Prepared by Malik Zahid Akbar Group # 610

Tooth extraction
Indications:
1. 2. 3. 4.

Grossly carious tooth which cannot be restored Acute/chronic pulpitis which cant be restored by RCT Periodontal diseases More than half of alveolar bone loss Fracture of tooth Root Longitudinal If tooth lies on jaw # line

Indication cont.. 5. Bony lesion lies over the tooth Cyst, Tumor,OM 6. Impacted tooth 7. Aesthetic indication 8. Orthodontic appliances Teeth crowding 9. Supernumerary and malposed teeth 10. Retained deciduous tooth if permanent successor is present 11. If tooth hurting the soft tissue Upper 3rd molar damaging the lower 3rd molar gum tissue

Contraindications: General 1. Cardiac diseases - Valvular heart diseases, RHD, Hypertension,Patients on anticoagulation therapy 2. Blood disorders (Severe anemia, Leukemia, Hemophilia) 3. Liver disease (Vitamin K deficiency, Clotting factor deficiency) 4. DM 5. Pregnancy- 1st and 3rd trimester 6. Epilepsy patient 7. Allergic to local anesthesia 8. Psychiatric patient 9. Very old patient 10. Uncooperative patient/ Lack of consent 11. Patient on steroids 12. High grade fever

Contraindication :
Local 1. Acute gingivitis 2. Acute periodontitis 3. Acute pericoronitis 4. Acute cellulitis 5. Acute osteomyelitis 6. Malignancy

Any acute infection except Acute pulpitis is not contra indication of tooth extraction but it is rather indication of extraction

Post extraction instructions: 1. Bite on cotton or gauge for half an hour 2. Dont spit or rinse as far as possible 3. Dont take hot water or food at least for 12 hour 4. No physical activity for 24 hours 5. Soft lukewarm comfortable foods 6. Intake of antibiotics and analgesics as prescribed by dentist 7. Cold compress with ice packs 8. No smoking / Alcohol / Tobacco 9. If any bleeding, pain or complications contact hospital or dentist immediately 10. Warm saline wash after 24 hrs for next 2 or 3 days
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Complications 1. Fracture of Crown, Root, Alveolar bone, Adjacent tooth 2. Dislocation of TMJ 3. Trauma to Gingiva, Lips, Tongue, Palate 4. Intraoperative and post operative hemorrhage 5. Trismus 6. Infection : local /systemic 7. Anesthesia related complication

Antibiotic prophylaxis:
Under L.A Amoxycillin 3gm 1 hour before surgery,If allergic to Amoxycillin then give Clindamycin 600mg Under G.A Amoxycillin IV + oral 1gm at induction and 0.5 gm 6 hours later,If allergic then Vancomycin IV infusion1gm over 1 hour+Gentamycin120mg IV
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Position

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Extraction movement Primary movement: Along longitudinal axis of root Secondary movement: Main extracting movement Rotatory Buccolingual or labiolingual Mesodistal Lifting the tooth

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Upper central and lateral incissor Rotation only Upper canine Rotation initially, some labiolingual movement may be needed Upper premolar and molar Buccopalatal movement

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Lower central and lateral incissor Labiolingual movement Lower canine Rotatory and labiolingual Lower premolar Rotatory Lower molar Buccolingual movement

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Nerve supply: Maxilla Posterior superior alveolar nerve: Molars Middle superior alveolar nerve: Premolars Anterior superior alveolar nerve: Canines and Incissor Sensory supply of palate from greater and lesser palatine nerves as well

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Mandibular nerve: Lingual nerve Inferior alveolar nerve : Enters the mandibular canal

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Dental block Types of blocks Supraperiosteal injection Mental nerve block Anterior superior alveolar (Infraorbital) nerve block Posterior superior alveolar nerve block Inferior alveolar nerve block

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Choice of anesthesia in dental procedure 2% lidocaine/Xylocaine with 1:100,000 epinephrine is a good choice. This provides about 1 hour of dental pulp analgesia 3 to 5 hours of soft-tissue analgesia For temporary relief of pain, the preferred agent is 0.5% Bupivacaine with 1:200,000 epinephrine 1 to 3 hours of dental pulp analgesia 4 to 9 hours of soft-tissue analgesia Duration of analgesia is less with supraperiosteal injections than with regional nerve blocks

