Treatment of Endodontic Infections, Cysts, and Flare-ups - J. CRAIG BAUMGARTNER, PAUL A. ROSENBERG, MICHAEL M. HOEN, LOUIS M. LIN
Periapical abscesses and cellulitis occur when microbes invade these tissues. The severity of the periapical infections is related to the virulence of the organisms and host resistance. An abscess is a localized collection of pus within a tissue or confined space.1 Cellulitis is a symptomatic edematous inflammatory process that spreads diffusely through connective tissue and fascial planes.1 Clinically, cellulitis and the associated abscess should be considered a continuum of the infectious inflammatory process.
After bacteria have invaded periapical tissues, an otherwise healthy patient will eventually exhibit clinical signs and symptoms of infection. The patient may experience swelling and mild to severe pain. As the infection and inflammatory response spreads further, the patient may experience systemic signs and symptoms such as chills, fever, lymphadenopathy, nausea, and headache. The tooth that is the reservoir of the endodontic infection will usually be sensitive to biting and percussion (touch), and eventually the overlying tissues will be sensitive to palpation. There may or may not be radiographic evidence of periapical disease. The pulp cavity of an infected tooth is the source of the infection spreading to periapical tissues and for secondary (metastatic) infection that may spread to facial spaces of the head and neck. Appropriate treatment includes removing the reservoir of infection either by debridement of the infected root canal system or removal of the tooth, along with drainage from swollen tissues. Adjunctive pharmacotherapeutics may also be indicated with cellulitis, progressive swellings, and systemic signs and symptoms of infection.
The spread of infection into facial spaces may be life-threatening. There are potential spaces between anatomic structures of the head and neck which may be involved in infection and inflammation. These facial spaces are recognized by their anatomic boundaries.2 An anatomic space that may be involved in mandibular infections is the mandibular buccal vestibule. The swelling occurs between the cortical plate and the buccinator muscle in the posterior of the mandible and the mentalis muscle in the anterior. Mandibular anterior teeth may produce swelling of the mental or submental spaces (Figure 1). The mental space is located between the mentalis muscle and the
[Figure 1. Mental, submental, and sublingual spaces.]
[Figure 2. Submandibular and sublingual spaces.]
platysma muscle. The submental space is between the mylohyoid muscle and the platysma muscle. Mandibular anterior teeth may also lead to swelling in the sublingual space (see Figure 1) located between the floor of the mouth and the inferiorly located mylohyoid muscle. The submandibular space (Figure 2) is between the mylohyoid and the platysma muscles. The source of infection in this space is usually a mandibular posterior tooth. Ludwig's angina is an infection that includes the submental, sublingual, and submandibular spaces. Cellulitis may extend to the pharyngeal and cervical spaces and produce airway obstruction.
Anatomic spaces involved in lateral face swelling include the maxillary buccal vestibule. This space is located between the cortical plate of the maxilla and the superior attachment of the buccinator muscle and associated with infections of maxillary posterior teeth. The buccal space (Figure 3) is between the lateral surface of the buccinator muscle and the overlying skin of the cheek. The source of the infection may be either a maxillary or a mandibular posterior tooth. The submasseteric space (see Figure 3) lies between the lateral surface of the ramus of the mandible and the masseter muscle. The source of the infection is usually the mandibular third molar. The deep temporal space is between the lateral surface of the skull and the medial surface of the temporal muscle while the superficial temporal space lies between the temporal muscle and the overlying fascia.
[Figure 3. Buccal, submasseteric, pterygomandibular, and parapharyngeal spaces.]
Anatomic spaces involved in the pharyngeal and cervical areas include the pterygomandibular space (see Figure 3). That space is usually associated with infection of the mandibular second or third molars. The pterygomandibular space is bounded by the lateral surface of the medial pterygoid muscle and the medial surface of the mandible. The bilateral parapharyngeal space is between the medial surface of the medial pterygoid muscle and the superior constrictor muscle. The superior border is the base of the skull and the inferior border is the hyoid bone. The carotid space contains the carotid artery, internal jugular vein, and the vagus nerve. The retropharyngeal space (Figure 4) is posterior to the superior constrictor muscle and extends to the mediastinum. The pretracheal space surrounds the trachea and extends from the thyroid cartilage to the level of the aortic arch. The retrovisceral space extends from the base of the skull into the posterior mediastinum. The danger space (see Figure 4) extends from the base of the skull into the posterior mediastinum. The prevertebral space surrounds the vertebral column.
The anatomic spaces involved in midface swellings are the palate, the base of the upper lip, the
[Figure 4. Pretracheal, prevertebral, and danger spaces.]
[Figure 5. Periorbital and canine spaces.]
infraorbital (canine) space, and the periorbital spaces. The source of infection for the palate is the maxillary teeth. Swelling of the base of the nose is typically caused by a maxillary central incisor with its root apex above the attachment of the orbicularis oris muscle. The infraorbital space (Figure 5) is between the levator anguli oris muscle and the levator labii superioris muscle. The source of the infection is usually the maxillary cuspid or first premolar. The periorbital space lies deep to the orbicularis oculi muscle and becomes involved as a result of the spread of infection from the buccal or infraorbital space. Infections of the midface are of special concern because of the possibility that they may result in cavernous sinus thrombosis. If the inflammation and resulting edema cause blood to back up into the cavernous sinus, the infected thrombi may escape into circulation and produce a life-threatening event.
Figure 1. Mental, submental, and sublingual spaces. Courtesy Dr. Wm. Girsch.0
Figure 2. Submandibular and sublingual spaces. Courtesy Dr. Wm. Girsch.0
Figure 3. Buccal, submasseteric, pterygomandibular, and parapharyngeal spaces. Courtesy Dr. Wm. Girsch.0
Figure 4. Pretracheal, prevertebral, and danger spaces. Courtesy Dr. Wm. Girsch.0
Figure 5. Periorbital and canine spaces. Courtesy Dr. Wm. Girsch.0
Treatment of Endodontic Abscesses/Cellulitis
Prompt diagnosis and removal of the reservoir of infection are important for the successful treatment of endodontic infections. Drainage of infectious material and inflammatory mediators associated with endodontic infections may be established through the tooth, soft tissues, or alveolus. Surgical methods for drainage include incision for drainage (I&D), needle aspiration, and trephination. In otherwise healthy patients, chemo-mechanical debridement of the root canal system and drainage of an associated swelling will lead to rapid improvement of the patient's signs and symptoms. Tooth extraction is the alternative treatment to removal of the reservoir of infection. After debridement of the root canal system, I&D is indicated for periapical swellings. A recent study found that even with drainage through the access opening into the pulp cavity, there was not a significant reduction in pain, percussion pain, swelling, or number of analgesics taken.3
[Figure 6. Drain sutured in place.]
