PANINEEYA DENTAL SCIENCES & RESEARCH CENTRE

PAIN CONTROL IN OPERATIVE

DENTISTRY

GUIDED BY-DR. P. KARUNAKAR (H.O.D)

DR.N.MADHAVI
MODERATOR-DR.RANGAREDDY (PROF)
 CONTENTS
 INTRODUCTION
 HISTORY OF PAIN
 DEFINITION OF PAIN
 CLASSIFICATION OF ORO FACIAL PAIN
 ETIOLOGY OF PAIN
 THEORIES OF PAIN
 PATHWAYS OF PAIN
 PAIN CINTROL IN OPERATIVE DENTISTRY-
LOCAL ANESTHESIA
ANALGESIA
HYPNOSIS
OTHER METHODS
CONCLUSION
REFERENCES
Introduction
 INTRODUCTION

 Pain is one of the most commonly experienced

symptoms in dentistry and as such, is a major
concern to the dentist.
 It is often spoken as a protective mechanism, since
it is usually manifested when an environmental
change occurs that cause injury to responsive
tissue.
 Although everyone has experienced pain and
described it as sharp, burning, aching, cramping,
dull or throbbing, actual pain experience varies as
a result of human emotions.
 HISTORICAL BACKGROUND

HOMER - pain was due to arrows shot by the gods.

ARISTOTLE – first to distinguish the 5 physical senses,

considered pain to be ‘a passion of the soul’ that resulted
from intensification of sensory experience.
FREUD - physical symptoms result from thought process
such symptoms as pain could develop as a solution to
emotional conflicts.

PLATO – pain and pleasure arose from within the

body, so it is considered as an emotional experience.
MERSKEY-reviewed some of the historical
background of modern pain concepts.
CHANGING CONCEPTS & DEFINITION

As Defined By The Medical Dictionary

A more or less localized sensation of discomfort,
distress or agony resulting from the stimulation of
specialized nerve endings. It serves as a protective
mechanism in so far as it induces the sufferer to
remove or withdraw from the source.
Unpleasant sensory or

Pain
emotional Experience
associated with
or without actual tissue
damage& described in terms of
such damage
 Traditionally pain is understood as localized
sensation of discomfort, distress or agony resulting
from stimulation of specialized nerve endings

 By International association for the study of pain

–WHO- An unpleasant sensory or emotional
experience associated with the actual or potential
tissue damage or described in terms of such
damage
 An unpleasant sensory or emotional experience
associated with the actual or potential tissue
damage defines the psychologic or physiologic
components.-COHEN
 FIELDS- unpleasant sensation that is perceived as
arising from a specific region of the body & it is
commonly produced by a processes that damage
or capable of producing damage.
 Classification of pain

 ODONTOGENIC NON
ODONTOGENIC

Pulpal & periradicular pain

due to damage to the pulp) (extension of the pulpal

disease into the
periradicular tissues)
 NON ODONTOGENIC ORIGIN

 Toothache of neurovascular region

 Toothache of neuropathic origin
 Toothache of maxillary sinus origin
 Toothache of myofacial origin
 Toothache of cardiac origin
 Classification of pain

 Classification based on Duration

 Acute pain
 Chronic pain
Classification based on Etiology
 Nociceptive pain
 Inflammatory pain
 Neuropathic Pain
 Classification of Oro facial pain

 Physical Conditions
 Somatic pain
 Superficial Somatic pain
 Cutaneous pain
 Mucogingival pain
 Deep Somatic pain
 Musculoskeletal pain
 TM Joint pain
 Periodontal Pain
 Osseous and periosteal pain
 Visceral pain
 Pulpal dental pain
 Vascular pain
 Neurovascular pain

 Neuropathic pain
 Episodic pain
 Continuous
 Psychological Pain
 Mood disorders
 Depression
 Anxiety disorders
 Post Traumatic disorders
 Somatoform disorders
 Conversion disorders
 Hypochondriasis
Acute pain –
The normal, predictable, appropriate response
to a noxious stimulus or disease process that
threatens or produces tissue injury, and that
abates following remission of the stimulus or
healing of the injury.
Chronic pain –
Pain associated with a chronic disorder or pain
that persists beyond resolution of an underline
disorder or healing of an injury and that is often
more intense than the underline process would
predict.
 Nociceptive pain  pain in response to a noxious
stimulus that alerts the organism to impending
tissue injury.

 Inflammatory pain  pain in response to tissue

injury and the resulting inflammatory process.

