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periapical pathologies- pulpal origin

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Gurmeen Kaur

Introduction, Classification, Definition, Etiology, Clinical features, Radiographic features, Diagnosis, Differential diagnosis, Bacteriology, Histopathology, Treatment, prognosis of various periapical pathologies of endodontic origin

Health & Medicine
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PERIAPICAL PATHOLOGIES I M D S , D E PA R T M E N T O F C O N S E R VAT I V E D E N T I S T R Y A N D E N D O D O N T I C S , A B S H E T T Y M E M O R I A L I N S T I T U T E O F D E N TA L S C I E N C E S , M A N G A LO R E . DR GURMEEN KAUR
• Introduction • Periapical Anatomy In Health – Cementum • Types • Matrix – Periodontal Ligament • Cells • Extra cellular Matrix – Alveolar Bone • Parts • Matrix • Intraoral periapical radiograph
PERIRADICULAR LESIONS • PULPAL ORIGIN • Changes in tissues • Irritants – Living – Non-living • Radiographic changes • Histologic changes • Endodontic implications • FISH Zones – Zone of stimulation – Zone of irritation – Zone of contamination – Zone of infection • Role of Bacteria
• Diagnosis – History & discussion with patient – Clinical examination – Clinical tests – Radiographic examination – Correlation of history, clinical, radiographic & test findings – Treatment plan • Classification- – Grossman – WHO – Weine’s – Ingle’s – Clinical classification – Nair’s classification
ACUTE APICAL PERIODONTITIS • Apical periodontitis –WHO classification • Acute apical periodontitis – Definition – Synonyms – Etiology • Vital tooth • Non-vital tooth • Primary • Secondary – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Bacteriology – Histopathology – Treatment – prognosis – Outcome
ACUTE ALVEOLAR ABSCESS – Definition – Synonyms – Etiology – Clinical features – Systemic reactions – complications – Radiographic features – Diagnosis – Differential diagnosis – Bacteriology – Histopathology – Treatment • Incision to establish drainage • Root canal treatment • Antibiotic therapy – prognosis – Consequences of untreated abscess
PHOENIX ABSCESS – Definition – Etiology – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Bacteriology – Histopathology – Treatment – prognosis
CHRONIC APICAL PERIODONTITIS – Definition – Etiology – Clinical features – Radiographic features – Histopathology – Zones of well established granuloma – Microbiologic features – Treatment – Prognosis – Outcome – Case report
CHRONIC ALVEOLAR ABSCESS – Definition – Synonyms – Etiology – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Histopathology – Treatment – prognosis
APICAL PERIODONTAL CYST – Cyst – Apical periodontal cyst • Definition • Epithelial lining • Pathogenesis • Theories of cyst formation – Nutritional deficient theory – Abscess theory • Periapical pocket cyst • Periapical true cyst – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Bacteriology – Histopathology – Cystic lumen – Treatment • Surgical • Endodontic • marsupilisation – Prognosis – Healing • Periapical pocket cyst • Periapical true cyst – complications
CONDENSING OSTEITIS – Definition – Etiology – Clinical features – Radiographic features – Histopathology – Treatment – prognosis
EXTERNAL ROOT RESORPTION • Definition • Classification of root resorption – Internal – External • External surface resorption • External inflammatory root resorption • External replacement resorption • Radiographic appearance • Histopathology • Clinical features • Differential diagnosis • Management • Follow-up & prognosis
POST-TREATMENT APICAL PERIODONTITIS • Etiology • Management – Retreatment – Surgery • Technical aspects of endodontic retreatment • Case reports • Persistent apical periodontitis – Causes – Bacteriology • Periapical scar/ Surgical defect
HYPERCEMENTOSIS • Clinical features • Radiographic features • Factors associated • Histopathology • Treatment • Prognosis • Lesions with non-endodontic origin with vital pulp • Non endodontic periradicular lesions
• Summary – Conditions and diagnosis – Management of symptomatic conditions • Previously Asked Questions
PERIRADICULAR TISSUES
CEMENTUM • Mineralized, avascular connective tissue • Consists of three different types- – Acellular afibrillar cementum- cementoenamel junction. – Acellular extrinsic fiber cementum- coronal half of the root. – Cellular intrinsic fiber cementum - apical half of the root.
M A T R I X • Released under certain conditions- – cementoblast proliferation, – migration, – differentiation during cementum wound healing • Cementoblasts: – Osteoblast-like phenotype; – responsive to osteotropic signals: PTH/PTHrP. – Cementum attachment protein, cementum-derived growth factor, and PLAP-1 • Bone matrix proteins: osteocalcin, osteopontin, and bone sialoprotein Periodontium and Periodontal Disease. Insulin- like Growth Factor-1 IGF-1 Fibroblas t Growth Factors FGFs Epiderm al Growth Factor EGF Bone Morpho genetic Proteins BMPs Transfor ming Growth Factor-β TGF-β Platelet- derived Growth Factor PDGF
PERIODONTAL LIGAMENT • Soft, specialized connective tissue- connects the cementum to the alveolar bone. . HETEROGENOUS CELL POPULATION- Osteoblasts, Osteoclasts, Fibroblasts, Cementoblasts, Epithelial cell rests of Malassez, Macrophages, Undifferentiated mesenchymal cells (stem cells). • Fibroblasts, osteoblasts, and epithelial cells - differentiated cellsundergo limited cell divisions and proliferation upon stimulation by appropriate signals • Multipotent mesenchymal stem cellsdifferentiate into cementoblast- like cells and periodontal ligament cells,osteoblasts EXTRACELLULAR MATRIX- Collagen fibers, Fibronectin, Elastin, other noncollagenous proteins, and proteoglycans. • The ECM serves as stratum for cell adhesion and promotes cell spreading and cytoskeletal organization Shafer’s textbook of Oral Pathology, 7th edition
The collagen fibers (Sharpey fiber) of the periodontal ligament connect the tooth with the alveolar bone. • Highly vascularized and innervated. Epithelial cell rests of Malassez (ERM), the remnants of the Hertwig epithelial root sheath- present in PDL after root formation. • Nests of epithelial cells connected as a network; surrounded by a basal lamina. • ERM - stimulated to proliferate in apical periodontitis. • Cellular source - can form radicular cysts. Shafer’s textbook of Oral Pathology, 7th edition
ALVEOLAR BONE • Houses the sockets for the teeth. • Outer cortical plate, a central spongy or cancellous bone, and bone lining the sockets – Alveolar Bone Proper : lines the alveolus or the bony sockets that house the roots of the teeth. – Supporting Alveolar Bone : Cancellous(spongy) bone adjacent to the alveolar bone proper covered by 2 outer tables of compact bone. • Lamina Dura- compact bone that lies adjacent to the periodontal ligament. – Radiopaque line surrounding the tooth root • Bone matrix contains IGFs, TGF-β, BMPs, FGF, and PDGF. – Essential for osteoblast progenitor cell proliferation, migration, and differentiation during bone wound healing.Shafer’s textbook of Oral Pathology, 7th edition
INTRAORAL PERIAPICAL RADIOGRAPH
PERIRADICULAR PATHOLOGIES
Depending on the – nature, – quantity of irritants, – duration of exposure of the periradicular tissues, following changes can occur • Degenerative – Fibrous – Resorptive – Calcific • Proliferative Irritants from infected root canal Noxious products of tissue necrosis and antigenic agents in root canal. Periradicular tissues PERIRADICULAR LESIONS
• Physical irritation of periradicular tissues- Overinstrumentation, Impact trauma, Hyperocclusion, Endodontic procedures and accidents, Pulp extirpation, Root perforation, and Overextension of filling materials. Irritants Living Bacteria Bacterial toxins Bacterial fragments Viruses Non-living Mechanical Thermal Chemical REVERSIBLE tissue damage Short-lived Self- limiting Transient, Mild to moderate injuries Destruction of periradicular tissues. Nonspecific and Specific Immunologic reactions can cause Persistent, Severe injuries
RADIOGRAPHICALLY Radiographically- Radiolucent areas around the portal(s) of exit of the main canal or lateral and/or accessory canals.
HISTOLOGICALLY Depending on their stage of development the periradicular pathologic tissues contain – polymorphonuclear neutrophils, – lymphocytes, – plasma cells, – macrophages, – mast cells, – immunoglobulins IgG, IgA, IgM,IgE, – complement. Reactions that may occur- • Anaphylactic, • Cytotoxic, • Antigen–antibody Complex, • Delayed Hypersensitivity.
PERIRADICULAR LESIONS OF PULPAL ORIGIN
ENDODONTIC IMPLICATIONS • Fish: Described the reaction of the periradicular tissues to noxious products of tissue necrosis, bacterial products, and antigenic agents from the root canal. • Experimental foci of infection in the jaws of guinea pigs by drilling openings in the bone and packing in wool fibers saturated with a broth culture of microorganisms. • Four well-defined zones of reaction were found: – Zone of infection – Zone of contamination – Zone of irritation – Zone of stimulation
Grossman’s endodontic practice: 11th edition Characterized by fibroblasts and osteoblasts. Periphery: Toxin mild enough to be a stimulant. Response: Collagen fibers laid down by fibroblasts Role of Collagen: as a wall of defense around the zone of irritation and as a scaffolding on which the osteoblasts built new bone. New bone- built in irregular fashion. Zone of Stimulation Characterized by macrophages and osteoclasts. Fish found evidence of irritation further from the central lesion as the toxins became more diluted. Distinguished by small, round cells, normal bone cells and osteoclasts could just about survive. The collagen framework was digested by phagocytic cells, the macrophages, while osteoclasts attacked the bone tissue. Histologic picture- body’s attempt to initiate repair. Zone of Irritation Characterized by round cell infiltration. Cellular destruction around the central zone from toxins discharged from the central zone. Toxins: Either tissue breakdown products or exotoxins. Dead bone cells- undergone autolysis, lacunae appeared empty. Lymphocytes: prevalent everywhere. Zone of Contamination Characterized by polymorphonuclear leukocytes. Infection- present in the center of the lesion, and microorganisms were found only in that area. The only microorganisms not disposed of by polymorphonuclear leukocytes were found in Haversian canals or in fissures in the bone matrix made by the bur. Zone of Infection
Zone of Infection Root canal Zone of Contamination: Microorganisms- multiply sufficiently to grow or the metabolic products or the toxic products of tissue necrosis get diffused to the periradicular tissues. Periradicular area- they are destroyed by the polymorphonuclear leukocytes. Microorganisms overwhelm the defensive mechanism Periradicular Lesion Zone of Irritation: Polymorphonuclear leukocytes destroy the microorganisms . The result is a chronic abscess. The toxic products of the microorganisms + the necrotic pulp in the root canal + dead polymorphonuclear leukocytes  irritate and destruct the periradicular tissue + produce pus. Zone of Stimulation Periphery of the destroyed area of osseous tissue toxic bacterial products- diluted enough  act as a stimulant. form granuloma. Fibroblasts fibrous tissue, osteoblastssclerotic bone. Epithelial rests of Malassez stimulated Cyst Grossman’s endodontic practice: 11th edition
ROLE OF BACTERIA Kakehashi et al. 1965 • Role of bacteria in progression of pulp and periapical diseases. • Pulp degeneration and necrosis following unrestored exposures to the oral environment in germ-free and germ- containing rats only developed when bacteria were present and they were able to contaminate the tooth and the pulp space. Korzen et al. • Bacterial invasion of the root canal Periapical tissue reactions periapical tissues not inflamed until root canal is infected. • Micro-organisms along entire length of root canal severe periapical inflammatory reaction • Limited inoculum  limited periapical tissue reaction. Sundqvist • Periapical lesions were found in 18 of 19 cases where microbes were present in the canal • Size of the periapical radiolucency was directly related to the number of strains that could be isolated from the affected tooth. Paul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics
THE GENERAL STAGES OF DISEASE PROGRESSION IN ANY TISSUE AS A RESULT OF A STIMULUS OR IRRITANT THAT IS NOT REMOVED OR TREATED Paul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics 2004, 8, 36–54
DIAGNOSIS
Procedure Result 1. History and discussion with patient Medical history Dental history Description of presenting complaint Details of any previous treatment of presenting complaint Provisional diagnosis of presenting condition 2. Clinical Examination Extra-oral signs Intra-oral signs Individual tooth assessment Restoration assessment Assess possible causative factors Provisional diagnosis of tooth status 3. Clinical Tests Pulp sensibility tests Percussion, mobility, palpation Provisional diagnosis of the status of the and/or the root canal system Provisional diagnosis of the periapical status 4. Radiographic Examination Confirm/assess causative factors Provisional diagnosis of periapical status 5. Correlation of the history, clinical, radiographic and test findings DEFINITIVE DIAGNOSIS - Pulp, root canal and periapical status - Cause(s) of the diseases TREATMENT PLAN Investigation/restoration removal Reassessment of the tooth and its prognosis Confirm the definitive diagnosis and cause(s) Finalize and continue the treatment plan
CLASSIFICATION OF PERIRADICULAR PATHOLOGIES
GROSSMAN’S CLASSIFICATION Symptomatic periradicular diseases Symptomatic apical periodontitis Vital tooth Nonvital tooth Acute alveolar abscess Acute exacerbation of asymptomatic apical periodontitis (phoenix abscess) Asymptomatic periradicular diseases Asymptomatic apical periodontitis Chronic alveolar abscess Radicular cyst Condensing osteitis External root resorption Persistent apical periodontitis Diseases of the periradicular tissues of nonendodontic origin
WHO CLASSIFICATION CODE NUMBER CATEGORY K04.4 Acute apical periodontitis K04.5 Chronic apical periodontitis (apical granuloma) K04.6 Periapical abscess with sinus (dentoalveolar abscess with sinus, periodontal abscess of pulpal origin)K04.60 Periapical abscess with sinus to maxillary antrum K04.61 Periapical abscess with sinus to nasal cavity K04.62 Periapical abscess with sinus to oral cavity Ko4.63 Periapical abscess with sinus to skin Ko4.7 Periapical abscess with out sinus Ko4.8 Radicular cyst(apical periodontal cyst, periapical cyst) Ko4.80 Apical & Lateral cyst Ko4.81 Residual cyst Ko4.82 Inflammatory Paradental cyst
WEINE’S CLASSIFICATION Painful pulpoperiapical pathosis Incipient acute apical periodontitis Advanced acute apical periodontitis Acute Periapical abscess Phoenix abscess Subacute Periapical abscess Non painful Periapical pathosis Condensing ostestis Incipient chronic apical periodontitis Advanced chronic apical periodontitis Periapical granuloma Chronic Periapical abscess Periapical cyst
INGLE’S CLASSIFICATION Painfulpulpoperiapicalpathosis Acute apical periodontitis Advanced acute apical periodontitis Acute apical abscess Phoenix abscess Suppurative apical periodontitis Nonpainfulpulpoperiapicalpathosis Condensing ostetis Chronic apical periodontitis Incipient Advanced Chronic apical periodontitis Periapical granuloma Apical cyst Suppurative apical periodontitis
CLINICAL CLASSIFICATION OF THE STATUS OF THE PERIRADICULAR TISSUES World Health Organisation. Application of the International Classification of Diseases to dentistry and stomatology, 3rd edn. Geneva: WHO, 1995: 66–67. Facial cellulitis Extra-radicular infection Foreign body reaction Periapical scar External root resorption Surface Inflammatory Replacement Invasive Pressure Orthodontic Physiological Clinically normal periapical/periradicul ar tissues Apical periodontitis Acute Primary Secondary (or acute exacerbation) Chronic Granuloma Condensing osteitis Periapical cyst True cyst Pocket cyst Periapical abscess Acute Primary Secondary Chronic
• Nair’s criteria included – the distribution and type of inflammatory cells within the lesion, – the presence or absence of epithelial cells, – whether the lesion had transformed into a cyst and, – if so, the relationship of the cyst-cavity to the apical foramen of the root canal of the affected tooth. Nair PNR. Apical periodontitis: a dynamic encounter between root canal infection and host response. Periodontology 2000 1997: 13: 121–148 Periapical Radiolucencies Acute Apical Periodontitis Primary Secondary Chronic Apical Periodontitis Apical Abscess Acute Chronic Periapical Cyst True Pocket
ACUTE APICAL PERIODONTITIS
APICAL PERIODONTITIS • Inflammation of the periodontal ligament around the root apex • Resorption of the periapical bone , root apex. - Acute depending upon the virulence of the microorganisms involved - Chronic the type and severity of the physical or chemical irritants, And host resistance • Common causes – Spread of infection following pulp necrosis, – Occlusal trauma from a high restoration or biting suddenly on a hard object, – Inadvertent endodontic procedures • Over instrumentation, • Pushing the infected material into the apical portion • Chemical irritation from root canal medicamentsPaul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics 2004, 8, 36–54
The World Health Organization has classified apical periodontitis in five categories: • Acute apical periodontitis of pulpal origin • Chronic apical periodontitis of pulpal origin • Periapical abscess with sinus • Periapical abscess without sinus • Radicular cysts Paul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics 2004, 8, 36–54
ACUTE APICAL PERIODONTITIS Painful inflammation of the periodontium as a result of trauma, irritation, or infection through the root canal, regardless of whether the pulp is vital or nonvital, producing clinical symptoms including painful response to biting and percussion. history of previous pulpitis. • Symptomatic Apical Periodontitis. Grossman’s endodontic practice: 11th edition
ETIOLOGY Vital tooth Occlusal trauma • Abnormal occlusal contacts • Recently inserted restoration extending beyond the occlusal plane • Wedging of a foreign object between the teeth, such as a toothpick or food • Traumatic blow to the teeth Nonvital tooth. Sequelae of pulpal diseases • Diffusion of bacteria and noxious products from inflamed or necrotic pulp Iatrogenic causes : • Root canal instrumentation forcing bacteria or debris inadvertently through the apical foramen • Forcing of irritating irrigants or medicaments through the apical foramen • Extension of obturating material through the apical foramen to impinge on periradicular tissues • Perforation of the root • Overinstrumentation during shaping and cleaning of root canals Grossman’s endodontic practice: 11th edition
Paul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics 2004, 8, 36–54
CLINICAL FEATURES • Pain and tenderness of the tooth. • Slightly sore ~ Sometimes only when it is percussed in a certain direction – Or the soreness may be severe. • The tooth may feel extruded and the patient may have pain on closure and mastication. • The tooth is slightly elevated in its socket – Due to the collection of inflammatory edema in the periodontal ligament – Causes tenderness while biting or even to mere touch. • Thermal change does not induce pain as in pulpitie • External pressure on tooth forces the edema fluid against already sensitized nerve endings  severe pain. Grossman’s endodontic practice: 11th edition
• symptoms are either the result of – irritation originating from endodontic treatment – caused by overinstrumentation, – medicinal irritants, – overfilling, in which case the tooth is pulpless, – result of noxious stimuli irritating the periodontal ligament, in which case the pulp is vital.
