A overview of local anesthesia and various advancement in its modern day approach. A post graduate periodontology approach to application of local anesthesia in day to day dental surgeries and various other dental and maxillofacial treatment procedures.

1. Dr. Soumyadeep Bandopadhyay
MDS-1st Year
Department of Periodontology

2. Local anesthesia is defined as a loss of sensation in
a circumscribed area of the body caused by
depression of excitation in nerve endings or an
inhibition of the conduction process in peripheral
nerves.

3. 1) It should not be irritating to tissues where it is
applied.
2) It shouldn’t cause any permanent alteration in
nerve structures.
3) Systemic toxicity should be low.
4) It should have short time of onset
5) It should have high level of effectiveness
regardless of the fact whether it is injected into
the tissue or applied locally to the mucous
membrane.

4. 6) It shouldn’t produce any allergic reactions.
7) It should be stable in solution and relatively
undergo biotransformation in the human body.
8) It should have sufficient duration of action to
enable the working process.
9) It shouldn’t be producing any permanent
damage or alteration of nervous structure.
10) It should have short time of onset.
11) It should be sterile or should be able to be
sterilized by heat without deterioration.
12) It should be stable in light.
13) It should have a longer shelf life.
14) It should have sufficient potency.

5.  Cocaine was the first anasthetic agent to be
used. It was derived from coca tree. Its
anasthetic action was first demonstrated by
Karl Koller in 1884.
 The first effective and widely used synthetic
anasthetic agent was Procaine and was
clinically used in 1905 by Braun
 Lidocaine was clinically used by Torsten Gordh
in 1949

6.  Classification of local anasthetic agents have
been done based on the following sub-group:
1) Chemical nature:
A) Ester:
i) Benzoic acid ester:
Benzocaine , cocaine, butacaine, tetracaine
ii) Para amino benzoic acid ester:
Procaine, chloroprocaine

7. B) Amide:
Lignocaine, Bupivacaine, Mepivacaine, Prilocaine,
Atricaine
C) Quinolone:
Centbucridine

8. 2) Mode of application:

9. 3) Potency:

10. 4)Biological site and mode of action :

11. 5) Duration of action :

13.  An initial phase of slow depolarization. The
electrical potential within the nerve becomes
slightly less negative.
 When the falling electrical potential reaches a
critical level, an extremely rapid phase of
depolarization results. This is termed threshold
potential, or firing threshold.
 This phase of rapid depolarization results in a
reversal of the electrical potential across the
nerve membrane. An electrical potential of +40
mV exists inside the nerve cell.

14.  After these steps of depolarization,
repolarization occurs. The electrical potential
gradually becomes more negative inside the
nerve cell relative to outside until the original
resting potential of −70 mV is again achieved.

15. IMPULSE SPREAD
 The propagated impulse travels along the nerve
membrane towards CNS. The spread of impulse differs
in myelinated and unmyelinated nerve fibers.
UNMYELINATED NERVES: The high resistance cell
membrane and extra cellular media produce a rapid
decrease in density of current with in a short distance of
depolarized segment.
 The spread of the impulse is characterized as a slow
forward-creeping process.
 Conduction rate is 1.2m/sec

16. Myelinated nerves:
Impulse conduction in myelinated nerves occurs by means
of current leaps from nodes to node this process is called
as SALTATORY CONDUCTION.
It is more rapid in thicker nerves because of increase in
thickness of myelin sheath and increase in distance
between adjacent nodes of ranvier.
If conduction of impulse is blocked at one node the local
current will skip over that node and prove adequate to
raise that membrane potential at next node to its firing
potential and produce depolarization.
Conduction rate of myelinated fibers is 120m/sec

19. Local anesthetics interferes with the excitation
process in a nerve membrane in one or more of
the following ways:
1. Altering the basic resting potential of the nerve
membrane
2. Altering the threshold potential (firing level)
3. Decreasing the rate of depolarization
4. Prolonging the rate of repolarization

20. 1)Acetylcholine theory: Acetylcholine is
involved in nerve conduction, in addition to
its role as a neurotransmitter at nerve
synapses.
Demerit: No evidence exists indicating that
acetylcholine is involved in neural
transmission along the body of the neuron.

21. 2) Calcium displacement theory:
Local anesthetic nerve block is
produced by the displacement of
calcium from some membrane site
that controls permeability to sodium.
Demerit: Varying the concentration
of calcium ions bathing a nerve does
not affect local anesthetic potency.
This has diminished the credibility of
this theory.

