INTRODUCTION:

An inter appointment flare-up is an unhappy event. After a root canal treatment appointment, the patient calls or returns to the dentist’s office in distress. This is upsetting to both the patient and the dentist and is disruptive to a busy practice. This is a complication which can be characterized by the development of pain, swelling or both, which commences within a few hours or days after root canal procedures and is of sufficient severity to require an unscheduled visit for treatment (1).

Various reasons have been attributed to these acute exacerbations of chronic conditions like

1) Alteration of local adaptation syndrome.

2) Microbial factors.

3) Changes in periapical tissue pressure.

4) Effects of chemical mediators

5) Immunological phenomena.

6) Numerous psychological factors.(2)

Occurrence of mild postoperative pain is relatively common even when the treatment has followed acceptable standards, and this should be expected and anticipated by patients. However, an inter-appointment flare- up has been demonstrated to be an unusual occurrence. It may spread to fascial spaces and even have such unfortunate sequelae as regional temporary paresthesia. The inter appointment flare-up is obviously a situation which both the patient and dentist would wish to avoid.

CLINICAL CONDITIONS:

Common clinical conditions associated with flare ups are

Apical peridontitis secondary to treatment:

The tooth which was symptomless before the initiation of endodontic treatment but becomes sensitive to percussion during the course of the treatment and causes for this condition most frequently are over instrumentation or over medication or forcing debris into the periapical tissues.

Incomplete removal of pulp tissues during the initial appointment:

In some instances due to lack of time factor the endodontic therapy may consist of incomplete pulpectomy after a diagnosis of acute or chronic pulpitis. This situation generally occurs when the radicular pulp is already inflamed.

Phoenix abscess:

It is a condition that occurs in teeth with necrotic pulps and apical lesions that are asymptomatic. There is a exacerbation of a previously symptomless per iradicular lesion. The reason for this phenomenon is thought to be due to the alteration of the internal environment of the root canal space during instrumentation which activates the bacterial flora.

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 micro organism of high virulence or poor host resistance.

ETIOLOGY:

Dr Seltzer discussed a number of hypothesis thought to be related to the etiology of flare ups

· Alteration of the local adaption syndrome.

· Changes in periapical tissue pressure.

· Microbial factors.

· Effects of chemical mediators.

· Changes in cyclic nucleotides.

· Immunological phenomena.

· Various psychological factors.

Among this microbial factors play an important role in endodontic flareups. Apical extrusion of contaminated debris to the periapical tissues is one of the principle cause of post operative pain (4). Studies of microbial flora of the root canal shows the presence of a considerable variety of microorganisms. According to Sundquist most strains found in the root canals with necrotic pulp are obligately anaerobic micro organism. These organisms can produce enzymes which are collagenolytic and fibrolytic. They also produce endotoxin which in turn activates Hageman factor, which leads to production of bradykinin a potent pain mediator. Chemical mediators which are activated during inflammation, such as histamine, serotonin, prostaglandin, platelet activating factor, leukotrienes etc are all capable of producing pain.

Microbial Causes:

The most important goal of root canal therapy is to minimize the number of microorganisms and pathologic debris in root canal systems to prevent or treat apical periodontitis (5). Many teeth present with infection and pain after endodontic intervension because of persisitent bacterial presence. Microorganisms play an important role in periradicular inflammation, both preoperatively and postoperatively. The mechanisms by which microorganisms cause flare-ups are many.

Failure of endodontic treatment and flare-ups can be attributed to microbial causes only if they are pathogenic, have sufficient numbers and have access to the periradicular tissues. The root canal system has an environment conducive for the survival of certain species of microorganisms. This environment is disrupted by endodontic treatment, by measures for disinfection, debridement, and intracnal medicaments. To survive in this altered environment where nutrient levels are low, bacteria must possess abilities to adapt themselves to the changed environment (6).

Bacteria residing in certain anatomical areas of the root canals such as isthmuses, apical ramifications, irregularities, deltas and dentinal tubules may be left untouched and unaffected by disinfection procedures (7, 8). These buried bacteria, after the canals are sealed, are killed or prevented from gaining access to the periradicular tissues by the root canal filling. Some bacteria can also remain viable by deriving nutrients from tissue remnants. An inadequate seal provided by the root canal filling can allow seepage of tissue fluids and provide a substrate for bacterial growth. The bacteria can also gain access to the periradicular area and cause inflammation (6). Many endodontic pathogens show an increased virulence when in association with other pathogenic species.

Mechanisms For Survival:

The bacteria have many mechanisms to withstand depletion of nutrients. In case of nitrogen depletion, bacteria that require ammonia as a source of nitrogen are able to scavenge traces of ammonia. This is enables by the Ntr gene system (9). In situations of oxygen depletion, the Arc system (Aerobic respiration regulatory) is activated which helps the bacteria shift from aerobic to anaerobic metabolism Under low glucose concentrations, bacteria can activate catabolite repressor system which enables production of enzymes from other sources (9). Under phosphate starvation, cells utilize organic phosphate compounds and scavenge trace amounts of inorganic phosphate (9).

Bacterial Populations in the Root Canal:

The microbiota in flare-ups and refractory or failed cases are different from untreated cases, the former having more of gram negative, facultatives and anaerobes and latter having more gram positive bacteria. The oxygen tension and oxidation-reduction potential are higher in coronal portion of the canals, thus housing facultatives and aero-tolerant anaerobes. Anaerobes are significantly higher in the apical third of the root canal due to the anaerobic conditions of the area (10).