 Neuropathic pain  pain produced by damage to

or dysfunction of neurons on the peripheral or
central nervous system.
Classification of facial pain
Trigeminal neuralgia type I(TN 1)
Facial pain of spontaneous onset with greater
than 50% limited to the duration of an episode of
pain (temporary pain).
Trigeminal neuralgia type II (TN 2)
Facial pain of spontaneous onset with greater
than 50%as a constant pain.
 Trigeminal neuropathic pain(TNP)
pain resulting from unintentional injury to the
trigeminal system from facial trauma, oral
surgery,ear,nose,skull base surgery, stroke etc.,

Trigeminal differentiation pain(TDP)

pain in a region of trigeminal numbness
resulting from intentional injury to the trigeminal
system from neurectomy ,gangliolysis, nucleotomy
and other denervating procedures.
 Symptomatic trigeminal neuralgia(STN)-
Pain resulting from multiple sclerosis.

Atypical facial pain(AFP)-

pain predominantly having a psychological rather
than a physiological origin.
 Etiology of Pain
 Pain has multi model etiology, but some specific pathological processes are
commonly associated with pain.
1. Inflammation
Tissue injury  chemical inflammatory mediators are released( Bradykinin,
Prostaglandin etc..)  Vasodilatation and Pain.
2. Muscle Pain  Non inflammatory  Spasm.
3. Vascular Pain  Vasodilatation & increase in vascular permeability  tissue
edema leads to  Ischemia  Pain
4. Spontaneous Pain without obvious cause
5. Allergic & Toxic conditions
6. Increase body temperature
7. Direct noxious, chemical, mechanical or thermal.
8. Psychogenic pain
9. Neural Pain
 Dimensions of Pain
 Cognitive – Represents the subject’s ability to comprehend
and evaluate the significance of the experience
 Emotional – Represents the feelings which are generated
 Motivational – Deals with the drive to terminate it
 Intensity of pain – Relates to the attention given to it at the
time of injury
 Emergency nature of pain – Relates more to the fear that it
generates than the actual injury
 THEORIES OF PAIN
 It is often assumed that pain is a warning that damage has
occurred where as no pain means that everything is all
right. But pain may occur when there is no obvious disease
as in primary neuralgias.

VARIOUS THEORIES ARE-

-Specificity theory
-Intensity theory
-Pattern theory
-Chemical theory
-Gate control theory
 SPECIFICITY THEORY
Descartes 1644 – straight channel from skin to the
brain which carried message from receptors to the pain
center. A pain center was thought to exist with in the
brain, which was responsible for all overt manifestations of
unpleasant experience.

INTENSITY THEORY
Pain is produced when any sensory nerve is stimulated
beyond a certain level.
This is true of nerves mediating the sensation of touch
when stimulated to an excessive degree.
It depends only on high intensity of stimulation.
 PATTERN THEORY
GOLD SCHEIDER(1894) – stimulus intensity and central summation
are critical.
Large cutaneous nerve comprises a specific touch system, small fibers
summate their input and transmit a pattern to the pain receptors.

CHEMICAL THEORY
Based on recently discovered chemical messenger.
They are endorphine, enkephalins.
GABA-These are produced in brain. These act as pain inhibitory
substance and increases the pain threshold.
substance-p –produced in sensory nerves, spinal cord pathway and some
part of brain. this act as pain stimulant and facilitates pain transmission.
 GATE CONTROL THEORY
Proposed By Melzack And Wall In 1965
Neural Mechanism In The Dorsal Horns Of Spinal Cord
Acts as a Gate that Increases or Decreases the Flow Of
Impulse from periphery to the Brain.
Proposes
1. Information about the presence of injury-PAIN
transmitted to the CNS by small peripheral nerves.
2. Cells in the spinal cord modulate these injury signals-
facilitate or inhibit.
3. Descending control systems from the brain modulate the
cells that transmit information about injury.
Source Of pain…
Source Of pain
Sight of Pain
Endodontic Pain Pathway

 Structures serving as source of primary Odontogenic Pain

- Pulp / Dentin Complex.
- Periradicular Tissues.

 Primary Nociceptors of Pulp that respond to Inflammation.

- Slow Conduction, High Threshold ‘C’ Fibers.

