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Edgar Schfer

Irrigation of the root canal

Key words
apical
periodontitis,
chlorhexidine,
disinfection,
smear layer,
sodium
hypochlorite

The root canal


system is
colonised with
microorganisms

in cases of apical periodontitis. Currently, it is impossible to totally eliminate these microbes


purely with mechanical instrumentation. Therefore, irrigants are required to eradicate
intraradicular infection. In this article, the different actions and in-teractions of the most commonly
used irrigants are discussed and a clinical protocol suggested. At least two different irrigants
should be used to achieve the most effective reduction of intraradicular microorganisms.

Edgar Schfer

Department of Operative
Dentistry,
University of Mnster,
Waldeyerstr. 30, D-48149
Mnster, Germany

Tel: +49 251 8347040


Email: eschaef@unimuen-ster.de

Introduction

Pulpitis versus apical periodontitis

In recent years, there have been major advances in improving


the properties of root canal instruments. Since the introduction
of nickel-titanium alloy (NiTi) into endodontics, nearly every
month a new rotary NiTi-system comes onto the dental market.
More-over, there are several new products and root canal filling
materials. Unfortunately, all these advances are focused on the
technical aspects of the root canal treatment. A more biologically
based approach has received less attention. There is a renewed
interest in the relationship between mechanical root canal instrumentation and intraradicular disinfection. Infec-tion control
during root canal treatment is important for successful outcome
in nonsurgical root canal treatment.

Therefore, the aim of this review is to analyse the relevant


literature on root canal irrigation. An irrigation protocol for
the everyday clinical practice is also proposed, including
other relevant recom-mendations.
ENDO 2007;1(1):11-27

The healthy pulp can be affected by several irritants such as dental


caries (bacteria and their products), traumatic injuries, iatrogenic
factors (dehydration of dentine, toxic influences from filling
materials, and leakage of the restoration) and, very seldom, systemic influences (nutritional deficiencies). Like all other connective
tissues in the body, the pulp reacts to these irritants with
inflammation. Most frequent-ly, an inflammatory reaction in the pulp
is caused by bacteria from a profound carious lesion, since denti-nal
tubules are portals of entry for these bacteria, bacterial antigens and
tissue breakdown products to reach the pulp tissue13. Thus an
inflammatory reac-tion in the pulp starts long before bacteria invade
the pulp tissue4. However, when further development of the
inflammatory process allows enough bacteria to reach the pulp, the
local inflammation is likely to be irreversible; but even at this stage,
the remaining vital pulp tissue will defend itself against the invad-ing
microbes5 and thus the infection will remain rel-

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atively superficial. In the more apical part of the root canal, most of the pulp tissue will be vital and free of bacteria at this
point of the disease6.

Due to this microbial aetiology of pulpitis, it is clear that the treatment of irreversible pulpitis, in other words the treatment of vital
cases, should focus on prevention of infection rather than an elimination of intraradicular infection4. As the apical part of the root
canal system is bacteria free, the aim is asepsis7. Under clinical conditions, the easiest and by far the most efficient methods to
guarantee asepsis during endodontic treatment are coronal disinfection of the tooth and mandatory use of rubber dam. Moreover,
sterilised burs and root canal instruments must be used, gloves must be worn, and the root canal obturation should if possible be
performed at the first visit68. Thus the pulpectomy procedure is basically aimed at preventing the development of a pulpal infection
and thereby preventing the development of an apical periodontitis6.

In contrast, in cases with radiographic and/or clinical signs of an apical periodontitis there can no longer be any doubts that the root
canal system harbours microorganisms6,911. There is over-whelming evidence that periradicular diseases are caused by
microorganisms in the necrotic root canal12. Hence, antisepsis must be the aim of ther-apy in order to eliminate all microbes within
the root canal system7. In cases of infected root canals, the key factor for clinical success and thus for promoting healing of the
apical periodontitis is efficient, and theoretically the complete, removal of intraradicular microorganisms13. Whether or not there is
a direct correlation between the number of viable microbes remaining in the root canal at the time of obturation and the outcome of
the thera-py remains controversial. Some studies have shown a significantly poorer prognosis for cases of apical periodontitis if
viable bacteria remain in the canal at the time of filling14,15. This finding has been sup-ported by a clinical study indicating that the
treat-ment outcome was significantly better in cases with apical periodontitis after intraradicular dress-ing versus one-visit
treatment14,15. On the other hand, a recent study failed to show any difference in residual microorganisms between one- and twovisit treatment16, an observation that is in agree-

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ias no difference

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in healing between teeth filled afterepositivezor

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negative root canal cultures was observed17.

Endodontic infection: localisation of microorganisms

In general, endodontic infection can be divided into primary (primary apical periodontitis) or secondary root canal infection
(previously root-filled teeth with apical periodontitis). In general, primary root canal infection is characterised by strictly anaerobic
bacteria and is typically polymicrobial12,1820. Predominant species are Bacteroides,

Porphyromonas, Prevotella, Fusobacterium, Treponema, Peptostreptococcus, Eubacterium and

Campylobacter12. Facultative streptococci are also commonly found in primary infection12. In general, about 110 different microbial
species have been de-tected in the root canal system in cases of apical pe-riodontitis; less than 1015 different species can be
expected in a single tooth12. In chronic periapical le-sions, the range of microbial species encountered is wider compared with a
more restricted number of species in cases of acute apical periodontitis or acute periapical abscess12,21,22.

Secondary intraradicular infection is usually caused by microbes that are not normally present in primary infection and have entered
the root canal system during or after endodontic treatment12. If these microorganisms are successful in colonising the root canal
system and survive the prevailing local conditions, a secondary infection becomes estab-lished. The composition of intraradicular
flora in sec-ondary infection is quite different from that found in primary infection. Usually, in the former, the flora is dominated by a
single species, or by fewer species when compared with primary infection12. In fact, monoinfection is not common in primary
infection4. Gram-positive bacteria predominate in secondary in-fection and fungi can also often be found12,2326. Sometimes
Enterococcus faecalis is found in pure culture in previously root-filled teeth with persistent apical periodontitis2528.

In approximately 8595% of all cases, the infec-tion is restricted to the root canal system containing necrotic pulp tissue 4,6,12; they are
protected from the

ENDO 2007;1(1):11-27

action of the cellular (phagocytes) and molecular

12,29

(antibodies, complement system) host defences


.
The microbes survive on pulp tissue remnants and
exudate from the periodontium20, the reason why in
most cases intraradicular microbes are mostly locat-ed
in the apical part of the root canal system23. These
microorganisms at the apical part of the root canal are
usually delineated from the inflamed periapical tissues
either by a dense accumulation of polymor-phonuclear
neutrophils or by an epithelial plug near the apical
foramen12,23. As a result, these microbes are protected
from the host defences. Within the root canal these
microorganisms are organised on the surface of the
canal walls as an aggregation in an ex-tracellular
polysaccharide matrix, the so-called biofilm30,31.
Unfortunately, microbes organised in a biofilm are
about 1000-fold more resistant to antimi-crobial agents
than their planktonic counterparts that exist in the root

Schfer Root canal irrigation

canal32.

When intraradicular infection is not adequately treated,


microorganisms will penetrate from the main root canal
into dentinal tubules, lateral canals, and other canal
irregularities. The invasion of dentine is es-timated to
occur in approximately 5080% of all teeth with apical
periodontitis, and the microbes involved are dominantly

Gram-positive cocci and rods30,3336 (Fig 1). Bacterial


invasion into the dentinal tubules can be observed up
to a depth of 400 m29,33,37, while bac-terial
components such as lipopolysaccharides can penetrate
even up to 1.2 mm into these tubules35. It is also worth
remembering that even in the absence of viable
bacteria, their products can cause a severe inflammatory response12. These indirect mechanisms of

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collagenase, hyaluronidase), exotoxins and metabot

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lites (e.g. butyrate, ammonium, sulphur compounds), and other bacterial


components, such as peptidogly-cans, teichoic acid and lipopolysaccharides 12,38.
The lipopolysaccharide, in particular, seems to be capable of causing severe
tissue destruction by stimulating the development of host immune reaction12. The
endo-toxin is located in the outer membrane of Gram-neg-ative bacteria and is
able, as mentioned above, to cause tissue damage even in the absence of viable
bacteria6. It has been shown in an animal model that placing lipopolysaccharide
in empty sterile root canals led to the development of periapical lesions 39. In pulp
tissue of teeth associated with apical periodontitis, high levels of
lipopolysaccharides were found40, and there was a strong association between
lipopolysac-charide levels and the prevalence of Gram-negative bacteria41.
These observations that bacterial metabo-lites and breakdown products play a

tissue damage are caused by bacteria enzymes (e.g.


i

significant role in the pathogenesis of apical periodontitis 6 confirmed the need for
a root canal irrigant capable of neutralis-ing lipopolysaccharides.

Microbes can also reside in the root canal system within the smear layer. This is
a thin surface film formed on the root canal wall after instrumentation. A smear
layer is produced on areas touched by root canal instruments. The smear layer
consists of den-tine particles, bacterial components, and remnants of vital or
necrotic pulp tissue42,43. Due to these organ-ic remnants, the microbes have easy
access to nutri-ents inside the smear layer. Therefore, it is clear that in infected
cases the smear layer should be ren

Fig 1 Gram-positive bacteria that have penetrated into the dentinal tubules (Gram; original magnifica-tion 400x).

