Pharmacology of

local anesthetics
Why are local anesthetics
different??
Local anesthetic, when used for
the management of pain, differs
from other drugs used in
dentistry in one important regard
i.e. almost all other drugs reach
blood stream & exert their effect,
while the action of local
anesthetics ceases when these
enter the blood stream.
 Uptake of local
anesthetic..
When injected into soft tissue, L.A.
exerts action on blood vessels of the
area.

Mostly producing vasodilatation, only

some can produce vasoconstriction..
E.g. Cocaine.

Procaine is probably the most potent

vasodilator, this property is used
Rotes of administration..
1. ORAL….
All L.A. Except cocaine are poorly
absorbed from G.I.T.
These undergo significant hepatic
first pass. e.g lidocaine. Approx 72%
of the absorbed dose is converted to
inactive metabolites..thereby
hampering its use as oral
antidysarhythmic.
Tocainide hydrochloride, analogue
2. Topical.…
Different rates of absorption for
different mucosa
ØTracheal mucosa- as rapid as i.v
ØPharyngeal mucosa- slow
ØEsophageal mucosa- slower then
pharyngeal.
Eg. Solarcaine, E.M.L.A – provides
anesthetic action to intact skin.
3. Injection….
Intravenous.. Clinically used
in primary management of
ventricular dysrhythmias.
Eg. Premature ventricular
contractions.
but these may cause toxic
reactions as well.
 Distribution…
From blood, L.A is distributed to body
tissues.
Highly perfused organs are:-
Ø Brain
Ø Liver
Ø Kidneys
Ø Lungs
Ø Spleen
Skeletal muscle, although not highly
perfused has higher distribution due to
 Blood levels of l.A
depend on…
q rate of absorption into C.V.S.
q rate of distribution to tissues
q rate of elimination.
Elimination half life of some L.A
agents:-
• Procaine -0.1 hrs
• Lidocaine-1.6 hrs
• Bupivacaine-3.5 hrs
All L.A readily cross B.B.B & placenta.
Metabolism/biotransform
ation…
There are two types of local
anesthetic

esters amides
with different types of
metabolism..
esters
Hydrolyzed in plasma by enzyme
pseudocholinesterase.
Rate of hydrolysis is different for
different compounds.
e.g. chlorprocaine is most rapidly
hydrolysed while tetracaine is
hydrolysed 16 times slowly.
PABA is the metabolic product causing
most of the allergic reactions.
Approx. 1 in 2800 people have atypical
form of pseudocholinesterase
Inability to hydrolysed LA & other
chemically related drugs.
atypical form of pseudocholinesterase
is hereditary trait so family history is
important.
amides
 Biotransformation
products
Significant in cases of renal &
cardiac failure.
e.g. orthotoluidine, a metabolite of
prilocaine , may cause clinically
significant methemoglobinemia.
Also, metabolites of lidocaine i.e.
monoethylglycinexylidide &glycine
xylidide may produce sedation.
excretion
Kidneys are primary excretory
organs.
A small dose may appear
unchanged in urine.
Esters are usually present as
metabolites while amides as parent
compounds.
Patients with severe renal impairment
pose a potential of toxicity
 Action of L.A.

Systemic local

L.A reversibly blocks action potential in

all membranes & thus C.V.S & C.N.S
are susceptible to their effects.
The actions of L.A depend on the
plasma concentration of the drug.
 Central nervous system
Rapidly cross BBB.
Pharmacologic action is depression.
3. Anticonvulsive property
Used especially in interrupting status
epilepticus at a dose of 2-3 mg/kg body wt,
given at a rate of 40-50mg/min.

