Clinical and pharmacological management of endodontic flare-up.

Knowledge of the causes of and mechanisms behind interappointment pain in endodontics is of utmost importance for the clinician to properly prevent or manage this undesirable condition. The causative factors of interappointment pain encompass mechanical, chemical, and microbial injuries to the pulp or periradicular tissues, which are induced or exacerbated during root canal treatment. This review article underlines the various treatment modalities for relief of pain and swelling in such situations, including premedication, drainage establishment, relief of occlusion, and intracanal and systemic medication.

A flare-up is defined as the occurrence of severe pain and swelling following an endodontic treatment appointment, requiring an unscheduled visit and active treatment. Flare-up is a well known complication that disturbs both patients and dentists. Mechanical and chemical injuries are often associated with iatrogenic factors. However, microbial injury caused by microorganisms and their products is the major and most common cause of interappointment flare-ups. A flare-up of infectious origin can sometimes occur even though root canal procedures have been performed judiciously and carefully. Regardless of the type of injury, the intensity of inflammatory responses is directly proportional to the intensity of tissue injury which causes interappointment flare-ups.

Cause of Interappointment Pain

The causative factors of interappointment pain comprise mechanical, chemical, and microbial injuries to the pulp or periradicular tissues which are induced (or) exacerbated during root canal treatment.[12]

Microbial causes

There are some special circumstances in which microorganisms can cause interappointment pain as a result of imbalance in host-bacteria relationship induced by intracanal procedures.

Development of pain precipitated by infectious agents can be dependent on several factors. These factors are as follows:

Presence of pathogenic bacteria

The bacterial species can be associated with symptomatic periradicular lesions. These include Porphyromonas endodontalis, Porphyromonas gingivalis, and Prevotella species.[3-7] A recent study revealed that F. nucleatum, Prevotella species, and Porphyromonas species were frequently isolated from flare-up cases.[8] The possibility exists that the bacterial species associated with flare-ups are the same as those involved with primarily infected root canals associated with symptomatic periradicular lesion.

Presence of virulent clonal types

A disease ascribed to a given pathogenic bacterial species is caused by specific virulent clone types of that species which can significantly diverge in their virulence ability.[910] Presence of virulent clones of endodontic pathogens in the root canal may be a predisposing factor for interappointment pain, provided that conditions are created for them to exert their pathogenicity.

Microbial synergism or additism

Most of the endodontic pathogens show virulence when they are in association with other species.[1112] This is because of synergistic or additive microbial interactions, which can certainly influence virulence and play a role in symptom causation.

Number of microbial cells

The microbial load is well recognized as an important factor for a microorganism to cause disease. If the host is faced with a higher number of microbial cells than it is used to an acute exacerbation of the periradicular lesion can occur.

Environmental cues

A great deal of evidence indicates that the environment exerts an important role in inducing microbial virulence genes. Studies have demonstrated that environmental changes can influence the behavior of some putative oral (and endodontic) pathogens, including P. gingivalis, F. nucleatum, Prevotella intermedia, and oral treponemes.[413] If the root canal environmental conditions are altered by intracanal procedures and become conducive, microbial virulence can be enhanced and interappointment pain can ensue.

Host resistance

Different individuals present different patterns of resistance to infections and such differences can certainly become evident during an individual's lifetime.[12] Individuals who have reduced ability to cope with infections are more prone to develop clinical symptoms after endodontic procedures in infected root canals. Herpes viruses have the ability to diminish the host resistance to infection.[1415] There are some situations during the endodontic treatment that can facilitate microorganisms to cause interappointment pain. These include: (a) apical extrusion of debris; (b) incomplete instrumentation leading to changes in the endodontic microbiota or in environmental conditions; and (c) secondary intraradicular infections.

Apical extrusion of debris

Extrusion of infected debris to the periradicular tissues during chemomechanical preparation is one of the principal causes of postoperative pain.[1617] In asymptomatic chronic periradicular lesions associated with infected teeth, there is a balance between microbial aggression from the infecting endodontic microbiota and the host defenses at the periradicular tissues. During chemomechanical preparation, if microorganisms are extruded into the periradicular tissues, the host would face a situation in which the host will be challenged by a larger number of irritants than it was before. Consequently, there would be a transient disruption in the balance between aggression and defense in such a way that an acute inflammatory response is mounted to re-establish equilibrium. The incidence of postoperative pain in re-treatment cases with periradicular lesions has been demonstrated to be significantly high.[118]

Forcing microorganisms and their products into the periradicular tissues can generate an acute inflammatory response, the intensity of which will depend on the quantitative (number) and qualitative (virulence) nature of the extruded microorganisms.

