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Marthaler (1970). Pulp anaesthesia of lower teeth through
intraseptal injection. Quintessence Int. 1 (2): 21–23.
(Note.No initial provided).
Masselink, B.H. (1910). The advent of painless dentistry.
Dent. Cosmos 52 (8): 868–872.
Matthews, R.W. and Stables, D.K. (1985). Intraligamentary
dental analgesia by dental therapists. Br. Dent. J. 159 (10):
329–330.
McLean, M.E., Wayman, B.E., and Mayhew, R.B. (1992).
Duration of anesthesia using the periodontal ligament
injection: a comparison of bupivacaine to lidocaine.
Anesth. Pain Control Dent. 1 (4): 207–213.
Medvedev, D., Petrikas, A., and Dyubaylo, M. (2012). Aspiration
in intra- ligamental anaesthesia of lower first molar teeth: a
pilot study. Oral Health Dent. Manag. 11 (3): 95–99.
Meechan, J.G. (1992). Intraligamentary anesthesia. J. Dent.
20 (6): 325–332.
Meechan, J.G. (2002). A comparison of ropivacaine and
lidocaine with epinephrine for intraligamentary
anesthesia. Oral Surg. Oral Med. Oral Pathol. 93 (4):
469–473.
Meechan, J.G., McCabe, J.F., and Carrick, T.E. (1990). Plastic
dental local anaesthetic cartridges: a laboratory
investigation. Br. Dent. J. 169 (2): 54–56.
Miles, T.S. (1983). Dental pain: self-
neurophysiologist. J. Endod. 19 (12): 613–615.
Miller, A.G. (1983). A clinical evaluation of the Ligmaject
periodontal ligament injection syringe. Dent. Update
10(10): 639–643.
Moore, K.D., Reader, A., Meyers, W.J. etal. (1987). A
comparison of the periodontal ligament injection using
2% lidocaine with 1:100,000 epinephrine and saline in
human mandibular premolars. Anesth. Prog. 34 (5):
181–186.
Mulkey, T.F. (1976). Outpatient treatment of hemophiliacs for
dental extractions. J. Oral Surg. 34 (5): 428–434.
Nakane, S. and Kamayama, Y. (1987). Root resorption caused
by mechanical injury of the periodontal soft tissues in rats.
J. Periodont. Res. 22 (5): 390–395.
Nelson, P.W. (1981). Injection system (letter). J. Am. Dent.
Assoc. 103 (5): 692.
Nevin, M. and Puterbaugh, P.G. (1949). Conduction,
Infiltration and General Anesthesia in Dentistry, 5e.
NewYork: Dental Items of Interest Publishing Co Inc.
235–243.
Nogué, R. (1907). L´anesthésie diploique– exposé de la
méthode– technique –résultats. Rev. Stomatol. (Paris) 13:
191–196.
Nusstein, J., Reader, A., Nist, R. etal. (1998). Anesthetic
efficacy of the supplemental intraosseous injection of 2%
lidocaine with 1:100,000 epinephrine in irreversible
pulpitis. J. Endod. 24 (7): 487–491.
observations by a
Nusstein, J., Kennedy, S., Reader, A. etal. (2003). Anesthetic
efficacy of the supplemental X- Tip intraosseous injection
in patients with irreversible pulpitis. J. Endod. 29 (11):
724–728.
Nusstein, J., Berlin, J., Reader, A. etal. (2004). Comparison of
injection pain, heart rate increase, and postinjection pain
of articaine and lidocaine in a primary intraligamentary
injection administered with a computeranesthetic delivery system. Anesth. Prog. 51 (4): 126–133.
Nusstein, J., Claffey, E., Reader, A. etal. (2005a). Anesthetic
effectiveness of the supplemental intraligamentary
injection, administered with a computer controlled local
anesthetic delivery system, in patients with irreversible
pulpitis. J. Endod. 31 (5): 354–358.
Nusstein, J., Wood, M., Reader, A. etal. (2005b). Comparison
of the degree of pulpal anesthesia achieved with the
intraosseous injection and infiltration injection using 2%
lidocaine with 1:100,000 epinephrine. Gen. Dent.
53(1): 50–53.
Parente, S.A., Anderson, R.W., Herman, W.W. etal. (1998).
Anesthetic efficacy of the supplemental intraosseous
injection for teeth with irreversible pulpitis. J. Endod. 24
(12): 826–828.
Parrot, A.H. (1914). Injection (intra- alveolar) anaesthesia in
conservative work. Translations of the six International
Dental Congress. London: Published by the Committee of
Organization. 561–567.
Pashley, D.H. (1986). Systemic effects of intraligamental
injections. J. Endod. 12 (10): 501–504.
Pashley, E.L., Nelson, R., and Pashley, D.H. (1981). Pressures
created by dental injections. J. Dent. Res. 60 (10):
1742–1748.
Pearce, J.H. (1976). Intraosseous injection for profound
anesthesia of the lower molar. J. Colo Dent. Assoc.
54(2): 25–26.
Peñarrocha, M., Oltra, M.J., Estarelles, B. etal. (1996).
Estudio comparativo entre la anestesia intraósea y las
técnicas de anestesia oral convencionales. Av.
Odontoestomatol. (Madrid) 12 (9): 597–609.
Peñarrocha, M., Oltra, M.J., Gay, C., and Berini, L. (1997).
