An unpleasant emotional experience usually initiated by a noxious stimulus & transmitted over a specialized neural network to the CNS where it is interpreted as such.

It is the structural & functional unit of the nervous system.

It transmits messages b/w the CNS and all parts of the body.

Depending upon the function: Sensory (afferent)

Motor (efferent).

Relay (Interneuron).

Depending upon number of poles: Unipolar neurons.

Bipolar neurons.

Multipolar neurons.

Depending upon the length of axon: Golgi type I.

Golgi type II.

They are capable of transmitting pain & consist of 3 main parts.

1. Dendritic zone-most distal segment, respond to stimulation, provoking an impulse centrally in the axon.

2. Axon-thin cable like structure which has similar arborizationslike that of the dendrites. They may be quite long (giant squid axon measures 100-200 cm)

3. Cell body-it is located away from the axon/the main pathway of impulse transmission in the nerve. Its main function is to provide vital metabolic support.

Resting potential

Stimulus

Slow Depolarization (0.3 msec)

Rapid Repolarization (0.7 msec)

Resting potential

Fiber class Subclass

Myelin Function

A a + Motor, propioception

b + Motor, propioception

g + Muscle tone

d + Pain, temperature, touch

B + Various autonomic functions

C sC - Various autonomic functions

d gC - Various autonomic functions; pain, temperature, touch

Classical description was provided by Descartes in 1644, when he conceived pain system as a straight through channel from skin to the brain.

The concept changed little until 19th century when Muller postulated the theory of information transmission only by the way of sensory nerves.

Von Frey developed the concept of specific cutaneousreceptors for the mediation of touch, heat, cold & pain.

Free nerve endings were implicated as pain receptors.

A pain centre was thought to exist within the brain, which was responsible for the development of all overt manifestations of the unpleasant experience.

In 1894 Goldscheider was the 1st to propose that stimulus intensity & central summation are the critical determinants of pain.

The theory suggested that particular patterns of nerve impulses that evoke pain are produced by summation of sensory input within the dorsal horn of the spinal column.

Pain results when the total output of cells exceeds a critical level.

For example, touch plus pressure plus heat might add up in such a manner that pain was the modality experienced.

The gate control theory, proposed by Melzack & Wall in 1965 & recently reevaluated, is presently receiving considerable attention.

Although the theory may be simply stated, its ramifications are extremely complex.

The gate control theory postulates:1. Information about the presence of injury is transmitted to the CNS by small

peripheral nerves.2. Cells in the spinal cord or nucleus of 5th cranial nerve, which are excited by

these injury signals, are also facilitated or inhibited by other large peripheral nerves that also carry information about innocuous events.

3. Descending control systems originating in the brain modulate the excitability of cells that transmit information about injury.

Therefore the brain receives messages about injury by the way of the gate control system, which is influenced by:

1. Injury signals.2. Other types of afferent impulses &3. Descending control.

Sensory nerve endings that mediate pain (nociceptor) are actually chemo receptors. It is currently believed that there are both mechano-receptive & chemo-receptive nociceptors.

Criteria for a substance to be classified as a chemical pain mediator are: General accessibility & activation as a consequence of injury,

infection or mechanical tissue damage. Suppression of mediator formation resulting in prevention of pain

fiber activation. Easy formation from labile precursors, release from sensitive storage

sites, and short half-life. Pain caused by exogenous application onto nociceptors.

All criteria are met within the dental pulp by the peptide, substance P. In other parts, other chemical agents are significant, with bradykinin being one of the most active.

Cyclooxygenasepathway

• vascular permeability. •sensitizes nociceptor

Cell injury tissue acidity Kallikrein Bradykinin vascular permeability

activates nociceptor

synthesis & release of prostaglandins

Substance P (released by free nerve endings) sensitize nociceptor

vascular perm., plasma extravasation

(neurogenic inflammation)

releases histamine (from mast cells)

Calcitonin gene related peptide (free nerve endings) dilation of peripheral capillaries

Serotonin (released from platelets & damaged endothelial cells) activates nociceptor

Cell injury potassium activates nociceptor.

Historically, the public has associated dental treatment with pain. This association is no longer valid because techniques for the elimination of pain, including atraumatic injection, have been available for years and are essential to a successful dental practice. Local anesthesia for operative dentistry must be profound, often to depths required for pulpal anesthesia.

