Pulpal and Periradicular Lesions (2) PDF

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Pharos University in Alexandria

Dr. Rasha Ahmed Abou Samra

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dental procedures pulpal lesions periradicular lesions dental health

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This document describes pulpal and periradicular lesions, covering topics such as the etiology, pathologies, clinical manifestations, diagnosis, and treatment of various dental conditions. It also includes the "mountain pass concept" analogy for understanding root canal infections and provides examples of various routes of draining a chronic apical abscess.

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PULPAL AND PERIRADICULAR LESIONS (2) DR. RASHA AHMED ABOU SAMRA Periradicular Tissue Periradicular tissue consists of cementum, periodontal ligament, and alveolar bone. Etiology of pathologies of periradicular tissues  As the inflammation progresses throughout the radicular pulp, it gr...

PULPAL AND PERIRADICULAR LESIONS (2) DR. RASHA AHMED ABOU SAMRA Periradicular Tissue Periradicular tissue consists of cementum, periodontal ligament, and alveolar bone. Etiology of pathologies of periradicular tissues  As the inflammation progresses throughout the radicular pulp, it gradually starts to affect the periapical tissues.  The progression of the pulp disease into the periapical tissues presents a major biological challenge to those tissues.  The PDL is a very thin, highly fibrous tissue that is confined within the bony crypt. Etiology of pathologies of periradicular tissues  As such, these tissues are not capable of mounting an immune response that can stop the advancing microbial ingress.  Therefore the hallmark of apical periodontitis is bone resorption to accommodate the formation of a soft tissue lesion, in which the immunologic reactions that can stop the advancing infection can be concentrated. Etiology of pathologies of periradicular tissues 1. Bacterial: Untreated pulpal infection leads to total pulp necrosis and further periapical infection. 2. Severe trauma to tooth and heat production during tooth preparation may cause immediate interruption of blood supply resulting in pulp necrosis and periapical infection. 3. Traumatic occlusion: Persistent periapical tissue compression from traumatic occlusion may lead to apical inflammatory response. 4. Improper manipulation of instruments within root canal or overinstrumentation can force dentinal debris, irrigating solution, and toxic components of necrotic tissue in the periapical tissues. Etiology of pathologies of periradicular tissues 5. Tissue irritating drugs used in treating canals may result in damage to the periapical tissues. 6. Mechanical irritation resulting from excess root filling may cause bone resorption in the periapical region during masticatory movement. Poor obturation with 7. Irritation resulting from interchange of periapical infection foreign proteins accumulating in poorly filled canals. Rickets and Dixon in 1931 postulated a hollow tube theory for RCT In poorly filled canals, periapical tissue fluids will accumulate in the empty space in the canal, stagnate, and later escape into the surrounding periapical tissues where they act as irritating products of protein degradation. Because of the close relationship between the pulp and periradicular tissue, it is easy to see that inflammation of the pulp may cause inflammation in the periodontal ligament, even before the entire pulp has become necrotic. When the necrosis is complete, bacteria with their toxins, immunological agents, and the products of pulp degeneration and tissue necrosis reach the periradicular zone through pathways (portals of exit) by which the pulp and periodontal tissue communicate. This gives rise to inflammatory and immunologic reactions in the periradicular tissues which are simply called lesions of endodontic origin. It is useful to recall the analogy provided in 1939 by Kronfeld THE MOUNTAIN PASS CONCEPT  The bacteria in the root canal can be compared to an army waiting behind high, inaccessible mountains, the walls of the canal.  Through the mountain pass the apical foramen, this army tries to invade the plain beyond the pass, the periodonal tissue and surrounding tissues.  Another army in the plain guards the pass, the granulation tissue, which tries to prevent the mountain army from progressing farther. It is useful to recall the analogy provided in 1939 by Kronfeld THE MOUNTAIN PASS CONCEPT  The defending army is represented by the white blood cells and other cells of the granulation tissue.  