ENDO 2007;1(1):11-27

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moved to achieve the greatest possible reduction of intraradicular


microorganisms.
Extraradicular infections may occur, but they are rare6,12. Usually, they may occur in
the form of an acute periradicular abscess or in cases of actinomycosis12. The
problem with extraradicular infection is that microbes are established in the
periradicular tissues, inaccessible to nonsurgical endodontic treatment procedures.
As a result, extraradicular infection may cause endodontic failure. There is
overwhelming evidence in the litera-ture that microorganisms left in the root canal
system after root canal preparation or re-infection of the root filled tooth (secondary
infection), are the main causes of endodontic failure4,7,14,25.

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Fig 3 Scanning electron micrograph of multiple accessory
foramina on the pulp chamber floor of a mandibular molar
(original magnification 80x).

Root canal instrumentation and bacterial


reduction

Due to its complex anatomy, with the multiple fins, isthmuses,


ramifications and accessory canals44 (Fig 2), it is virtually impossible
for mechanical root canal instrumentation to shape and clean the
entire root canal system45. Intraradicular microbes may be lodged in
these areas, which are inaccessible to in-strumentation6. In addition,
this complex environ-ment prevents irrigants from exerting their full
an-timicrobial potential4. Approximately 79% of all per-manent
molars have accessory canals in the furcation area46 (Fig 3). These
canals may have diameters of up

steel files and sterile saline resulted in a 1001000-fold reduction of


intraradicular microorganisms, but it was not possible to predictably
obtain bacteria-free root canals47. These results were supported by
fur-ther investigations, which showed that the sole use of manual
stainless steel instruments does not render root canals bacteriaFig 2 Post-operative radiograph showing a lateral root canal that is
partially filled with sealer and associated with a lateral lesion (see circled
area).

to 200 m, so microbes can easily penetrate from the root canal


system into the periodontal tissues or vice versa. Therefore,
nowadays an adhesive seal of the pulp chamber floor, after the
obturation of the root canal space, is recommended to avoid reinfection of the root canal system via the periodontium46.
Classic Scandinavian studies by Bystrm and Sundqvist clearly
indicated that mechanical instru-mentation is able to reduce
4749

significantly the number of microbes in the root canal system


.
These stud-ies showed that hand instrumentation using stainless

free5052. These investigations convincingly demonstrated the limited


antibacterial effect of mechanical preparation.

The introduction of more flexible alloys like NiTi led to the


development of rotary systems. It was as-sumed that these
improvements would result in more effective removal of bacteria
from infected root canals compared with conventional hand
instruments6. Re-cently, several studies have been conducted to
com-pare the level of intraradicular bacterial reduction of hand
instruments (stainless steel or NiTi) compared with rotary NiTi
instruments with greater tapers than ISO .02 taper. Nearly all of
these studies failed to show significant differences between hand
and rotary in-strumentation50,5158. Only about one- third of the instrumented canals were found to be free of bacteria

ENDO 2007;1(1):11-27

Reduction of intraradicular microorganisms and neutralisation of


endotoxins.
Dissolution of vital or necrotic pulp tissue.

Lubrication of canal walls and instruments.

Removal of dentine particles.


and in general both preparation techniques were not
able to predictably render canals bacteria-free50,51,58.
The following are requirements of a root canal irrigant:

In summary, predictable and complete bacterial


elimination does not appear to be possible, either
with traditional hand instrumentation or with newer

A broad antimicrobial spectrum.

rotary NiTi-systems6,50. Irrigation of the root canal is


essential for effective elimination of bacteria.

Biocompatibility.

Objectives and requirements of


irrigants

Tissue-dissolution capability.

The aims of root canal irrigation are:

Antimicrobial irrigation solutions

Clinical studies performed in Scandinavia showed


that copious irrigation with an antimicrobial solution
during mechanical root canal preparation has an
essential effect on the reduction of intraradicular
microorganisms47,48,55. Mechanical root canal
preparation using saline as an irrigant leaves only
about 20% of canals bacteria-free. The percentage
of bacteria-free canals was increased to up to 50%
when NaOCl was used for irrigation. Ultrasonic
activation of sodium hypochlorite achieved a further
reduction of intraradicular microbes, with
approximately 70% of all canals bacteria-free.
These studies confirmed the paramount importance
of antibacterial irrigation solutions. The employment
of one or more antimicrobial irrigation solutions
during root canal treatment is good clinical practice.

Sodium hypochlorite

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Sodium hypochlorite (NaOCl) is the most widely


used irrigation solution in endodontics. Currently

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. In water, NaOCl dissociates int

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to Na+ and OCl-, the hypochlorite ion. Between pH 4 and pH 7, chlorine from
NaOCl exists predomi-nantly as HClO (hypochlorous acid), whereas above
pH 9, OCl- predominates4,59. Although the antimi-crobial effectiveness of
hypochlorous acid is greater than that of hypochlorite59, in the clinically used
NaOCl solutions, the entire available chlorine is in the form of OCl-, as the

available evidence strongly indicates that NaOCl is


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pH of the solution is normally about 127,60. Unfortunately, due to several


technical problems (e.g. stability of the solution), NaOCl solu-tions with a
lower pH, which would increase the amount of available hypochlorous acid,
are not com-mercially available at present7.

In endodontic therapy, NaOCl solutions are used in concentrations varying


from 0.5% to 5.25%4. Also available are unbuffered solutions at pH 1112 in
concentrations ranging between 0.5% and 5.25%, or the so-called Dakins
solution, which is a buffered 0.5% solution at pH 9.04,59. There is no
difference between these two solutions with respect to tissue dissolution or
antibacterial efficiency4,61. Although allergic reactions to NaOCl are rare7,
there have been several case studies on the potential risk of hypersensitivity reactions6264.

NaOCl dissolves pulpal remnants (vital and necrotic pulp tissue), organic
compounds of dentine, and the organic components of the smear layer6569.
The tissue-dissolving capability of NaOCl is signifi-cantly better than all other
commonly used irrig-ants65 (Fig 4). Moreover, neutralisation or inactiva-tion
of lipopolysaccharides has been reported with NaOCl7072. However, NaOCl
is not able to remove the smear layer73,74.
Sodium hypochlorite is characterised by having strong antibacterial activity
with comparably short contact times4,7. Even the resistant Candida albi-cans
was killed in vitro by both 5% and 0.5% NaOCl solutions75. Several in vitro

investiga-tions7577 and one clinical study26


confirmed the sus-ceptibility of C. albicans to
NaOCl. In addition, sev-eral Gram-negative
anaerobic bacteria, typically found in primary root

ENDO 2007;1(1):11-27

canal infection, displayed a high susceptibility to NaOCl in concentrations


rang-ing from 0.5% to 5%77. In contrast, based on the re-sults of both
laboratory studies76,78 and one clinical report evaluating microbiological
samples of previ-

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Figt4 Canal wall

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after preparation

with rotary nickel-

titanium instru-

ments: a) using

NaCl as an irrigant,

b) using NaOCl for

irrigation. Notice

that when using

NaOCl nearly no

remnants of pulpal

tissue or debris

were found on the

canal wall (original

magnification 40x).

biofilms7981. In a comparative study on the effect of different irrigants


against E. faecalis biofilms, both 6% and 1% NaOCl killed more than
99.7% of bac-teria after contact times of 1 or 5 minutes, while 2%
chlorhexidine and MTAD killed only 60.5% and 16% of the biofilm
bacteria respectively80. Therefore cur-rent evidence indicate that
NaOCl is distinctly more effective in rendering biofilm bacteria
nonviable and in physically removing the biofilm compared with other
26

ously root-filled teeth with apical periodontitis , E. faecalis is much


more resistant to NaOCl than the aforementioned microbes.
However, despite the re-duced effectiveness of NaOCl against E.
faecalis, NaOCl has the unique ability to disrupt or to remove

commonly used irrigants81.

The tissue-dissolution capability and the antimi-crobial efficiency as well


as the toxicity of NaOCl is dependent on the concentration of the
solution. The higher the concentration of the solution the greater the
cytotoxicity8284. A 5.25% NaOCl solution demonstrated greater
cytotoxicity than 0.5% or 1% NaOCl solutions83. Most in vivo studies
showed no significant difference in antibacterial activity between 0.5%,
1%, 2.5% and 5% solutions against both E. faecalis

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and a mixed

anaerobic flora47,49,85. Com-parative studies failed to show any significant


differ-ence in the tissue-dissolving ability between higher and lower
concentration NaOCl solutions86,87. In fact, based on laboratory
investigations, 1% NaOCl is sufficient for dissolving pulp tissue 88. The
tissue-dissolution capacity is reliant on regularly refreshing the irrigant
solution rather than the concentration of the solution. Therefore, the
NaOCl solution must be regularly replenished during treatment. In
summary,

Instead of using a more concentrated solution, the effectiveness of


NaOCl could be improved by increasing the temperature of a less
concentrated solution7. Several studies reported that warmed NaOCl
dissolved organic tissues significantly better than unheated solutions 86,88
91

. It was found that a 1% solution at 45C dissolved pulp tissue as effectively as 5.25% NaOCl at 20C, and a 1% solution at 60C was
significantly more effective than an un-heated full-strength solution 86.
Warmed solutions also exhibited significantly greater antimicrobial efficacy compared with unheated solutions. A 100-fold in-crease in the killing of
E. faecalis was observed be-tween corresponding NaOCl solutions (1%,
2.62%, and 5.25%) at 20C and at 45C86. It seems reason-able to use
lower concentration NaOCl solutions in order to ensure a good margin of
safety, but its ef-fectiveness may be improved by warming the solution7,88. It must be kept in mind that NaOCl solution once heated but not
used must be discarded, as its effectiveness will be exhausted90.

