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Local Anesthesia in Dentistry

Ritu Bahl
School of Dental Medicine, University of Connecticut Health Center, Farmington, Connecticut

This paper was the First Place winning Contest for 2003.


of the ADSA Student Essay Award

Pain and dentistry are often synonymous in the minds of patients, especially those with poor dentition due to multiple extractions, periodontal disease requiring surgery, or symptomatic teeth requiring endodontic therapy. Members of the public perceive a good dentist as a practitioner who causes little or no discomfort. In turn, dental practitioners identify a good anesthetic as one that allows them to focus solely on operative procedures without distractions from pain-induced patient movements. The everyday practice of dentistry is therefore based upon achieving adequate local anesthesia. Research has shown that the fear of pain associated with dentistry is closely associated with the most common method for blocking pain during dental procedures-intraoral administration of local anesthetics. This is considered aversive due to the pain associated with the injection and the perceived threat of needle puncture prior to the injection.1 Another survey finding was that those individuals who reported themselves as highly fearful of dentistry were worried about receiving oral injections and demonstrated an association between high dental anxieties and missed or delayed appointments.2 Pain is a result of stimulation of nociceptors that are receptors preferentially sensitive to a noxious stimulus or a stimulus that will become noxious if prolonged. When nociception reaches the cerebral cortex, it may be perceived as pain. Pain may be abolished by interrupting the pathways that carry the information of the stimulus from the periphery of the body to the central nervous system, by blocking the central nervous system, or by removing the stimulus. Local anesthetics block sensory neuronal conduction of noxious stimuli from reaching the central nervous system.
Received June 20, 2003; accepted for publication July 12, 2004. Address correspondence to Ritu Bahl, School of Dental Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030; Anesth Prog 51:138-142 2004 ) 2004 by the American Dental Society of Anesthesiology

The sensory supply to the teeth, jaws, and oral mucosa is derived from the maxillary and mandibular division of the trigeminal (fifth cranial) nerve, whose cell bodies are found in the Gasserian ganglion. The maxillary nerve carries purely sensory fibers, exits the skull through the foramen rotundum, and enters the pterygo-palatine fossa. At this point the maxillary nerve gives branches to the sphenopalatine ganglion. Among the nerves that pass through the sphenopalatine ganglion is the nasopalatine nerve (also called the long sphenopalatine nerve) that passes along the nasal septum and emerges at the incisive foramen on the anterior hard palate. It supplies sensation to the gingival soft tissues of the anterior hard palate. The greater and lesser palatine nerves also pass through the sphenopalatine ganglion and course through the greater and lesser foramina, respectively. The greater palatine innervates the palatal mucoperiosteum and the gingiva from the molars to the area near the cuspid region that abuts tissue supplied by the nasopalatine nerve. The lesser palatine nerve supplies the tissues of the soft palate and uvula. The maxillary nerve also gives rise to the posterior superior alveolar nerve, which supplies sensation to the buccal gingiva and periodontium adjacent to the maxillary molar teeth and the pulps of all molar teeth except the mesiobuccal pulp of the upper first molar. That mesio-buccal pulp is supplied by another branch of the maxillary nerve, the middle superior alveolar nerve, which also innervates the pulps, buccal gingiva, and peridontium of the maxillary premolars. The final branch of the maxillary nerve, the anterior superior alveolar nerve, supplies the pulps of the upper incisors and cuspid along with the associated buccal gingiva and periodontium.3,4 Unlike the maxillary division, the mandibular division of the trigeminal nerve is a mixed motor and sensory nerve. The mandibular nerve exits the skull through the foramen ovale to enter the infratemporal fossa. It then
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Anesth Prog 51:138-142 2004



Chemical Classification and Duration of Action of Local Anesthetic Agents Local Anesthetic Classification Lidocaine Amide Prilocaine Amide Mepivacaine Amide Bupivacaine Amide Etidocaine Amide Articaine Amide with an ester side chain Procaine Ester

Duration Intermediate Intermediate Intermediate Long-acting Long-acting Intermediate


divides into anterior and posterior divisions. The anterior division has some sensory branches: the long buccal nerve that supplies the buccal mucosa and the gingiva adjacent to the lower molar and second premolar teeth. Other fibers supply sensation to the skin of the cheek. The posterior division is primarily sensory. It branches to give the auriculotemporal, lingual, and inferior alveolar dental nerves. The lingual nerve innervates the lingual gingiva, floor of the mouth, and anterior two thirds of the tongue. The inferior alveolar nerve supplies sensation to the pulp and periodontium of all the molar and premolar teeth on 1 side of the mouth. Near the mental foramen, the inferior alveolar nerve branches into the incisive and mental nerves. The mental nerve innervates the buccal gingiva and the mucosa from the mental foramen forward to the midline, including the skin of the lower lip and chin. The incisive nerve supplies the pulps of the first premolar, canine, and incisor teeth.3,4

