3. Introduction
Most widely used method of pain control in
dental practice
Even with major advances in sedative and
General anesthesia techniques ,local
anesthetics remain the pharmacological
mainstay of a typical oral surgery practice
4. History
Horace Wells (1844) ,first used nitrous oxide for
anesthesia in tooth extraction.
First local anesthetic to be described was cocaine.
Albert Niemann (1859),German chemist-first to extract
and isolate cocaine.
On 15th September of 1884 ,Koller used cocaine for
treating glaucoma.
William Halsted,American surgeon,developed principles
of nerve block.
In November 1884,he performed infraorbital and inferior
alveolar nerve block.
1901 –Epinephrine ,first used as vasoconstrictor along with
local anesthetics.
6. Advantages
Patient remains awake and co-operative
Low incidence of morbidity
Patient leaves the office unescorted
No additional trained personnel required
Techniques not difficult to master
Percentage of failure is small
No additional expense to patients
Patient need not omit the previous meal
Little distortion of normal physiology,used to
advantage on poor risk patients
7. Indications:
Extraction of teeth
Odontectomy or surgical removal of teeth
Alveoloplasty & Alveolectomy
Incision and drainage
Cavity preparation - in deeper painful cavities
Pulpotomy and Pulpectomy
Periodontal and Gingival surgeries
Cyst enucleation and Marsupialization
Removal of residual infection , small neoplastic growths , salivary
stones
For relief from sore spots of dentures
Treatment of trismus
Therapy in trigeminal neuralgia
In radiotherapy when patient is gagging due to placement of film
For anesthesia of oral cavity and jaw bones in treatment of fracture
8. Contraindications
Fear and apprehension
Infection rules out the use of regional anesthesia
Allergic to local anesthetics
Below the age of reason
Patient with mental deficiencies
Major oral surgery makes it unfeasible
Anamolies makes it difficult or impossible
Patients with cardiac problems, Liver disorders,
Renal disorders
Specific local anesthetics in famial disorders
9. Ideal Properties
Non irritating
Not cause permanent alteration of nerve structure
Low systemic toxicity
Effective when injected or locally applied
Time of onset should be short
Sufficient duration of action
Potency sufficient to give complete anesthesia
Free from producing allergic reactions
Should be stable in solution and undergo
biotransformation readily
Sterile or capable of being sterlized by heat
without deterioration
Action must be reversible
10. Classification
1. According to the biological site
a . Agents acting at the receptor site on the external
surface of nerve membrane
Tetrodotoxin,saxitoxin
b. Acting on receptor site on the internal surface of
nerve membrane
quarternary ammonium analogues of Lidocaine,
scorpion venom
c. Agents acting by a receptor independent physio-
chemical mechanism
Benzocaine
d. Agents acting by combination of receptor and
receptor independent mechanism
Lidocaine, mepivacaine, prilocaine
11. 2. According to the duration of action
a. Ultra short-acting (<30 mins)
Procaine without vasoconstrictor
2% chloroprocaine without vasoconstrictor
b. Short acting(45-75 mins)
2% lidocaine with 1:100000 epinephrine
2% mepivacaine with 1:20000 levonordefrine
c. Medium acting(90-150 mins)
4% prilocaine with 1:200000 epinephrine
d.Long acting(180 mins or longer)
5% Bupivacaine with 1:200000 epinephrine
12. 3. According to chemical groups
Ester groups –
Benzoic acid ester - cocaine
benzocaine
Para aminobenzoic acid ester
procaine , tetracaine
propoxycaine
Non –ester group –
a. Anilides – bupivacaine
etidocaine
lidocaine
mepivacaine
prilocaine
13. 4. According to sources
a. Natural : cocaine
b. Synthetic nitrogenous :