Blood levels of lidocaine- anticonvulsive

anticonvulsive 0.5-4µg/ml
preseizure signs & symptoms 4.5-7µg/ml
tonic clonic seizures >7.5µg/ml
2. Analgesia
Earlier used as i.v. analgesic but not
used now due to low safety margin.
3. Mood elevation
Cocaine has been long used for
inducing euphoria & lessening
fatigue. Since cocaine causes
habituation it is no longer used.
 Cardiovascular system
L.A. have direct action on myocardium &
peripheral vasculature.
2. DIRECT ACTION ON MYOCARDIUM:-
L.A. produce myocardial depression,
decrease the conduction rate,
decrease the force of contraction.
Therapeutic advantage of this is taken in
managing the hyperexcitable
myocardium.
Therapeutic plasma levels for lidocaine
are1.8-6µg/ml. levels >6µg/ml lead to
2. Direct effect on peripheral
vasculature.
Cocaine causes vasoconstriction,
ropivacaine causes cutaneous
vasoconstriction, almost all others
cause vasodilatation.
The primary effect of L.A. on blood
pressure is hypotension- depression
of myocardium & relaxation of
 Local actions
No / minimal local irritant action.
Injected around a nerve cause
anesthesia.
Both sensory & motor nerves are
equally sensitive.
Order of pain blockade is pain,
temperature, touch, deep pressure
sense.
Applied to tongue bitter taste is lost
INDVIDUAL DRUGS IN LOCAL
ANESTHESIA & LOCAL
ANESTHESTICS IN DENTISRY
What are local anesthetics?
• Local anesthetic: drugs that have
little
no irritating effects when injected
into the
tissues & that will temporarily
interrupt
conduction when absorbed into the
nerve.
 CLASSIFICATION OF LOCAL
ANESTHETICS
• ESTERS AMIDES
Procaine Lidocaine
Prpoxycaine Etidocaine
2-chloroprocaine Bupivacaine
Tetracaine Mepivacaine
 Structures of Amides and Esters
• The amine end is hydrophilic (soluble in water), anesthetic
molecule dissolve in water in which it is delivered from the
dentist’s syringe into the patient’s tissue. It’s also
responsible for the solution to remain on either side of the
nerve membrane.
• The aromatic end is lipophilic(soluble in lipids). Because
nerve cell is made of lipid bilayer it is possible for
anesthetic molecule to penetrate through the nerve
membrane.
Differences of Esters and Amides
ESTERS AMIDES
result from the combination results from the combination
of para- amino benzoic acid of an aromatic amine & an
& an amino alcohol. Amino acid.
unstable in a solution stable in a solution
diffuse poorly through diffuse readily through
tissues tissues.

Pka value high pka value low

rmetabolisedby plasma metabolised in liver only

cholinestrases & liver.
produce less intense & produce more intense &
shorter lasting anaesthesia longer lasting anaesthesia.

allergic rxncan occur rarely cause allergic rxn

 Mechanism
• The mechanism of local anesthetics involves the ion channels,
nerve, and depolarization.
• Local anesthetics block the conduction in peripheral nerves that
inhibited the nerve to get excited and creates anesthesia.
• The anestheicis having a reversible action.
• The anesthetics inhibit the sodium ion influx across the
neuronal cell membrane .

• As a result, the nerve loses depolarization and the capacity to

create the impulse, the patient loses sensation in the area
supplied by the nerve.
 Factors Affect the action of Local Anesthetics
Lipid solubility
• All local anesthetics have weak bases. Increasing the lipid
solubility leads to faster nerve penetration, block sodium
channels, and speed up the onset of action.
• The more tightly local anesthetics bind to the protein, the
longer the duration of onset action.
• Local anesthetics have two forms, ionized and nonionized.
The nonionized form can cross the nerve membranes and
block the sodium channels.
• More non ionisedform present lead to faster onset of action.

pH influence
• Usually at range 7.6 – 8.9
• Decrease in pH shifts equilibrium toward the ionized form,
delaying the onset action.
• Lower pH, solution more acidic, gives slower onset of action
 Factors Affect the Reaction of Local
Anesthetics (cont.)
Vasodilation
greater vasodilator activity = increased blood flow through
the region=rapid removal of anesthetic molecule from the
injection site.
thus decreased anesthetic potency & decreased duration

• Vasoconstrictor is a substance used to keep the anesthetic

solution in place at a longer period and prolongs the action
of the drug
• vasoconstrictor delays the absorption which slows down the
absorption into the bloodstream
• Lower vasodilator activity of a local anesthetic leads to a
slower absorption and longer duration of action
• Vasoconstrictor used the naturally hormone called
epinephrine (adrenaline). Epinephrine decreases
vasodilation.

