal is lost • Regardless of the initial cause, the sum of all causes is leakage.
  • 121. Surgical or Nonsurgical? • Nonsurgical retreatment (NSRCT) is an endodontic procedure used to ▫ remove materials from the root canal space ▫ address deficiencies ▫ repair defects that are pathologic or iatrogenic • Nonsurgical endodontic retreatment efforts are directed toward eliminating microleakage.
  • 122. Surgical or Nonsurgical? • In NRSCT, endodontic failures are evaluated for ▫ coronal leakage ▫ fractures ▫ missed canals • Pathologic and iatrogenic events can be repaired non- surgically.
  • 123. Periradicular SurgeryProcedure To remove a portion of the root with undebrided canal space or to retro seal the canal when a complete seal can not be obtained with conventional endodontics.
  • 124. Periradicular Surgery• Indications ▫ NSRCT is not feasible ▫ Failure of a NSRCT ▫ Retreatment will not produce a better result ▫ Biopsy is indicated ▫ Persistent periapical pathosis ▫ Periapical lesion that enlarges after NSRCT ▫ Overextension of obturation material interfering with healing ▫ Apical portion of the root with apical lesion cannot be cleaned, shaped, and obturated.
  • 125. Periradicular Surgery • Contraindications ▫ Treatment of choice is NSRCT ▫ Unidentified cause of treatment failure ▫ Anatomic Factors  Inaccessibility to the surgical site  Spaces such as maxillary sinus or proximity of neurovascular bundles
  • 126. Periradicular SurgerySequence of Procedures• Flap design • Root-end filling• Incision and reflection ▫ MTA (Pro Root)• Apical access • Flap replacement and suturing• Periradicular curettage • Post-operative care and• Root-end resection instructions• Root-end cavity preparation • Suture removal and evaluation ▫ Ultrasonic instruments offer advantages of control and ease of use and permits less apical root beveling and uniform depth of preparation.
  • 127. Vital Pulp Therapy• Treatment to maintain and preserve the vitality of the tooth.• Highly recommended in teeth with incomplete formed roots and young teeth.
  • 128. Pulpectomy• Pulp extirpation• The complete removal of the vital dental pulp.
  • 129. Open Apex• The developing root of Open Apex immature teeth until apical closure occurs.• Apex closes approximately 3 years after eruption. Thin Walls
  • 130. Open Apex• These teeth are difficult to Open Apex treat.• Difficulties: ▫ The canal is wider apically than coronally ▫ A modified access is needed. ▫ The canal walls are thin and susceptible to fracture.• Long-term prognosis is questionable. Thin Walls
  • 131. Apexogenesis• A vital pulp therapy procedure performed to enable continued physiological development and formation of the root end. Calcium Hydroxide/MTA
  • 132. Apexogenesis• A vital pulp therapy procedure performed to enable continued physiological development and formation of the root end.• In young teeth it allows root formation and dentin deposition to have a good Calcium crown–root ratio and an Hydroxide/MTA adequate thickness of the root in order to avoid possible root fractures.
  • 133. Apexification• A method to induce a calcified or artificial barrier in a root with an open apex or the continued apical development of an incompletely formed root in Calcium Hydroxide/ MTA teeth with necrotic pulps.
  • 134. Pulp Therapy• The stage of development influences the type of pulp therapy rendered when pulp injury occurs.
  • 135. Vital Pulp Therapy: Requirements• Treatment of a non inflamed pulp• Proper Diagnosis• Clinical Judgment Histologic appearance of the pulp within 24 hours of a traumatic exposure. There is approximately 1.5 mm of inflamed pulp below the surface of the fracture.
  • 136. Vital Pulp TherapyIndications• Trauma• Some mature teeth• RCT and subsequent restoration not affordable• Teeth with calcification of the pulp chamber and canals are not candidates• Bacteria tight seal ▫ Most critical factor for a successful treatment
  • 137. Vital Pulp Therapy  Pulp capping  Pulpotomy  Partial pulpotomy (Cvek pulpotomy)  Cervical pulpotomy
  • 138. Vital Pulp TherapyDressingsCalcium Hydroxide [Ca(OH)2] ▫ Antibacterial ▫ Causes liquefaction necrosis ▫ Promotes hard tissue formationMineral Trioxide Aggregate (MTA) ▫ Excellent results reported ▫ Dentinal bridging ▫ Earlier dentin deposition
  • 139. Vital Pulp Therapy  Pulp capping  Indirect  Procedure in which a material is placed on a thin partition of remaining carious dentin that if removed might expose the pulp.  Step-Wise Excavation of Caries.