 ‘C’ Fibers don’t respond to normal / Non-Pathologic

Stimulation

 Pain occurs in tooth only when the Stimulus is intense

enough to reach the Threshold.
 Tissue Inflammation

Sensitisation of Nerve Fibers

Firing Threshold of Aδ &‘C’ Fibers

Pain Perceived by Patient

Pain of Periradicular Origin
 Easy to localize since numerous mechanoreceptors are in PDL
 Most densely concentrated in apical 3rd
 Once inflammation sets into PDL from pulp , pt are able to locate
the source of pain more easily

Inflammation

PDL sensitized

Pain – dull, throbbing / aching& should resolve completely with LA

If doesn’t respond to LA – pain is of non odontogenic origin.
 Neurotransmitters

 Serotonin
 Median raphae of the brain stem
 Blood platelets
 In the CNS synthesized by L- tryptophan

 The activation of the seretonergic pathways in the brain

stem by tricyclic antidepressants yields paralleling
analgesic effects.
 Rapid acting small molecule
 Modulates chronic pain only.
 Substance P
 Slow acting large molecule
 Polypeptide composed of 11 amino acids.
 Released at the central terminals of the primary neurons
 Centrally excitatory for nociceptive impulses.
 Released by nerve fibers and excites neurons in the dorsal horn that
are activated by noxious stimulus.

 Opiate like substances secreted in the brain have shown to

produce analgesia and they are
 Beta-Endorphin
 Met-enkephalin
 Leu-enkephalin
 Dynorphin.
 Enkephalins are more powerful in relieving
sudden,excessive and shooting type of pain. Inhibit
the activity of the thalamic projections at the post
synaptic sites.

 Beta Endorphins- the effect is long lasting,requires

latent period and has high anti nociceptive
activity. Modulates acute pain only.
 PERIPHERAL NERVES

 A fibers -MYELINATED FIBERS

INNERVATE DENTIN
alpha- 13-20micro meters in diameter
conduction rate- 70-120mts/sec
proprioception& somatic motor function
beta- 6-13 micro meter in diameter
conduction rate- 40-70mts/sec
touch& pressure
gamma- 3-8 micro meter in diameter
conduction rate-15-40mts/sec
motor to muscle spindle
delta – conduct fast or first pain ( 100 mts per sec)
pain, temperature, touch
 B fibers – 3-14 mts per sec, 1-3 micro meters in diameter

 C fibers- UNMYLINATED FIBERS

INNERVATES BODY OF THE
PULP&BLOOD VESSELS
conduct slow or second pain(0.5 – 2 mts per sec)
0.5-1 micro meter in diameter
pain associated with necrotic pulp
Dual Nature of Pain
 Referred pain
Often a person feels pain in a part of his body that
is considerably far from the tissues causing the
pain called referred pain.
 Diagnosis
 An accurate history is the Characteristics of the
most important aspect of pain
diagnosing obscure pain. – Quality of the pain
 Location – Intensity
 Localized – Bright
 Diffused
– Dull
 Onset of the pain
 Trauma
– Pricking
 Caries – Burning
 Duration – Itching
 Continuous – Tenderness
 Intermittent – Pulsating
 Recurrent
 Treatment Modalities
 Analgesics
Ultrasound (Trans
 Non-narcotics oral lithotrophy)
 Narcotics Manual technique
 Anesthetic agents Massage
 Anti inflammatory agents Exercise
 Muscle-relaxants Strech technique
 Antidepressants Psychological
 Physical modalities technique
 Sensory stimulation Counselling
(TENS) Relxation training
WHO Pain Management Guidelines
The Pain Management ladder

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WHO guidelines for treatment of Pain

Severe Eg. Morphine

pain Add powerful opioid to NSAID
Intensity of pain

Moderate Eg. Ibuprofen + codeine

Add mild opioids to NSAIDs
pain

Administer
AdministerNSAIDs
NSAIDs Eg. Ibuprofen – fast
Mild pain onset of action,
powerful action
Treatment of pain - WHO guidelines

1. First step is administration of any NSAID. Ibuprofen

is suitable because of its fast onset of action and
powerful inhibitory action on cyclo-oxygenase

2. Second step: If pain persists even after the dose is

optimized, an opioid should be added, not
substituted.
 Final step is for more moderate to severe pain where a
powerful opioid (powerful enough to relieve moderate to
severe pain i.e. morphine) may be administered in addition to
ibuprofen

Interventional strategies, as last resort interventions “when all

else fails” include anesthetic nerve blocks, epidural steroid
injections, continuous spinal pain-relieving techniques with
implanted catheters and external pumps, neurodestructive
techniques and implantable devices for pain such as spinal
cord stimulators and morphine pumps
Treatment of Acute Pain

 Only two classes of drugs can be considered

mainstays for acute pain treatment: opioids and

nonsteroidal anti-inflammatory drugs (NSAIDs)