RADIOGRAPHIC APPEARANCE Trauma Abnormal Occlusal Contacts Orthodontic Treatment Nonvital tooth: A slight widening of the apical periodontal ligament space and loss of the apical lamina dura of the involved pulpless tooth may be seen Vital tooth: No radiographic changes with normal periradicular structures Grossman’s endodontic practice: 11th edition
Periodontitis caused due to carious exposure Grossman’s endodontic practice: 11th edition
DIAGNOSIS • Look for decay, fracture lines, swelling, sinus tracts, orientation of tooth, hyperocclusion Visual • mucosa overlying the root apex: may or may not be tender to palpation. Tooth: tender on percussion or slight pressure • Moderate mobility- check for periodontal condition Mobility: slight to no mobility • Response not prolonged- consider traumatic occlusion • Response prolonged- irreversible pulpitis • No response- necrotic pulp Thermal test • Response- pulp is vital • No response- pulp non vital Electric pulp testing Grossman’s endodontic practice: 11th edition
DIFFERENTIAL DIAGNOSIS • Acute alveolar abscess – represents a further stage in development of disease – breakdown of periradicular tissue,. • The patient’s history, symptoms, and clinical test results help the clinician to differentiate these diseases. Grossman’s endodontic practice: 11th edition
HISTOPATHOLOGY Acute trauma Transient inflammation • neutrophils release stimulate osteoclasts resorb the surrounding bone detectable periapical radiolucency Inflammatory reaction in pdl Dilation of blood vessels infiltration with polymorphonuclear leukocytes transmigration from the blood vessels into perivascular tissue space Accumulation of serous exudate Distension of Pdl & extrusion of tooth, slight tenderness If continuous irritation occurs, loss of alveolar bone
BACTERIOLOGY • Blow, occlusal trauma, or chemical or mechanical irritation during endodontic treatment.  The pulp and periradicular tissues may be sterile • Bacteria or toxic bacterial products present in the root canal may either be forced through or grow beyond the apical foramen and may irritate the apical periodontal tissues Grossman’s endodontic practice: 11th edition
TREATMENT AND PROGNOSIS Immediate line of management Determining the cause and relieving the Symptoms Occlusal trauma Relieved by selective occlusal grinding. Non vital infected pulp Endodontic treatment to drain the exudate. When the acute phase has subsided, the tooth is treated by conservative means. Prognosis: Generally favorable. The occurrence of symptoms during endodontic treatment in no way affects the ultimate outcome of the treatment
OUTCOME Paul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics 2004, 8, 36–54
ACUTE ALVEOLAR ABSCESS
ACUTE ALVEOLAR ABSCESS An inflammatory reaction to pulpal infection and necrosis characterized by rapid onset, spontaneous pain, tenderness of the tooth to pressure, pus formation, and eventual swelling of associated tissues. • Synonyms: Acute abscess, acute apical abscess, acute dentoalveolar abscess, acute periapical abscess, and acute radicular abscess.
ETIOLOGY • Bacterial invasion of dead pulp tissue. • Trauma • chemical or mechanical irritation • Because the pulp tissue is solidly enclosed, no drainage is possible and the infection continues to extend in the direction of least resistance, i.e., through the apical foramen, and thereby involves the periodontal ligament and the periradicular bone.
CLINICAL FEATURES • Purulent material accumulates within alveolusSymptomatic • Tenderness: • Relieved by continued slight pressure on the extruded tooth to push it back into the alveolus First symptom • Spontaneous, severe, throbbing pain, exacerbated by lying down with attendant swelling of the overlying soft tissue. Later • More pronounced, extends beyond original site. • Tooth: more painful, elongated, and mobile. • At times, the pain may subside or cease entirely while the adjacent tissue continues to swell. Swelling • Infection progresses to chronic apical abscess  Contained pus may break through to form a sinus tract, opening in labial or buccal mucosa. If left unattended • osteitis, periosteitis, cellulitis, or osteomyelitis. May further progress • Adjacent tissues close to the affected tooth. • Extensive  cellulitis may distort the patient’s appearance grotesquely. Swelling Grossman’s endodontic practice: 11th edition
Maxillary teeth: drain through buccal or palatal bone into oral cavity or maxillary sinus or the nasal cavity. Anterior tooth: cuspid swelling of the upper lip may extend to one or both the eyelids.Posterior tooth  the cheek may swell to an immense size, distorting the patient’s facial features Mandibular teeth: drain through the buccal or lingual bone into the oral cavity. Anterior tooth swelling can involve the lower lip and chin, and in severe cases, the neck. Posterior tooth swelling of the cheek may extend to the ear or even around the border of the jaw into the submaxillary region Infectious process extend into fascial spaces of the head and neck  cellulitis and systemic signs and symptoms, with consequent complications. Grossman’s endodontic practice: 11th edition José F. Siqueira, Jr., Isabela N. Rôças . Microbiology and Treatment of Acute Apical Abscesses. Clinical Microbiology Reviews, April 2013;26 (2):255-273
(A) An individual with spread acute apical abscess. (B) A bone radiolucent lesion is visible around the root apexes of the mandibular second molar, which is the source of infection. (C) Incisional drainage is essential for management of these conditions. In this complicated case, it was performed extraorally. • (Courtesy of Craig Baumgartner.) José F. Siqueira, Jr., Isabela N. Rôças . Microbiology and Treatment of Acute Apical Abscesses. Clinical Microbiology Reviews, April 2013;26 (2):255-273
• Swelling : taut and inflamed; • Pus formation : liquefaction  proteolytic enzymes: trypsin and cathepsin. • Pressure of the underlying pus rupture from pressure  extrude through a tiny opening beginning of a chronic alveolar abscess. • Elimination of the infection  Sinus tract: heals by granulation Grossman’s endodontic practice: 11th edition
SYSTEMIC REACTIONS • Pt may appear pale, irritable & weakened due to pain & loss of sleep. • Mild cases- slight rise in temp (99-100˚C) • Severe cases- temp above normal (102-103˚C) • Fever: preceded or accompanies by chills. • Intestinal stasis: orally- coated tongue & foul breath. • Headache & malaise Grossman’s endodontic practice: 11th edition
COMPLICATIONS • 60% of all nontraumatic dental emergencies are associated • Mortality: result of sepsis or airway obstruction, but death due to a spreading infection leading to massive hemorrhage from the subclavian vein into the pleural cavity has been reported. • Fascial plane infections- – Sublingual, Submandibular, Buccal, Pterygomandibular spaces, Temporal – Masseteric, Lateral pharyngeal, Retropharyngeal • Brain abscess • Septicemia in a patient with multiple myeloma • deep neck infection • Mediastinitis • necrotizing fasciitis • orbital abscess • cervical spondylodiscitis with spinal epidural abscess • Host-related factors: Contribute toward increased morbidity and mortality diabetes, chronic alcohol and tobacco consumption, malnourishment, and the use of illicit substances
RADIOGRAPHIC FEATURES • Acute reaction - develops very quickly • May not show radiographic evidence of periradicular bone destruction. • Radiographic periradicular radiolucency: abscess is result of exacerbation of a previous chronic asymptomatic condition • Thickening of the apical periodontal ligament • Ill-defined radiolucency Zcm, nevilleOral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
DIAGNOSIS • clinical examination and from the subjective history. • Early stages: difficult to locate the tooth because of the absence of clinical signs and the presence of diffuse, annoying pain. • Progressed infection periodontitis & extrusion tooth easily located • Radiograph: Cavity / defective restoration / slight widening of the apical periodontal ligament space of the involved tooth. • No response to cold, heat or EPT • tender to percussion, Pain while chewing • Apical mucosa: tender to palpation Grossman’s endodontic practice: 11th edition
DIFFERENTIAL DIAGNOSIS • Periodontal abscess : – Infection from periodontium accumulation of pus along the root surface – Periodontal pocket ; swelling and mild pain. – Pressure pus may exude near the edematous tissue or through the sulcus. – Swelling : opposite the midsection of the root and gingival border – Generally associated with vital tooth • Tests for pulp vitality are useful in establishing a correct diagnosis.
BACTERIOLOGY • Concentration of microorganisms: unusually large. • Total bacterial loads per abscess case have been reported to range from 104 to 109 cells • Streptococci and staphylococci are generally recovered • Draining purulent material  Sterile : dead leukocytes, dead bacteria. • An analysis of 100 consecutive cases of acute alveolar abscess failed to show a relationship between any specific type of organism and the abscess. José F. Siqueira, Jr., Isabela N. Rôças . Microbiology and Treatment of Acute Apical Abscesses. Clinical Microbiology Reviews, April 2013;26 (2):255-273
José F. Siqueira, Jr., Isabela N. Rôças . Microbiology and Treatment of Acute Apical Abscesses. Clinical Microbiology Reviews, April 2013;26 (2):255-273
HISTOPATHOLOGY • Active infection  Marked infiltration of polymorphonuclear leukocytes; rapid accumulation of inflammatory exudate  distention of PDL  elongation of tooth. • Periodontal fibers separate  mobility. • Bone resorption at root apex- polymorphonuclear leukocytes die X microorganisms Pus • Microscopically: suppuration empty space; surrounded by viable leukocytes, occasional lymphocytes, cellular debris, necrotic materials and bacterial colonies. • Root canal: appears devoid of tissue,; clumps of microorganisms and debris may be observed • Dilatation of the blood vessels in PDL & marrow spaces of the bone. • Marrow spaces- inflammatory cell infiltrate. • Tissue around area of suppuration: serous exudate. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition Shafer’s textbook of Oral Pathology, 7th edition
TREATMENT • Incision for drainage • Root canal treatment or extraction of the involved tooth to remove the source of infection • Decisive triad for the successful management of complications of acute dental abscesses – early diagnosis, – initiation of empirical antibiotic therapy, and – timely surgical intervention Grossman’s endodontic practice: 11th edition
I) Immediate task: Relieve pressure  drainage opening up the pulp chamber. • Gaining access - difficult - tooth is often extremely tender. • Gently grip the tooth - use small, round, diamond bur • Immediate relief - pus drains feely from an access cavity. • If drainage is not immediate- explore apical foramen with very fine (size 08 or 10) file. – Foramen not be instrumented or enlarged, and if drainage does not result the procedure should not be persevered. Endodontics: Part 3. Treatment of endodontic emergencies. P. Carrotte. BRITISH DENTAL JOURNAL VOLUME 197 NO. 6 SEPTEMBER 25 2004
INCISION TO ESTABLISH DRAINAGE • Soft-tissue swelling Pointing intra-orally Incision. • Use of copious amounts of surface analgesia. – Regional anaesthesia may not be effective due to the presence of pus. – local analgesic solution may spread the infection further into the tissues. • Incise the swelling with a Bard Parker No. 11 or 15 scalpel blade • Aspirate using a wide bore needle and disposable syringe. It may be possible to aspirate the abscess via the root canal as well. • Sample can be sent for bacteriological examination • Drain: piece of quarter-inch or half-inch selvage gauze may be used. • Same criteria when extra-oral drainage is indicated. Endodontics: Part 3. Treatment of endodontic emergencies. P. Carrotte. BRITISH DENTAL JOURNAL VOLUME 197 NO. 6 SEPTEMBER 25 2004
TREPHINATION • In the absence of swelling • Surgical perforation of the alveolar cortical plate. • to release the accumulated inflammatory and infective tissue exudate from between the cortical plates • Engine-driven perforator entering through the cortical  cancellous bone – without the need for an incision, – provide pathway for drainage from the periradicular tissues. • Care to guard against injury to the tooth root or surrounding structures Cohen’s Pathways of the Pulp,11th edition
ROOT CANAL TREATMENT Access and initial drainage; Isolation using rubber dam Irrigation: Sodium hypochlorite remove superficial organic and inorganic debris considerable pain relief. Ultrasonically activated endodontic files - effectively flush infected debris from the root canal system.. Do not to push necrotic debris beyond the apex – • Positive-pressure irrigation methods- needle-and-syringe irrigation: risk of expressing debris or solution out of the apex. • Electronic apex locators- accuracy in determining working length measurements  thorough canal debridement and less apical extrusion. • Crown-down instrumentation- remove most of the debris coronally rather than pushing it out the apex Endodontics: Part 3. Treatment of endodontic emergencies. P. Carrotte. BRITISH DENTAL JOURNAL VOLUME 197 NO. 6 SEPTEMBER 25 2004
Canals dried with paper points Dry sterile cotton wool pledget placed in the pulp chamber to prevent ingress of the temporary dressing. Access cavity sealed to prevent re-infection of the canals from the oral cavity. Patient must be recalled within 48 hours complete instrumentation ; Intracanal calcium hydroxide dressing
ANTIBIOTICS • Not necessary in most cases of localized and uncomplicated apical abscesses. • Analgesics: pain control. • Antibiotics are indicated – abscesses associated with systemic involvement, including fever, malaise, and lymphadenopathy; – disseminating infections resulting in cellulitis, progressive diffuse swelling, and/or trismus; – abscesses in medically compromised patients who are at increased risk of a secondary (focal) infection following bacteremia. Endodontics: Part 3. Treatment of endodontic emergencies. P. Carrotte. BRITISH DENTAL JOURNAL VOLUME 197 NO. 6 SEPTEMBER 25 2004
Penicillins : first choice for treatment of endodontic infections •Most of the bacterial species involved with endodontic infections, including abscesses, are susceptible to penicillins •Penicillin V or amoxicillin •Amoxycillin: 250 mg three times a day until the infection is under control Amoxicillin + Clavulenic acid/ Metronidazole (the spectrum of action extended to include penicillin- resistant Strains) Metronidazole: alternative where the penicillins are contraindicated. Clindamycin: strong antimicrobial activity against oral anaerobes •effective alternative in patients allergic to penicillin or when treatment with amoxicillin resulted in failure. Moxifloxacin: fluoroquinolone- good antibacterial activity against Gram-positive and Gram-negative aerobic and anaerobic bacteria isolated from odontogenic infections •A clinical trial : significantly better pain reduction and overall clinical response than clindamycin for patients with dental abscesses Oral cephalosporins and macrolides: little use- decreased activity against Fusobacterium and nonpigmented Prevotella species José F. Siqueira, Jr., Isabela N. Rôças . Microbiology and Treatment of Acute Apical Abscesses. Clinical Microbiology Reviews, April 2013;26 (2):255-273
• Facial photographs. (A) Preoperative. (B) A decrease in inflammation is observed two days after the first treatment appointment. (B) Postoperative. (D) Follow-up at 16 months • Radiographic examination. (A) Preoperative. (B) Postoperative. Follow-up at (C) 1 month and (D) 16 months. Jesús Alejandro Quiñones Pedraza, Maria Argelia Akemi Nakagoshi Cepeda, Jorge Jaime Flores Treviño, Idalia Rodriguez Delgado, Sergio Eduardo Nakagoshi Cepeda and Rosalva González Meléndez . Endodontic management of acute apical abscess: A case report. International Journal of Applied Dental Sciences 2017; 3(4):
PROGNOSIS • The prognosis for the tooth is generally favorable, depending on the degree of local involvement and the amount of tissue destruction. Although the symptoms of an acute alveolar abscess may be severe, pain and swelling generally subside if adequate drainage is established. • In most cases, the tooth can be saved by endodontic treatment, and the severity of the symptoms need not bear any relation to the ease or difficulty of treatment. • When purulent material has been discharged through the gingival sulcus and the periodontium has been extensively destroyed, the prognosis is guarded. In selected cases, combined periodontal and endodontic treatment will restore the tooth to functional health. Grossman’s endodontic practice: 11th edition
CONSEQUENCES OF UNTREATED ABSCESS Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition • With progression, the abscess spreads along the path of least resistance. • The purulence may extend through the medullary spaces away from the apical area, osteomyelitis, • it may perforate the cortex and spread diffusely through the overlying soft tissue  cellulitis • Perforation of cortical plate  permits entrance into the oral cavity sessile swelling or drain through an intraoral sinus  a mass of subacutely inflamed granulation tissue  parulis
PERIAPICAL PATHOLOGIES
PHOENIX ABSCESS – Definition – Etiology – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Bacteriology – Histopathology – Treatment – prognosis
CHRONIC APICAL PERIODONTITIS – Definition – Etiology – Clinical features – Radiographic features – Histopathology – Zones of well established granuloma – Microbiologic features – Treatment – Prognosis – Outcome – Case report
CHRONIC ALVEOLAR ABSCESS – Definition – Synonyms – Etiology – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Histopathology – Treatment – prognosis
APICAL PERIODONTAL CYST – Cyst – Apical periodontal cyst • Definition • Epithelial lining • Pathogenesis • Theories of cyst formation – Nutritional deficient theory – Abscess theory • Periapical pocket cyst • Periapical true cyst – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Bacteriology – Histopathology – Cystic lumen – Treatment • Surgical • Endodontic • marsupilisation – Prognosis – Healing • Periapical pocket cyst • Periapical true cyst – complications
CONDENSING OSTEITIS – Definition – Etiology – Clinical features – Radiographic features – Histopathology – Treatment – prognosis
EXTERNAL ROOT RESORPTION • Definition • Classification of root resorption – Internal – External • External surface resorption • External inflammatory root resorption • External replacement resorption • Radiographic appearance • Histopathology • Clinical features • Differential diagnosis • Management • Follow-up & prognosis
POST-TREATMENT APICAL PERIODONTITIS • Etiology • Management – Retreatment – Surgery • Technical aspects of endodontic retreatment • Case reports • Persistent apical periodontitis – Causes – Bacteriology • Periapical scar/ Surgical defect
HYPERCEMENTOSIS • Clinical features • Radiographic features • Factors associated • Histopathology • Treatment • Prognosis • Lesions with non-endodontic origin with vital pulp • Non endodontic periradicular lesions
• Summary – Conditions and diagnosis – Management of symptomatic conditions • Previously Asked Questions
PHOENIX ABSCESS
ACUTE EXACERBATION OF ASYMPTOMATIC APICAL PERIODONTITIS • Named after the mythical bird that would die, only to arise again from its own ashes. • In progressive periapical granulomas, the enlargement often is not continuous but occurs in spurts associated with periodic acute exacerbations. • Etiology 1.When state of equillibrium in granuloma /cyst is upset by: • Influx of bacteria/necrotic products of high virulence and antigenicity • Lowering of host defenses 2. Mechanical irritation during RCT. Acute inflammatory reaction superimposed on an existing asymptomatic apical periodontitis.
CLINICAL FEATURES • exacerbated and exaggerated pain. • may or may not be associated with pus & suppuration • Initially, tooth may be tender on palpation. • Loss of Vitality • As inflammation progresses, tooth gets elevated from the socket & becomes sensitive. • Mucosa over the radicular area may appear red & swollen & sensitive to palpation. • Most commonly associated with initiation of root canal therapy. • Mobility may be observed Endodontics: Part 3. Treatment of endodontic emergencies. P. Carrotte. BRITISH DENTAL JOURNAL VOLUME 197 NO. 6 SEPTEMBER 25 2004
DIAGNOSIS • Associated with the initiation of root canal therapy in a completely asymptomatic tooth. • The radiograph shows a well- defined periradicular lesion • History of trauma  discoloring of the tooth ; postoperative pain that had subsided until then. • Negative response to vitality tests: necrotic pulp. – Rare occasions- +ve electric pulp test  fluid in the root canal or in a multirooted tooth. Grossman’s endodontic practice: 11th edition
DIFFERENTIAL DIAGNOSIS • symptoms similar to those of an acute alveolar abscess. • Because the treatment of both lesions is the same, no differential diagnosis is needed. • Pulp vitality: Painful pulpitis • Acute alveolar : widening of the periodontal ligament space is the only radiographic change seen. Grossman’s endodontic practice: 11th edition
BACTERIOLOGY • An abscess usually forms as a result of microbial infection, although some abscesses, called sterile abscesses, form in the absence of bacteria. • The periradicular lesions are usually devoid of bacteria, except for transient bacteria. Grossman’s endodontic practice: 11th edition
HISTOPATHOLOGY • Phoenix abscesses can maintain a soft tissue component; • Subacutely inflamed periapical granulomas or cysts intermixed with areas of significant abscess formation. • In these cases the pathologist typically diagnoses the primary lesion but comments about the abscess formation. • Areas of liquefaction necrosis + disintegrating polymorphonuclear neutrophils and cellular debris (pus) • Surrounded by infiltration of macrophages; some lymphocytes and plasma cells. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition Grossman’s endodontic practice: 11th edition
TREATMENT AND PROGNOSIS • Same as acute alveolar abscess. • The prognosis for the tooth is good once the symptoms have subsided Grossman’s endodontic practice: 11th edition
CHRONIC APICAL PERIODONTITIS
Asymptomatic apical periodontitis is the symptomless sequelae of symptomatic apical periodontitis and is characterized radiographically by periradicular radiolucent changes and histologically by the lesion dominated with macrophages, lymphocytes, and plasma cells. • Low-grade infection; Most common sequelae of pulpitis or acute periapical periodontitis. • If the acute process is left untreated, it is incompletely resolved and becomes chronic proliferative. • Spread of pulp infection - usually- periapical direction. • Lateral or accessory root canals opening on the lateral surface of the root at any level - ‘lateral’ granuloma or related inflammatory lesion.