Figure 6. Drain sutured in place. Courtesy Dr. Craig Baumgartner.0
INCISION FOR DRAINAGE
Successful resolution of an infection requires removal of the source of infection and drainage of the accumulated exudate. Drainage from a swelling caused by an abscess/cellulitis decreases the number of bacteria, bacterial by-products, and inflammatory mediators associated with the swelling. The removal of pockets of purulence and edematous fluid also improves circulation and allows delivery of prescribed antibiotics in a minimum inhibitory concentration. An I&D or needle aspiration of a swelling associated with cellulitis will often reveal accumulations of purulence consistent with an abscess. An incision provides a pathway for additional drainage to prevent the further spread of the abscess/cellulitis. Nerve block anesthesia should be used and if necessary supplemented with local infiltration (see Chapter 22).
To achieve drainage from a swelling, a stab incision through the periosteum is made at the most dependent site of the swelling. A periosteal elevator or hemostat is then used for blunt dissection to allow drainage of any accumulated exudate and inflammatory mediators. Except for very small localized swellings, a drain should be sutured into place (Figure 6).
[Figure 7. Top drain is a capillary drain, middle is a penrose drain, bottom is a rubber dam drain.]
Drains may be a piece of rubber dam, a Penrose drain, or a capillary drain (Figure 7). The latter is ribbed and seems to stay under the tissues better than the non-ribbed drains. Non-latex drains should be used for those allergic or sensitive to latex. A sutured drain keeps the incision open for continued drainage and encourages compliance by the patient to return for follow-up evaluations. The use of warm intraoral rinses may help promote drainage. The drain can usually be removed in 1 or 2 days when there is improvement in the patient's clinical signs and symptoms. Consultation with, and referral to other specialists in the management of facial infections, is indicated for severe or persistent infections.
Figure 7. Top drain is a capillary drain, middle is a penrose drain, bottom is a rubber dam drain. Courtesy Dr. Craig Baumgartner.0
Needle aspiration may be described as the use of suction to remove fluids from a cavity or space. It is a surgical procedure that may provide information as to the presence and volume of exudate, cystic fluid, or blood. Aspirated samples may be used for microbial isolation and identification, using either culturing or molecular methods4-6 (Figure 8). In addition, the sample may be used for immunohistochemical analysis (Figure 9). In 1995, Simon et al.7 described the clinical use of needle aspiration for intraoral swelling as an alternative technique to I&D. Following regional and local anesthesia, the technique involved the use of a syringe with an 18-gauge needle to aspirate the contents of a swelling. Clinical advantages of needle aspiration over I&D include reduced scarring, evaluation of volume and character of the aspirate, use of the aspirate for culture and sensitivity testing, and the lack of postoperative drain removal.
[Figure 8. Aspirate from abscess/cellulitis.]
Figure 8. Aspirate from abscess/cellulitis. Courtesy Dr. Mike Hoen.0
Figure 9. The aspirated sample is injected through the stopper into an anaerobic transport vial. Courtesy Dr. Craig Baumgartner.0
ANTIBIOTICS IN ENDODONTICS
The vast majority of infections of endodontic origin can be effectively managed without the use of antibiotics. Systemically administered antibiotics are not a substitute for timely endodontic treatment. Chemo-mechanical debridement of the infected root canal system with drainage through the root canal and by incision and drainage of swollen tissues will decrease the bioburden so that a normal healthy patient can
[Figure 9. The aspirated sample is injected through the stopper into an anaerobic transport vial.]
[Table 1. Conditions not Requiring Adjunctive Antibiotics]
begin the healing process. Antibiotics are not recommended for healthy patients with symptomatic pulpitis, symptomatic apical periodontitis, a draining sinus tract, a localized swelling of endodontic origin, or following endodontic surgery8-13 (Table 1). An antibiotic regimen should be prescribed in conjunction with endodontic treatment when there are systemic signs and symptoms of infection or a progressive/persistent spread of infection. The presence of a fever (>100°F), malaise, cellulitis, unexplained trismus, and progressive swelling are all signs and symptoms of systemic involvement and spread of infection (Table 2). Under these circumstances, an antibiotic is indicated in addition to debridement of the root canal harboring the infecting microbes and drainage of any accumulated purulence. Patients with serious endodontic infections should be closely followed on a daily basis. Their conditions will usually improve rapidly once the source of the infection is removed. Because of the lack of circulation, systemically administered antibiotics are not effective against a reservoir of microorganisms within an infected root canal system. Furthermore, a minimum inhibitory concentration of an antibiotic may not reach an anatomic space filled with purulence and edematous fluid because of poor circulation and the diffusion gradient that it must traverse. Pus consists mainly of neutrophils, cellular debris, bacteria, bacterial by-products, enzymes, and edematous fluid. An I&D will allow drainage of the purulent material and improve circulation to the area. Drainage provides a pathway for removal of inflammatory mediators and helps prevent further spread of cellulitis.
[Table 2. Indications for Adjunctive Antibiotics (Antimicrobial Therapy)]
Empirical selection of an antibiotic (antimicrobial agent) should be based on knowledge of which bacteria are most commonly associated with endodontic infections and their antibiotic susceptibility.4,5,14-18 The clinician must be knowledgeable about the antibiotic and inform the patient of its benefits, possible side effects, and possible sequelae of failing to take the recommended dosage. A loading dose is important to provide an initial adequate therapeutic blood level of antibiotic. It should generally be continued for 2 to 3 days following resolution of the major clinical signs and symptoms of the infection. Following removal of the source of the infection and adjunctive antibiotic therapy, significant improvement in the patient's status should be seen in 24 to 48 hours. A prescription written for a 7-day regimen of antibiotic therapy is usually adequate.
Penicillin VK is the antibiotic of choice because of its effectiveness against both facultative and anaerobic microorganisms commonly found in polymicrobial endodontic infections.4,5,14,17-19 However, up to 10% of the population may be allergic to this medication, so a careful history of drug hypersensitivity is important. A loading dose of 1,000 mg of penicillin VK should be orally administered followed by 500 mg every 4 to 6 hours.
Amoxicillin has an expanded spectrum of activity that includes bacteria not routinely associated with infections of endodontic origin.4,5,15,16 It is rapidly absorbed and provides sustained serum levels which make it ideal for use with medically compromised patients who require antibiotic prophylaxis. The usual oral dosage for amoxicillin to treat infections is 1,000-mg loading dose followed by 500 mg every 8 hours. An alternate dosage for amoxicillin is 875 mg every 12 hours.
