Flare up in endodontics

Flowchart
 Introduction
 Definition
 Incidence
 Criteria
 Risk factors
 Etiology
 Prevention
 Management

Introduction
 An inter appointment flare-up is an unhappy
event both for the patient and the dentist.
 After a root canal treatment appointment, the
patient calls or returns to the dentist’s office in
distress.
 Patients might even consider postoperative
pain and flare-up as a benchmark against which
the clinician’s skills are measured.

 The flare-up phenomenon is complex and
involves a number of aspects.
 Hence, It would be desirable to understand the
phenomenon to know how to prevent the
occurrence and be able to manage this event.
 This seminar discusses these many facets of the
flare-up: definition, incidence, factors,
prevention and how to manage the patient once
the flare-up occurs.

Definition
 Flare up is defined as an unscheduled
emergency appointment necessitated by pain &
swelling combined or by either alone.
Morse (1990)
 Flare up is defined as pain or discomfort or
swelling that requires an unscheduled patient
visit and active intervention by the dentist.
Walton & Foad (1992)

 Flare up is an acute exacerbation of
periradicular pathosis after the initiation or
continuation of root canal treatment.
AAE (1998)
 Flare-up is moderate-to-severe postoperative
pain or moderate to severe swelling that begins
12 to 48 hours after treatment and lasts at least
48 hours.
Pickenpaugh et al. (2001)

Incidence
 Fortunately, the frequency of this emergency
event occurs following only a small percentage
of root canal treatment appointments.
 The overall incidence of flare-ups is low.
(ranges from 1.5% to 5.5%)
 Lowest frequency a vital pulp without
periapical pathosis;
 Highest frequency patients who
preoperatively present with more severe pain
and swelling, particularly with pulp necrosis
and acute apical abscess.

RICHARD E. WALTON
Interappointment flare-ups:incidence,
related factors,prevention, and management
ENDODONTIC TOPICS 2002.1601-1538

Survey reports:
 Morse reported (1987) - 2.2%
 Walton reported (1992) - 3.17%
 Mura reported (1995) - 1.58%
 Kakahura reported ( 2001) - 1.23%
 Pickenpaugh (2001) -1.58% to 9%

 The studies with the best experimental design
show that the incidence, when considering all
pretreatment diagnoses together, ranges from
1.5% to 5.5%
Richard E Walton, Interappointment flare-
ups:incidence, related factors,prevention,
and management, Endodontic Topics 2002,
3, 67–76

Criteria
 Within a few hours to a few days after an
endodontic procedure, a patient has significant
increase in pain or swelling or a combination of
the two.
 The problem is of such severity that the patient
initiates contact with the dentist.
 The dentist determines that the problem is of
such significance that the patient must come
for an unscheduled visit.
RICHARD E. WALTON

 Pain is a subjective perception that is difficult
to quantify let alone compare between
different individuals and as such is a
problematic marker for detecting flare-up.
 In an effort to quantify and measure pain, the
visual analogue scale (VAS) has been proposed
by Seymour et al.
 This is a mathematical progression from 0 to
100, 0 being no pain and 100 being the most
severe pain imaginable.

 A flare-up is defined as an increase of 20 or
more points on the visual analogue scale for a
given tooth, within the periods of 4 h and 24 h
after the initial treatment appointment.
Ernest H. Ehrmann,Harold H. Messer, Robert
M. Clark, Aust Endod J 2007; 33: 119–130

 ‘Flare-up Index’ by RIMMER
– This extends from 0 to 45 and encompasses nine
variables. These include not only different
degrees of pain but also swelling and trismus.
– This index has not found acceptance as it is
altogether too complicated.
 Flare -up index attempts to show the
effectiveness of the treatment or infectiveness
of the treatment.