CLINICAL FEATURES • nonvital • slightly tender to percussion • Percussion- dull sound • mild pain on biting or chewing on solid food • the tooth feels slightly elongated in its socket • Sensitivity- due to hyperemia, edema, and inflammation of the apical periodontal ligament. Many cases are entirely asymptomatic. No perforation of overlying bone and oral mucosa with the formation of a fistulous tract unless the lesion undergoes an acute exacerbation.
RADIOGRAPHIC FEATURES • Earliest periapical change -thickening of the ligament at the root apex. • Radiolucent area of variable size - attached to the root apex: Well- circumscribed, definitely demarcated from the surrounding bone. • Thin radiopaque line  a zone of sclerotic bone may sometimes be seen outlining the lesion  periapical lesion is a slowly progressive and long standing one that has probably not undergone an acute exacerbation • Thickening of the apical periodontal membrane - large carious lesion involving the dental pulp Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
• Periapical radiolucencies destruction of bone and replacement by granulation tissue. (A) maxillary central incisor: carious lesion of the distal surface that involves the pulp. (B) mandibular incisors: traumatic injury with loss of pulp vitality and subsequent formation of diffuse periapical granulomata. • Periphery: Diffuse blending of the radiolucent area with the surrounding bone. – Due to the difference in cellular activity around the margins of the lesion • Root resorption- occasionally observed. Shafer’s Textbook of Oral Pathology, 7th edition
HISTOPATHOLOGY • Chronic process from the onsetdoes not pass through acute phase. • Hyperemia and edema of the PDL; infiltration of chronic inflammatory cells. • Inflammation + Increased vascularity  resorption of the supporting bone proliferation of fibroblasts and endothelial cells formation of more tiny vascular channels & numerous delicate connective tissue fibrils. • Homogeneous lesion: – predominantly of macrophages, lymphocytes, and plasma cells – less frequently with mast cells and eosinophils, – qualifies as an immune-type granuloma. • Athanassiades and Spears, and Page et al.: – more lymphocytes and plasma cells than non-immune granulomas relatively pure collections of macrophages and giant cellsShafer’s Textbook of Oral Pathology, 7th edition
Typical periapical granuloma: (A) delicate fibrillar stroma with intense lymphocytic and plasma cell infiltration (A) polymorphonuclear leukocytes as well as many small capillaries (B) Collections of macrophages that are often filled with lipoid material (C) Cholesterol slits in the tissue (D) Surrounded by a connective tissue ‘capsule’ Shafer’s Textbook of Oral Pathology, 7th edition
Shafer’s textbook of Oral Pathology, 7th edition
• Majority of the small lymphocytes (81%) was designated non-B lymphocytes. • Plasma cells contained Russell bodies, some of which were subsequently extruded and could be found extracellularly. • The non-B lymphocytes  T cells of the cellular arm of the immune system, expression of delayed type hypersensitivity. • T cell activity bone and tooth resorption through the production of osteoclast activating factor (OAF). • Presence of antibody-producing lymphocytes and plasma cells- antibodies - specificity provide clues to the antigens causes of periapical granulomas and cysts • Macrophages and other mononuclear phagocytes are the hallmarks • Dendritic cells – Kaneko T et al: associated with local defense reactions as stronger antigen presenting than macrophages. Shafer’s textbook of Oral Pathology, 7th edition
• Phagocytes- ingest lipid material Foam cells • Abundant mast cells. • Deposits of cholesterol as well as hemosiderin  derived from the breakdown of extravasated red blood cells. • Cholesterol crystals : clear needle like spaces or clefts – associated with multinucleated giant cells of the foreign body type
Giant-cell hyaline angiopathy. • described by Dunlap and Barker • consists of inflammatory cell infiltration, collections of foreign body type giant cells, and the presence of ring like structures known as Rushton bodies, composed of an eosinophilic material resembling hyalinized collagen. • King and Mincer et al.: Fragments of foreign material, sometimes resembling vegetable matter such as legumes pulse granuloma’ • Dunlap and Barker : Earliest change - acute vasculitis with subsequent thickening and hyalinization of vessel walls. – Not confined to periapical granulomas – Reported in granulomas in edentulous jaws, in a nasopalatine duct cyst, and in chronic periostitis. • Chen and his colleagues : endogenous in origin- studied by both electron microscopy and immunoperoxidase procedure. Shafer’s textbook of Oral Pathology, 7th edition
ZONES OF WELL ESTABLISHED GRANULOMA
MICROBIOLOGIC FEATURES • Pre-extraction cultures: – few instances through the root canal or the alveolar plate – relatively free of actual contamination. • Burket : The microorganisms generally found in the oral cavity, such as Streptococcus viridans, Streptococcus hemolyticus, nonhemolytic streptococci, Staphylococcus aureus, Staphylococcus albus, Escherichia coli, and pneumococci. • Seldom can microorganisms actually be demonstrated histologically in the periapical granuloma. • Some investigatiors: Dental granuloma is usually a sterile lesion. • Current evidence: many lesions may be infected before and after endodontic treatment Shafer’s textbook of Oral Pathology, 7th edition
Iwu et al. 88% or 14 of 16 periapical granulomas were bacteria positive Mixed infections - not been possible to associate particular types of microorganisms with specific periapical lesions, based upon either clinical or histologic evaluation. Sebati M and Slots J 34 periapical lesions, that most teeth with necrosed pulp and periapical lesions harbored human cytomegalovirus and Epstein-Barr virus in periapical granulomatous tissue, along with the endodontopathic bacteria Slots J and coworkers 25 symptomatic and 19 nonsymptomatic periapical lesions- human cytomegalovirus (HCMV) in 100% of symptomatic and 37% of non-symptomatic periapical lesions and Epstein- Barr virus (EBV) only in lesions infected with HCMV. induction of cytokine and lymphokine induction from inflammatory or connective tissue cells or by impairing the local host defenses which increase the virulence of resident bacterial pathogens.Shafer’s textbook of Oral Pathology, 7th edition
TREATMENT • Reduction and control of the offending organisms. – If the tooth can be maintained, then root canal therapy can be performed. • Non restorable teeth: Extracted, followed by curettage of all apical soft tissue. • Symptomatic cases: (NSAIDs) are beneficial; – use of systemic antibiotic medications is not recommended unless associated swelling or systemic changes are present. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
• Teeth treated endodontically should be evaluated at 1- and 2-year intervals (at a minimum) to rule out possible lesional enlargement and to ensure appropriate healing. • Evaluations at 1, 3, and 6 months are appropriate. Follow-up • failure can occur in cases with excellent endodontic therapy but poor coronal restoration. Coronal restoration is critical • endodontic retreatment represents the best approach for minimizing the bacterial contamination and should be considered before periapical surgery. If initial conventional therapy is unsuccessful • lesions larger than 2 cm • teeth not appropriate for conventional endodontic therapy. • thorough curettage of all periradicular soft tissue, amputation of the apical portion of the root, and sealing the foramen of the canal. Periapical surgery • histopathologic examination and diagnostic confirmation are mandatory. Surgical sites: failed to respond to appropriate therapy Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
OUTCOME Asymptomatic apical periodontitis Repair of after root canal therapy severe periapical tissue destruction acute exacerbati on abscess - draining sinus tract cellulitis. Grossman’s endodontic practice: 11th edition
• Chief complaint- painful swelling left temporal region; trismus • medical history - osteoporosis, no medication. • Diffuse, elastic soft, and painful swelling at the left side of the temporal region • Intraorally- left maxillary second molar : tender on percussion and gingival tenderness of apical area Sayaka Yoshiba, Takaaki Kamatani, Tatsuo Shirota. Temporal Fossa Abscess Caused by Apical Periodontitis: A Case Report. Open Journal of Clinical Diagnostics, 2018, 8, 47-51
• Leukocytes - 10,300/μl ; C-reactive protein (CRP) 11mg/dl • Albumin- decreased difficult food intake by trismus. • Computed tomography: low density area range from pterygomandibular region to temporal region – abscess formation suspected. • Diagnosis- Temporal fossa abscess due to the periapical periodontitis of the upper left second molar.
Immediate treatment Hospitalized for anti-inflammatory treatment. Day 1 Drainage : incision line designed at temporal skin Fusobacterium species detected in pus. Day 1 to Day 4 Ampicillin 3 g/day IV. Day 5 Since the drainage amount was reduced, Ampicillin - 2 g/day. Day 9 Leukocytes - 5500/μl ; CRP - 0.5 mg/dl. Mouth opening training inter-incisal distance- 5 mm to 20 mm. Day 12 extraction of the upper left side of the second molar Day 15 patient recovered satisfactory and left hospital Follow up The patient continues to mouth opening training in the outpatient.
CHRONIC ALVEOLAR ABSCESS
A chronic alveolar abscess is a longstanding, low-grade infection of the periradicular alveolar bone generally symptomless and characterized by the presence of an abscess draining through a sinus tract. Synonyms – Chronic suppurative apical periodontitis, – Suppurative periradicular periodontitis, – chronic apical abscess, – chronic periradicular abscess, – chronic periapical abscess Grossman’s endodontic practice: 11th edition
CAUSES • Necrosed pulp • Preexisting acute abscess Grossman’s endodontic practice: 11th edition
SYMPTOMS • Generally asymptomatic, or only mildly painful. • Detected only during routine radiographic examination or because of the presence of a sinus tract, which can be either intraoral or extraoral. • The sinus tract usually prevents exacerbation or swelling by providing continual drainage of the periradicular lesion • The point at which the pus breaks into the mouth depends on the thickness of the alveolar bone and the overlying soft tissues. • Obviously, the confined pus takes the path of least resistance Cohen’s Pathways of the Pulp,11th edition
Upper jaw,: along the labial alveolar plate which is thinner than the palatal plate of bone. upper lateral incisors , palatal root of a maxillary molar: palatally because these roots lie in closer proximity to the palatal plate of bone lower jaw: Vestibule -along the buccal alveolar plate -may occur along the lingual alveolar wall in the case of lower molars Grossman’s endodontic practice: 11th edition
DIAGNOSIS • Patient may remember a sudden, sharp pain that subsided & not recurred, or he or she may relate a history of traumatic injury. • Clinical examination: a cavity, a composite or metallic restoration, or a full coverage crown • Slight pain in relation to the tooth, particularly during mastication. • Non vital teeth: negative electric pulp test or to thermal tests. • At times, the sinus tract is several teeth away from the cause. • Open cavity  drainage by root canal. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
RADIOGRAPHIC FEATURES • The first sign of osseous breakdown is radiographic evidence seen during routine examination or discoloration of the crown of the tooth. • radiograph taken after the insertion of a gutta-percha cone into the sinus tract often shows the involved tooth by tracing the sinus tract to its origin • Diffuse area of bone rarefaction- so diffuse as to fade indistinctly into normal bone • Nondiagnostic. • Periodontal ligament is thickened.
DIFFERENTIAL DIAGNOSIS • CYST: presence of a diffuse area indicated an abscess, a circumscribed area indicated an asymptomatic apical periodontitis, and a sclerotic bony outline was a sign of a cyst • however, all attempts to correlate the radiographic appearance of an area with its histopathologic features failed. • As a result, a proper and accurate diagnosis can be made only when a tissue specimen has been examined histologically.
HISTOPATHOLOGY• Progression of infective process into periradicular tissues detachment or loss of periodontal fibers at the root apex  destruction of the apical periodontal ligament. • The apical cementum may also become affected. • The root canal itself may appear to be empty, or cellular debris may be present. Bacteria were found infrequently on microscopic examination of 230 periapical tissue specimens removed during root resection. Center: Polymorphonuclear leukocytes, Mononuclear cells.Periphery: Lymphocytes and plasma cells Capsule: Fibroblasts
• Suppurative material from the interior of the abscess is discharged on the mucosa or gingiva. – may or may not be continuous. • Intermittent: discharge preceded by swelling • Stoma formation: Pressure from pus rupture the thin wall of soft tissue discharge of suppurative material into mouth – The opening may heal and may close again – May reopen: pressure from the contained pus overcomes the resistance of the undermined layer of soft tissue. • Parulis: Small elevation of the mucosa – In conjunction with infection of the deciduous and permanent teeth
• Sinus tract - surface of the face -young person. • Associated with lower anterior teeth opens near the symphysis of the jaw, • Associated with posterior teeth - chiefly the first molar along the inferior border of the mandible • Rare cases: purulent material encounters least resistance along the root  into the gingival sulcus impression of a pocket of periodontal origin
TREATMENT • Elimination of infection. • Cleaning, shaping of root canal, intracanal medicament sealed in to reduce the bacterial flora sinus tract closes up and disappears
Chronic alveolar abscess in relation to a maxillary central incisor with a history of surgical endodontic therapy. Gutta-percha tracing being done through the labial sinus opening. Tracing indicative of periradicular infection in relation to the apical third of the involved tooth. Retreatment of the root canal completed Complete resolution of the sinus after completion of the treatment. Three-year follow- up radiograph showing healing of the periradicular region
PROGNOSIS • Depends on proper cleaning, shaping, and obturation of the root canals. • Periodontal status, restorative needs, and potential for functional rehabilitation
APICAL PERIODONTAL CYST
CYST • A cyst is a closed cavity or sac internally lined with epithelium, the center of which is filled with fluid or semisolid material • Cysts of the jaws are divided into • Odontogenic- arise from odontogenic epithelium – Follicular, arising from the enamel organ or follicle, – Radicular, arising from the cell rests of Malassez. • Nonodontogenic- – Fissural, arising from epithelial remnants entrapped in the fusion of the facial processes – Nasopalatine, arising from the remnants of nasopalatine duct. • Nonepithelial- bony cavities that are not lined with epithelium and, therefore, are not truly cysts. – traumatic cysts – idiopathic bone cavities – aneurysmal bone cysts.
APICAL PERIODONTAL CYST RADICULAR CYST, PERIAPICAL CYST, ROOT END CYST • slowly growing epithelial sac at the apex of a tooth that lines a pathologic cavity in the alveolar bone • most common odontogenic cyst • usual but not inevitable sequela of the periapical granuloma • true cyst- epithelial lining is derived from the epithelial rests of Malassez • Epithelium may be derived in some cases from – Respiratory epithelium of the maxillary sinus when the periapical lesion communicates with the sinus wall – Oral epithelium from a fistulous tract – Oral epithelium proliferating apically from a periodontal pocket.
PATHOGENESIS • Lumen: lined by stratified squamous epithelium • Wall: made up of condensed connective tissue. • Inflammation in the periapical granuloma  Stimulus for the proliferation of epithelium – Induced by the keratinocyte growth factor elaborated by the stromal cells of the periodontal ligament, or inflammatory stimulus. • Gao et al: Activated T cells in the periapical granulomas produce lymphokines act on the rest of Malassez  proliferation and altered differentiation  Cyst formation Shafer’s textbook of Oral Pathology, 7th edition
NUTRITIONAL DEFICIENT THEORY: T cells in the periapical granulomas produce lymphokines Act on the cell rest of Malassez Proliferation and altered differentiation leading to cyst formation Irregular pattern of growth Epithelial mass increases in size by division of the cells on the periphery Cells in the central portion of the mass separated from source of nutrition Central cells fail to obtain sufficient nutrients Eventually degenerate, become necrotic, and liquefy Epithelium-lined cavity filled with fluid THE APICAL PERIODONTAL CYST
ABSCESS THEORY Abscess cavity in connective tissue Surrounded with proliferating epithelial tissue Formation of Cyst. Grossman’s endodontic practice: 11th edition
Paul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics 2004, 8, 36–54
• Epithelial-lined cavity  open towards the root canal of the affected tooth. • initiated by accumulation of neutrophils around the apical foramen • Microabscess- enclosed by the proliferating epithelium, forming a collar with epithelial attachment on contacting the root tip. • Apical pouch seals off infected root canals with microabscess from periapical tissue milieu PERIAPICAL POCKET CYST: (ORIGINALLY BAY CYST) Grossman’s endodontic practice: 11th edition
PERIAPICAL TRUE CYST: • cavities completely enclosed in epithelial lining • totally independent of the root canal of the affected tooth Grossman’s endodontic practice: 11th edition
CLINICAL FEATURES • Asymptomatic • Age: 20-60 years, involve deciduous teeth. • Maxilla: 75% – incisors, 62%; cuspids, 7%; premolars, 20%; and molars, 11%. • Mandible,: 25% – incisors, 16%; cuspids, 2%; premolars, 34%; and molars, 48%. • Non-vital tooth; deep carious lesion or a restoration • Develops only over a prolonged period of time. – Acute exacerbation  abscess  cellulitis or form a draining fistula. Cohen’s Pathways of the Pulp,11th edition
RADIOGRAPHIC FEATURES • identical in most cases with that of the periapical granuloma • Cyst > granuloma in size, by virtue of its longer duration X • Occasionally : a thin, radiopaque line around the periphery of the radiolucent area, and this indicates a reaction of the bone to the slowly expanding mass • Cone beam computed tomography > biopsy Cohen’s Pathways of the Pulp,11th edition
DIAGNOSIS • Non-vital pulp • Previous history of pain. • Radiographic diagnosis- – loss of continuity of the lamina dura with an area of rarefaction. – radiolucent area is generally round in outline, except where it approximates adjacent teeth, in which case it may be flattened and may have an oval shape. • The radiolucent area may be larger than a chronic apical abscess and may include more than one tooth Grossman’s endodontic practice: 11th edition
DIFFERENTIAL DIAGNOSIS Asymptomatic apical periodontitis Incisive foramen
Globulomaxill ary cyst • marsupialized and enucleated without Traumatic bone cyst/ hemorrhagic or extravasation cyst: • aspiration of fluid through surgical cavity Lateral periodontal cyst: • periodontal signs and symptoms
BACTERIOLOGY • A cyst may or may not be infected. • Represents a defensive reaction of the tissue to a mild irritant • Actinomyces organisms have been isolated from a periapical cyst. Bacterial colonies in the cyst lumen, surrounded by inflammatory Cells, Ricucci D, Bergenholtz G: Histologic features of apical periodontitis in human biopsies, Endod Topics 8:68, 2004, Fig. 6
HISTOLOGICAL FEATURES • Similar to Periapical granuloma • Epithelial lining • Epithelial thickness • Rete ridges • Inflammatory infiltrate • Rushton body • Cholesterol clefts Shafer’s textbook of Oral Pathology, 7th edition
• Martin A Rushton: 1955 • Peculiar Hyaline bodies- exclusively in odontogenic cysts • tiny linear or arc-shaped bodies, associated with the lining epithelium • amorphous, eosinophilic, and brittle in nature • No clinical or diagnostic significance; origin is unknown, but may represent some type of epithelial product. (Allison, 1977) • Sedano (1968) and Gorlin reported a marked morphologic and histochemical similarity between these bodies and red blood cells, suggesting that they arise from thrombus formation in small capillaries, being formed chiefly from these red blood cells—a rouleau phenomenon. Babburi S, Rudraraju AR, V A, P S. Rushton bodies: an update. J Clin Diagn Res. 2015;9(2):ZE01– ZE3. doi:10.7860/JCDR/2015/10990.5533 RUSHTON BODY:
• wall of the lesion- dystrophic calcifications and collections of cholesterol slits with associated multinucleated giant cells • collections of lipid-filled macrophages or even macrophages containing hemosiderin are present. Shafer’s textbook of Oral Pathology, 7th edition
CONTENTS OF CYST LUMEN- • watery, straw-colored, blood tinged fluid to semisolid materials • Protein: low conc. - stains palely eosinophilic. • Shimmering effect: Cholesterol • Keratin: Rare instances, limited amounts • Blood - rare finding, except associated with surgical procedure involved in removing the cyst. Cohen’s Pathways of the Pulp,11th edition
TREATMENT Surgical Therapy • The affected tooth is either preserved by root canal treatment or is removed. • Mucoperiosteal flap lying over the cyst is raised and a window is opened in the bone which gives sufficient access. • The cyst is then separated from the bony wall. • The edges off the cavity are smoothened and the cavity is washed to clean the debris. • After the bleeding is controlled, the flap is replaced back and sutured. Endodontic Method • 80–98% of the radicular cysts undergo resolutions after root canal treatment and do not require surgery. • The treatment of choice Cohen’s Pathways of the Pulp,11th edition
Marsupialisation • Aims at producing self cleansing cavity which becomes the ground for oral tissues. • Cyst is cut open for enucleation but the epithelial lining is stitched on to the mucous membrane at margins of opening. • Cavity is plugged with ribbon gauze in the beginning. • Once the margins get healed, the cavity closes when the surrounding tissues start growing back along with new bone • large cyst which will require decompression, and where the jaw has chances of getting fractured.