 Other classes of drugs, such as antidepressants and

anticonvulsants, are sometimes used as adjuvants

The Need for Pain & Inflammation Relief

Inflammation
Drug Mechanism of Action Pain Relief
Relief
Inhibition of COX-I & COX-II
NSAIDs isoenzymes, inhibits PG Yes Yes
synthesis
Decrease pain & fever through
Paracetamol Yes No
inhibition of COX-3
Bind to opioid receptors,
Opioids producing agonist action that Yes No
inhibits pain impulses
Mixed actions-opioid agonist
Tramadol plus norepinephrine/ serotonin Yes No
reuptake inhibitor
Selective
Selective for COX-2 isoenzyme
COX-II Yes Yes
inhibition
inhibitors
Synergistic Effects of Analgesic Combinations

•Additive or

Decreasing opioid use

synergistic analgesia
can provide better
pain control
•Lower doses of
individual agents may
be used
•Opioid-sparing Opioid alone Multimodal approach
IN Operative

DENTISTRY……..?
 DETAILS OF PAIN PATHWAY:
(BASICS OF PAIN TRNSMISSION)
pain sensation to reach the cortex from the nociceptors
it requires three neuron sets.
 FIRST ORDER NEURONS :
Pain receptors

SPINAL CORD

• Three classes of nociceptive afferent neurons provide the

input whereby the brain perceives pain.
1. Mechanothermal afferents are primarily A∂ fibers respond
to intense thermal and mechanical stimuli.
2. Poly model afferent c fibers, conduct more slowly, respond
to mechanical, thermal and chemical stimuli.
3. High Threshold mechanoreceptive afferents are chiefly A ∂
Fiber normal respond to intense mechanical stimuli.
 2nd Order neurons :
Dorsal horn of spinal cord
The primary afferent neuron 2nd Order neurons (Transmission cells)

transfer the impulse on to higher centers.

Types :
1. Low Threshold mechanosensitive neuron (LTM) -- light
touch, pressure & proprioception.
2. Nociceptive Specific neurons (NS) -- exclusively carry
impulse related to noxious stimulation.
3. Wide dynamic range neuron (WDR) -- Neurons are able to
respond to a wide range of stimulus intensities from
nonnoxious to noxious.
Dual pain pathways of pain in
the spinal cord and brain stem :
On entering the spinal cord, the pain signals take two
pathways to brain 1. Neospinothalamic.
2. Paleospinothalamic.
NEURONAL TRANSMISSION IN THE
HEAD AND NECK REGION :
PAIN PATHWAY OF
HEAD AND NECK REGION

FROM THE ANTERIOR ASPECT FROM THE POSTERIOR ASPECT

FACE, MOUTH, TEETH AND EYES POSTERIOR ASPECT OF

HEAD AND NECK

Through cranial nerves. Through spinal nerves.

(Gasserian ganglion) (Dorsal root ganglion)
PATHWAYS OF PAIN FROM OROFACIAL REGION

TRIGEMINAL PATHWAY SPINOTHALAMIC PATHWAY

BRAIN STEM SPINAL CORD

THALAMUS THALAMUS

CORTEX
 PATHWAYS OF PAIN TO OROFACIAL
REGION
CRANIAL AND CERVICAL NERVES THAT PROVIDE
SOMATIC AND VISCERAL SENSATION TO THE ORO
FACIAL AREA;
NERVES AREA SUPPLIED

TRIGEMINAL N (V) Skin of face, fore head, scalp conjunctiva, oral

and nasal mucosa, anterior 2/3 of tongue,
masticatory muscles, TMJ.
FACIAL N (VII) Skin of the hollow of the auricle of external ear
and small area of skin behind ear.
GLOSSOPHARYNGEAL N (IX) Mucosa of pharynx, palatine tonsils, posterior
1/3rd of tongue, skin of external ear.
VAGUS N (X) Pharynx, larynx, skin at the back of the ear,
posterior wall of external auditory meatus.
CERVICAL (2 & 3) Lateral, posterior and back of the head and neck.
 The Trigeminal system – BELL
 Sensory input from
face and mouth
carried by 5th cranial
nerve.
 The cell bodies of
Trigeminal afferent
neurons located in
the large gasserian
ganglion.
Sensory afferent pass to
1. Mesencephalic nucleus – Proprioception.
2. Principal nucleus - Touch, Pressure.
3. Spinal nucleus - Pain, Temp.

Fibers from all 3 divisions

Ascending Br. Descending Br.

Touch, Pressure. Touch, Pressure, Pain, Temp.

Principal nucleus Spinal tract of Trigeminal N.

( C-2 or 4)
Pathway from dental pulp to cortex :- (mand. molar)
• Once the nociceptors located in the pulp activated,

• the impulse is carried into the CNS by primary afferent neuron in the
mandibular branch of 5th nerve.

GASSERIAN OR TRIGEMINAL GANGLION.

nucleus caudalis.
(The nucleus oralis may also play imp., role in nociception of intra-oral
structure).
.