The practice of various psychological, physical, and chemical approaches to the prevention and treatment of preoperative, operative, and postoperative anxiety and pain.

Anesthetic agents

Inhalation sedation

Anti anxiety agents

Intravenous sedation

General anesthesia

Injection is used to achieve local anesthesia in restorative dentistry.

The administration of local anesthesia to all tissues in the operating site is recommended for most patients to eliminate pain and reduce salivation associated with tooth preparation and restoration.

To administer effective anesthesia, the dentist must have a thorough knowledge of the patient’s physical and emotional status and an understanding of the effects of the drug to be injected and the advantages and disadvantages of adding vasoconstrictors.

A therapeutic dose of a drug is the smallest amount that is effective when properly administered and does not cause adverse reactions. An overdose of a drug is an excessive amount that results in an overly elevated local accumulation or blood level of the drug, which causes adverse reactions.

The normal healthy patient can safely receive five to eight cartridges of anesthetic per appointment.

Each 1.8-mL cartridge contains anesthetic, with or without a vasoconstrictor (e.g., lidocaine 2% [anesthetic] with epinephrine 1 : 100,000 [vasoconstrictor], lidocaine 2% plain [no vasoconstrictor]).

The number of permissible cartridges increases as body weight increases. According to Malamed, the maximum recommended dose of 2% lidocaine with epinephrine 1 : 100,000 is 4.4 mg/kg, or 2 mg/lb, to an absolute maximum of 300 mg.

Maximum Recommended Dosages (MRDs) of Local Anesthetics Available in North AmericaMANUFACTURER’S AND FDA (MRD)Local Anesthetic mg/kg mg/lb MRD, mgArticaineWith vasoconstrictor 7.0 3.2 None listedBupivacaineWith vasoconstrictor None listed None listed 90With vasoconstrictor (Canada) 2.0 0.9 90LidocaineWith vasoconstrictor 7.0 3.2 500MepivacaineNo vasoconstrictor 6.6 3.0 400With vasoconstrictor 6.6 3.0 400PrilocaineNo vasoconstrictor 8.0 3.6 600With vasoconstrictor 8.0 3.6 600CALCULATION OF MILLIGRAMS OF LOCAL ANESTHETIC PER DENTAL CARTRIDGE (1.8 ml CARTRIDGE)Local Anesthetic Percent Concentration mg/ml × 1.8 ml = mg/CartridgeArticaine 4 40 72*Bupivacaine 0.5 5 9Lidocaine 2 20 36Mepivacaine 2 20 363 30 54Prilocaine4 40 72

Local anesthetics have different durations of action for pulpal and soft tissue anesthesia. Pulpal (deep) anesthesia varies from 30 to 90 or more minutes.

Soft tissue anesthesia varies from 1 to 9 hours, depending on the specific agent and whether or not a vasoconstrictor is included. Local anesthetics are selected on the basis of the estimated length of the clinical procedure and the degree of anesthesia required.

Two (or more) anesthetic agents can be administered when needed.

The total dose of both anesthetics should not exceed the lower of the two maximum doses for the individual agents.

Anesthetics also are available in amide and ester types. Hypersensitivity and allergic reactions in affected patients are

much less frequent with the amide type of local anesthetic.

Short Duration (Pulpal anesthesia approximately 30 minutes) Mepivacaine, HCL 3%

Prilocaine, HCL 4% (by infiltration)

Intermediate Duration (Pulpal anesthesia approximately 60 minutes) Articaine, HCL 4% + epinephrine 1 : 100,000

Articaine, HCL 4% + epinephrine 1 : 200,000

Lidocaine, HCL 2% + epinephrine 1 : 50,000

Lidocaine, HCL 2% + epinephrine 1 : 100,000

Mepivacaine, HCL 2% + levonordefrin 1 : 20,000

Mepivacaine, HCL 2% + epinephrine 1 : 200,000

Prilocaine, HCL 4% (via nerve block only)

Prilocaine, HCL 4% + epinephrine 1 : 200,000

Long Duration (Pulpal ≥90 minutes) anesthesia approximately 90+ minutes Bupivacaine 0.5% + epinephrine 1 : 200,000

Cardiovascular System

Patient's heart rate, blood pressure (BP). and pulse rate should be evaluated. A patient having heart disease like

valvular defect should be operated under antibiotic coverage.(in conservative dentistry, endodontology or sub gingival

caries

Large amount of anesthetic drugs may cause decreased blood pressure which leads to unconsciousness

due to reduced oxygen supply to the brain. Generally. local anesthetic preparations contain 1:80.000 to

200.000 concentration of adrenaline and 2 percent local anesthetic salt, which have good safety margin. The

increased concentration of adrenaline may cause increase in blood pressure, rise in heart rate and arrhythmia also. In

cardiac patients local anesthetic solution without adrenaline should be used.