Naturally the soldiers of the defending army are grouped closely around the opening of the pass through which the enemy is trying to come; for the same reason the white blood cells accumulate near the opening of the apical foramen. It is useful to recall the analogy provided in 1939 by Kronfeld THE MOUNTAIN PASS CONCEPT  For a long time there may be no action.  Occasionally, a few soldiers of the mountain army descend through the pass, the apical foramen, but they are usually captured and destroyed by the defenders, the white blood cells.  Then suddenly the mountain army makes a mass attack and a battle occurs.  Such a battle between invading bacteria and body tissues is known as acute inflammation. It is useful to recall the analogy provided in 1939 by Kronfeld THE MOUNTAIN PASS CONCEPT The outcome of this battle may vary  The bacteria may win and invade the plain; then the clinical manifestations are an acute periapical abscess, or even a general septic infection.  Or the defenders (WBCS) may be successful; they may overcome the invading bacteria, and afterwards the rest of the mountain army will again be confined to the canal, for which the WBCS have no access. It is useful to recall the analogy provided in 1939 by Kronfeld THE MOUNTAIN PASS CONCEPT If the attacking mountain army, the bacteria, are eliminated, either by:  Extraction of the tooth, or by  Root canal treatment.  the defending army is no longer needed!!!  The granulations shrink, and the soldiers, the WBCS, leave and return into the general circulation. This explains why the apical granulation tissue disappears after extraction or after successful RCT.  So the granuloma is a defense against spread of infection Periapical Tests Clinical tests that can localize pain to the offending tooth are essential tools for diagnosis of the periapical inflammatory status. These include: 1) Palpation over the apex. Percussion is performed by tapping 2) Light percussion with the end of the on the incisal or occlusal surfaces of the teeth either with the finger mirror handle. or with the handle of the mirror 3) Digital pressure on teeth (preferred if the patient reports severe pain on mastication). Periapical Tests Palpation of soft tissue using digital pressure. Percussion of tooth using gloved finger. Clinical classification of periradicular diseases 1) Normal apical tissues. 2) Symptomatic apical periodontitis. 3) Asymptomatic apical periodontitis. 4) Acute apical abscess. Phoenix Abscess Acute Exacerbation of Asymptomatic Apical Periodontitis 5) Chronic apical abscess. 6) Condensing Osteitis (1) Normal apical tissues This classification is the standard against which all of the other apical disease processes are compared. 1. In this category the patient is asymptomatic. 2. The tooth responds normally to percussion and palpation testing. 3. The radiograph reveals an intact lamina dura and periodontal ligament space around all the root apices. 4. No sinus tract, or swelling or complaint of painful symptoms. 5. There is no evidence of apical pathosis clinically or radiographically. (2) Symptomatic Apical Periodontitis (Acute Apical Periodontitis)  Symptomatic apical periodontitis is defined as 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. It is an inflammation around the apex of a tooth. Etiology 1. In vital tooth, it is associated with occlusal trauma and high points in the restoration. 2. In non-vital tooth, it is associated with sequelae to pulpal diseases. 3. Iatrogenic causes can be overinstrumentation of root canal, pushing debris and microorganisms beyond apex, overextended obturation, and root perforations. (2) Symptomatic Apical Periodontitis (Acute Apical Periodontitis) Signs and Symptoms 1. Tooth is tender on percussion or palpation. 2. Pain on mastication. 3. It may or may not respond to vitality tests. Pain on percussion indicates inflamed periodontium Radiographic picture may show no change, it may show widening of apical periodontal ligament space or a small radiolucency may be evident radiographically. (2) Symptomatic Apical Periodontitis (Acute Apical Periodontitis) Treatment 1. If cause is irreversible pulpitis or necrotic pulp, initiate endodontic treatment. 2. If cause is hyperocclusion, adjust the occlusion for immediate relief. 