Anestesia intraósea oral. Av. Odontoestomatol. (Madrid)
13(1): 19–30.
Peñarrocha-
(2012). Side effects and complications of intraosseous
anesthesia and conventional oral anesthesia. Med. Oral
Patol. Oral Cir. Bucal 17 (3): e430–e434.
Pereira, L.A.P., Groppo, F.C., Bergamaschi, C.C. etal. (2013).
Articaine (4%) with epinephrine (1:100,000 or 1:200,000) in
intraosseous injections in symptomatic irreversible pulpitis
of mandibular molars: anesthetic efficacy and
cardiovascular effects. Oral Surg. Oral Med. Oral Pathol.
116 (2): e85–e91.
Oltra, D., Ata- Ali, J., Oltra- Moscardó, M.J. etal.
controlled local
t.me/Dr_Mouayyad_AlbtousH

https://t.me/med1917
342
Peterson, J.E., Matsson, L., and Nation, W. (1983). Cementum
and epithelial attachment response to the sulcular and
periodontal ligament injection techniques. Pediatr. Dent.
5w(4): 257–260.
Peurach, J.C. (1985). Pulpal response to intraligamentary
injection in the cynomologus monkey. Anesth. Prog. 32
(2): 73–75.
Pin, P.J.A. (1987). The use of intraligamental injections in
haemophiliacs. Br. Dent. J. 162 (4): 151–152.
Plamondon, T.J., Walton, R., Graham, G.S. etal. (1990). Pulp
response to the combined effects of cavity preparation and
periodontal ligament injection. Oper. Dent. 15 (3): 86–93.
Primosch, R.E. (1986). The role of pressure syringes in the
administration of intraligamentary anesthesia. Comp.
Cont. Edu. Dent. 7 (5): 340–348.
Rakusin, H., Lemmer, J., and Gutmann, J.L. (1986).
Periodontal ligament injection: clinical effects on tooth and
periodontium of young adults. Int. Endod. J. 19 (5):
230–236.
Rawson, R.D. and Orr, D.L. II (1985). Vascular penetration
following intraligamental injection. J. Oral Maxillofac.
Surg. 43 (8): 600–604.
Reader, A., Nusstein, J., and Drum, M. (2011). Successful
Local Anesthesia. For Restorative Dentistry and Endodontics.
Chicago: Quintessence Publishing Co, Inc. 99, 114.
Reisman, D., Reader, A., Nist, R. etal. (1997). Anesthetic
efficacy of the supplemental intraosseous injection of 3%
mepivacaine in irreversible pulpitis. Oral Surg. Oral Med.
Oral Pathol. 84 (6): 676–682.
Reitz, J., Reader, A., Nist, R. etal. (1998). Anesthetic efficacy
of the intraosseous injection of 0.9mL of 2% lidocaine
(1:100,000 epinephrine) to augment an inferior alveolar
nerve block. Oral Surg. Oral Med. Oral Pathol. 86 (5):
516–523.
Remmers, T., Glickman, G., Spears, R., and He, J. (2008). The
efficacy of IntraFlow intraosseous injection as a primary
anesthesia technique. J. Endod. 34 (3): 280–283.
Replogle, K., Reader, A., Nist, R. etal. (1997). Anesthetic
efficacy of the intraosseous injection of 2% lidocaine
(1:100,000 epinephrine) and 3% mepivacaine in
mandibular first molars. Oral Surg. Oral Med. Oral Pathol.
83 (1): 30–37.
Replogle, K., Reader, A., Nist, R. etal. (1999). Cardiovascular
effects of intraosseous injections of 2 percent lidocaine
with 1:100,000 epinephrine and 3 percent mepivacaine.
J. Am. Dent. Assoc. 130 (5): 649–657.
Roahen, J. and Marshall, F.J. (1984). Pulpal and periodontal
tissue effects of the periodontal ligament injection.
J. Endod. 10 (3): 122. (abstract no. 18).
Roahen, J.O. and Marshall, F.J. (1990). The effects of
periodontal ligament injection on pulpal and periodontal
tissues. J. Endod. 16 (1): 28–33.
Roberts, D.H. and Sowray, J.H. (1987). Local Analgesia in
Dentistry, 3e. Bristol (UK): Wright. 90–93.
Saadoun, A.P. and Malamed, S. (1985). Intraseptal anesthesia
in periodontal surgery. J. Am. Dent. Assoc. 111 (2): 249–256.
Sachs, S.A., Lipton, R., and Frank, R. (1978). Management of
ambulatory oral surgical patients with hemophilia. J. Oral
Surg. 36 (1): 25–29.
Sauvez, E. (1905). L’anesthésie locale pour l’extraction des
dents. Paris: Vigot Fréres Editeurs. 1–34, 178. (Note. The
author’s name is Emil. Not provided in the bibliography).
Schleder, J.R., Reader, A., Beck, M., and Meyers, W.J. (1988).
The periodontal ligament injection: a comparison of 2%
lidocaine, 3% mepivacaine, and 1:100,000 epinephrine to
2% lidocaine with 1:100,000 epinephrine in human
mandibular premolars. J. Endod. 14 (8): 397–404.
Schmitt, E. (1936). Intraseptal anesthesia. Dent. Cosmos 78:
1190–1192.
