Intracanal Medicaments Treatment: Presently- single-visit treatment: vital pulp, necrotic pulp & necrotic pulp with apical periodontal tissue involved (acutely infected or abscessed) Recommendation - Vital pulp - a single visit therapy (endodontic access, chemomechanical preparation, canal obturation); Necrotic pulp - two visit treatment: 1 visit: endodontic access, biochemo-mechanical preparation + intracanal medical dressing + temporary filling; 2 visit: canal obturation Root canal infection mechanism: carious pulp infected & inflamed infection pulp necrosis lost defense capability obligate anaerobes colonize root canal spread to dentinal tubules & anatomic variables commonly in apical third of RC periradicular lesion, not inflamed dental pulp is sterile!!! Goal: eradication of RC infection in aseptic manner during RCT Treatment of infected root canals: antibiotics (when vascularized periradicular tissues accessed) + chemical & mechanical procedures Endodontic treatment steps: chemomechanical preparation, intracanal medication, root canal obturation. Chemomechanical preparation: removal of bacteria from main root canal with mechanical action of instruments & canal irrigation Irrigant propertiess: antibacterial Intracanal medication: against viable bacteria , destroy remaining bacteria, limit growth of new ones, useful in apical periodontitis Properties of root canal disinfentant: effective germicide & fungicide, non-irritating to periapical tissues, stable in solution, prolonged antimicrobial action, remain active in presence of blood & pus, low surface tension, not interfere with repair of periradicular tissues, not stain tooth, capable of inactivation of culture bacteria, not induce immune response. Classification of intracanal medicaments: Phenolic compounds Essential oils Aldehydes Halogens Quaternary ammonium compounds Antibiotics and corticosteroids Calcium hydroxidePhenols & their derivatives: Action: denaturation of bacterial protein and inactivation of bacterial enzymes; toxic impact on apical periodontal tissues. Properties: loss of antibacterial action after 24 hours due to contact with tissue fluids. Application: because phenol derivatives are vapored compounds, they can be placed into pulp chamber to obtain bactericidal effect up to 14mm down in apical direction to reduce harmful action on apical periodontal tissues, cresophene for 1 week in cotton pellet for necrotic pulp Specimens: Camphorated Parachlorphenol, Camphorated Monochlorophenol -CPMC, Camphocresol, Camphor mentol, Cresophene, Dikamfen, Endotine (parachlorphenol). Not recommended: high toxicity, low efficacyEssential oils – Action: some antibacterial effects, severe irritant impact on periradicular tissues Aldehydes: Action: bacterial protein denaturation effective canal desinfectant; cytotoxic; mutagenic; carcinogenic Not recommended: high toxicity, low efficacy Specimens: Formaldehyde, paraformaldehyde, glutaraldehyde Halogens – Chlorine –in NaOCl & Iodine compoundsIodine compounds: Action: iodine binds to bacterial proteins, has oxidative influence through oxygen formation as the result iodine reaction with water and hydrogen iodide formation. Application: intracanal dressing, iontophoresis. Specimens: iodine potassium iodide- IPI 2% & 4% with H2O, Lugol’s Solution. Attention: possible allergy; good antibacterial effect but easily inactivated.Quaternary ammonium compounds: Action: lower surface tension of solution, mildly effective disinfectantsAntibiotic-Corticoids pastes:Ledermix: is a glucocorticosteroid-antibiotic compound: 1% triamcinolone (a synthetic corticosteroid) + 3% demeclocycline (broad spectrum tetracycline). Optimal time of use: 4-6 weeks. Ledermix + Calcium Hydroxide: 50-50 mixture does not alter pH mixture will act in similar manner to when calcium hydroxide is used alone.Septomixine forte: 2 antibiotics: neomycin & polymixin B sulphate +2 corticosteroids: dexamethasone + tyrothricin. Action: inappropriate spectrum against commonly reported endodontic bacteria Not recommended for treatment of infected root canals.Pulpomisine (Dexadent): 2 antibiotics: framycetine B and Polimyxine B + Dexamethasone (corticoid). Action: Antibacterial and anti-inflammatory action.Metronidazole: nitroimidazole compound, broad spectrum of activity against protozoa & anaerobic bacteria, strong antibacterial activity anaerobic cocci, as well as gram-negative & gram-positive bacilli, it has bed used both systemically and topically in the treatment of periodontal disease; readily permeates bacterial cell membrane; binds to DNA, disrupting its helical structure, very rapid cell death; excellent activity against anaerobes isolated from odontogenic abscess but no activity against aerobes. Action: antibacterial against anaerobic bacteria, damage of bacterial cells, change of pH in alkaline direction. Easily inactivated. Application: 0’5% solution for canal irrigation during mechanical canal preparation;

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10% paste as intracanal medication for 2-3 days or in acute condition for 24 hours and change of the dressing. Specimens: grinazole, metronidazole 10% paste.Calcium Hydroxide: pH – 12,5 - most endodontopathogens are unable to survive in highly alkaline environment, blood, exudate & tissue fluids reduce pH & decrease its efficacy after 2-3 weeks Activity: antimicrobial - release of hydroxyl ions in aqueous environment, facilities washing out swelling of necrotic tissue. Antibacterial mechanism: Damage to the bacterial cytoplasmic membrane Protein denaturation Damage to the DNA Combined with: CPMC, CHX, or IPI; increase antimicrobial spectrum of Ca(OH)2 - additive or synergistic effects. Recommendation: Two visit treatment: First visit: larger mechanical canal preparation- 3 files sizes over than in canal with vital pulp; it helps to remove the most infected the root dentin; canal irrigation with antibacterial irrigants; intracanal dressing with calcium hydroxide for 1 week (up to 3 weeks). Second visit: canal obturation, if asymptomatic tooth. Treatment: Short-term: for 1-3 weeks intracanal dressing (temporary canal filling). Sealed temporary filling (thickness of material layer 4-5 mm) Long-term: 3 to 12 months with the exchange of calcium hydroxide paste in RC every 2-3 months periapical lesion; unmatured teeth (not finished root canal development)- apexification; external/external resorption; re-treatment; Calcium Hydroxide points: 1. Calcium Hydroxide Points. 2 Calcium Hydroxide Plus Points: additionally contain sodium chloride and tensides. The tensides reduce the surface stress of liquids thereby allowing a more efficient penetration into the dentinal tubules. Thus these points are capable of maintaining a high pH over a long period. Advantages: minimal or no residue left, no smearing around access cavity during insertion, firm for easy insertion & flexible enough to follow natural canal curvature, insertion of points down the apex is easy & ensures that calcium hydroxide is released throughout the canal. 3x more Ca release than regular points, due to highly water soluble components like tensides & sodium chloride, superior pH values & increased wettability of canal surfaces, sustained alkaline pH for 7 days as against 3 days which was seen with calcium hydroxide points.Vitapex: contains: Iodoform 40,4% Calcium hydroxide 30,3% Silicone 22,4% Action: excellent antibacterial; used in pulpectomies & infected root canal, when extruded into furcal or apical areas can either diffuse away or be resorbed in part by macrophages, in 1-2 weeks, bone regeneration clinically & histologically documented, used in infected root canals & pulpectomy treatment in primary teeth. Advantages: no spatulation, radiopacity, excellent accessibility, no chemical & physical changesCalplus - premixed Ca(OH)2 paste with iodoform with improved radiopacity & increased antimicrobial effectChlorhexidine: 2% gel CHX, 2% solution CHX as canal irrigant, Points CHX.Chlorhexidine gutta-percha points: gutta-percha matrix with 5% chlorhexidine diacetate for applying CHX directly into canal, highly effective against bacteria, yeasts & fungi (in low concentrations), Use: intra-canal medication & prevention of reinfection, radiopaque, easy to apply & remove.