Side effects of epinephrine

• Epinephrine acts on the heart, causes the heart beat
 Factors of circulation levels
• Factors of circulation levels are the rates of
absorption,, distribution and metabolism.
• . Absorption depends on the speed of
administration and levels of the doses.
• Distribution allows absorption to occur in
three phases. First, the drug occurs at
highly vascular tissues in the lungs and
kidneys. Then it appears in less vascular,
muscle and fat.
• Then the drug is metabolized.
• Metabolism involves in the chemical
structure based on two classes, amide and
ester as discussed earlier.
• Rapid metabolism leads to decreased
 Toxicity
• Toxicity is the peak circulation levels of local anesthetics
• Levels of local anesthetic concentration administered to
patients are varied according to age, weight, and health.
• Maximum dose for an individual is usually between 70mg to
500mg
• The amount of dose also varied based on the type of
solution used and the presence of vasoconstrictor
Example:
---For adult whose weight is 150lbs and up, maximum dose
Articaine and lidocaine is about 500mg
---For children, the dosage reduced to about 1/3 to ½
depending on their weight.
The doses are not considered lethal.
Some common toxic effects:
--light headedness ---shivering or twitching --seizures
--hypotension (low blood pressure) --numbness
 HISTORY
• Cocaine was the first drug tried to produce surface anaesthesia.

• An ophthalmologist Carl Koller realized the importance of the

alkaloid’s anesthetic effect on mucous membranes.

• In 1884, he used the first local anesthetic on a patient with

glaucoma.

• Freud, Halsted, and Koller became addicted to the drug through

self-experimentation.

• Though having strong addicting CNS action but it was widely Used,
neverthless for 30 yr.

• Modification of cocaine molecule has been responsible for

producing vast no of local anesthetichs.

• Certain structural changes may increase toxicity or irritancy

without Increasing potency.
Aim in synthesis of new compound is to produce more potent
drug With decreased systemic & local toxicity
• However,if the structural change responsible for increased
potency also increases the rate of biotransformation, the toxicity
 Procaine replaced Novocaine
cocaine Problems
• In 1898, Professor Heinrich • Took too long to set (i.e. to
Braun introduced procaine produce the desired anesthetic
as the first derivative of result)
cocaine, also known as the • Wore off too quickly, not nearly
first synthetic local as potent as cocaine
anesthetic drug • Classified as an ester; esters
• Trade name is Novocaine® have high potential to cause
allergic reactions
• Caused high conc. of adrenaline
resulted in increasing heart rate,
make people feel nervous
Most dentists preferred not to used
any local anesthetic at all that
time; they used nitrous oxide
gas.
Today, procaine is not even
available for dental procedures.
PROCAINE(NOVACAINE)

• A diethyl amino ethyl ester of PABA

• Synthesised by german chemist EINHON 1905
• POTENCY-1( Procaine=1)
• TOXICITY- 1(procaine=1)
• METABOLISM-hydrolysed in plasma by plasma pseudocholine -estrase.
• EXCREATION- more than 2% unchanged in urine.
• VASODILATING PROPERTIES-produces the greatest vasodilatation of
all curently used local anesthetics.
ONSETOF ACTION- 6TO 10 min.
EFECTIVE DENTAL CONC-2% to 4%
SYSTEMIC EFFECTS-
CNS- crosses blood brain barrier it first stimulate the CNS & Latter on
can produce CNS depression.
CVS- no effect on CVS except vasodilatation of the microcirculation in the
injectin site.
RESPIRATORY SYSTEM-Large doses depresees the system
• PROPOXYCAINE 2 –CHLOROPOCAINE
• CHEMICAL FORMULA
2-diethyl amino ethyl -4 amino beta – diethyl amino
ethyl
2-prpoxy benzoate hydrochloride 2- chloro 4- amino
benzoate
POTENCY-7to8(procaine) 2 times potent than
procaine
TOXICITY-7to8(procaine) less toxic than that of

