Flare-up is described as the occurrence of pain, swelling or the combination of these during the course of root canal therapy, which results in unscheduled visits by patient. Pain may occur soon after initiating endodontic treatment for an asymptomatic tooth or shortly after the initial emergency treatment or during the course of treatment.
Acute periapical inflammation is the most common cause of mid treatment pain and swelling. Mid treatment emergencies are usually due to irritants left within root canal system or iatrogenic factors such as operator’s fault and host factors. The occurrence of mild pain is relatively common following root canal therapy; it should be expected and anticipated by patients, whereas severe pain and swelling associated with flare-up is a rare occurrence (Fig. 21.1).
ETIOLOGY
The occurrence of flare-ups during the endodontic therapy is a polyetiologic phenomenon
Causative Factors
Comprise mechanical, chemical and/or microbial injury to the pulp or periapical tissues resulting in the release of myriad of inflammatory mediators. Pain then occurs due to the direct stimulation of the nerve fibers by these mediators or edema resulting in an increase in the hydrostatic pressure with consequent compression of nerve endings.
Mechanical Injury
Mechanical injury may occur in form of:
• Overinstrumentation—most common cause of mid treatment flare-ups (Fig. 21.2).
• Inadequate debridement or incomplete removal of pulp tissue can result in pain (Fig. 21.3)
• Periapical extrusion of debris can lead to periapical inflammation and flare-ups (Fig. 21.4).
Chemical Injury
Chemical injury to the periapical tissues may be caused by:
• Irrigants
• Intracanal medicaments
• Overextended filling materials (Fig. 21.5).
Microbial Induced Injury
Microbial induced injury is considered as the most significant factor in the flare-up pathogenesis. Microbial factors may be combined with iatrogenic factors to cause inter-appointment pain.
The cause of injury may vary, but the intensity of inflammatory response is usually directly proportional to the intensity of tissue injury.
Contributing Factors for Flare-ups
Age of the Patient
Patients in the 40–59 years range have the most flare-ups and those under the age of 20 have the least.
Gender
A higher percentage of females than males have been reported with the postoperative pain in a number of studies.
Systemic Conditions
Medical status of the patient is an important variable in the occurrence of flare-ups. Patients with allergies to various substances (sulfa medication, pollen, dust and food stuffs) have a higher frequency of inter-appointment pain.
Tooth Type
Mandibular teeth are more associated with inter-appointment emergencies than maxillary teeth.
Anxiety
Anxious patients are likely to have more pain during the course of the treatment.
Presence of Preoperative Pain and/or Swelling
Patients taking analgesics and anti-inflammatory drugs so as to prevent preoperative pain have shown higher incidence of flare-ups.
Pulpal/Periapical Status (Fig. 21.6)
Teeth with vital pulps show lower incidence of flare-ups as compared to teeth with necrotic pulp. Periradicular status of the tooth can also predict the flare-up rates, with incidence of 3.4 percent in chronic apical periodontitis, 4.8 percent in acute apical periodontitis and 13.1 percent in case of acute apical abscess. Presence of a sinus tract is not associated with the development of flare-up.
Number of Visits
If proper case selection is not done, more flare-ups occur after multi-visit approach as compared to single visit approach to endodontics.
Retreatment Cases
Chances of flare-ups are 10 fold higher in the retreatment cases because of extrusion of infected debris or solvents into periapical tissues (Fig. 21.7).
MECHANISMS FOR FLARE-UPS
Seven microbiological and immunological factors are seen to be responsible for flare-ups (Seltzer et al. 2004):
• Alteration of local adaptation syndrome.
• Changes in periapical tissue pressure.
• Microbial factors.
• Chemical mediators.
• Changes in cyclic nucleotides.
• Immunological responses. Psychological factors
Alteration of Local Adaptation Syndrome
Selye has shown that when a new irritant is introduced in a chronically inflamed tissue, a violent reaction may occur because of disturbance in local tissue adaptation to applied irritants. For example in case of chronic pulpal diseases, the inflammatory lesion is adapted to irritants but during root canal therapy, a new irritant in form of medicament get introduced in the lesion leading to flare-up.