3. To control postoperative pain following initial endodontic therapy, analgesics are prescribed. Symptomatic apical Periodontitis Secondary to Treatment An asymptomatic tooth before initiation of endodontic treatment becomes sensitive to percussion during treatment which can be due to: 1. Overinstrumentation 2. Forcing debris into periapical tissues Management: An intracanal corticosteroid–antibiotic medication is carried on paper point and applied with a pumping action so as to reach the inflamed periapical tissues. Anti-inflammatory corticoid triamcinolone acetonide (lower the inflammation). The broad-spectrum antibiotic Demeclocycline (control the infection ). Management of Pulpal Necrosis With Symptomatic Apical Periodontitis CRYOTHERAPY  A randomized clinical trial used final Digital irrigation with 20 mL sterile cold (2.5°C) thermometer saline solution delivered to the working length with a sterile, cold (2.5°C) EndoVac microcannula for 5 minutes.  They concluded that cryotherapy reduced the incidence of postoperative pain and the need for medication in patients presenting with a diagnosis of necrotic pulp and symptomatic apical periodontitis. A final irrigation with cold saline using a needle with gauge size 30. (2) Symptomatic Apical Periodontitis (Acute Apical Periodontitis)  It is noteworthy, however, that after restorative procedures on a vital normally responsive pulp, if the occlusion on the tooth is inadvertently left high, the tooth is rendered tender to percussion. In these cases, the occlusion needs to be adjusted, and the pulpal condition is considered reversible.  It is strongly recommended that whenever symptomatic apical periodontitis is suspected, the percussion test should be performed by gently percussing the tooth with the tip of the index finger instead of using the handle of a mirror, just to confirm the involved tooth. (3) Asymptomatic Apical Periodontitis (Chronic Apical Periodontitis)  After an initial period of primary acute apical periodontitis, and if the tooth has not been treated, the periapical inflammation can become chronic.  After several months, this usually manifests as a periapical radiolucency.  Bone is resorbed to create space for the inflammatory reaction to occur so there are usually no, or only occasional mild symptoms or an occasional “awareness” of the tooth feeling different to the other teeth. (3) Asymptomatic Apical Periodontitis (Chronic Apical Periodontitis) This condition is defined as inflammation and destruction of apical periodontium that is of pulpal origin; it appears as an apical radiolucent area and does not produce clinical symptoms.  This tooth does not usually respond to pulp sensibility tests.  The radiograph or image of the tooth will exhibit an apical radiolucency (cyst or granuloma).  The tooth is generally not sensitive to biting pressure but may “feel different” to the patient on percussion. (3) Asymptomatic Apical Periodontitis (Chronic Apical Periodontitis) Clinical features: 1. Tooth is non vital. 2. Usually asymptomatic. Radiographic findings  Periapical radiolucency will be present.  some cases may have evidence of previous endodontic treatment. (3) Asymptomatic Apical Periodontitis (Chronic Apical Periodontitis) Histologically: The radiolucent area associated with asymptomatic apical periodontitis will be either a granuloma or a cyst. These two histopathologic entities are radiographically indistinguishable.  In response to persistent low grade aggression from the root canal, bone is resorbed and an apical granuloma is formed.  Epithelial proliferation in some granulomas may give rise to cyst formation.  As long as the irritating substances are not removed from the root canals, resorption of the bony trabeculae and resorption of the radicular cementum and apical dentin may occur. (3) Asymptomatic Apical Periodontitis (Chronic Apical Periodontitis) Granuloma and Cyst The distinction cannot be made radiographically, but only histologically. Granuloma and cyst are lesions of endodontic origin. Apical Granuloma contains granulation tissue and chronic inflammatory cells. It arises in response to infection or inflammation of the Histopathology of periapical granuloma periapical tissue caused by pulp necrosis. Granuloma is the most common histopathologic form of apical periodontitis. (3) Asymptomatic Apical Periodontitis (Chronic Apical Periodontitis) Granuloma Therapy requires removal of the infected canal contents, disinfection of the endodontic space, and sealing of every portal of exit. This leads to the gradual neoformation of bony trabeculae Apical granuloma until a new lamina dura has been formed. During extraction, the granuloma very often remains adherent to the root apex. (3) Asymptomatic Apical Periodontitis (Chronic Apical Periodontitis) Apical cyst Epithelial cell rests