Derivatives of PABA: Procaine, Benzocaine
Derivatives of acetanilide:Lidocaine
Quinoline derivatives:Cinchocaine
Acridine derivatives: Bucricaine
c.Synthetic non-nitrogenous :
Benzyl alcohol ,
d. Miscellaneous drugs with local action:
Clove oil, phenol, chlorpromazine,
antihistaminics like Diphenhydramine
14. 5. According to potency and duration of
action
a. Low potency & short duration
Procaine, chloroprocaine
b. Intermediate potency & duration
Lidocaine, Mepivacaine
c. High potency & long duration
Tetracaine, Bupivacaine
16. Mode and site of action :
Theories of Regional Anesthesia:
1. Acetyl choline theory
2. Calcium displacement theory
3. Surface charge theory
4 .Membrane expansion theory
5. Specific receptor theory
20. Mechanism of action
Following sequence is proposed for the
mechanism of action
1. Displacement of calcium ions from nerve receptor
site
2. Binding of local anesthetic molecule to this
receptor site
3. Bockade of the sodium channel
4. Decrease in sodium conductance
5. Depression of rate of electrical depolarization
6. Failure to achieve the threshold potential level
7. Lack of development of propogated action
potential
8. Conduction blockade
21. Mechanism of action in normal pH
L.A available as solutions of acid salts of weak bases
L.A weak base(BNHOH) combined with strong acid(HCL) to
make acid salt(BNHCL) solouble for use in solution
Acid salt(BNHCL) must dissociate into free base
Charged amino group(BNH+) dissociates outside nerve sheath
resulting in non-ionised Lipophilic molecule(BN)
Diffuses readily through the lipid composed nerve sheath
Combines with hydrogen ion(H+) produced from the Buffer
system
Results in the formationof an ionised hydrophyllic L.A
molecule(BNH+)
Displaces calcium gate
Provides a more impermeable gate for the influx of sodium
ions
22. In infected or inflamed areas
Inflammatory process produces acidic
products
pH is 5 to 6 (normal tissue pH-7.4)
Prevents deprotonization (conversion of
RNH+ to RN ) and liberation of free base
Results in poor anesthesia
23. Biotransformation
Ester type local anesthetics are hydrolysed in plasma by
pseudocholinesterase. Procaine, tetracaine, chloroprocaine
Some hydrolysis also occurs in liver
Atypical pseudocholinesterase –heriditary trait-relative
contraindication
Excreted in small concentrations in urine
Amide type of L.A- primary site of biotransformation is
Liver (70% of dose injected)
Relative contraindication in patients with Liver, Hepatic,
and cardiac failures
Present in urine as the parent compound in greater %
33. Local complications
1. Needle breakage
2. Pain on injection
3. Burning on injection
4. Persistent anesthesia or Paresthesia
5. Trismus
6. Hematoma
7. Infection
8. Edema
9. Sloughing of tissues
10. Lip chewing
11. Facial nerve paralysis
12Post anesthetic intraoral lesions
34. Systemic complications
1.Syncope
2.Toxicity Overdosage
Predisposing factors
Patient factors Drug factors
-age - vasoactivity
- weight - concentration
- other drugs - dose
- sex - route of admn
- diseases - rate of injection
- genetics - vascularity of inj site
- mental attitude - vasoconstrictors
35. Toxic effects on C .N. S-
Cortical stimulation
Cortical depression
Medullary stimulation
Medullary depression
Toxic effects on C. V .S -
36. Toxic effects on respiratory system
Allergic reactions:
Symptoms
Treatment
Prevention
37. Elevated blood levels of L.A may result
from:
1.Large dose administration
2. Rapid absorbtion from the site of injection
3. Intravascular administration of L.A
4.Unusually slow Biotransformation of the
drug
5.Decreased rate of elimination of the drug
39. References
Monheim”s :Local anesthesia & pain
control in Dental practice
Stanley.F.Malamed:Hand book of L.A
Allan Donald : Dental Analgesia &
anesthesia
Tripathi:Pharmacology