Root canal Irrigation: Goals: Before using instruments in the root canal, it should be cleaned of the mass of necrotic, gelatinous material comprised of pulp remnants, bacteria, and tissue fluids. Copious irrigation with an irrigant eliminates most of this toxic material. Most instruments cut better in a wet environment than in a dry one. Irrigation should also follow the use of each instrument, and extended final irrigation should remove all loose debris from the canal. Removal of the smear layer just before filling enhances the final result. Canal irrigation is performed with syringe and special designed needles. Gelatinous mass of necrotic debris should be eliminated from the pulp canal before instrumentation. Forcing this infected material through the apical foramen leads to acute apical periodontitis and/or an acute apical abscess. Principles: Only irrigate under usage of rubber dam. Irrigate following the use of each file. Canal preparation should allow for the irrigation tip to lie at two thirds of the radiographic working length. The needle tip should not bind to the walls of the canal. Allow for adequate time in the canal system for optimal action. Always check for leakage around the protected areas. The needle is loose in the canal to allow backflow. Notched needle tip (inset) eliminates pressure. ProRinse irrigating needles irrigate through a side vent. By rotating the needle in the canal, the spray reaches all regions of the canal. This eliminates the water-cannon effect of open-end needles. Conventional irrigation: syringe + notched needle Vibringe - sonic irrigation system - It enables activation of the irrigant solution acoustic streaming. Activation of the irrigant improves of the canal debridement and distrupts the smear layer.Canal irrigants: Sodium hypochlorite (NaOCl): irrigant of choice, lubricant, disinfectant, tissue dissolvent, broad-spectrum antimicrobial activity; kill rapidly vegetative bacteria, spore-forming bacteria, fungi, protozoa, viruses, bacterial spores different concentration: 0,5-5,25%. Full-strength NaOCl 5,25%

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dissolves both necrotic and vital pulp remnants. Half-strength NaOCl 2,6% dissolves only necrotic tissue. Both solutions are effective antibacterial. Irrigation should also follow the use of each instrument, and NaOCl should then be left in the canal to act as a lubricant for the next instrument. Combination: NaOCl + hydrogen peroxide produces a debriding, foaming action. NaOCl + CHX gluconate destroys half again as many bacteria as NaOCl alone. Hydrogen peroxide (3% H2O2): It’s alone also effectively “bubbles” out debris and mildly disinfects the canal. Because of the potential for gaseous pressure from residual hydrogen peroxide, it must always be neutralized by the sodium hypochlorite and not sealed in the canal. 10(15)-17% Ethylene Diamine Tetraacetic Acid (EDTA): EDTA buffered to a pH of 7,3. It removes only calcified tissue, whereas sodium hypochlorite removes organic material, weak antibacterial 0,2% Chlorhexidine gluconate: It’s an effective endodontic antimicrobial agent. It possesses a broad-spectrum antimicrobial action and a relative absence of toxicity. However, chlorhexidine gluconate is not known to possess a tissue-dissolving property. Saline (0’9% NaCl). 40-50% Citric acid. MTAD (doxycycline, citric acid, Polysorbate): It’s a mixture of 3% doxycycline, 4’25% citric acid, and detergent (Tween-80). It has combined chelating and antibacterial properties. It has low pH, 2’15. QMix: 2 in 1 solution contains a mixture of a bisbiguanide antimicrobial agent, a polyaminocarboxylic acid calcium-chelating agent, and a surfactant. It is effective as 17% EDTA in removal of smear layer and is highly effective as antimicrobial agent. It kills planktonic bacteria within seconds, and it is capable of penetrating biofilms due to its unique blend of antibacterial substance and their combined synergistic effect. Efficacy of different endodontic procedures (% bacteria-free canals) Ultrasounds – 70% bacteria free canals NaOCl – 50% bacteria free canals NaCl 0,9% - 20% bacteria free canals

Endodontic errors and mishaps: Procedural accidents: During Access preparation. During root canal preparation. During obturation. During post space preparation. Endodontic mistakes: Access related: treating the wrong tooth, missed canals, damage to existing restoration, access cavity perforations, crown fracture Instrument related: ledge formation, cervical canal perforation, midroot perforations, apical perforations, separated instruments & foreign objects, canal blockage Obturation related: over or under-extended root canal fillings, nerve paresthesia, vertical root fractures Miscellaneous: post space perforations, irrigant related mishaps, tissue emphysema, instrument aspiration & ingestionA Access related:1 Treating the wrong tooth: Causes: misdiagnosis, tooth adjacent to one scheduled for treatment was inadvertently opened Recognition: Re-evaluation of the patient who continues to have symptoms after treatment. When the rubber dam has been removed. Correction: Appropriate treatment of both teeth: the one incorrectly opened and the one with the original pulpal problem. Prevention: Arrive at the correct diagnosis. Marking the tooth to be treated. It is easily prevented- mark the tooth with a felt-tip pen.2 Missed canals: Causes: Incorrect endodontic access.3 Failure to remove all caries and unsupported structures: Causes: Leads to contamination and re infection of the prepared root canal with saliva and bacteria conducting to endodontic failure. Correction: According to the case, sometimes retreatment may be needed. Prevention: Careful remove of all caries and unsupported tooth structure.4 Damage to existing restoration: Causes: In preparing an access cavity through a porcelain or porcelain-bounded crown, will sometimes chip. Correction: Minor porcelain chip can at time be repaired by bounded composite resin to the crown; however, the longevity of such repairs is unpredictable. Prevention: Placing a rubber dam clamp directly on the margin of porcelain crown is preventing damage to the crown margin and/or fracture of porcelain. Solution: Remove the permanently cemented crown before treatment with little or no damage to the crown. Porcelain crowns are the most susceptible to chipping and fracture. When one is present, use a water-cooled, smooth diamond point and do not force the stone. Do not place a rubber dam clamp on the gingiva of any porcelain or porcelain-faced crown. 5 Access cavity perforations: Searching for canal orifices perforations of crown occur: Peripherally through the side of the crown. Floor of the chamber. It’s an iatrogenic error. Recognition: Above the periodontal attachment: the first sign of an accidental perforation will often be the presence of leakage: either saliva into the cavity or irrigating solution into the mouth. Reason: Lack of knowledge of tooth anatomy. Lack of attention. Misdirection of the instruments. Prognosis: Location of the perforation. Time the perforation is open. Ability to seal the perforation. Correction: Perforations of the coronal walls above the alveolar crest can generally be repaired intracoronally without for surgical intervention. Perforations into the periodontal ligament should be done as soon as possible to minimize the injury to the tooth’s

