Pulp And Periapical Pathosis PDF

PULP AND PERIAPICAL PATHOSIS 4 a low-compliance system; therefore, a small increase in tissue pressure causes passive compression and even comp...

PULP AND PERIAPICAL PATHOSIS 4 a low-compliance system; therefore, a small increase in tissue pressure causes passive compression and even complete col- lapse of the venules at the site of pulpal injury.52 Pressure increases occur in small “compartmentalized” regions and progress slowly. Therefore, the dental pulp does not degener- ate by extensive increases in pressure, with subsequent strangulation.52,53 Pain is often caused by several factors. The release of medi- ators of inflammation causes pain directly by lowering the sensory nerve threshold. These substances also cause pain indirectly by increasing both vasodilation in arterioles and vascular permeability in venules, resulting in edema and ele- vation of tissue pressure. This pressure acts directly on sensory nerve receptors. Increased tissue pressure, the inability of the pulp to expand, and the lack of collateral circulation may result in pulpal Fig. 4.9 Some plasma cells stain positively for IgM in inflamed necrosis and the development of subsequent periradicular human dental pulp, indicating immunologic activity. pathosis. CLASSIFICATION OF PULPAL DISEASES Because there is little or no correlation between the histologic findings of pulpal pathosis and clinical symptoms,54 the diag- nosis and classification of pulpal diseases are based on clinical signs and symptoms rather than histopathologic findings. Pulpal conditions can be classified as normal pulp, reversible and irreversible pulpitis, hyperplastic pulpitis, necrosis, and previously treated pulp. Hard tissue responses include calci- fication and resorption. Normal Pulp A tooth with a normal pulp is clinically symptom free and responds normally to vitality tests. Such a tooth does not reveal any radiographic signs of pathosis. Fig. 4.10 Many dendritic cells (arrows) are present in an inflamed dental pulp. (Courtesy Dr. M. Jontell.) Reversible Pulpitis By definition, reversible pulpitis is a clinical condition associ- ated with subjective and objective findings indicating the pres- ence of mild inflammation in the pulp tissue. If the cause is indicates that delayed hypersensitivity reactions can also eliminated, the inflammation reverses and the pulp returns to occur in this tissue.20 Despite their protective mechanisms, its normal state. immune reactions in the pulp can result in the formation of Mild or short-acting stimuli can cause reversible pulpitis, small necrotic foci and eventual total pulpal necrosis. such as incipient caries, cervical erosion, or occlusal attrition; most operative procedures; deep periodontal curettage; and Lesion Progression enamel fractures resulting in exposure of dentinal tubules. Mild injuries may not result in significant pulpal changes. However, moderate to severe injuries to the pulp result in Symptoms localized inflammation50 and the release of a high concentra- Reversible pulpitis is usually asymptomatic. However, when tion of inflammatory mediators. An increase in protease inhib- present, symptoms usually follow a particular pattern. Appli- itors in moderately to severely inflamed pulps indicates the cation of stimuli, such as cold or hot liquids or air, may presence of natural modifiers.33 As a consequence of the produce sharp, transient pain. Removal of these stimuli, which release of a large quantity of inflammatory mediators, do not normally produce pain or discomfort, results in imme- increased vascular permeability, vascular stasis, and migration diate relief. Cold and hot stimuli produce different pain of leukocytes to the site of injury occur. Current research data responses in normal pulp.55 When heat is applied to teeth with show that the sensory neuropeptide, CGRP, is responsible for uninflamed pulp, the initial response is delayed; the intensity the increase in blood flow during pulpal inflammation.51 of pain increases as the temperature rises. In contrast, pain Elevated capillary pressure and increased capillary perme- in response to cold in normal pulp is immediate; the intensity ability move fluids from blood vessels into the surrounding tends to decrease if the cold stimulus is maintained. Based tissues. If removal of fluids by venules and lymphatics does on these observations, pulpal responses in both health and not coincide with the filtration of capillaries, an exudate disease apparently result largely from changes in intrapulpal forms. Pulp is encased in rigid surrounding tissues, forming pressures. 