Ultrasonic activation of NaOCl is a very promising alternative approach to


improve the effectiveness of this irrigant. A detailed review of the use of
ultrasound for irrigation can be found in this issue of the journal.

NaOCl at concentrations between 0.5% and 1% is recommended for


routine clinical use4,7. These con-centrations represent the best
balance between tissue-dissolution capability, antimicrobial activity
and bio-compatibility. There is currently no convincing scien-tific
evidence for using NaOCl at higher concentra-tions or at full

The question of the duration required for irrigants to work optimally is still
open to debate. Unfortu-

strength (5.25%)4,7.

ENDO 2007;1(1):11-27

The volume of irrigant is also clinically relevant. The scientific evidence on this matter is
sparse. However, an increase in the volume of the irrigant used is corre-lated with a
reduction of intraradicular microorganisms and improved canal cleanliness 93,94.
Yamada et al73 recommended at least 1020 ml of irrigant for each canal, followed by a
final high volume flush after the shaping procedure has been completed (Table 1).

nately, data are limited7 and most studies are not representative of the clinical situation. In a biofilm mod-el
using C. albicans, both 1% and 5% NaOCl need-ed 60
minutes to kill all the microbes. After only 30 minutes,

The chemical stability and activity of NaOCl so-lutions may be adversely affected
by many fac-tors95. Piskin and Turkun95 conducted a study on the stability of
various NaOCl solutions and pointed out that all solutions showed degradation
with time. High-concentration NaOCl (5%) decom-posed far more rapidly when
stored at 24C com-pared with 0.5% NaOCl. Solutions containing 0.5% and 5%
chlorine stored at 4C displayed sat-isfactory stability at 200 days95. Therefore it is
rec-ommended to store NaOCl solutions in a refrigera-

both concentrations failed to remove the biofilm92.


These observations are in agreement with another
study assessing the effect of different irriga-tion
solutions on biofilms of root canal isolates79. It was
reported that 2.25% NaOCl solution required 60 minutes
of contact time to achieve a total elimi-nation of all
microorganisms, including E. faecalis79. Therefore for
effective biofilm removal, NaOCl should be allowed a
contact time of at least 30 to 60 minutes79,92.

Irrigation protocol

Size of apical preparation: at least size 35

After access cavity: flush the canals with NaOCl

Between instruments: 25 ml of NaOCl per canal


After shaping: 510 ml of NaOCl per canal
h

After shaping: irrigation with 5 ml of EDTA per canal for


1 minute (or with citric acid)

Final rinse with 2 ml NaOCl per canal

Optional: final irrigation with chlorhexidine


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Optional: rinse with alcohol before obturation


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Table 1 Suggested irrigation protocol.

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Fig 5 Ecchymosis due to accidentally injection of NaOCl be-yond the apex. Clinical situation
two weeks after this com-plication.

tor and in dark bottles to avoid degradation caused by light.


NaOCl is caustic if accidentally extruded into pe-riapical tissues or adjacent anatomical
structures such as the maxillary sinus96. In the case of accidental in-jection of NaOCl
into periapical tissues, emphysema may develop within 1020 minutes. Furthermore,
oedema and paraesthesia may result due to the tis-sue-dissolving capability of
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NaOCl96. An even more serious development is ecchymosis, which is associ-ated with


severe pain, profuse interstitial bleeding, and haemorrhage under the skin (Fig 5).
Fortunate-ly, most of these symptoms will regress within 2 weeks96. A more detailed
overview of complications occurring during root canal irrigation with NaOCl was

published by Hlsmann96.

Chlorhexidine
e

It is generally accepted that as an irrigant chlorhexi-dine gluconate (CHX) should be


used in a concentra-tion of 2%97,98. CHX has a wide antimicrobial spec-trum and is
effective against Gram-positive and Gram-negative bacteria as well as yeasts 4. CHX is
able to permeate the cell wall or outer membrane and attacks the bacterial cytoplasmic
or inner mem-brane or the yeast plasma membrane4.

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ENDO 2007;1(1):11-27

CHX solutions in concentrations of 0.22% are considered toxicologically safe 99,100. For
instance, a 2% solution has been used as a subgingival irrigant without any adverse
effects101. In an animal study on rats, the root canals of teeth with experimentally induced apical periodontitis were temporarily filled with 2% CHX gel 102. Histological
evaluations after 7 days

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revealed that the use of CHX resulted in good periapi-cal regeneration and no
102

indication of inflammation . These findings were supported by a histopathological


study on dogs, evaluating the periapical regeneration using 2% CHX as root canal

irrigation103. A more re-cent study also confirmed the biocompatibility of 2% CHX 104.
CHX was injected into the peritoneal cavity of mice and the inflammatory response
was evaluated. CHX was found to be biocompatible since this solution did not
induce a significant inflammatory response104.

Although sensitivity to CHX is rare65, there are reports that CHX has the
potential to cause anaphy-lactic reactions105 and even anaphylactic
shock65. Hypersensitivity reactions described in the literature include
contact dermatitis and photosensitivity. Both application of CHX to mucous
membranes and to intact skin can cause allergic reactions. Therefore it is
important to remember this potential risk of CHX.

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According to several in vitro studies, CHX has a marked antimicrobial effect on E.


faecalis after a short contact time even in comparatively low concentrations75,78,97,107. Under these in vitro conditions, CHX was better at killing E.
faecalis than NaOCl. CHX was also found to be a very effective antifungal agent. In
several studies, CHX was very effective in killing C. albicans under in vitro
conditions108111. These two microorganisms (E. faecalis and C. albi-cans) are
reported to be responsible for endodontic failures24,112,116 in approximately 75% of
retreatment cases associated with apical periodontitis. Since CHX is highly effective
against the Gram-positive bacteria and both E. faecalis and C. albicans, the use of
CHX is recommended for retreatment cases.

Due to its cationic properties, CHX can bind to dentine and enamel113,114 and is
gradually released over time. Owing to this phenomenon of substantiv-ity, which has
not been observed with any other irri-gant, CHX has prolonged antimicrobial
activity7,60. After 10 minutes of irrigation, a prolongation of the antimicrobial effect of
about 12 weeks was ob-served115. Hence, CHX is the only irrigant whose antimicrobial effect outlasts the duration of irrigation.
h

Although not yet fully understood, the combina-tion of CHX and hydrogen
peroxide was reported to be better at killing E. faecalis in dentinal tubules compared with NaOCl or CHX alone116. In a further study, the observation of
synergistic effect was sup-

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thanzfor

E. faecalis in concentrations much lowere

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each component alone117. Although this synergistic


mechanism of CHX and hydrogen peroxide has not been
elucidated in detail, it may be speculated that CHX denatures
the bacterial cell walls and creates pores in the membrane,
resulting in a more perme-able cell wall117, which then allows
hydrogen perox-ide to penetrate the microbes and damage
intracel-lular organelles such as DNA 117. A similar synergistic
effect has also been shown for CHX and hydrogen peroxide
when used as an antiplaque mouth rinse118. However, there
are no clinical studies at present that have investigated the
potential synergistic effect of these irrigants against
intraradicular microbes4. Since a combination of CHX and
carbamide peroxide was found to be additive in their
u

cytotoxicity119, an as-sessment of the biocompatibility of this


combination is urgently required before any clinical
recommenda-tions are made4.

killed all

ported, as the two irrigants in combinationi

Unlike NaOCl, CHX does not possess any tissuedissolving ability4,120, and is unable to remove the smear
layer or neutralise lipopolysaccharides, which are obvious
benefits of NaOCl. It is only because of these differences
that CHX cannot be a substitute for NaOCl as the gold
standard of root canal irrig-ants. Also, CHX seems to be
less effective against Gram-negative bacteria (which

predominate in pri-mary endodontic infection)121. Further weaknesses of CHX


include its susceptibility to the presence of organic material; the antimicrobial
effect of CHX is strongly reduced by the presence of dentine, in-flammatory
exudates, serum albumin, dentine ma-trix, and heat-killed cells of E. faecalis
and C. albi-cans58,122124. These findings may explain the poor in vivo
performance of CHX compared with in vitro re-sults4. As yet, there have been
no controlled clinical studies on CHX to show increased antimicrobial ac-tivity
against E. faecalis compared with NaOCl. In a randomised clinical trial, 2.5%
NaOCl was signifi-cantly more effective than 0.2% CHX77. Direct con-tact

ENDO 2007;1(1):11-27

between NaOCl and CHX should be avoided, otherwise


red CHX crystals will precipitate immedi-ately (Fig 6).

In summary, a 2% CHX solution is an alternative ir-rigant


because of its potent antimicrobial activity4, but it certainly
cannot replace NaOCl. CHX is useful as a final flush (Table
1)7,60 in retreatment-cases.

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alone. In other words, the combination of the solui

tions killed E. faecalis in concentrations much lower


t

ssen

than each irrigant could alone116,117. Certainly this topic warrants further investigation as the mecha-nism has yet to be fully
understood4.

In conclusion, there is no scientific evidence indi-cating that H2O2 may be superior to other irrigants4.
concentration between 3% and 5% is preferred. Solutions of H2O2 are
chemically stable and H2O2 is active against bacte-ria, yeasts, and

viruses4 due to the production of hy-droxy free radicals ( OH). These


radicals attack sev-eral cell components such as proteins and DNA 4,59.

