LOCAL ANAESTHESIA

IN
DENTISTRY

Dr Ahmed Osman

BDS 3 Semester 1- 2014

1

Objectives of the course
On completion of this course you should be able to demonstrate:
•An awareness of patients’ attitudes towards, motivations for, and
apprehension of dental treatment.
•Knowledge of a range of methods now available for the control of
apprehension and pain during dental treatment.
•An understanding of how these methods can improve the quality of dental
treatment
•The ability to evaluate a patient’s general condition and select the appropriate
pain control method to be used for their treatment.
•Competence in dealing with problems and emergencies arising during dental
treatment (BDS4).
2

Definitions
Anaesthesia: “reversible lack of awareness”.
It is the loss of sensation obtained by the
(local) administration of a certain chemical
that temporarily prevents the conduction of
pain impulses to the brain, without the loss of
consciousness
 Pain: is an unpleasant sensation created by a
stimulus and mediated along specific nerve
pathways into the CNS where it is interpreted
as such.

3

Question: does it lead to complete lack of “awareness” ?

developed the Lidocaine 1943 developed as a derivative of xylidine. cocaine. cannabis. Swedish chemist “Nils Löfgren”. Procaine was the first injectable man-made local anesthetic first synthesized in 1898 by the German chemist “Alfred Einhorn”. More than 500 yrs ago Abu al-Qasim and Ibn Zuhr (Avenzoar). were first to use inhalant anaesthesis and performed hundreds of surgeries with the use of narcoticsoaked sponges.History of Anaesthesia         Herbal 4200 BC : opium. 19th century :1844 nitrous oxide discovered by Horace Wells. 4 . 1846: Morton applied sulphuric ether 1872 intravenous anesthesia 1884 Karl Koller introduced the topical and regional anaesthesia (cocaine to eye surgery).

Uses of LA 5 .

Advantages of LA administration 6 .

LA VS GA Awake  Anyone  Day visit  One doctor  Low risk  Eating  Clinic  Alone  Cheap  7 Asleep Only healthy heart& lungs hospital stay two doctors high risk fasting OT Accompanied Expensive .

from injured free nerve endings.What causes pain at nerve endings?   Physical /Chemical Insults > Injury > tissue damage > release of Cytokines.   8 Question: What is hyperalgesia? Can LA cure or cause further damage? . inflammatory mediators (defense mechanism) Release of substance-P.

5 gm. And distilled water 100 cc. Vehicle: Ringer’s solution: Sodium chloride 0.Chemistry of LA       LA – Active agent Preservative: Antibacterial : Methylparaben (Bacterioststic) Antifungal : Thymoral Vasoconstrictor: adrenaline. The addition of vasoconstrictor and sodium metabisulfite lowers local anesthetic solution pH. Buffer: hydroxide resulting inSodium a slower onset of action and an increased “burning” sensation during injection (necessitating the addition of buffers) 9 .02gm. Reducing agent (VC preservative): Sodium Meta bisulfite. potassium chloride 0. nor-adrenaline. felypressin.

10 .Structure of LA An organic compound that is basically a tertiary Amine having 1.2 or the 3 hydrogen atoms have been replaced by organic radicals.

Structure of LA 1. 2. 3. 11 A Lipophilic Group: an aromatic portion that provides lipid solubility A Hydrophilic Group: a terminal amide that provide water solubility An Intermediate chain with either Ester or Amide linkage .

12 .Structure of LA  The aromatic end is lipophilic (soluble in lipids). anesthetic molecule dissolve in water in which it is delivered from the dentist’s syringe into the patient’s tissue. Because nerve cell is made of lipid bilayer it is possible for anesthetic molecule to penetrate through the nerve membrane.  The amine end is hydrophilic (soluble in water).

LA Action Action relies on: • Diffusion of LA base through tissue and nerve sheath • Binding at receptor site of nerve 13 .

: Metabolized in liver* and. Amide type –NH. and is very stable in solution (more resistant to hydrolysis) eg. Mepivacaine. Lidocaine. to a lesser extent. Prilocaine. * By microsomal P-450 enzymes in the liver (N-dealkylation and hydroxylation) 14 .: Readily hydrolysed in plasma through pseudocholinesterases and not stable in solution eg. Cocaine. Procaine . in other tissues.Types of anasethetic agents:    The intermediate chain can be of: Ester type -COO.

15 .

Types of anasethetic agents: 16 .

Thiophene Ring 17 .

18 .All commonly used local anaesthetics in dentistry have some vasodilator activity that leads to the following: •Increased rate of absorption into the blood stream decreased duration of action and effectiveness •Increased bleeding at the site of injection. •And possible overdose reactions due to high blood levels.