of Malassez, the remnants of Hertwig's epithelial root sheath that disintegrates after tooth development, are natural components of the attachment apparatus of the tooth and are present in the periodontal ligament near the root surface in all teeth after root formation. They can be stimulated to proliferate in apical periodontitis. Under the irritative stimulus, they may proliferate and constitute the nucleus of a cystic formation. (3) Asymptomatic Apical Periodontitis (Chronic Apical Periodontitis) Apical cyst is an inflammatory lesion of endodontic origin that is characterized by the presence of a cavity lined by epithelial cells. Radicular cysts may appear in two configurations: A pocket cyst is a sac shaped apical inflammatory lesion, with the epithelium-lined cystic cavity in direct contact with the root canal system via apical foramen or lateral foramina. True apical cysts is a periradicular lesion with a distinct pathologic cavity completely enclosed by the epithelial lining, without any communication with the root canal system Types of radicular cysts. (3) Asymptomatic Apical Periodontitis (Chronic Apical Periodontitis) Schematic representation of a periapical Schematic representation of a periapical true pocket cyst showing communication of the cyst. There is no communication between the lumen of the cyst with the root canal system cyst lumen and the root canal system (3) Asymptomatic Apical Periodontitis (Chronic Apical Periodontitis)  Cysts are usually asymptomatic.  If they reach a significant size, they may present as swellings.  Their pressure may cause loosening of the diseased tooth.  If not treated, the cyst can expand at the expense of the mandibular or maxillary bone.  The cyst may appear to involve the apices of the nearby teeth whose roots may also be subjected to external resorption.  The diagnosis is based on radiographic findings. Negative responses to all pulp tests confirm the odontogenic nature of the cyst. (3) Asymptomatic Apical Periodontitis (Chronic Apical Periodontitis)  Cysts are treated by endodontic therapy. Healing of the cyst following nonsurgical treatment is due to spontaneous disintegration of its walls.  The treatment of choice of cysts is therefore not surgical enucleation, but endodontic therapy of the diseased necrotic tooth, followed as always by periodic check-ups and radiographs.  Surgical treatment is indicated only after traditional nonsurgical therapy has failed or if new symptoms.  A reason for the failure of nonsurgical therapy of odontogenic cysts may be failure to achieve complete drying of the canal, an essential pre- requisite for a good apical seal. (3) Asymptomatic Apical Periodontitis (Chronic Apical Periodontitis) Treatment of asymptomatic apical periodontitis 1. Removal of irritants (necrotic pulp) and obturation of the root canals usually result in resolution of asymptomatic apical periodontitis. 2. Surgical removal of periapical pathology may be needed. 3. Extraction of the tooth in some cases. There are no diagnostic means currently available to distinguish a granuloma from a cyst except histologically. The appearance of the radiolucent area in conventional radiographs cannot predict its histological diagnosis. Granuloma A. Preoperative radiograph of the upper left lateral incisor. The shape, degree of radiolucency, sharp borders, and size suggest a cystic lesion. B. A palatal swelling is present. C. Histologic appearance of the lesion (A)Preoperative radiograph of a first molar shows pulpal necrosis and asymptomatic apical periodontitis. (B)A postoperative radiograph 1 year after root canal therapy showing complete resolution of the periradicular pathosis. (4) Acute apical abscess caries  Acute apical abscess is characterized by a severe inflammatory reaction to root canal infection.  It is a sequel to symptomatic apical periodontitis, and is characterized by formation of a purulent inflammatory exudate in response to bacteria egressing from the apical foramen.  An extraradicular infection is established in these cases. (4) Acute apical abscess Signs and symptoms: 1. It has a rapid onset. 2. The results of pulp tests are negative. Swelling of mandibular area 3. Percussion gives positive results. because of apical abscess. 4. It is associated with pain, pus formation, mobility and swelling of the associated soft tissues. 5. Pain is usually spontaneous, throbbing and localized, exacerbated by chewing. (4) Acute apical abscess Signs and symptoms: 6. Systemic involvement may occur, including fever, malaise, and regional lymphadenitis. 