Fast pain Slow pain

Thalamus Reticular formation

Sensory cortex
 TOUCH

pressure warmth vibration pain

 CAUSATIVE FACTORS OF PAIN IN
OPERATIVE DENTISTRY:
 Patient behavior
 Armamentarium, instruments, materials
 Pulp-dentin organ
 Improper handling of tissues
 HOW TO OVERCOME?
 Gaining the confidence of the patient.
 Ideal instrumentation & proper
implementation.
 Use of cooling devices
 Use of palliative drugs& obtundents.
 Desiccation of dentin
 Pressure anesthesia with cocaine
 LOCAL ANESTHESIA
 ANALGESIA
 INHALATION SEDATION
 HYPNOSIS& PSYCOTHERAPY
 GENERAL ANESTHETICS
 1.CAVITY PREPARATION:
 The heat generated by grinding procedures of tooth
structure has been sited as greatest single cause of pulp
damage during cavity preparation.
 Intra pulpal temperature of 5.5˚c-causes 15% loss of tooth
vitality.
 Basic factors in rotary instrumentation that cause temp
raise in pulp:
 1.Force applied by the operator
 2.Size,shape, condition of cutting cool.
 3.Revolutions per min
 4.Duration of actual cutting time
Ideal instrumentation & proper implementation

 Hand cutting or rotary cutting instruments .

1. Hand cutting-
Principle- concentrate the force in a very thin cross section of the
instrument at the cutting edge.
Thinner the cross section

More sharper the instrument

More efficient of the cutting edge

 Dull or blunt instruments required more pressure
to cut the tooth structure.

Patient elicits more pain

 Sharp instrument a force of 10 lb=200lbs

 Dull instrument 10lb=20lb
 Rotary instruments
 1.Speed
 2.Vibration
 3.Pressure
 4.Heat production
 Stanley & Swerdlow-speed of 50,000rpm& over were
found to be less traumatic to the human pulp than
techniques using 6000- 20,000rpm.
 If air alone is using as a coolant at 200,000rpm-It is
possible to”burn” the pulp in 11min.

 Peyton& henry- teperature rose upto 110˚F at 15,000rpm

if no coolant was used while cutting with a no.37 bur at
0.5pound load.
 STANLEY-Emphacised the distructive intervention of
cavity preparation.
 Conclusion-demise of the pulp begins with a chronic lesion
turned acute by insult of cavity preparation (stressed
pulp).
 ZACH-increase in the intrapulpal temparature of 20˚F
may result in irriversible danafe.
 low speed drilling with no coolants-least acceptable
method.
 Ultraspeed with no coolants.
 STANLEY &SWERDLOW- Degree of cellular
displacement of odontoblastic nuclei into the cut dentinal
tubules is the best indication of the severity of the pulp
inflammation initially.

 This displacement of the cells caused by build up of

intrapulpal pressure by an inflammatory response & the
edema, hyperemia, &exudation occurring in proximity to
the pulp wall forced the odontoblastic nuclei &blood cells
into the dentinal tubules.
 GOODCARE- thermal elevation
 Low speed< high speed <ultra high speed.

 OTTL&LAUER-
 1.Carbide burs <diamond bur
 2.fine diamond bur <coarse diamond bur
 DEPTH OF PREPARATION:
 Deeper the preparation more extensive is the pulpal
inflammation.
 SEELIG& LEFKOWITZ-Degree of pulp response is the
inversly praportional to the remaining dentin thickness.
 PULPHORN EXTENSION:
 STANLEY&SWERDLOW- incresed importence of air-water
coolant as the dentin is thinned & the pulp is approached.
 Cervical pulphorn: 66.8-96.3%
First & second molars
Reprsents real danger in cavity preparation.
 Cervical pulphorn: 66.8-96.3%
First & second molars,
Present at the each axial line angle or centered buccally/
palatally.
High incidence at the mesiobuccal pulphorn –classV
&crown preparations should be redesigned.

Represents real danger in cavity preparation.