Clavulanate is a competitive inhibitor of betalactamase. Antibiotic susceptibility tests have shown excellent results against bacteria isolated from endodontic infections when clavulanate is used in combination with amoxicillin (Augmentin).4,5,15,16 This combination should be considered for patients who are immunocompromised. The usual oral dosage for amoxicillin with clavulanate is 1,000-mg loading dose followed by 500 mg every 8 hours. An alternate dosage is 875 mg every 12 hours.
Erythromycin has traditionally been the alternative choice for patients allergic to penicillin, but it is not effective against anaerobes associated with endodontic infections. Clarithromycin and azithromycin are macrolides like erythromycin, with some advantages over the latter. They have a spectrum of antimicrobial activity that includes facultative bacteria and some anaerobic bacteria associated with infections of endodontic origin. They also have less gastrointestinal upset than erythromycin. The oral dosage for clarithromycin is a 500-mg loading dose followed by 250 mg every 12 hours. The oral dosage for azithromycin is a 500-mg loading dose followed by 250 mg once a day.
Clindamycin is effective against both facultative and strict anaerobic bacteria associated with endodontic infections. It is well distributed throughout the body, especially to bone, where its concentration approaches that of plasma. Both penicillin and clindamycin have been shown to produce good results in treating odontogenic infections.4,5,20 Clindamycin is rapidly absorbed even in the presence of food in the stomach.21 The oral adult dosage for serious endodontic infections is a 600-mg loading dose followed by 300 mg every 6 hours.
Metronidazole is a nitroimidazole that is active against parasites and anaerobic bacteria. However, it is ineffective against facultative bacteria.4,5,22 It is a valuable antimicrobial agent in combination with penicillin when penicillin alone has been ineffective.22 The usual oral dosage for metronidazole is a 1,000-mg loading dose followed by 500 mg every 6 hours. Consultation with, and referral to other specialists in the management of facial infections, is indicated for severe or persistent infections.
Cephalosporins are usually not indicated for the treatment of endodontic infections. First-generation cephalosporins do not have activity against the anaerobes usually involved in endodontic infections. Second-generation cephalosporins have some efficacy for anaerobes, however, there is a possibility of cross-allergenicity of cephalosporins with penicillin.
Doxycycline occasionally may be indicated when the above antibiotics are contraindicated. However, many strains of bacteria have become resistant to the tetracyclines.
Ciprofloxacin is a quinilone antibiotic that is not effective against anaerobic bacteria usually found in endodontic infections. With a persistent infection, it may be indicated if culture and sensitivity tests demonstrated the presence of susceptible organisms.
PROPHYLACTIC ANTIBIOTICS FOR MEDICALLY COMPROMISED PATIENTS
Prophylactic antibiotic coverage may be indicated for medically compromised patients requiring endodontic treatment. The American Heart Association (AHA) and the American Academy of Orthopaedic Surgeons have made guidelines for prophylactic antibiotic coverage.23,24 The guidelines are meant to aid practitioners but are not intended as the standard of care or as a substitute for clinical judgment. The incidence of endocarditis following most procedures on patients with underlying cardiac disease is low (see Chapter 7 "Microbiology of Endodontic Disease"
A reasonable approach for prescribing prophylactic antibiotics considers the degree to which the underlying disease creates a risk for endocarditis, the apparent risk for producing a bacteremia, adverse reactions to the prophylactic antibiotic, and the cost-benefit aspect of the regimen.23 Antibiotic prophylaxis is employed to prevent surgical infections or their postoperative sequelae, to prevent metastatic bacteremias, and to prevent accusation that "all was not done for the patient."25 It is suspected that antibiotic prophylaxis is often prescribed to prevent malpractice claims.25
How antibiotics quickly kill bacteria in the blood is difficult to answer when many antibiotics are only effective with actively dividing bacteria. It is speculated that antibiotics may reduce metastatic infections by preventing adhesion of bacteria to tissues or inhibiting growth after attachment.26 The principles of antibiotic prophylaxis state that the antibiotic must be in the system prior to an invasive procedure. If a patient has not taken the prescribed antibiotic, he or she should be rescheduled or wait an hour after administration of the antibiotic for treatment. However, there is data to support the use of an antibiotic up to 2 hours after the onset of bacteremia.25
The incidence of bacteremia has been shown to be low during root canal therapy. A transient bacteremia can result from the extrusion of microorganisms from the root canal to the periapical tissues of the tooth.27-31 In addition, positioning rubber dam clamps and accomplishing other dental procedures may produce bleeding and can lead to a bacteremia. Medically compromised dental patients who are at risk of infection should receive a regimen of antibiotics that either follows the recommendations of the AHA or an alternate regimen determined in consultation with the patients' physicians.23 Chapter 24 gives the antibiotic regimens recommended for dental procedures. It is believed that amoxicillin, ampicillin, and penicillin V are equally effective against alpha-hemolytic streptococci; however, amoxicillin is recommended because it is better absorbed from the gastrointestinal tract and provides higher and more sustained serum levels.23
For cardiac conditions associated with endocarditis, prophylaxis is recommended for both non-surgical and surgical endodontic procedures.23 Antibiotic prophylaxis is recommended for cardiac conditions associated with endocarditis at a high or moderate risk category (see Chapter 24). Dental procedures for which antibiotic prophylaxis is recommended (see Chapter 24) include endodontic instrumentation beyond the apex or surgery, but not intracanal endodontic treatment, post-placement and buildup.23 From a practical standpoint, it is difficult to determine with certainty that endodontic instruments do not pass beyond the apical foramen. Also included for prophylaxis antibiotics is intraligamentary periodontal ligament (PDL) local anesthetic injections, but not non-intraligamentary ones.23
In 2003, a joint committee of the American Dental Association and American Academy of Orthopaedic Surgeons published their first advisory statement on antibiotic prophylaxis for patients with prosthetic joints. The dental procedures of concern and the antibiotic regimens are the same as for endocarditis Chapter 24. Patients of potential increased risk of having a hematogenous total joint infection include all patients during the first 2 years following joint replacement, immunocompromised/immunosuppressed patients, and patients with comorbidities as shown in Chapter 24.32
COLLECTION OF A MICROBIAL SAMPLE
Adjunctive antibiotic therapy for endodontic infections is most often prescribed empirically based on knowledge of the bacteria most often associated with endodontic infections. At times, culturing may provide valuable information to better select the appropriate antibiotic regimen. For example, an immunocompromised/immunosuppressed patient (not immunocompetent) or patients at high risk of developing infections (e.g., history of infective endocarditis) following a bacteremia require close monitoring. These patients may have an infection caused by bacteria usually not associated with the oral cavity. Other examples include a seemingly healthy patient who has persistent or progressive symptoms following surgical or non-surgical endodontic treatment. An aseptic microbial sample from a root canal is collected by first isolating the tooth with a rubber dam and disinfecting the tooth surface and rubber dam with sodium hypochlorite or other disinfectant. Sterile burs and instruments must be used to gain access to the root canal system. Intracanal irrigation should not be used until after the microbial sample has been taken. If there is drainage from the canal, it may be sampled with a sterile paper point or aspirated into a sterile syringe with a sterile 18- to 25-gauge needle, depending on the viscosity of the exudate. The aspirate should either be taken immediately to a microbiology laboratory in the syringe or injected into pre-reduced transport media. To sample a dry root canal, a sterile syringe should be used to place some pre-reduced transport medium into the canal. A sterile endodontic instrument is then used to scrape the walls of the canal to suspend microorganisms into the medium.