Flare - up index questionnaire
Questionnaire For range
Existence of pain after the first visit 0 - 1
No of days with pain X pain degree / day 0 - 21
How many days were analgesic taken? 0 - 7
How many times emergency treatment was needed? 0 - 7
Does pain still exist in what degree? 0 - 3
Are Analgesic still being taken? 0 - 1
Did Swelling appear and what degree? 0 - 3
Existence of limitation of mouth opening 0 - 1
Systemic involvement (temp, fatigue) 0 - 1
TOTAL 0-45

 These generally are categorized as
– patient related (demographic);
 pulpal/periapical diagnosis;
 presenting signs and symptoms;
– treatment procedures

 Interestingly, the literature clearly and
consistently shows that some of the patient
presenting factors are much more powerful
than treatment procedures as related to the risk
for developing a endodontic flare-up
Richard E Walton, Endodontic topics, 2002

1.Patient presenting factors
 Patient demographics
– Age groupings and gender have been
examined.

gender
 Several studies found higher numbers of post-
treatment pain and flare-ups in females
 Genet J, Hart A, Wesselink P, Thoden Van
Velzen S. Preoperative and operative factors
associated with pain after the first
endodontic visit. Int Endod J 1987: 20: 53–64.
 Torabinejad M, Kettering J, McGraw J,
Cummings R,Dwyer T, Tobias T. Factors
associated with endodontic
interappointment emergencies of teeth with
necrotic pulps.J Endod 1988: 14: 261–266.

age
 Age does not seem to be a significant factor.
 Several investigations have failed to find any
evidence indicating that age is a risk factor for
development of flare-ups.
 Imura N, Zuolo M. Factors associated with
endodontic flare-ups: a prospective study.
Int Endod J 1995: 28: 261– 265.
 Walton R, Fouad A. Endodontic
Interappointment flareups.a prospective
study of incidence and related factors. J
Endod 1992: 18: 172–177.

 Patients in the age group of 40-59 years had the
most flare ups and those under the age of 20
had the least.

 Mor C et al suggested that the incidence of
interappointment emergency associated with
endodontic therapy was 4.2% and unrelated to
patients sex , age or the tooth location .
Mor C, Rotstein I, Friedman S.Incidence of
interappointment emergency associated
with endodontic therapy.J Endod ;18:10,1992
509-511

2.Systemic conditions
 This aspect has been largely uninvestigated.
 A study reported that allergies were
significantly related to flare-ups
 Although this could not be replicated in
another study BY WALTON.

3.Pulp and periapical status
 Teeth with a vital pulp have relatively few flare-
ups.
 In contrast, teeth with pulpal necrosis have a
much higher incidence of flare-ups.
 It is generally accepted that the flare-up rate
after the extirpation of a vital pulp is either
non-existent or very low, even if the pulps were
painful before instrumentation.
Negm et al

RICHARD E. WALTON
Interappointment flare-ups:incidence, related
factors,prevention, and management
ENDODONTIC TOPICS 2002.1601-1538

 The periapical diagnosis of acute apical
abscess and acute apical periodontitis, both
painful entities, have been shown in most
studies to also result in a significantly higher
flare-up rate
 In addition, the radiographic presence of a
periapical lesion, particularly larger lesions,
also serves as a risk factor for development of
flare-ups.

Factors related to a reduced risk for developing
a post-endodontic flare-up

 Interestingly, the presence of a sinus tract
virtually ensures that a flare-up will not occur.
 Although this is indicative of an abscess,
apparently the tract functions as a relief valve,
releasing pressure, reducing tissue levels of
inflammatory mediators, and thereby
preventing the sudden increase in pain.

Treatment plan
 Factors related to the treatment plan include
– whether the case involves conventional vs.
retreatment,
– if the dentist chooses single or multiple visits,
– performs partial vs. complete debridement.
– treatment procedure

Retreatment
 There is no universal agreement as to whether
retreatment results in a higher incidence of
post-treatment pain or more flare-ups than
conventional root canal treatment
 Most studies indicate that there is no difference
 Mor C, Rotstein J Endod 1992: 18: 509–511.
 Mattscheck D, Law A, Noblett W.
Retreatment versus initial root canal
treatment: factors affecting post-
treatmentpain. Oral Surg Oral Med Oral
Path Oral Radiol Endod 2001: 92: 321–324.

 Study found high incidence of flare up in
retreatment cases 13.6%
 Trope . IEJ 1991.

No. of visits
There is no consistency in the literature; some
studies show numbers of visits to be a factor .
 Imura N, Zuolo M. Factors associated with
endodontic flare-ups: a prospective study.
Int Endod J 1995: 28: 261–265.
 Eleazer P, Eleazer K. Flare-up rate in
pulpally necrotic molars in one-visit versus
two-visit endodontic treatment. J Endod
1998: 24: 614–616.