 SELTZER-noted irritation dentin under restoration then
under caries.
 It is more amorphous & irregular.
 Asssociated odontoblastic nuclei were grossly altered in
structure.
 A. Low speed

 Application of more pressure on the cutting surface

Increase Amplitude & decreases frequency

Increase In the vibration

Increase Friction

Increase Heat production

 High speed –advantages

 Efficient rapid cutting

 Convenient to operator & patient
 Minimal vibration &low frictional heat with
coolants
 Longevity of cutting instruments
 Less pressure & sensitivity
 Disadvantages
 Over cutting
 Visibly hampered
 Lesser tactile sensation
 Use of cooling devices
 They minimize the pain &maximize the
efficiency with high speed.
Air
Water
Combination of the both
 HYPERSENSITIVITY

hhhhh
In 1935, Grossman suggested the criteria for the ideal
desensitizing agent.
Desensitizing agents should be
Nonirritating to the pulp,
Relatively pain less on application,
Easily applied,
Rapid in action
Permanently effective,
Consistently effective and
Cause no staining.
Hot olive oil, formaldehyde, silver nitrate, zinc chloride,
sodium carbonate, and sodium fluoride were used in the
1950s, many of these materials are used to stimulate the
formation of secondary dentin, and some are adhesive and
used for covering the sensitive areas.

2 mechanisms of action of desensitizing agents.

1.One involves blocking fluid movements by occluding dental

tubules.

2.The other involves blocking pulpal nerve activity by

altering the excitability of sensory nerves.
Dental conditions with symptoms similar to dentine
hypersensitivity :
Cracked tooth syndrome
Fractured restorations
Chipped teeth
Dental caries
Post-restorative sensitivity
Teeth in acute hyperfunction
Office treatments for dentinal hypersensitivity :
Cavity varnishes Stannous fluoride
Anti-inflammatory agents Strontium chloride
Burnishing of dentin Potassium oxalate
Silver nitrate Restorative resins
Zinc chloride - potassium ferrocyanide Dentin bonding agents
Calcium hydroxide
Diabasic calcium phosphate
Fluoride compounds
Sodium fluorides
 Burnishing of dentin :
Burnishing of dentin with tooth pick or orange wood stick
will create a partial smear layer on dentin surface, there by
occluding the orifices of dentinal tubules.
 Lasers
Types used : Argon, Co2, Ho:YAG, Nd:YAG, erbium YAG
etc. These
Mechanism of Action :
Blocks the tubules probably by fusion of crystals
(Hydroxyapatite), as low intensity defocused beam is used.
Side effects :
Tubules may act as optical fibers causing damage to the pulp
LOCAL ANESTHESIA
 CLASSIFICATION OF LOCAL ANESTHETICS
 I) Based on the mode of administration
 i) Injectable ii) Surface Anesthetics
  

 a) Low potency short duration a) Soluble

Eg. Procaine Eg. Cocaine
Lidocaine Lidocain
Tetracaine
Chloroprocaine b) Insoluble

 b) Intermediate potency and Eg: Benzocain

 duration
Eg. Oxythiazine
Lignocaine
Prilocaine
 c) High potency, long duration
Eg. Tetracaine
Bupivacaine
Dubocaine
 VI) Based on the duration of action

 Short acting (1/2 to 1 hour)

Eg: Primacaine, Duocaine, Nesacaine, Monocaine.
 Medium acting (1 to 2 1/2 hours)
Eg: Metycaine, Unacaine, Pontocaine, Primacaine,
Duocaine, Dynacaine, Citanest.
 Long acting (21/2 hours and longer)
Eg: Kincaine, Xylocaine, Carbocaine, Ravocaine.
 Ideal properties of local anesthesia
 Action must be reversible
 Nonirritating to the tissues and produce no secondary reactions
 Should have low systemic toxicity
 Rapid action should be of sufficient duration
 Should have a potency to give complete anesthesia
 Sufficient penetrating properties to be effective as topical
anesthetic
 Relatively free of producing allergic reactions
 Should be stable and readily under go biotransformation with in
the body
 Should be sterile or being sterilized by heat with out deterioration
 Sequence of action of local anesthetia
Displacement of calcium ions from the sodium channel
receptor site

Binding of the local anesthetic molecule to this receptor

site

Blockade of sodium channel

Decrease in sodium conductance

Depression of the rate of electrical depolarization

Failure of achieve the threshold potential level

Lack of development of propagated action potentials

Conduction blockade
Advantages:
•The safest method of administering drugs to
prevent pain.
•Permits to gain patient’s cooperation which is
necessary for some forms of dental treatment.
•Simple and cheaper method for pain prevention
which can be delivered without the aid of another
person (or) assistance.
•Addition of a vasoconstrictor agent helps to reduce
hemorrhage during surgical treatment.
•Permits prolonged treatments as additional
injections may be given.
Indications for use of Local Anesthesia:

•To make the dental treatments pain less.

•For diagnostic purposes in identifying the cause of

obscure facial pain when a particular nerve can be
blocked with a local anesthetic and patient’s reaction
noted.
•As a diagnostic procedure when usual tests fail to
enable one to identify the offending tooth. The
objective is to anesthetize a single tooth at a time
until the pain disappears and is localized to a specific
tooth.
Relative contra indications:

•Unsuitable when patient is unable to cooperate for

example very young child.