7. Pain becomes severe when the purulent collection is still intraosseous or has reached the sub-periosteal space. 8. A dramatic relief in pain occurs as the purulent exudate breaks through the periosteum and reaches the supraperiosteal soft tissues. (4) Acute apical abscess Radiographically  Radiographic changes range from a widening of the periodontal ligament space, to a radiolucent area around the root apex.  If the abscess develops as an exacerbation of a longstanding asymptomatic apical periodontitis (the so-called “phoenix” abscess) radiographs reveal a radiolucent area around the root apex. If the abscess develops as a direct extension of pulp necrosis and infection, the PDL space may appear only thickened. Management of acute apical abscess: 1. Complete canal debridement and disinfection to remove the source of the infection. Speed of recovery will rely on canal debridement 2. Swelling may be controlled by establishing drainage through the root canal or by incising the fluctuant swelling. 3. Antibiotics may be prescribed when there are systemic manifestations of the infection, such as fever and malaise. 4. Do not leave tooth open between appointments. The access cavity should be properly sealed. 5. Relieve the tooth out of occlusion. 6. NSAIDs should be prescribed to control postoperative pain. The principal modality for managing swelling secondary to endodontic infections is to achieve drainage and remove the source of the infection. Complete canal debridement and disinfection are paramount for success regardless of observable drainage, because the presence of any bacteria remaining within the root canal system will compromise the resolution of the acute infection. A. Preoperative radiograph of the lower central incisor with an acute alveolar abscess B. At the opening of the access cavity the pus has spontaneously drained, and the pain resolved instantaneously Immediate relief is obtained as pus drains from an access cavity. When the swelling is localized, the preferred avenue is drainage through the root canal. Penetration of the apical foramen with small files (up to file #25) may initiate drainage and release of pressure. An incision for drainage allows: 1. Decompression of the increased tissue pressure associated with edema. 2. Provides significant pain relief. 3. Drainage of edematous fluid and purulent exudate improves circulation to the tissues associated with an abscess or cellulitis, providing better delivery of the antibiotic to the area. Management of pulp necrosis with acute apical abscess with localized intraoral swelling for a 60-year-old female patient A, Preoperative radiograph of #30 with sulcular sinus tract. B, Preoperative photograph of intraoral swelling. C, Photograph of incision. D, Blunt dissection. E, Postoperative radiograph of completed obturation and access restoration at second visit. In some cases, the host defenses do not succeed in confining the infection to the periradicular tissues and the abscess can spread to anatomical spaces of the head and neck and even give rise to life- threatening conditions. FASCIAL SPACE INFECTIONS  If bacteria from the infected root canal gain entry into the periradicular tissues and the immune system is unable to suppress the invasion, the patient eventually shows signs and symptoms of an acute apical abscess, which can, in turn, evolve to cellulitis.  Clinically, the patient experiences swelling and mild to severe pain. Limited opening, pain and difficulty in swallowing, may also occur.  The patient may also have systemic manifestations, such as: Fever- Chills- Lymphadenopathy- Headache-Nausea.  The involved tooth may or may not show radiographic evidence of a widened periodontal ligament space because the reaction to the infection may occur quickly.  The tooth elicits a positive response to percussion in most cases.  The periradicular area is tender to palpation. Phoenix Abscess Acute Exacerbation of Asymptomatic Apical Periodontitis Phoenix abscess is defined as an acute inflammatory reaction superimposed on an existing asymptomatic apical periodontitis. Etiology Chronic periradicular lesions such as granulomas are in a state of equilibrium during which they can be completely asymptomatic. But sometimes, influx of necrotic products from diseased pulp or bacteria and their toxins can cause the dormant lesion to react. This leads to initiation of acute inflammatory response. Lowered body defenses also trigger an acute inflammatory response. Phoenix Abscess Acute Exacerbation of Asymptomatic Apical Periodontitis Symptoms Clinically, often indistinguishable