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supporting tissues. The material used for the repair should provide a good seal and does not cause further tissue damage. Materials used: Cavit. Amalgam. Calcium hydroxide paste. Super EBA. Glass ionomer. Gutta-percha. Haemostatic agents. Operative error: The first of an access cavity perforation is blood in the cavity or the patient complaining of a taste of NaOCl. This most frequently happens in the chamber floor of molar preparations when one is searching for a third or fourth canal. When the crown is perforated into the periodontal ligament, bleeding into the access cavity is often the first indication of an accidental perforation. To confirm the perforation place a small file through the opening and take a radiograph. The site of the perforation must be found, the floor of the preparation cleansed, the bleeding stopped, and mineral trioxide aggregate (MTA) or amalgam applied to the perforation. Because MTA takes more than 3 hours to set, it should be covered with a fast-setting cement. The other canal orifices should be protected by placing paper points or an instrument in the canals to prevent blockage. In the event MTA cannot be immediately applied, it is best to stop the bleeding, place calcium hydroxide over the “wound”, place a good temporary filling, and set an appointment with the patient, the sooner the better. The perforation area will be dry at the next appointment; then MTA can be applied and treatment continued. Prevention: Thorough examination of diagnostic preoperative radiographs. Close attention to the principles of access cavity preparation: adequate size and correct location, permitting direct access to the root canals. A thorough knowledge of tooth anatomy.6 Crown fractures: Preparing an endodontic access cavity in a tooth, particularly in molar or premolar with a large restoration, materially weakens the crown. Infrequently the crown fractures, either during preparation or at a next appointment. One of the frequent causes is failure to relieve the occlusion. If the fracture is chisel shaped and a cusp breaks off down to the periodontal ligament, the tooth can usually be saved. If the fracture extends through the pulp chamber and down into the root, the cases is hopeless and the tooth should be extracted. Causes: Preexisting infraction. Recognition: By direct observation. Treatment: Tooth extraction. Prevention: Reduce the occlusion before working length is established. Infracted crown should be supported with circumferential bands or temporary crowns.B Instrumentation related mistakes: Under-instrumentation and over-instrumentation (cleaning and shaping) can lead to many mishaps: Reduction of the working length. Zipping. Perforations. Injure of periodontal tissues. Inflammation of periodontal tissues. The iatrogenic accidents such as zipping and perforations begin with ledging during canal preparation1 Ledge formation: Ledge is an internal transportation of the canal which prevents positioning of an instrument to the apex in an otherwise patent canal. Causes: a. Using straight instruments in curved canal. b. Packing debris in the apical portion of the canal. c. Rapid advancement in files sizes or skipping file size. d. Inadequate access the operator does not have complete control over the direction of the tip of the instrument and tip of the instrument cuts into the wall of the canal starting a ledge; newer instruments with noncutting tips reduce this problem, because the rounded tip slips by the wall, not cut it. e. Curved roots stiffer instruments start a ledge that can develop into a perforation; but small, flexible instruments with noncutting tips negotiate the curves; if the instrument can no longer be inserted into the canal to full working length, there is suspicion that a ledge has been formed; there also is a change engaging the walls. STOP! Take a radiograph with the instrument in place. The major causes of ledge formation include: Inadequate straight-line access into the canal. Inadequate irrigation or lubrication. Excessive enlargement of a curved canal with files. Packing debris in the apical portion of the canal. Recognition: When the instrument cannot reach to the full working length. There may be a loss of normal tactile sensation at the tip of the instrument, loose feeling instead of binding in the canal. A radiograph of the tooth with the instrument in place will provide additional information. Correction: Use of a small file, Nº 10 or 15 with a small bend at the tip of the instrument. Penetrate the file carefully into the canal. Once the tip of the file is apical to the ledge, it’s moved in and out of the canal utilizing ultra-short push-pull movement with emphasis on staying apical to the defect.2 Broken instrument: Separated instruments & foreign objects : instrument breakage is a common and frustrating problem in endodontic treatment which occurs by improper or overuse of instruments. When an instrument fracture occurs during root canal preparation procedures, the clinician has to evaluate the treatment options with consideration for the pulp status, the root canal infection, the root canal anatomy, the position and type of fractured instrument. In the root canal can break different objects, most often files and reamers, lentulo spirals, Gates-Glidden drills and burs. It is caused by unrealistic strains placed upon them, especially in severely curved canals and at higher rotary speeds. Symptoms: Canal blockage. Short length of the instrument. Treatment: If a broken instrument can be grasped, it may be removed with forceps. Use of a small tipped ultrasonic instrument to loosen and float out the broken piece. Attempt to