22. 3) Surface charge (repulsion) theory:
Local anesthetics act by binding to the nerve membrane and changing
the electrical potential at the membrane surface.
Demerit: Cationic (RNH+)drug molecules are aligned at the
membrane-water interface, and because some of the local anesthetic
molecules carry a net positive charge, they make the electrical
potential at the membrane surface more positive, thus decreasing the
excitability of the nerve by increasing the threshold potential

23. Resting potential of the nerve membrane is unaltered by
local anesthetics (they do not become hyperpolarized),
and that conventional local anesthetics act within
membrane channels rather than at the membrane surface.
Also, the surface charge theory cannot explain the activity
of uncharged anesthetic molecules in blocking nerve
impulses.
(e.g., benzocaine)

24. Membrane expansion theory:
Local anesthetic molecules diffuse to hydrophobic
regions of excitable membranes, producing a
general disturbance of the bulk membrane
structure, expanding some critical region(s) in the
membrane, and preventing an increase in
permeability to sodium ions.
Lee AG. Model for action of local anesthetics. Nature.
1976;262:545–548.
Seeman P. The membrane actions of anesthetics and tranquilizers.
Pharmacol Rev. 1972;24:583–655

26. Local anesthetics that are highly lipid soluble can
easily penetrate the lipid portion of the cell
membrane, producing a change in configuration
of the lipoprotein matrix of the nerve membrane.
This results in a decreased diameter of sodium
channels, which leads to inhibition of both
sodium conductance and neural excitation.
 Limitation: No direct evidence suggests that
nerve conduction is entirely blocked by
membrane expansion per se.

27.  Specific receptor theory:
It proposes that local anesthetics act by binding to
specific receptors on the sodium channel.
Both biochemical and electrophysiologic studies
have indicated that a specific receptor site for
local anesthetics exists in the sodium channel
either on its external surface or on the internal
axoplasmic surface.
Strichartz GR, Ritchie JM. The action of local anesthetics on ion
channels of excitable tissues. In: Strichartz GR, ed. Local Anesthetics.
New York: Springer-Verlag; 1987.
Scholz A. Mechanisms of (local) anaesthetics on voltage-gated
sodium and other ion channels. Br J Anaesth. 2002;89(1):52–61.

29.  Local anesthetics are available as salts (usually
hydrochlorides) for clinical use.
 The salts, both water soluble and stable, is dissolved
in either sterile water or saline.
 In this solution it exists simultaneously as
unchanged molecule (RN), also called base and
positively charged molecules (RNH
+
) called cations.
RNH
+
==== RN+ H
+

30. The relative concentration of each ionic form in the
solution varies in the pH of the solution or surrounding
tissue.
In the presence of high concentration of hydrogen ion
(low pH) the equilibrium shifts to left and most of the
anesthetic solution exists in cationic form.
RNH+
> RN+
+ H+
As hydrogen ion concentration decreases (higher pH)
the equilibrium shifts towards the free base form.
RNH+
< RN + H+

31. The relative proportion of ionic form also depends on
pKa or DISSOCIATION CONSTANT, of the specific
local anesthetic.
The pKa is a measure of molecules affinity for H
+
ions.
When the pH of the solution has the same value as pKa
of the local anesthetic, exactly half the drug will exists
in the RNH
+
form and exactly half in RN form.
The percentage of drug existing in either form can be
determined by Henderson Hasselbalch equation
Log base/acid = pH - pKa

32. Local anesthetic agent (xylocaine, lignocaine 2%)
Vasoconstrictor (adrenaline 1: 80,000)
Reducing agent (sodium metabisulphite)
Preservative (methylparaben)
Fungicide (thymol)
Vehicle (distilled water,NaCl)

33. Vasoconstrictors constrict blood vessels and decrease
blood flow to the site of injection.
Absorption of LA into bloodstream is slowed,
producing lower levels in the blood.
Lower blood levels lead to decreased risk of overdose
(toxic) reaction.
Higher LA concentration remains around the nerve
increasing the LA's duration of action.