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Inferior alveolar nerve block Most widely used anesthetic procedure in dentistry All mandibular teeth to midline Anterior 2/3 of tongue Floor of oral cavity Complication: Infection Patient having tendency to bite tongue or lips

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Aim is to deposit solution around the inferior alveolar nerve as it enters the mandibular foramen underneath the lingula The patient's mouth must be widely open, inferior border being parallel to ground Palpate the landmarks of external and internal oblique ridges and note the line of the ptyerygomandibular raphe

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Index finger is used to stretch the tissues over the injection site, maximizing visibility and minimizing the pain of the injection. Orient the syringe so that the barrel is in the opposite corner of the mouth, resting on the premolars Aim toward your index finger and slowly penetrate the mucosa until bone is contacted, usually a distance of about 2.5 cm Needle should be parallel to occlusal surface

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Withdraw

slightly and aspirate If no blood is returned, inject 1.5 to 2 mL of anesthetic If aspiration is positive, pull back and redirect slightly, then repeat If a lingual nerve block is required 0.5 ml of LA is injected after withdrawal of 0.5cm of the needle

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Supraperiosteal infiltration Also called local infiltration Teeth affected Any maxillary tooth Only can anesthetize 2 or 3 adjacent teeth Poor option for mandibular tooth because of relatively high density

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The

aim is to deposit LA supraperiosteally in as close proximity as possible to the apex of the tooth to be anaesthetized. The LA will diffuse through periosteum and bone to bathe the nerves entering the apex. Reflect the lip or cheek to place mucosa on tension and insert the needle along the long axis of the tooth aiming towards bone. At approximate apex of tooth, withdraw slightly and deposit LA slowly

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Mental nerve block Apex of the second premolar Tissue and teeth affected Buccal soft tissues from 2nd mandibular premolar to midline skin of lower lip and chin

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Infraorbital block Just inferior to the infraorbital notch Teeth affected Incisors Canines premolars

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Local Anesthetics in Dentistry

What are local anesthetics?

Local

anesthetic: produce loss of sensation to pain in a specific area of the body without the loss of consciousness

History

Coca leaves from the genus Erythroxylum Erythroxylum contains high concentration of alkaloid up to 0.7-1.8% Alkaloid has natural nitrogen bases found in the coca leaves, also known as cocaine Genus Erythroxylum discovered in South America, Venezuela, Bolivia, and Peru since pre-Columbian periods Earliest cultivation and use of the coca leaf went back to about 700 BC in Bolivia and Andes regions New discoveries showed humans used coca more than 5,000 years ago in Ecuador

History (cont.)
Spanish conquistadors and explorers witnessed the consumption of coca in South America Spaniards, such as Alfred Buhler, hypothesized a tribe in the Negro River area called Arhuaco was the original discoverers of the properties and functions of the drugs. In 1571, Pedro Pizarro, a conquistador of Inca, observed nobles and high rank officials of the Inca empire consumed the coca plant. After the fall of the Inca empire, coca consumption spread widely to the population

Development of general and local anesthesia

Took place in Western Europe from 1750 to 1850 Chemists and physicians collected sample of coca leaves for experiments Isolated active principle of coca leaf, synthesized to a drug for patients to feel more relief of pain when taking surgeries In 1860, German chemist Albert Niemann successfully isolate the active principle of coca leaf; he named it cocaine

Development of general and local anesthesia (cont.)