Changes in Periapical Tissue Pressure
Studies have shown that in teeth with increased periapical pressure, excessive exudate creates pain by causing pressure on nerve endings. Root canals of such teeth when kept open, exudate comes out but in teeth with less periapical pressure, microorganisms and other irritants gets aspirated into periapical area leading to pain.
Microbial Factors
Gram-negative anaerobes (most commonly seen Prevotella and Porphyromonas species) produce a variety of enzymes and release endotoxins which are neurotoxic. These organisms also activate the Hageman factor to release bradykinin, a potent pain mediator. Teichoic acid, present in the cell wall and plasma membranes of many gram- positive bacteria is potent immunogen, producing humoral antibodies IgM, IgG, IgA and releases various chemical, mediators that cause pain.
Microbial Mechanisms in the Induction of Flare-ups
• Apical extrusion of infected debris: Extrusion of micro- organisms and their products during the endodontic procedures may disrupt the balance between microbial aggression and host defence leading to acute periapical inflammation (Figs 21.8A and B). 
• Changes in the endodontic microflora and/or in environmental conditions (Fig. 21.9): Incomplete chemo mechanical preparation disrupts the balance between the various microbial communities within the root canal system that may favor the overgrowth of certain species. These bacteria when present in sufficient number and express virulence genes, can lead to the development of flare-up.
• Secondary intraradicular infection (Figs 21.10A and B): Penetration of the new microbial species, more microbial cells and substrate from saliva into the root canal system during treatment may lead to a secondary infection and can be a cause of flare-up.
• Increase of oxidation-reduction potential (Fig. 21.11): Alteration of oxidation-reduction potential in the root canal during treatment may favor the overgrowth of facultative bacteria that resisted chemomechanical procedures and lead to flare-ups.
Effect of Chemical Mediators
Chemical mediators can be in form of cell mediators, plasma mediators and in form of neutrophils products (Fig. 21.12). Cell mediators include histamine, serotonin, prostaglandins, plateletactivating factor and lysosomal components which may lead to pain. The plasma mediators are present in circulation in inactive precursor form and get activated on coming in contact with irritants. For example Hageman factor when gets activated after in contact with irritants, produce multiple effects like production of bradykinin and activation of clotting cascade which may cause vascular leakage.
Changes in Cyclic Nucleotides
Bourne et al have shown that character and intensity of inflammatory and immune response is regulated by hormones and the mediators. For example increased levels of cAMP inhibits mast cell degranulation which helps in reducing pain where as increase in cGMP levels stimulate mast cell degranulation which results in increase in pain (Fig. 21.13). Studies have shown that during flare-up, there is increased level of cGMP over cAMP concentrations.
Immunological Response
In chronic pulpitis and periapical disease, presence of macrophages and lymphocytes indicates both cell mediated and humoral response. Despite of their protective effect, the immunologic response also contributes to destructive phase of reaction which can occur, causing perpetuation and aggravation of inflammatory process.
Psychological Factor
Anxiety, apprehension, fear and previous history of dental experience appears to play an important role in mid treatment flare-ups.
CLINICAL CONDITIONS RELATED TO FLARE-UP
Flare-ups in endodontics may be grouped as:
• Interappointment flare-ups.
• Postobturation flare-ups.
Inter-appointment Flare-ups
These conditions are encountered during the course of the endodontic treatment.
Apical Periodontitis Secondary to Treatment
An asymptomatic tooth before the initiation of endodontic treatment becomes sensitive to percussion during the course of treatment. In this condition, pain may become severe causing a throbbing or gnawing pain. The cause of this pain may be:
• Overinstrumentation
• Overmedication
• Forcing debris into periapical tissues.
Confirmatory test: Apply the rubber clamp and use a sterile paper point. Access and mark the working length. Then, place the paper point in the canal. If over instrumentation has happened by fault, then the paper point will go beyond the working length without obstruction. On withdrawal, tip of the point will show a reddish or brownish color indicating inflamed tissue in the periapical region and absence of stop in apical preparation (Fig. 21.14). 
Management: An intracanal corticosteroid-antibiotic medi- cation is given to the patient for symptomatic relief. The medication is carried on the paper point and applied with a pumping action so as to reach the inflammed periapical tissues. Routine endodontic therapy may be continued after 2 to 5 days after readjusting the working length.