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bypass it with a small file or reamer. Bypassing is made easier with a lubricant. If successful, the canal preparation can be completed and the can filled, thus the instrument segment becomes part of the filling material. If the fragment extends past the apex an efforts to remove it none surgically are unsuccessful, the corrective treatment will probably include apical surgery.3 Canal blockage: It can occur during canal enlargement. Files compact debris at the apex and working length is shorter because the instruments are working against the packed mass at the apex. A radiograph will confirm this suspicion. Correction is made by recapitulation starting with finer instruments and using a chelating agent- EDTA. On the other hand, sterile dentin chips at the apex, formed during preparation, help to block the foramen and prevent overcompaction, and stimulate cementum formation at the apex.Injure of apical periodontal tissues: After the enlargement of the bent canal, a greater amount of dentin is removed, and as result the previously correct working length becomes shorter and the instrument is too long and can injure apical periodontal tissues.Root perforations: These are usually caused by three errors: Creating a ledge and persisting until a perforation develops. Wearing a hole in the lateral surface of the midroot by overinstrumentation (canal stripping). Using too long instrument and perforating the apex. Identification of perforation place: Paper points confirming strip perforation. The area of bleeding marked on the paper point indicates the area where the strip occurred. Types of perforations:4 Cervical canal perforations: Causes: During the process of locating and widening the canal orifice or inappropriate use of gate-glidden burs. Recognition: Sudden appearance of blood in the cavity. Magnification with loupes, endoscope, or microscope is useful. Correction: The bleeding is stopped and MTA is applied to perforation. Cotton should be placed in the chamber and a good temporary filling is placed to allow time for the MTA to set (> 3 hr). Preparation is continued at a subsequent appointment.5 Midroot perforations: Commonly occur in the carved canal when a ledge has formed during instrumentation, or along inside the curvature of root canal, as it straightened out. Recognition: Blood in the canal indicates that a perforation has occurred. Management: MTA is the material of choice to close the perforation.6 Apical perforations: Causes: The file is not passing a curved canal. Not establishing accurate working length. Overinstrumentation. Detection: Patient suddenly complains of pain during treatment. The canal becomes flooded with haemorrhage. The tactile resistance of the confines space is lost. Paper point inserted to the apex will confirm a suspected apical perforation (bleeding at the tip of paper point). Radiographically with the instrument inside. Treatment: If the perforation create new foramen: One is now dealing with two foramina: one natural and the other lateral. Obturation of both of these foramina and of the main body of the canal requires the vertical compacting techniques with heat-softened gutta-percha. If the perforation is caused by over instrumentation: corrective treatment include Re-establishing tooth length short of the original length and then enlarging the canal with larger instruments, to that length. The canal is then cautiously filled to that length. Steps: Apical perforation destroys the resistance form, it means that the tip of the primary gutta-percha point must be blunted and fit to place so that it does not extend beyond the orifice, even when compaction during obturation is used. Deposition tiny pack of MTA or BIODENTINE at the apex and checking its placement radiographically. During the next appointment after the MTA has set and plugs the apical foramen. This new plug (resistance form) allows compaction of the gutta-percha. Later, MTA o BIODENTINE will encourage cementum formation at the apex.C Obturation-related mishaps: Over or underextended root canal fillings. Causes: Over extended filling: Apical perforation. Under extended filling: Failure to fit the master gutta-percha point accurately. Poorly prepared canal, particularly in the apical part of the canal. Recognition: When a post treatment radiograph is examined. Correction: Underextended filling: treatment by, removal of the old filling followed by proper preparation and obturation of the canal. Overextended filling: is more difficult. An attempt to remove the over extension is sometimes successful if the entire point can be removed with one tug. If the overextended filling cannot be removed through the canal, it will be necessary to remove the excess surgically.D Miscellaneous mishaps:1 Irrigant-Related Mishaps: Forcibly injecting NaOCl or any other irriganting solution into the apical tissue can be disastrous. The patient may immediately complain of severe pain. Swelling can be violent and alarming. Symptoms: Immediately severe pain. Swelling is violent and alarming. Severity of symptoms depends of concentration of irrigant. Paraesthesia, scarring, and muscle weakness. Management: Antihistamines, ice packs, intramuscular steroids, even hospitalization and surgical

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intervention may be needed. Prevention: Is the only solution. Using passive placement of a modified needle. The needle must not be wedged in the canal.2 Tissue Emphysema: Causes: A blast of air to dry a canal. Exhaust air from a high-speed drill directed toward the tissue and not evacuated to the rear of the handpiece during apical surgery. Symptoms: Rapid swelling. Erythema. Crepitus. If the air pocket breaks through into the neck region, there is a sudden swelling of the neck, the voice sounds brassy, and the patient has difficulty breathing. If it breaks through into the mediastinum, a crunching noise is heard on auscultation. Death can follow. Prevention: Use paper points to dry the canal. Do not blow air directly down an open canal.3 Instrument Aspiration and Ingestion: Prevention: Always use a rubber dam. Procedure: If instrument aspiration or ingestion is apparent, the patient must be taken immediately to a medical emergency facility for examination, and the dentist must accompany the patient. This examination should include radiography of the thorax and abdomen. It is helpful if the dentist takes a sample file along so the radiologist has a better idea of what to look for. The results may be disastrous. Be prepared for a session in a court.

Radiographs Types: 1) Intraoral radiographs in periapical projection: Paralleling technique: film is placed parallel to long axis of tooth; film is exposed to X-rays. Which are perpendicular to its surface, requires special film holders. Bisecting angle technique: x-rays pass perpendicular to angular bisector by long axis of tooth and x-ray film, no film holder is required. 2) Digital radiography: Advantages: Reduced exposure to radiation. Increased speed of obtaining image. Possibility for digital enhancement. Storage as digital data in computers. Ease of transmissibility. Elimination of manual processing steps. Digital image enhancement. Inversion. Contrast. Pseudocolor. Flash light. Magnification. Measurement of angle of root curvature. Linear measurement. Diagnostic Radiographs: ideally, paralleling angle technique, high quality, no forshortening or elongation , they help in proper diagnosis of case, & determining prognosis by comparison with post-operative & follow up radiographs. Working radiographs: with bisecting angle technique, used for determining position of instruments, taken without removing rubber dam Intraoral images: Examination of dentition and associated structure. Number, sequence, appearance, root structure. Crown-caries, defective enamel. Interproximal areas and restorations. Bone rarefication. Describing lesion: Size: Measure lesion with a ruler; if you must estimate, use surrounding structure as guide. Measure in two dimensions, width and high in mm. Shape: Regular shape like round, triangular, rhomboid. Irregular shape. Location: Localized or generalized. Unilateral or bilateral. Where is lesion in relation to other structures & anatomic landmarks. In terms: Mesial, distal. Inferior, superior. Posterior, anterior. Density: Is lesion radiopaque, radiolucent or mixed density? Remember that opacity is relative to adjacent structure. If lesion is of mixed density, describe appearance. Borders: Well or poorly demarcated. Punched out (no bone reaction). Corticated (thin opaque border). Sclerotic (wide, uneven opaque border). Hyperostetic (increased density of trabecylation). Internal architecture: Is lesion uniform? Internal structure such as septae or loculations (numerous small compartments). Effect on adjacent structures: Is lesion causing: Resorption. Displacement. Scalloping. Effacement. Destruction. Space occupying lesions displace other structure. Remodeling. Expansion. Thinning/thickening.

Morphology and function of periradicular tissues Periodontal tissues: PDL, cementum, alveolar processPeriodontal Ligament (PDL): ~ width 0,2mm; dense fibrous connective tissue that occupies periodontal space between root of tooth & alveolus, derived from dental follicle; above alveolar crest - continuous with connective tissues of gingiva; apical foramen it is continuous with dental pulp. Composition: Collagenous fibers: running from the cementum to the alveolus. Blood vessels: forming loops and amortizes a pressure onto the tooth. Nerves: the sensory coming from the nerve V and are associated with mechanoreception; the autonomic nerves are associated with the supply of the periodontal blood vessels. Cells: fibroblasts, cementoblasts and cementoclasts; osteoblast and osteoclast; epithelial cells- the rest of Malassez and defense cells- macrophages. Mast cells, eosinophils. Sharpery’s fibers of PDL: Dentoalveolar crest fibers. Horizontal fibers. Oblique fibers. Apical fibers. Gingival fibers. Interseptal fibers.Functions: supports tooth in alveolar socket & provides physiological mobility of tooth, amortizes action of mastication forces, contributes in permanent reconstruction of cementum, mediates in receiving of sensory agents.