Rapid onset of action Suitable duration of action Active whether applied topically or injected Nonirritant Causes no permanent damage No systemic toxicity High therapeutic ratio Chemically stable and a long shelf life Ability to combine with other agents without loss of properties * Sterilizable without loss of properties * Nonallergenic * Nonaddictive * * * * * * * * *
In spite of the major advances made in the field of anesthesia, the ideal local anesthetic agent does not exist. Local anesthetic agents can be classified in several ways (as shown in the Table):

LOCAL ANESTHESIA Local anesthesia is defined as a loss of sensation in a circumscribed area of the body by a depression of excitation in nerve endings or an inhibition of the conduction process in the peripheral nerves. In clinical practice a localized loss of pain sensation is desired. Although the terms dental anesthesia and dental analgesia are used synonymously in dentistry, local analgesia is more accurate. Local anesthesia can be achieved by a number of mechanisms including mechanical trauma, anoxia, and use of neurolytic agents in addition to traditional local anesthetic drugs. However, clinically only reversible local anesthetic agents and other reversible techniques such as temperature reduction or electronic stimulation are useful to prevent pain. The use of reversible local anesthetic chemical agents is the most common method to achieve pain control in dental practice.5 Some ideal properties of local anesthetics are as follows:
* Specific action * Reversible action

* Chemical structure: local anesthetics are classified usually as either esters or amides. * Duration of action: local anesthetics maybe classified as short acting, intermediate-acting, or long-acting. The injectable local anesthetics used in dentistry have a common core structure consisting of5,6 * Hydrophilic amino terminal * Intermediate chain * Lipophilic aromatic terminal

The combination of hydrophilic and lipophilic properties in 1 molecule is essential for an injectable local anesthetic to be effective. The hydrophilic portion of the molecule consists of a substituted secondary or tertiary amine. Solubility in water is essential for 2 reasons-to allow for the dissolution in a solvent to permit injection, and to allow penetration through interstitial fluid following administration.5,6 The intermediate chain consists of either an amide or ester linkage. This allows spatial separation of the hydrophilic and lipophilic components of the molecule. The older agents, procaine and cocaine, are ester-based


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drugs but are no longer widely used as dental anesthetics due to their unwanted side effects, such as toxic or allergic reactions. The lipophilic part of the local anesthetic agent is an aromatic residue that is essential for its ability to penetrate fatty tissue such as the lipid sheath of nerves in order to gain access to the nerve cell membrane to reach its site of action. Different drugs have different proportions of hydrophilic and lipophilic components. These differences modify the characteristics and/or the properties of the anesthetic agents in the following ways:

the nerve fibers. Thin fibers are anesthetized more rapidly as compared with thick fibers, possibly because the nodes of Ranvier are closer together. Duration of action: duration of action of anesthesia is dependent on the rate of diffusion along a concentration gradient away from its site of action-the ion channels in the nerves. Effects on other tissues including toxicity: the functions of lipid-containing organs and tissues such as the brain and heart may be affected by high levels of local anesthetics. Rate of degradation, both systemically and locally: most amide local anesthetic agents are broken down by hepatic dealkylation and hydrolysis and are subsequentially conjugated with glucuronic acid and excreted in the urine. Esters are metabolized by esterases that are widely distributed in the body.

Intrinsic anesthetic potency: the minimum concentration of local anesthetic required to reduce the nerve amplitude by half its amplitude within 5 minutes. It is a measure of pharmacologic action of the agent. Onset of anesthesia: the onset of anesthesia is dependent on the speed at which the agent passes through the tissue, the proximity of site of injection to the nerve to be anesthetized, and the diameter of

constrictor and acts by competing with the vasoconstrictor for oxygen available in the solution. The most commonly used reducing agent is sodium metabisulfite. * Preservative: a bacteriostatic preservative prolongs the shelf life of the solution, but since preservatives can provoke allergic reactions, they are no longer contained in dental local anesthetic cartridges in the United States. The typical shelf life of an anesthetic without preservative is approximately 18 months to 2 years. * Fungicide: Thymol is used occasionally as a fungicide. * Carrier solution: an acidic aqueous solution dissolves the local anesthetic salt and maintains it at an acceptable pH.


All local anesthetic agents used in dentistry work by obstructing the exchange in Na+ permeability, which is essential for the initial phases of a neuronal action potential. This mechanism prevents the development and propagation of the action potential by preventing the wave of depolarization.

