Oral Pathology Lecture Notes: Pulpal & Periapical Disease PDF

Oral pathology 1 MAJD & SHATHA Lecture 12 BY : MAJD & SHATHA ORAL PATHOLOGY 1 LECTURE : 12 0 Oral pathology 1 MAJD & SHATHA Lecture 12 Pulpal & Periapical Disease II...

Oral pathology 1 MAJD & SHATHA Lecture 12 BY : MAJD & SHATHA ORAL PATHOLOGY 1 LECTURE : 12 0 Oral pathology 1 MAJD & SHATHA Lecture 12 Pulpal & Periapical Disease II Pulpal & Periapical Disease Pulpitis & Pulp Necrosis Pulpal Calcifications Periapical Inflammatory Disease (Granuloma; Cyst; Abscess) Cellulitis Osteomyelitis Condensing Osteitis Osteomyelitis with Proliferative Periostitis Periapical Inflammatory Disease PERIAPICALGRANULOMA PERIAPICAL CYST PERIAPICAL ABSCESS ACUTEPE PERIAPICAL PERIODONTITIS 1  Oral pathology 1 MAJD & SHATHA Lecture 12 PERIAPICAL GRANULOMA (CHRONIC APICAL PERIODONTITIS) The term periapical granuloma refers to a mass of chronically or subacutely inflamed granulation tissue at the apex of a nonvital tooth. This commonly used name is not totally accurate because the lesion does not show true granulomatous inflammation microscopically. Although the term chronic apical periodontitis may be more appropriate, it may prove confusing to the clinician. Formation of apical inflammatory lesions represents a defensive reaction secondary to the presence of microbial infection in the root canal with spread of related toxic products into the apical zone. Initially, the defense reaction eliminates noxious substances that exit the canals. With time, however, the host reaction becomes less effective with microbial invasion or spread of toxins In the early stages of infection, neutrophils predominate and radiographic alterations are not present; this phase of periapical inflammatory disease is termed acute apical periodontitis. The involved neutrophils release prostaglandins, which activate osteoclasts to resorb the surrounding bone, leading to a detectable periapical radiolucency. 2  Oral pathology 1 MAJD & SHATHA Lecture 12 With time, chronic inflammatory cells begin to dominate the host response. Spread of pulpal infection into bone can lead to serious complications or systemic sepsis with life threatening complications. Periapical granulomas may arise after quiescence of a periapical abscess or may develop as the initial periapical pathosis. These lesions are not necessarily static. In addition to possible periapical cyst formation, a worsening of the pulpal infection can lead to a reappearance of inflammation, redevelopment of symptoms, and possible enlargement of the associated radiolucency. Secondary acute inflammatory changes within a periapical granuloma have been termed a phoenix abscess, 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. è Clinical and Radiographic Features The initial phase of periapical inflammatory disease— acute periapical periodontitis—creates a constant dull, throbbing pain. The associated tooth responds negatively to vitality testing or reveals a delayed positive result. 3  Oral pathology 1 MAJD & SHATHA Lecture 12 Typically, pain on biting or percussion is present, and no obvious radiographic alterations are noted initially. If the acute inflammatory process evolves into a chronic pattern, then the associated symptoms diminish. In many instances, chronic periapical inflammatory disease is detected without any previous recollection of a prior acute phase. Most periapical granulomas are asymptomatic, but pain and sensitivity can develop if acute exacerbation occurs. Typically, the involved tooth does not demonstrate mobility or significant sensitivity to percussion, the soft tissue overlying the apex may or may not be tender. The tooth does not respond to thermal or electric pulp tests unless the pulpal necrosis is limited to a single canal in a multirooted tooth. Most lesions are discovered on routine radiographic examination. Associated radiolucencies are variable, ranging from small lesions to ones exceeding 2 cm in diameter. Affected teeth typically reveal loss of the apical lamina dura. 4  Oral pathology 1 MAJD & SHATHA Lecture 12 The lesion may be circumscribed or ill-defined and may or may not demonstrate a surrounding radiopaque rim (depending on frequency of subacute or acute exacerbation). Root resorption is not uncommon. Although lesions greater than 2 cm in diameter often represent periapical cysts, numerous investigators have been unable to distinguish periapical granulomas from periapical cysts simply on the basis of size and radiographic appearance. Because periapical inflammatory disease is not static and granulomas can transform into cysts or abscesses (and vice versa) without significant radiographic change, it is not surprising that the radiographic features are not diagnostic. è Histopathologic Features Inflamed granulation tissue surrounded by a fibrous connective tissue wall. 5  Oral pathology 1 MAJD & SHATHA Lecture 12 The granulation tissue demonstrates a variably dense lymphocytic infiltrate that is intermixed frequently with neutrophils, plasma cells, histiocytes, and, less frequently, mast cells and eosinophils. Collections of cholesterol clefts, with associated multinucleated giant and areas of red blood cell extravasation with hemosiderin pigmentation, may be present. è Treatment and Prognosis Apical inflammatory lesions result from the presence of microorganisms OR their toxic products in the root canal, the apical tissues, or both. Non-restorable teeth must be extracted, followed by curettage of all apical soft tissue. 