PROGNOSIS Depends on – Particular tooth – Extent of bone destroyed – Accessibility for treatment. Grossman’s endodontic practice: 11th edition
HEALING OF LESIONS - APICAL POCKET CYST • Hypothesis I: – Overinstrumentation of canal beyond apexacute inflammatory response in cystic area destroy the epithelial lining  Resolution. – Rejected: healing usually occurs from the periphery to the center of the lesion. • Hypothesis II: – Instrument into the cyst puncture of cyst wall Drainage. – Drainage reduces the pressure on walls of osseous cavity  stimulates fibroplasia  repair from the periphery of the lesion Grossman’s endodontic practice: 11th edition
APICAL TRUE CYST • Hypothesis: – Subsided inflammatory process  drainage  fibroplasia  collagen. – Pressure of the proliferating collagen  reduced blood supply to epithelium by compressing the vascular network of the granulomatous tissue. – Collagen  entraps epithelial lining degeneration Removal by Macrophages • Current and most feasible hypothesis: – Periapical lesions- inflammatory responses to antigen content of root canal system, – Epithelial proliferation- response to irritating materials, – Removal of source of irritation  Destruction and removal of proliferating epithelial cells by immune system Grossman’s endodontic practice: 11th edition
COMPLICATIONS • Fractured jaw • Damage to surrounding structures • Infection in the wound. • Fatal cysts might not be removed properly with added tissue. • Remains of cyst  Recurrence of cyst formation. Grossman’s endodontic practice: 11th edition
CONDENSING OSTEITIS
• Asymptomatic apical periodontitis with reactive bone formation = Chronic osteomyelitis with proliferative periostitis. • long-term, low-grade inflammation/ infection or a high resistance of local tissue to inflammation/ infection. • Inflammation induces reactive bone formation of alveolar trabecular or spongy bone around the periapex of endodontically involved teeth. Cohen’s Pathways of the Pulp,11th edition Grossman’s endodontic practice: 11th edition Condensing osteitis is a diffuse radiopaque lesion believed to represent a localized bony reaction to a low-grade inflammatory stimulus, usually seen at the apex of a tooth in which there has been a long-standing pulpal pathosis.
CLINICAL FEATURES • young patients • Mandibular first molar • gross carious lesions • vital or nonvital. • usually asymptomatic. • Radiographically- – radiopaque mass associated with the apex of an endodontically involved tooth. – Lamina dura - usually intact Cohen’s Pathways of the Pulp,11th edition
HISTOPATHOLOGY • There is an excessive apposition of bone mass without bone resorption in the apical area. • As the bone marrow spaces become smaller and obliterated, the bone resembles compact bone that is infiltrated by a small number of lymphocytes. • The compact bone has few lacunae, and many of them are empty of osteocytes. • It has many prominent resting and reversal lines, similar to an idiopathic osteosclerosis or a Pagetoid appearance. Cohen’s Pathways of the Pulp,11th edition
TREATMENT • Removal of the irritant stimulus is recommended. • Endodontic treatment should be initiated if signs and symptoms of irreversible pulpitis are diagnosed. Prognosis • long-term retention: excellent if root canal therapy is performed and if the tooth is restored satisfactorily. • Lesions may persist after endodontic treatment. Grossman’s endodontic practice: 11th edition
EXTERNAL ROOT RESORPTION
• lytic process occurring in the cementum or cementum and dentin of the roots of teeth. Grossman’s endodontic practice: 11th edition
Grossman’s endodontic practice: 11th edition CLASSIFICATION Tooth resorption: internal and external. External tooth resorption- A. External surface resorption B. External inflammatory root resorption C. External replacement resorption or ankylosis
RADIOGRAPHIC FEATURES • radiolucent, concave, ragged bowl-shaped excavations along the root surface, • corresponding and associated radiolucencies in the adjacent alveolar bone. • Complete loss of the lamina dura is seen in the area of the resorption. • Initial signs : as early as 3 to 4 weeks after a TDI involving the periodontal tissues – EIR is always seen within 1 year after the injury. • Areas of replacement resorption or ankylosis: – resorbed root – no periodontal ligament space – bone replacing the defects. Cohen’s Pathways of the Pulp,11th edition
“Moth-eaten” radiolucent alteration- reimplanted after traumatic avulsion Diffuse external resorption after initiation of orthodontics. Extensive external resorption - impacted right maxillary cuspid. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
First molars in all four quadrants demonstrate extensive radicular external resorption. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
HISTOLOGIC APPEARANCE • Cementum & Dentin: Saucer or bowl-shaped areas of resorption • Inflammation in the adjacent periodontal membrane. • Resorption cavities: Howship lacunae – lacunae sometimes are occupied by odontoclasts. • PDL inflammation: intense – consists of a mixed-cell infiltrate - plasma cells, lymphocytes, and polymorphonuclear leukocytes in a granulation tissue matrix. – Proliferation of capillaries • EIR can be identified histologically 1 week after experimental replantation of teeth. Cohen’s Pathways of the Pulp,11th edition
CLINICAL FEATURES • Tooth in question may look normal • No response to vitality testing. • Advanced cases: signs of pulpal and/or periapical periodontitis – discolored tooth – sinus present – tenderness to percussion and/or palpation Cohen’s Pathways of the Pulp,11th edition
DIFFERENTIAL DIAGNOSIS • External resorption – radiograph blunt apex, – “scooped-out” area on the side of the root, – if the area is superimposed on the root canal, the root canal clearly traverses the area of resorption. • Internal resorption – root canal with a well-demarcated, enlarged “ballooning” area of resorption. • internal resorption  perforated the root surface • external resorption penetrated the pulpal cavity Grossman’s endodontic practice: 11th edition Difficult to diagnose
MANAGEMENT • Effective removal of the causal agent • Root canal treatment • Exception: Replanted teeth with closed apices – Root canal treatment should be carried out 7 to 10 days after replantation, even if there are no radiographic signs of EIR. PROGNOSIS: • Depends on early diagnosis and treatment. • Long-term dressing of the root canal with calcium hydroxide may be beneficial – associated risk of root fracture. Cohen’s Pathways of the Pulp,11th edition
FOLLOW-UP AND PROGNOSIS • Healing - cessation of the resorption process – resolution of the radiolucency in the adjacent bone – reestablishment of the PDL space. • Untreated cases- entire root can be resorbed within 3 months. • The prognosis is especially poor for untreated immature teeth Cohen’s Pathways of the Pulp,11th edition
POST-TREATMENT APICAL PERIODONTITIS
The occurrence of signs and/or symptoms of disease in association with root canal-treated teeth • Emergent (if developed after treatment) • Persistent (if persisted despite treatment) • Recurrent (if developed after having healed). • usually observed after endodontic treatments that have not followed acceptable standards for prevention and control of the root canal infection • occur in 5-15% of teeth with pre-operative apical periodontitis even when treatment has followed proper standards J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
ETIOLOGY • Persistent intraradicular infection • Secondary intraradicular infection – Coronal leakage – Extraradicular infection • Microbial cause – Intraradicular infection – Extraradicular infection • Procedural errors – Fractured instrument, – Ledge – Perforation – Overfilling J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
MANAGEMENT Retreatment: teeth with inadequa te root canal treatment available coronal access Surgery:teeth with well-treated canals where retreatment offers no better prognosis retreatment is not feasible because coronal access to the apical canal is impossible high risk of accidents (extensive restorations, fractured instruments, perforations , ledges, etc) teeth that have already been subjected to retreatment; and cases where there is a need for biopsy. J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
TECHNICAL ASPECTS OF ENDODONTIC RETREATMENT J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
repeated abscesses- right mandible, swelling, pain. Tooth 46 -crown, asymptomatic at the visit. Radiograph - root canal-treated, but the apical distal canal was clearly untreated and the mesial canals underinstrumented. - well-fitted metal-ceramic crown Endodontic retreatment Crown removed and access to the canals achieved. J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
Obturation materials were removed, and new working lengths established; Appearance of the pulp chamber just before root canal obturation Canals obturated after 48 days of Ca(OH)2 medication with cold gutta-percha laterally compacted and sealer J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
Postoperative radiograph Two-year follow-up radiograph. Only a minor radiolucency is present on the mesial root Radiograph taken after ten years Normal periradicular conditions J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
recurrent abscess left upper jaw. Maxillary first premolar - root canal-treated 6 years before. Buccal sinus tract A large mesio- occlusal-distal (MOD) composite restoration; carbon fibre post seen at the occlusal surface Inadequate root canal treatment with the apical canals untreated; Post in the palatal canal J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
Endodontic retreatment- Rubber dam isolation, core material removed, post drilled out with burs for post space preparation in the coronal portion, and with ultrasonic diamond tips in the deepest part Working length determination. Two canals joined- common apical canal. Ca(OH)2 paste in saline intracanal medicament placed After one week- sinus tract disappeared, tooth was comfortable The canals were obturated J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
maxillary left first molar –single visit root canal-treated three months before. Buccal sinus tract never disappeared after the treatment , tooth was painful. Tooth was not restored permanently Periapical radiographs- poor instrumention and obturation, large radiolucency around the mesio- buccal root apex.
Isolation with a rubber dam, temporary remaining restorative materials removed, abundant carious tissue appeared on the pulp chamber floor and in the rest of the cavity; Fissure connecting the mesiobuccal and palatal root canal orifices Additional canals were present in the mesial root, negotiated with #10 files. Calcification adhered to the pulp chamber floor One ribbon- shaped canal at the entrance of the mesial root
uninstrumented canal (MB2) was found ending considerably short of the radiographic apex Removal of the obturation material in the mesio-buccal canal and working length determination obturated after three weeks of Ca(OH)2 medication; the tooth became asymptomatic, sinus tract disappeared Follow-up radiograph taken after three years and seven months. J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
PERSISTENT APICAL PERIODONTITIS • Persistent apical periodontitis is a post-treatment apical periodontitis in an endodontically treated tooth Grossman’s endodontic practice: 11th edition
CAUSES • Anatomical complexity of pulp space system with regions that cannot be reached with instruments or with irrigants or intracanal medicaments. • Cannot be obturated with conventional techniques. • Nair: extraradicular factors that contribute to persistent apical periodontitis. – Apical biofilms (periapical plaque)  – Actinomycosis infection – Cholesterol crystals – Foreign body reaction to gutta-percha – Cellulose granuloma – Periapical scar tissue Grossman’s endodontic practice: 11th edition
BACTERIOLOGY • Yeasts and Candida albicans in post-treated cases. • Grampositive cocci, rods and filaments, genera Actinomyces, Enterococccus, and Propioniobacterium have also been implicated. • E. faecalis : – most consistently reported organism that can survive prolonged starvation – can grow as a monoinfection in endodontically treated teeth. – Considered as a therapy-resistant microbe among the potential etiological agents of post-treatment apical periodontitis. Grossman’s endodontic practice: 11th edition
• Fourteen year old female patient • All mandibular incisors were painful with swelling of soft tissue • Endodontic treatment two years ago. • Exacerbation with pain and swellingperiapical surgery on teeth 42, 41 and 31 without endodontic retreatment of involved teeth. Patient x-ray before emergency treatment. X-ray image after root canals obturation with Gutta Flow sealer and Gutta-percha master point X-ray image two month after treatment X-ray image ten month after treatment Nedim S. Management of Acute Periapical Lesions at Four Mandibular Incisors a Case Report. Adv Dent & Oral Health. 2017; 5(1): 555654. DOI:10.19080/ADOH.2017.05.555654
PERIAPICAL SCAR
PERIAPICAL SCAR • Defect created by periapical inflammatory lesions may fill with dense collagenous tissue rather than normal bone • occur most frequently when both the facial and lingual cortical plates have been lost – occasionally arise in areas with intact cortical plates. – Both plates missing, patient should be informed of the possibility of scar formation. – development of a periapical scar is not an indication for future surgery. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
DISEASES OF THE PERIRADICULAR TISSUES OF NONENDODONTIC ORIGIN
Lesions of nonendodontic origin with vital pulps include: • Periapical cemental dysplasia or cementoma • Cementoblastoma • Odontogenic cysts • Fissural cysts • Central giant cell granuloma • Metastatic malignant tumors or ameloblastomas: – aggressive lesions – excessive bone loss, mobility of teeth, extensive root resorption, and loss of pulp vitality. Grossman’s endodontic practice: 11th edition
HYPERCEMENTOSIS
HYPERCEMENTOSIS • Cemental hyperplasia • nonneoplastic deposition of excessive cementum that is continuous with the normal radicular cementum. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
CLINICAL FEATURES • May be isolated, involve multiple teeth, or appear as a generalized process. • Mandibular molars – followed by the mandibular and maxillary second premolars – mandibular first premolars. • Adulthood, and the frequency increases with age • Occurrence reported in younger patients  familial clustering, suggesting hereditary influence. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
RADIOGRAPHIC FEATURES • Thickening or blunting of the root • Cementum and dentin demonstrate similar radiodensities • surrounded by the radiolucent PDL space and the adjacent intact lamina dura. • Enlargement may be significant enough to suggest the possibility of a cementoblastoma • cementoblastoma : associated pain, cortical expansion, and continued enlargement Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
FACTORS ASSOCIATED WITH HYPERCEMENTOSIS Local Factors • Abnormal occlusal trauma • Adjacent inflammation (e.g., pulpal, periapical, periodontal) • Unopposed teeth (e.g., impacted, embedded, without antagonist) • Repair of vital root fracture Systemic Factors • Acromegaly and pituitary gigantism • Arthritis • Calcinosis • Paget disease of bone • Rheumatic fever • Thyroid goiter • Gardner syndrome • Vitamin A deficiency (possibly) Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
HISTOPATHOLOGIC FEATURES • Excessive cementum deposition- periphery of the root. • Hypocellular or exhibit areas of osteocementum • Arranged in concentric layers • Entire root or be limited to the apical portion. • Routine light microscopy: distinguishing between dentin and cementum is difficult, • Polarized light: discriminate between the two different layers A, Dental root exhibiting excessive deposition of cellular and acellular cementum. The dividing line between dentin and cementum is indistinct. B, Polarized light demonstrating the sharp dividing line between the tubular dentin and osteocementum. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
TREATMENT AND PROGNOSIS • Patients with hypercementosis require no treatment. • Because of a thickened root, occasional problems have been reported during the extraction of an affected tooth. • Sectioning of the tooth may be necessary in certain cases to aid in removal Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
NON ENDODONTIC PERIRADICULAR LESIONS Odontogenic cysts: • Dentigerous cyst • Lateral periodontal cyst • Odontogenic keratocyst • Residual cyst Bone Pathologies: • fibro-osseous lesions • Periradicular cemental dysplasia • Osteoblastoma • Cementoblastoma • Cementifying & ossifying fibroma Odontogenic tumours: Non-odontogenic • Central giant cell granuloma • Nasopalatine duct cyst • Globulomaxillary cyst • Simple bone cyst • Enostosis
SUMMARY
Captain Scott B. McClanahan, DC, USN, Captain James D. Johnson, DC, USN, and Captain Robert E. Blundell, Jr., DC, USN. Pulpal and periradicular diagnostic terminology. Clinical Update. January 2002. Vol. 24, No. 1
Grossman’s endodontic practice: 11th edition
PREVIOUSLY ASKED QUESTIONS • Classification of Periradicular pathologies • Phoenix abscess • Management of acute alveolar abscess • Theories of cyst formation • Histopathology of radicular cyst (10 marks, NITTE University, 2019)

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periapical pathologies- pulpal origin

  • 1. PERIAPICAL PATHOLOGIES I M D S , D E PA R T M E N T O F C O N S E R VAT I V E D E N T I S T R Y A N D E N D O D O N T I C S , A B S H E T T Y M E M O R I A L I N S T I T U T E O F D E N TA L S C I E N C E S , M A N G A LO R E . DR GURMEEN KAUR
  • 2. • Introduction • Periapical Anatomy In Health – Cementum • Types • Matrix – Periodontal Ligament • Cells • Extra cellular Matrix – Alveolar Bone • Parts • Matrix • Intraoral periapical radiograph
  • 3. PERIRADICULAR LESIONS • PULPAL ORIGIN • Changes in tissues • Irritants – Living – Non-living • Radiographic changes • Histologic changes • Endodontic implications • FISH Zones – Zone of stimulation – Zone of irritation – Zone of contamination – Zone of infection • Role of Bacteria
  • 4. • Diagnosis – History & discussion with patient – Clinical examination – Clinical tests – Radiographic examination – Correlation of history, clinical, radiographic & test findings – Treatment plan • Classification- – Grossman – WHO – Weine’s – Ingle’s – Clinical classification – Nair’s classification
  • 5. ACUTE APICAL PERIODONTITIS • Apical periodontitis –WHO classification • Acute apical periodontitis – Definition – Synonyms – Etiology • Vital tooth • Non-vital tooth • Primary • Secondary – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Bacteriology – Histopathology – Treatment – prognosis – Outcome
  • 6. ACUTE ALVEOLAR ABSCESS – Definition – Synonyms – Etiology – Clinical features – Systemic reactions – complications – Radiographic features – Diagnosis – Differential diagnosis – Bacteriology – Histopathology – Treatment • Incision to establish drainage • Root canal treatment • Antibiotic therapy – prognosis – Consequences of untreated abscess
  • 7. PHOENIX ABSCESS – Definition – Etiology – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Bacteriology – Histopathology – Treatment – prognosis
  • 8. CHRONIC APICAL PERIODONTITIS – Definition – Etiology – Clinical features – Radiographic features – Histopathology – Zones of well established granuloma – Microbiologic features – Treatment – Prognosis – Outcome – Case report
  • 9. CHRONIC ALVEOLAR ABSCESS – Definition – Synonyms – Etiology – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Histopathology – Treatment – prognosis
  • 10. APICAL PERIODONTAL CYST – Cyst – Apical periodontal cyst • Definition • Epithelial lining • Pathogenesis • Theories of cyst formation – Nutritional deficient theory – Abscess theory • Periapical pocket cyst • Periapical true cyst – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Bacteriology – Histopathology – Cystic lumen – Treatment • Surgical • Endodontic • marsupilisation – Prognosis – Healing • Periapical pocket cyst • Periapical true cyst – complications
  • 11. CONDENSING OSTEITIS – Definition – Etiology – Clinical features – Radiographic features – Histopathology – Treatment – prognosis
  • 12. EXTERNAL ROOT RESORPTION • Definition • Classification of root resorption – Internal – External • External surface resorption • External inflammatory root resorption • External replacement resorption • Radiographic appearance • Histopathology • Clinical features • Differential diagnosis • Management • Follow-up & prognosis
  • 13. POST-TREATMENT APICAL PERIODONTITIS • Etiology • Management – Retreatment – Surgery • Technical aspects of endodontic retreatment • Case reports • Persistent apical periodontitis – Causes – Bacteriology • Periapical scar/ Surgical defect
  • 14. HYPERCEMENTOSIS • Clinical features • Radiographic features • Factors associated • Histopathology • Treatment • Prognosis • Lesions with non-endodontic origin with vital pulp • Non endodontic periradicular lesions
  • 15. • Summary – Conditions and diagnosis – Management of symptomatic conditions • Previously Asked Questions
  • 17. CEMENTUM • Mineralized, avascular connective tissue • Consists of three different types- – Acellular afibrillar cementum- cementoenamel junction. – Acellular extrinsic fiber cementum- coronal half of the root. – Cellular intrinsic fiber cementum - apical half of the root.