To prevent contamination by the normal oral flora, a microbial sample from a soft tissue swelling should be obtained before making an I&D. Once profound anesthesia is achieved, the surface of the mucosa should be dried and disinfected with an iodophor swab. A sterile 16- to 20-gauge needle and syringe is used to aspirate the exudate. The aspirate should be handled as described above. A sample can be collected on a swab after the I&D has been made, but great care must be taken to prevent microbial contamination with normal oral flora. After collecting the specimen on a swab, it should be quickly placed in pre-reduced medium for transport to the laboratory.
Good communication with the laboratory personnel is important. The sample should be Gram-stained to demonstrate which types of microorganisms predominate. The culture results should show the prominent isolated microorganisms and not just be identified as "normal oral flora." Antibiotics can usually be chosen to treat endodontic infections based on the identification of the prominent microorganisms in the culture. With persistent infections, susceptibility testing can be undertaken to establish which antibiotics are the most effective against resistant microbial isolates. At present, it may take 1 to 2 weeks to identify anaerobes using conventional methods. Some laboratories may have molecular methods available to rapidly detect and identify known opportunistic bacteria.
Cortical trephination is defined as the surgical perforation of the alveolar cortical plate to release accumulated tissue exudates.1 Its use is indicated for patients with severe pain of endodontic origin without intraoral or extraoral swelling and when drainage cannot be accomplished through the root canal, for example, in the presence of posts, filling material, or ledging. Cortical trephination involves exposing the cortical bone, making an opening in the bone, and making a pathway through the cancellous bone to the root end.33-40 Occasionally, an instrument may be used to penetrate the mucosa and cortical plate without an incision (Figure 10 A). Several studies have demonstrated that a patient with severe periapical pain without swelling will have significant relief following trephination.34,41-43 A technique for trephination recommended by Henry and Fraser41 involves a submarginal horizontal full thickness flap to access the alveolar bone, the use of a surgical high speed round bur to access the involved root apex and abscessed area, and the placement of a sutured drain.
[Figure 10. A, Trephination using a #3 spreader. B, Radiograph showing tip of a #3 spreader near root end.]
Some studies have shown cortical trephination may not be predictable in relieving periapical pain.36-38 A prospective randomized blinded clinical trial raised concern about the assumed clinical effectiveness of trephination.38 In that study, pain logs were evaluated after non-surgical endodontic treatment and either real or simulated trephination. It was found that the routine use of trephination for the reduction of pain or swelling in symptomatic necrotic pulps in teeth with periapical radiolucencies was not predictable. A systematic review of the literature concerning the emergency management of acute apical periodontitis in the permanent dentition also concluded that routine cortical trephination did not show significant benefit.44 While there is no higher level of evidence justifying the routine use of surgical trephination, there are limited instances in which it is a reasonable treatment alternative. Patients with severe periapical pain of endodontic origin without swelling may benefit from the procedure.
Figure 10. A, Trephination using a #3 spreader. B, Radiograph showing tip of a #3 spreader near root end. Courtesy Dr. Craig Baumgartner.0
DECOMPRESSION: ASPIRATION AND IRRIGATION
The terms decompression and marsupialization are often used interchangeably. Decompression is the surgical exposure of a cyst wall and insertion of a tube or other type of drain to decompress the lesion during healing.1 It is not uncommon for chronic periapical pathosis to remain clinically asymptomatic and develop a bony defect of significant size. If left undiagnosed and untreated, periapical pathosis may develop into self-perpetuating entities that erode osseous supporting structures and encroach on adjacent teeth, sinus cavities, neurovascular bundles, and even the nasal cavity. Bony lesions radiographically exceeding 200 mm2 have a higher statistical chance of being cystic.45 There are radicular cysts that may have progressed to the extent that they are truly independent, and non-surgical endodontic treatment may no longer be enough to result in bony healing.46,47 When non-surgical endodontics does not resolve apical pathosis, surgical intervention is an alternative treatment recommendation.
Surgical treatment, including the enucleation of extensive bony lesions, may involve unintentional interruption of periapical vascular and neural structures, development of soft tissue defects, and damage to adjacent anatomic structures. Decompression is a more conservative treatment option that allows the progressive reduction in lesion size and may eliminate the necessity for surgical enucleation. Decompression is intended to disrupt the integrity of the lesion wall, reduce the internal osmotic pressure, and permit osseous regeneration (Figure 11).
In 1982, Suzuki48 suggested treating jaw cysts using an irrigational technique. In that study, the contents of 36 cysts were irrigated weekly for months and even years. This irrigation method involved the use of Ringer's solution, glucose, and antibiotics. The fluids aspirated from the cysts were quantitatively analyzed for electrolytes, inorganic substances, proteins, and lipids. Irrigation of the lesions eventually resulted in the reduction in the volume and size of the cysts. The irrigation method is effective for the treatment of cysts in jaws.48 Large cysts have been decompressed using acrylic stents, obturators, and tubing that extends into the lesion.49-53 Acrylic stents or tubing was often left in for months with irrigation of the lesion. Neaverth and Berg52 described several cases of large lesion decompression that lasted from several weeks to more than a year. The method used radiopaque tubing in conjunction with water irrigation by the patient. The tube was removed once there was evidence of elimination of the cystic lesion.
A surgical technique was described in case series format by Wong54 in 1991. After flap reflection, a surgical fenestration was used to obtain some tissue for biopsy, but the majority of bony defect was left intact. Copious drainage was accomplished and the defect irrigated with saline prior to suturing. This surgical treatment was effective in producing healing while avoiding potential complications.54 Rees55 in 1997 reviewed and highlighted the treatment of large maxillary cysts by root canal treatment and subsequent decompression. The described technique used a drain made from surgical suction tubing. This seems to be the consensus treatment sequence currently in the dental literature. Figure 12 shows the radiographic and clinical appearance of decompression tube that was left in position for 1 week and the 6-month follow-up radiograph after non-surgical root canal filling.
