Jist of pain control

2.  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.

4.  It is the structural & functional unit of the
nervous system.
 It transmits messages b/w the CNS and all
parts of the body.

5.  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.

7.  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 arborizations
like 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.

8. Resting
potential
Stimulus
Slow Depolarization
(0.3 msec)
Rapid Repolarization
(0.7 msec)
Resting potential

9. Fiber class Subclas
s
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

11.  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 cutaneous
receptors 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.

12.  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.

13.  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.

14.  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.

15. Cyclooxygenase
pathway
• vascular
permeability.
•sensitizes
nociceptor

16.  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.

18.  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.

19.  Anesthetic agents
 Inhalation sedation
 Anti anxiety agents
 Intravenous sedation
 General anesthesia

20.  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.

21.  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.

22. Maximum Recommended Dosages (MRDs) of Local Anesthetics Available in North
America
MANUFACTURER’S AND FDA (MRD)
Local Anesthetic mg/kg mg/lb MRD, mg
Articaine
With vasoconstrictor 7.0 3.2 None listed
Bupivacaine
With vasoconstrictor None listed None listed 90
With vasoconstrictor (Canada) 2.0 0.9 90
Lidocaine
With vasoconstrictor 7.0 3.2 500
Mepivacaine
No vasoconstrictor 6.6 3.0 400
With vasoconstrictor 6.6 3.0 400
Prilocaine
No vasoconstrictor 8.0 3.6 600
With vasoconstrictor 8.0 3.6 600
CALCULATION OF MILLIGRAMS OF LOCAL ANESTHETIC PER DENTAL CARTRIDGE
(1.8 ml CARTRIDGE)
Local Anesthetic Percent Concentration mg/ml × 1.8 ml = mg/Cartridge
Articaine 4 40 72*
Bupivacaine 0.5 5 9
Lidocaine 2 20 36
Mepivacaine 2 20 36
3 30 54
Prilocaine4 40 72

23.  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.

24.  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

26.  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.

27.  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

28. 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.

29.  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.

30.  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.

31.  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