  • 140. Vital Pulp Therapy  Pulp Capping  Indirect  Treatment to avoid pulp exposure.  Promote dentinal sclerosis.  Stimulate reparative dentin.  Allows the pulp to protects itself against caries.
  • 141. Indirect Pulp CappingIndications• None or minimal pulpal inflammation. ▫ Vital tooth. ▫ No spontaneous pain. ▫ No periapical pathology.• Deep carious lesion that will expose pulp if removed completely.
  • 142. Indirect Pulp CappingFollow -Up• Reevaluate in 6 to 8 weeks.• Check of pulpal status• Remove remaining caries using rubber dam.• Restore permanently.
  • 143. Vital Pulp Therapy  Pulp capping  Direct  Treatment of an exposed vital pulp by sealing the pulpal wound a with a dental material placed in direct contact with the exposure to facilitate the formation of reparative dentin and maintenance of the vital pulp.
  • 144. Direct Pulp CappingIndications Mechanical and traumatic exposures ▫ Immature permanent teeth. ▫ Mature permanent teeth with a simple restorative plan. None or minimal pulpal inflammation ▫ Normal or reversible pulpitis. ▫ Asymptomatic ▫ No periapical pathology.
  • 145. Direct Pulp Capping• Dressing directly on pulp exposure.• Mechanical exposures have better prognosis than carious exposures.• If the exposure is on the axial wall, a pulpotomy or pulpectomy should be performed rather than a pulp cap.• In caries, the larger the exposure, the poorer the prognosis.• On trauma, the size of the exposure does not influence healing.
  • 146. Direct Pulp CappingFollow-up• Vitality testing at 3 weeks, 3, 6, and 12 months and yearly thereafter• Radiographic examination• Prognosis: success in the 80% range
  • 147. Partial Pulpotomy(Cvek Pulpotomy) • Differs from pulp capping in that a portion of the remaining pulp is removed. • Indications are similar to pulp capping. • Inflammation zone has extended more than two millimeters apically from exposition. • Success rate is 94 to 96%.
  • 148. Partial Pulpotomy(Cvek Pulpotomy)• Indications are similar to pulp capping• Inflammation zone has extended more than two millimeters apically from exposition• Success rate is 94 to 96%
  • 149. Successful Vital Pulp Therapy• Non-inflamed vital pulp• Continued apical growth of the root with a normal or nearly normal apex is expected in immature treated teeth.• Maintenance of positive sensitive tests
  • 150. Treatment Failure• Cessation of growth and/or apical disease• Inflamed pulp or necrosis• Further treatment: ▫ Root-end closure  Apexification  MTA plug ▫ Root canal treatment
  • 151. Open Apex• Treatment alternatives for necrotic teeth ▫ Apexification ▫ MTA plug ▫ Revascularization
  • 152. Open Apex• Open apex is found: ▫ In developing roots of immature teeth. ▫ In necrotic teeth before root development is complete. ▫ As a result of extensive resorption of a mature apex due to different causes:  Orthodontic movement  Periradicular inflammation  Cysts
  • 153. Apexification• The process of inducing a calcified barrier in a necrotic tooth with an open apex.• Indicated for immature teeth in which standard instrumentation techniques cannot create an apical stop.• Allows a calcified barrier to form across the open apex.• Results in blunting of the end of the root.
  • 154. Apexification: Procedure The Ca(OH)2 is packed against the apical soft tissue with a plugger to initiate hard tissue formation.
  • 155. Apexification: Follow-up• A radiograph is taken at 3-month intervals up to one year to evaluate whether a hard-tissue barrier has formed• Successfully treated teeth are characterized by the following: ▫ Absence of signs or symptoms of periradicular pathosis. ▫ Presence of a calcified barrier across the apex as demonstrated by radiographs or, more often, by careful tactile probing with a file.
  • 156. MTA Plug• Clean and prepare canal.• Calcium hydroxide left for at least two weeks.• Remove Ca(OH)2.• MTA is carried into the canal.• Create a 3 to 4 mm apical plug.• In a subsequent appointment, obturate canal with gutta-percha• Final restoration.
  • 157. MTA Barrier The mix is condensed to the apical extend using pluggers or paper points to create a 3 to 4 mm apical plug. MTA placed In a subsequent appointment, the remainder of the canal is obturated with gutta percha and a final restoration is placed.