 Whereas others show no difference , when
combining and considering all diagnoses, signs
and symptoms.
 Walton R, Fouad A. Endodontic
interappointment flareups.a prospective
Endod 1992: 18: 172–177.

 Compelling evidence indicating a significantly
different prevalence of postoperative pain/
flare-up of either single- or multiple-visit root
canal treatment is lacking
 Sathorn C, Parashos P, Messer H. The
prevalence of postoperative pain and flare-
up in single- and multiple-visit endodontic
treatment: a systematic review.
International Endodontic Journal, 41, 91–99,
2008.

 Majority of endodontists have found that single
visit endodontics does not cause more Flare-
ups than multi - visit treatments.
 Based on clinical and scientific principles, the
practitioner must decide if root canal
treatment is to be completed in one or more
appointments according to each specific case.

 Teeth without apical periodontitis did not flare-
up and may be treated in a single visit;
 Teeth with apical periodontitis but no previous
root treatment can be treated in a single visit,
with a low probability of a flare-up occurring;
 Teeth with apical periodontitis which need
retreatment, the flare-up rate was highest and
single-visit root treatment would be
inadvisable.
M. TROPE

Debridement
 Incomplete debridement has been traditionally
assumed to be a cause of flare-ups.
 However, studies have shown this factor to be
unrelated to the risk of developing a flare-up
 Balaban F, Skidmore A, Griffin J. Acute
exacerbations followinginitial treatment of
necrotic pulps. J Endod 1984:10: 78–81.

CONTRIBUTING FACTORS FOR FLARE UPS????
 Inadequate debridement
 Over instrumentation
 Periapical extrusion of debris

 Overfilling
 Periapical lesion
 Re-treatment
 Host factors

Therapeutics
 Studies showed prophylactic antibiotics to be
unrelated to flare-ups .
 Pickenpaugh L, Reader A, Beck M, Meyers
W, Peterson L. Effect of prophylactic
amoxicillin on endodontic flare-up in
asymptomatic, necrotic teeth. J Endod 2001:
27: 53–56.
 Walton R, Chiappenelli J. Prophylactic
penicillin; effect on post treatment
symptoms following root canal treatment
of asymptomatic periapical pathosis. J
Endod 1993: 19: 466–470.

 Another study reported that patients taking
antibiotics were more likely to have a flare-up
than those that were not.
 Fouad A.Walton R, Endodontic
interappointment flareups. a prospective
Endod 1992: 18: 172–177.

 Analgesics
 There is good evidence that pretreatment
analgesics minimize inter and post treatment
pain .
 Pretreatment pain and anxiety control,
including analgesics, may reduce incidence of
flare-ups

Mata et al. (1985) suggests
Following factors may be etiologically involved in
the production of pain and swelling following
endodontic therapy.
 entrance of oxygen into the root canal during
access may induce facultative aerobic bacteria to
proliferate and produce inflammatory agents.
 Instrumentation and the air syringe can force
bacteria into the canal and perhaps through the
apical foramen.
 The use of local anesthetic or instrumentation
might act as local irritants that cause an
inflammatory response.

Aetiology of flare ups
 1) Alteration of local adaptation syndrome.
 2) Changes in periapical tissue pressure.
 3) Microbial factors
 4) Effects of chemical mediators.
 5) Immunological phenomena.
 6)Changes in cyclic nucleotides and
 7)Numerous psychological factors.
SELTZER .NAIDORF.FLARE UPS IN
ENDODONTICS:ETIOLOGIC FACTORS.JOE
2004

1.Alteration of local adaptation
 Selye has shown that there is a local tissue
adaptation to applied irritants.
 Ordinarily, the connective tissues become
inflamed when they are exposed to an irritant.
 Chronic inflammation persists if the irritant is
not removed; there is local adaptation.

 When a new irritant is introduced to inflamed
tissue, a violent reaction may occur.
 In a patient with a tooth with chronic pulpitis
or periapical periodontitis, the inflammatory
lesion may be adapted to the irritant, and
chronic inflammation may exist without
perceptible pain or swelling.

 However, when endodontic therapy is
performed ,new irritants in the form of
medicament ,irrigating solutions, or chemically
altered tissue proteins may be introduced into
the granulomatous lesion.
 A violent reaction may follow, leading to
necrosis, indicative of an alteration of the local
adaptation syndrome.