Smith, A.E. (1920). Block Anesthesia and Allied Subjects. With
Special Chapters on the Maxillary Sinus, the Tonsils, and
Neuralgias of the Nervous Trigeminus for Oral Surgeons,
Dentists, Laryngologists, Rhinologists, Otologists, and
Students. St Louis (Mo): CV Mosby Co. 439.
Smith, G.N. and Pashley, D.H. (1983d). Periodontal ligament
injection: evaluation of systemic effects. Oral Surg. Oral
Med. Oral Pathol. 56 (6): 571–574.
Smith, N. and Smith, S.A. (1983a). Intrapulpal injection:
distribution of an injected solution. J. Endod. 9 (5):
167–170.
Smith, G.N. and Walton, R.E. (1983b). Periodontal ligament
injection: distribution of injected solutions. Oral Surg. Oral
Med. Oral Pathol. 55 (3): 232–238.
Smith, G.N., Walton, R.E., and Abbott, B.J. (1983c). Clinical
evaluation of periodontal ligament anesthesia using a
pressure syringe. J. Am. Dent. Assoc. 107 (6): 953–956.
Spuller, R.L. (1988). Use of the periodontal ligament injection
in dental care of the patient with haemophilia– a clinical
evaluation. Spec. Care Dent. 81 (1): 28–29.
Stabident instruction manual. Miami; Fairfax Dental
Inc. 2001.
Susi, L., Reader, A., Nusstein, J. etal. (2008). Heart rate
effects of intraosseous injections using slow and fast rates
of anesthetic solution deposition. Anesth. Prog. 55
(1): 9–15.
Tagger, E., Tagger, M., Sarnat, H., and Mass, E. (1994a).
Periodontal ligament injection in the dog primary
dentition: spread of local anaesthetic solution. Int.
J. Paediatr. Dent. 4 (3): 159–166.
Tagger, M., Tagger, E., and Sarnat, H. (1994b). Periodontal
ligament injection: spread of the solution in the dog.
J. Endod. 20 (4): 283–287.
Torabinejad, M., Peters, D.L., Peckham, N. etal. (1993).
Electron microscopic changes in human pulp after
t.me/Dr_Mouayyad_AlbtousH

343
https://t.me/med1917
intraligamental injection. Oral Surg. Oral Med. Oral Pathol.
76 (2): 219–224.
Van Gheluwe, J. and Walton, R. (1997). Intrapulpal injection.
Oral Surg. Oral Med. OralPathol. 83 (1): 38–40.
Villette, A. (2003). Untersuchungs-
Intention durchgeführten Trans-
Schweitz Monatsschr. Zahnmed. 113 (11): 1211–1214.
Walmsley, A.D., Lloyd, J.M., and Harrington, E. (1989).
Pressures produced invitro during intraligamentary
anaesthesia. Br. Dent. J. 167 (10): 341–344.
Walton, R.E. (1990). The periodontal ligament injection as a
primary technique. J. Endod. 16 (2): 62–66.
Walton, R.E. and Abbott, B.J. (1981). Periodontal ligament
injection: a clinical evaluation. J. Am. Dent. Assoc. 103 (4):
571–575.
Walton, R.E. and Garnick, J.J. (1982). The periodontal
ligament injection: histological effects on the periodontium
in monkeys. J. Endod. 8 (1): 22–26.
bilanzaus 500in erster
kortikalelis- Anästhesien.
White, J.J., Reader, A., Beck, M., and Meyers, W.J. (1988). The
periodontal ligament injection: a comparison of the
efficacy in human maxillary and mandibular teeth.
J. Endod. 14 (10): 508–514.
Wood, M., Reader, A., Nusstein, J. etal. (2005). Comparison
of intraosseous and infiltration injections for venous
lidocaine blood concentrations and heart rate changes after
injection of 2% lidocaine with 1:100,000 epinephrine.
J. Endod. 31 (6): 435–438.
Woodmansey, K.F., White, R.K., and He, J. (2009).
Osteonecrosis relates it intraosseous anesthesia: report of a
case. J. Endod. 35 (2): 288–291.
X-
Tip (2010). X- Tip Intraosseous Anesthesia Delivery System.
Ballaigues (Switzerland): Dentsply Mailleffer.
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19
FailureofDentalLocalAnesthesia
Despite scientific advances, there is, unfortunately, no
infallible technique for ensuring local anesthesia in dentistry, and failures generally reflect specific situations such
as anatomical variations, pathological abnormalities (e.g.
local inflammation), considerable patient anxiety, and failures associated with the dentist. In this chapter, we address
the area of failure of dental anesthesia and its causes and
examine the means at our disposal to overcome it.
Frequency
It is difficult to quantify how often dental local anesthesia
fails because pulpal anesthesia, the most difficult type of
anesthesia to achieve, is hampered by various factors.
1) Type of stimulus. The pain stimulus differs depending on
whether the procedure is obturation (especially if it is not
very deep), extraction, incision of soft tissue, or an endodontic procedure in a vital tooth. It is much easier to
anesthetize the soft tissues or alveolar process than the
dental pulp (Phillips1943). We believe that the electric
pulp meter is the most reliable experimental stimulus for
evaluating the efficacy of local pulpal anesthesia since it
reaches deep levels and its findings are reproducible.
Therefore, in this book, we have selected studies whose
results are based on the application of this approach.