Bacteroides Melaninogenicus:

In a study done by Sundqvist et al in necrotic dental pulps, a relationship was established between certain microorganisms and painful teeth. After utilizing anaerobic techniques to identify these organisms, most of the strains were found to be obligately anaerobic. In all cases of flare-up, an anaerobic gram negative rod, Bacteroides melaninogenicus was found (11). Also, Grifee et al did a study to reveal that symptomless infected teeth did not contain this organism (12). This organism has been found to produce collagenolytic, fibrinolytic enzymes which activate Hageman factor to produce bradykinin which is a potent pain mediator. Sudqvist also found combinations of bacteria that were responsible for transmissible infections, one such combination was B.melaninogenicus and Bacteroides asaccharolyticus. This showed the bacterial synergism that maintains bacteroides infections (13).

Fusobacterium nucleatum:

A study was done to determine the association of Fusobacterium nucleatum and endodontic flare-ups. The cases were pre-operatively asymptomatic with periapical lesions. Root canal samples were taken after the occurrence of flare-ups and the bacterial findings were correlated with the pain intensity recorded on a visual analog scale. All teeth in patients who reported with severe pain and swelling had Fusobacterium nucleatum. Samples from teeth with less pain did not have F.nucleatum. Thus, F.nucleatum appeared to be associated with development of the most severe forms of flare-ups. Bacteria that were also frequently recovered from the samples were Prevotella species and Porphyromonas species (14).

Enterococcus Faecalis:

Enterococcus faecalis has been only occasionally found in cases of primary endodontic infections but frequently isolated or detected in cases in which the endodontic therapy has failed. Enterococcus faecalis is the most isolated or detected species from oral infections, including marginal periodontitis, infected root canals, and periradicular abscesses (15,16)

Enterococcus faecalis is a persistent organism that makes up a small portion of the endodontic microflora but has a major role in the etiology of persistent periradicular infection (17). These are facultative anaerobes that can survive in harsh environments including extremely alkaline pH. Studies have shown that E.faecalis is present in 4 to 40% of primay endodontic infections. The likeliness of its presence in failed root canal treatment was found to be nine times higher. E.faecalis has been detected at 67-77% in a PCR detection method (18). It is known to be resistant to the action of calcium hydroxide intracanal medicament. It can survive in the presence of calcium hydroxide due to the presence of a proton pump and its ability to passively maintain pH homeostasis. It has displayed resistance to essentially every useful antimicrobial agent. The resistance may be intrinsic or acquired via gene transfer. The genes for intrinsic resistance, like other species characteristics, reside on the chromosome.(19)

Actinomyces radicidentis:

A new bacterial species has been identified with failed endodontic treatment by Kalfas et al. In two patients with failed endodontic treatment and persistent signs and symptoms, the root fillings were removed and the samples were grown in pure culture. The bacteria were similar to each other and were classified as Actinomyces radicidentis (20).

PREVENTION OF FLARE UP:

Flare ups causes a dilemma to the clinican when it is difficult for the patient to comprehend that they enter the office pain free, but experience a sustained increase or severe pain during or after treatment. Certain pre caution taken by a clinican can prevent flare-ups in most instances. Proper diagnosis- Identify the correct tooth causing pain. Ascertain whether tooth is vital or non vital. Identify if tooth is associated with periapical lesion. Determine correct working length- Radiographs. Apex locaters Complete extirpation of vital pulp. Irrigation- Preferably with combination of irrigants such as sodium hypochlorite and chlorohexedine. Avoid filing too close to the radiographic apex. Pre form apical trephination only if necessary. Reduce tooth from occlusion especially if apex is severely violated by over instrumentation. The Placement of intra canal medicaments, Prescription of mild analgesics and antibiotics whenever condition warrants it.

TREATMENT:

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. (21,22). Various studies have evaluated the effectiveness of cortical trephination to prevent and relieve post-treatment pain. (23-25). Chestner et al. (26) 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.

Antibiotics:

In a review on the use of systemic antibiotics for the control of post-treatment endodontic pain, Fouad 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.(27)

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. [28,29] The NSAIDs have been shown to be very effective for managing pulpal and periradicular pain.(28,30). 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.(29). 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.(28,29,31,32). If pain is not controlled by NSAIDs and acetaminophen, narcotic analgesics are required. These may be given in combination with NSAIDs for additive effects.(32,33).

CONCLUSION

The occurrence of mild pain and discomfort following endodontic treatment is common even when the treatment rendered is of the highest standard. It is the duty of the clinican to explain it to the patient. Prompt and effective treatment of flare- ups is an essential part of the overall endodontic treatment. When a flare-up occurs and is managed, the patient should be contacted daily until symptoms subside. Communication may usually be made by telephone Those patients with more severe or persistent problems (not resolving) and requiring additional measures should have follow-up appointments and additional treatment when needed. When symptoms are persistent and severe and can- not be controlled, these patients should be referred to a specialist. Frequently, other treatment measures such as periradicular apical surgery are necessary.

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Received on 11.06.2015 Modified on 21.06.2015

Research J. Pharm. and Tech. 8(11): Nov., 2015; Page 1588-1592

DOI: 10.5958/0974-360X.2015.00283.8