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Cementum: thin layer of calcified tissue covering dentin of root, derived from inner layer of dental follicle, no blood vessels & nerves, between 10&70 years of life cementum layer increases 3-fold. Composition: Inorganic material: 65% calcium phosphate (hydroxyapatite), Organic material: 23% (collagen, proteins), Water: 12% Classification: Cellular: apical region, cementoblasts, cementoclasts, fibers. Acellular: cervical region, fibers. Functions: give attachment to collagen fibers of PDL, help in maintenance of root integrity, involve in tooth repair & regeneration.Alveolar process: Classification: Compact: cortical and cancellous. or Spongy. Composition: Inorganic material: 65% carbonated hydroxyapatite. Organic material: 25% proteins, collagen, cells (osteoblast, osteocytes, osteoclasts). Water: 15%. In dental socket, tooth surrounded by thin layer of compact bone in which are numerous openings - alveolar sieve. Through alveolar sieve, at acute inflammation of apical periodontal tissues, exudate penetrates & reaches spongy bone. Bone is covered by periosteum, well innervated fibrous tissue. Normally invisible in radiograph, but in pathology gains osteogenic property periosteal reaction. Function: continuous remodeling & adaptation to changing functional situations due to resorption & proliferation (stratification): Norm: balanced processes. Pathology: osteoclasts activity increased osteoporosis or osteolysis of bone. At enhanced osteoblasts activity/inhibition of physiological process of destruction osteosclerosis occurs

Diseases of apical periodontal tissues - pathological processes, which involve PDL & bone of alveolar process. Healthy apical periodontal tissues – barrier. Inflamed periodontal tissues systemic diseases Periradicular lesions: consequence of pathologic changes in dental pulp & root canal system, that harbor numerous irritants. Irritants can initiate formation & progression of periradicular lesions. If transient irritants - inflammatory process is short-lived & self-limiting. If excessive amount of irritants or persistent exposure - nonspecific & specific immunologic reactions can cause destruction of periradicular tissues. Causative factors of periradicular lesions: infective: mostly bacterial. Non infective.Periradicular lesions of pulpal origin: Irritants: Irritation of pulpal or periradicular tissues inflammation. Classification: Living irritants: various microorganisms and viruses. Non-living irritants: mechanical (trauma), thermal, and chemical irritants. Mild to moderate injuries of short duration reversible tissue damage recovery Persistent and/or severe injuries irreversible changes in pulp periradicular lesions Living irritants: bacteria, bacterial toxins, bacterial fragments, viruses; they egress apically from root canal system into periradicular tissues inflammation & tissue alteration by immunological reaction. Gangrenous pulp - anaerobic bacteria (65-90%): Bacteroides intermedius, denticola, gingivalis, endodontalis, buccae. Eubacterium, Actinomyces. Non-living irritants: Mechanical irritants: Occlusal trauma: tooth has vital pulp & reveals significant mobility Traumatic occlusion: premature contact with opposing tooth widened periodontal spaces; alveolar bone loss due to periodontal disease. Iatrogenic trauma: gutta-percha point overfilled pain & inflammation Spreading ways of periradicular tissues infection: from main root canal, from gingival pocket, through lateral canal or perforation, via blood.Acute Apical Periodontitis: Symptoms: Symptoms of pulpitis or necrosis + pain on bite, Clinical examination: Pain on percussion, may or may not respond to pulp vitality testing X-ray: Thickening of periodontal ligament space, no periradicular radiolucency. Treatment: RCT.Chronic Apical Periodontitis: Symptoms: Asymptomatic or slight discomfort. Clinical examination: Little or pain on percussion, no response to pulp vitality testing X-ray: Interruption of lamina dura or apical radiolucency Treatment: RCT.Acute Apical Abscess (closed): Symptoms: Severe discomfort, swelling, fever, some degree of mobility, tenderness of cervical & submandibular LNs Clinical examination: Swelling in mucobuccal fold & facial tissues adjacent to tooth, pain on bite, percussion & palpation, no response to pulp vitality testing, X-ray: Radiolucent lesion (localization). Anything from widened PDL to periradicular radiolucency Treatment: RCT, drainage (antibiotics).Suppurative Apical Periodontitis (open): Symptoms: Asymptomatic (drain), swelling Clinical examination: Fistula, swelling, no response to pulp vitality testing, no pain on bite on percussion X-ray: Radiolucent lesion (localization with gutta-percha). Treatment: RCT.Classification of apical periodontal tissues diseases, acc. to Polish Textbook: Acute Chronic, Serous or Purulent | Chronic Exacerbation Acute | Serous Purulent | Chronic Fibrous or Granulous | Fibrous Granulous | Granulous Cystitis or Purulent | Cystitis Purulent

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Ingle’s classification of periradicular lesions: Symptomatic (acute) Apical Periodontitis SAP. Asymptomatic (chronic) Apical Periodontitis AAP. Apical Abscess.AASymptomatic Apical Periodontitis (SAP): localized inflammation of PDL in apical region. Causes: irritant diffusing from inflamed or necrotic pulp, egress of irritants: bacteria, bacterial toxins, disinfecting medications, debris pushed into periradicular tissues, physical irritation of periapical tissues, impact trauma. Pain: intensity comparable to advanced acute pulpitis, but lasts longer, constant, gnawing, pounding, throbbing pain, tooth elevated in its socket. Examination: No pulp reaction to stimuli (necrotic pulp), pain on percussion, painful to touch, supraocclusion Radiograph: widened PDL, no radiolucency Treatment: Give long-acting block anesthesia. Relieve occlusion in opposite arch if possible. Opening of tooth gives release; even small amount of fluid gives immediate relief.Endodontic access & chemo-mechanical preparation of canal. Intracanal dressing with antibiotic & corticoid. Place small dry cotton pellet in chamber & thin temporary filling; re-check occlusion. If pain unbearable at night, instruct patient how to remove temporary filling, watching in mirror & using safety pin bent at right angle; relieve pressure. Give antibiotics & NSAIDs: ibuprofen. RCT should not be undertaken until all acute symptoms subsided. Asymptomatic Apical Periodontitis (AAP): Granuloma& Cyst: may be preceded by SAP or apical abscess, frequently asymptomatic. Causes: inadequate RCT, gradually release of noxious agents with low-grade pathogenicity or in low concentration by necrotic pulp Symptoms: non-significant pain, little or no pain on percussion, if AAP perforates cortical plate of bone, palpation of superimposed tissues may cause discomfort; negative pulp response for electrical or thermal stimuli (necrotic pulp) Radiograph: periradicular radiolucent changes ranging from thickening of PDL & resorption of lamina dura to destruction of apical bone resulting in well-demarcated radiolucency Local effects: Bone & periodontal ligament replaced by inflammatory tissue, destructive & healing processes occur simultaneously in asymptomatic apical lesions. Extent of lesion depends on potency of the irritants within RC system & activity level of defensive factors in this region. Balance maintained asymptomatic. If causative factors overcome defensive elements symptomatic periradicular lesion superimposed on asymptomatic one - phoenix abscess. Systemic Effects: it is not a focus of systemic diseases via immune complexes, but SAP systemic immunologic reactions & some systemic disease. Condensing osteitis - Chronic Facial Sclerosing Osteomyelitis: radiographic variation of AAP – Inflammation stimulates osteoclastic & osteoblastic activities; predominant osteoblastic (formative) activity; unknown reason, possibly special balance between host tissues & RC irritants; localized overproduction of apical bone; low-grade inflammation of periradicular tissues. Location - observed around apices of mandibular posterior teeth with pulp necrosis or chronic pulpitis. Symptoms: various - associated with variety of pulpal & periradicular lesions, may be asymptomatic or sensitive to stimuli, may or may not respond to electrical & thermal stimuli. Radiograph: well-circumscribed radiopaque area around 1 or all of roots; often indicative of chronic pulpitis; radiopaque changes return to normal after successful RCT, additional bony trabeculae formed, marrow spaces reduced to minimum. PDL space visible,despite increased radiopacity of nearby bone. Periradicular granuloma: mass of chronically inflamed granulation tissue of apex of non-vital tooth, may arise after acute condition like periapical abscess becomes quiet or de novo; lesion is not static; may transform into periapical cyst or undergo acute exacerbation. Pain: painless, or relatively painless Examination: negative pulp vitality test (pulp necrosis by trauma or caries).with transillumination tooth appears darker than its neighbour, percussion is of little value Radiograph: well-defined periapical lesion, variable size, external resorption usually not destroyed root end, loss of lamina dura. Histology: Predominantly of granulation inflammatory tissue with many small capillaries, fibroblasts, numerous connective tissue fibers, inflammatory infiltrate, & usually connective tissue capsule. Capsule is replacing periodontal ligament, apical bone, & sometimes root cementum & dentin; infiltrated by plasma cells, lymphocytes, mononuclear phagocytes &occasional neutrophils. Lesion shows inflamed granulation tissue containing a dense lymphocytic infiltrate mixed with PMNL’s (polymorphonuclear leukocyter), plasma cells & macrophages. Epithelial rests of Malassez may be seen within granulation tissues. Cholesterol clefts may be seen along with associated multinucleated giant cells. Areas of extravasation of RBCs and hemosiderin pigmentation are also common. Conditions: low virulence bacteria in canal, well controlled by layers of periapical inflammatory lesion, can spring into violence if virulent bacteria take over & phoenix abscess develops, or it may develop into an apical cyst. Treatment: RCT, surgery not necessary, curettage to speed up healing Periradicular cysts: inflammatory process stimulates epithelial resting cells of Malassez, cystic cavity filled with cholesterol & fluid develops around apex, may grow by expansion from fluid, may become infected Examination: radiograph, may be unnoticed until starts moving teeth (pathognomonic) or becomes infected & abscess