A 20-patient cohort study of decompression results by Enislidis et al.56 is perhaps the best evidence of the technique's effectiveness. The authors described the advantages as ease of treatment, confirmed diagnosis with biopsy, low morbidity, and low incidence of complications. The quickest evidence of successful decompression was related by Loushine et al.57 in 1991. This case report related the removal of the decompression tube after only 2 days with follow-up examinations showing progressive osseous repair at 3, 6, and 12 months. The use of decompression to treat odontogenic keratocyst (OKC) has been reported by August et al.58 A pediatric nasal airway was modified and placed in 14 OKCs for an average of 8.4 months. They were irrigated twice a day with chlorhexidine. At the time of cystectomy, 9 of 14 no longer showed histological features of OKCs. The epithelium had dedifferentiated and lost cytokeratin 10 production in 64% of the patients.
Mejia et al.59 reported, in a case series format, the use of a vacuum system within the root canal system. The technique produced a vacuum effect capable of removing copious amounts of exudate and inflammatory fluids. Perhaps, the removal of the rather high osmolarity fluid and disruption of the bony defect lining is the impetus for subsequent healing.
The combination of aspiration and irrigation as an alternative to surgical endodontic treatment was reported by Hoen et al.60 in 1990. This case series demonstrated successful outcomes using a single-visit aspiration and saline irrigation of non-healing bony lesions associated with previously endodontically treated teeth. Following profound anesthesia, mucosa disinfection and aspiration of the cyst contents was accomplished using a 16- or 18-gauge needle attached to a syringe. Several milliliters of viscous aspirate was routinely obtained. The aspirates were submitted for aerobic and anaerobic culturing, Gram-staining, and immunoglobulin quantification. The level of immunoglobulin (Ig) G was significantly elevated in each specimen. Above normal levels of IgG have been shown to be consistent with cyst fluid.61 It has also been shown there is a high level of albumin and globulin in cysts compared to "granulomas".62 No bacteria were seen or cultured from any of the aspirates. At the 1-year follow-up appointments, the patients were asymptomatic and significant bony healing was seen on radiographs. It is important to develop a clear differential diagnosis and to have timely re-evaluations of the patient's signs and symptoms to determine if further treatment is needed.60
An additional use of aspiration is to obtain a biopsy sample. August et al.58 concluded that the use of needle aspiration for biopsy is a useful technique to distinguish between malignant and benign intraosseous jaw lesions. The described technique involved the use of a 10-mL syringe containing 1 or 2 mL of air attached to 23- or 25-gauge needles. Once within the lesion, suction was applied and several quick passes were performed to obtain cellular
[Figure 11. A, Surgical window into cyst. B, Healed surgical window. C, Acrylic stint in place for decompression. D, Biopsy from window consistent with radicular cyst. E, Palatal radiographs showing loss of bone on left and bone fill after 3 months of decompression.]
[Figure 12. A, A 20-mm piece of nasogastric tubing in cyst for decompression. B, Tubing used next to ruler was in place for 1 week. C, Six-month follow-up after non-surgical root canal filling.]
material. The specimens were then placed on glass slides for smear preparation. The authors suggested that aspiration may be the diagnostic tool of choice in a hospital setting due to its simplicity, suitability as an outpatient procedure, rapidity of interpretation, and minimal morbidity.63 The accuracy of fine-needle aspiration biopsy of head and neck tumors has been reviewed in 218 patients.64 The technique was determined to be a useful modality for the diagnosis of head and neck tumors. The use of such a technique requires coordination with a pathologist familiar with needle biopsy specimens.
Figure 11. A, Surgical window into cyst. B, Healed surgical window. C, Acrylic stint in place for decompression. D, Biopsy from window consistent with radicular cyst. E, Palatal radiographs showing loss of bone on left and bone fill after 3 months of decompression. Courtesy Dr. Craig Baumgartner.0
Figure 12. A, A 20-mm piece of nasogastric tubing in cyst for decompression. B, Tubing used next to ruler was in place for 1 week. C, Six-month follow-up after non-surgical root canal filling. Courtesy Dr. Craig Baumgartner.0
The American Association of Endodontics' Glossary of Endodontic Terms offers the following definition: "A flare-up is an acute exacerbation of an asymptomatic pulp/or periapical pathosis after the initiation or continuation of root canal treatment."1 Treating similar teeth in patients with comparable medical and dental histories is no assurance of a common outcome. While one patient remains asymptomatic, another may have a flare-up. The contrasting clinical outcomes may seem to occur in a random manner or lead to erroneous conclusions about the cause-effect relationship of endodontic procedures to the flare-up. The development of moderate to severe inter-appointment pain, with or without swelling, is an infrequent but challenging problem. The severe pain and swelling associated with flare-ups represent the clinical manifestation of complex pathologic changes occurring at a cellular level. There is increasing evidence pointing to multiple complex factors involved in producing a flare-up. These factors include mechanical, microbial, chemical, immunological, gender, and psychological components. The regulation of periapical inflammation is highly complex and is another factor in patients' response to endodontic procedures.22,65-70
The reported incidence of inter-appointment emergencies ranges from 1.4 to 19%.66,69-74 While one study found pain and swelling occurred in as many as 20 to 40% of patients,75 the incidence of severe pain conditions is most frequently reported at less than 5%.65,70,76,77 Variations in the findings are the result of a number of factors. For example, differences exist in the definition of a flare-up. Some investigators have used swelling as the sole criteria for a flare-up after treating asymptomatic teeth with pulp necrosis and chronic apical periodontitis.71 Others have used broader definitions of a flare-up which do not require swelling.65,66,69,70 Some investigators used a retrospective approach in their research,69,73 while others used prospective methodologies.65,66,70 There have also been variations in sample size, treatment procedures, number of visits, endodontic medications, and other variables that are neither well-defined nor controlled.
AGE OF PATIENT
There is a lack of agreement concerning the influence of age on the incidence of flare-ups. Prospective studies assessing the incidence of flare-ups in endodontic patients found no correlation between flare-ups and the age of the patient.70 However, a large retrospective study reached a different conclusion. Records of 2,000 patients were examined, and it was determined that when age was evaluated (20-39, 40-59, over age 60), a significant difference was found among age groups (p = 0.0001). Patients in the 40- to 59-year range had the most flare-ups and those under the age of 20 had the least.69 Conflicting conclusions regarding the influence of age on the incidence of flare-ups can be attributed to variations in research methodologies, definitions, sample size, and clinical procedures.