In 1865, Willhelm Lossen determine the correct molecular formula of cocaine (C17H21NO4) Niemann discovered the effect of numbness of the tongues caused by alkaloid in 1860 Based on Niemanns discovery, Russian physician Basil Von Anrep did experiments on animals, such as rats, dogs, and cats. He injected small quantity of 1% solution to his tongue; tongue became insensitive He concluded cocaine is a good drug for surgical anesthetic William Steward Halsted and Richard John Hall developed the inferior dental nerve block techniques for dentistry

Cocaine Addiction

More physicians began to do research of cocaine in the clinic trials. The physician Sigmund Freud used the stimulant effect of cocaine to treat the morphine addiction in patients An ophthalmologist Carl Koller realized the importance of the alkaloids 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

Side Effects of Cocaine and Solutions

Minor: Addiction Intoxication Solutions: Used nitrous oxide gases and ether for minor surgery in dentistry Give a low concentration of cocaine; it slows down the release of the drug into the bloodstream causing little side effects

Severe: Death

Procaine replaced cocaine

Novocaine Problems
Took too long to set (i.e. to produce the desired anesthetic result) Wore off too quickly, not nearly as potent as cocaine Classified as an ester; esters 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.

In 1898, Professor Heinrich Braun introduced procaine as the first derivative of cocaine, also known as the first synthetic local anesthetic drug Trade name is Novocaine

Lidocaine

In 1940, the first modern local anesthetic agent was lidocaine, trade name Xylocaine It developed as a derivative of xylidine Lidocaine relieves pain during the dental surgeries Belongs to the amide class, cause little allergenic reaction; its hypoallergenic Sets on quickly and produces a desired anesthesia effect for several hours Its accepted broadly as the local anesthetic in United States today

Differences of Esters and Amides

All local anesthetics are weak bases. Chemical structure of local anesthetics have an amine group on one end connect to an aromatic ring on the other and an amine group on the right side. The amine end is hydrophilic (soluble in water), and the aromatic end is lipophilic (soluble in lipids) Two classes of local anesthetics are amino amides and amino esters. Amides: Esters: --Amide link b/t intermediate --Ester link b/t intermediate chain and chain and aromatic ring aromatic ring --Metabolized in liver and very --Metabolized in plasma through soluble in the solution pseudocholinesterases and not stable in the solution --Cause allergic reactions

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 dentists syringe into the patients tissue. Its 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. The trick the anesthetic molecule must play is getting from one side of the membrane to the other.

Mechanism

The mechanism of local anesthetics connects with the ion channels, nerve, and depolarization. Local anesthetics block the conduction in peripheral nerves that inhibited the nerve to excited and created anesthesia. The anesthetic is a reversible reaction. It binds and activates the sodium channels. The sodium influx through these channels and depolarizes the nerve cell membranes. It also created high impulses along the way. 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 Reaction 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. So, the more nonionized presented, the faster the onset 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 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 vasodilator. Side effects of epinephrine Epinephrine circulates the heart, causes the heart beat stronger and faster, and makes people feel nervous.

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 depending on their weight. The doses are not considered lethal.

Some common toxic effects:

--light headedness ---shivering or twitching --hypotension (low blood pressure) --numbness --seizures

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 less in 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. Decreasing the potential toxicity resulted in rapid metabolism.

Three special drugs used in dental anesthesia

Bupivicaine (Marcaine

--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 showed by 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 --most toxic local anesthetic drug

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 of lidocaine --Used with vasoconstrictor. --Enters blood barrier smoothly --The drug is widely used in most nations today

Conclusion
Anesthetic pKa Onset Duration (with Epinephrine) in minutes Max Dose (with Epinephrine)

Procaine
Lidocaine

9.1
7.9

Slow
Rapid

45 - 90
120 - 240

8mg/kg 10mg/kg
4.5mg/kg 7mg/kg 2.5mg/kg 3mg/kg 5mg/kg 7.5mg/kg 4.0mg/kg 7mg/kg

Bupivacaine Prilocaine Articaine

8.1 7.9 7.8

Slow Medium Rapid

4 hours 8 hours 90 - 360 140 - 270

References
Peter

C. Meltzer, Shanghao Liu, Heather S. Blanchette, Paul Blundell, Bertha K. Madras. Design and Synthesis of an Irreversible Dopamine-Sparing Cocaine Antagonist. @ Bioorganic & Medicinal Chemistry Volume 10, Issue 11 , November 2002, Pages 35833591 www.who.org Don R Revis, Jr. Local Anesthetics. October 14,2004: (Medline) http://www.emedicine.com/ent/topic20.htm