2.Changes in periapical tissue pressure
 Various pathological conditions usually produce
a wide range of positive pressures
 The experiments of Mohom et al have indicated
that endodontic therapy may also cause a
change in the periapical tissue pressure.

 It is possible that, in teeth with increased
periapical pressure, excessive exudate, not
resorbed by the lymphatics, would tend to
create pain by exerting pressure on nerve
endings.
 In contrast, should the periapical pressure be
less than atmospheric pressure, it is conceivable
that microorganisms and altered tissue proteins
could be aspirated into the periapical area in
accentuation of the inflammatory response and
cause severe pain.

Bacterial, chemical and physical irritants likely act in combination to
produce changes at the periapex that result in inflammation and ultimately
pain and/or swelling.

3.Microbial Factors
 Microbial injury caused by microorganisms and
their products that egress from the root canal
system to the periradicular tissue is
conceivably the major and most common cause
of interappointment flare ups
 Bartels ,Seltzer

 Bacteriodes, Fusobacteria and
peptostreptococci are the most frequent
anaerobic isolates in flare – up.
 F.nucleatum is associated with the development
of most severe forms of inter appointment
endodontic flare ups
 B. melanogenicus acts synergistically with other
obligate anaerobes and facultative anaerobes.

From: Chavez de Paz L. Fusobacterium in endodontic flare-ups. Oral Surg Oral
Med Oral Path Oral Radiol Endod 2002:

 In asymptomatic chronic periradicular lesions
associated with infected teeth there is a balance
between microbial aggression and host defense
in the particular tissues
 During chemomechanical preparation ,micro
organisms are apically extruded, and the host
will face a situation in which it has to deal with
a large number of irritants than it was before.

 Consequently there will a transient disruption
in the balance between aggression and defense
in such a way that the host will mobilize an
acute inflammation to reestablish the
equilibrium

 Iatrogenic over instrumentation
 1)Promotes the enlargement of the apical
foramen
– Permits the increased influx of exudates and
blood into the root canal
Chavez de Paz Villanueva 2002
– Enhances the nutrient supply to the remaining
bacteria within the root canal that can then
proliferate and cause exacerbation of a chronic
periradicular lesion.

 Also can cause mechanical injury to the
periradicular tissue
– which is usually coupled with the apical
extrusion of significant debris
– Forcing microorganisms and their products
into periradicular tissues can generate
inflammatory response whose intensity will
depend on the number and virulence of micro
organisms

 All instrumentation techniques have been
shown to promote apical extrusion of debris,
 Crown down techniques usually extrude less
debris and should be elected for
instrumentation of root canals.
DUMMER AND FAVIERI
 Hence. Quantitative factor is more likely to
be under the control of the therapist.

 Qualitative factor is more difficult to control.
 When virulent clonal types of pathogenic
bacterial species are present and are propelled
to the periradicular tissues –even a small
amount of infected debris will have the
potential to cause or exacerbate the
periradicular inflammation.
QUALITATIVEQUANTITATIVE

Changes in environmental conditions/
endodontic microbiota
 Ideally the chemomechanical preparation
should be completed in one appointment and
between visits, an intracanal medication should
be left in the root canal.
 Incomplete chemomechanical preparation can
disrupt the balance within the microbial
community by eliminating some of the
inhibitory species and leaving behind other
previously inhibited species, which can then
overgrow.

 If overgrown strains are virulent and / or reach
sufficient numbers, damage to the periradicular
tissues can be intensified which may result in
exacerbation.
 When microorganisms are not totally
eliminated environmental changes have the
potential to induce virulent genes to be turned
on/off .

Secondary infections-
 Introduction of new microorganisms into the
root canal system during treatment usually
occurs following a breach of aseptic chain.
 remnants of dental plaque,
 calculus caries on the tooth crown,
 leaking rubber dam
 contaminated endodontic instruments,
 leaking temporary restoration

Increase of oxidation-reduction potential
 When tooth is opened oxygen penetrates into
root canal system and microbial growth
pattern changes from anaerobic to aerobic
conditions.
MATUSOW
 If facultative anaerobes such as streptococci are
present in root canal infection and resist intra
canal procedures, they may overgrow as a result
of increase in the redox potential and deflagrate
acute periradicular infection.