34. Vasoconstrictors are of two types:

35. Concentrations of Vasoconstrictor in Local Anesthetics
- 1:50,000 ,1:100,000, 1:200,000 - 0.020mg/ml
,0.010mg/ml, 0.005 mg/ml
Max dose of vasoconstrictors :
 With Ephinephrine:
- Healthy patient approximately 0.2mg
- Patient with significant cardiovascular history:
0.04mg
 With Norephinephrine:
I. With healthy patient approximately 0.34mg
II. Patient with significant cardiovascular history is
0.14mg

36.  Vasoconstrictors are unstable in solution and may
oxidize especially on prolong exposure to sunlight
this results in turning of the solution brown and this
discoloration is an indication that such a solution
must be discarded.
 To overcome this problem a small quantity of
sodium metabisulphite is added - competes for the
available oxygen.
 It increases shelf life.

37.  Modern local anesthetic solution are very stable and
often have a shelf of two years or more. Their
sterility is maintained by the inclusion of small
amount of a preservative such as capryl
hydrocuprienotoxin.
 Some preservative such as methylparaben have
been shown to allergic reaction in sensitized
subjects.

38.  In the past some solutions tended to become cloudy
due to the proliferation of minute fungi.
 In several modern solutions a small quantity of
thymol is added to serve as fungicide and prevent
this occurrence.

39.  The anesthetic agent and the additives referred to
above are dissolved in distilled water & sodium
chloride.
 This isotonic solution minimizes discomfort during
injection.

40. The molecular structure of all local anesthetics
consists of 3 components: (a) lipophilic aromatic
ring,(b) intermediate ester or amide linkage, and
(c) tertiary amine.

41.  Typically range from 0.5-4%.
 Reason: Lipid solubility that enhances diffusion
through nerve sheaths and neural membranes.
 Example : Bupivacaine is more lipid soluble
and potent than atricaine, allowing its
formulation as a 0.5% conc. (5mg/ml) rather
than a 4% ( 40 mg/ml).
Daniel E Becker,Kenneth L Reed. Local Anesthetics: Review of Pharmacological Considerations. The
Journal of sedation and anasthesiology in dentistry. 2012 Summer; 59(2): 90–102.
doi: 10.2344/

42. When injected into soft tissue most local anesthetics
produce dilation of vascular bed.
Cocaine is the only local anesthetic that produces
vasoconstriction, initially it produces vasodilation
which is followed by prolonged vasoconstriction.
Vasodilation is due to increase in the rate of absorption
of the local anesthetic into the blood, thus decreasing
the duration of pain control while increasing the
anesthetic blood level and potential for over dose

43. ORAL ROUTE:
 Except cocaine, local anesthetics are poorly
absorbed from GIT
 Most local anesthetics undergo hepatic first-pass
effect following oral administration.
 72% of dose is biotransformed into inactive
metabolites
 TOCAINIDE HYDROCHLORIDE an analogue of
lidocaine is effective orally

44. TOPICAL ROUTE:
 Local anesthetics are absorbed at different rates after
application to mucous membranes.
 In the tracheal mucosa uptake is as rapid as with
intravenous administration.
 In pharyngeal mucosa uptake is slow
 In bladder mucosa uptake is even slower
 Eutectic mixture of local anesthesia (EMLA) has been
developed to provide surface anesthesia for intact skin.

45. INJECTION PATHWAY:
 The rate of uptake of local anesthetics after injection is
related to both the vascularity of the injection site and the
vasoactivity of the drug.
 IV administration of local anesthetics provide the most
rapid elevation of blood levels and is used for primary
treatment of ventricular dysrhythmias.
Once absorbed in the blood stream local anesthetics are
distributed through out the body to all tissues.
Highly perfused organs such as brain, head, liver, kidney, lungs
have higher blood levels of anesthetic than do less higher
perfused organs. All local anesthetic agents readily cross the
blood-brain barrier, they also readily cross the placenta.

46. ESTER LOCALANESTHETICS:
 Ester local anesthetics are hydrolyzed in the plasma
by the enzyme pseudocholinesterase.
 Chloroprocaine the most rapidly hydrolyzed, is the
least toxic.
 Tertracaine hydrolyzed 16 times more slowly than
Chloroprocaine ,hence it has the greatest potential
toxicity.

47. AMIDE LOCALANESTHETICS
 The metabolism of amide local anesthetics is more
complicated then esters. The primary site of
biotransformation of amide drugs is liver.
 Entire metabolic process occurs in the liver for
lidocaine, articaine, etidocaine, and bupivacaine.
 Prilocaine undergoes more rapid
biotransformation then the other amides.