GENDER AND FLARE-UPS
An extensive review concerning gender variation in clinical pain experience reported that women are more likely than men to experience a variety of recurrent pain.78 In most studies, women have reported more severe levels of pain, more frequent pain, and pain of longer duration than men.79 While a number of studies found a significantly higher percentage of females than males had postoperative pain,69,70,75,80 others have not found gender to be a significant factor.66,81 It should be noted that there are considerable variations between different types of clinical pain.82 Experimental pain, produced under controlled conditions by brief, noxious stimuli, differs from procedural and post-surgical pain. These differences make the study of pain more complex.79
It seems reasonable to assume that host resistance, for example, medical status of the patient, is an important variable in the occurrence of flare-ups. Unfortunately, there is little conclusive evidence concerning the relationship between host resistance and flare-ups. One study found a highly significant association between flare-ups and the presence of allergies to various substances (sulfa medication, pollen, dust, and foodstuffs) and the frequency of inter-appointment pain.69 It was suggested that this could have been due to an immediate hypersensitivity reaction occurring in the periapical tissues in response to the egress of antigens from the root canal. Although the components of the immediate hypersensitivity reactions (IgE, mast cells, and mast cell-derived mediators) have been found in periapical lesions, evidence is lacking as to whether these reactions actually occur in the periapical tissues and are responsible for inter-appointment pain.68 An association between allergy and inter-appointment pain has not been confirmed.70
Examining the incidence of flare-ups by tooth groups or between arches (maxillary versus mandibular) has usually shown no significant difference.66,70,80 An exception was a retrospective study of 2,000 patients who had received root canal treatment for necrotic pulps. Mandibular teeth were associated with more inter-appointment emergencies than their maxillary counterparts (p = 0.0247). Mandibular premolars followed by mandibular incisors were the most problematic teeth after cleaning and shaping of their root canals.69
A high incidence of fear and anxiety among patients concerning an endodontic procedure may have a marked effect on the patient's intra-operative and postoperative response to treatment. It has been shown that if a patient expects pain to occur during dental treatment, this increases the likelihood of pain being perceived.83 An anxious patient with a previous memory of dental pain is more likely to expect pain during subsequent treatment. The slightest pressure on the tooth can be interpreted as pain and initiate a pain reaction. Anxiety may also lead to increased sympathetic activity and muscle tension that may cause more pain.79 Patients' descriptions of their pain can be influenced by their level of anxiety and complicate the diagnostic process.79
A multivariate analysis of the effectiveness of local anesthesia in pediatric patients indicated anxiety as the strongest predictor of poor pain control.84 A large retrospective study noted an association between apprehension and postoperative pain.72 The dental procedures causing the highest levels of stress and anxiety are oral surgery and endodontics. There is a high probability that endodontic patients are anxious and expect to experience pain during treatment79 (see Chapter 22).
PREOPERATIVE HISTORY OF THE TOOTH
Most studies have found a highly significant relationship between the presence of preoperative pain and/or swelling and the incidence of inter-appointment emergencies.65,66,69,70 Studies have also shown a statistically significant higher incidence of flare-ups in patients taking analgesics and anti-inflammatory drugs.66,70 It is reasonable to assume that patients taking those drugs were having preoperative pain.
There is no universal agreement concerning the influence of pulp status and/or the presence of a periapical lesion on the incidence of inter-appointment emergencies. A prospective study found that teeth with vital pulps resulted in relatively few flare-ups, with an overall percentage of 1.3%.66,70 In contrast, pulp necrosis correlated to an incidence of flare-ups of 6.5%, a statistically significant increase when compared to vital pulps. A low number of flare-ups following root canal treatment of teeth with vital pulps is consistent with findings in other studies.73,74
The periapical diagnosis of acute apical abscess was also related to significantly greater incidence of flare-ups when compared with less symptomatic or less severe apical pathosis.70 As one might expect, the presence of a sinus tract did not correlate with flare-ups.69,70 Investigators found the presence of a periapical radiolucency was significantly related to inter-appointment flare-ups.65,66,71,74 These findings are in contrast to others who found a higher incidence of inter-appointment emergencies in teeth without apical radiolucencies.69,81,85,86 The differences in findings may be attributable to variations in research methodologies, sample size, clinical procedures, patients studied, and definition of flare-ups.
NUMBER OF TREATMENT VISITS
A number of studies have determined that less postoperative pain results from a single-visit approach to endodontics than a multi-visit course of treatment.66,87,88 Other investigators concluded that little or no difference occurred between single- and multiple-visit endodontic therapy.70,89-91 Significant variables exist among the studies that may account for the different conclusions.
CAUSES OF INTER-APPOINTMENT PAIN
Inter-appointment pain is caused by mechanical, chemical, and/or microbial injury to the pulp or periapical tissues that are induced or exacerbated during endodontic treatment.68,69,92 The cause of injury may vary, but the intensity of the inflammatory response is usually directly proportional to the intensity of tissue injury.93 Mechanical and chemical injuries are often associated with iatric factors, but microbial-induced injury is a major cause of inter-appointment pain.68,92,94 Microbial factors may be combined with iatric factors to cause inter-appointment pain. Even when endodontic procedures are performed within accepted guidelines, microbes can cause a flare-up.68 Development of pain precipitated by microbial factors can depend on the interrelationship of several factors that are discussed in Chapter 7.
TREATMENT OF TEETH WITH VITAL AND NON-VITAL PULPS
Treatment of teeth with vital (pulpitis) and non-vital (necrotic) pulps represent pathological conditions that require different approaches to therapy.95 It has been suggested that if the pulp is free of infection, the endodontic treatment should be completed in one visit if other factors permit. Temporization after removal of a vital pulp entails the risk of micro-leakage and contamination of the canal.95 A high level of asepsis during pulpectomy and subsequent obturation is an essential part of treatment. Although asepsis is also an important part of treating a tooth with a non-vital pulp, the principle concern is the presence of bacteria in the root canal system. Infected canals may contain 10 to 100 million bacterial cells.95-97 Clinicians are faced with the challenge of disinfecting the canal system through instrumentation, irrigation, and medication without pushing debris into the periapical tissues.