Iatrogenic overinstrumentation promotes the enlargement of apical foramen, which may permit an increased influx of exudate and blood into the root canal.[18] This will enhance the nutrient supply to the remaining bacteria within the root canal, which can then proliferate and cause exacerbation of a chronic periradicular lesion. Virtually all instrumentation techniques promote apical extrusion of debris.[1920]

Steps to prevent the apical extrusion of debris, crown-down techniques, irrespective of whether hand- or engine-driven instruments are used, which extrudes less debris and should be selected for the instrumentation of infected root canals. Therefore, the quantitative factor is more likely to be under the control of the practitioner. The qualitative factor is more difficult to be controlled.

Incomplete chemomechanical preparation leading to the following

Changes in the endodontic microbiota

The endodontic microbiota is usually established as a mixed consortium, and alteration of part of this consortium will affect both the environmental and the remaining species. Positive and negative interactions among the members of the microbial community allow the community to be relatively stable and in balance. However, incomplete chemomechanical preparation can disrupt the balance within the microbial community by eliminating some inhibitory species and leaving behind other previously inhibited species, which can then overgrow.[21] If overgrown strains are virulent and reach sufficient numbers, damage to the periradicular tissues can be intensified. This results in exacerbation of the lesion. As a result of the increase in microbial virulence, a previously asymptomatic case may become symptomatic.

Increase of the oxidation–reduction potential

Another form of environmental change induced by endodontic intervention refers to the entrance of oxygen in the root canal. It has been suggested that this can alter the oxidation–reduction potential (Eh) in the root canal and, as a consequence, acute exacerbation can occur.[22] This theory is based on the fact that the increase in Eh would induce microbial growth pattern to change from anaerobic to aerobic. Energy yield of facultative anaerobe is more marked in the presence of oxygen than under anaerobic condition and a faster growth rate is expected with consequent overgrowth of facultative anaerobic bacteria. This theory is considered speculative and there is no scientific evidence indicating it is valid.

Secondary intraradicular infections

Secondary intraradicular infections are caused by microorganisms that were not present in the primary infection and have gained entry into the root canal system during treatment, between appointments, or even after the conclusion of the endodontic treatment,[2324] the most common being a breach of the aseptic chain during treatment.[25] If the microorganisms that gain access to the root canal are successful in surviving into and colonizing such a new environment, a secondary infection will establish itself and may be one of the causes of postoperative pain.

Non-microbial causes

Non-microbial causes are represented by chemical or physical factors that can inflict damage to the periradicular tissues, and thereby can be responsible for the development of interappointment pain. The intensity of pain will depend on several aspects, including intensity of the injury, intensity of tissue damage, and intensity of the inflammatory response. All these three phenomena are interconnected, as one is directly dependent on the other.

Mechanical irritation causing periradicular inflammation includes mainly overinstrumentation and overextended filling materials. Chemical irritation includes apical extrusion of irrigants or intracanal medications. Most irrigants and medications are cytotoxic to the host tissues. In spite of being cytotoxic, clinical trials have shown that substances used for irrigation or intracanal medication may have no influence on the occurrence of postoperative symptoms. The larger the amount of overextended material, the greater is the intensity of damage to the periradicular tissues.

Inflammatory events leading to interappointment pain

Interappointment pain is almost exclusively due to the development of acute inflammation at the periradicular tissues. Following injury to the periradicular tissues, a myriad of chemical substances are released or activated, which will mediate characteristic events of inflammation, such as vasodilatation, increase in vascular permeability, and chemotaxis of inflammatory cells. The chemical mediators of inflammation include vasoactive amines, prostaglandins, leukotrienes, cytokines, neuropeptides, lysosomal enzymes, nitric oxide, oxygen-derived free radicals, and plasma-derived factors (complement, kinin, and clotting systems.[25])

Although some mediators can cause pain through direct stimulation of sensory nerve fibers, the major inflammatory event responsible for periradicular pain appears to be the increase in vascular permeability, resulting in exudation and edema formation.[2627]

Treatment of interappointment pain

Re-instrumentation

Definitive treatment may involve re-entering the symptomatic tooth. The access cavity should then be opened. Working lengths should be reconfirmed, patency to the apical foramen obtained and a thorough debridement with copious irrigation performed. Remaining tissue, microorganisms, and toxic products or their extrusion are arguably the major elements responsible for the post-treatment symptoms. Drainage will allow for the exudative components to be released from the periradicular tissues, thus reducing localized tissue pressure.