  • 18. M A T R I X • Released under certain conditions- – cementoblast proliferation, – migration, – differentiation during cementum wound healing • Cementoblasts: – Osteoblast-like phenotype; – responsive to osteotropic signals: PTH/PTHrP. – Cementum attachment protein, cementum-derived growth factor, and PLAP-1 • Bone matrix proteins: osteocalcin, osteopontin, and bone sialoprotein Periodontium and Periodontal Disease. Insulin- like Growth Factor-1 IGF-1 Fibroblas t Growth Factors FGFs Epiderm al Growth Factor EGF Bone Morpho genetic Proteins BMPs Transfor ming Growth Factor-β TGF-β Platelet- derived Growth Factor PDGF
  • 19. PERIODONTAL LIGAMENT • Soft, specialized connective tissue- connects the cementum to the alveolar bone. . HETEROGENOUS CELL POPULATION- Osteoblasts, Osteoclasts, Fibroblasts, Cementoblasts, Epithelial cell rests of Malassez, Macrophages, Undifferentiated mesenchymal cells (stem cells). • Fibroblasts, osteoblasts, and epithelial cells - differentiated cellsundergo limited cell divisions and proliferation upon stimulation by appropriate signals • Multipotent mesenchymal stem cellsdifferentiate into cementoblast- like cells and periodontal ligament cells,osteoblasts EXTRACELLULAR MATRIX- Collagen fibers, Fibronectin, Elastin, other noncollagenous proteins, and proteoglycans. • The ECM serves as stratum for cell adhesion and promotes cell spreading and cytoskeletal organization Shafer’s textbook of Oral Pathology, 7th edition
  • 20. The collagen fibers (Sharpey fiber) of the periodontal ligament connect the tooth with the alveolar bone. • Highly vascularized and innervated. Epithelial cell rests of Malassez (ERM), the remnants of the Hertwig epithelial root sheath- present in PDL after root formation. • Nests of epithelial cells connected as a network; surrounded by a basal lamina. • ERM - stimulated to proliferate in apical periodontitis. • Cellular source - can form radicular cysts. Shafer’s textbook of Oral Pathology, 7th edition
  • 21. ALVEOLAR BONE • Houses the sockets for the teeth. • Outer cortical plate, a central spongy or cancellous bone, and bone lining the sockets – Alveolar Bone Proper : lines the alveolus or the bony sockets that house the roots of the teeth. – Supporting Alveolar Bone : Cancellous(spongy) bone adjacent to the alveolar bone proper covered by 2 outer tables of compact bone. • Lamina Dura- compact bone that lies adjacent to the periodontal ligament. – Radiopaque line surrounding the tooth root • Bone matrix contains IGFs, TGF-β, BMPs, FGF, and PDGF. – Essential for osteoblast progenitor cell proliferation, migration, and differentiation during bone wound healing.Shafer’s textbook of Oral Pathology, 7th edition
  • 24. Depending on the – nature, – quantity of irritants, – duration of exposure of the periradicular tissues, following changes can occur • Degenerative – Fibrous – Resorptive – Calcific • Proliferative Irritants from infected root canal Noxious products of tissue necrosis and antigenic agents in root canal. Periradicular tissues PERIRADICULAR LESIONS
  • 25. • Physical irritation of periradicular tissues- Overinstrumentation, Impact trauma, Hyperocclusion, Endodontic procedures and accidents, Pulp extirpation, Root perforation, and Overextension of filling materials. Irritants Living Bacteria Bacterial toxins Bacterial fragments Viruses Non-living Mechanical Thermal Chemical REVERSIBLE tissue damage Short-lived Self- limiting Transient, Mild to moderate injuries Destruction of periradicular tissues. Nonspecific and Specific Immunologic reactions can cause Persistent, Severe injuries
  • 26. RADIOGRAPHICALLY Radiographically- Radiolucent areas around the portal(s) of exit of the main canal or lateral and/or accessory canals.
  • 27. HISTOLOGICALLY Depending on their stage of development the periradicular pathologic tissues contain – polymorphonuclear neutrophils, – lymphocytes, – plasma cells, – macrophages, – mast cells, – immunoglobulins IgG, IgA, IgM,IgE, – complement. Reactions that may occur- • Anaphylactic, • Cytotoxic, • Antigen–antibody Complex, • Delayed Hypersensitivity.
  • 29. ENDODONTIC IMPLICATIONS • Fish: Described the reaction of the periradicular tissues to noxious products of tissue necrosis, bacterial products, and antigenic agents from the root canal. • Experimental foci of infection in the jaws of guinea pigs by drilling openings in the bone and packing in wool fibers saturated with a broth culture of microorganisms. • Four well-defined zones of reaction were found: – Zone of infection – Zone of contamination – Zone of irritation – Zone of stimulation
  • 30. Grossman’s endodontic practice: 11th edition Characterized by fibroblasts and osteoblasts. Periphery: Toxin mild enough to be a stimulant. Response: Collagen fibers laid down by fibroblasts Role of Collagen: as a wall of defense around the zone of irritation and as a scaffolding on which the osteoblasts built new bone. New bone- built in irregular fashion. Zone of Stimulation Characterized by macrophages and osteoclasts. Fish found evidence of irritation further from the central lesion as the toxins became more diluted. Distinguished by small, round cells, normal bone cells and osteoclasts could just about survive. The collagen framework was digested by phagocytic cells, the macrophages, while osteoclasts attacked the bone tissue. Histologic picture- body’s attempt to initiate repair. Zone of Irritation Characterized by round cell infiltration. Cellular destruction around the central zone from toxins discharged from the central zone. Toxins: Either tissue breakdown products or exotoxins. Dead bone cells- undergone autolysis, lacunae appeared empty. Lymphocytes: prevalent everywhere. Zone of Contamination Characterized by polymorphonuclear leukocytes. Infection- present in the center of the lesion, and microorganisms were found only in that area. The only microorganisms not disposed of by polymorphonuclear leukocytes were found in Haversian canals or in fissures in the bone matrix made by the bur. Zone of Infection
  • 31. Zone of Infection Root canal Zone of Contamination: Microorganisms- multiply sufficiently to grow or the metabolic products or the toxic products of tissue necrosis get diffused to the periradicular tissues. Periradicular area- they are destroyed by the polymorphonuclear leukocytes. Microorganisms overwhelm the defensive mechanism Periradicular Lesion Zone of Irritation: Polymorphonuclear leukocytes destroy the microorganisms . The result is a chronic abscess. The toxic products of the microorganisms + the necrotic pulp in the root canal + dead polymorphonuclear leukocytes  irritate and destruct the periradicular tissue + produce pus. Zone of Stimulation Periphery of the destroyed area of osseous tissue toxic bacterial products- diluted enough  act as a stimulant. form granuloma. Fibroblasts fibrous tissue, osteoblastssclerotic bone. Epithelial rests of Malassez stimulated Cyst Grossman’s endodontic practice: 11th edition
  • 32. ROLE OF BACTERIA Kakehashi et al. 1965 • Role of bacteria in progression of pulp and periapical diseases. • Pulp degeneration and necrosis following unrestored exposures to the oral environment in germ-free and germ- containing rats only developed when bacteria were present and they were able to contaminate the tooth and the pulp space. Korzen et al. • Bacterial invasion of the root canal Periapical tissue reactions periapical tissues not inflamed until root canal is infected. • Micro-organisms along entire length of root canal severe periapical inflammatory reaction • Limited inoculum  limited periapical tissue reaction. Sundqvist • Periapical lesions were found in 18 of 19 cases where microbes were present in the canal • Size of the periapical radiolucency was directly related to the number of strains that could be isolated from the affected tooth. Paul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics
  • 33. THE GENERAL STAGES OF DISEASE PROGRESSION IN ANY TISSUE AS A RESULT OF A STIMULUS OR IRRITANT THAT IS NOT REMOVED OR TREATED Paul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics 2004, 8, 36–54
  • 35. Procedure Result 1. History and discussion with patient Medical history Dental history Description of presenting complaint Details of any previous treatment of presenting complaint Provisional diagnosis of presenting condition 2. Clinical Examination Extra-oral signs Intra-oral signs Individual tooth assessment Restoration assessment Assess possible causative factors Provisional diagnosis of tooth status 3. Clinical Tests Pulp sensibility tests Percussion, mobility, palpation Provisional diagnosis of the status of the and/or the root canal system Provisional diagnosis of the periapical status 4. Radiographic Examination Confirm/assess causative factors Provisional diagnosis of periapical status 5. Correlation of the history, clinical, radiographic and test findings DEFINITIVE DIAGNOSIS - Pulp, root canal and periapical status - Cause(s) of the diseases TREATMENT PLAN Investigation/restoration removal Reassessment of the tooth and its prognosis Confirm the definitive diagnosis and cause(s) Finalize and continue the treatment plan
  • 37. GROSSMAN’S CLASSIFICATION Symptomatic periradicular diseases Symptomatic apical periodontitis Vital tooth Nonvital tooth Acute alveolar abscess Acute exacerbation of asymptomatic apical periodontitis (phoenix abscess) Asymptomatic periradicular diseases Asymptomatic apical periodontitis Chronic alveolar abscess Radicular cyst Condensing osteitis External root resorption Persistent apical periodontitis Diseases of the periradicular tissues of nonendodontic origin
  • 38. WHO CLASSIFICATION CODE NUMBER CATEGORY K04.4 Acute apical periodontitis K04.5 Chronic apical periodontitis (apical granuloma) K04.6 Periapical abscess with sinus (dentoalveolar abscess with sinus, periodontal abscess of pulpal origin)K04.60 Periapical abscess with sinus to maxillary antrum K04.61 Periapical abscess with sinus to nasal cavity K04.62 Periapical abscess with sinus to oral cavity Ko4.63 Periapical abscess with sinus to skin Ko4.7 Periapical abscess with out sinus Ko4.8 Radicular cyst(apical periodontal cyst, periapical cyst) Ko4.80 Apical & Lateral cyst Ko4.81 Residual cyst Ko4.82 Inflammatory Paradental cyst
  • 39. WEINE’S CLASSIFICATION Painful pulpoperiapical pathosis Incipient acute apical periodontitis Advanced acute apical periodontitis Acute Periapical abscess Phoenix abscess Subacute Periapical abscess Non painful Periapical pathosis Condensing ostestis Incipient chronic apical periodontitis Advanced chronic apical periodontitis Periapical granuloma Chronic Periapical abscess Periapical cyst
  • 40. INGLE’S CLASSIFICATION Painfulpulpoperiapicalpathosis Acute apical periodontitis Advanced acute apical periodontitis Acute apical abscess Phoenix abscess Suppurative apical periodontitis Nonpainfulpulpoperiapicalpathosis Condensing ostetis Chronic apical periodontitis Incipient Advanced Chronic apical periodontitis Periapical granuloma Apical cyst Suppurative apical periodontitis
  • 41. CLINICAL CLASSIFICATION OF THE STATUS OF THE PERIRADICULAR TISSUES World Health Organisation. Application of the International Classification of Diseases to dentistry and stomatology, 3rd edn. Geneva: WHO, 1995: 66–67. Facial cellulitis Extra-radicular infection Foreign body reaction Periapical scar External root resorption Surface Inflammatory Replacement Invasive Pressure Orthodontic Physiological Clinically normal periapical/periradicul ar tissues Apical periodontitis Acute Primary Secondary (or acute exacerbation) Chronic Granuloma Condensing osteitis Periapical cyst True cyst Pocket cyst Periapical abscess Acute Primary Secondary Chronic
  • 42. • Nair’s criteria included – the distribution and type of inflammatory cells within the lesion, – the presence or absence of epithelial cells, – whether the lesion had transformed into a cyst and, – if so, the relationship of the cyst-cavity to the apical foramen of the root canal of the affected tooth. Nair PNR. Apical periodontitis: a dynamic encounter between root canal infection and host response. Periodontology 2000 1997: 13: 121–148 Periapical Radiolucencies Acute Apical Periodontitis Primary Secondary Chronic Apical Periodontitis Apical Abscess Acute Chronic Periapical Cyst True Pocket
  • 44. APICAL PERIODONTITIS • Inflammation of the periodontal ligament around the root apex • Resorption of the periapical bone , root apex. - Acute depending upon the virulence of the microorganisms involved - Chronic the type and severity of the physical or chemical irritants, And host resistance • Common causes – Spread of infection following pulp necrosis, – Occlusal trauma from a high restoration or biting suddenly on a hard object, – Inadvertent endodontic procedures • Over instrumentation, • Pushing the infected material into the apical portion • Chemical irritation from root canal medicamentsPaul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics 2004, 8, 36–54
  • 45. The World Health Organization has classified apical periodontitis in five categories: • Acute apical periodontitis of pulpal origin • Chronic apical periodontitis of pulpal origin • Periapical abscess with sinus • Periapical abscess without sinus • Radicular cysts Paul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics 2004, 8, 36–54
  • 46. ACUTE APICAL PERIODONTITIS Painful inflammation of the periodontium as a result of trauma, irritation, or infection through the root canal, regardless of whether the pulp is vital or nonvital, producing clinical symptoms including painful response to biting and percussion. history of previous pulpitis. • Symptomatic Apical Periodontitis. Grossman’s endodontic practice: 11th edition
  • 47. ETIOLOGY Vital tooth Occlusal trauma • Abnormal occlusal contacts • Recently inserted restoration extending beyond the occlusal plane • Wedging of a foreign object between the teeth, such as a toothpick or food • Traumatic blow to the teeth Nonvital tooth. Sequelae of pulpal diseases • Diffusion of bacteria and noxious products from inflamed or necrotic pulp Iatrogenic causes : • Root canal instrumentation forcing bacteria or debris inadvertently through the apical foramen • Forcing of irritating irrigants or medicaments through the apical foramen • Extension of obturating material through the apical foramen to impinge on periradicular tissues • Perforation of the root • Overinstrumentation during shaping and cleaning of root canals Grossman’s endodontic practice: 11th edition
  • 48. Paul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics 2004, 8, 36–54
  • 49. CLINICAL FEATURES • Pain and tenderness of the tooth. • Slightly sore ~ Sometimes only when it is percussed in a certain direction – Or the soreness may be severe. • The tooth may feel extruded and the patient may have pain on closure and mastication. • The tooth is slightly elevated in its socket – Due to the collection of inflammatory edema in the periodontal ligament – Causes tenderness while biting or even to mere touch. • Thermal change does not induce pain as in pulpitie • External pressure on tooth forces the edema fluid against already sensitized nerve endings  severe pain. Grossman’s endodontic practice: 11th edition
  • 50. • symptoms are either the result of – irritation originating from endodontic treatment – caused by overinstrumentation, – medicinal irritants, – overfilling, in which case the tooth is pulpless, – result of noxious stimuli irritating the periodontal ligament, in which case the pulp is vital.
  • 51. RADIOGRAPHIC APPEARANCE Trauma Abnormal Occlusal Contacts Orthodontic Treatment Nonvital tooth: A slight widening of the apical periodontal ligament space and loss of the apical lamina dura of the involved pulpless tooth may be seen Vital tooth: No radiographic changes with normal periradicular structures Grossman’s endodontic practice: 11th edition
  • 52. Periodontitis caused due to carious exposure Grossman’s endodontic practice: 11th edition
  • 53. DIAGNOSIS • Look for decay, fracture lines, swelling, sinus tracts, orientation of tooth, hyperocclusion Visual • mucosa overlying the root apex: may or may not be tender to palpation. Tooth: tender on percussion or slight pressure • Moderate mobility- check for periodontal condition Mobility: slight to no mobility • Response not prolonged- consider traumatic occlusion • Response prolonged- irreversible pulpitis • No response- necrotic pulp Thermal test • Response- pulp is vital • No response- pulp non vital Electric pulp testing Grossman’s endodontic practice: 11th edition
  • 54. DIFFERENTIAL DIAGNOSIS • Acute alveolar abscess – represents a further stage in development of disease – breakdown of periradicular tissue,. • The patient’s history, symptoms, and clinical test results help the clinician to differentiate these diseases. Grossman’s endodontic practice: 11th edition
  • 55. HISTOPATHOLOGY Acute trauma Transient inflammation • neutrophils release stimulate osteoclasts resorb the surrounding bone detectable periapical radiolucency Inflammatory reaction in pdl Dilation of blood vessels infiltration with polymorphonuclear leukocytes transmigration from the blood vessels into perivascular tissue space Accumulation of serous exudate Distension of Pdl & extrusion of tooth, slight tenderness If continuous irritation occurs, loss of alveolar bone
  • 56. BACTERIOLOGY • Blow, occlusal trauma, or chemical or mechanical irritation during endodontic treatment.  The pulp and periradicular tissues may be sterile • Bacteria or toxic bacterial products present in the root canal may either be forced through or grow beyond the apical foramen and may irritate the apical periodontal tissues Grossman’s endodontic practice: 11th edition
  • 57. TREATMENT AND PROGNOSIS Immediate line of management Determining the cause and relieving the Symptoms Occlusal trauma Relieved by selective occlusal grinding. Non vital infected pulp Endodontic treatment to drain the exudate. When the acute phase has subsided, the tooth is treated by conservative means. Prognosis: Generally favorable. The occurrence of symptoms during endodontic treatment in no way affects the ultimate outcome of the treatment
  • 58. OUTCOME Paul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics 2004, 8, 36–54
  • 60. ACUTE ALVEOLAR ABSCESS An inflammatory reaction to pulpal infection and necrosis characterized by rapid onset, spontaneous pain, tenderness of the tooth to pressure, pus formation, and eventual swelling of associated tissues. • Synonyms: Acute abscess, acute apical abscess, acute dentoalveolar abscess, acute periapical abscess, and acute radicular abscess.