Incomplete Removal of the Pulp Tissue
Whenever a pulpotomy or partial pulpectomy has been done, the patient may experience pain due to incomplete removal of inflammed pulp tissue (Fig. 21.15). In this condition, sensitivity to hot and cold or pain on percussion is usually seen. 
Confirmatory test: Apply rubber dam, place a sterile paper point, ofcourse short of working length. When paper point is removed, it will display brownish discoloration indicative of inflamed seeping tissue.
Management: The working length is re-established and the remaining pulp tissue is removed
Recrudescence of Chronic Apical Periodontitis (Phoenix Abscess)
It is a condition that occurs in teeth with necrotic pulps and apical lesions that are asymptomatic. There is no exacerbation of previously asymptomatic periradicular lesion. The reason for this phenomenon is thought, to be due to the alteration of the internal environment of root canal space during instrumentation which activates the bacterial flora. Mobility, tenderness and swelling are usually the sign and symptoms found in phoenix abscess.
Management: The tooth is opened under rubber dam and allowed to drain. Irrigation with warm sterile saline or water helps to encourage the drainage. Drainage is allowed until the exudation ceases or a slight clear serum drains. The canal is then irrigated with sodium hypochlorite, dried with paper point; filled with an appropriate intracanal medicament (calcium hydroxide paste) and sealed with a dry cotton pellet and a temporary filling.
Recurrent Periapical Abscess
It is a condition where a tooth with an acute periapical abscess is relieved by emergency treatment after which the acute symptoms return. In some cases, the abscess may recur more than once, due to microorganism of high virulence or it results in resistance.
Management: The management and treatment are the same as for discussed above for phoenix abscess.
Flare-ups Related to Necrotic Pulp (Fig. 21.16)
Teeth with necrotic pulp often develop as acute apical abscess after the initial appointment. As the lesion, is confined to bone, there occurs severe pain. 
Management: The drainage is established, canal copiously irrigated, and the tooth sealed after placing an intracanal medicament of calcium hydroxide. Increasing the appointment time allows more exposure of the bacteria to irrigants like hydrogen peroxide and sodium hypochlorite, thus reducing the chances of flare-ups.
Postobturation Flare-ups
Postobturation flare-ups are relatively infrequent as compared to interappointment flare-ups. Only one-third of the endodontic patients experience some pain after obturation. A mild pain is usually present which may resolve spontaneously. Patients experiencing preoperative pain are more likely to suffer from postobturation flare-ups. Another cause of postobturation flare-ups may be over-extended root canal fillings.
Management: Mild to moderate pain may be controlled with analgesics. For cases with severe pain, retreatment is indicated. When nonsurgical retreatment is not possible, surgical intervention is required.
MANAGEMENT OF FLARE-UPS
As the etiology of flare-ups is multifactorial, many treatment options have been empirically advocated for the prevention and alleviation of symptoms during the root canal therapy
Management of flare-ups can be categorized as:
• Preventive.
• Definitive.
Preventive Management
Proper Diagnosis
Before initiating endodontic therapy, proper diagnosis of the condition should be made so as to prevent incorrect treatment that may lead to pain, swelling or both to the patient.
Long Acting Local Anesthetics
Long acting anesthetics, e.g. bupivacaine, provide increased period of analgesia for up to 8-10 hours during the immediate postoperative period.
Determination of the Proper Working Length
Inaccurate measurement of the working length may lead to under or overinstrumentation and extrusion of debris, irrigants, medicaments or filling materials beyond the apex.
Complete Debridement (Fig. 21.17)
Thorough cleaning and shaping of the root canal system may decrease the incidence of flare-ups. Maintenance of apical patency and crown-down preparation technique are two important factors in the management of flare-ups. 
Occlusal Reduction
It is a valuable pain preventive strategy in appropriate cases. The relief of pain provided by occlusal reduction is due to the reduction of mechanical stimulation of sensitized nociceptors.