2) Type of local anesthetic solution. Different outcomes
are achieved by varying the concentration of anesthetic
and/or vasoconstrictor, as well as by using different
local anesthetics or vasoconstrictors. This is particularly
important in infiltrative techniques (Annex 21),
although generally of little relevance in mandibular
block (Annex 24). Therefore, we have selected the two
most widely used solutions today: the one we have
referred to throughout the book as the standard solution,
i.e. lidocaine 2% with epinephrine 1:100 000 (10 μg/ml)
(L- 100) or 1:80 000 (12.5 μg/ml) (L- 80), and a potent
solution, i.e. articaine 4% with epinephrine 1:100 000
(10
μg/ml) (A- 100).
3) The amount of solution administered (in milliliters
[ml]). We selected the standard quantities on which
current clinical evaluations are based (generally slightly
higher than recommended in textbooks) and which are
those used in daily clinical practice.
4) Area of the mouth. The results are very different for the
maxillary and the mandibular arches and are very different for the anterior teeth (canines and incisors) and posterior teeth (molars and premolars). Therefore, we have
drawn a distinction between these four areas and have
taken the lateral incisor and first molar as a reference.
Table19.1 summarizes the percentage of failures in healthy
teeth that respond to an electric stimulus despite being anesthetized. A study from 2002in patients receiving dental treatment over 5years found that treatment was painful in more
than 40%. In addition, the pain was moderate or intense in
more than half (20% of the total) (Maggirias and Locker2002).
Consequently, dental local anesthesia could be improved.
ConsequencesofFailure
Failure of dental locoregional anesthesia is important for
various reasons:
1) Dental treatment cannot be administered.
2) Patients lose trust not only in their dentist, but also in
modern dental techniques for controlling pain
(Kaufman etal.1984).
3) Failure is especially important in children because trau-
matic experiences (e.g. pain during dental procedures
resulting from insufficient anesthesia) generate psychological effects, i.e. patients become very fearful of dental
treatment and may develop phobias during adulthood
(Molin and Seeman 1970; Kleinknecht et al. 1973;
Cohen etal.1993; Berggren and Meynert1984).
Local Anesthesia in Dentistry: A Locoregional Approach, First Edition. Jesús Calatayud and Mana Saraghi.
© 2024 John Wiley & Sons Ltd. Published 2024 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Calatayud/local
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Table19.1 Summary offailures.
Tooth Anesthetictechnique ml/LAS/time(min) Failure Reference
Maxillary teeth
Incisors Buccal infiltration 1.0/L-
Buccal infiltration 1.0/A-
First molar Buccal infiltration 1.8/L-
Mandibular teeth
Incisors Buccal infiltration 1.8/L-
Buccal infiltration 1.8/ADouble infiltration 1.8/LDouble infiltration 1.8/AMandibular block 1.8/LMandibular block 3.6/L-
First molar Mandibular block 1.8/L-
Mandibular block 3.6/LMandibular block +
complementary
buccal infiltration
Percentage of failures with the most frequently used techniques in healthy teeth. The lowest percentages of failure are shown in bold.
Evaluation is with electrical stimulation.
ml/LAS/time, milliliters/local anesthetic solution/time in minutes; L- 100, lidocaine 2% with epinephrine 1:100 000 (10 μg/ml); A- 100, articaine
4% with epinephrine 1:100 000 (10 μg/ml).
100/5′ 5% Annex 21
100/5′ 2% Annex 21
100/5′ 13% Annex 21
1.8/A-
100/5′ 5% Annex 21 (estimated)
100/5–10′ 45% Annex 31
100/5–10′ 20% Annex 31
100/5–10′ 10% Annex 31
100/5–10′ 2% Annex 31
100/10–15′ 65–70% Annex 25
100/10–15′ 60–70% Annex 25
100/10–15′ 35–40% Annex 25
100/10–15′ 30–35% Annex 25
100/10–15′
1.8/L-
1.8/A-
100/5–10′
5% Table16.5
Chapter16
Failures:GeneralCauses
Many failures are associated with patient- specific
situations.
HighlyAnxiousPatients
As we saw in Chapter8, around 10% of patients are highly
anxious and fear dental treatment. Anxiety reduces the
pain threshold and increases the possibility that nonpainful stimuli are interpreted as being painful (Pinkham and
Schroeder 1975; Wepman 1978; Woolgrove 1983; Sokol
et al. 1985; Van Wijk and Makkes 2008). It is therefore
important to bear in mind that local anesthetics are very
effective for anesthetizing painful stimuli but are much
less effective with sensations of temperature and pressure.
In addition, they are poorly effective with the nerve fibers
that transmit proprioceptive stimuli (de Jong 1977;
Wildsmith1986). In such patients, it is necessary to follow
various steps:
1) Inform the patient that he/she should distinguish
between “painful” stimuli, which can be easily anesthetized, and sensations of touch, pressure, and temperature, which are more difficult to anesthetize. Thus, we
can help the patient to interpret these sensations in
two ways:
● Extraorally:
○ The dentist can take the patient’s hand by the wrist
in his/her own hand, move it from side to side, and
ask the patient if he/she notices this and if it hurts.
The patient will reply that he/she does notice it but
that it does not hurt.
○ The dentist presses the patient’s hand with his/
her own and asks if the patient notices pressure
and if this is painful. The patient will reply that
he/she does notice the pressure but that it is not
painful.