53 4 ENDODONTICS Treatment also be associated with intermittent or continuous episodes of The removal of irritants and sealing and insulating the exposed spontaneous pain (with no external stimuli). Pain resulting dentin or vital pulp usually result in diminished symptoms from an irreversibly inflamed pulp may be sharp, dull, local- and reversal of the inflammatory process in the pulp tissue ized, or diffuse and can last anywhere from a few minutes up (Fig. 4.11). Nevertheless, if irritation of the pulp continues or to a few hours. Localization of pulpal pain is more difficult increases in intensity for the reasons stated earlier, moderate than localization of periradicular pain and becomes more dif- to severe inflammation develops, with resultant irreversible ficult as the pain intensifies. Application of external stimuli, pulpitis and eventually pulpal necrosis. such as cold or heat, may result in prolonged pain. Accordingly, in the presence of severe pain, pulpal responses Irreversible Pulpitis differ from those of uninflamed teeth or teeth with reversible Irreversible pulpitis may be classified as symptomatic or pulpitis. For example, application of heat to teeth with irre- asymptomatic. It is a clinical condition associated with sub- versible pulpitis may produce an immediate response; also, jective and objective findings indicating the presence of severe occasionally with the application of cold, the response does inflammation in the pulp tissue. Irreversible pulpitis is often not disappear and is prolonged. Application of cold in patients a sequel to and a progression from reversible pulpitis. Severe with painful irreversible pulpitis may cause vasoconstriction, pulpal damage from extensive dentin removal during opera- a drop in pulpal pressure, and subsequent pain relief. Although tive procedures or impairment of pulpal blood flow as a result it has been claimed that teeth with irreversible pulpitis have of trauma or orthodontic movement of teeth may also cause lower thresholds to electrical stimulation, Mumford found irreversible pulpitis. Irreversible pulpitis is a severe inflamma- similar pain perception thresholds in inflamed and uninflamed tory process that does not resolve, even if the cause is removed. pulps.56 The pulp is incapable of healing and slowly or rapidly becomes necrotic. Irreversible pulpitis can be symptomatic with spon- Tests and Treatment taneous and lingering pain. It can also be asymptomatic, with If inflammation is confined to the pulp and has not extended no clinical signs and symptoms. periapically, teeth respond within normal limits to palpation and percussion. The extension of inflammation to the PDL Symptoms causes percussion sensitivity and allows better localization of Irreversible pulpitis is usually asymptomatic. However, pain. Root canal treatment or extraction is indicated for teeth patients may report mild symptoms. Irreversible pulpitis may with signs and symptoms of irreversible pulpitis. A B C Fig. 4.11 A, Mechanically exposed pulp horns of a mandibular molar with signs of reversible pulpitis were capped with mineral trioxide aggregate. B, Immediate postoperative radiograph. C, Follow-up radiograph 5 years later shows no calcific 54 metamorphosis in the pulp chamber, closure of apexes, and normal responses during clinical examination.  PULP AND PERIAPICAL PATHOSIS 4 Hyperplastic Pulpitis Hard Tissue Changes Caused by Hyperplastic pulpitis (pulp polyp) is a form of irreversible Pulpal Inflammation pulpitis that originates from overgrowth of a chronically As a result of irritation, one of two distinct hard tissue changes inflamed young pulp onto the occlusal surface. It is usually may occur: calcification or resorption. found in carious crowns of young patients (Fig. 4.12, A). Ample vascularity of the young pulp, adequate exposure for Pulp Calcification drainage, and tissue proliferation are associated with the for- Extensive calcification (usually in the form of pulp stones or mation of hyperplastic pulpitis. Histologic examination of diffuse calcification) occurs as a response to trauma, caries, hyperplastic pulps shows surface epithelium overlying the periodontal disease, or other irritants. Thrombi in blood inflamed connective tissue (Fig. 4.12, B). Cells of the oral vessels and collagen sheaths around vessel walls are possible epithelium are implanted and grow over the exposed surface sources for these calcifications. to form an epithelial covering. Another type of calcification is the extensive formation of Hyperplastic pulpitis is usually asymptomatic. It appears as hard tissue on dentin walls, often in response to irritation or a reddish, cauliflower-like outgrowth of connective tissue into death and replacement of odontoblasts. This process is called caries that has resulted in a large occlusal exposure. It is calcific metamorphosis (Fig. 4.13). As irritation increases, the occasionally associated with clinical signs of irreversible pul- amount of calcification may also increase, leading to partial pitis, such as spontaneous pain, in addition to lingering pain or complete radiographic (but not histologic) obliteration of to cold and heat stimuli. The threshold to electrical stimula- the pulp chamber and root canal.57 A yellowish discoloration tion is similar to that found in normal pulps. These teeth of the crown is often a manifestation of calcific metamorpho- respond within normal limits when palpated or percussed. sis. The pain threshold to thermal and electrical stimuli usually Hyperplastic pulpitis can be treated by pulpotomy, root canal increases; often the teeth are unresponsive. treatment, or extraction. Palpation and percussion are usually within normal limits. In contrast to soft tissue diseases of the pulp, which have no radiographic signs and symptoms, calcification of pulp tissue is associated with various degrees of pulp space obliteration. A reduction in coronal pulp space followed by a gradual nar- rowing of the root canal is the first sign of calcific metamor- phosis. This condition is not pathologic in nature and does not require treatment. Internal (Intracanal) Resorption Inflammation in the pulp may initiate resorption of adjacent hard tissues. The pulp is transformed into a vascularized A B Fig. 4.12 A, Pulp polyp, also known as hyperplastic pulpitis. The involved tooth is usually carious with extensive loss of tooth structure; the pulp remains vital and proliferates from the exposure Fig. 4.13 Calcific metamorphosis does not represent pathosis site. B, Histologic examination of hyperplastic pulpitis shows per se and may occur with aging or low-grade irritation. It also may surface epithelium and underlying inflamed connective tissue. occur subsequent to a traumatic injury to the tooth. 55 4 ENDODONTICS inflammatory tissue with dentinoclastic activity; this condi- due to an increase in intrapulpal pressure, as is the case in tion leads to the resorption of the dentinal walls, advancing teeth with vital pulps. This pressure registers zero after heat from its center to the periphery.58 Most cases of intracanal application to teeth with necrotic pulps. It is commonly resorption are asymptomatic. Advanced internal resorption believed (but is unlikely) that applying heat to teeth with involving the pulp chamber is often associated with pink spots liquefaction necrosis causes thermal expansion of gases in the crown. present in the root canal space, which provokes pain.60 In fact, Teeth with intracanal resorptive lesions usually respond cold, heat, or electrical stimuli applied to teeth with necrotic within normal limits to pulpal and periapical tests. Radio- pulps usually produce no response. graphs reveal the presence of radiolucency with irregular enlargement of the root canal compartment (Fig. 4.14). Imme- Tests and Treatment diate removal of the inflamed tissue and completion of root By definition, the pulp of a tooth with necrotic pulp should canal treatment are recommended; these lesions tend to be be nonresponsive to vitality testing. However, various degrees progressive and eventually perforate to the lateral periodon- of inflammatory response are possible, ranging from revers- tium. When this occurs, pulp necrosis ensues, and treatment ible pulpitis to necrosis in teeth with multiple canals, and of the tooth becomes more difficult. this may occasionally cause confusion during testing for responsiveness. Furthermore, the effects of necrosis are Pulpal Necrosis seldom confined within canals. Because of the spread of As stated before, pulp is encased in rigid walls, it has no col- inflammatory reactions to periradicular tissues, teeth with lateral blood circulation, and its venules and lymphatics col- necrotic pulps are often sensitive to percussion. Sensitivity lapse under increased tissue pressure. Therefore, irreversible to palpation is an additional indication of periradicular pulpitis leads to liquefaction necrosis. If exudate produced involvement. Root canal treatment or extraction is indicated during irreversible pulpitis is absorbed or drains through for these teeth. caries or through a pulp exposure into the oral cavity, necrosis is delayed; the radicular pulp may remain vital for a long time. Previously Initiated Root Canal Therapy In contrast, closure or sealing of an inflamed pulp induces This condition represents a clinical diagnostic category in rapid and total pulpal necrosis and periradicular pathosis.59 In which the tooth has had either partial or complete endodontic addition to liquefaction necrosis, ischemic necrosis of the therapy. The teeth in this category can be symptomatic or pulp occurs as a result of traumatic injury from disruption of asymptomatic, depending on pulpal and periapical conditions. the blood supply. Necrotic pulp is a clinical condition associ- Completion of partial root canal therapy or retreatment of ated with subjective and objective findings indicating death of failed root canal treatment, endodontic surgery, or