6  Oral pathology 1 MAJD & SHATHA Lecture 12 If the tooth can be maintained, then root canal therapy can be performed. Successful treatment depends on the reduction and control of the offending organisms. In addition to the quality of endodontic treatment, the coronal restoration is critical, and failure can occur in cases with excellent endodontic therapy but poor coronal restoration. Changes that may occur around the apex of a non-vital tooth: 7  Oral pathology 1 MAJD & SHATHA Lecture 12 PERIAPICAL CYST (RADICULAR CYST; APICAL PERIODONTAL CYST) Epithelial rests of Malassez at the apex of a nonvital tooth presumably can be stimulated by inflammation to form an epithelium-lined cyst, the periapical cyst. Cyst development is common with a wide range of prevalence. The lumen of the periapical cyst contains fluid and cellular debris. Fluid enters the lumen to equalize the osmotic pressure, and slow enlargement occurs. Most periapical cysts grow slowly and do not attain a large size. Lateral Radicular Cyst & Residual Periapical Cyst On occasion, a similar cyst, best termed a lateral radicular cyst, may appear along the lateral aspect of the root. § Like the periapical cyst, this lesion also usually arises from rests of Malassez, and the source of inflammation may be periodontal disease or pulpal necrosis with spread through a lateral foramen. 8  Oral pathology 1 MAJD & SHATHA Lecture 12 A periapical inflammatory lesion that is not curetted at the time of tooth removal may give rise to an inflammatory cyst called a residual periapical cyst. è Clinical and Radiographic Features ü Periapical Cyst Typically, patients with periapical cysts have no symptoms unless there is an acute inflammatory exacerbation. Or, if the cyst reaches a large size, then swelling and mild sensitivity may be noted. Movement and mobility of adjacent teeth are possible as the cyst enlarges. The tooth from which the cyst originated does not respond to thermal and electric pulp testing. The radiographic pattern is identical to that of a periapical granuloma. A loss of the lamina dura is seen along the adjacent root, and a rounded radiolucency encircles the affected tooth apex. Root resorption is common. Periapical cysts can also involve deciduous teeth. 9  Oral pathology 1 MAJD & SHATHA Lecture 12 ü Lateral Radicular Cyst Appears as a discrete radiolucency along the lateral aspect of the root associated with loss of lamina dura. Radiographically, these cysts mimic developmental lateral periodontal cysts. Before performing any surgery for such laterally positioned lesions, a thorough evaluation of the periodontal status and vitality of adjacent teeth should be performed. 10  Oral pathology 1 MAJD & SHATHA Lecture 12 ü Residual Periapical Cyst Appears as a round-to-oval radiolucency of variable size within the alveolar ridge at the site of a previous tooth extraction. è Histopathologic Features The histopathologic features of all three types of inflammatory cysts are similar. The cyst is lined by stratified squamous epithelium. Scattered mucous cells or areas of ciliated pseudostratified columnar epithelium may be noted. The cyst lumen may be filled with fluid and cellular debris. The wall of the cyst consists of dense fibrous connective tissue—often with an inflammatory infiltrate (lymphocytes and variable numbers of neutrophils, plasma cells, and histiocytes). 11  Oral pathology 1 MAJD & SHATHA Lecture 12 Dystrophic calcification, cholesterol clefts with multinucleated giant cells, red blood cells, and areas of hemosiderin pigmentation may be present in the lumen, wall, or both. è Treatment and Prognosis A periapical cyst is treated in the same manner as a periapical granuloma. Depending on restorability of the tooth, extraction or endodontic therapy is performed. Biopsy is indicated in to rule out other possible pathologic processes for the last 2 options. As with any periapical inflammatory lesion, minimal follow-up at 1 and 2 years is advised strongly. Residual periapical cysts should be excised surgically because some odontogenic and non odontogenic cysts and tumors can mimic their appearance radiographically. 12  Oral pathology 1 MAJD & SHATHA Lecture 12 In addition, carcinomatous transformation can rarely occur in odontogenic cysts, including periapical and residual periapical cysts. All inflammatory foci in the area of a lateral radicular cyst should be eliminated and the patient observed in a manner like that described for the periapical cyst. ACUTE APICAL PERIODONTITIS In the earliest stage of all forms of periapical inflammatory disease, the periapical periodontal ligament (PDL) fibers may exhibit acute inflammation but no frank abscess formation. This localized alteration, best termed acute apical periodontitis, may or may not proceed to abscess formation. Although this process often occurs in association with a nonvital tooth, acute apical periodontitis may be found in vital teeth secondary to trauma, high occlusal contacts, or wedging by a foreign object. The clinical presentation often closely resembles that of a periapical abscess and must be considered in the differential diagnosis. 