The antimicrobial efficiency and the tissue-dis-solving capacity of


Fig 6 Precipitation of chlorhexidine when mixed with NaOCl.

Hydrogen peroxide

H2O2 are poor in comparison with NaOCl. It was previously


thought that an irri-gation protocol employing NaOCl and H2O2
alter-nately could have beneficial effects on canal clean-liness and
reduce intraradicular microorganisms, but this has not been
substantiated scientifically. Sever-al studies showed that a
combination of NaOCl and H2O2 resulted in a marked reduction in
both the tis-sue dissolution capacity and the antibacterial effi-

Hydrogen peroxide (H2O2) is used in dentistry in various


concentrations ranging from 1% to 30%4. For endodontic treatment, a

ciency of NaOCl116,125. In fact, a combination of these two solutions


resulted in a bubbling effect as a result of the chemical reaction.

Oxygen evapo-rates from the aqueous peroxide and NaOCl reacts

There seems to be some evidence that IPI is effec-tive against E.

with sodium chloride126, rendering both irrigation solutions useless.

faecalis28,129 and biofilms of root canal isolates79. At the same time, the
biocompatibility of this irrigant is good since iodine compounds are less
cytotoxic and irritating to vital tissues than other com-monly used

H2O2 + NaOCl O2 + H2O + NaCl

Although there is no obvious synergism between H2O2 and


NaOCl, a combination including H2O2 has been reported to be
promising. Recent studies on combining CHX and H2O2 at low
concentrations found significantly greater antimicrobial activity
against E. faecalis than the tested medicaments

irrigants82,128. However, there are two main problems associated with


the clinical use of io-dine compounds as a root canal irrigant. Firstly,
iodine is a very potent allergen so there is a high risk of an al-lergic
reaction. Secondly, substances commonly found in the root canal
inhibit the antimicrobial efficiency of iodine. For example, dentine
powder, organic dentin matrix, heat-killed cells of E. faecalis and C.

albicans displayed an inhibitory effect on both 0.2% and 0.4% IPI122,129.


A minor problem is that iodine has also the potential to stain dentine.
For these reasons, IPI can-not be considered an irrigant of first choice.

MTAD
Iodine compounds

Iodine can penetrate into microorganisms and at-tacks cell molecules


such as proteins, nucleotides, and fatty acids4, resulting in cell death.
Iodine com-pounds are bactericidal, fungicidal and virucidal4. Since
aqueous iodine solutions are unstable, and mo-lecular iodine (I2)
displays the most marked antimi-crobial activity, iodine potassium
iodine (IPI) is used (2% iodine in 4% potassium iodine) in
endodontics4.

MTAD is a mixture of tetracycline (doxycycline, 3%), citric acid


(4.25%), and detergent (Tween 80, 0.5%), with a pH of 2.15;
the commercial product is Biop-ure (Tulsa Dentsply, Tulsa OK,
USA). When assessing the properties of MTAD on the basis of
the current-ly available literature, it should be kept in mind that
most of the studies conducted on MTAD were per-formed by its
creators, Mahmoud Torabinejad and co-workers.

MTAD was reported to be effective in remov-ing the smear layer


due to its low pH, and showed

ENDO 2007;1(1):11-27

When introducing a new irrigant, the key require-ment is its


antimicrobial efficiency. Some studies found that MTAD has

20

Schfer Root canal irrigation

a good antibacterial activity against E. faecalis135137, but this


was not supported by other investigations. NaOCl solutions
(5%) and CHX were both more effective against E. faecalis
and C. albicans than MTAD138,139. Both 1% and 6% NaOCl
were found to be more efficient in eliminat-ing E. faecalis
biofilms than MTAD80; this has been supported by another

tissue-dissolving action as long as the canal was rinsed with NaOCl during
mechanical prepara-tion130,131. It is interesting that MTAD displayed good
tissue-dissolving capability only when NaOCl was used during
instrumentation131. Therefore, the clinical recommendation is to use 1.3%
NaOCl during instrumentation, followed by MTAD as a fi-nal irrigation. MTAD
seems to be less cytotoxic than 3% H2O2, 5.25% NaOCl, CHX mouth wash,
and EDTA, but more cytotoxic than 2.63% and 1.31% NaOCl132. Moreover,
MTAD seems to ad-versely influence the physical properties of dentine or the
bonding strength of adhesives to den-

recently published report81. In this study, the intraradicular


content from 10 extract-ed teeth associated with a chronic
apical periodonti-tis was collected and cultured on sections
of root apices to generate a polymicrobial biofilm. The sections were immersed in 6%, 3%, and 1% NaOCl, 2%
chlorhexidine, sterile phosphate buffered solu-tion, and 1%
NaOCl followed by MTAD. While 6% and 3% NaOCl were
able to disrupt and remove the biofilm, 1% NaOCl and 1%
NaOCl followed by MTAD were capable of disrupting the
biofilm but not eliminating the bacteria. Chlorhexidine was
not ca-pable of disrupting the biofilm. Viable bacteria were
not found in sections immersed in 6% NaOCl, 2%
chlorhexidine, and 1% NaOCl followed by MTAD. The
authors concluded that 6% NaOCl was the only irrigant
capable of both rendering bacteria nonviable and physically
removing the biofilm81.

tine133,134.
A preliminary report found the alternating use of NaOCl and
MTAD might potentially cause iatrogenic tetracycline staining

of teeth140. Another concern is the high concentration of tetracycline in MTAD; resistance to tetracycline is not uncommon among bac-teria isolated from root
canals141. In fact, a higher in-cidence of tetracycline-resistant bacteria must be
ex-

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Phenolic compounds

These irrigants are relatively ineffective under clinical

of antibi-

pected in future years. The local applicationi

conditions142, and from reports of numerous studies there


is clear scientific evidence that solutions con-taining
camphorated paramonochlorophenol are ir-ritating and
display toxic effects on healthy tis-sues82,143,144. The
application of these irrigants in the root canal results in
systemic distribution145. In gen-eral, phenolic compounds
are assessed as incompat-ible with a biologic approach
to endodontic treat-ment146.

Therefore, phenolic compounds must be seen as


obsolete147 and will not be discussed further in this
review.

vorbehalten

Irrigation solutions to remove the


smear layer
t

EDTA

otics must be viewed very critically, as theespectrumsz

Ethylenediaminetetraacetic acid (EDTA) as a 17%


solution (pH 7) effectively removes the smear layer by
chelating the inorganic components of the den-tine4,148.
EDTA has almost no antibacterial activity4, is highly
biocompatible, can demineralise intertubu-lar dentine
and reduces the surface hardness of root canal wall
dentine7,149. Some caution should be ex-ercised when
using EDTA inside root canals because prolonged

ssen

of some antibiotics are narrower than commonly used antimicrobial


irrigating solutions7,59. According to Zehnder, the use of antibiotics
instead of biocides such as hypochlorite or chlorhexidine appears unwarranted7.

ENDO 2007;1(1):11-27

exposure to EDTA may weaken root den-tine150 and


thereby increase the risk of creating a per-foration during
mechanical root canal instrumenta-tion.

According to the results of preliminary studies, irrigation


of the root canal using alternately NaOCl and EDTA
appears to be very promising151. This combination seems
to enhance the tissue-dissolution capability of
NaOCl151,152 and is more

efficient in reducing intraradicular microbes than


NaOCl alone49. EDTA retains its calcium-complexing
ability when mixed with NaOCl, but EDTA causes

NaOCl to lose its tissue-dissolving capacity155.


Therefore EDTA and NaOCl should be used
separately and EDTA should never be mixed with
NaOCl7,153. Furthermore, chelating agents like EDTA
can disrupt the biofilm adhering to the root canal
wall7,154. After irrigation of the canals with EDTA, 2 ml
of NaOCl should be finally used to neutralise the
acidic effects of EDTA and to allow NaOCl to
penetrate into the dentinal tubules, which are opened
after the use of EDTA.

Schfer Root canal irrigation

Citric acid

Concentrations ranging from 140% have been used in


endodontics to remove the smear layer after root canal
preparation (Fig 7). Compared with EDTA, 10% citric acid
seems to be more effective in remov-ing the smear

layer155,156 and in dissolving powdered dentine157.


Moreover, citric acid solutions display an-timicrobial
effects157, although it is questionable whether or not this
property might have any clinical significance. In contrast,
other studies have failed to show a significant difference
between EDTA and cit-ric acid in removing the smear
layer158,159. As citric acid demineralises the intertubular
dentine around the opening of the tubules, they are
enlarged148.
t21

In summary, both EDTA and citric acid can re-move the


smear layer effectively4,148. The removal of the smear
layer is a crucial step to facilitate disinfec-

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embedded in the smear layer are eliminated and


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canal cleanliness is improved. Secondly, it has been shown that the removal of
the smear layer improves the antimicrobial effect of intraradicular medica-ments
in the deeper layer of dentine34,160. Therefore, either EDTA or citric acid should
be included in the ir-rigation regimen (Table 1).