  • 61. ETIOLOGY • Bacterial invasion of dead pulp tissue. • Trauma • chemical or mechanical irritation • Because the pulp tissue is solidly enclosed, no drainage is possible and the infection continues to extend in the direction of least resistance, i.e., through the apical foramen, and thereby involves the periodontal ligament and the periradicular bone.
  • 62. CLINICAL FEATURES • Purulent material accumulates within alveolusSymptomatic • Tenderness: • Relieved by continued slight pressure on the extruded tooth to push it back into the alveolus First symptom • Spontaneous, severe, throbbing pain, exacerbated by lying down with attendant swelling of the overlying soft tissue. Later • More pronounced, extends beyond original site. • Tooth: more painful, elongated, and mobile. • At times, the pain may subside or cease entirely while the adjacent tissue continues to swell. Swelling • Infection progresses to chronic apical abscess  Contained pus may break through to form a sinus tract, opening in labial or buccal mucosa. If left unattended • osteitis, periosteitis, cellulitis, or osteomyelitis. May further progress • Adjacent tissues close to the affected tooth. • Extensive  cellulitis may distort the patient’s appearance grotesquely. Swelling Grossman’s endodontic practice: 11th edition
  • 63. Maxillary teeth: drain through buccal or palatal bone into oral cavity or maxillary sinus or the nasal cavity. Anterior tooth: cuspid swelling of the upper lip may extend to one or both the eyelids.Posterior tooth  the cheek may swell to an immense size, distorting the patient’s facial features Mandibular teeth: drain through the buccal or lingual bone into the oral cavity. Anterior tooth swelling can involve the lower lip and chin, and in severe cases, the neck. Posterior tooth swelling of the cheek may extend to the ear or even around the border of the jaw into the submaxillary region Infectious process extend into fascial spaces of the head and neck  cellulitis and systemic signs and symptoms, with consequent complications. Grossman’s endodontic practice: 11th edition José F. Siqueira, Jr., Isabela N. Rôças . Microbiology and Treatment of Acute Apical Abscesses. Clinical Microbiology Reviews, April 2013;26 (2):255-273
  • 64. (A) An individual with spread acute apical abscess. (B) A bone radiolucent lesion is visible around the root apexes of the mandibular second molar, which is the source of infection. (C) Incisional drainage is essential for management of these conditions. In this complicated case, it was performed extraorally. • (Courtesy of Craig Baumgartner.) José F. Siqueira, Jr., Isabela N. Rôças . Microbiology and Treatment of Acute Apical Abscesses. Clinical Microbiology Reviews, April 2013;26 (2):255-273
  • 65. • Swelling : taut and inflamed; • Pus formation : liquefaction  proteolytic enzymes: trypsin and cathepsin. • Pressure of the underlying pus rupture from pressure  extrude through a tiny opening beginning of a chronic alveolar abscess. • Elimination of the infection  Sinus tract: heals by granulation Grossman’s endodontic practice: 11th edition
  • 66. SYSTEMIC REACTIONS • Pt may appear pale, irritable & weakened due to pain & loss of sleep. • Mild cases- slight rise in temp (99-100˚C) • Severe cases- temp above normal (102-103˚C) • Fever: preceded or accompanies by chills. • Intestinal stasis: orally- coated tongue & foul breath. • Headache & malaise Grossman’s endodontic practice: 11th edition
  • 67. COMPLICATIONS • 60% of all nontraumatic dental emergencies are associated • Mortality: result of sepsis or airway obstruction, but death due to a spreading infection leading to massive hemorrhage from the subclavian vein into the pleural cavity has been reported. • Fascial plane infections- – Sublingual, Submandibular, Buccal, Pterygomandibular spaces, Temporal – Masseteric, Lateral pharyngeal, Retropharyngeal • Brain abscess • Septicemia in a patient with multiple myeloma • deep neck infection • Mediastinitis • necrotizing fasciitis • orbital abscess • cervical spondylodiscitis with spinal epidural abscess • Host-related factors: Contribute toward increased morbidity and mortality diabetes, chronic alcohol and tobacco consumption, malnourishment, and the use of illicit substances
  • 68. RADIOGRAPHIC FEATURES • Acute reaction - develops very quickly • May not show radiographic evidence of periradicular bone destruction. • Radiographic periradicular radiolucency: abscess is result of exacerbation of a previous chronic asymptomatic condition • Thickening of the apical periodontal ligament • Ill-defined radiolucency Zcm, nevilleOral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 69. DIAGNOSIS • clinical examination and from the subjective history. • Early stages: difficult to locate the tooth because of the absence of clinical signs and the presence of diffuse, annoying pain. • Progressed infection periodontitis & extrusion tooth easily located • Radiograph: Cavity / defective restoration / slight widening of the apical periodontal ligament space of the involved tooth. • No response to cold, heat or EPT • tender to percussion, Pain while chewing • Apical mucosa: tender to palpation Grossman’s endodontic practice: 11th edition
  • 70. DIFFERENTIAL DIAGNOSIS • Periodontal abscess : – Infection from periodontium accumulation of pus along the root surface – Periodontal pocket ; swelling and mild pain. – Pressure pus may exude near the edematous tissue or through the sulcus. – Swelling : opposite the midsection of the root and gingival border – Generally associated with vital tooth • Tests for pulp vitality are useful in establishing a correct diagnosis.
  • 71. BACTERIOLOGY • Concentration of microorganisms: unusually large. • Total bacterial loads per abscess case have been reported to range from 104 to 109 cells • Streptococci and staphylococci are generally recovered • Draining purulent material  Sterile : dead leukocytes, dead bacteria. • An analysis of 100 consecutive cases of acute alveolar abscess failed to show a relationship between any specific type of organism and the abscess. José F. Siqueira, Jr., Isabela N. Rôças . Microbiology and Treatment of Acute Apical Abscesses. Clinical Microbiology Reviews, April 2013;26 (2):255-273
  • 72. José F. Siqueira, Jr., Isabela N. Rôças . Microbiology and Treatment of Acute Apical Abscesses. Clinical Microbiology Reviews, April 2013;26 (2):255-273
  • 73. HISTOPATHOLOGY • Active infection  Marked infiltration of polymorphonuclear leukocytes; rapid accumulation of inflammatory exudate  distention of PDL  elongation of tooth. • Periodontal fibers separate  mobility. • Bone resorption at root apex- polymorphonuclear leukocytes die X microorganisms Pus • Microscopically: suppuration empty space; surrounded by viable leukocytes, occasional lymphocytes, cellular debris, necrotic materials and bacterial colonies. • Root canal: appears devoid of tissue,; clumps of microorganisms and debris may be observed • Dilatation of the blood vessels in PDL & marrow spaces of the bone. • Marrow spaces- inflammatory cell infiltrate. • Tissue around area of suppuration: serous exudate. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition Shafer’s textbook of Oral Pathology, 7th edition
  • 74. TREATMENT • Incision for drainage • Root canal treatment or extraction of the involved tooth to remove the source of infection • Decisive triad for the successful management of complications of acute dental abscesses – early diagnosis, – initiation of empirical antibiotic therapy, and – timely surgical intervention Grossman’s endodontic practice: 11th edition
  • 75. I) Immediate task: Relieve pressure  drainage opening up the pulp chamber. • Gaining access - difficult - tooth is often extremely tender. • Gently grip the tooth - use small, round, diamond bur • Immediate relief - pus drains feely from an access cavity. • If drainage is not immediate- explore apical foramen with very fine (size 08 or 10) file. – Foramen not be instrumented or enlarged, and if drainage does not result the procedure should not be persevered. Endodontics: Part 3. Treatment of endodontic emergencies. P. Carrotte. BRITISH DENTAL JOURNAL VOLUME 197 NO. 6 SEPTEMBER 25 2004
  • 76. INCISION TO ESTABLISH DRAINAGE • Soft-tissue swelling Pointing intra-orally Incision. • Use of copious amounts of surface analgesia. – Regional anaesthesia may not be effective due to the presence of pus. – local analgesic solution may spread the infection further into the tissues. • Incise the swelling with a Bard Parker No. 11 or 15 scalpel blade • Aspirate using a wide bore needle and disposable syringe. It may be possible to aspirate the abscess via the root canal as well. • Sample can be sent for bacteriological examination • Drain: piece of quarter-inch or half-inch selvage gauze may be used. • Same criteria when extra-oral drainage is indicated. Endodontics: Part 3. Treatment of endodontic emergencies. P. Carrotte. BRITISH DENTAL JOURNAL VOLUME 197 NO. 6 SEPTEMBER 25 2004
  • 77. TREPHINATION • In the absence of swelling • Surgical perforation of the alveolar cortical plate. • to release the accumulated inflammatory and infective tissue exudate from between the cortical plates • Engine-driven perforator entering through the cortical  cancellous bone – without the need for an incision, – provide pathway for drainage from the periradicular tissues. • Care to guard against injury to the tooth root or surrounding structures Cohen’s Pathways of the Pulp,11th edition
  • 78. ROOT CANAL TREATMENT Access and initial drainage; Isolation using rubber dam Irrigation: Sodium hypochlorite remove superficial organic and inorganic debris considerable pain relief. Ultrasonically activated endodontic files - effectively flush infected debris from the root canal system.. Do not to push necrotic debris beyond the apex – • Positive-pressure irrigation methods- needle-and-syringe irrigation: risk of expressing debris or solution out of the apex. • Electronic apex locators- accuracy in determining working length measurements  thorough canal debridement and less apical extrusion. • Crown-down instrumentation- remove most of the debris coronally rather than pushing it out the apex Endodontics: Part 3. Treatment of endodontic emergencies. P. Carrotte. BRITISH DENTAL JOURNAL VOLUME 197 NO. 6 SEPTEMBER 25 2004
  • 79. Canals dried with paper points Dry sterile cotton wool pledget placed in the pulp chamber to prevent ingress of the temporary dressing. Access cavity sealed to prevent re-infection of the canals from the oral cavity. Patient must be recalled within 48 hours complete instrumentation ; Intracanal calcium hydroxide dressing
  • 80. ANTIBIOTICS • Not necessary in most cases of localized and uncomplicated apical abscesses. • Analgesics: pain control. • Antibiotics are indicated – abscesses associated with systemic involvement, including fever, malaise, and lymphadenopathy; – disseminating infections resulting in cellulitis, progressive diffuse swelling, and/or trismus; – abscesses in medically compromised patients who are at increased risk of a secondary (focal) infection following bacteremia. Endodontics: Part 3. Treatment of endodontic emergencies. P. Carrotte. BRITISH DENTAL JOURNAL VOLUME 197 NO. 6 SEPTEMBER 25 2004
  • 81. Penicillins : first choice for treatment of endodontic infections •Most of the bacterial species involved with endodontic infections, including abscesses, are susceptible to penicillins •Penicillin V or amoxicillin •Amoxycillin: 250 mg three times a day until the infection is under control Amoxicillin + Clavulenic acid/ Metronidazole (the spectrum of action extended to include penicillin- resistant Strains) Metronidazole: alternative where the penicillins are contraindicated. Clindamycin: strong antimicrobial activity against oral anaerobes •effective alternative in patients allergic to penicillin or when treatment with amoxicillin resulted in failure. Moxifloxacin: fluoroquinolone- good antibacterial activity against Gram-positive and Gram-negative aerobic and anaerobic bacteria isolated from odontogenic infections •A clinical trial : significantly better pain reduction and overall clinical response than clindamycin for patients with dental abscesses Oral cephalosporins and macrolides: little use- decreased activity against Fusobacterium and nonpigmented Prevotella species José F. Siqueira, Jr., Isabela N. Rôças . Microbiology and Treatment of Acute Apical Abscesses. Clinical Microbiology Reviews, April 2013;26 (2):255-273
  • 82. • Facial photographs. (A) Preoperative. (B) A decrease in inflammation is observed two days after the first treatment appointment. (B) Postoperative. (D) Follow-up at 16 months • Radiographic examination. (A) Preoperative. (B) Postoperative. Follow-up at (C) 1 month and (D) 16 months. Jesús Alejandro Quiñones Pedraza, Maria Argelia Akemi Nakagoshi Cepeda, Jorge Jaime Flores Treviño, Idalia Rodriguez Delgado, Sergio Eduardo Nakagoshi Cepeda and Rosalva González Meléndez . Endodontic management of acute apical abscess: A case report. International Journal of Applied Dental Sciences 2017; 3(4):
  • 83. PROGNOSIS • The prognosis for the tooth is generally favorable, depending on the degree of local involvement and the amount of tissue destruction. Although the symptoms of an acute alveolar abscess may be severe, pain and swelling generally subside if adequate drainage is established. • In most cases, the tooth can be saved by endodontic treatment, and the severity of the symptoms need not bear any relation to the ease or difficulty of treatment. • When purulent material has been discharged through the gingival sulcus and the periodontium has been extensively destroyed, the prognosis is guarded. In selected cases, combined periodontal and endodontic treatment will restore the tooth to functional health. Grossman’s endodontic practice: 11th edition
  • 84. CONSEQUENCES OF UNTREATED ABSCESS Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition • With progression, the abscess spreads along the path of least resistance. • The purulence may extend through the medullary spaces away from the apical area, osteomyelitis, • it may perforate the cortex and spread diffusely through the overlying soft tissue  cellulitis • Perforation of cortical plate  permits entrance into the oral cavity sessile swelling or drain through an intraoral sinus  a mass of subacutely inflamed granulation tissue  parulis
  • 86. PHOENIX ABSCESS – Definition – Etiology – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Bacteriology – Histopathology – Treatment – prognosis
  • 87. CHRONIC APICAL PERIODONTITIS – Definition – Etiology – Clinical features – Radiographic features – Histopathology – Zones of well established granuloma – Microbiologic features – Treatment – Prognosis – Outcome – Case report
  • 88. CHRONIC ALVEOLAR ABSCESS – Definition – Synonyms – Etiology – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Histopathology – Treatment – prognosis
  • 89. APICAL PERIODONTAL CYST – Cyst – Apical periodontal cyst • Definition • Epithelial lining • Pathogenesis • Theories of cyst formation – Nutritional deficient theory – Abscess theory • Periapical pocket cyst • Periapical true cyst – Clinical features – Radiographic features – Diagnosis – Differential diagnosis – Bacteriology – Histopathology – Cystic lumen – Treatment • Surgical • Endodontic • marsupilisation – Prognosis – Healing • Periapical pocket cyst • Periapical true cyst – complications
  • 90. CONDENSING OSTEITIS – Definition – Etiology – Clinical features – Radiographic features – Histopathology – Treatment – prognosis
  • 91. EXTERNAL ROOT RESORPTION • Definition • Classification of root resorption – Internal – External • External surface resorption • External inflammatory root resorption • External replacement resorption • Radiographic appearance • Histopathology • Clinical features • Differential diagnosis • Management • Follow-up & prognosis
  • 92. POST-TREATMENT APICAL PERIODONTITIS • Etiology • Management – Retreatment – Surgery • Technical aspects of endodontic retreatment • Case reports • Persistent apical periodontitis – Causes – Bacteriology • Periapical scar/ Surgical defect
  • 93. HYPERCEMENTOSIS • Clinical features • Radiographic features • Factors associated • Histopathology • Treatment • Prognosis • Lesions with non-endodontic origin with vital pulp • Non endodontic periradicular lesions
  • 94. • Summary – Conditions and diagnosis – Management of symptomatic conditions • Previously Asked Questions
  • 96. ACUTE EXACERBATION OF ASYMPTOMATIC APICAL PERIODONTITIS • Named after the mythical bird that would die, only to arise again from its own ashes. • In progressive periapical granulomas, the enlargement often is not continuous but occurs in spurts associated with periodic acute exacerbations. • Etiology 1.When state of equillibrium in granuloma /cyst is upset by: • Influx of bacteria/necrotic products of high virulence and antigenicity • Lowering of host defenses 2. Mechanical irritation during RCT. Acute inflammatory reaction superimposed on an existing asymptomatic apical periodontitis.
  • 97. CLINICAL FEATURES • exacerbated and exaggerated pain. • may or may not be associated with pus & suppuration • Initially, tooth may be tender on palpation. • Loss of Vitality • As inflammation progresses, tooth gets elevated from the socket & becomes sensitive. • Mucosa over the radicular area may appear red & swollen & sensitive to palpation. • Most commonly associated with initiation of root canal therapy. • Mobility may be observed Endodontics: Part 3. Treatment of endodontic emergencies. P. Carrotte. BRITISH DENTAL JOURNAL VOLUME 197 NO. 6 SEPTEMBER 25 2004
  • 98. DIAGNOSIS • Associated with the initiation of root canal therapy in a completely asymptomatic tooth. • The radiograph shows a well- defined periradicular lesion • History of trauma  discoloring of the tooth ; postoperative pain that had subsided until then. • Negative response to vitality tests: necrotic pulp. – Rare occasions- +ve electric pulp test  fluid in the root canal or in a multirooted tooth. Grossman’s endodontic practice: 11th edition
  • 99. DIFFERENTIAL DIAGNOSIS • symptoms similar to those of an acute alveolar abscess. • Because the treatment of both lesions is the same, no differential diagnosis is needed. • Pulp vitality: Painful pulpitis • Acute alveolar : widening of the periodontal ligament space is the only radiographic change seen. Grossman’s endodontic practice: 11th edition
  • 100. BACTERIOLOGY • An abscess usually forms as a result of microbial infection, although some abscesses, called sterile abscesses, form in the absence of bacteria. • The periradicular lesions are usually devoid of bacteria, except for transient bacteria. Grossman’s endodontic practice: 11th edition
  • 101. HISTOPATHOLOGY • Phoenix abscesses can maintain a soft tissue component; • Subacutely inflamed periapical granulomas or cysts intermixed with areas of significant abscess formation. • In these cases the pathologist typically diagnoses the primary lesion but comments about the abscess formation. • Areas of liquefaction necrosis + disintegrating polymorphonuclear neutrophils and cellular debris (pus) • Surrounded by infiltration of macrophages; some lymphocytes and plasma cells. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition Grossman’s endodontic practice: 11th edition
  • 102. TREATMENT AND PROGNOSIS • Same as acute alveolar abscess. • The prognosis for the tooth is good once the symptoms have subsided Grossman’s endodontic practice: 11th edition
  • 104. Asymptomatic apical periodontitis is the symptomless sequelae of symptomatic apical periodontitis and is characterized radiographically by periradicular radiolucent changes and histologically by the lesion dominated with macrophages, lymphocytes, and plasma cells. • Low-grade infection; Most common sequelae of pulpitis or acute periapical periodontitis. • If the acute process is left untreated, it is incompletely resolved and becomes chronic proliferative. • Spread of pulp infection - usually- periapical direction. • Lateral or accessory root canals opening on the lateral surface of the root at any level - ‘lateral’ granuloma or related inflammatory lesion.