•Should not be used where injection site is acutely

infected.

•In hemophiliacs and patients with hemorrhagic

diathesis unless the condition is properly controlled

•Used with caution in patients suffering from certain

diseases Eg: Liver failure (or) being treated with
certain drugs Eg: anti –arrhythmic drugs
 Contraindications: of local
anesthesia:
 Absolute contraindications
 Local anesthetic allergy
 Bisulfite allergy
 Pseudocholinesterase deficiency[ester compounds]
 Relative contraindications
 Methemoglobinemia
[idiopathic/congenital]
 Significant cvs disease
 Significant liver dysfunction
 Clinical hyperthyroidism
 Significant renal dysfunction
 Each 1.8ml cartridge contains anesthetic, with are without a
vasoconstrictor.
eg.lidocaine2% with epinephrine 1:100,000.
• Normal healthy patient can receive 5-8 cartridge of anesthesia per
appointment.
• The number of permissible cartridges increases as body weight increases.
• According to malamed -max recommended dose of 2%lidocaine with
epinephrine 1:100,000 is 4.4mg.
absolute max dose-300mg.
 DURATION OF ACTION:
 It depends upon the presence of vasoconstictor.
 Pulpal anesthesia varies from 30-90min.
 Soft tissue anesthesia 1-9hrs & it depends upon th specific
agents.
 PATIENT FACTORS:
CVS
CNS
RESPIRATORY
ALLERGY
 CARDIOVASCULAR SYSTEM:
 According to latest guidelines: less than 160/100 are good candidates for dental
procedures.
 Pulse rate less then 60beats/min or greater than 110 beats/min be questioned
further.
 Lower heart rate may indicate heart block.
 5/ more Missed beats (pre mature ventricular contraction) – indication for medical
consultation.
 Patients with valvular disease, infective endocarditis-prophylactic antibiotic regimen
recommended according to AMERAICAN HEART ASSICIATION.
 Over dose of any vasoconstrictor causes an increase in BP, heart rate, possible
dysarthemias. these symptoms may also seen with retraction card treated with
epinephrine resulting in rapid uptake of drug into the circulatory system.


 CENTRAL NERVOUS SYSTEM:

 It is more easily affected by an overdose of injected

anesthetic drugs than the cardiovascular system.
 Anesthetics depress the CNS, but when administer properly
it causes no depression.
 At minimal to moderate overdose levels, depression is
manifested in exitation (eg; Talkativeness, apprehension,
sweating, elevated blood pressure& heart rate, elevated
respiratory rate)or drowsiness.
 Moderate to high overdose levels – tonic-clonic seizures.
 RESPIRATORY SYSTEM

 High doses- Depressed blood pressure

Reduced heart rate

Depressed blood pressure

Respiratory arrest
 ALLERGY:
 Anaphylactic shock from an allergic reaction can
be immediate & life threatening.
 Fast injection & IV injection of anesthetic are
reasons for allergy like reaction.

Demonstrated positive reaction to Methylparaben and

negative reactions to amide anesthetic without the
preservative.(Aldrete & Johnson (1970)

Clinical manifestations:
1. Dermatological reactions.
2. Respiratory
3. Generalized Anaphylaxis
 Drug interactions with vasoconstrictors:
drug Adverse effect
Tricyclic Increase cadiovascular response
antidepressents,amphitylin,
Nonselective B blockers Hypertention ,bradicardia
Nadolol,propranalol
cocaine Increased cardiovascular response
Antiadrenergic Increased CVS response
drugs,glunadrel,guanethadine
Nonselective alpha Increase CVS response
blockers,chlorpromazine,clozapine,
haloperidol
digitalis dysarythmias
Thyroid harmones,levothyroxine dysarythmias
TECHINIQUES OF REGIONAL ANESTHESIA

Local infiltration

Field block

Nerve block
 MAXILLARY NERVE BLOCKS:
Supra Periosteal/ Infiltration Technique.
 3) Infra orbital nerve block

 4. Greater palatine nerve block

 5. Nasopalatine nerve block

 Techniques of Mandibular anesthesia

1. Inferior alveolar nerve block:

a. Intra oral Techniques.
b. Extra oral Techniques.
Gow-Gates mandibular Nerve Block Technique.