Irrigants for drying the root canal


tion of the root canal system. Firstly, microorganisms
i

Rinsing the root canal with alcohol before obturation has been anecdotally
practised161. The basic premise is that alcohol reduces the surface tension of
irrigants and root canal sealers162. Lowering the surface ten-sion of a fluid or a
sealer will increase the fluid flow into the dentinal tubules. Thus alcohol will spread
into the dentinal tubules and dry the root canal as it evaporates. Therefore alcohol
might affect sealer penetration and leakage of the root canal filling. In a recently
published study it was shown that a final rinse with 95% alcohol before root canal
obturation resulted in increased sealer penetration and conse-quently decreased
leakage161. This is in agreement with another study demonstrating that a final rinse
with alcohol allowed better sealer coverage than dry-ing with paper points 163.

Therefore a final rinse of approximately 3 ml of 95% ethyl alcohol per


canal can be recommended in order to improve the sealing ability of the
root canal filling (Table 1).

Fig 7 Opened dentinal tubules of root canal dentine: the smear layer was removed with citric acid.

ENDO 2007;1(1):11-27
8

of the working length.

22

Schfer Root canal irrigation

py

Fig 8 Flexible 30-gauge irrigation nee-dles with safety tips


(NaviTips, Ultradent, Munich, Germany).

Fig 9 Curved root canal enlarged with rotary nickel-titanium


FlexMaster (VDW, Munich, Germany) to an apical size of 02/35.
Even in this curved canal a pre-bent 30-gauge needle can be
inserted

to about 12 mm short

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g

vorbehalten
h

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b
9

Clinical and technical aspects of irrigation

The most important technical aspect of root canal irri-gation is the


correlation between the diameter of the irrigating needle and the apical
preparation size. Inside the root canal the effect of irrigation is limited
to 34 mm apical from the needle tip. In an in vitro study, it was shown
that the introduction of an irrigation nee-dle 1 mm short of working
length resulted in signifi-cantly fewer remaining bacteria in the root

canal com-pared with using a needle 6 mm short of the working


length164. The aim is to introduce the needle as near as possible to
working length to improve the irrigation efficiency. Since the smallest
needle recommended for root canal irrigation is a 30-gauge needle
(Fig 8) (di-ameter of 0.3 mm, corresponding to ISO size 30), the apical
preparation should be size 35 to 407,165. Even in severely curved
canals, an apical preparation of size 35 to 40 can be achieved with
modern rotary nickel-tita-nium instruments without the risk of canal
aberrations or canal straightening166,167. Flexible irrigation needles with
a safety tip are recommended, so that the needle can be pre-bent
according to the canal curvature to al-low proper cleaning of the apical
part of curved root canals (Fig 9).

When trying to insert the needle tip as close as possible to the working
length, the needle might be-come jammed in the root canal and the
pressure ex-erted can easily result in extrusion of NaOCl or H2O2 into
the periapical tissue. Hence when resistance to the needle is felt, it
should be pulled back approxi-mately 2 mm to ensure space between
the canal wall and needle to allow the irrigant to flow out of the

canal (Fig 10). This will minimise the risk of injecting


irrigation solutions beyond the apex and into the periapical
tissue.
Based on this review, the following irrigation pro-tocol is
suggested (Table 1)4,7:
Apical root canal preparation should be to at least size 35
and a 30-gauge needle should be used.
After access cavity preparation: flush the cavity and the canals with
NaOCl. Canals must always be filled with NaOCl because this will
increase work-ing time available for the irrigant. At the same time,
cutting efficiency of root canal instruments is enhanced due to the
lubrication effect168.

Fig 10 When introducing the irrigation needle there must be enough space
between the canal wall and the needle to allow the irrigant to flow out of the
root canal.

ENDO 2007;1(1):11-27

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Between instruments: 25 ml of NaOCl per canal.


13.
u

Chugal NM, Clive JM, Spngberg LS. A prognostic modeli

for assessment of the outcome of endodontic treatment:n

NaOCl should always be employed throughout

effect of biologic and diagnostic variables. Oral Surg Oral


t

mechanical root canal preparation.

Med Oral Pathol 2001;91:342-352.

ssen

14.

After root canal shaping: 510 ml of NaOCl per

Sjgren U, Figdor S, Persson S, Sundqvist G. Influence of in-

fection at the time of root filling on the outcome of en-

canal. When the shaping procedure is complet-

dodontic treatment of teeth with apical periodontitis. Int

ed, flush with a high volume of NaOCl73.

Endod J 1997;30:297-306.

15.
Katebzadeh N, Sigurdsson A, Trope M. Radiographic eval-

After shaping: irrigation with 5 ml of EDTA per

uation of periapical healing after obturation of infected root

canal for 1 minute (or with citric acid). After a fi-

canals: an in-vivo study. Int Endod J 2000;33:60-66.

16.
Kvist T, Molander A, Dahlen G, Reit C. Microbiological eval-

nal rinse of NaOCl, the canals should be irrigat-

uation of one- and two-visit endodontic treatment of teeth

ed with either EDTA or citric acid to remove the

with apical periodontitis: a randomized, clinical trial. J

Endod 2004;30:572-576.

smear layer.

17.
Peters LB, van Winkelhoff AJ, Buijs JF, Wesselink PR. Effects

Final rinse: irrigation with 2 ml of NaOCl per canal

of instrumentation, irrigation and dressing with calcium hy-

droxide on infection in pulpless teeth with periapical bone

to neutralise the acidic effect of EDTA and to al-

lesions. Int Endod J 2002;35:13-21.

low NaOCl to penetrate into the opened tubules.


18.
Fabricius L, Dahlen, G, Holm SE, Mller AJ. Influence of

Optional, final irrigation especially in retreat-

combinations of oral bacteria on periapical tissues of mon-

keys. Scand J Dent Res 1982;90:200-206.

ment cases: chlorhexidine. Rinse with water to re19.


Fabricius L, Dahlen, G, Ohman AE, Mller AJ. Predominant

move NaOCl and then with a 2% chlorhexidine

indigenous oral bacteria isolated from infected root canals

after varied times of closure. Scand J Dent Res

solution.
20.
1982;90:134-144.

Optional, before root canal filling: rinse with 3 ml

Sundqvist G. Taxonomy, ecology, and pathogenicity of the

root canal flora. Oral Surg Oral Med Oral Pathol

of alcohol per canal to dry the root canal.

1994;78:522-530.

21.
Baumgartner JC, Falkler WA. Bacteria in the apical 5 mm of

infected root canals. J Endod 1991;17:380-383.

22.

Gomes BPFA, Lilley JD, Drucker DB. Clinical significance of

dental root canal microflora. J Dent 1996;24:47-55.

23.
Nair PN. Pathogenesis of apical periodontitis and the cause

of endodontic failures. Crit Rev Oral Biol Med

2004;15:348-381.

24.
Waltimo TM, Siren EK, Torkko HL, Olsen I, Haapasalo MP.

References

Fungi in therapy-resistant apical periodontitis. Int Endod J

1997;30:96-101.

Bergenholtz G. Pathogenic mechanisms in pulpal disease. J 25. Molander A, Reit C, Dahlen G, Kvist T. Microbiological staLangeland K. Tissue response to dental caries. Endod Dent Traumatol
1987;3:149-171.
Endod 1990;16:98-101.

tus of root-filled teeth with apical periodontitis. Int Endod J 1998;31:1-7.


Jontell M, Okiji T, Dahlgren U, Bergenholtz G. Immune de-fence
mechanisms of the dental pulp. Crit Rev Oral Biol Med 1998;9:179-200.
Peciuliene V, Reynaud A, Balciuniene I, Haapasalo M. Isolation of yeasts
and enteric bacteria in root-filled teeth with chronic apical periodontitis. Int
Endod J 2001;34: 429-434.
Haapasalo M, Endal U, Zandi H, Coil J. Eradication of en- 27. Peciuliene V, Balciuniene I, Eriksen HM, Haapasalo M.
Walker A. A definite and dependable therapy for pulpless teeth. J Am Dent
Assoc 1936:23:1418-1425.
dodontic infection by instrumentation and irrigation solu-tions. Endodontic
Topics 2005;10:77-102.

Hahn CL, Best AM, Tew JG. Cytokine induction by Streptococcus mutans
and pulpal pathogenesis. Infect Immun 2000;68:6785-6789.

Trope M, Bergenholtz G. Microbiological basis for en-dodontic treatment: can a


maximal outcome be achieved in one visit? Endodontic Topics 2002;1:40-53.

Zehnder M. Root canal irrigants. J Endod 2006;32:489-398.

Kakehashi S, Stanley H, Fitzgerald R. The effects of surgical exposures of


dental pulps in germ-free and conventional laboratory rats. Oral Surg Oral
Med Oral Pathol 1965;20:340-349.

Bergenholtz G. Micro-organisms from necrotic pulp of trau-matized teeth.


Odontol Revy 1974:25:347-358.

Sundqvist G. Bacteriological studies of necrotic dental pulps. Ume


University Odontological Dissertation No. 7. Sweden: University of Ume,
1976.

Siqueira JF. Endodontic infections: concepts, paradigms, and perspectives.


Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;94:281-293.

Nair PN. Light and electron microscopic studies of root canal flora and
periapical lesions. J Endod 1987;13: 29-39.

Isolation of Enterococcus faecalis in previously root-filled canals in a


Lithuanian population. J Endod 2000: 26: 593-595.

Costerton JW, Lewandowski Z, DeBeer D, Caldwell D, Korber D, James G.


Biofilms, the customized microniche. J Bacteriol 1994;176:2137-2142.

Siqueira JF Jr. Rocas IN. Polymerase chain reaction-based analysis of


microorganisms associated with failed endodon-tic treatment. Oral Surg
Oral Med Oral Pathol Oral Radiol Endod 2004;97:85-94.