FAILURE OF ANESTHESIA Failure of local anesthetics to achieve profound analgesia may be related to:
* inaccurate anatomic placement of local anesthetic solution * placing too little solution * allowing insufficient time for it to diffuse and take effect * injecting into inflamed or infected tissues * using an outdated or improperly stored anesthetic solution.
It is recommended that a local anesthetic not be injected in infected tissue because of the risk of spreading the infection and the increased probability of achieving less than effective anesthetic results owing to the low pH within the infected tissue maintaining the ionized, nonlipid-soluble state to the anesthetic.

The general constituents of thetic solution are:

* *

dental cartridge of


Local anesthetic agent Vasoconstrictor: this is sometimes included to delay the removal of the anesthetic from the tissues by decreasing the blood flow through adjacent blood vessels. A vasoconstrictor produces the following advantages: (a) longer duration of local anesthetic action, (b) reduced bleeding of a surgical site, and (c) reduced systemic effects. The most commonly used vasoconstrictors are epinephrine (adrenaline) and octapressin (felypressin). Only epinephrine is available in the United States. Reducing agent: this prevents oxidation of the vaso-


Complications of local anesthetic administration include both local effects and systemic effects.7 Local complications include:

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* Spread of infection: occasionally infection may be spread into the tissues by the needle passing through a contaminated tissue or by the needle being contaminated before use. * Hematoma: damage of a blood vessel by the tip of a needle may lead to bleeding into the tissues, resulting in the formation of a hematoma. Significant bleeding may produce swelling, act as an irritant to the tissues, and cause pain and trismus. Theoretically, the localized collection of blood becomes an ideal culture medium for bacteria, although infection of a hematoma is unusual. * Nerve damage: rarely, during an injection the needle may pierce a nerve bundle during placement, producing an immediate electric shock sensation to the patient. It is usually followed by a partial sensory deficit, but subsequently a complete return to normal sensation usually follows. * Blockade of the facial nerve: if the injection is given in close proximity to the facial nerve, a motor blockade causing temporary paralysis of the muscles of facial expression may occur. The effect may last for 12 hours. In such circumstances, the desired branch of the trigeminal nerve will not be anesthetized, and a subsequent injection will be required at the correct anatomic location to achieve the desired effect.



metabolism of these drugs is impaired. Ester-type local anesthetics are no longer routinely used for dental procedures. * Methemoglobinemia: this is a rare complication caused by a metabolite of prilocaine that oxidizes the ferrous component of heme in red blood cells to the ferric state. This reduces their oxygen-delivering capacity and results in tissue hypoxia.


Systemic complications include:

* Regional or systemic infection: the spread of infection within the perioral tissues can be potentially spread through planes of the head and neck by passage of a needle through an infected area. * Endocarditis risk: injections such as the intraligamentary injection can force bacteria into the systemic circulation and cause bacterial endocarditis. * Cardiovascular disease: patients with ischemic heart disease (angina pectoris, previous myocardial infarction) or who have had previous cardiac surgery or circulatory dysfunction such as cardiac failure, show higher plasma levels of lidocaine when compared with healthy subjects given the same dose. Therefore it is recommended that the maximum safe dose be halved in such patients.8 Low plasma potassium levels and acidosis also potentiate adverse effects of local anesthetics on the myocardium.7 * Liver disease: patients with reduced hepatic function may exhibit an abnormally decreased rate of metabolism of amide local anesthetics, resulting in potentially toxic blood levels. Dosage levels must therefore be reduced for these patients. * Pseudocholinesterase deficiency: local anesthetics of the ester type (eg, procaine) should be avoided in patients who have this rare familial enzyme defect as

The adverse drug reactions during pregnancy may affect either the mother or the fetus. Hypersensitivity, allergy, or toxicity reactions in the mother may compromise her health and limit her ability to support a pregnancy. Fortunately, doses of local anesthetics in dentistry are usually relatively small and are generally unlikely to cause complications during pregnancy. All local anesthetics cross the placenta to some degree.9-11 Highest concentrations in the fetal circulation follow injection of prilocaine, and the lowest follow bupivacaine, with lidocaine in between.12."3 Felypressin, which is a derivative of vasopressin and is related to oxytocin, has the potential to cause uterine contractions. Although this is a highly unlikely effect at the low dose of felypressin used in local anesthetics, it is best avoided during pregnancy. Lidocaine with epinephrine is commonly used for pregnant dental patients. The performance of common dental treatments for a pregnant patient is highly variable. In a telephone survey using a standardized questionnaire, 78 resident dentists in Germany, Switzerland, and Austria were interviewed with respect to several aspects of the dental treatment of pregnant women. Only 58% of the interviewees decided clearly in favor of using local anesthetics, 59% supported the use of analgesics, 70% supported a possible antibiotic therapy, and 33% would agree with a radiological examination during pregnancy.9"13 In addition, according to references in the specialist literature, guidelines for the dental treatment, drug therapy, and radiological diagnosis of pregnant women are presented.12 The local anesthetics should have a high plasma protein bonding capability (Articaine, bupivacaine, etidocaine) and minimum epinephrine concentrations. Acetaminophen is the usual analgesic of choice for pregnant dental patients. If an antibiotic treatment is required, penicillin, cephalosporin, and erythromycin are recommended. In particular, during the first 3-month period, radiological examinations should be restricted to the absolute minimum and performed only if no rea-