procaine because of
rapid
hydrolysis.
METABOLISM-
hydrolysed in the both hydrolysed in the
presence
plasma & the liver of plasma choline
estrases
 Lidocaine
• In 1940, the first modern local
anesthetic agent came in use that is
lidocaine , trade name Xylocaine®
• It developed as a derivative of
xylidine
• dental surgeries
• Belongs to the amide class, cause
little allergenic reaction; it’s
hypoallergenic
• Sets on quickly and produces a
desired anesthesia effect for several
hours
• It’s accepted broadly as the local
anesthetic in United States today
• POTENCY-2( compared with procaine)
• TOXICITY-2( Compared with procaine)
• METABOLISM-In liver by microsomal
fixed
function oxidases , to mono ethyl
glycerine
& xylidine.
EXCREATION- Via kidneys
 SYSTEMIC EFFECTS
• NERVOUS SYSTEM-
Lidocaine, in toxic doses,first produces stimulation
then depression of the CNS.
Lidocaineadminister I.V is capable of producing a
degree of analgesia & even general anesthesia.
RESPIRATORY SYSTEM-
small doses of lidocaine have a mild bronchodilating
effect
respiratory arrest is the most common cause of death
related to over dose of local anesthetics.
CARDIOVASCULAR SYSTEM-
Effect of lidocaine on the cvs varies in acc with dose
- the drug, indoses of 50 to 100mg (1.5mg /kg) is givaen I.V during
general anesthesia & surgery to correct ventricular arrhythmias.
In general moderately large doses produces a
-decrease in the electrical excitability force of ofthe myocardium
-decrease in the force of contraction( negative inotropic effect)
-decrease in the rate of electrical impulse conduction( negative
chronotropic effect)
Although these effects make lidocaine one of the most popular anti
arrhythmic agent.
 Three special drugs used in dental
• Bupivicaine (Marcaine®anesthesia
--Produce very long acting anesthetic effect to delay the post operative pain
from the surgery for as long as possible
--0.5% solution with vasoconstrictor
--toxicity slowed because the pKa is very basic
--Onset time is longer than other drugs b/c most of the radicals (about 80%) bind
to sodium channel proteins effectively
--less than four times that of lidocaine.

• Prilocaine (Citanest®)
--Identical pKa and same conc. with lidocaine
--Almost same duration as lidocaine
--Less toxic in higher doses than lidocaine b/c small vasodilatory activity

• Articaine (Septocaine®)
--newest local anesthetic drug approved by FDA in 2000
--Same pKa and toxicity as lidocaine, but its half life is less than about ¼ of
lidocaine
--Used with vasoconstrictor.
--Enters blood barrier smoothly
--The drug is widely used in most nations today
Conclusion
COMPLICATIONS OF LA.

Dr. Manu Gupta

M.D.S – I
Deptt. Of Oral &
Maxillofacial
Surgery
 Reactions to Local
Anesthesia
• Syncope • Loss of blood flow-
fainting-
Trendelburg
position

• Toxic • High level of drug

in circulation-
agitation-restless-
HR& BP up-then
CNS depression-
nonester have
depression only
 Reactions to Local
Anesthesia
• Allergic • Immediate- target
lungs and
circulatory
• Delayed-minor
type-hours to days
after - IM or IV or
oral
antihistamines-
Benadryl 50 mg
either IM or per
oral
 Complications of Injections
• Injury to nerve • Broken needle
– Inferior alveolar – Infrequent,removal
block • Infections
– Burning sensation – previously used
lip needle
• Injury to blood – passage of needle
vessels thru infected area
– Torn vessel- • Idiosyncrasy
hematoma – unknown reaction
– warm rinse/warm
compress reduce
 Anesthetic complications
Anesthetic complication may be defined
as any deviation from the normally
expected pattern during or after the
securing of regional analgesia.
CLASSIFICATION OF
COMPLICATIONS:
 
These complications may be classified
as follows.
Primary or secondary
 Complications may be further subdivided into
two groups.
– These attributed to the solution used.
– These attributed to the insertion of the
needles.
COMPLICATION OF LOCAL ANESTHETICS
SOLUTION

• Syncope (fainting)
• Muscle trismus
• Pain or hyperalgesia an infections.
• Edema
• Infections
• Broken needles
• Prolonged anaesthesia
• Hematoma
• Sloughing of tissues
• Facial nerve paralysis
• Soft tissue injury
Broken needles
Hematoma
Soft tissue injury
 Effects of over dosage of local
anesthesia
On CNS
On CVS
•Anxiety, restlessness
•Cardiac muscle
•Sighing respiration, beats
tremors less effectively

•Generalized •Cardiac output falls

convulsions
•Many LA’s produce
•Disorganized vasodilatation
respiration leading to
pallor of skin &
Death
Overdose
Predisposing factors
I. Patient factors
1. Age
2. Weight
3. Other drugs
4. Sex
5. Presence of disease
6. Genetics
7. Mental attitude & environment.
II. Drug factors

1. Concentration
2. Dose
3. Route of ad.
4. Rate of injection
5. Vascularity of the injection site
6. Presence of vacsoconstrictors.
Causes of Overdose
2. Biotransformation & elimination.
3. Excessive total dose.
4. Rapid absorption into the
circulation.
5. Intravascular injection.
 Classification of
Orofacialanesthetic
techniques:
I. LOCAL INFILTRATION
II. FIELD BLOCK
III. NERVE BLOCK
I. LOCAL INFILTRATION
• Technique that anesthetizes the terminal nerve
endings of the dental plexus.