Wilson M. Susceptibility of oral bacterial biofilms to antimi-crobial agents. J


Med Microbiol 1996;44:79-87.

Haapasalo M, Udnaes T, Endal U. Persistent, recurrent and acquired infection of


the root canal system posttreatment. Endodontic Topics 2003;6:29-56.

ENDO 2007;1(1):11-27

Shovelton DH. The presence and distribution of microorgan-isms within non-vital


teeth. Br Dent J 1964;117:101-107.

rstavik D, Haapasalo M. Disinfection by endodontic irrig-ants and dressings of


experimentally infected dentinal tubules. Endod Dent Traumatol 1990;6:142-149.

py

Alle

24
Schfer Root canal irrigation

Rechte

35.

Peters LB, Wesselink PR, Moorer WR. Penetration of bacteria


57.
u

Rollinson S, Barnett F, Stevens RH. Efficacy of bacterial re-

in bovine root dentine in vitro. Int Endod J 2000;33:28-36.

moval from instrumented root canals innvitro relatedvorbehaltento in-

36.
Peters LB, Wesselink PR, Buijs JF, Van Winkelhoff AJ. Viable

strumentation technique and size. Oral SurgeOral MedzOral

bacteria in root dentinal tubules of teeth with apical peri-

Pathol Oral Radiol Endod 2002;94:366-371.

ssen

odontitis. J Endod 2001;27:76-81.


58.
Siqueira JF Jr, Rocas IN, Santos SR, Lima KC, Magalhaes FA,

37.
Love RM, Jenkinson HF. Invasion of dentinal tubules by oral

de Uzeda M. Efficacy of instrumentation techniques and ir-

bacteria. Crit Rev Oral Biol Med 2002;13:171-183.

rigation regiments in reducing the bacterial population

38.
Nair SP, Meghji S, Wilson M, Reddi K, White P, Henderson

within root canal. J Endod 2002;28:181-184.

B. Bacterially induced bone destruction: mechanisms and


59.
McDonnell G, Russell D. Antiseptics and disinfectants: ac-

misconceptions. Infect Immun 1996;64:2371-2380.

tivity, action, and resistance. Clin Microbial Rev

39.
Dwyer TG, Torabinejad M. Radiographic and histologic

1999;12:147-179.

evaluation of the effect of endotoxin on the periapical tis-60. Frais S, Ng YL, Gulabivala K. Some factors affecting the

sues of the cat. J Endod 1981;7:31-35.

concentration of available chlorine in commercial sources of

40.
Schein B, Schilder H. Endotoxin content in endodontically

sodium hypochlorite. Int Endod J 2001;34:206-215.

involved teeth. J Endod 1975;1:19-21.


61.
Zehnder M, Kosicki D, Luder H, Sener B, Waltimo T. Tissue-

41.
Dahln G, Bergenholtz G. Endotoxin activity in teeth with

dissolving capacity and antibacterial effect of buffered and

necrotic pulp. J Dent Res 1980;59:1033-1040.

unbuffered hypochlorite solutions. Oral Surg Oral Med

42.
Grandini S, Balleri P, Ferrari M. Evaluation of Glyde File Prep

Oral Pathol Oral Radiol Endod 2002;94:756-762.

in combination with sodium hypochlorite as a root canal ir-62. Kaufman AY, Keila S. Hypersensitivity to sodium hypochlo-

rigant. J Endod 2002;28:300-303.

rite. J Endod 1989;15:224-226.

43.
West JD, Roane JB, Goerig AC. Cleaning and shaping the
63.

Caliskan MK, Turkun M, Alper S. Allergy to sodium

root canal system. In: Cohen S, Burns RC (eds). Pathways

hypochlorite during root canal therapy: a case report. Int

of the Pulp. 6th ed. St. Louis, USA: Mosby Year Book,

Endod J 1994;27:163-167.

1994.
64.
Dandakis C, Lambrianidis T, Boura P. Immunologic evalua-

44.
Hess W. Zur Anatomie der Wurzelkanle des menschlichen

tion of dental patient with history of hypersensitivity reac-

Gebisses mit Bercksichtigung der feinen Verzweigungen

tion to sodium hypochlorite. Endod Dent Traumatol

am Foramen apikale. Schweiz Vierteljahresschr Zahnheilk

2000;16:184-187.

1917;1:1-53.
65.
Naenni N, Thoma K, Zehnder M. Soft tissue dissolution ca-

45.
Peters OA. Current challenges and concepts in the preparation

pacity of currently used and potential endodontic irrigants.

of root canal systems: a review. J Endod 2004;30:559-567.

J Endod 2004;30:785-787.

46.
Dammaschke T, Witt M, Ott K, Schfer E. Scanning elec66.
Baumgartner JC, Mader CL. A scanning electron microscop-

tron microscopic investigation of incidence, location, and

ic evaluation of four root canal irrigation regimens. J Endod

size of accessory foramina in primary and permanent mo-

1987;13:147-157.

lars. Quintessence Int 2004;35:699-705.


67.
Gutierrez JH, Jofre A, Villena F. Scanning electron micro-

47.
Bystrm A, Sundqvist G. Bacteriologic evaluation of the ef-

scope study on the action of endodontic irrigants on bacte-

fect of 0.5 percent sodium hypochlorite in endodontic ther-

ria invading the dentinal tubules. Oral Surg Oral Med Oral

apy. Oral Surg Oral Med Oral Pathol 1983;55:307-312.

Pathol 1990;69:491-501.

48.
Bystrm A, Sundqvist G. Bacteriologic evaluation of the ef68.
Haikel Y, Gorce F, Allemann C, Voegel JC. In vitro efficien-

ficacy of mechanical root instrumentation in endodontic

cy of endodontic irrigation solutions on protein desorption.

therapy. Scand J Dent Res 1981;89:321-328.

Int Endod J 1994;27:16-20.

49.
Bystrm A, Sundqvist G. The antibacterial action of sodium
69.
Andersen M, Lund A, Andreasen JO, Andreasen FM. In vitro

hypochlorite and EDTA in 60 cases of endodontic therapy.

solubility of human pulp tissue in calcium hydroxide and sodi-

Int Endod J 1985;18:35-40.

um hypochlorite. Endod Dent Traumatol 1992;8:104-108.

50.
Nair PW, Henry S, Cano V, Vera J. Microbial status of apical
70.
Silva IA, Leonardo MR, Assed S, Tanomaru Filho M.

root canal system of human mandibular first molars with

Histological study of the effect of some irrigating solutions

primary apical periodontitis after one-visit endodontic

on bacterial endotoxin in dogs. Braz Dent J 2004;15:109-

treatment. Oral Surg Oral Med Oral Pathol Oral Radiol

114.

Endod 2005;99:231-252.
71.
Sarbinoff JA, OLeary TJ, Miller CH. The comparative effec-

51.
Dalton BC, rstavik D, Phillips C, Pettiette M, Trope M.

tiveness of various agents in detoxifying diseased root sur-

Bacterial reduction with nickel-titanium rotary instrumenta-

faces. J Periodontol 1983;54:77-80.

tion. J Endod 1998;24:763-767.

72.
Buttler TK, Crwawford JJ. The detoxifying effect of varying

52.
rstavik D, Kerekes K, Molven O. Effects of extensive api-

concentrations of sodium hypochlorite on endotoxins. J

cal reaming and calcium hydroxide dressing on bacterial in-

Endod 1982;8:59-66.

fection during treatment of apical periodontitis: a pilot


73.
Yamada RS, Armas A, Goldman M, Lin PS. A scanning elec-

study. Int Endod J 1991;24:1-7.

tron microscopic comparison of a high volume final flush

53.
Chuste-Guillot MP, Badet C, Peli JF, Perez F. Effect of nick-

with several irrigating solutions: Part 3. J Endod

el-titanium rotary file techniques on infected root dentin re-

1983;9:137-142.

duction. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
74.
McComb D, Smith DC, Beagrie GS. The results of in vivo

2006;102:254-258.

endodontic chemomechanical instrumentation: a scan-

54.
Siqueira JF Jr, Lima KC, Magalhaes FA, Lopes HP, de Uzeda

ning electron microscopy study. J Br Endod Soc

M. Mechanical reduction of the bacterial population in the

1976;9:11-18.

root canal by three instrumentation techniques, J Endod


75.
Waltimo TM, rstavik D, Siren EK, Haapasalo MP. In vitro

1999;25:332-335.

susceptibility of Candida albicans to four disinfectants and

55.
Pataky L, Ivanyi I, Grigar A, Fazekas A. Antimicrobial effica-

their combinations. Int Endod J 1999;32:421-429.

cy of various root canal preparation techniques: an in vitro


76.
Radcliffe CE, Potouridou L, Quereshi R, Habahdeh N,

comparative study. J Endod 2002:28:603-605.

Qualthrough A, Worthington H, Drucker DB. Antimicrobial

56.
Shuping GB, rstavik D, Sirgurdsson A, Trope M.

activity of varying concentrations of sodium hypochlorite

Reduction of intracanal bacteria using nickel-titanium ro-

on the endodontic microorganisms Actinomyces israelii, A.

tary instrumentation and various medications. J Endod

maeslundii, Candida albicans and Enterococcus faecalis.

2000;26:751-755.

Int Endod J 2004;37:438-446.

ENDO 2007;1(1):11-27
Dunavant TR, Regan JD, Glickman GN, Solomon ES, Honeyman AL. Comparative
evaluation of endodontic irri-gants against Enterococcus faecalis biofilms. J Endod
2006;32:527-531.