○ The dentist asks the patient if his/her hand is cold
or warm. The patient replies that it is warm.
○ Finally, the dentist points out to the patient that he/
she felt the movement of the hand, the pressure, and
the temperature, but no pain. The same will be true of
the mouth, that is, the patient will notice sensations
(movement, pressure, temperature) but not pain.
● Intraorally. The word “pain” is now taboo, and the
euphemism “discomfort” is used instead.
○ The dentist shows the patient his/her right hand
with the fist closed and the index finger extended
and says, “Look at my finger.”
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○ The dentist then inserts the finger into the patient’s
mouth and presses on the injection site and says
“Here is where I’ll place the anesthesia. Can you
feel where I’m touching you? The patient will reply
that he/she does notice it. Observe that the dentist
says “place” the anesthesia and not “inject,” which
is taboo.
○ The dentist says that when the anesthetic is placed
in this area, the patient will notice it or perhaps will
feel some “discomfort” (euphemism for pain, now
a taboo word).
2) The dentist must exercise great care when administer-
ing local anesthetic to minimize the pain of the injection (see sections “Insertion of the Needle” and
“Injection”, Chapter13). In addition, it is advisable to
administer a larger quantity of anesthetic.
3) If necessary, the patient should receive an anxiolytic or
sedative drug, although therapy of this type is beyond
the scope of this book.
4) If the patient continues to feel pain for any reason dur-
ing treatment, supplementary techniques can be applied
to address failure (see Chapter18).
However, if the level of anxiety is very high or the patient
is phobic (irrational and uncontrolled fear), then he/she
must be treated by a psychologist or psychiatrist. Such
patients may require psychiatric drugs or general anesthesia, both of which approaches are beyond the scope of
this book.
PatientswithDrugAddictionandAlcoholism
Patients who are addicted to alcohol or other drugs such as
heroin, cocaine, or tranquilizers have a very low tolerance
of stress (nervousness) and pain because of psychological
and physiological abnormalities affecting the central nervous system (Scheutz 1982; Chemical 1987; Stewart and
Finn1995; Fiset et al. 1997; Lindroth etal. 2003). These
patients require greater amounts of anesthesia, and anesthesia fails twice as often as in patients who do not have
addictions (Scheutz 1982; Chemical 1987; Stewart and
Finn1995). In addition, they are often difficult to manage
and require both medical and psychological treatment.
This group of patients should be treated in the same way
as highly anxious patients (see above).
TeethAffectedbyIrreversibleAcutePulpitis
The pulp of teeth affected by acute pulpitis (symptomatic
irreversible pulpitis) is both inflamed and hypersensitive
(called a “hot tooth”). The frequency of failure of local anesthetic is higher, i.e. double or triple that of patients without
Table19.2 Percentage offailures after local anesthesia
inmolars withirreversible acute pulpitis compared withhealthy
molars.
Anesthetic
technique
Maxillary teeth
Buccal
infiltration
“ 1.8/A-
Mandibular teeth
Mandibular
block
Mandibular
block
ml/LAS/time, milliliters/local anesthetic solution/time in minutes;
L- 100, lidocaine 2% with epinephrine 1:100 000 (10 μg/ml); A- 100,
articaine 4% with epinephrine 1:100 000 (10 μg/ml).
ml/LAS/time
(min)
100/5–10′ 13% 35%
1.8/L-
100/5–10′ 5% 25%
1.8/L-
100/10–15′ 35–40% 70%
100/10–15′ 30–35% 55%
3.6/L-
Reference Table19.1 Annex 35
Failurehealthy
molars
Failuremolars
withpulpitis
pulpitis (Table19.2), given that the tooth is more difficult to
anesthetize. In Table19.2, failure in healthy molars is evaluated based on an electric pulp meter; however, in molars
affected by irreversible acute pulpitis, failure is evaluated in
endodontic procedures when the pulp chamber is opened
and during cleaning because negative electrical stimulation
is no guarantee of a painless endodontic procedure in these
cases (Dreven etal. 1987; Reisman et al.1997; Nusstein
etal.1998; Tortamano et al.2009). It is also important to
highlight that the more severe the symptoms are in teeth
with pulpitis (more pain), the greater the percentage of failures will be (Aggarwal etal.2015).
ReasonsforFailureofAnesthesiainAcutePulpitis
1) Structural abnormalities affecting peripheral nerves.
These nerves are affected by inflammation (Kimberly
and Byers1988; Byers etal.1990; Taylor and Byers1990;
Sorensen etal.2004), and their thresholds of excitability
and of electrolyte exchange in the membrane are
altered, thus rendering the membrane hyperexcitable
(Brown1981; Rood and Pateromichelakis1981). These
neurodegenerative changes affect not only the axonal
membrane exposed to inflammation, but also the whole
nerve pathway, therefore truncal block at some distance
from the inflammation also fails (Najjar1977; Wallace
etal.1985; Luo etal.2008).
2) Local factors:
● Tissue pH in inflamed or purulent areas is lower and
may reach 5–6.6 (Schade et al. 1921; de Jong and
Cullen1963) instead of the 7.4 observed in healthy
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tissue, therefore the acid environment leaves very little free base for the anesthetic to penetrate the cell
membrane (Bieter 1936; de Jong 1977; Walton and
Torabinejad1992; Wong and Jacobsen1992).