Cortical trephination

Cortical trephination is defined as the surgical perforation of the alveolar bone in an attempt to release accumulated periradicular tissue exudates.[2829] Various studies have evaluated the effectiveness of cortical trephination to prevent and relieve post-treatment pain.[30-32] Chestner et al.[33] reported pain relief in patients with severe and recalcitrant periradicular pain when cortical trephination was performed.

Incision and drainage (I and D)

The rationale for an I and D procedure is to facilitate the evacuation of pus, microorganisms, and toxic products from the periradicular tissues. Moreover, it allows for the decompression of the associated increased periradicular tissue pressure and provides significant pain relief. In teeth where the endodontic treatment has not yet been completed, it may be advisable to re-enter the root canal system. If the abscess occurs after the obturation of the root canal system, incision of the fluctuant tissue is perhaps the only reasonable emergency treatment, provided the root canal filling is adequate. Antibiotics are usually not indicated in cases of a localized abscess, but they can be used to supplement clinical procedures in cases where there is poor drainage and if the patient has a concomitant trismus, cellulitis, fever, or lymphadenopathy. In addition, aggressive incision for drainage has been advocated for any infection with acellulitis, regardless of whether it is fluctuant or indurated.

Intracanal medicaments

Clinical studies have demonstrated that post-treatment pain is neither prevented nor relieved by medicaments such as formocresol, camphorated paramonochlorophenol, eugenol, iodine potassium iodide, Ledermix, or calcium hydroxide.[13334] However, the use of intracanal steroids, nonsteriodal anti-inflammatory drugs (NSAIDs),[35] or a corticosteroid–antibiotic compound[36] has been shown to reduce post-treatment pain. In a study conducted by Walton et al. steroids and NSAIDs, when placed within the root canal system after debridement procedures, can reduce or prevent post-treatment pain.[37]

Occlusal reduction

There appears to be minimal agreement in the dental literature as to the benefit of reducing the occlusion to prevent post-endodontic pain. Rosenburg et al.[38] demonstrated that in teeth with pain upon biting, occlusal reduction was effective in reducing postoperative pain. Sensitivity to biting and chewing is perhaps due to increased levels of inflammatory mediators that stimulate periradicular nociceptors. Occlusal reduction may therefore alleviate the continued mechanical stimulation of the sensitized nociceptors.[29]

Drugs

Antibiotics

In a review on the use of systemic antibiotics for the control of post-treatment endodontic pain, Fouad[39] concluded that their use is without justification. Current advances in our understanding of the biology of the infectious and inflammatory process, along with the known risks associated with antibiotics, such as the emergence of multiresistant bacterial strains, strongly indicate that the clinician should seriously re-evaluate their prescribing habits.[39]

Non-narcotic analgesics

Non-narcotic analgesics, NSAIDs and acetaminophen, have effectively been used to treat patients with endodontic pain. These drugs produce analgesia by their actions on both the peripherally inflamed tissues as well as on certain regions of the brain and spinal cord.[4041] The NSAIDs have been shown to be very effective for managing pulpal and periradicular pain.[4042] In patients with known sensitivity to NSAIDs or aspirin, and in those who have gastrointestinal ulcerations or hypertension due to renal effects of NSAIDs, acetaminophen should be considered for post-treatment pain.[41] Pre-treatment with NSAIDs for irreversible pulpitis should have the effect of reducing pulpal and periradicular levels of the inflammatory mediator prostaglandin E2 (PGE2). Administration of NSAIDs alone is usually sufficient for most endodontic pain for patients who can tolerate this drug class. The combination of an NSAID and acetaminophen, taken together, shows additive analgesia for treating dental pain.[40414344] If pain is not controlled by NSAIDs and acetaminophen, narcotic analgesics are required. These may be given in combination with NSAIDs for additive effects.[4445]

Conclusion

Even though it has been demonstrated that a flare-up has no significant influence on the outcome of endodontic treatment, its occurrence is extremely undesirable for both the patient and the clinician, and can undermine clinician–patient relationships. Therefore, clinicians should employ proper measures and follow appropriate guidelines in an attempt to prevent the development of interappointment flare-up.