• The procedure is performed in the direct vicinity

of the site of infiltration.

• Anesthetic fluid is injected deep the vestibular

fold and deposited on the periosteum of the
alveolar bone overlying the root apex
(supraperiosteal injection).

• In general, a localized tooth block may be

attempted on any tooth that has a vestibular
alveolar plate of bone thin enough to permit
 II. FIELD
BLOCK
• anesthetizes the terminal nerve branches in the
area.

• The deposition of local anesthetic at the apex of a

tooth for the purposes of achieving pulpal and
soft tissue anesthesia is often employed by many
dental and maxillofacial professionals.

• While this is commonly termed “local infiltration,”

it is important to note this is a misnomer. Terminal
nerve branches are anesthetized in this technique
and it is therefore correctly termed a field block.
 III. NERVE
BLOCK
• Larger areas and several teeth may be
anesthetized by blocking a main nerve.

• The anesthetic solution is deposited adjacent to a

main peripheral nerve.

• Will obviously produce a greater effect because

the farther proximally a nerve is blocked, the
greater the area anesthetized.
 Equipments
• Topical Anesthetic
Cartridge
• anesthesia cartridge
containers
•

•
 SYRINGE and NEEDLE

• t
Needle assembling
 Techniques of
Maxillary Regional
 I. Local Infiltration
• a. Supraperiosteal Injection
• b. Periodontal Ligament Injection
• c. Intraseptal Injection
• d. Intrapulpal Injection
• e. Local Palatal infiltration
•

II. Nerve block

• a. PSAN block
• b. ASAN block or Infraorbital Nerve
block
• c. Greater Palatine Nerve block
• d. Nasopalatine Nerve block
•
Techniques of Anesthesia for Treatment
of a Localized Area or 1 or 2 Teeth
 Supraperiosteal (Local)
Infiltration
- simplest and most commonly employed

Injection Site: Height of the mucobuccal fold above the

tooth

Technique:
• Insert the needle at the injection site to a depth of
no more than to a depth of no more than a few
millimeters and aspirate. Then inject one third to
one half (0.6-1.2cc) of a cartridge of anesthetic
solution slowly, over the course of thirty seconds.
Supraperiosteal (Local)
Infiltration
Periodontal Ligament
(Intraligamentary
- useful adjunct to the nerve block.

Injection Site: Sulcus between the gingiva and the

tooth

Technique:
• Insert the needle (bevel facing the root), to the
depth of the gingival sulcus
• Advance the needle until resistance is met. A small
amount of anesthetic (0.2cc) is then administered
slowly over the course of twenty to thirty seconds.
It is normal to experience resistance to the flow of
anesthetic.
 Periodontal Ligament
(Intraligamentary Injection)
 Intrapulpal
Injection
- involves anesthesia of the nerve within the
pulp canal of the individual tooth to be treated.
- may be used once the pulp chamber is open.

Injection Site: Pulp Chamber

Technique:
• Advance the needle into the pulp canal and
deposit another 0.2cc of local anesthetic solution.
• It may be necessary to bend the needle in order
to gain access to the chamber.
Local Palatal Infiltration

Injection Site: five to ten millimeters palatal

area of tooth

Technique:
• While maintaining pressure behind the
injection site, deposit anesthetic solution as
the soft tissue is penetrated. Advance the
needle until bone is contacted
Local Palatal Infiltration
Techniques of Anesthesia for Treatment of
Upper Quadrant for Multiple Teeth
 PSAN Block
• Also known as the tuberosity block or the
zygomatic block,

Injection site: height of the mucobuccal fold over the

2nd molar

Technique:
• Insert the needle at the injection site at a 45 degree
angle directed superiorly, medially, and posteriorly
(one continuous movement).