● Increase of inflammatory mediators (such as prosta-
glandins, calcitonin gene-
related peptide, substance
P, neurokinin A, neuropeptide Y, vasoactive intestinal
polypeptide) that sensitize the sodium channels of
the free nerve endings by facilitating depolarization
with less intense stimuli (hyperalgesia), therefore
local anesthetics are less efficacious for blocking
them (Bowles etal. 2003; Lai et al. 2004; CaviedesBucheli etal.2006).
● Modifications in the sodium channels of the dental
pulp lead to a threefold multiplication of the subtype
or isoform Na
1.9 (Wells etal.2007), which requires
v
2.5–5 times more anesthetic for the block to be effective (Scholz etal.1998); six to eightfold of the subtype
1.8 (Renton etal.2005; Warren etal.2008) and
Na
v
also the subtype Na
● Regional vasodilation favors rapid removal of the
1.7 (Luo etal.2008).
v
anesthetic solution at the affected site as a result of it
entering the systemic circulation (Kramer and
Mitton1973; Meechan1999).
Approach
1) Administer a nonsteroidal anti- inflammatory drug
(NSAID) 45–60
most widely used NSAID is ibuprofen at 400–800
minutes before local anesthesia. The
mg,
although any NSAID can be used (Annex 35; Modaresi
et al. 2006). When NSAIDs cannot be used (e.g. in
patients with gastrointestinal ulcer, pregnant women,
patients taking oral anticoagulants, aspirin- sensitive
asthmatics), acetaminophen can be administered at
1000 mg, although the outcome is somewhat more modest (Annex 35; Modaresi etal.2006). In addition, two
meta-
analyses have shown that NSAIDs taken 1 hour
before the procedure improve anesthesia in mandibular
block. This finding was statistically significant (Li
etal.2012; Shirvani etal.2017).
2) Administration of local anesthesia (Annex 35).
● Use potent solutions such as articaine 4% with epi-
nephrine 1:100 000 (10 μg/ml) (A- 100) instead of
the standard solution of lidocaine (Annex 35).
Three meta- analyses have demonstrated the superiority of A- 100 over the standard lidocaine solution
(L- 100 or L- 80) in patients with irreversible acute
pulpitis (Kung et al. 2015; Su et al. 2016; de Geus
etal.2020).
● In maxillary teeth:
○ Anterior teeth. Buccal infiltration with 1.8 ml of
A- 100 complemented by a small amount
administered via the area of the palate. Wait a little
longer, 5–10 minutes.
○ Posterior teeth. Buccal infiltration with more than
1.8
ml of A- 100 (75% success rate [Annex 35]) and
complement with 0.3–0.4
ml via the palate to
enhance anesthesia of the palatal roots (Ulusoy
and Alacam2014; Askari etal.2016).
● In mandibular teeth:
○ Anterior teeth. Double infiltration (buccal and lin-
gual) of 1.8–3.6
ml of A- 100. Wait 5–10 minutes for
the anesthetic to take effect.
○ Posterior teeth. Mandibular block with1.8 ml of
A-
100. Wait 5minutes to ensure that the lower lip
is anesthetized. At this point, inject a further 1.8
of A-
100 as mandibular block (two cartridges,
3.6
ml, have now been injected) and use complementary anesthesia in the buccal region with a
further 1.8 ml of A- 100 (three cartridges have
now been injected). Wait 5–10
minutes in total). It is important to take two
(10–15
minutes longer
aspects into account:
■ If the second mandibular block is performed
using the Gow-
Gates technique instead of the
conventional technique used for the first block,
it increases efficacy and the number of teeth
anesthetized (Saatchi etal.2018).
■ It is interesting to observe that mandibular block
is more painful in these cases (McCartney
etal. 2007; Fan et al.2009; Kreimer etal.2012;
Annex 23), therefore the technique should be
performed meticulously.
3) Anesthesia with supplementary techniques. If the
above approach is insufficient and the anesthetic fails to
take effect.
Failure of mandibular block affects the dentine in
30% of cases (pain is felt when the burr reaches the dentine), therefore it is too early to apply the intrapulpal
technique and it is necessary to turn to other supplementary techniques (Annex 35).
We can turn to the periodontal ligament technique
(PDL) and the intraosseous technique (IO), again using
100, which we have used so far (it is important to
Aremember not to mix two local anesthetics at the same
point of action, Chapter5). The initial success with the
first injection is greater with the IO technique than with
the PDL (85% vs. 65%), although the cumulative effect
after the second injection (if the first fails) is very similar (almost 100%) (Annex 35). However, the supplementary technique may sometimes have to be repeated as
many as three times (Nusstein etal.1998). The PDL has
the advantage that if a rubber dam is in place, it is not
necessary to remove it for administration (Walton and
ml
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Abbott 1981; Khedari 1982); the advantage of the IO
technique is that is has fewer adverse effects
(Chapter18).
In patients with irreversible acute pulpitis, supplementary techniques can be painful because of the high
sensitivity of the teeth, even if all the tissue is anesthetized (Nusstein etal.2003).
It is also noteworthy that other methods are currently being sought, such as inhalation of nitrous oxide,
for which data seem promising (Fullmer et al. 2014;
Chompu-
Finally, remember that endodontic procedures are considered to be successful when the anesthetized teeth do
not hurt or only do so minimally, so that the procedure
can be performed with the drill able to penetrate the
enamel and dentine and reach the pulp chamber (Annex
35). These teeth may subsequently require intrapulpal
anesthesia.
inwai etal.2018).