extraction the dental pulp. is indicated for these teeth. Symptoms Pulpal necrosis is usually asymptomatic but may be associ- PERIAPICAL PATHOSIS ated with episodes of spontaneous pain and discomfort or pain (from the periradicular tissues) on pressure. In teeth with As a consequence of pulpal necrosis, pathologic changes can necrotic pulps, pain provoked with application of heat is not occur in the periradicular tissues. In contrast to pulp, perira- dicular tissues have an almost unlimited source of undifferen- tiated cells that participate in inflammation and repair. In addition, these tissues have a rich collateral blood supply and lymphatic drainage system. The interaction between the irri- tants emanating from the canal space and the host defense results in the activation of an extensive array of reactions to protect the host. Despite the benefits of this process, some of these reactions are associated with destructive consequences, such as periradicular bone resorption. Resorption of the bone provides a separation between the irritants and the bone, thereby preventing osteomyelitis. Depending on the severity of irritation, its duration, and the host response, periradicular pathoses may range from slight inflammation to extensive tissue destruction. The reactions involved are highly complex and are usually mediated both by nonspecific mediators of inflammation and by specific immune reactions (Fig. 4.15).38 Nonspecific Mediators of Periapical Lesions Nonspecific mediators of inflammatory reactions include neu- ropeptides, fibrinolytic peptides, kinins, complement frag- ments, vasoactive amines, lysosomal enzymes, arachidonic acid metabolites, and various cytokines.31 Neuropeptides Fig. 4.14 Hard tissue resorption that causes disappearance of have been demonstrated in inflamed periapical tissues of normal radiographic evidence of the root canal usually indicates an experimental animals, and it appears that these substances 56 internal resorption defect. play a role in the pathogenesis of periradicular pathosis.34 4 ENDODONTICS in periapical lesion formation. Matrix metalloproteinases (MMPs) are a class of endopeptidases that significantly con- tribute to degradation of extracellular matrix components.76 Elevated levels of MMPs have been reported in lesions iso- lated from animals77 and humans.78 MMP-9 (also known as gelatinase-B), in particular, which removes the collagenous layer from bone, has been isolated in chronic and acute lesions.79 Another key protein that plays a major role in bone resorp- tion is nuclear factor-κB ligand (RANKL). RANKL binds to its receptor (RANK), resulting in osteoclast differentiation. This interaction is inhibited by osteoprotegerin (OPG), a decoy protein that binds to the receptor. Levels of RANKL and the ratio of RANKL to OPG both peak at 2 to 3 weeks, concurrent with the progression of periapical bone destruc- Fig. 4.16 Using the anticomplement immunofluorescence tion.80 RANKL production tapers off between weeks 4 and 8, technique, immune complexes are identified (arrows) in human whereas production of OPG increases during this time, creat- periapical lesions. ing a negative feedback loop that limits the amount of bone destruction caused by bacterial infection. The RANKL- RANK interaction is involved in both physiologic and patho- logic bone resorption.81 In periapical tissues, a significant increase in RANKL levels has been found in granulomatous lesions compared to healthy controls.82,83 CLASSIFICATION OF PERIAPICAL LESIONS Periapical lesions have been classified on the basis of their clinical and histologic findings. As with pulpal disease, little correlation exists between the clinical signs and symptoms and duration of lesions and the histopathologic findings.84 Because of these discrepancies and for convenience, these lesions are classified into six main groups: normal periapical tissues, symptomatic (acute) apical periodontitis, asymptom- atic (chronic) apical periodontitis, condensing osteitis, acute apical abscess, and chronic apical abscess. Lesions associated with significant symptoms, such as pain or swelling, are Fig. 4.17 T lymphocytes (red membrane cells) are identified in a referred to as acute (symptomatic), whereas those with mild human periapical lesion by an immunohistochemical technique. or no symptoms are identified as chronic (asymptomatic). Normal Periapical Tissues sensitization.31 The presence of potential antigens in root The normal periapical tissue group represents a clinical and canals, IgE, and mast cells in pathologically involved pulp and radiographic diagnostic category in which the tooth has periradicular lesions indicates that a type I immunologic reac- normal periapical tissues and is not abnormally sensitive to tion may occur. percussion or palpation testing. The teeth in this category have Various classes of