13  Oral pathology 1 MAJD & SHATHA Lecture 12 ü PERIAPICAL ABSCESS The accumulation of acute inflammatory cells at the apex of a nonvital tooth. Acute inflammatory lesions with abscess formation may arise as the initial periapical pathosis OR from an acute exacerbation of a chronic periapical inflammatory lesion (periapical granuloma or cyst). Frequently, the source of the infection is obvious. On occasion, pulpal necrosis may be trauma related, and the tooth may contain neither a cavity nor a restoration. è Clinical and Radiographic Features Periapical abscesses are best designated as symptomatic or asymptomatic based on their clinical presentations. Periapical abscesses become symptomatic as the purulent material accumulates within the alveolus. The initial stages produce tenderness of the affected tooth that often is relieved by direct application of pressure. With progression, the pain becomes more intense, often with extreme sensitivity to percussion, extrusion of the tooth, and swelling of the tissues. 14  Oral pathology 1 MAJD & SHATHA Lecture 12 Radiographically, abscesses arising as the initial periapical pathosis (primary periapical abscesses) may demonstrate a thickening of the apical periodontal ligament, an ill-defined radiolucency, or both. Often no appreciable alterations can be detected because insufficient time has occurred for significant bone destruction. Abscesses arising from pre-existing chronic lesions (phoenix abscesses) demonstrate the outline of the original chronic lesion, with or without an associated ill-defined bone loss. The offending tooth DOES NOT respond to cold or electric pulp testing. Headache, malaise, fever, and chills may be present. The purulent material can accumulate in the connective tissue overlying the bone and can create a sessile swelling. The purulent material can perforate through the surface epithelium and drain through an intraoral sinus. 15  Oral pathology 1 MAJD & SHATHA Lecture 12 At the intraoral opening of a sinus track, a mass of subacutely inflamed granulation tissue often is found, known as a parulis (gum boil). Occasionally, the nonvital tooth associated with the parulis may be difficult to determine, and insertion of a gutta-percha point into the track can aid in detection of the offending tooth during radiographic examination. With progression, the abscess spreads along the path of least resistance. The purulence may extend through the medullary spaces of bone away from the apical area, resulting in osteomyelitis, or it may perforate the cortex and spread diffusely through the overlying soft tissue as cellulitis. Dental abscesses also may channelize through the overlying skin and drain via a cutaneous sinus. Most dental-related abscesses perforate buccally because the bone is thinner on the buccal surface. However, infections associated with maxillary lateral incisors, the palatal roots of maxillary molars, and mandibular second and third molars typically drain through the lingual cortical plate. If a chronic path of drainage is achieved, a periapical abscess typically becomes asymptomatic because of a lack of accumulation of purulent material within the alveolus. 16  Oral pathology 1 MAJD & SHATHA Lecture 12 Occasionally, such infections are discovered during a routine oral examination after detection of a parulis or drainage through a large carious defect. If the drainage site becomes blocked, then signs and symptoms of the abscess frequently become evident in a short time. On occasion, periapical infections can spread through the bloodstream and result in systemic symptoms, such as fever, lymphadenopathy, and malaise. The risk of dissemination appears to be less for periapical abscesses that drain freely. è Histopathologic Features Biopsy specimens from pure abscesses are uncommon because the material is in liquid form. Abscesses consist of a sea of polymorphonuclear leukocytes often intermixed with inflammatory exudate, cellular debris, necrotic material, bacterial colonies, or histiocytes. 17  Oral pathology 1 MAJD & SHATHA Lecture 12 In the later stages of irreversible pulpitis, the pain increases in intensity and is experienced as a throbbing pressure that can keep patients awake at night. At this point, heat increases the pain; however, cold may produce relief. The tooth responds to electric pulp testing at higher levels of current or demonstrates no response. Mobility and sensitivity to percussion are usually absent because significant inflammation has not spread yet to the apical area. è Histopathologic Features Often demonstrates congestion of the venules that results in focal necrosis. This necrotic zone contains polymorphonuclear leukocytes and histiocytes. The surrounding pulp tissue usually exhibits fibrosis and a mixture of plasma cells, lymphocytes, and histiocytes. v Pulpal Necrosis Death of cells and tissues in the pulp chamber of a tooth. Pulpal necrosis should be suspected when the tooth fails to respond to electric or thermal sensitivity testing. 18  Oral pathology 1 MAJD & SHATHA Lecture 12 è Treatment and Prognosis Treatment of the patient with a periapical abscess consists of drainage and elimination of the focus of infection. Abscesses associated with a patent sinus track may be asymptomatic but, nevertheless, should be treated. If the affected tooth is extruded, then reduction of the occlusion is recommended. Unless contraindicated, treatment with NSAIDs usually is appropriate. Antibiotic coverage should be reserved for the medically compromised and patients with significant cellulitis or clinical evidence of dissemination (i.e., fever, lymphadenopathy, malaise). Once the infection has been resolved by extraction or appropriate endodontic therapy, the affected bone typically heals. Usually, a sinus track resolves spontaneously after the offending tooth is extracted or endodontically treated. Sinus tracks that persist contain sufficient infectious material to maintain the surface granulation tissue, and surgical removal with curettage of the track is required for resolution. 19