  • 105. CLINICAL FEATURES • nonvital • slightly tender to percussion • Percussion- dull sound • mild pain on biting or chewing on solid food • the tooth feels slightly elongated in its socket • Sensitivity- due to hyperemia, edema, and inflammation of the apical periodontal ligament. Many cases are entirely asymptomatic. No perforation of overlying bone and oral mucosa with the formation of a fistulous tract unless the lesion undergoes an acute exacerbation.
  • 106. RADIOGRAPHIC FEATURES • Earliest periapical change -thickening of the ligament at the root apex. • Radiolucent area of variable size - attached to the root apex: Well- circumscribed, definitely demarcated from the surrounding bone. • Thin radiopaque line  a zone of sclerotic bone may sometimes be seen outlining the lesion  periapical lesion is a slowly progressive and long standing one that has probably not undergone an acute exacerbation • Thickening of the apical periodontal membrane - large carious lesion involving the dental pulp Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 107. • Periapical radiolucencies destruction of bone and replacement by granulation tissue. (A) maxillary central incisor: carious lesion of the distal surface that involves the pulp. (B) mandibular incisors: traumatic injury with loss of pulp vitality and subsequent formation of diffuse periapical granulomata. • Periphery: Diffuse blending of the radiolucent area with the surrounding bone. – Due to the difference in cellular activity around the margins of the lesion • Root resorption- occasionally observed. Shafer’s Textbook of Oral Pathology, 7th edition
  • 108. HISTOPATHOLOGY • Chronic process from the onsetdoes not pass through acute phase. • Hyperemia and edema of the PDL; infiltration of chronic inflammatory cells. • Inflammation + Increased vascularity  resorption of the supporting bone proliferation of fibroblasts and endothelial cells formation of more tiny vascular channels & numerous delicate connective tissue fibrils. • Homogeneous lesion: – predominantly of macrophages, lymphocytes, and plasma cells – less frequently with mast cells and eosinophils, – qualifies as an immune-type granuloma. • Athanassiades and Spears, and Page et al.: – more lymphocytes and plasma cells than non-immune granulomas relatively pure collections of macrophages and giant cellsShafer’s Textbook of Oral Pathology, 7th edition
  • 109. Typical periapical granuloma: (A) delicate fibrillar stroma with intense lymphocytic and plasma cell infiltration (A) polymorphonuclear leukocytes as well as many small capillaries (B) Collections of macrophages that are often filled with lipoid material (C) Cholesterol slits in the tissue (D) Surrounded by a connective tissue ‘capsule’ Shafer’s Textbook of Oral Pathology, 7th edition
  • 110. Shafer’s textbook of Oral Pathology, 7th edition
  • 111. • Majority of the small lymphocytes (81%) was designated non-B lymphocytes. • Plasma cells contained Russell bodies, some of which were subsequently extruded and could be found extracellularly. • The non-B lymphocytes  T cells of the cellular arm of the immune system, expression of delayed type hypersensitivity. • T cell activity bone and tooth resorption through the production of osteoclast activating factor (OAF). • Presence of antibody-producing lymphocytes and plasma cells- antibodies - specificity provide clues to the antigens causes of periapical granulomas and cysts • Macrophages and other mononuclear phagocytes are the hallmarks • Dendritic cells – Kaneko T et al: associated with local defense reactions as stronger antigen presenting than macrophages. Shafer’s textbook of Oral Pathology, 7th edition
  • 112. • Phagocytes- ingest lipid material Foam cells • Abundant mast cells. • Deposits of cholesterol as well as hemosiderin  derived from the breakdown of extravasated red blood cells. • Cholesterol crystals : clear needle like spaces or clefts – associated with multinucleated giant cells of the foreign body type
  • 113. Giant-cell hyaline angiopathy. • described by Dunlap and Barker • consists of inflammatory cell infiltration, collections of foreign body type giant cells, and the presence of ring like structures known as Rushton bodies, composed of an eosinophilic material resembling hyalinized collagen. • King and Mincer et al.: Fragments of foreign material, sometimes resembling vegetable matter such as legumes pulse granuloma’ • Dunlap and Barker : Earliest change - acute vasculitis with subsequent thickening and hyalinization of vessel walls. – Not confined to periapical granulomas – Reported in granulomas in edentulous jaws, in a nasopalatine duct cyst, and in chronic periostitis. • Chen and his colleagues : endogenous in origin- studied by both electron microscopy and immunoperoxidase procedure. Shafer’s textbook of Oral Pathology, 7th edition
  • 114. ZONES OF WELL ESTABLISHED GRANULOMA
  • 115. MICROBIOLOGIC FEATURES • Pre-extraction cultures: – few instances through the root canal or the alveolar plate – relatively free of actual contamination. • Burket : The microorganisms generally found in the oral cavity, such as Streptococcus viridans, Streptococcus hemolyticus, nonhemolytic streptococci, Staphylococcus aureus, Staphylococcus albus, Escherichia coli, and pneumococci. • Seldom can microorganisms actually be demonstrated histologically in the periapical granuloma. • Some investigatiors: Dental granuloma is usually a sterile lesion. • Current evidence: many lesions may be infected before and after endodontic treatment Shafer’s textbook of Oral Pathology, 7th edition
  • 116. Iwu et al. 88% or 14 of 16 periapical granulomas were bacteria positive Mixed infections - not been possible to associate particular types of microorganisms with specific periapical lesions, based upon either clinical or histologic evaluation. Sebati M and Slots J 34 periapical lesions, that most teeth with necrosed pulp and periapical lesions harbored human cytomegalovirus and Epstein-Barr virus in periapical granulomatous tissue, along with the endodontopathic bacteria Slots J and coworkers 25 symptomatic and 19 nonsymptomatic periapical lesions- human cytomegalovirus (HCMV) in 100% of symptomatic and 37% of non-symptomatic periapical lesions and Epstein- Barr virus (EBV) only in lesions infected with HCMV. induction of cytokine and lymphokine induction from inflammatory or connective tissue cells or by impairing the local host defenses which increase the virulence of resident bacterial pathogens.Shafer’s textbook of Oral Pathology, 7th edition
  • 117. TREATMENT • Reduction and control of the offending organisms. – If the tooth can be maintained, then root canal therapy can be performed. • Non restorable teeth: Extracted, followed by curettage of all apical soft tissue. • Symptomatic cases: (NSAIDs) are beneficial; – use of systemic antibiotic medications is not recommended unless associated swelling or systemic changes are present. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 118. • Teeth treated endodontically should be evaluated at 1- and 2-year intervals (at a minimum) to rule out possible lesional enlargement and to ensure appropriate healing. • Evaluations at 1, 3, and 6 months are appropriate. Follow-up • failure can occur in cases with excellent endodontic therapy but poor coronal restoration. Coronal restoration is critical • endodontic retreatment represents the best approach for minimizing the bacterial contamination and should be considered before periapical surgery. If initial conventional therapy is unsuccessful • lesions larger than 2 cm • teeth not appropriate for conventional endodontic therapy. • thorough curettage of all periradicular soft tissue, amputation of the apical portion of the root, and sealing the foramen of the canal. Periapical surgery • histopathologic examination and diagnostic confirmation are mandatory. Surgical sites: failed to respond to appropriate therapy Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 119. OUTCOME Asymptomatic apical periodontitis Repair of after root canal therapy severe periapical tissue destruction acute exacerbati on abscess - draining sinus tract cellulitis. Grossman’s endodontic practice: 11th edition
  • 120. • Chief complaint- painful swelling left temporal region; trismus • medical history - osteoporosis, no medication. • Diffuse, elastic soft, and painful swelling at the left side of the temporal region • Intraorally- left maxillary second molar : tender on percussion and gingival tenderness of apical area Sayaka Yoshiba, Takaaki Kamatani, Tatsuo Shirota. Temporal Fossa Abscess Caused by Apical Periodontitis: A Case Report. Open Journal of Clinical Diagnostics, 2018, 8, 47-51
  • 121. • Leukocytes - 10,300/μl ; C-reactive protein (CRP) 11mg/dl • Albumin- decreased difficult food intake by trismus. • Computed tomography: low density area range from pterygomandibular region to temporal region – abscess formation suspected. • Diagnosis- Temporal fossa abscess due to the periapical periodontitis of the upper left second molar.
  • 122. Immediate treatment Hospitalized for anti-inflammatory treatment. Day 1 Drainage : incision line designed at temporal skin Fusobacterium species detected in pus. Day 1 to Day 4 Ampicillin 3 g/day IV. Day 5 Since the drainage amount was reduced, Ampicillin - 2 g/day. Day 9 Leukocytes - 5500/μl ; CRP - 0.5 mg/dl. Mouth opening training inter-incisal distance- 5 mm to 20 mm. Day 12 extraction of the upper left side of the second molar Day 15 patient recovered satisfactory and left hospital Follow up The patient continues to mouth opening training in the outpatient.
  • 124. A chronic alveolar abscess is a longstanding, low-grade infection of the periradicular alveolar bone generally symptomless and characterized by the presence of an abscess draining through a sinus tract. Synonyms – Chronic suppurative apical periodontitis, – Suppurative periradicular periodontitis, – chronic apical abscess, – chronic periradicular abscess, – chronic periapical abscess Grossman’s endodontic practice: 11th edition
  • 125. CAUSES • Necrosed pulp • Preexisting acute abscess Grossman’s endodontic practice: 11th edition
  • 126. SYMPTOMS • Generally asymptomatic, or only mildly painful. • Detected only during routine radiographic examination or because of the presence of a sinus tract, which can be either intraoral or extraoral. • The sinus tract usually prevents exacerbation or swelling by providing continual drainage of the periradicular lesion • The point at which the pus breaks into the mouth depends on the thickness of the alveolar bone and the overlying soft tissues. • Obviously, the confined pus takes the path of least resistance Cohen’s Pathways of the Pulp,11th edition
  • 127. Upper jaw,: along the labial alveolar plate which is thinner than the palatal plate of bone. upper lateral incisors , palatal root of a maxillary molar: palatally because these roots lie in closer proximity to the palatal plate of bone lower jaw: Vestibule -along the buccal alveolar plate -may occur along the lingual alveolar wall in the case of lower molars Grossman’s endodontic practice: 11th edition
  • 128. DIAGNOSIS • Patient may remember a sudden, sharp pain that subsided & not recurred, or he or she may relate a history of traumatic injury. • Clinical examination: a cavity, a composite or metallic restoration, or a full coverage crown • Slight pain in relation to the tooth, particularly during mastication. • Non vital teeth: negative electric pulp test or to thermal tests. • At times, the sinus tract is several teeth away from the cause. • Open cavity  drainage by root canal. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 129. RADIOGRAPHIC FEATURES • The first sign of osseous breakdown is radiographic evidence seen during routine examination or discoloration of the crown of the tooth. • radiograph taken after the insertion of a gutta-percha cone into the sinus tract often shows the involved tooth by tracing the sinus tract to its origin • Diffuse area of bone rarefaction- so diffuse as to fade indistinctly into normal bone • Nondiagnostic. • Periodontal ligament is thickened.
  • 130. DIFFERENTIAL DIAGNOSIS • CYST: presence of a diffuse area indicated an abscess, a circumscribed area indicated an asymptomatic apical periodontitis, and a sclerotic bony outline was a sign of a cyst • however, all attempts to correlate the radiographic appearance of an area with its histopathologic features failed. • As a result, a proper and accurate diagnosis can be made only when a tissue specimen has been examined histologically.
  • 131. HISTOPATHOLOGY• Progression of infective process into periradicular tissues detachment or loss of periodontal fibers at the root apex  destruction of the apical periodontal ligament. • The apical cementum may also become affected. • The root canal itself may appear to be empty, or cellular debris may be present. Bacteria were found infrequently on microscopic examination of 230 periapical tissue specimens removed during root resection. Center: Polymorphonuclear leukocytes, Mononuclear cells.Periphery: Lymphocytes and plasma cells Capsule: Fibroblasts
  • 132. • Suppurative material from the interior of the abscess is discharged on the mucosa or gingiva. – may or may not be continuous. • Intermittent: discharge preceded by swelling • Stoma formation: Pressure from pus rupture the thin wall of soft tissue discharge of suppurative material into mouth – The opening may heal and may close again – May reopen: pressure from the contained pus overcomes the resistance of the undermined layer of soft tissue. • Parulis: Small elevation of the mucosa – In conjunction with infection of the deciduous and permanent teeth
  • 133. • Sinus tract - surface of the face -young person. • Associated with lower anterior teeth opens near the symphysis of the jaw, • Associated with posterior teeth - chiefly the first molar along the inferior border of the mandible • Rare cases: purulent material encounters least resistance along the root  into the gingival sulcus impression of a pocket of periodontal origin
  • 134. TREATMENT • Elimination of infection. • Cleaning, shaping of root canal, intracanal medicament sealed in to reduce the bacterial flora sinus tract closes up and disappears
  • 135. Chronic alveolar abscess in relation to a maxillary central incisor with a history of surgical endodontic therapy. Gutta-percha tracing being done through the labial sinus opening. Tracing indicative of periradicular infection in relation to the apical third of the involved tooth. Retreatment of the root canal completed Complete resolution of the sinus after completion of the treatment. Three-year follow- up radiograph showing healing of the periradicular region
  • 136. PROGNOSIS • Depends on proper cleaning, shaping, and obturation of the root canals. • Periodontal status, restorative needs, and potential for functional rehabilitation
  • 138. CYST • A cyst is a closed cavity or sac internally lined with epithelium, the center of which is filled with fluid or semisolid material • Cysts of the jaws are divided into • Odontogenic- arise from odontogenic epithelium – Follicular, arising from the enamel organ or follicle, – Radicular, arising from the cell rests of Malassez. • Nonodontogenic- – Fissural, arising from epithelial remnants entrapped in the fusion of the facial processes – Nasopalatine, arising from the remnants of nasopalatine duct. • Nonepithelial- bony cavities that are not lined with epithelium and, therefore, are not truly cysts. – traumatic cysts – idiopathic bone cavities – aneurysmal bone cysts.
  • 139. APICAL PERIODONTAL CYST RADICULAR CYST, PERIAPICAL CYST, ROOT END CYST • slowly growing epithelial sac at the apex of a tooth that lines a pathologic cavity in the alveolar bone • most common odontogenic cyst • usual but not inevitable sequela of the periapical granuloma • true cyst- epithelial lining is derived from the epithelial rests of Malassez • Epithelium may be derived in some cases from – Respiratory epithelium of the maxillary sinus when the periapical lesion communicates with the sinus wall – Oral epithelium from a fistulous tract – Oral epithelium proliferating apically from a periodontal pocket.
  • 140. PATHOGENESIS • Lumen: lined by stratified squamous epithelium • Wall: made up of condensed connective tissue. • Inflammation in the periapical granuloma  Stimulus for the proliferation of epithelium – Induced by the keratinocyte growth factor elaborated by the stromal cells of the periodontal ligament, or inflammatory stimulus. • Gao et al: Activated T cells in the periapical granulomas produce lymphokines act on the rest of Malassez  proliferation and altered differentiation  Cyst formation Shafer’s textbook of Oral Pathology, 7th edition
  • 141. NUTRITIONAL DEFICIENT THEORY: T cells in the periapical granulomas produce lymphokines Act on the cell rest of Malassez Proliferation and altered differentiation leading to cyst formation Irregular pattern of growth Epithelial mass increases in size by division of the cells on the periphery Cells in the central portion of the mass separated from source of nutrition Central cells fail to obtain sufficient nutrients Eventually degenerate, become necrotic, and liquefy Epithelium-lined cavity filled with fluid THE APICAL PERIODONTAL CYST
  • 142. ABSCESS THEORY Abscess cavity in connective tissue Surrounded with proliferating epithelial tissue Formation of Cyst. Grossman’s endodontic practice: 11th edition
  • 143. Paul V. Abott, Classification, diagnosis and clinical manifestations of apical Periodontitis. Endodontic Topics 2004, 8, 36–54
  • 144. • Epithelial-lined cavity  open towards the root canal of the affected tooth. • initiated by accumulation of neutrophils around the apical foramen • Microabscess- enclosed by the proliferating epithelium, forming a collar with epithelial attachment on contacting the root tip. • Apical pouch seals off infected root canals with microabscess from periapical tissue milieu PERIAPICAL POCKET CYST: (ORIGINALLY BAY CYST) Grossman’s endodontic practice: 11th edition
  • 145. PERIAPICAL TRUE CYST: • cavities completely enclosed in epithelial lining • totally independent of the root canal of the affected tooth Grossman’s endodontic practice: 11th edition
  • 146. CLINICAL FEATURES • Asymptomatic • Age: 20-60 years, involve deciduous teeth. • Maxilla: 75% – incisors, 62%; cuspids, 7%; premolars, 20%; and molars, 11%. • Mandible,: 25% – incisors, 16%; cuspids, 2%; premolars, 34%; and molars, 48%. • Non-vital tooth; deep carious lesion or a restoration • Develops only over a prolonged period of time. – Acute exacerbation  abscess  cellulitis or form a draining fistula. Cohen’s Pathways of the Pulp,11th edition
  • 147. RADIOGRAPHIC FEATURES • identical in most cases with that of the periapical granuloma • Cyst > granuloma in size, by virtue of its longer duration X • Occasionally : a thin, radiopaque line around the periphery of the radiolucent area, and this indicates a reaction of the bone to the slowly expanding mass • Cone beam computed tomography > biopsy Cohen’s Pathways of the Pulp,11th edition
  • 148. DIAGNOSIS • Non-vital pulp • Previous history of pain. • Radiographic diagnosis- – loss of continuity of the lamina dura with an area of rarefaction. – radiolucent area is generally round in outline, except where it approximates adjacent teeth, in which case it may be flattened and may have an oval shape. • The radiolucent area may be larger than a chronic apical abscess and may include more than one tooth Grossman’s endodontic practice: 11th edition
  • 150. Globulomaxill ary cyst • marsupialized and enucleated without Traumatic bone cyst/ hemorrhagic or extravasation cyst: • aspiration of fluid through surgical cavity Lateral periodontal cyst: • periodontal signs and symptoms
  • 151. BACTERIOLOGY • A cyst may or may not be infected. • Represents a defensive reaction of the tissue to a mild irritant • Actinomyces organisms have been isolated from a periapical cyst. Bacterial colonies in the cyst lumen, surrounded by inflammatory Cells, Ricucci D, Bergenholtz G: Histologic features of apical periodontitis in human biopsies, Endod Topics 8:68, 2004, Fig. 6
  • 152. HISTOLOGICAL FEATURES • Similar to Periapical granuloma • Epithelial lining • Epithelial thickness • Rete ridges • Inflammatory infiltrate • Rushton body • Cholesterol clefts Shafer’s textbook of Oral Pathology, 7th edition
  • 153. • Martin A Rushton: 1955 • Peculiar Hyaline bodies- exclusively in odontogenic cysts • tiny linear or arc-shaped bodies, associated with the lining epithelium • amorphous, eosinophilic, and brittle in nature • No clinical or diagnostic significance; origin is unknown, but may represent some type of epithelial product. (Allison, 1977) • Sedano (1968) and Gorlin reported a marked morphologic and histochemical similarity between these bodies and red blood cells, suggesting that they arise from thrombus formation in small capillaries, being formed chiefly from these red blood cells—a rouleau phenomenon. Babburi S, Rudraraju AR, V A, P S. Rushton bodies: an update. J Clin Diagn Res. 2015;9(2):ZE01– ZE3. doi:10.7860/JCDR/2015/10990.5533 RUSHTON BODY:
  • 154. • wall of the lesion- dystrophic calcifications and collections of cholesterol slits with associated multinucleated giant cells • collections of lipid-filled macrophages or even macrophages containing hemosiderin are present. Shafer’s textbook of Oral Pathology, 7th edition
  • 155. CONTENTS OF CYST LUMEN- • watery, straw-colored, blood tinged fluid to semisolid materials • Protein: low conc. - stains palely eosinophilic. • Shimmering effect: Cholesterol • Keratin: Rare instances, limited amounts • Blood - rare finding, except associated with surgical procedure involved in removing the cyst. Cohen’s Pathways of the Pulp,11th edition
  • 156. TREATMENT Surgical Therapy • The affected tooth is either preserved by root canal treatment or is removed. • Mucoperiosteal flap lying over the cyst is raised and a window is opened in the bone which gives sufficient access. • The cyst is then separated from the bony wall. • The edges off the cavity are smoothened and the cavity is washed to clean the debris. • After the bleeding is controlled, the flap is replaced back and sutured. Endodontic Method • 80–98% of the radicular cysts undergo resolutions after root canal treatment and do not require surgery. • The treatment of choice Cohen’s Pathways of the Pulp,11th edition
  • 157. Marsupialisation • Aims at producing self cleansing cavity which becomes the ground for oral tissues. • Cyst is cut open for enucleation but the epithelial lining is stitched on to the mucous membrane at margins of opening. • Cavity is plugged with ribbon gauze in the beginning. • Once the margins get healed, the cavity closes when the surrounding tissues start growing back along with new bone • large cyst which will require decompression, and where the jaw has chances of getting fractured.