immunoglobulins have been found in normal lamina dura and periodontal ligament structures. inflamed lesions.31,70 These include specific antibodies against a number of bacterial species in infected root canals.71,72 In Symptomatic Apical Periodontitis addition, numerous types of immunocompetent cells, such as Etiology antigen-presenting cells (Ia antigen-expressing nonlymphoid The first extension of pulpal inflammation into the periradicu- cells), macrophages,73 PMN leukocytes, and B and T cells, lar tissues is called symptomatic apical periodontitis (SAP). have been found in human periradicular lesions.74 The pres- Eliciting irritants include inflammatory mediators from an ence of immune complexes (Fig. 4.16) and immunocompetent irreversibly inflamed pulp or egress of bacterial toxins from cells (e.g., T cells; Fig. 4.17) indicates that various types of necrotic pulps, chemicals (e.g., irrigants or disinfecting immunologic reactions (types II to IV) can initiate, amplify, agents), restorations in hyperocclusion, overinstrumentation or perpetuate these inflammatory lesions.31 of the root canal, and extrusion of obturating materials. The pulp may be reversibly inflamed, irreversibly inflamed, or Lesion Progression necrotic. As previously stated, bone resorption during periapical lesion formation allows bone to retreat from infection sites to prevent Signs and Symptoms bacterial invasion of alveolar osseous tissues that could lead Clinical features of SAP are moderate to severe spontaneous to the development of osteomyelitis.75 A wide variety of discomfort, in addition to pain on biting or percussion. If SAP 58 factors have been implicated in the bone resorption observed is an extension of pulpitis, its signs and symptoms include  PULP AND PERIAPICAL PATHOSIS 4 responsiveness to cold, heat, and electricity. Cases of SAP Histologic Features caused by a necrotic pulp do not respond to vitality tests. Histologically, AAP lesions are classified as either granulo- Application of pressure by the fingertip or tapping with the mas or cysts. A periapical granuloma consists of granuloma- butt end of a mirror handle (percussion) can cause marked to tous tissue infiltrated by mast cells, macrophages, lymphocytes, excruciating pain. SAP is not associated with an apical radio- plasma cells, and occasionally, PMN leukocytes (Fig. 4.20). lucency. Occasionally there may be slight radiographic Multinucleated giant cells, foam cells, cholesterol clefts, and changes, such as a “widening” of the PDL space or a very epithelium are often found. small radiolucent lesion; however, usually there is a normal The apical (radicular) cyst has a central cavity filled with PDL space with an intact lamina dura. an eosinophilic fluid or semisolid material and is lined by stratified squamous epithelium (Fig. 4.21). The epithelium is Histologic Features surrounded by connective tissue containing all cellular ele- With SAP, PMN leukocytes and macrophages are visible ments found in the periapical granuloma. Therefore, an apical within a localized area at the apical region of the pulp. At times cyst is a granuloma that contains a cavity or cavities lined with there may be a small area of liquefaction necrosis (abscess). epithelium. The origin of the epithelium is the remnants of Bone and root resorption may be present histologically; Hertwig’s epithelial sheath, the cell rests of Malassez. These however, resorption is usually not visible radiographically. cell rests proliferate in response to inflammatory stimuli. The actual genesis of the cyst is unclear. Treatment The reported incidence of various classes of endodontic Adjustment of occlusion (when there is evidence of hyperoc- lesions is inconsistent. Variations may be due to sampling clusion), removal of irritants or a pathologic pulp, or removal methods and the histologic criteria used for diagnosis. Nobu- of periapical exudate usually results in relief. hara and del Rio examined periapical biopsies that were refractory to root canal treatment and showed most to be Asymptomatic Apical Periodontitis granulomas (59%), with some cysts (22%), a few scars (12%), Etiology and a scattering of other types of lesions (7%).85 However, Asymptomatic apical periodontitis (AAP) results from pulp percentages such as these are misleading. Many lesions share necrosis and usually is a sequel to SAP. combined features of granulomatous inflammatory lesions, cysts, and areas of scarring. The samples usually do not Signs and Symptoms include abscesses, because their intact recovery is difficult By definition, AAP is a clinical, asymptomatic condition of during surgery. In fact, in the majority of cases, the entire pulpal origin associated with inflammation and destruction of lesion typically is not recovered for biopsy, and only frag- periapical tissues. Because the pulp is necrotic, teeth with ments are