4.Effect of chemical mediators
 During the inflammatory response, chemicals
can be derived from cells or plasma.
Cell Mediators
 histamine,
 serotonin (5-hydroxytryptamine (5-HT),
 prostaglandins (PGs),
 platelet-activating factor (PAF),
 leukotrienes (LTs)
 various lysosomal components,
 and some lymphocyte products called
lymphokines,
PAIN

Plasma Mediators
 Plasmin
 fibrinopeptides and fibrin degradation products
 Bradykinin
 Prekallikrein activator
 Hageman factor
PAIN

Neutrophil Products
 hydrolytic enzymes
 lysozyme,
 collagenases,
 cathepsins,
 f3-glucuronidase,
 peroxidase,
 amylases,
 lipases,
 ribonucleases,
 deoxyribonucleases, and
 lactic dehydroenases.

5.IMMUNOLOGICAL PHENOMENA
 In chronic pulpitis and apical periodontitis, the
presence of macrophages and lymphocytes
indicates that both cell-mediated and humoral
immune reactions are involved.
 Despite their protective effects, immunological
mechanisms may contribute to the destructive
phase of inflammation.
 The type of clinical response may be dictated by
the type of immunoglobulin elaborated.

 Should the dominant immunoglobulin in the
pulp or periapical lesion be lgG,there is a
possibility of an Arthus-type reaction, after
complement activation, owing to the local
formation of immune complexes.
 On the other hand, if the dominant
immunoglobulin is IgA, complement-fixing
activity is low.
 Pain and destruction are the result of a shift in
the production of lgG over IgA, causing
perpetuation and aggravation of the
inflammatory process.

6.CHANGES IN CYCLIC NUCLEOTIDES
 According to the hypothesis of Bourne et al, the
character and intensity of inflammatory and
immune responses is regulated by certain
hormones and mediators.
 This regulation is mediated by a general
inhibitory action of cyclic AMP on the release of
mediators from mast cells. basophils, monocytes,
and polys.
 Increased intracellular levels of cyclic AMP,
induced by PGs and histamine, may inhibit
degranulation of mast cells and help in reducing
pain.

 Where as an increase in cyclic GMP stimulates
mast cell degranulation which results in
increase in pain.
 It has been seen that during flare up there is
increase in level of cGMP over cAMP
concentrations.

7.PSYCHOLOGICAL FACTORS
 Fear of dentists and dental procedures, anxiety,
apprehension, and many other psychological
factors influence the patient’s pain perception
and reaction thresholds .
 Previous traumatic dental experiences appear
to be significant factors in the production of
anxiety and apprehension in dental patients.
 These factors predispose individual to flare ups.

Clinical conditions associated with flare upsClinical conditions associated with flare ups

 A tooth which was symptomless
before the initiation of endodontic
treatment but becomes sensitive
to percussion during the course of
the treatment.
 Causes for this condition most
frequently are over
instrumentation or forcing debris
into the periapical tissues.
Apical periodontitis secondary to treatment

Incomplete removal of pulp tissues during the
intial 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 periradicular 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.

Preventive measuresPreventive measures
Occlusal reduction
Intracanal medicaments
Drugs

Relief of Occlusion
 Occlusal relief prior to endodontics has been
advocated by Cohen for the prevention of
endodontic pain.
 Other endodontists (Olgivle AL, Nichols E.) have
recommended occlusal relief
Occlusal Reduction

 Routine prophylactic occlusal reduction as a
prevention of postoperative pain is ineffective.
– Creech J, Walton R, Kaltenbach R. Effect of
occlusal relief on endodontic pain. J Am Dent
Assoc 1994: 109: 64–67.
– Jostes J, Holland G. The effect of occlusal
reduction after canal preparation on patient
comfort. J Endod 1989: 10: 34–37.

 Occlusal reduction in teeth with pain upon
mastication is effective in reducing
postoperative pain
 Whether this would prevent flare-ups in
symptomatic teeth was not examined, but is
unlikely.
Rosenberg P, Babick P, Schertzer L, Leung A.
Effect of occlusal reduction on pain after
instrumentation. J Endod 1998: 24: 492–496.

 Although this procedure has not been studied
with flare-ups, it is unlikely that this would
have any benefit.
– Walton R, Hutter J. Endodontic emergencies.
In: WaltonR, Torabinejad M, eds. Principles
and practice of endodontics, Chapter 17, 3rd
edn Philadelphia: Saunders, 2002, 306–308.