CENTRAL NERVOUS SYSTEM

Side effects of the local anesthesia are more common in central nervous system. Therapeutic dose generally may

cause depression. Very high dose may cause tonic-clonic seizure, decreased blood pressure and respiratory arrest

leading to death.

dose should be given.

Allergy Most dangerous complication is allergy, because it is life-threatening in most of the cases. Hence, proper history about allergy is mandatory before administering local anesthesia.

Pregnancy: It is better to use minimum amount of local anesthetic drug specially during pregnancy,

Hepatic dysfunction: In hepat ic dysfunction, the biotransformation cannot take place properly. It causes high level of local anesthetic in the blood. Therefore, low doses of local anesthetic should be administered, or using material that not biotransformation in the lever.

Renal dysfunction: In patients with kidney diseases, local anesthetics do not cause any extra problem to the patient.

Thyroid diseases: Careful f inding for uncontrolled hyperthyroidism is required because such patients exhibit increased response to the vasoconstrictor (adrenaline) present with local anesthetics. Therefore solutions without adrenaline should be used.

Age: In very young and extremely old persons, less than the normal therapeutic

1. Better patient co-operation: If the region or tooth is fully anesthetized patient does not feel pain. It removes fear

and apprehension. Patient appears relaxed and gives better cooperation and dental procedure can be done in a

calm environment

2. Control of saliva: Increased flow of saliva during dental procedure is the consequence of "touch" sensation to

various parts of the oral cavity during t reatment .Under local anesthesia, there is reduction of sensation

which results in decreased salivary flow.

3. Control of bleeding: In the local anesthesia, a vasoconstrictor, usually epinephrine or adrenaline is added

mainly for increasing the period of anesthesia by decreasing flow of blood at the site of injection. This

temporary reduction in blood flow helps in controlling bleeding during any dental procedure.

4. Operative efficiency: By the use of local anesthesia, pain disappears, which is associated with reduced

blood flow and apprehension. Under local anesthesia, the patient is most cooperative. Therefore, the

confidence and work efficiency is increased.

The most appropriate method of preventing pain is by blocking the nerve pathways capable of conducting nerve impulses.

For patients who have a low threshold of pain and are apprehensive (hyper-responders), raising the threshold by inhalation sedation is an adjunctive aid to anesthesia by injection.

The use of nitrous oxide and oxygen is one method of inhalation sedation.

The operator should understand that this method of pain control has definite limitations.

Analgesia should not be thought of as general anesthesia in any stage or depth. It is simply a condition in which the pain threshold is elevated.

With inhalation sedation, the patient is conscious of the activities around him or her.

The fear of pain associated with dental procedures sometimes can be controlled by hypnosis.

A favorable mental attitude may be established through suggestions of relaxation.

The dentist and the patient may derive certain benefits through hypnosis. The dentist has the opportunity to work on a more relaxed and

cooperative patient and has better control over patient habits such as talking and rinsing and oral tissue tension.

The patient who is relaxed is less fatigued at the end of the appointment and has no specific recollection of having experienced discomfort.

Hypnosis has some merit under certain circumstances and has produced satisfactory results for some practitioners when it is properly applied. Before hypnosis is attempted, the operator must know how to recognize and cope with conditions associated with psychological, emotional, and mental factors and must be thoroughly familiar with all of the principles involved in hypnosis.

Hypnosis is not a way to eliminate all other accepted means of minimizing dental pain or discomfort, but it may be a valuable adjunct in improving accepted procedures. Also, post-hypnotic suggestion has been found to be successful in alleviating certain noxious dental habits.

Sturdvent

Ada’s journal on anxiety and pain control

Journal on pain management, American society of endodontics

Journal on pain control in dentistry,

Pickard’s manual of operative dentistry

Pain control in operative dentistry, Dr Ann Elrich