48.  Kidneys are the primary excretory organs for both the local
anesthetic and its metabolites
 A percentage of given dose of local anesthetic drug is
excreted unchanged in the urine.
 Esters appear in only very small concentration as the parent
compound in urine.
 Procaine appears in the urine as PABA (90%) and 2%
unchanged.
 10% of cocaine dose is found in the urine unchanged.
 Amides are present in the urine as a parent compound in a
greater percentage then are esters.

49. 1.) The Syringe
2.) The Needle
3.) The Cartridge
4.) Other Armamentarium
- Topical Anesthetic (strongly recommended) -
ointments, gels, pastes, sprays
- Applicator sticks
- Cotton gauze

53. The Needle Gauge: the larger the gauge the smaller the
internal diameter of the needle Usual dental needle
gauges are 25,27, & 30 Length:
1-Long(approximately 40mm)
2-Short(20-25 mm).
3-Extra-short(approximately 15 mm).

54. Maxillary Region:
1) Supraperiosteal
2) PDL
3) Intraseptal Injection
4) Intracrestal Injection
5) Intraosseous Injection
6) PSA Nerve Block
7) MSA Nerve Block
8) ASA Nerve Block
9) Maxillary Nerve Block
10) Greater Palatine Nerve Block
11) Nasopalatine Nerve Block

55. Mandibular Region:
 Inferior Alveolar Nerve block
 Buccal nerve Block
 Mandibular nerve block techniques:
- Gow Gates technique
- Vazirani Akinosi closed mouth mandibular block
 Mental nerve block
 Incisive nerve block
 Lingual nerve block

72. It can be
broadly
divided into
two parts:
•Local
•Systemic

73. Needle breakage :
 Do not use short needles for inferior alveolar nerve
block in adults or children.
 Do not use 30-gauge needles for inferior alveolar nerve
block in adults or children.
 Do not bend needles when inserting them into soft
tissue.
 Do not insert a needle into soft tissue to its hub, unless
it is absolutely essential for the success of the injection.
 Observe extra caution when inserting needles in
younger children or in extremely phobic adult or child
patients.

74. Paraesthesia
 Strict adherence to injection protocol
 Most paraesthesia resolve within approximately 8
weeks to 2 months without treatment.
 Determine the degree and extent of paraesthesia.
 Explain to the patient that paraesthesia
 Record all findings
 Second opinion
 Examination every 2 months.

75. Facial Nerve palsy
 Reassure the patient
 Contact lenses should be removed until muscular
movement returns.
 An eye patch should be applied to the affected eye until
muscle tone returns
 Record the incident on the patient's chart.
 Although no contraindication is known to
reanesthetizing the patient to achieve mandibular
anesthesia, it may be prudent to forego further dental
care at this appointment

77. Trismus
 Prescribe heat therapy by hot moist towel to affected area for
every 20 minutes every hourly , warm saline rinses,
analgesics (Aspirin 325 mg)
 If necessary, muscle relaxants to manage the initial phase of
muscle spasm - Diazepam (approximately 10 mg bid) or
chloroxazone 250 mg TDS.
 Initiate physiotherapy. Sugarless chewing gums to provide
lateral movement of TMJ.
 Antibiotics should be added to the treatment regimen
described and continued for 7 full days
 Patients report improvement within 48 to 72 hours.avoid
further treatment in involved area until symptoms get
resolved.

79. Injection pain
 Adhere to proper techniques of injection, both anatomic
and psychological.
 Use sharp needles.
 Use topical anesthetic properly before injection.
 Use sterile local anesthetic solutions.
 Inject local anesthetics slowly.
 Make certain that the temperature of the solution is
correct
 Buffered local anesthetics, at a pH of approximately 7.4,
have been demonstrated to be more comfortable on
administration

80. Burning on Injection
 By buffering the local anesthetic solution to a pH of
approximately 7.4 immediately before injection, it is
possible to eliminate the burning sensation that
some patients experience during injection of a local
anesthetic solution containing a vasopressor.
 Slowing the speed of injection also helps.

81. Infection :
 Use sterile disposable needles.
 Properly care for and handle needles.
 Properly prepare the tissues before penetration.
 Prescribe 29 (or 41, if 10 days) tablets of penicillin
V (250-mg tablets).
 Erythromycin may be substituted if the patient is
allergic to penicillin.