ResistancetoLocalAnesthetics
Cases of resistance to the action of various local anesthetics have been reported. In both medical practice (Miller
etal.1981; Kavlock and Ting2004) and in dental practice
(Beckett and Gilmour 1990), resistance takes the form of
short duration of effect or insufficient effect. In dental
practice (Beckett and Gilmour1990) this cannot be attributed to the traditional causes of failure addressed in this
chapter, but rather to genetic abnormalities that lead to
structural abnormalities in some of the isoforms of the
sodium channels (Panigel and Cook 2011; Clendenen
et al. 2016). The frequency of resistance is unknown,
although it must be low, and in some cases it has been
overcome using local anesthetics in which the concentration of the anesthetic component is high (Beckett and
Gilmour1990).
CausesofMaxillaryFailure
1) Excessive thickening of the maxillary bone cortex. This
mainly affects the superior central incisors via the anterior nasal spine (Figure 19.1) if this is very wide and
covers the apices. However, such a situation is highly
unlikely (Jastak et al.1995). This situation may also
arise in the first molars owing to thickening of the zygomatic crest (Evers and Haegerstam1981; Roberts and
Sowray1987; Jastak et al.1995) or thickening of the
outer bone plate, which is typical of patients with
bruxism.
2) Excessive separation of the palatal roots of the molars,
premolars, and lateral incisor as they course toward the
palate. In the posterior teeth, the distance separating
the palatal roots and the buccal roots may be very great.
In fact, the maxillary sinus may even lie between the
palatal and the buccal roots (Figure19.2), thus hampering diffusion of the anesthetic solution toward the palatal root (Evers and Haegerstam 1981; Haglund and
Evers1985). Very rarely, the root of the lateral incisor
may be inclined toward the palate.
3) Accessory innervation via the nasopalatine nerve to the
pulp of the incisors and, occasionally, the canines. This
branch of the nasopalatine root was proposed initially
by Otto Hofer from Vienna (Hofer1922) and supported,
albeit without demonstration, by various authors
(Phillips and Maxmen 1941; Cook 1949). In 1943, the
Department of Anatomy of the University of Wayne
reported having found this branch in dissections
(Phillips1943), although other studies based on dissection did not (Olsen etal.1955), therefore these contradictory results created an atmosphere of distrust
(FitzGerald and Scott 1958; Westwater 1960;
Sicher1950). More recently, it was suggested that fibers
OtherCausesofFailure
Other proposed causes of failure include hematoma in
mandibular block that could dilute the anesthetic solution
in the pterygomandibular space (Traeger1979), although
this seems highly unlikely.
SpecificFailuresAfterMaxillary
Infiltration
Failure of local anesthesia is less frequent after infiltration
in maxillary teeth than after mandibular block. Below, we
present the causes and the means to overcome them.
Figure19.1 Thickening of the anterior nasal spine covering
the apices of the maxillary central incisors.
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Maxillary sinus
Buccal ar
Pala
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● Children. Complementary anesthesia can also be
administered via the palate, but using L-
50 and transpapillary injection, which is typical in children
(Chapter15).
3) Supplementary techniques. If the two methods pro-
posed above fail after a further 5
minutes (complementary anesthesia and complementary anesthesia
administered via the palate), then the PDL and/or the
IO technique is used.
ea
Figure19.2 Maxillary sinus entering the space between the
palatal and buccal roots.
of the superior dental plexus can join the nasopalatine
nerve right at the nasal floor and reach the apices of the
central incisors (Roda and Blanton1994).
4) Accessory innervations of the pulp via branches of the
greater palatine nerve of the palatal roots of the molars
and premolars (Ulusoy and Alacam2014).
Approach
If pulpal anesthesia has not been achieved 5minutes after
injection, the available options are as follows:
1) Complementary anesthesia:
● Adults. If articaine 4% with epinephrine 1:100 000
(A-
100) was used, i.e. the first choice in adults, repeat
the injection with a greater quantity at the same sites.
● Children. If the standard solution of lidocaine 2%
with epinephrine 1:100 000 (10 μg/ml) (L- 100) was
used, i.e. the solution indicated for children, repeat
the injection with a greater quantity at the same sites,
but use lidocaine 2% with epinephrine 1:50 000 (20 μg/
ml) (L- 50), which contains double the amount of epinephrine, thus rendering its effect more potent. Note
that the anesthetic is the same, since two different
anesthetics should not be mixed at the same site.
2) Complementary palatal anesthesia.
● Adults. Complementary anesthesia administered via
the palate in small amounts (±0.2–0.3 ml) of
A- 100increases both the efficacy and the duration of
pulpal anesthesia, especially in posterior teeth with
palatal roots (Aggarwal etal.2011a,2011b; Guglielmo
etal.2011; Ulusoy and Alacam2014).
In children, supplementary techniques such as the PDL
or the IO technique can be used, although only in permanent teeth (not in temporary teeth, so as not to affect the
buds of the underlying permanent teeth).
SpecificFailuresAfterMandibular
Block
As we have seen, mandibular block is only used to achieve
pulpal anesthesia in molars and premolars (posterior
teeth), where the results are acceptable (Annex 25). Below,
we present the reasons for failure and the means to
address it.