  • 158. Revascularization• Technique to treat immature teeth with apical periodontitis.• Canal disinfected• Mix of antibiotics• Apex irritated-blood clot• Coronal tight seal
  • 159. Treatment Summary Reversible Irreversible pulpitis pulpitis Necrotic pulp Vital Pulp therapy Closed apex Open apex Pulp capping or pulpotomy Root Canal Root end closure: Therapy CaOH2 MTA plug. Revascularization
  • 160. Definition of a Perio-Endo Lesion ▫ At least one necrotic, not simply irreversible inflamed, canal is to be expected when a moderate to large periapical lesion is present. ▫ There must be a periodontal defect that can be probed to either the apex of the tooth or to the area of an involved lateral canal. • Both root canal therapy and periodontal treatment are required to resolve the entirety of the lesion.
  • 161. Primary Endodontic Lesions• Endodontic lesions resorb bone apically, laterally, and destroy the attachment apparatus adjacent to a non vital tooth.• Inflammatory process in the periodontium occurring as a result of root canal infection may not only be localized at the apex, but may also appear along the lateral aspect of the root and in furcation areas of two and three-rooted teeth.
  • 162. Primary Endodontic Lesions• Because this lesion is an endodontic problem that has merely fistulated through the periodontal ligament, complete resolution is usually anticipated after routine root canal treatment.
  • 163. Primary Periodontal Lesions• Clinically, there is tooth mobility• The affected tooth respond positively to pulp testing.• Careful periodontal examination will usually reveal pocket formation and an accumulation of plaque and calculus.• Prognosis depends exclusively on the outcome of periodontal therapy.
  • 164. Perio-Endo: Treatment Decision Conical with narrow probing at base of defect True Combined Perio-Endo LesionGiven: bone loss Conical Pulpless tooth with separatefrom the CEJ to or Non periodontal defectnear the apex Vital WNL Probing Endo only Single Endo only Pulp Narrow Endo only Radiograph Tests Possible vertical Fracture Multiple/Conical Perio only WNL Vital Probing Pathosis; possible biopsy Narrow Exceptions: Enamel spurs Developmental grooves Defect after trauma
  • 165. Restoration of Endodontically TreatedAnterior Teeth • Intact, non vital anterior teeth that have no loss of tooth structure beyond the endodontic access are at minimal risk of fracture and do not require a crown. • A non vital anterior tooth that has lost significant tooth structure requires a crown. • Placement of dowel and core depends on the amount of remaining tooth structure.
  • 166. Restoration of Endodontically TreatedPosterior Teeth • Restoration must be planned to protect posterior teeth against fracture. • The functional forces against molars require crown or onlay protection. • Placement of dowels (posts) and core depends in the amount of remaining tooth structure. • When there is sufficient tooth structure to retain the core and the crown, dowels are not needed.
  • 167. Dowels (post) • Dowel is a post or other relatively rigid, restorative material placed in the root of a non vital tooth. CROWN • Purpose of the dowel is to CORE provide retention for the core and coronal restoration. • Dowel does not strengthen the DOWEL tooth and is not necessary when (POST) substantial tooth structure is present. • Tooth is weakened if dentin is sacrificed to place a large Gutta diameter dowel. Percha
  • 168. Conventional Dowels • Always use RD during post preparation. CROWN • Passive CORE • Cemented into place • Residual dentin should DOWEL undergo minimal alteration (POST) • Length and diameter should be the minimum dimension needed to withstand functional loading. ▫ At least 5 mm of filling material should be left at apex.
  • 169. Coronal Coverage • Coronal restorations reestablish function and prevent microleakage. • As a general rule, endodontically treated posterior teeth and anterior teeth where extensive tooth structure is missing and integrity, function and esthetics must be restored, should be restored with coronal coverage. • Crowns should restore function without harm to the remaining root or the periodontal attachment.
  • 170. Ferrule Effect FERRULE • Ideal characteristics: ▫ Minimum of 2 mm in 2 mm height ▫ Parallel axial walls ▫ Completely encircle the tooth ▫ End on tooth structure ▫ Not invade the attachment apparatus of the tooth
  • 171. Standards of Success• The patient should be asymptomatic and able to function equally well on both sides.• The periodontium should be healthy including a normal attachment apparatus.• Radiographs should demonstrate healing or progressive bone fill over time.• The principles of restorative excellence should be satisfied.
  • 172. Questions??????