Clegg MS, Vertucci FJ, Walker C, Belanger M, Britto LR. The effect of exposure to irrigant solutions
on apical dentin biofilms in vitro. J Endod 2006;32:434-437.

Vianna ME, Gomes BP, Berber VB, Zaia AA, Ferraz CC, de
Souza-Filho FL. In vitro evaluation of the antimicrobial activity
of chlorhexidine and sodium hypochlorite. Oral Surg Oral Med
Oral Pathol Oral Radiol Endod 2004;97:79-84.

Gomes BP, Ferraz CC, Vianna ME, Berber VB, Teixeira FB, de
Souza-Filho FJ. In vitro antimicrobial activity of several
concentrations of sodium hypochlorite and chlorhexidine gluconate
in the elimination of Enterococcus faecalis. Int Endod J
2001;34:424-428.

Spratt DA, Pratten J, Wilson M, Gulabivala K. An in vitro


evaluation of the antimicrobial efficacy of irrigants on biofilms of
root canal isolates. Int Endod J 2001;34:300-307.

Spngberg L, Engstrm B, Langeland K. Biologic effects of dental materials. 3. Toxicity and


antimicrobial effect of en-dodontic antiseptics in vitro. Oral Surg Oral Med Oral Pathol
1973;36:856-871.

Pashley EL, Birdsong, NL, Bowman K, Pashley DH. Cytotoxic effects of NaOCl on vital
tissue. J Endod 1985;11:525-528.

Chang YC, Huang FM, Tai KW, Chou MY. The effect of sodium hypochlorite and
chlorhexidine on cultured human periodontal ligament cells. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 2001;92:446-450.

Cvek M, Nord CE, Hollender L. Antimicrobial effect of root canal debridement in teeth with
immature root: a clinical and microbiologic study. Odontol Revy 1976;27:1-10.

Sirtes G, Waltimo T, Schaetzle M, Zehnder M. The effects of


temperature on sodium hypochlorite short-term stability, pulp
dissolution capacity, and antimicrobial efficacy. J Endod
2005;31:669-671.

py
Moorer WR, Wesselink PR. Factors promoting the tissue
dissolving capability of sodium hypochlorite. Int Endod J
1982;15:187-196.

Cunningham WT, Balekjian AY. Effect of temperature on


collagen-dissolving ability of sodium hypochlorite en-dodontic
irrigant. Oral Surg Oral Med Oral Pathol 1980;49:175-177.

Kamburis JJ, Barker TH, Barfield RD, Eleazer PD. Removal of


organic debris from bovine dentin shavings. J Endod
2003;29:559-561.

Cunnigham WT, Joseph SW. Effect of temperature on the


bactericidal action of sodium hypochlorite endodontic ir-rigant.
Oral Surg Oral Med Oral Pathol 1980;50:569-571.

Abou-Rass M, Oglesby SW. The effects of temperature,


concentration, and tissue type on the solvent ability of sodi-um
hypochlorite. J Endod 1981;7:376-377.

Sen BH, Safavi KE, Spngberg LS. Antifungal effects of sodium hypochlorite and chlorhexidine in root canals. J Endod
1999;25:235-238.

Baker NS, Eleazer PD, Overbach RD, Seltzer S. Scanning electron


microscopic study on the efficacy of various irriga-tion solutions. J
Endod 1975;1:127-135.

Sedgley CM, Applegate B, Nagel AC, Hall D. Real-time im-aging


and quantification of bioluminescent bacteria in root canals in vitro.
J Endod 2004;30:893-898.

Piskin B, Turkun M. Stability of various sodium hypochlorite


solutions. J Endod 1995;21:253-255.
g

Hlsmann M, Hahn W. Complications during root canal irrigation: literature review and case reports. Int Endod J
2000;33:186-193.

Schfer Root canal irrigation

25

vorbehalten
Alle

Rechte

97.

Schfer E, Bssmann K. Antimicrobial efficacy of chlorox-

ylenol and chlorhexidine in the treatment of infected root

phylaxis: case report and review of the literature. Contact

canals. Am J Dent 2001;14:233-237.

Dermatitis 2004;50:113-116.

99.
98.

Yesilsoy C, Whitaker E, Cleveland D, Phillips E, Trope M.

Krautheim AB, Jermann TH, Bircher AJ. Chlorhexidine ana-

ssen

Antimicrobial and toxic effects of established and potential

root canal irrigants. J Endod 1995;21:513-515.

periodontal pickets. J Periodontol 1989;60:302-309.

101.
100. Southard SR, Drisko CL, Killoy WJ, Cobb CM, Tira DE. The

effect of 2.0% chlorhexidine digluconate irrigation on clin-

ical parameters and the level of Bacteroides gingivales in

Schfer E, Bssmann K. Antimicrobial efficacy of chlorhexi-

dine and two calcium hydroxide formulations against

Enterococcus faecalis. J Endod 2005;31:53-56.

102.
Dammaschke T, Schneider U, Stratmann U, Mokrys K, Yoo

103.
Tanomaru Filho M, Leonardo MR, Silva LAB, Anibal FF,

JM, Schfer E. Effect of root canal dressings on the repair of


Facciolo LH. Inflammatory response to different endodon-

inflamed periapical tissue. Acta Odontol


Scand

tic irrigation solutions. Int Endod J 2002;35:735-739.

104.
2005;63:143-152.

Zamany A, Safavi K, Spngberg LS. The effect of chlorhex-

idine as an endodontic disinfectant. Oral Surg Oral Med


allergy. Acta Anaesthesiol Scand 2001;45:1290-1294.

Oral Pathol Oral Radiol Endod 2003;96:578-581.

106.
Basrani B, Santos JM, Tjaederhane L, Grad H, Gorduysus O,

105.
Garvey LH, Roed-Petersen J, Husum B. Anaphylactic reac-

Huang J et al. Substantive antimicrobial activity in chlorhex-

tions in anaesthetised patients: four cases of chlorhexidine

idine-treated human root dentin. Oral Surg Oral Med Oral

Pathol Oral Radiol Endod 2002;94:240-245.

108.
Tanomaru Filho M, Leonardo MR, da Silva LAB. Effect of ir-

107.
Oncag O, Hosgor M, Hilmioglu S, Zekioglu O, Eronat C,

rigation solution and calcium hydroxide root canal dressing

Burhanoglu D. Comparison of antibacterial and toxic effects

on the repair of apical and periapical tissues of teeth with

of various root canal irrigants. Int Endod J 2003;36:423-432.

periapical lesion. J Endod 2002;28:295-299.

110.
Hamers AD, Shay K, Hahn BL, Sohnle PG. Use of a mi-

109.
Barkvoll P, Attramadal A. Effect of nystatin and chlorhexicrotiter plate assay to detect the rate of killing of adherent

dine digluconate on Candida albicans. Oral Surg Oral Med


Candida albicans by antifungal agents. Oral Surg Oral

Oral Pathol 1989;67:279-281.


Med Oral Pathol Oral Radiol Endod 1996;81:44-49.

111.

Siren EK, Haapasalo MP, Ranta K, Salmi P, Kerosuo EN.

112.
Rlla G, Loe H, Schiott CR. Retention of chlorhexidine in

Microbiological findings and clinical treatment procedures


the human oral cavity. Arch Oral Biol 1971;16:1109-1116.

in endodontic cases selected for microbiological investiga-

113.
Rlla G, Loe H, Schiott CR. The affinity of chlorhexidine for

tions. Int Endod J 1997;30:91-95.


hydroxyapatite and salivary mucins. J Periodontal Res

1970;5:90-95.

Dona BL, Grundemann LJ, Steinfort J, Timmerman MF, van

114.

der Weijden GA. The inhibitory effect of combining

White RR, Janer LR, Hays GL. Residual antimicrobial activi-

chlorhexidine and hydrogen peroxide on 3-day plaque acty associated with a chlorhexidine endodontic irrigant used

cumulation. J Clin Periodontol 1998;25:879-883.


with sodium hypochlorite. Am J Dent 1999;12:148-150.

115.

116.
Heling I, Chandler MP. Antimicrobial effect of irrigant combi-

against Streptococcus sobrinus, Streptococcus faecalis

nations within dentinal tubules. Int Endod J 1998;31:8-14.

and

Staphylococcusaureus.J

Rehabil

117.
Steinberg D, Heling I, Daniel I, Ginsburg I. Antibacterial

1999;26:151-156.

synergistic effect of chlorhexidine and hydrogen peroxide

ENDO 2007;1(1):11-27

Oral

Beltz RE, Torabinejad M, Pouresmail M. Quantitative analy-sis of


the solubilizing action of MTAD, sodium hypochlorite, and EDTS
on bovine pulp and dentin. J Endod 2003;29:334-337.
26

Schfer Root canal irrigation


Torabinejad M, Cho Y, Khademi AA, Bakland LK, Shabahang S.
The effect of various concentrations of sodi-um hypochlorite on the
ability of MTAD to remove the smear layer. J Endod 2003;29:233239.

Babich H, Wurzburger BJ, Rubin YL, Sinensky MC, Blau L. An in vitro study on the
cytotoxicity of chlorhexidine diglu-conate to human gingival cells. Cell Biol Toxicol
1995;11:79-88.