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sonable alternative is available, although the radiological burden on the fetus falls 500,000 times short of the limit value of 50 mgray (5 rad) in the case of a microradiogram, and 50,000 times short of the limit value in the case of an orthopantomogram.2

Fixed pediatric dosage recommendations for a given age range are no longer endorsed for local anesthetic and sedative agents. Available data suggest that adverse reactions in pediatric patients are commonly caused by inadequate dosage reduction.14 Maximum recommended doses of local anesthetics is based upon the weight of the child, usually expressed as milligrams per kilogram of body weight. For very obese children, the maximum dose should be calculated on the basis of leanbody weight or ideal weight, not the true body weight. The specific number of milligrams per kilogram used for calculating the maximum recommended dose differs among the various local anesthetics.
It is incumbent upon every dental practitioner to treat his or her patients in an appropriate way, taking into consideration both their dental needs and any special precautions related to their past medical history. To prevent any implication of negligence, a practitioner must administer appropriate treatment. Furthermore the patient should receive adequate information about the proposed dental treatment and must submit themselves willingly to a local anesthetic as a part of the proposed dental treatment after the benefits and risks are explained. Medico-legal complaints arising from administration of local anesthesia are few in number. There are, however, some particular complications arising directly from the local anesthetic drugs or their delivery that merit consideration. Persisting anesthesia or paresthesia due to damage to various branches of the trigeminal nerve is a common complication in dental surgical procedures, especially associated with lower third molar removal. Cases relating to sensory loss of lingual nerve and inferior alveolar nerve following inferior dental block injections for restorative procedures have occasionally been presented as a legal complaint. In a study of over 12,000 inferior dental block injections, all given for restorative treatment, 18 patients

(0.15%) were found to have some lingual sensory disturbance following treatment. Of these 18 patients, 17 patients totally regained normal sensation within 6 months, and 1 patient still had a loss of sensation after 1 year (0.008%). Of the 12,000 patients, 856 (7%) experienced an "electric shock" type feeling in the tongue at the time of injection, suggesting that the tip of the anesthetic needle had touched the lingual nerve.3 Although the medico-legal issues tend to frighten the dental practitioner, statistical data demonstrate that if the current standards of practice are observed, the dentist is unlikely to run into these types of problems. REFERENCES
1. Rosenberg ES. A computer-controlled anesthetic delivery system in a periodontal practice: patient satisfaction and acceptance. J Esthet Restor Dent. 2002;14:39-46. 2. Robinson PD, Pitt Ford TR, McDonald F. Local anesthesia in dentistry. London: Reed Educational and Professional Publishing; 2000. 3. Kraft TC, Hickel R. Clinical investigation into the incidence of direct damage to the lingual nerve caused by local anesthesia. J Craniomaxillofac Surg. 1994;22:294-296. 4. Dionne RA, Phero JC, Becker DE. Management of pain and anxiety in the dental office. Philadelphia: WB Saunders; 2002. 5. Haas DA. An update on local anesthetics in dentistry. J Can Dent Assoc. 2002;68:546-551. 6. Meechan JG, Robb ND, Seymour RA. Pain and anxiety control for the conscious dental patient. London: Oxford University Press; 1998. 7. Chen AH. Toxicity and allergy to local anesthesia. J Calif Dent Assoc. 1998;26:683-692. 8. Preshaw PM, Rowson JE. The use of lignocaine local anesthetic. Br Dent J. 1996;181:240. 9. Pertl C, Heinemann A, Pertl B, et al. The pregnant patient in dental care. Survey results and therapeutic guidelines. Schweiz Monatsschr Zahnmed. 2000; 110:37-46. 10. Lawrenz DR, Whitley BD, Helfrick JF. Considerations in the management of maxillofacial infections in the pregnant patient. J Oral Maxillofac Surg. 1996;54:474-485. 11. Avraamides EJ, Craen RA, Gelb AW. Anesthetic management of a pregnant, post liver transplant patient for dental surgery. Anesth Intens Care. 1997;25:68-70. 12. Johnson CG. Local anesthetics and pregnancy. J Am Dent Assoc. 1985;110:302. 13. Watson AK. Local anesthetics in pregnancy. Br Dent J. 1989;166:36. 14. Hunter ML, Hood CA, Hunter B, Kingdon A. Oral health advice: reported experience of mothers of children aged 5 years and under referred for extraction of teeth under general anesthesia. Int J Pediatr Dent. 1998;8:13-27.