Placement of Intracanal Medicament in Multi-visit Root Canal Treatment (Figs 21.18A to C)
Calcium hydroxide has been recommended as an intracanal medicament for the prevention or the treatment of flare-up (Fig. 21.19). It serves the following purposes:
• Antimicrobial action: Calcium hydroxide hydroxylates the lipid moiety of bacterial lipopolysaccharide, rendering it incapable of producing biologic effects and complement activation. It absorbs carbon dioxide thus nutritionally depriving the capnophilic bacteria in the root canal system. The antimicrobial effect of calcium hydroxide remains in the canal for one week.
• It obliterates the root canal space which minimizes the ingress of tissue exudates, a potential source of nourishment of remaining bacteria.
• Extrusion of calcium hydroxide periapically reduces inflammatory reaction by reducing substrate adherence capacity of macrophages.
• Calcium hydroxide has soft tissue dissolving property because of its high pH. Its denaturing effect on the necrotic tissue, allows sodium hypochlorite to dissolve remaining tissue more easily. 
Chlorhexidine gluconate and iodine potassium iodide are other primary medicaments that can be considered. The use of phenolic medicaments that have an immunologic potential should be avoided to prevent the occurrence of flare-ups.
Medications
• Systemic antibiotics: These are not indicated in the prevention of flare-ups for healthy patients with localized infections. Antibiotics should be recommended only in cases of medically compromised patients at high risk levels and in cases of spreading infection that indicates failure of local host responses to control bacterial irritants. The commonly prescribed antibiotics include penicillin, erythromycin or cephalosporin. Metronidazole, tinidazole, ornidazole and clindamycin are also used because of their efficacy against anaerobic bacteria.
• Analgesics: Nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen are the most commonly used drugs to reduce pain. Treatment with an NSAID before a procedure has shown to reduce postoperative pain. Most commonly used drugs include ibuprofen, diclofenac sodium and ketorolac.
Closed Dressing
Leaving a tooth open for drainage is contraindicated as it can cause contaminations from the oral cavity and lead to flare- ups. Drainage should be allowed under the rubber dam, and the tooth closed immediately after the treatment to prevent secondary infections.
Behavioral Management
Providing information about the procedure in an important step in reducing patient anxiety. 
Definitive Treatment
Drainage through the Coronal Access Opening
The first step in relieving the pain is to establish drainage through the root canal, when it has not been obturated or poorly obturated. Sometimes apical trephination may be needed to establish drainage. In patients with periradicular abscess but no drainage through the canal, penetration of the apical foramen with small files (up to no. 25) may establish drainage that helps in reducing the periapical pressure and thus alleviating the symptoms (Fig. 21.20).
Proper Instrumentation
Under profound local anesthesia, working length should be re-established, apical patency obtained and thorough chemomechanical preparation is done. This removes the necrotic tissue, microorganisms and toxic products responsible for causing pain.
Trephination
When drainage through the canal is not possible due to restorative issues, or in case of certain conditions like failing treatments or necessary correction of procedural accidents, surgical trephination can be used as a palliative measure. It involves the surgical perforation of the alveolar cortical plate over the root-end to release the accumulated exudates to release pain. However, it is not the first line of treatment because of the additional trauma, invasiveness and questionable beneficial result.
Intracanal Medicaments
Use of corticosteroid-antibiotic combination as an intracanal medicament has been recommended to reduce pain, especially in cases of over instrumentation.
Analgesics and Antibiotics
For most of the patients, NSAIDs are sufficient to control pain. However, if the pain cannot be controlled with NSAIDs, opoid analgesics can be used to supplement with NSAIDs. Commonly used opoids include morphine, codeine, meperidine, tramadol and propoxyphene. Antibiotics are prescribed for the treatment of flare-ups only when indicated as discussed before. Use of antihistaminics for treatment of flare-ups has also been suggested.
CONCLUSION
The development of flare-up after the endodontic treatment appointment is an extremely undesirable and a challenging problem. Despite judicious and careful treatment procedures, severe pain, swelling or both may occur. The clinician should employ proper measures and follow appropriate guidelines to prevent these undesirable occurrences. Psychological preparation of the patient, thorough cleaning and shaping of the root canal system, use of long acting anesthetic solutions and analgesics may decrease the incidence of flare-ups. Prompt and effective treatment of flare-ups is essential to alleviate patient’s symptoms and prevent its recurrence.
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