Intracanal Antimicrobial agents
 Since microorganisms are responsible for
exacerbating inflammation, it would appear
that the intracanal placement of root canal
antiseptics and germicides should at least
indirectly reduce inter and post treatment pain.
 According to Seltzer, intracanal medication
reduces the possibility of flare ups due to the
forcing of infected debris into the periapical
tissues

 Such does not appear to be the case in most
instances. The anodyne properties of calcium
hydroxide ,formocresol, cresatin, eugenol,
camphorated monochlorphenol, and iodine-
potassium iodide have been studied.
 Maddox DL, Walton RE, Davis CO. Incidence
of posttreatment endodontic pain related to
medicaments and other factors. J Endodon
1977;3:447.
 Kleier DJ, Mullaney TP. Effects of
formocresol on posttreatment pain of
endodontic origin in vital molars. J Endodon
1980;6:566.

 There were no significant differences in the
flare-up rates at 4 hr and 24-h periods between
the three modalities- Ledermix, calcium
hydroxide and no medication.
 H Ernest, M Robert, H Harold Messer Aust
Endod J 2007; 33: 119-130.

Irrigating solutions
 Since the induction of pain in endodontic
therapy is multifactorial, it is difficult to
attribute a lower pain incidence specifically to
the use of any particular irrigant.
 Harrison et al. found that there was a higher
incidence and degree of pain in patients whose
canals were either not irrigated or irrigated
with saline solution, compared with those
irrigated with 5.25% sodium hypochlorite and
3% H2O2

Corticosteriods
 The anti-inflammatory activity of
corticosteroids is based partly on their ability to
retard lysosomal release from cells by inhibiting
fusion of lysosomes with their target
membranes.
 In addition,corticosteroids inhibit the
liberation of free arachidonic acid from the
phospholipids of the cell membrane by
phospholipases

 A number of investigators have reported that
corticosteroids placed into the root canal
control pain successfully.
 Langeland K, Langeland LK, Anderson DM.
Corticosteroids in dentistry.Int Dent J
1977;27:217.
 Moskow A, Morse DR, Krasner P, Furst ML.
Intracanal use of a corticosteroid solution
as an endodontic anodyne. Oral Surg
1984;58:600.

Ledermix(Lederle Laboratories Gosport, Hants,
UK)
A paste that combines
1% triamcinolone acitonide (a corticosteroid)
demethylchlorotetracycline (demeclocycline, a
tetracycline analog).
Still there is no conclusive evidence that flare up
can be prevented by intracanal placement of
corticosteroids.

 There is no demonstrated benefit in placing
medicaments or any other substance in canals
to help prevent or resolve a flare-up.
– RICHARD E. WALTON, ENDODONTIC
TOPICS 2002

 Steroids, administered in a single dose (e.g. 4–
6mg of dexamethasone) may also be of benefit
to reduce pain.
 Leisinger A, Marshall FJ, Marshall JG. Effect
of variabledoses of dexamethasone on post
treatment endodontic pain. J Endod 1993: 19:
35–39.

Antibiotics
 Although antibiotics are widely used in treating
a localized abscess, prospective clinical trials
show they are of no benefit for reducing
postoperative pain or risk of developing a flare-
up.
 there are no significant studies which show that
any specific antibiotic is capable of reducing or
eliminating painful exacerbations during
endodontic therapy.

Analgesics
 There is good evidence that pretreatment
analgesics minimize inter and post treatment
pain.
 Dionne R. Preemptive vs. preventive
analgesia: which approach improves
clinical outcomes? Compend Contin Educ
Dent 2000: 21: 51–456.
 Gottschalk A, Smith DS. New concepts in
acute pain therapy:preemptive analgesia.
Am Fam Physician 2001: 63:1979–1984.

 Pretreatment pain and anxiety control,
including analgesics, may reduce incidence of
flare-ups
 Torabinejad M, Cymerman J, Frankson M,
Lemon R,Maggio J, Schilder H. Effectiveness
of various medications on postoperative
pain following complete instrumentation.J
Endod 1994: 20: 345–354.

Placebo
 Placebos are pharmacologically inert
substances that nonetheless have a therapeutic
effect
 A placebo does not have to be a medication. It
can be a person, a procedure, a place, or a ritual.