ReasonsforFailureAfterMandibularBlock
FailureOwingtoInappropriateTechnique
This failure arises when soft tissue anesthesia of half of the
ipsilateral lower lip is not achieved 5 minutes after injection (Cohen et al. 1993; Hersh et al. 1995; Nusstein
etal.1998). This is the most frequent cause and may arise
in up to 10% of cases (Annex 28).
Logically, this failure is particularly common among
dentistry students (Rood and Sowray1980) since the technique is not easy to apply and requires the acquisition of
appropriate skills. Failure may also arise among experienced professionals, although it has been demonstrated
that the frequency of this type of failure decreases with
experience and the number of years the dentist has been
working (Keetley and Moles 2001). Nonetheless, cases of
failure are reported.
FailureforAnatomicalReasons
Accessory Mandibular Foramina
foramina are found in the region of the condyle and the
mandibular foramen (Barker 1972a; Haveman and
Tebo1976). In some cases, accessory branches, which are
smaller than the inferior alveolar nerve, may enter some
foramina at higher levels and supply the inferior molars.
These branches may not be affected by conventional
mandibular block.
Most accessory mandibular
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Very High Lingula A very high lingula means that the
inferior alveolar nerve does not come into contact with the
solution because the anesthetic cannot be appropriately
placed in the pterygomandibular space, as in conventional
mandibular block (Coleman and Smith1982). The finding
of a lingula greater than 11
mm occurs in 0.1% of cases
(Kay1974) and in up to 5% of cases (Bremer1952). To avoid
this, it is recommended that the level of needle contact
with bone should be slightly superior to the lingula.
Double (Bifid) Mandibular Canal and/or Foramen Bifid
mandibular canal and/or foramen was initially described
in isolated cases (Kiersch and Jordan1973; Patterson and
Funke1973). Trifid canal/foramen is even rarer (Mizbah
etal.2012). It is important to remember that this situation
arises because the mandibular canal originates from the
junction of three separate canals during embryonic
development (Chavez-
Lomeli etal.1996). Such anatomical
anomalies are thought to hamper the efficacy of
conventional mandibular block (Kiersch and Jordan1973;
Grover and Lorton1983; Neves et al.2013), especially in
cases of bifid foramina (Nortjé et al. 1977; Langlais
etal.1985; Bogdan etal.2006; Correr etal.2013). Modern
tomography- based techniques have made it possible to
identify these anomalies (mean length of 10–15
30% of mandibular canals (Annex 34).
Bifid mandibular canals are important because they can
sometimes escape mandibular block (Grover and
Lorton1983; Neves etal.2013).
Sphenomandibular Ligament Sometimes, deposition of
local anesthetic where it is separated from the inferior
alveolar nerve by the sphenomandibular ligament
(Figure 3.14, Chapter 3) or other fibrous tissue in the
pterygomandibular space may impede diffusion (Barker
and Davies 1972b; Garg and Townsend 2001; Shiozaki
etal.2007; Khoury etal.2010,2011; Simonds et al. 2017).
To avoid this, it is recommended that the level of needle
contact with bone should be slightly superior to the lingula
(Khoury etal.2010,2011).
FailureArisingfromAccessoryInnervation
Mylohyoid Nerve
The mylohyoid nerve is mainly a motor
nerve that supplies the mylohyoid muscle and the anterior
belly of the digastric muscle, therefore anesthesia of this
nerve causes some discomfort when swallowing (Barker
and Davies 1972b). The nerve emerges from the inferior
alveolar nerve before entering the mandibular foramen. It
was initially thought to emerge at a very low level, some
5 mm before entering the mandibular foramen
(Jeffries1944; Barker and Davies1972b), therefore it was
systematically anesthetized during mandibular block.
mm) in
Figure19.3 Variant of the mylohyoid nerve emerging at a high
level and penetrating a specific canal.
Thanks to meticulous dissection studies, we now know
that it emerges much higher, at around 15 mm (5–23 mm)
(Wilson et al. 1984; Bennett and Townsend 2001).
Consequently, it is often not anesthetized (Figure 19.3);
furthermore, it may be protected from the anesthetic
solution by the interpterygoid fascia (i.e. it penetrates the
fascia) or by the sphenomandibular ligament (Stein
etal.2007).
In 1904, in Vienna, Schumacher proposed that the mylohyoid nerve could give off branches to the mandibular
symphysis to supply the inferior incisors (Schumacher1904).
Dissection studies have shown that up to 20% of its fibers
are sensitive to pain and temperature, and supply the skin
of the chin (Sicher1946; Frommer etal.1972; Roberts and
Harris 1973). In 15–50% of cases, it may also supply the
pulp of the mandibular teeth (Novitzky1938; Sicher1946;
Carter and Keen 1971; Madeira et al. 1978; Wilson
etal.1984). The pulpal branches penetrate the bone via the
foramina along the mylohyoid groove of the internal aspect
of the mandible, along which the nerve courses. Thus, we
have the following (Figure19.4):
● Branches for molars (Frommer etal.1972), which pene-
trate via the posterior foramina and are found in more
than 80% of mandibles (Haveman and Tebo1976).
● Branches for premolars (Carter and Keen 1971;
Chapnick 1980; Bennett and Townsend 2001), which
penetrate via the foramina in the area of the bicuspids of
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