Effect of LA agent on BVs 19 .

bronchodilatation and VD of cardiac and skeletal muscle arteries and with depressed GIT motility and gluconeogenesis. salivary glands and gut)  Beta stimulation causes: increased Ht rate.000 &1:100.000 & 1:80.000 Acts on alpha and beta adrenergic receptors*  * Alpha stimulation leads to: contraction of smooth muscle cells (VC of skin. Adrenaline Most commonly used vasoconstrictor Concentration in LA range from 1:50. 20 .000 1:200.Chemistry of LA: (Vasoconstrictors):    1.

While epinephrine exerts both alpha and beta effects where the beta 2 stimulation vasodilates the skeletal muscles which decreases the diastollic BP compensating somehow to the alpha effects. 21 . * Epinephrine is preferred than norepinephrine and levonordefrin as these exert an excessive alpha 1 stimulation causing more peripheral VC >>BP.Chemistry of LA: (Vasoconstrictors):   2.Noradrenaline Similar to adrenaline Acts on alpha more than beta adrenergic receptors and constricts almost all blood vessels(small and large)* thus care must be taken when given to a hypertensive pt.

Therefore not use in pregnancy patients. thus stimulates uterine smooth muscle contraction.Chemistry of LA: (Vasoconstrictors): 3. Felypressin (octapressin)    Commonly used vasoconstrictor A synthetic analogue of the ADH vasopressin Has Oxytocic effect. 22 .

Duration of action: 23 .

Mode of action of LA (Theories)     MECHANICAL (the free base causes temporary coagulation of lipoid content of nerve) METABOLIC ( the base interferes with oxygen intake causing distorted intracellular oxidation of glucose causing paralysis) PHARMACOLOGIC: toxicity of the solution is “selective” to nerve tissue causing cessation of function. ELECTRIC: (depolarization theory) 24 .

ions  extracellulary Local anesthetic base diffuses through tissue and nerve sheath and binds to sodium receptors thus decreases the permeability of nerve membranes to sodium ions and prevents the influx of Na+ . Decrease rate of depolarization process and therefore preventing the conduction of impulses  25 .Conduction of nerve impulses  Resting potential across membrane    -60 to -90 mV K+ ions  intracellularly Na+. Cl.

Variation in neural response to LA 26 .

Effectiveness of LA depend on         Prior experience of pain Type of LA Concentration Volume given Vascularity of site Vasoconstrictor? pH of tissue at site of injection Correct Technique 27 .

 There are two major steps in drug metabolism. Phase I in which the drug molecule becomes ‘activated’ in the blood stream and local tissues by either oxidation. in highly vascular tissues such as skeletal muscle). reduction or hydrolysis.Absorption. the lungs. 28 . but this also takes place in the mucosa of the gut. Phase II takes place after activation and occurs usually in the liver. in the form of conjugation of the drug with some other chemicals to render it more water soluble in readiness for excretion. where a proportion of it becomes bound to plasma proteins while the free (unbound) anaesthetic agent becomes (re)distributed to tissues throughout the body (esp. biotransformation and elimination  The liver is the major organ for the biotransformation of LA drugs. blood plasma and kidneys.  Once it is absorbed by local circulation it enters the bloodstream to be transported to liver.

i.Absorption.e. 29 . biotransformation and elimination  Ester-type: are hydrolysed rapidly in the plasma by cholinesterase enzymes and is dissociated into ParaaminoBenzoic acid (PABA) and alcohol . Elimination: Both the ester and amide local anaesthetics and their metabolites (conjugated and unconjugated products) are excreted by the kidneys. oxidation and hydrolysis takes place mostly in tissues .e. Phases I and II both occur in the liver for the majority of amide anaesthetics. they are not broken down in blood stream but rather in the presence of catalysts in the liver ( microsomal P450 enzymes) then products are further oxidized and some are conjugated with glucuronic acid. In healthy individuals only a small percentage of the anaesthetic agent is excreted unchanged as the primary compound.i.  Amide-type: is more complex and takes longer than the breakdown of esters. And then it is further broken down in the liver before excretion. and in blood (where they are bound to plasma proteins but 2% are unbound –free) and to a lesser extent in liver) .

Clinical hint:   All nerve fibers are sensitive to local anesthetics. Thus. a differential block can be achieved (i. non-myelinated axons. those with a smaller diameter tend to be more sensitive than larger fibers.g. then large myelinated axons.e. Local anesthetics block conduction in the following order: small myelinated axons (e. but generally. those carrying nociceptive impulses). pain sensation is blocked more readily than other sensory modalities). 30 .

References 31 .

Best wishes 32 .