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develops; does not respond to thermal or electric stimulation; may be slightly discolored in transillumination; negative percussion, but if grown to size where it perforates cortical plate may be palpated. Radiograph: round or ovoid radiolucency with sclerotic border; if infection supervenes, margin becomes indistinct like in granuloma. Histology: Central cavity lined by incomplete & ulcerated stratified squamous epithelium; lumen contains pale eosinophilic fluid & occasionally some cellular debris. Connective tissue – capsule surrounding epithelium contains cellular & extracellular elements of periradicular granuloma. Inflammatory cells are also present within epithelial lining of this lesion. Presence of dental epithelium-lined cavity filled with fluid or semisolid material. Treatment: RCT & periapical surgery Differential diagnosis: Periapical granuloma. Periapical cemento-osseous displasia (early lesion) Types of periapical (radicular) cysts: Apical, Lateral, residual radicular cyst Classification of cysts acc. to WHO: 1. Odontogenic: A. Developmental Odontogenic keratocyst (primodial cyst) Dentigerous (follicular) cyst Eruption cyst Lateral periodontal cyst Gingival cyst of infants (Epstein pearls) Gingival cyst of adults Glandular odontogenic cyst; sialo-odontogenic cyst Orthokeratinized odontogenic cyst B. Inflammatory Radicular (periapical) cyst: apical, lateral, residual Paradental cyst 2. Non-odontogenic: Nasopalatine (incisive canal) duct cyst Nasolabial (nasoalveolar) cyst Apical Abscesses: localized collection of pus in cavity formed by disintegration of tissues: Symptomatic & Asymptomatic Symptomatic Apical Abscess (SAA): sudden egress of bacterial irritants, accompanied by exudate formation within lesion. Cause: rapid influx of microorganism, or their products, from root canal system. Pain: in pain, fever, increased WBCs, not as painful as SAP, pressure from accumulation of exudate within confining tissue severe pain Swelling: Gentle palpation reveals early swelling. Spread of lesion toward surface, erosion of cortical bone & extension of abscess through periosteum & into soft tissues is usually accompanied by swelling & some relief. Swelling localized, but may become diffuse & spread widely (cellulitis); depends on virulence & incubation period of involved bacteria, & host’s resistance. Location of swelling determined by relation of apex of involved tooth to adjacent muscle attachments. Tooth examination: No pulp reaction to stimuli (necrotic pulp). Percussion: varying degrees of sensitivity to percussion and palpation. Redness of mucosa & later “pointing” of abscess. Clinical: Initial stage: tenderness of affected tooth. Later: pain becomes intense with extreme sensitivity to percussion. Extrusion of tooth from its socket. Systemic findings: fever, chills… Radiograph: No gross radiographic changes may be noted at first, but later in the process, rapid bone loss shows up as radiolucency. Therefore, the x-ray picture varies from no obvious signs of pathosis through a thickening of the periodontal ligament space to a frank periradicular lesion. Spread of inflammatory response into the cancellous bone results in apical bone resorption; since inflammation is not confined to the periodontal ligament but has spread to the bone, the patient now has an acute osteitis. Course: Immunologic or no-immunologic inflammatory responses contribute to the breakdown of the alveolar bone and cause disruption of the blood supply, which, turn, produces more soft and hard tissue necrosis. The suppuration process finds lines of least resistance and eventually perforates the cortical plate; when it reaches the soft tissue, the pressure on the periosteum is relieved, usually with a reduction of symptoms. Once this drainage through bone and mucosa is obtained, supportive apical periodontitis or an asymptomatic periradicular abscess is established. Treatment: Early stages – drain canal with slight opening with reamer, if it doesn’t work antibiotic therapy; frequent hot rinses, once abscess becomes fluctuant, incision & drainage is employed to drain abscess, once whole area “quiets down”, RCT may be completed. Asymptomatic Apical Abscess (AAA): Features: abscess from low virulence; long-standing fistulous draining abscess continuously or intermittently by draining sinus tract, drained into oral cavity as stoma on oral mucosa but occasionally extraorally as fistula on skin of face, cutaneous fistula; exudate can also drain through gingival sulcus of involved tooth, mimicking a periodontal lesion with “pocket”, asymptomatic – patient often tolerate condition for months or even years, may also develop acute exacerbation, the so-called phoenix abscess Examination: If draining fistula is present, process is quite apparent. One should probe fistulous track with a gutta-percha point, using a radiograph as a guide. Often what is thought to be the obvious tooth may not actually be the culprit. Pulp test reveal the necrotic pulp. Radiographs: diffuse radiolucency, sometimes of enormous size. Treatment: RCT. Often fistula stops draining after 1st visit, abscess area heal to new bone. Surgery root apex is “chewed-up” by inflammatory resorption. Open apex- difficult to obturate; so, surgery & root-end filling. Removing all chronic inflammatory cells from region - speed up healing. Apical Scar (Fibrous Scar): Variation in healing process. Norm - surgical site fills with blood clot- organizes, mineralizes & remodels like surrounding bone. Occasionally it fails, patient asymptomatic, no treatment.