Re-treatment cases, in most studies, have had a significantly higher incidence of flare-ups than conventional cases69,70 (Figure 13). One study found an extremely high incidence of flare-ups (13.6%) in re-treatment teeth with apical periodontitis.77 It can be hypothesized that re-treatment cases are often technically difficult to treat, and there is a tendency to push remnants of gutta-percha, solvents, and other debris into the periapical tissues. Microbes may also be pushed apically during the re-treatment process. Extrusion of infected debris or solvents into the periapical tissues during preparation of the canals is allegedly one of the principal causes of postoperative pain.92,96,98 Re-treatment cases are usually associated with a persistent or secondary root canal infection by therapy-resistant microorganisms that may be more difficult to eradicate when compared to primary infections.67,98,99 In contrast, others have found no statistical significance in the relation of re-treatment to flare-ups.70
Figure 13. Swelling associated with flare-up following revision of previous endodontic treatment. Courtesy Dr. Paul Rosenberg.0
The apical portion of the root canal system has been considered the most critical anatomic area with regard to the need for cleaning, disinfection, and sealing.67,100
Overextension should be avoided as it can result in postoperative pain.67 Teeth with non-vital (necrotic) pulps associated with a periapical lesion, as well as root-filled teeth with recalcitrant lesions, represents a different biological challenge.67 In these cases, microorganisms may be at or near the apical foramen and accessory foramina that are in close contact with the periapical tissues.67,101-104 Thus, correct working length in infected teeth is essential.67,105 Inaccurate working length or inadvertent over- or under-instrumentation can result in negative outcomes for the patient. Over-instrumentation may force infected debris into the periapical tissues eliciting a severe inflammatory response and pain. Under-instrumentation will leave microorganisms in close proximity to the apical foramina where they or their virulence factors can gain access to the periapical tissues67,106 (see Chapter 7). Incomplete instrumentation can disrupt the balance within the microbial flora and allow previously inhibited species to overgrow.107 If those strains of bacteria are virulent and/or reach sufficient numbers, damage to the periapical tissues may be intensified and result in an exacerbation of the lesion. Furthermore, environmental changes, induced by incomplete debridement, have the potential to activate virulence genes.68
[Figure 13. Swelling associated with flare-up following revision of previous endodontic treatment.]
A change in host resistance or microbial virulence may allow a previously asymptomatic situation to become symptomatic.68 Clinical studies, however, have not linked incomplete canal preparation to flare-ups.70,91,108,109
Overfilling can cause postoperative pain particularly when a substantial amount of filling material extrudes through the apical foramen. Gross overfilling involves the introduction of excess sealer (and its cytotoxic components) into the periapical tissues causing tissue damage and inflammation.67 A recent study found that overfilling was significantly associated with increased rate of pain and percussion sensitivity in 1-week follow-up examinations in comparison with teeth not overfilled.110 Scheduling of the obturation visit in relation to instrumentation may be another important factor. Obturation in the presence of acute apical periodontitis can be considered to be a predictor of postoperative pain. In order to avoid increased postoperative pain, patients who present for obturation but have significant acute apical periodontitis should have the procedure postponed until the tooth is more comfortable. Relief of pain can be achieved by treatment directed at reducing tissue levels of factors that stimulate peripheral terminals of nociceptors or by reducing mechanical stimulation of sensitized nociceptors (e.g., occlusal adjustment). Thus by deferring obturation of a tooth with pericementitis, further stimulation of sensitized nociceptors is avoided.111,112
Strategies to Prevent Flare-ups
The causes of endodontic flare-ups are varied, and an effective preventive strategy must be multifaceted (see Chapter 23). There is a well-documented relationship between anxiety, pain threshold, and postoperative pain.72,79,83,84
In preoperative patients, high levels of stress, anxiety, or pessimism predict poor outcomes in measures that range from speed of wound healing to duration of hospital stay. Over 200 studies indicate that preemptive behavioral intervention, to decrease anxiety before and after surgery, reduces postoperative pain intensity and intake of analgesics improves treatment compliance, cardiovascular and respiratory indices, and accelerates recovery.113 In a landmark study, it was found that preoperative discussion of likely post-surgical treatments and associated discomfort halved the requirement for postoperative morphine and reduced time to discharge. Patients in that study also received instructions in a relaxation technique.114
Providing information about the procedure is an important step in preparing patients for endodontic treatment. Information about profound dental anesthesia and preventive pain strategies is an important anxiety reduction technique. Perhaps most importantly, the dentist should assure the patient that pain prevention is a primary concern. It was determined that patients given a running commentary concerning procedures and associated sensations rated themselves as less anxious and experiencing less pain than a normal control group.115 Information about sensations experienced during treatment as well as a description of procedures appears to have a significant impact in reducing patient anxiety.115 Patients should not be allowed to watch surgical procedures in a mirror.
Occlusal reduction is a valuable pain preventive strategy in appropriate cases.116,117 Some earlier studies raised questions concerning the value of prophylactic occlusal reduction as a pain preventive measure.118,119 The results of a more recent study indicated that occlusal reduction should result in less post-treatment pain in patients whose teeth exhibit pulp vitality, preoperative pain, percussion pain, or absence of a periapical radiolucency.120 While the presence of all four conditions is the strongest predictor, the presence of any one or more of the conditions is enough to indicate the need for occlusal reduction (Figure 14).
Occlusal reduction when performed in appropriate cases is a highly predictable, simple strategy for the prevention of postoperative pain and relief of pain due to acute apical periodontitis. There is a biologic rationale for the relief of pain provided by the occlusal reduction. Mechanical allodynia (i.e., sensitivity to percussion or biting forces) is due to tissue levels of mediators that stimulate peripheral terminals of nociceptors. Occlusal adjustment, in either arch, reduces mechanical stimulation of sensitized nociceptors.120,121
[Figure 14. Effect of occlusal reduction on pain.]
Figure 14. Effect of occlusal reduction on pain. Courtesy Dr. Paul Rosenberg.0
Pharmacologic Strategies for Flare-ups
Antibiotics are frequently prescribed to endodontic patients without a rational biologic basis.122,123 An evidence-based review determined that the use of systemic antibiotics for the prevention of post-treatment endodontic pain should be discouraged.124 Antibiotic treatment is generally not recommended for healthy patients with localized endodontic infections. Systemic antibiotics should be considered if there is a spreading infection that indicates failure of local host responses to control bacterial irritants or the patient has a medical condition that compromises defense mechanisms and could expose the patient to higher systemic risks.124
NSAIDS AND ACETOMINOPHEN
Nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to be effective for managing pulpal and periapical pain.111,125 However, due to the renal effects of NSAIDs as well as interactions with many anti-hypertensive drugs, acetaminophen should be considered for post-treatment pain in patients with known sensitivity to NSAIDs or aspirin. Acetaminophen should also be considered for those with the following disorders: ulcers, ulcerative colitis, asthma, or hypertension. Pretreatment with NSAIDs or acetaminophen has also been shown to be effective for reducing postoperative pain.68,121 Pretreatment with NSAIDs for irreversible pulpitis should have the effect of reducing pulpal levels of the inflammatory mediator prostaglandin E2 (PGE2).68,71
It is advisable to have endodontic patients take their analgesics "by the clock" rather than on an "as needed basis".121 Patients should take an NSAID or acetaminophen just prior to, or immediately after, treatment. If they wait to take medication until after the onset of pain, there is usually a delay of up to 1 hour before they experience pain relief. It has been suggested that instructing patients to take their analgesics by the clock for the first few days provides a more consistent blood level of the drug and may contribute to more consistent pain relief.121 The combination of ibuprofen and acetaminophen taken together has been shown to produce additive analgesia when treating dental pain.111,121,126-128 Opioids may be added when indicated (see Chapter 22).