obtained during curettage. AAP do not respond to electrical or thermal stimuli. Percus- sion produces little or no pain. There may be slight sensitivity Treatment to palpation, indicating an alteration of the cortical plate of Removal of inciting irritants (necrotic pulp) and complete bone and extension of AAP into the soft tissues. Radiographic obturation of the root canal system usually result in resolution features range from interruption of the lamina dura (Fig. 4.18) of AAP (Fig. 4.22). There is no evidence that apical cysts to extensive destruction of periapical and interradicular tissues resist resolution after adequate root canal treatment or (Fig. 4.19). extraction. Fig. 4.18 After cementation of a three-unit bridge, the premolar Fig. 4.19 Chronic apical periodontitis. Extensive tissue developed clinical signs and symptoms of acute apical destruction in the periapical area of a mandibular first molar has periodontitis. Radiograph shows a widened periodontal ligament occurred as a result of pulpal necrosis. Lack of symptoms and the space (arrow). presence of a radiographic lesion are diagnostic. 59 4 ENDODONTICS A B C D E F Fig. 4.20 A, Lymphocytes (small arrows). Plasma cells (large arrows) have an eccentric nucleus with adjacent “clear zone” and a basophilic outer rim of cytoplasm. B, A plasma cell with an accumulation of immunoglobulins within the cytoplasm. C, Polymorphonuclear (PMN) leukocytes are concentrated in this field. They have multilobed nuclei, and many of them are degenerating and have disrupted cell walls. D, Giant cells (arrows) with multiple nuclei. Macrophages (M) with lighter-stained nuclei and diffuse cytoplasm. E, Macrophages (arrows) are larger and often have ingested material, as indicated by a “foamy” cytoplasm in these cells. F, Lymphocytes, with their densely basophilic nuclei, dominate this field. (Courtesy Dr. C. Kleinegger.) Condensing Osteitis pulp inflammation or necrosis. However, condensing osteitis Etiology can occur in association with the apex of any tooth. Condensing osteitis, a variant of asymptomatic apical peri- odontitis, represents an increase in trabecular bone in response Signs and Symptoms to persistent irritation. The irritant diffusing from the root Depending on the cause (pulpitis or pulpal necrosis), condens- canal into periradicular tissues is the main cause of condens- ing osteitis may be either asymptomatic or associated with ing osteitis. This lesion is usually found around the apices of pain. Pulp tissue of teeth with condensing osteitis may or may 60 mandibular posterior teeth, which show a probable cause of not respond to electrical or thermal stimuli. Furthermore,  PULP AND PERIAPICAL PATHOSIS 4 these teeth may or may not be sensitive to palpation or percus- Root canal treatment, when indicated, may result in the sion. Radiographically, the presence of a diffuse, concentric complete resolution of condensing osteitis.87 Condensing arrangement of radiopacity around the root of a tooth is osteitis is often confused with enostosis (sclerotic bone), a pathognomonic (Fig. 4.23). Histologically, there is an increase nonpathologic entity. in irregularly arranged trabecular bone and inflammation.86 Acute Apical Abscess Etiology Acute apical abscess (AAA) is a localized (Fig. 4.24, A) or diffuse (Fig. 4.24, B) liquefaction lesion of pulpal origin that destroys periradicular tissues and a severe inflammatory response to microbial and nonbacterial irritants from a necrotic pulp. Signs and Symptoms AAA is characterized by rapid onset and spontaneous pain. Depending on the severity of the reaction, patients with AAA usually have moderate to severe discomfort and/or swelling. There often is no swelling if the abscess is confined to bone. In addition, they occasionally have systemic manifestations of an infective process, such as elevated temperature, malaise, and leukocytosis. Because these findings are only observed in association with a necrotic pulp, electrical or thermal stimula- tion produces no response. However, these teeth are usually painful to percussion and palpation. Depending on the degree Fig. 4.21 A region of human apical cyst consists of a central of hard tissue destruction inflicted by irritants, radiographic cavity filled with eosinophilic material (EM) and a wall lined with features of AAA range from no changes to widening of the epithelium. PDL space to an obvious radiolucent lesion. A B C Fig. 4.22 A, Preoperative radiograph of a second molar with pulpal necrosis and evidence of chronic apical periodontitis. B, Postoperative radiograph of the tooth. C, Postoperative radiograph 2 years after root canal therapy shows complete resolution of the periradicular pathosis. 