82. Edema
If edema occurs in any area where it compromises breathing, treatment
consists of the following:
 P (position): if unconscious, the patient is placed supine.
 A-B-C (airway, breathing, circulation): basic life support is administered,
as needed.
 D (definitive treatment): emergency medical services (e.g., 9-1-1) is
summoned.
 Epinephrine is administered: 0.3 mg (0.3 mL of a 1:1000 epinephrine
solution) (adult), 0.15 mg (0.15 mL of a 1:1000 epinephrine solution)
(child [15 to 30 kg]), intramuscularly (IM) or 3 mL of a 1:10,000
epinephrine solution intravenously (IV-adult), every 5 minutes until
respiratory distress resolves.
 Histamine blocker is administered IM or IV.
 Corticosteroid is administered IM or IV.
 Preparation is made for cricothyrotomy if total airway obstruction
appears to be developing. This is
 extremely rare but is the reason for summoning emergency medical
services early.
 The patient's condition is thoroughly evaluated before his or her next
appointment to determine the cause of the reaction.

83. Hematoma :
 Hematoma is not always preventable. Whenever a
needle is inserted into tissue, the risk of inadvertent
puncturing of a blood vessel is present.
 When swelling becomes evident during or immediately
after a local anesthetic injection, direct pressure should
be applied to the site of bleeding.
 For most injections, the blood vessel is located between
the surface of the mucous membrane and the bone;
localized pressure should be applied for not less than 2
minutes. This effectively stops the bleeding.
 Ice may be applied to the region immediately on
recognition of a developing hematoma.

85. Soft tissues injury due to needle prick
 Analgesics, antibiotics, lukewarn saline rinse,
petroleum jelly
 Cotton roll placed between lips and teeth, secured
with dental floss, minimizes risk of accidental
mechanical trauma to anesthetized tissues.

87. Adverse drug reaction
 Toxicity Caused by Direct Extension of the Usual
Pharmacologic Effects of the Drug:
1) Side effects
2) Overdose reactions
3) Local toxic effects
 Toxicity Caused by Alteration in the Recipient of the Drug:
1) A disease process (hepatic dysfunction, heart failure, renal
dysfunction)
2) Emotional disturbances
3) Genetic aberrations (atypical plasma cholinesterase, malignant
hyperthermia)
4) Idiosyncrasy
 Toxicity Caused by Allergic Responses to the Drug

88. LOW TO MODERATE OVERDOSE LEVELS:
Confusion
Talkativeness
Apprehension
Excitement
Slurred speech
Generalized stutter
Muscular twitching, tremor of face and extremities
Elevated BP, heart rate and respiratory rate

89. MODERATE TO HIGH BLOOD LEVELS:
Generalized tonic clonic seizure, followed by
Generalized CNS depression
Depressed BP, heart rate and respiratory rate
Headache
Light headedness
Auditory disturbances
Dizziness
Blurred vision
Numbness of tongue and perioral tissues
Loss of consciousness

90. Basic emergency management : A-B-C-D approach
Allergy : Medical history questionnaire is important.
Elective dental care
Emergency dental care:
Protocol no.1 : no treatment of an invasive nature
Protocol no.2 : use general anesthesia
Protocol no.3: Histamine blockers

91. Pediatric cases:
The maximum safe dose of lidocaine for a child is
4.5 mg/kg per dental appointment.
Local infiltration of anesthesia is sufficient for all
dental treatment procedures in 90% of cases even in
the mandible

92. Handicapped Patient:
choose a shorter needle and/or a larger
gauge needle which is less likely to be bent
or broken.
better to use general anesthesia.

93. Patient with bleeding
disorders:
Oral procedures must be
done at the beginning of the
day allowing delayed re-
bleeding episodes, usually
occurring after 24-48 h.
•Regional nerve blocks should be avoided when possible.
•Local vasoconstriction may be encouraged by infiltrating a
small amount of local anesthetic containing adrenaline
(epinephrine) close to the site of surgery.
Local anesthetic containing a
vasoconstrictor should be
administered by infiltration
or by intraligamentary
injection wherever practical.

94. PREGNANCY:
Lidocaine + vasoconstrictor: most common local
anesthetic used in dentistry extensively used in pregnancy
with no proven ill effects, Esters are better to be used.
Accidental intravascular injections of lidocaine pass
through the placenta but the concentrations are too low to
harm fetus.