LONG-ACTING LOCAL ANESTHETICS
Long-acting local anesthetics (e.g., bupivicaine) can provide an increased period of post-treatment analgesia beyond the usual duration of anesthesia.129,130 By blocking the activation of unmyelinated C-fiber nociceptors, the anesthetic decreases the potential for central sensitization.121 Long-acting local anesthetics can provide a period of analgesia for up to 8 to 10 hours following block injections and may reduce pain even 48 hours later.121,129 Use of long-acting local anesthetics is a valuable biologically based strategy that provides analgesia during the immediate postoperative period.121 Endodontic treatment by itself can be expected to provide significant pain relief (see Chapter 22).
Treatment of Endodontic Flare-ups
Selecting the appropriate treatment after an endodontic flare-up is dependent upon understanding its biological cause. For example, the clinician must determine if a flare-up is primarily iatrogenic in nature, as in the case of inaccurate measurement control, or microbiologically based, as in an infected necrotic situation.
DIAGNOSIS AND DEFINITIVE TREATMENT
History of the onset of pain is important in determining if the pain is spontaneous or provoked by a specific stimulus. For example, if a tooth had a history of acute apical periodontitis and its occlusion had not been reduced, that could be identified as a probable cause of postoperative pain, appropriate treatment should be provided.120 In contrast, a complaint of swelling, pressure, and throbbing in the interproximal area might suggest a periodontal component of the problem that should be explored. If inaccurate measurement control was used or proper measurement not maintained, the clinician must determine if the canal was under- or over-instrumented. Working length should be reconfirmed, patency to the apical foramen obtained, and thorough debridement with copious irrigation completed. Remaining tissue, microorganisms and their products, and extrusion beyond the apex are major factors responsible for post-treatment symptoms.94 Pain relief in the over-instrumented case is often dependent on an analgesic strategy. The under-instrumented case may require further instrumentation to the correct measurement, as well as the use of analgesics.
Drainage Through the Coronal Access Opening
A cardinal principle in the treatment of suppurative lesions is the establishment of drainage (Figure 15). Drainage, upon access to the pulp cavity, releases purulent or hemorrhagic exudate from the periapical tissues and may reduce periapical pressure in symptomatic teeth with radiolucent areas.131 Obtaining drainage through the coronal access opening has been advocated as a means of reducing pain following treatment in some necrotic cases.132 Interestingly, a retrospective study examined the effect of drainage upon access on postoperative endodontic pain and swelling in symptomatic necrotic teeth. It was determined that drainage upon access (average of 1.85 minutes) did not significantly (p > 0.05) reduce pain, percussion pain, swelling, or the number of analgesic medications taken, for symptomatic teeth with periapical radiolucencies.131 It is possible that pre-existent apical periodontitis was a factor in the cases studied and was not addressed by the establishment of drainage. Occlusal relief may also have been required to address that symptom.
Figure 15. Purulent drainage upon access to the pulp cavity. Courtesy Dr. Craig Baumgartner.0
The goal of emergency treatment for an endodontic flare-up with a swelling is to achieve drainage.132 The object of drainage is to evacuate exudate from the periapical spaces (Figure 16). Drainage is best achieved through a combination of canal instrumentation and I&D. Even in cases where an I&D is to be implemented, the canal should be accessed, instrumented, irrigated, medicated, and closed as soon as active drainage stops. Systemic antibiotics can be expected to be more effective once the canal has been debrided, medicated, and closed.133,134
[Figure 15. Purulent drainage upon access to the pulp cavity.]
[Figure 16. Purulent drainage following incision of a fluctuant abscess involving a mandibular anterior tooth]
Figure 16. Purulent drainage following incision of a fluctuant abscess involving a mandibular anterior tooth (Courtesy Dr. John Ingle).0
After considering the biological cause of the flare-up, the clinician may decide to re-enter the symptomatic tooth. Profound local anesthesia is necessary before re-entry. Enhanced magnification and illumination are helpful in reassessing the chamber morphology for canals that might have been missed at the prior visit.135-137 Working lengths should be reconfirmed, patency to the apical foramen obtained, and a thorough debridement with copious irrigation performed.68 Remaining necrotic tissue, microorganisms, and toxic products are important factors responsible for flare-ups.94 Enlarging the apical constriction has been advocated to encourage drainage.138 Others have found that instrumenting through the apical foramen does not ensure drainage of periapical exudation.68,138
In some cases, however, drainage may be established through the root canal system upon instrumentation. Drainage allows for exudate to be released from the periapical tissues thus reducing localized tissue pressure and pain.131 Leaving a tooth open after drainage is complete will result in re-infection from oral microbes.73,94
As discussed earlier in the chapter, trephination is the surgical perforation of the alveolar cortical plate over the root end, to release accumulated tissue exudate that is causing pain.1 It may be indicated for patients with a flare-up when there is exquisite pain, no swelling, and drainage cannot be accomplished through the tooth.
The clinician must be sensitive to the potential of nonodontogenic pain being confused with a flare-up. For example, the words "tingling" or "burning" when used as descriptors of pain are signals of non-odontogenic pain rather than a flare-up. Similarly, although rare, it is possible for a tooth, other than one undergoing endodontic treatment, to suddenly become painful and confuse the diagnosis. A previously undetected periodontal component may also pose a diagnostic problem.
Bacterial Factors Associated with Flare-ups
Bacteria are capable of acting as irritants and induce non-specific innate or specific adaptive immune responses in the host.139,140 The host's responses to a bacterial challenge depend largely on virulence factors and the numbers of pathogens, as well as the host's innate and adaptive immunity. If the host's defense mechanisms are capable of overcoming a bacterial challenge, bacteria will be eliminated. In contrast, if the bacterial challenge overwhelms the host's defense mechanisms, an inflammatory response, as a result of innate or adaptive immunity, will occur. Microorganisms have been suggested as the major causative agents of flare-ups.68,92,94 Unlike elsewhere in the body, bacteria in the root canal system are well protected from the host's immune defenses and antimicrobial agents. The microbes and virulence factors associated with pulpal and periapical infections are discussed in Chapter 7 "Microbiology of Endodontic Disease."
The bacterial community in an infected root canal is closely related to the nutrient supply, bacteria