61 4 ENDODONTICS Histologic Features directly with the apical foramen; frequently an abscess does Histologic examination of AAA usually shows a localized not drain through an accessed tooth. destructive lesion of liquefaction necrosis containing numer- Removal of the underlying cause, release of pressure ous disintegrating PMN leukocytes, debris, and cell remnants (drainage where possible), and routine root canal treatment and an accumulation of purulent exudate (see Fig. 4.24, C). lead to resolution of most cases of AAA. Surrounding the abscess is granulomatous tissue; therefore, the lesion is best categorized as an abscess within a granu- Chronic Apical Abscess loma. Notably, the abscess often does not communicate The chronic apical abscess (CAA) is an inflammatory lesion of pulpal origin characterized by the presence of a long- standing lesion that has resulted in an abscess that drains to a mucosal (sinus tract) or skin surface. Etiology CAA has a pathogenesis similar to that of AAA. It also results from pulpal necrosis and is usually associated with chronic apical periodontitis that has formed an abscess. The abscess has “burrowed” through bone and soft tissue to form a sinus tract stoma on the oral mucosa (Fig. 4.25, A) or sometimes onto the facial dermis. The histologic findings in these lesions are similar to those found in SAP (Fig. 4.25, B). CAA may also drain through the periodontium into the sulcus and may mimic a periodontal abscess or pocket (see Chapter 7). Signs and Symptoms Because drainage exists, CAA is usually asymptomatic, except when there is occasional closure of the sinus pathway, which can cause pain. Clinical, radiographic, and histopatho- Fig. 4.23 Condensing osteitis. Chronic inflammation of the pulp logic features of CAA are similar to those described for AAP. of the first molar has resulted in radiopacity of periapical tissue. An additional feature is the sinus tract, which may be lined A C B Fig. 4.24 A, Localized vestibular swelling resulting from the necrotic pulp in the right lateral incisor. B, An acute apical abscess (AAA) has created diffuse facial swelling. C, Histologic examination of the AAA shows edematous tissue heavily 62 infiltrated by degenerating PMN leukocytes.  PULP AND PERIAPICAL PATHOSIS 4 A B Fig. 4.25 A, Sinus tract stoma associated with a necrotic pulp in the left central incisor. B, Histologic examination of the periapical tissue shows numerous lymphocytes, plasma cells, and macrophages (foam cells). A B Fig. 4.26 A, Sclerotic dentin, which appears as an irregularly organized, mineralized tissue and stains lighter than normal tubular dentin with antibody against dentin sialoprotein (DSP). B, Dentin bridge; also, secondary dentin, deposited along canal wall after a pulp capping procedure, which shows a tubular structure and stains similarly to the primary dentin with antibody against DSP. partially or completely by epithelium surrounded by inflamed Extent of Healing connective tissue.88 The level of healing is proportional to the degree and extent of tissue injury and the nature of tissue destruction. When injury to the underlying tissues is slight, little repair or regen- HEALING OF PULP AND PERIAPICAL TISSUES eration is required. On the other hand, extensive damage requires substantial healing (see Fig. 4.22). In other words, Regeneration is a process by which altered tissues are com- pulp and periradicular repair ranges from a relatively simple pletely replaced by tissues native to their original architecture resolution of an inflammatory infiltrate to considerable reor- and function. Repair is a process by which altered tissues are ganization and repair of a variety of tissues. not completely restored to their original structures. Histologic examination of most tissue sections in experimental animals Process of Pulp Healing and humans shows that healing of periradicular lesions after In the absence of irritants, a healthy pulp has tremendous root canal therapy is by repair rather than regeneration of the capacity to heal. Andelin and associates used immunostaining periradicular tissues. Inflammation and healing are not two with dentin sialoprotein (DSP) to determine the type of tissue separate entities; in fact, they constitute part of one process that forms after pulp capping procedures.89 DSP is present in in response to tissue injury. On the molecular and cellular both bone and dentin but is expressed at an approximately levels, they are inseparable. Inflammation dominates the early 400-fold higher level in dentin than in bone.90 Andelin’s study events after tissue injury, shifting toward healing after the showed that, depending on the capping material used, dentin early responses have subsided. However, for convenience and healing may occur through regeneration of dentin (identified to simplify the complex inflammatory-resorptive process, they through heavy DSP staining; Fig. 4.26, A) or through repair are studied as two separate entities. with an amorphous mineralized scar tissue (light DSP 63