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Resorption of dental root - physiologic or pathologic factors leading to loss of hard dental tissues & bone tissue.Classification of root resorption Based on nature: Pathologic: seen in both, deciduous and permanent dentition. Physiologic: seen in deciduous dentition. Based on anatomical occurrence of region: Internal. External: Apical, Lateral, Cervical Based on causes: Local. Inflammation: External & Internal Pressure: Orthodontic, Tooth movement, Tumor, Cyst Replacement or dentoalveolar ankyloses. Systemic. Idiopathic.Resorption process: In physiologic condition the mineralized dental tissue of the permanent teeth are not normally resorbed. They are protected in the root canal by the predentin and the odontoblasts and on the root surface by the precementum and the cementoblasts. In pathologic condition, if the predentin or the precementum becomes mineralized or in case of precementum is mechanically damaged or scraped off- the osteoclast- like cells will colonize the mineralized or denuded surface and resorption will develop. However, resorbing cells require continuous stimulation during phagocytosis, and stimulation by a denuded dentin or cement surface is not sufficient to support the resorptive process for long. Therefore, a phagocytic colonization of denuded areas of the root will be transient without additional stimulation of the cells, and repair with cement- like tissue will occur both in the root canal and on the root surface. This type of resorption is named a transient root resorption. Phases: 1. An injury (mechanical or chemical) to the protective tissues covering the root (precementum or predentin) which initiates the resorption process. 2. A continued stimulation of the resorptive process by either infection or pressure.External resorption: Pathologic loss of tooth structure resulting in a defect in the root and adjacent bone, it is initiated in the periodontium. Etiology: Chronic inflammation of periradicular tissues. Necrotic pulp. Mechanical injury- trauma. Tooth replantation. Orthodontic treatment. Impacted teeth. Internal bleaching. Idiopathic- unknown cause.Histologically: Scalloped border lined with osteoclasts.Radiographically: Defect is rough. Asymmetric. Moth-eaten appearance.Types according to causative agents:Inflammatory: periradicular lesions always result in resorption of both bone and tooth, and after replantation of the tooth. Root resorption supported by infection can occur: In the root canal internal resorption. On the tooth surface external resorption and cervical resorption. Depending on whether the bacterial stimuli come from the gingival sulcus or from the root canal.External inflammatory resorption: A commonly occurring complication following displacement of the teeth (after luxation and avulsion, injuries leading to a disruption of the pulpal blood vessels at the apical foramina and to ischemic pulp necrosis). It can be initiated by mechanical trauma resulting in the removal of cementoblasts, precementum, and sometimes cementum in areas of the root surface. The resorptive process is then maintained by bacterial products from the infected root canal which provide the necessary continuous stimulation of the resorbing cells. If the resorptive process progress, the tooth may be destroy completely in a few months Due to tooth traumatic injure: mechanical stimulation of osteoclasts to support a progressive resorption is seen, for example, in root-fractured teeth there sharp edges of the root fragments are selectively resorbed. Only when fragments are well rounded and cause no further tissue irritation will the resorption stop Pulpal infection root resorption: following infection, the presence of bacteria in the dentinal tubules is the stimulating factor of the osteoclastic inflammatory response that takes place in the dentin bone. Treatment: Ca(OH)2 is placed in the canal for 6-12 months or MTA. Diagnosis: radiographically, there is a radiolucency on external root surface and adjacent bone or on internal root canal walls.External Cervical Resorption: Periodontal infection root resorption: external root resorption that occurs after injury of the precementum below the epithelial attachment, and contamination by bacteria from the sulcus. Consequently, resorbing cells penetrate into the damaged areas of the root, causing resorption inside the root and in the adjacent alveolar bone. Initially, this does not penetrate into the root canal but may do so at later stages. Radiographically: a single radiolucency in the dentin at crestal bone level. Treatment: surgically expose the resorptive area and remove the granulation tissue, followed by restoration with resin composite or amalgam. The root canal treatment in necessary only if canal is perforated.Post traumatic injury: following severe traumas (avulsion or intrusion), healing with cementum may not be possible. Therefore, bone comes into contact with the dentin without an intermediate protective layer (cementum) and the dentin becomes part of the normal bone remodeling process. Causes: Trauma. Idiopathic.

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Clinically: The ankylosed tooth lacks physiologic mobility, has metallic percussion sound, and may be in infraocclusion.Radiographically: There is no PDL. No radiolucent areas. The root becomes replaced by boneTreatment: there is not. Treatment of idiopathic resorption : Use the same method as for inflammatory resorption. Prognosis depends on extent and location, sometimes unpredictable. Prevention: The goal with severe traumas such as avulsions is to minimize damage to PDL cells by either immediately replanting the tooth into the socket, or placing the tooth into a suitable storage media until the tooth can be replanted. Cervical tooth resorption: damage of epithelial attachment, it begins on root surface and may extend and form the chamber and canal perforations.Pressure: in the permanent teeth the pressure resorption may be seen during: Teeth eruption, especially of maxillary canines and mandibular third molars. The presence of certain tumors impinging on the roots of the teeth. Orthodontic movement of the teeth, usually in the form of apical resorption and a shortening of the roots. Pressure resorption may be quite destructive if diagnosed late on. However, the resorptive process will be arrested when the stimulation of the resorbing cells stops. Orthodontic teeth movement: apical root resorption resulting from pressure applied during orthodontic movement. Teeth are asymptomatic and vital. Most root resorption is minimal and ceases after the appliances are removed. Treatment: discontinue orthodontic treatment. Endodontic treatment is not necessary. Impacted tooth/tumor pressure: pressure applied from erupting permanent teeth (mainly canines and mandibular 3rd molars) or tumors causes resorption of adjacent roots. The teeth affected are most often vital and asymptomatic. Radiographically: resorptive area is next to the impacted tooth or tumor. Treatment: surgery.Replacement resorption/ ankylosis: pathologic loss of tooth structure with the ingrowth of bone into the defect fusion of bone to cementum or dentin Causes: trauma, idiopathic Following severe traumas (avulsion or intrusion), healing with cementum may not be possible.Therefore, bone comes into contact with the dentin without an intermediate protective layer (cementum) and the dentin becomes part of the normal bone remodeling process. Clinically, the ankylosed tooth lacks physiologic mobility, has metallic percussion sound, and may be in infraocclusion. Radiographically, there is no PDL, and no radiolucent areas, and the root becomes replaced by bone. No treatmentSurface/transient: Physiologic process causing small superficial defects in the cement and dentin that undergo repair by deposition of new cement. Pathologic process is initiated by a denudated area of the root surface and supported by mechanical irritation, increased pressure in the tissue or infection of the root canal and tubules of the crown and root dentin. Usually too small to be detected on a radiograph and without clinical importance.