• Advance the needle, aspirate, and inject

• Prior to injecting, one should aspirate in two planes

to avoid accidental injection into the pterygoid plexus
Posterior Superior Alveolar
Nerve Block
 Anterior Superior Alveolar
Nerve Block/Infraorbital Nerve
• the ASA nerve may also innervate the premolar
teeth and mesiobuccal root of the 1st molar.

Injection site: ht. of the mucobuccal fold above the

max. 1st premolar
Technique:
• Identify the infraorbital notch and inferior to it is the
infraorbital foramen in line with the second premolar.

• Insert the needle at the injection site and The

syringe should be angled toward the infraorbital
foramen and kept parallel with the long axis of the
1st premolar to avoid hitting the maxillary bone
prematurely.
 Anterior Superior Alveolar
Nerve Block/Infraorbital Nerve
 Greater Palatine Nerve
Block
• is useful when treatment is necessary on the palatal
aspect of the maxillary premolar and molar dentition.

• This technique targets the area just anterior to the

greater palatine canal.

• The greater palatine nerve exits the canal and travels

forward between the bone and soft tissue of the
palate.

• Location of the greater palatine foramen is done by

placing it on a cotton swab the palatal tissue
approximately one centimeter medial to the junction
of the 2nd and 3rd molar
Greater Palatine Nerve
Block
Nasopalatine Nerve Block
• known as the incisive nerve block and
sphenopalatine nerve block,
• anesthetic solution is deposited in the area of the
incisive foramen.

Injection Site: lateral to the incisive papilla is the

injection site

Technique-:
• With a cotton swab, hold pressure over the incisive
papilla.
• Insert the needle just lateral to the papilla with the
bevel against the tissue.
• Advance the needle slowly toward the incisive
foramen while depositing small volumes of
anesthetic and maintaining pressure on the papilla.
Nasopalatine Nerve Block
Techniques of
Mandibular
• I. Local Infiltration
• a. Supraperiosteal Injection
• b. Periodontal Ligament Injection
• c. Intraseptal Injection
• d. Intrapulpal Injection
• are executed in the same manner as described above for maxillary
anesthesia.
• II. Nerve block
• a. Inferior Alveolar Nerve Block
• b. Buccal Nerve Block
• c. Gow-Gates Technique
• d. Vazirani-Akinosi
Closed Mouth Mandibular Block
• e. Mental Nerve Block
• f. Incisive Nerve Block
 Techniques of Anesthesia for
Treatment of Lower Quadrant for
Multiple Teeth
Inferior Alveolar Nerve
Block
Most commonly employed technique

This technique carries a high failure rate

The target for this technique is the mandibular

nerve as it travels on the medial aspect of the
ramus, prior to its entry into the mandibular
foramen.

The lingual, mental, and incisive nerves are also

anesthetized.

A 25 gauge long needle is preferred for this

 Inferior Alveolar Nerve
Block
• Technique- With the mouth open maximally,
identify the coronoid notch and the
pterygomandibular raphe.
• Bring the needle to the injection site from the
contralateral premolar region.
• Advance the needle until bone is contacted. Once
bone is contacted, withdraw the needle 1mm and
redirect the needle posteriorly by bringing the
barrel of the syringe towards the occlusal plane .
• Advance the needle to three quarters of its depth,
aspirate, and inject three quarters of a cartridge
of anesthetic solution slowly over the course of
one minute. As the needle is withdrawn, continue
to deposit the remaining one quarter of
anesthetic solution so as to anesthetize the
Inferior Alveolar Nerve
Block
 The buccal nerve block
• The buccal nerve block, otherwise known as the
long buccal or buccinator block
Technique-

• Identify the most distal molar tooth on the

side to be treated. The tissue just distal and
buccal to the last molar tooth is the target area
for injection . Needle should parallel to the
occlusal plane on the side of the injection. The
needle is inserted into the soft tissue and a few
drops of anesthetic solution are administered.
• 0.2cc of local anesthetic solution is deposited.
The buccal nerve block
 Mental Nerve Block
• The mental nerve block is indicated for
procedures where manipulation of buccal soft
tissue anterior to the mental foramen is
necessary.
Technique-

• The target area is the height of the

mucobuccal fold over the mental foramen .
• The foramen can be manually palpated by
applying gentle finger pressure to the body of the
mandible in the area of the premolar apicies.
• The needle is directed toward the mental
foramen with the bevel facing the bone.
Mental Nerve Block
Thank you.