Nair PN, Sjgren U, Krey G, Kahnberg KE, Sundqvist G. Intraradicular bacteria and fungi in
root-filled, asympto-matic human teeth with therapy-resistant periapical lesions: a long-term
light and electron microscopic follow-up study. J Endod 1990;16:580-588.

Emilson CG. Susceptibility of various microorganisms to chlorhexidine. Scand J Dent Res


1977;85:255-265.
Ringel AM, Patterson SS, Newton CW, Miller JM. In vivo evaluation of chlorhexidine
gluconate solution and sodium hypochlorite solution as root canal irrigants. J Endod
1982;8:200-204.
Portenier I, Haapasalo H, rstavik D, Yamauchi M, Haapasalo M. Inactivation of the
antibacterial activity of io-dine potassium iodide and chlorhexidine digluconate against
Enterococcus faecalis by dentin, dentin matrix, type-I collagen, and heat-killed microbial
whole cells. J Endod 2002;28:634-637.

Portenier I, Haapasalo H, Rye A, Waltimo T, rstavik D, Haapasalo M. Inactivation of root


canal medicaments by dentine, hydroxylapatite and bovine serum albumin. Int Endod J
2001;34:184-188.

Zhang W, Torabinejad M, Li Y. Evaluation of cytotoxicity of MTAD


using the MTT-tetrazolium method. J Endod 2003;29:654-657.

Machnik TK, Torabinejad M, Munoz CA, Shabahang A. Effect of


MTAD on the bond strength to enamel and dentin. J Endod
2003;29:818-827.

Machnik TK, Torabinejad M, Munoz CA, Shabahang A. Effect of


MTAD on flexural strength and modulus of elas-ticity of dentin. J
Endod 2003;29:747-750.

Shabahang S, Pouresmail M, Torabinejad M. In vitro an-timicrobial


efficacy of MTAD and sodium. J Endod 2003;29:450-452.
Shabahang S, Torabinejad M. Effect of MTAD on Enterococcus
faecalis-contaminated root canals of extract-ed human teeth. J
Endod 2003;29:576-579.

Torabinejad M, Shabahang S, Aprecio RM, Kettering JD. The


antimicrobial effect of MTAD: an in vitro investigation. J Endod
2003:29:400-403.

Cannell JS. The use of antimicrobial in the mouth. J Int Med Res 1981;9:277-282.

Siqueira JF Jr, Machado AG, Silveira RM, Lopes HP, de Uzeda M. Evaluation of the
effectiveness of sodium hypochlorite used with three irrigation methods in the elim-ination of
Enterococcus faecalis from the root canal, in vitro. Int Endod J 1997;30:279-282.

Baumgartner JC, Ibay AC. The chemical reactions of irrigants used for root canal debridement. J
Endod 1987;13:47-51.

Molander A, Reit C, Dahlen G. The antimicrobial effect of calcium hydroxide in root


canals pretreated with 5% iodine potassium iodide. Endod Dent Traumatol 1999;15:205209.

Spngberg L, Rutberg M, Rydinge E. Biologic effects of en-dodontic antimicrobial agents. J Endod


1979;5:166-175.

Haapasalo HK, Siren EK, Waltimo TM, rstavik D, Haapasalo MP. Inactivation of local
root canal medicaments by dentine: an in vitro study. Int Endod J 2000;33:126-131.

py

Rechte

Alle

138. Kho P, Baumgartner JC. A comparison of the antimicro-

bial efficiency of

NaOCl/BiopurenMTADvorbehaltenversus

NaOCl/EDTA against

. J
Endod

Enterococcus faecalise

2006;32:652-655.

140.
Tay FR, Mazzoni A, Pashley DH, Day TE, Ngoh EC, Breschi

ssen

L. Potential iatrogenic tetracycline staining of endodontical-

ly treated teeth via NaOCl/MTAD irrigation: a preliminary

report. J Endod 2006;32:354-358.

139.
Ruff ML, McClanahan SB, Babel BS. In vitro antifungal ef-

141.
Dahlen G, Samuelsson W, Molander A, Reit C.
ficacy of four irrigants as a final rinse. J Endod

Identification and antimicrobial susceptibility of Enterococci


2006;32:331-333.

isolated from the root canal. Oral Microbiol Immunol

2000;15:309-312.

144.
Powell DL, Marshall FJ, Melfi RC. A histopathologic evalu-

ation of tissue reaction to the minimum effective doses of

some endodontic drugs. Oral Surg Oral Med Oral Pathol


142.
Messer HH, Chen RS. The duration of effectiveness of root

1973;36:261-272.

canal medicaments. J Endod 1984;10:240-245.

143.
Torneck CD. Reaction of hamster tissue to drugs used in

145.
sterilization of the root canal. Oral Surg Oral Med Oral

Pathol 1961;14:730-747.

Fager FK, Messer HH. Systemic distribution of champorat-

ed monochlorphenol from cotton pellets sealed in pulp

chambers. J Endod 1986;12:225-230.

root canal therapy reconsidered. J Endod 2005;31:817-

820.
146.
Spngberg L. Intracanal medication. In: Ingle JI, Bakland

LK. Endodontics. 4th edn. Baltimore: Williams & Wilkins

1994;627-640.

149.
Hlsmann M, Heckendorfff M, Lennon A. Chelating agents

in root canal treatment: mode of action and indications for

their use. Int Endod J 2003;36:810-830.


147.
European Society of Endodontology. Quality guidelines for

endodontic treatment. Int Endod J 1994;27:115-124.

150.
148.
Zehnder M, Schmidlin P, Sener B, Wlatimo T. Chelation in

Calt S, Serper A. Time-dependent effects of EDTA on dentin

structures. J Endod 2002;28:17-19.

with EDTA and NaOCl solutions. Int Endod J 2002;35:934-

939.

151.
Yamashita JC, Tanomaru Filho M, Leonardo MR, Rossi MA,

Silva LA. Scanning electron microscopic study of the clean-

153.
ing ability of chlorhexidine as a root-canal irrigant. Int

Endod J 2003;36:391-394.

Grawehr M, Sener B, Waltimo T, Zehnder M. Interaction of

ethylenediamine tetraacetic acid with sodium hypochlorite

in aqueous solutions. Int Endod J 2003;36:411-417.

154.
152.

Bonsor SJ, Nichol R, Reid TM, Pearson GJ. An alternative reg-

Niu W, Yoshioka T, Kobayashi C, Suda H. A scanning elec-

imen for root canal disinfection. Br Dent J 2006;22:101-105.


tron microscopic study of dentinal erosion by final irrigation

155.
Gutmann JL, Saunders WP, Nguyen L, Gou IY, Saunders

157.
EM. Ultrasonic root-end preparation. Part 1. SEM analysis.

Int Endod J 1994;27:318-324.

Yamaguchi M, Yoshida K, Suzuki R, Nakamura H. Root

canal irrigation with citric acid solution. J Endod

1996;22:27-29.

156.
Machado-Silveiro LF, Gonzales-Lopes S, Gonzales-

Rodriguez MP. Decalcification of root canal dentine by cit-

158.
Di Lenarda R, Cadenaro M, Sbaizero O. Effectiveness of 1

ric acid, EDTA and sodium citrate. Int Endod J 2004;37:365mol L-1 citric acid and 15% EDTA irrigation on smear layer

369.

removal. Int Endod J 2000;33:46-52.

2003;95:234-236.

159.
Scelza MF, Teixeira AM, Scelza P. Decalcifying effect of

EDTA-T, 10% citric acid, and 17% EDTA on root canal

dentin. Oral Surg Oral Med Oral Pathol Oral Radiol Endod

ENDO 2007;1(1):11-27
Sedgley CM, Nagel AC, Hall D, Applegate B. Influence of irrigant needle depth in removing
bioluminescent bacteria inoculated into instrumented root canals using real-time im-aging in vitro.
Int Endod J 2005;38:97-104.

Haapasalo M, rstavik D. In vitro infection and disinfec-tion of


dentinal tubules. J Dent Res 1987;66:1375-1379.

py

Stevens RW, Strother JM, McClanaban SB. Leakage and sealer


penetration in smear-free dentin after a final rinse with 95%
ethanol. J Endod 2006;32:785-788.

Cunningham WT, Cole JS, Balekjian AY. Effect of alcohol on the


spreading ability of NaOCl endodontic irrigant. Oral Surg Oral Med
Oral Pathol 1982;54:333-335.

Wilcox LR, Wiemann AH. Effect of a final alcohol rinse on


sealer coverage of obturated root canals. J Endod
1995;21:256-258.

Schfer

Root canal irrigation

Q
h

t27

vorbehalten
Alle

165. McGurkin-Smith R, Trope M,

Rechte
u

Caplan D, Sigurdsson A.

ssen

Reduction of intracanal bacteria using GT rotary instrumen-

166. Hlsmann M, Peters OA, Dummer


n

PMH. Mechanical

tation, 5.25% NaOCl, EDTA,


and
Ca(OH)2. J Endod
t

preparation of root canals: shaping goals, techniques and

means. Endodontic Topics 2005;10:30-76.

167. Schfer E, Vlassis, M. Comparative investigation of two ro-tary nickel-titanium


instruments: ProTaper versus RaCe. Part 2. Cleaning effectiveness and shaping ability in
severe-ly curved root canals of extracted teeth. Int Endod J 2004;37:239-248.
2005;31:359-363.
168. Tepel J, Schfer E, Hoppe W. Kunststoffe als Modellmaterial in der Endodontie. Dtsch
Zahnrztl Z 1993;48:736-738.

ENDO 2007;1(1):11-27

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