Internal resorption: associated with a long-standing chronic inflammation in pulp,occurs sometimes during chronic pulpitis or due to injure as a result of damage of the odontoblasts layer. The predentin is mineralized and becomes sensitivity on the action of the osteoblast-like cells. The loss of dentin (dentin decay is called as the resorption lacuna) in more or less regular shape is occurred, which is filled by granular tissue. The dental pulp is changed into the granulation tissue with presence of giant cells. Predisposing factors: Unknown, the process appears to be associated with a pulpal inflammation. Features: Preceded by disappearance of the odontoblastic layer of cells, followed by an invasion of macrophage- like dentin-resorbing cells. Internal resorption is usually asymptomatic and is discovered on routine radiographs. The resorptive process may progress slowly, rapidly or intermittently with periods of activity and inactivity. Mechanism: Pulp stimulated by irritants Inflammation. Undifferentiated cells of pulp become osteoclasts and macrophages. Dentinal resorption.Types: Surface/ transient : is associated with a long-standing chronic inflammation in the pulp. It occurs if the odontoblasts in an area of the root canal are destroyed so that the predentin becomes mineralized. No detectable radiographically. Inflammatory: (internal granuloma, internal progressive resorption, pink tooth, pink spot). The enlargement of the dental cavity size in oval shape lacuna. Often in pulp chamber is necrotic pulp, however, the early performed root canal treatment can inhibit the resorption progression. In case of the progressive internal resorption, the resorptive activity is sustained by infection of necrotic tissue coronally in the root canal. Etiology: chronic pulpitis, disorders of blood circulation followed by a trauma, vital pulpotomy with calcium hydroxide. Unknown reason: idiopathic resorption. Histologically: the dental pulp is changed into granular tissue with presence of giant cells, which resorb dentin. Location: Type A&B- non perforated, Type C- perforated Type A: resorption in dental crown. The only clinical symptom

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can be a pink spot, which is the result of shining the richly vascularization granular tissue through the thin enamel without supporting dentin. On the radiograph the ampulla enlargement of chamber is observed. Type B: resorption in root canal wall. Type C: perforation of root dentin by granulation tissue. Diagnosis: occasionally radiograph taken. When the resorption decay is spread from labial or lingual root canal surface it is difficult to distinguish the internal resorption from external one based on radiograph. The affected teeth for a long time normally react on thermical and mechanical agents, asymptomatic course; in case of perforating resorption dental pulp is infected and necrotic. Management: Non-perforated (A,B): 1. Pulp removal and canal preparation: Coronal access modified or enlarged to allow greater penetration of the NaOCl. Copious irrigation with (NaOCl). Ultrasonic instrumentation coupled with high volume flushing. Interim CaOH if difficult to remove at 1st visit. 2. Canal obturation: Small or moderate defect: use vertical compaction with warm gutta-percha, thermoplasticized gutta-percha, or pressure syringe injection. Large defect: use same techniques with more pressure required. Near perforation: use same techniques with avoid excessive pressure, use CaOH-based root canal scaler. Perforated (C): Determined of perforation: Clinically: Continue hemorrhage after all the pulp has been removed. Blood in paper pints at side. Radiographically: Lateral radicular lesion at resorptive defect. Nonsurgical repair: defect is far apical to epithelial attachment. Technique: Calcium hydroxide paste into the canal until a hard-tissue barrier is formed, then obturation with MTA. Surgical repair: making a flap, area is curetted, cleaned and obturated with an alloy, composite resin, glass ionomer restoration or MTA. Perforating: a communication between the root canal and the periodontal ligament due to a perforation of the root by progressive internal resorption. It can be misdiagnosed as cervical external resorption when the perforating internal resorption is located in pulpal chamber. Replacement: irregular widening of dental cavity is observed. Histologically: dental pulp metaplasia into bone tissue is found. Resorption:

INTERNAL EXTERNALMargins Smooth and well-defined Rough & mouth-eatenSymmetric Symmetrical AsymmetricalCanal anatomy Altered + size Unaltered

X-ray projection: different horizontal beam angles

The relationship of the canal to the defect will remain the same, regardless of the angle

The relationship of the defect to the canal will shift as the horizontal angle of the beam is altered

Identification and differentiation:Internal: regular, round, outline of canal is distorted, centeredExternal: irregular, moth eaten outline of canal is normal, off centerExternal resorptionType Differential diagnosis Treatment PrognosisTransient – Surface

Small excavation is separated from bone by periodontal ligamentPulp is responsive

No treatment is necessary Excellent

Pressure Pulp is responsive Resorption stops when pressure is discontinued

Correction and discontinuance or pressureNo RCT

Excellent when etiologic pressure is discontinued

Type Differential diagnosis Treatment PrognosisReplacement - Ankylosis

There is no periodontal space at the resorptive siteMargins of the defect are irregularCanal maintains regular form Pulp responsiveness may vary depending on etiological injury

No predictable direction of therapyRCT usually neccesary owing to etiologic injury

Poor

Inflammatory

There is a radiolucency next to the resorptionMargin of the resorption varies from smooth to ragged but is not comparable to the irregular defect of

RCT Excellent

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ankylosis Multiple angulation x-ray films will shift lesion when superimposed over pulp.Canal maintains original form, tissue may be fluctuant or a fistula may be present owing to nonresponsive pulp.

Internal resorptionType Differential diagnosis Treatment PrognosisIntracanal resorption with no external perforation

Ampullar enlargement of pulp chamber or canalResorptive pulp during active phase

RCT Excellent

Intracanal resorption with infraosseus perforation

Ampullar enlargement extends to periodontal tissuesThere is a radiolucency at site of perforationPulp is nonresorptiveTissue may demonstrate fluctulance or fistula

Root canal debridementCa(OH)2 paste inserted into canal until tissues repair occursMTA inserted at the site of resorptionWell condensed filling of the canal and resorptive defect

Far to excellent depending on the quality of obturation of the canal space and resorptive defect

Type Differential diagnosis Treatment PrognosisIntracanal resorption with supraosseus perforation

Ampullar enlargement extends to or near the oral environment Periodontal breakdown extends to perforationPulp is nonresorptiveTissue may demonstrate fluctulance

RCT- root canal treatment & surgical repair

Depends on location surgical access and periodontal defect will repair

Extracanal invasive resorptionType Differential diagnosis Treatment PrognosisExtracanal invasive resorption

There is an irregular radiolucency within the tooth, often superimposed over pulp canalRadiolucency becomes more regular in advanced stageCanal maintains original formPulp remains responsive

RCT; Debridement of defect through coronal access opening with slow-speed round burFilling with loose mix of silver alloy, composite or GI or better with MTA

Poor to good depending on the quality to debride the defect and the quality of the filling

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