Prevention through treatment procedures
SIQUEIRA J.F. MICROBIAL CAUSES OF ENDODONTIC FLARE UPS .
IEJ 2003

 When a flare-up occurs, management is in
three phases:
– Psychological
– Localized treatment
– Pharmaco therapeutics.

 And perhaps the most important, aspect of treatment
The Big is criticalR eassurance

 The dentist must explain that flare-ups do
occur and are treatable.
 Next, the patient must be made comfortable by
breaking the pain cycle.
 Important to psychological management is
good local anesthesia.

Localized teatment.
Establishment of drainage
 In the presence of suppuration, drainage of
exudate is the most effective method for
reducing pain and swelling.
 In most instances, the accumulated exudate will
surge from the root canal, affording immediate
relief.
 However, upon occasion, no exudate will
emerge; it may be blocked by packed dentinal
shavings in the apical third of the root canal.

 After adequate anaesthsia passing a root canal
instrument, such as a file or reamer, through
the caked material may help to establish the
flow of exudate.
 During drainage canal is left open for about 15
mins .or until exudation has ceased or a slight
clear serum drains.
 After adequate drainage and irrigation the root
canal can then be resealed, usually without
further discomfort to the patient.

 Many endodontists prefer to leave the root
canal open until symptoms have subsided.
 According to Seltzer ,Weine and August this
exposure to the oral flora serves no useful
purpose and may actually cause subsequent
flare-ups when additional treatment is
undertaken.

 Exposure of the root canal to salivary products
logarithmically
 increases bacterial growth,
 introduces new microorganisms,
 activates the alternate complement pathway,
and
 may enhance bradykinin production
LEADING TO THE EXACERBATION OF PAIN.

 In exceptional cases, the exudate is either
absent or cannot be evacuated through the root
canal.
 Surgical intervention is then necessary.
 The removal of the alveolar bone over the apex
of the tooth root (creation of an artifical sinus
tract), or a soft tissue incision when swelling
has occurred usually affords relief.

 Following the administration of the appropriate
block and/or infiltration anesthesia, the
surgical area should be isolated with sterile 2 ×
2 gauze sponges.
 The incision should be horizontal and placed at
the dependent base of the fluctuant area.
 The incision should be made using a scalpel
blade that is pointed,such as a No. 11 or No. 12,
rather than a rounded No. 15 blade.

 Probing with a curette or hemostat into the
incisional wound to release exudate entrapped
in tissue compartments will facilitate a more
effective result
Scalpel blades for surgical incisions. From top:
, No. 15, No. 12, No. 11.

 The use of drains following an I & D procedure is
controversial.
 McDonald andHovland have stated that the
incision alone will usually provide the needed
drainage
 Frank et al. recommended the use of a rubber
drain to maintain the patency of the surgical
opening.
– Rubber dam drain
– Penrose drain
– Caillary drain-ribbed

 Gutmann and Harrison stated that the use of
drains following I & D procedures has been
greatly abused.
 Patients with localized or diffuse intraoral
swellings ,even if mild extra oral swelling is
present, do not usually require drains following
I & D procedures.

 The drain may be made of either iodoform
gauze or rubber dam material cut in an “H” or
“Christmas tree” shape
A self-retentive ‘Christmas tree’ drain mae from a sterilized rubber dam.

Trephination
 Cortical trephination involves making an
incision through muco-periosteal tissues and
perforating through the cortical plate with a
rotary instrument
 The objective is to create a pathway through the
cancellous bone to the vicinity of the involved
periradicular tissues.

 Gutmann and Harrison recommend using
either a No.6 or No. 8 round bur in a high-
speed handpiece to penetrate the cortical plate.
 A reamer or K-type file is then passed through
the cancellous bone into the vicinity of the
periradicular tissues

Specific Treatment measures
 These depend on previous diagnosis and
Current findings.
 Previous diagnosis includes vital or necrotic
pulp with or without swelling.

Vital pulp
 Flare-ups seldom occur in these situations, but
when they do, the problem likely is related to
tissue remnants that have become inflamed.
 Working lengths should be verified and the
canals carefully cleaned with copious irrigation
 A dry cotton pellet is then placed followed by a
temporary restoration.
 The pain will usually subside rather quickly and
predictably following administration of
analgesics.