95. GERIATRIC PATIENT:
•When choosing an anesthetic, we are largely concerned
with the effect of the anesthetic agent upon the patient's
cardiovascular and respiratory systems.
•increased tissue sensitivity to drugs acting on the CNS
•Decreased hepatic size and blood flow may reduce
hepatic metabolism of drugs
•hypertension is common and can reduce renal function
•Same prevention procedures used with children

96. LIVER DISORDERS:
•Advanced liver diseases include:
•Liver cirrhosis - Jaundice
•- Potential complications:
•1 . Impaired drug detoxication e.g. sedative, analgesics, general
anesthesia.
•2. Bleeding disorders ( decrease clotting factors, excess fibrinolysis,
impaired vitamin K absorption).
•3. Transmission of viral hepatitis.
•Management
•Avoid LA metabolized in liver: Amides (Lidocaine, Mepicaine), esters
should be used.

97. Modern day advancements in Local Anesthesia delivery
devices, newer technologies has been developed to assist the
dentist in providing patients with enhanced pain relief with
reduced injection pain and minimum adverse effect
First is the introduction of articaine hydrochloride as an
injectable local anesthetic. Although articaine is an amide, its unique
structure allows the drug to be quickly metabolized, reducing toxicity
associated with repeated injections over time. The second
development is the formulation of a lidocaine and prilocaine
dental gel for topical anesthesia of the periodontal pocket. This
product may significantly reduce the need for anesthetic injections
during scaling and root planing. Finally, the use of triazolam as an
oral sedative/anxiolytic is reviewed. The recent administration of
triazolam in multiple doses has extended the availability of anxiety
control to many dental patients, but unknowns about the safety of the
technique as practiced by some dentists remains a concern.

98. Eutectic mixture of local anesthesia (EMLA):
The Eutectic Mixture of Local Anesthetics
(EMLA) is a topical application, which has
proved to be a useful medication for providing
pain relief among children. It is an emulsion
containing a 1:1 mixture of lidocaine and
prilocaine.

100.  The DentiPatch® system is applied to the
buccal mucosa to provide topical anesthesia by
releasing lidocaine. Lidocaine stabilizes the
neuronal membrane by inhibiting the ionic
fluxes required for the initiation and
conduction of impulses, thereby effecting local
anesthetic action.

102. DentalVibe Gen4 Comfort Injection system is designed to
reduce injection pain by applying pressure and vibration at the
injection site.
Their concept is to reduce the pain of needle injection by
applying pressure, vibration, microoscillations or a
combination of them. The applied physical stimuli are
hypothesised to modify or interfere with pain signals by
closing the neural gate of cerebral cortex, aimed to decrease the
pain perception due to distraction.

106. Computer-controlled local anesthetic delivery (CCLAD) is one the
method to reduce patient pain during local anesthesia; it is a device that
slowly administers anesthetics by using a computerized device to control
the injection speed.
CCLAD can reduce pain by controlling anesthetic injection speed, which
permits continuous administration of a small amount of anesthetic at a
slow speed, which can reduce pain not only from resistance felt in the
tissues, but also from anesthesia taking effect simultaneously with
injection, which in turn allows the anesthetic to be injected into tissue
that has already been anesthetized. Thus, owing to this series of
processes, the patient feels less pain.

108. Ultra Safety Plus® is a sterile, single use, self-
aspirating syringe system. This syringe system is
used for the routine administration of local dental
anesthetics and is specifically designed to prevent
needle stick injuries.

110. 1. Handbook of local anesthesia – Stanley F Malamed
– 6th edition
2. Essentials of Local Anesthetic Pharmacology :
Daniel E Becker: Anesth Prog. 2006 Fall; 53(3):
98–109.
3. Lee AG. Model for action of local anesthetics.
Nature.1976;262:545–548.
4. Seeman P. The membrane actions of
anesthetics and tranquilizers.Pharmacol Rev.
1972;24:583–655

111.  Advances in dental local anesthesia techniques and devices: An
update ; Payal Saxena et al: National Journal of Maxillofacial
Surgery | Vol 4 | Issue 1 | Jan-Jun 2013.
 Daniel E Becker,Kenneth L Reed. Local Anesthetics: Review
of Pharmacological Considerations. The Journal of sedation
and anasthesiology in dentistry. 2012 Summer; 59(2): 90–
102.doi: 10.2344/
 Strichartz GR, Ritchie JM. The action of local anesthetics on
ion channels of excitable tissues. In: Strichartz GR, ed. Local
Anesthetics. New York: Springer-Verlag; 1987.
 Scholz A. Mechanisms of (local) anaesthetics on voltage-
gated sodium and other ion channels. Br J Anaesth.
2002;89(1):52 61.