  • 158. PROGNOSIS Depends on – Particular tooth – Extent of bone destroyed – Accessibility for treatment. Grossman’s endodontic practice: 11th edition
  • 159. HEALING OF LESIONS - APICAL POCKET CYST • Hypothesis I: – Overinstrumentation of canal beyond apexacute inflammatory response in cystic area destroy the epithelial lining  Resolution. – Rejected: healing usually occurs from the periphery to the center of the lesion. • Hypothesis II: – Instrument into the cyst puncture of cyst wall Drainage. – Drainage reduces the pressure on walls of osseous cavity  stimulates fibroplasia  repair from the periphery of the lesion Grossman’s endodontic practice: 11th edition
  • 160. APICAL TRUE CYST • Hypothesis: – Subsided inflammatory process  drainage  fibroplasia  collagen. – Pressure of the proliferating collagen  reduced blood supply to epithelium by compressing the vascular network of the granulomatous tissue. – Collagen  entraps epithelial lining degeneration Removal by Macrophages • Current and most feasible hypothesis: – Periapical lesions- inflammatory responses to antigen content of root canal system, – Epithelial proliferation- response to irritating materials, – Removal of source of irritation  Destruction and removal of proliferating epithelial cells by immune system Grossman’s endodontic practice: 11th edition
  • 161. COMPLICATIONS • Fractured jaw • Damage to surrounding structures • Infection in the wound. • Fatal cysts might not be removed properly with added tissue. • Remains of cyst  Recurrence of cyst formation. Grossman’s endodontic practice: 11th edition
  • 163. • Asymptomatic apical periodontitis with reactive bone formation = Chronic osteomyelitis with proliferative periostitis. • long-term, low-grade inflammation/ infection or a high resistance of local tissue to inflammation/ infection. • Inflammation induces reactive bone formation of alveolar trabecular or spongy bone around the periapex of endodontically involved teeth. Cohen’s Pathways of the Pulp,11th edition Grossman’s endodontic practice: 11th edition Condensing osteitis is a diffuse radiopaque lesion believed to represent a localized bony reaction to a low-grade inflammatory stimulus, usually seen at the apex of a tooth in which there has been a long-standing pulpal pathosis.
  • 164. CLINICAL FEATURES • young patients • Mandibular first molar • gross carious lesions • vital or nonvital. • usually asymptomatic. • Radiographically- – radiopaque mass associated with the apex of an endodontically involved tooth. – Lamina dura - usually intact Cohen’s Pathways of the Pulp,11th edition
  • 165. HISTOPATHOLOGY • There is an excessive apposition of bone mass without bone resorption in the apical area. • As the bone marrow spaces become smaller and obliterated, the bone resembles compact bone that is infiltrated by a small number of lymphocytes. • The compact bone has few lacunae, and many of them are empty of osteocytes. • It has many prominent resting and reversal lines, similar to an idiopathic osteosclerosis or a Pagetoid appearance. Cohen’s Pathways of the Pulp,11th edition
  • 166. TREATMENT • Removal of the irritant stimulus is recommended. • Endodontic treatment should be initiated if signs and symptoms of irreversible pulpitis are diagnosed. Prognosis • long-term retention: excellent if root canal therapy is performed and if the tooth is restored satisfactorily. • Lesions may persist after endodontic treatment. Grossman’s endodontic practice: 11th edition
  • 168. • lytic process occurring in the cementum or cementum and dentin of the roots of teeth. Grossman’s endodontic practice: 11th edition
  • 169. Grossman’s endodontic practice: 11th edition CLASSIFICATION Tooth resorption: internal and external. External tooth resorption- A. External surface resorption B. External inflammatory root resorption C. External replacement resorption or ankylosis
  • 170. RADIOGRAPHIC FEATURES • radiolucent, concave, ragged bowl-shaped excavations along the root surface, • corresponding and associated radiolucencies in the adjacent alveolar bone. • Complete loss of the lamina dura is seen in the area of the resorption. • Initial signs : as early as 3 to 4 weeks after a TDI involving the periodontal tissues – EIR is always seen within 1 year after the injury. • Areas of replacement resorption or ankylosis: – resorbed root – no periodontal ligament space – bone replacing the defects. Cohen’s Pathways of the Pulp,11th edition
  • 171. “Moth-eaten” radiolucent alteration- reimplanted after traumatic avulsion Diffuse external resorption after initiation of orthodontics. Extensive external resorption - impacted right maxillary cuspid. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 172. First molars in all four quadrants demonstrate extensive radicular external resorption. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 173. HISTOLOGIC APPEARANCE • Cementum & Dentin: Saucer or bowl-shaped areas of resorption • Inflammation in the adjacent periodontal membrane. • Resorption cavities: Howship lacunae – lacunae sometimes are occupied by odontoclasts. • PDL inflammation: intense – consists of a mixed-cell infiltrate - plasma cells, lymphocytes, and polymorphonuclear leukocytes in a granulation tissue matrix. – Proliferation of capillaries • EIR can be identified histologically 1 week after experimental replantation of teeth. Cohen’s Pathways of the Pulp,11th edition
  • 174. CLINICAL FEATURES • Tooth in question may look normal • No response to vitality testing. • Advanced cases: signs of pulpal and/or periapical periodontitis – discolored tooth – sinus present – tenderness to percussion and/or palpation Cohen’s Pathways of the Pulp,11th edition
  • 175. DIFFERENTIAL DIAGNOSIS • External resorption – radiograph blunt apex, – “scooped-out” area on the side of the root, – if the area is superimposed on the root canal, the root canal clearly traverses the area of resorption. • Internal resorption – root canal with a well-demarcated, enlarged “ballooning” area of resorption. • internal resorption  perforated the root surface • external resorption penetrated the pulpal cavity Grossman’s endodontic practice: 11th edition Difficult to diagnose
  • 176. MANAGEMENT • Effective removal of the causal agent • Root canal treatment • Exception: Replanted teeth with closed apices – Root canal treatment should be carried out 7 to 10 days after replantation, even if there are no radiographic signs of EIR. PROGNOSIS: • Depends on early diagnosis and treatment. • Long-term dressing of the root canal with calcium hydroxide may be beneficial – associated risk of root fracture. Cohen’s Pathways of the Pulp,11th edition
  • 177. FOLLOW-UP AND PROGNOSIS • Healing - cessation of the resorption process – resolution of the radiolucency in the adjacent bone – reestablishment of the PDL space. • Untreated cases- entire root can be resorbed within 3 months. • The prognosis is especially poor for untreated immature teeth Cohen’s Pathways of the Pulp,11th edition
  • 179. The occurrence of signs and/or symptoms of disease in association with root canal-treated teeth • Emergent (if developed after treatment) • Persistent (if persisted despite treatment) • Recurrent (if developed after having healed). • usually observed after endodontic treatments that have not followed acceptable standards for prevention and control of the root canal infection • occur in 5-15% of teeth with pre-operative apical periodontitis even when treatment has followed proper standards J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
  • 180. ETIOLOGY • Persistent intraradicular infection • Secondary intraradicular infection – Coronal leakage – Extraradicular infection • Microbial cause – Intraradicular infection – Extraradicular infection • Procedural errors – Fractured instrument, – Ledge – Perforation – Overfilling J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
  • 181. MANAGEMENT Retreatment: teeth with inadequa te root canal treatment available coronal access Surgery:teeth with well-treated canals where retreatment offers no better prognosis retreatment is not feasible because coronal access to the apical canal is impossible high risk of accidents (extensive restorations, fractured instruments, perforations , ledges, etc) teeth that have already been subjected to retreatment; and cases where there is a need for biopsy. J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
  • 182. TECHNICAL ASPECTS OF ENDODONTIC RETREATMENT J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
  • 183. repeated abscesses- right mandible, swelling, pain. Tooth 46 -crown, asymptomatic at the visit. Radiograph - root canal-treated, but the apical distal canal was clearly untreated and the mesial canals underinstrumented. - well-fitted metal-ceramic crown Endodontic retreatment Crown removed and access to the canals achieved. J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
  • 184. Obturation materials were removed, and new working lengths established; Appearance of the pulp chamber just before root canal obturation Canals obturated after 48 days of Ca(OH)2 medication with cold gutta-percha laterally compacted and sealer J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
  • 185. Postoperative radiograph Two-year follow-up radiograph. Only a minor radiolucency is present on the mesial root Radiograph taken after ten years Normal periradicular conditions J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
  • 186.
  • 187. recurrent abscess left upper jaw. Maxillary first premolar - root canal-treated 6 years before. Buccal sinus tract A large mesio- occlusal-distal (MOD) composite restoration; carbon fibre post seen at the occlusal surface Inadequate root canal treatment with the apical canals untreated; Post in the palatal canal J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
  • 188. Endodontic retreatment- Rubber dam isolation, core material removed, post drilled out with burs for post space preparation in the coronal portion, and with ultrasonic diamond tips in the deepest part Working length determination. Two canals joined- common apical canal. Ca(OH)2 paste in saline intracanal medicament placed After one week- sinus tract disappeared, tooth was comfortable The canals were obturated J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
  • 189.
  • 190. maxillary left first molar –single visit root canal-treated three months before. Buccal sinus tract never disappeared after the treatment , tooth was painful. Tooth was not restored permanently Periapical radiographs- poor instrumention and obturation, large radiolucency around the mesio- buccal root apex.
  • 191. Isolation with a rubber dam, temporary remaining restorative materials removed, abundant carious tissue appeared on the pulp chamber floor and in the rest of the cavity; Fissure connecting the mesiobuccal and palatal root canal orifices Additional canals were present in the mesial root, negotiated with #10 files. Calcification adhered to the pulp chamber floor One ribbon- shaped canal at the entrance of the mesial root
  • 192. uninstrumented canal (MB2) was found ending considerably short of the radiographic apex Removal of the obturation material in the mesio-buccal canal and working length determination obturated after three weeks of Ca(OH)2 medication; the tooth became asymptomatic, sinus tract disappeared Follow-up radiograph taken after three years and seven months. J. F. Siqueira Jr, I. N. Rôças, D. Ricucci2 And M. Hülsmann . Causes And Management Of Post-treatment Apical Periodontitis. BRITISH DENTAL JOURNAL March 2014; 2(6): 305-312
  • 193. PERSISTENT APICAL PERIODONTITIS • Persistent apical periodontitis is a post-treatment apical periodontitis in an endodontically treated tooth Grossman’s endodontic practice: 11th edition
  • 194. CAUSES • Anatomical complexity of pulp space system with regions that cannot be reached with instruments or with irrigants or intracanal medicaments. • Cannot be obturated with conventional techniques. • Nair: extraradicular factors that contribute to persistent apical periodontitis. – Apical biofilms (periapical plaque)  – Actinomycosis infection – Cholesterol crystals – Foreign body reaction to gutta-percha – Cellulose granuloma – Periapical scar tissue Grossman’s endodontic practice: 11th edition
  • 195. BACTERIOLOGY • Yeasts and Candida albicans in post-treated cases. • Grampositive cocci, rods and filaments, genera Actinomyces, Enterococccus, and Propioniobacterium have also been implicated. • E. faecalis : – most consistently reported organism that can survive prolonged starvation – can grow as a monoinfection in endodontically treated teeth. – Considered as a therapy-resistant microbe among the potential etiological agents of post-treatment apical periodontitis. Grossman’s endodontic practice: 11th edition
  • 196. • Fourteen year old female patient • All mandibular incisors were painful with swelling of soft tissue • Endodontic treatment two years ago. • Exacerbation with pain and swellingperiapical surgery on teeth 42, 41 and 31 without endodontic retreatment of involved teeth. Patient x-ray before emergency treatment. X-ray image after root canals obturation with Gutta Flow sealer and Gutta-percha master point X-ray image two month after treatment X-ray image ten month after treatment Nedim S. Management of Acute Periapical Lesions at Four Mandibular Incisors a Case Report. Adv Dent & Oral Health. 2017; 5(1): 555654. DOI:10.19080/ADOH.2017.05.555654
  • 198. PERIAPICAL SCAR • Defect created by periapical inflammatory lesions may fill with dense collagenous tissue rather than normal bone • occur most frequently when both the facial and lingual cortical plates have been lost – occasionally arise in areas with intact cortical plates. – Both plates missing, patient should be informed of the possibility of scar formation. – development of a periapical scar is not an indication for future surgery. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 199. DISEASES OF THE PERIRADICULAR TISSUES OF NONENDODONTIC ORIGIN
  • 200. Lesions of nonendodontic origin with vital pulps include: • Periapical cemental dysplasia or cementoma • Cementoblastoma • Odontogenic cysts • Fissural cysts • Central giant cell granuloma • Metastatic malignant tumors or ameloblastomas: – aggressive lesions – excessive bone loss, mobility of teeth, extensive root resorption, and loss of pulp vitality. Grossman’s endodontic practice: 11th edition
  • 202. HYPERCEMENTOSIS • Cemental hyperplasia • nonneoplastic deposition of excessive cementum that is continuous with the normal radicular cementum. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 203. CLINICAL FEATURES • May be isolated, involve multiple teeth, or appear as a generalized process. • Mandibular molars – followed by the mandibular and maxillary second premolars – mandibular first premolars. • Adulthood, and the frequency increases with age • Occurrence reported in younger patients  familial clustering, suggesting hereditary influence. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 204. RADIOGRAPHIC FEATURES • Thickening or blunting of the root • Cementum and dentin demonstrate similar radiodensities • surrounded by the radiolucent PDL space and the adjacent intact lamina dura. • Enlargement may be significant enough to suggest the possibility of a cementoblastoma • cementoblastoma : associated pain, cortical expansion, and continued enlargement Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 205. FACTORS ASSOCIATED WITH HYPERCEMENTOSIS Local Factors • Abnormal occlusal trauma • Adjacent inflammation (e.g., pulpal, periapical, periodontal) • Unopposed teeth (e.g., impacted, embedded, without antagonist) • Repair of vital root fracture Systemic Factors • Acromegaly and pituitary gigantism • Arthritis • Calcinosis • Paget disease of bone • Rheumatic fever • Thyroid goiter • Gardner syndrome • Vitamin A deficiency (possibly) Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 206. HISTOPATHOLOGIC FEATURES • Excessive cementum deposition- periphery of the root. • Hypocellular or exhibit areas of osteocementum • Arranged in concentric layers • Entire root or be limited to the apical portion. • Routine light microscopy: distinguishing between dentin and cementum is difficult, • Polarized light: discriminate between the two different layers A, Dental root exhibiting excessive deposition of cellular and acellular cementum. The dividing line between dentin and cementum is indistinct. B, Polarized light demonstrating the sharp dividing line between the tubular dentin and osteocementum. Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 207. TREATMENT AND PROGNOSIS • Patients with hypercementosis require no treatment. • Because of a thickened root, occasional problems have been reported during the extraction of an affected tooth. • Sectioning of the tooth may be necessary in certain cases to aid in removal Oral and Maxillofacial Pathology, Neville, Damm, Allen, Chi, 4th edition
  • 208. NON ENDODONTIC PERIRADICULAR LESIONS Odontogenic cysts: • Dentigerous cyst • Lateral periodontal cyst • Odontogenic keratocyst • Residual cyst Bone Pathologies: • fibro-osseous lesions • Periradicular cemental dysplasia • Osteoblastoma • Cementoblastoma • Cementifying & ossifying fibroma Odontogenic tumours: Non-odontogenic • Central giant cell granuloma • Nasopalatine duct cyst • Globulomaxillary cyst • Simple bone cyst • Enostosis
  • 210. Captain Scott B. McClanahan, DC, USN, Captain James D. Johnson, DC, USN, and Captain Robert E. Blundell, Jr., DC, USN. Pulpal and periradicular diagnostic terminology. Clinical Update. January 2002. Vol. 24, No. 1
  • 212. PREVIOUSLY ASKED QUESTIONS • Classification of Periradicular pathologies • Phoenix abscess • Management of acute alveolar abscess • Theories of cyst formation • Histopathology of radicular cyst (10 marks, NITTE University, 2019)

Editor's Notes

  1. does not normally undergo remodeling. Performs two essential functions: Attachment of the tooth to the alveolar bone by insertion of periodontal ligament fibers; Prevent root resorption during remodeling of the periodontium
  2. irritants egress apically from the root canal system into the periradicular tissues and initiate inflammation and tissue alterations.
  3. Since this classification does not account for the structural aspects of periapical lesions, Nair proposed an alternative classification in 1997, which was based on the histopathology and dynamics of these lesions with strict criteria to define each entity.
  4. rather than merely an inflammatory reaction of the periodontal ligament
  5. pathology shafer
  6. Grossman
  7. Firmicutes and Bacteroidetes together contribute to more than 70% of the species found in abscesses
  8. During the clinical examination tooth #30 had a painful response to percussion and was nonresponsive to the pulp vitality test. Periodontal probing was within the normal limits. Radiographic examination revealed periapical radiolucency
  9. histologically identical with the periapical granuloma---Epithelium lining- usually stratified squamous- Newly formed cysts- epithelial thickness is uneven, shows hyperplasia- Established cysts- regular appearance, fairly even thickness.--Few cells thick, or exceedingly thick with a great deal of proliferation into the adjacent connective tissue.---- Actual rete ridge formation sometimes occurs. The epithelial lining many times is discontinuous, frequently missing over areas of intense inflammation.
  10. Complications might occur after the removal of radicular cysts.
  11. Several radiographs taken at different angles may help to resolve the question. When bone adjacent to the area of resorption is involved and the resorbed area is externally concave and when the root canal is intact, as seen in the radiograph, external resorption is present.