Previously necrotic pulp with no swelling
 These teeth may develop a flare-up after the
appointment.
 The abscess is confined to bone and is
generally very painful.
 Management
– Anaesthesia
– Opening tooth
– Drainage
– Irrigation
– Medicament
– Resealing

Necrotic pulps with swelling
 Localised swelling
– The tooth should be opened and the canals
re-debrided and closed.
– Incision and drainage.

 Non localized swelling
– Non-localized swellings, that is, rapidly
spreading into spaces, and those patients
with systemic signs of infection, require
antibiotics.
– If the spread of infection is alarming,
extraoral drainage may be performed and
the patient may even be hospitalized.

Pharmaco-therapeutics
 Analgesic
a drug that selectively relieves pain by acting on
the central nervous system or on peripheral
pain mechanism without significantly altering
consciousness.
Analgesics are broadly classified into-
1. Opioid/ narcotic/ morphine like analgesics
2. Non opioid/ non-narcotic/ aspirin like/
antipyretic anti- inflammatory analgesics

 There is no specific analgesic that is
preferentially effective for the pain induced
during root canal therapy.
 Avoid indiscriminate usage of opiod/steroidal
analgesics.
 NSAIDs are shown to be effective in reducing
pain in most of the situations.For severe pain, a
combination approach (steroidal and
nonsteroidal) is most effective.

Who analgesic ladder
 If pain is moderate to severe, opioid should be
employed along with the non-opioid analgesics,
but at this stage use a low potency opioid. E.g.
Codeine ,oxycodone, hydrocodone is used first.
 If treatment pain is inadequate (or) patients
presents with severe pain, a high potency opioid
[morphine, hydromorphine) should be selected
and prescribe along with the non-opioid
analgesics.

Flexible prescription strategy
Modified from: Hargreaves
KM & Seltzer S. Pharmacological
control of dental pain. In: Hargreaves
KM, Goodis HE, eds. Seltzer
and Bender’s dental pulp. Chicago:
Quintessence, 2002: 205–226

 Combination of flurbiprofen (100mg loading
followed by 50mg each 6h) and tramadol
(100mg each 6h) seems to be effective in
managing pain in emergency patients.
– Doroschak A, Bowles W, Hargreaves K.
Evaluation of the combination of
flurbiprofen and tramadol for management
of endodontic pain. J Endod 2001: 25: 660–
663.

Oxford League table of Analgesic Efficacy.
Analgesic N > 50%pain relief NNT
Ibuprofen 800 76 100 1.6
Ketorolac 20 69 57 1.8
Diclofenac 100 411 67 1.9
Piroxicam 40 30 80 1.9
Acetaminophen1000 197 57 2.2
Codeine 60
Diclofenac 50 738 63 2.3
Oxycodone IR 15 60 73 2.3
Ibuprofen 600 203 79 2.4
Ibuprofen 400 4703 56 2.4
Aspirin 1200 279 61 2.4
Acetaminophen 500 561 61 3.5
Acetaminophen 1500 138 65 3.7
Analgesic efficacy

ANALGESIC TRADE NAME
DOSE RANGE
(MG)
DOSAGE/DAY
(MG)
Acetaminophen
Tylenol,
others
325-1000 4000
Aspirin Many 325-1000 4000
Diflunisal Dolobid 250-1000 1500
Diciofenac
potassium
Cataflam 50-100 150-200
Etodolac Lodine 200-400 1200
Fenoprofen Nalfon 200 1200
Flurbiprofen Ansaid 50-100 200-300
Ibuprofen Motrin, 200-400 2400
Ketoprofen Orudis 25-75 300
Ketorolac Toradol 30-60 60
Naproxen Na Anaprox, 220-550 165O

CONCLUSION
 Flare ups may occur with the best of the
therapy, but most flare ups occur when
improper treatment is rendered or when
insufficient time is allowed for specific
modalities in therapy according to Franklin S
Weine
 Flare ups causes a dilemma to the clinician and
also 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

 It would be desirable to understand the
phenomenon to know how to prevent the
occurrence and be able to manage this event
 However, the flare-up phenomenon is complex
and involves a number of aspects.
 Taking all precautions at every step to prevent a
flare up is required to avoid this unforeseen
emergency .

Flare up in endodontics

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