from acute apical abscess. Tenderness of tooth to percussion. Tenderness on palpating the apical soft tissue Diagnosis Pulp tests show negative response Radiographs show large area of radiolucency in the apex. Phoenix abscess should be differentiated from acute alveolar abscess by patient’s history, symptoms, and clinical tests results. (5) Chronic apical abscess This condition is defined as an inflammatory reaction to pulpal infection and necrosis characterized by gradual onset, little or no discomfort, and the intermittent discharge of pus through an associated sinus tract. The sinus tract can appear intraorally or extraorally. In general, a tooth with a chronic apical abscess will not present with clinical symptoms. The tooth will not respond to pulp sensibility tests, and the radiograph or image will exhibit an apical radiolucency. Usually the tooth is not sensitive to biting pressure but can “feel different” to the patient on percussion. This entity is distinguished from asymptomatic apical periodontitis because it will exhibit intermittent drainage through an associated sinus tract. (5) Chronic apical abscess  To trace the sinus tract, a size #25 gutta- percha cone is threaded into the opening of the sinus tract. Although this may be slightly uncomfortable to the patient, the cone should be inserted until resistance is felt.  After a periapical radiograph is exposed, the termination of the sinus tract is determined by following the path taken by the gutta- percha cone. This will direct the clinician to which tooth is involved, and more specifically, which root of that tooth is the source of the pathosis. (5) Chronic apical abscess Once the causative factors related to the development of the sinus tract are removed, the stoma and the sinus tract will close within just a few days. The opening of the sinus tract may be found on the mucosa overlying the tooth that sustains it , but it may also often be found at considerable distance from the diseased tooth. (5) Chronic apical abscess Examples of various routes of draining of a chronic apical abscess to the oral environment: (a) Through the alveolar bone. (b) Along the periodontal ligament. A. Cutaneous sinus in the right submandibular region. B. Preoperative radiograph of the ipsilateral lower first molar. The tooth had been “opened” one month before and left open “to drain”. Note the small radiopacity at the center of the access cavity, due to a residuum of the chamber roof left in place. C. Clinical appearance of the access cavity: three openings have been made in the roof of the pulp chamber! One, corresponding to the distal canal, is shaped like an “8”; the two round ones correspond to the mesial canals: the pulp horns have been misdiagnosed for canal orifices. D. Postoperative radiograph. E. Healing of the sinus tract two years later with complete absence of any scarring. (6) Condensing Osteitis  This condition represents a radiographic feature of the periapex of some teeth with pulpal pathosis.  In these cases, the bone surrounding the apical region is more sclerotic than that surrounding neighboring teeth.  Pulp can be chronically inflamed or necrotic.  It is thought that low-grade irritation of the bone may result in sclerosis rather than in resorption. (6) Condensing Osteitis Diagnosis Usually discovered on routine radiograph, it appears as localized area of radiopacity surrounding the offending tooth apex. Histopathology Dense bone around root apex Treatment  Endodontic treatment may result in complete resolution.  Radiopacity may or may not disappear after endodontic treatment or tooth extraction. Periapical Scar A periapical scar is not a disease or a pathological condition. It is a healing response where fibrous, connective tissue forms instead of bone and/or PDL. Typically the radiolucency reduces in size over time but it does not completely disappear. Clinicians should recognize that this condition does occur and it should be part of the differential diagnosis of a persistent radiolucency following endodontic treatment. A. Preoperative radiograph shows a large radiolucency. B. One year after root canal treatment, the radiolucency is much smaller. C. The radiolucency has remained of a similar size when reviewed after three more years. A: Extensive lesion in the region of the mesial root of tooth 36. B: Completed root canal filling. C: Follow-up radiograph 1 year later. Significant, but yet incomplete healing. The periodontal ligament space appears to be widened. The tooth was symptom-free.

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