Vazirani-Akinosi Closed mouth Mandibular Nerve Block

Extra oral Mandibular Block

 SUPPLEMENTAL TECHNIQUES
 Intra-osseous injection

 Intra-Pulpal injection
Intra- Septal Injection

Intra- Ligamentary Injections

 Topical anesthesia:
 Renders the free nerve endings in accessible
structures (mucous membrane,abraded
skin,cornea of eyes)
 Application of solution directly on to the surface.
 Dentipatchs are available
 LOCAL COMPLICATIONS AND
MANAGEMENT
 
 Needle breakage
 Pain on injection
 Burning on injection
 Persistent anesthesia (or) Paraesthesia
 Trismus
 Hematoma
 Infection
 Edema
 Sloughing of the tissues
 Soft tissue injury
 Facial Nerve paralysis
 Post anesthetic intra-oral lesions
 SYSTEMIC COMPLICATIONS
 Causes of adverse drug reactions: 
 OVERDOSE REACTIONS
 1. Pre- Disposing Factors.
 A. Patient’s factors:
 Age , Weight, Sex, Presence of Disease, Genetics & mental attitude.
 B. Drug Factors:
 Vasoactivity, Concentration, Route of Administration, Rate of
absorption, vascularity of site, presence of vasoconstrictors
 Signs – Talkativeness, apprehension, excitability, slurred speech,
muscle twitching, euphoria, nystagmus, sweating, vomiting, elevated
B.P., heart rate and respiratory rate.

 
 EPINEPHRINE OVERDOSE:
 Optimum concentration- 1:250000 with lidocaine.
 Overdose reactions are seen when used in gingival cords
(22.5Mg. Epinephrine/inch of cord).

 Management:
 Terminate treatment, erect position of patient, check vital
signs.
 Management:
 P – position

A – airway

B – breathing

C– circulation

D– definitive care(diazepam,
medazolam)
 REASONS FOR FAILURE

 Pharmaceutical Reasons

 Treatment Reasons

 Anatomical Reasons

 Pathological Reasons

 Psychological Reasons

 
 Substitutes for LA agents
 
 Local anesthetic activity of Anti-Histamine reported in
1939.

 In 1947 Halpern, Perrin & Dews showed that Anti-

Histamines do possess local anesthetic activity.

 In 1957 Naranjaro studied various Anti-Histamines as L.A

substitutes and found that every Anti-Histamine tested was
more potent that procaine which was generally the standard
for comparison of potency of LA.
.
 They also showed that chlorpromazine is effective at 0.1
to 0.2% concentrations as a L.A where as procaine;
Lidocaine etc are used in 1% -2% concentration.
 ALTERNATIVE METHODS TO PAIN CONTROL:

 1. PREMEDICATION WITH ANTIANXIETY AGENTS

OR SEDATIVES
 2. INHALATION SEDATION
 3. HYPNNOSIS
 4. ELECTRONIC DENTAL ANAESTHESIA (EDA)
 1. PREMEDICATION WITH ANTIANXIETY AGENTS OR
SEDATIVES :

 This technique can be employed as an adjunct to local anesthesia

in order to calm the patient during the dental treatment.
 The agents used are:
1. Diazepam: 2-10mg orally- one hour prior to the dental
appointment.
2. Alprazolam: 0.25- 0.5mg -one hour prior to the dental
appointment.
3. Midazolam: 2-5mg -one hour prior to the dental appointment.
 2. INHALATION SEDATION

 Mild to moderate dental treatment can benefit

from this consious sedation with nitrous oxide &
oxygen.
 The patients pain threshold is elevated while he is
consious of surroundings.
 Safe & alternative to GA.
3. HYPNOSIS

Another adjunct to local anesthesia.

Patient can be made more relaxed & co-operative.
Audio-analgesia is advantageous as White noise
reduces pain where as Music relieves fear and
anxiety and as a result complete relaxation occurs
(neil 1998)
 4. ELECTRONIC DENTAL ANAESTHESIA (EDA):
It is a recently available techinque to control pain.
Works on the principle of gate control theory of pain transmission.
Used at high frequency of more than 120hz.
 EDA –MECHANISM OF ACTION:
1.Acts by stimulating the larger diameter A-fibers which transmit the
sensation of touch, pressure& temperature.
This inhibits the transmission of pain impulses produced by the high
speed drill which are transmitted by the smaller
A – δ & C- fibers.
When the pain impulses fail to reach the brain, the sensation of the pain
does not occur.
 2.it occurs during high frequency stimulation is
that blood levels of serotonin & endorphins are
increased.
 They play a secondary role in controlling pain
during dental treatment.
 INDICATIONS CONTRA INDICATIONS
1.Needle phobic patients. 1.patients with cardiac
pacemakers.

2.Patients allergic to local 2.Nurological disorders like

anesthesia. epilepsy.

3.Pain control prior to 3.Very young& very old

administration of local patients.
anesthesia ,especially for palatal
injections.
4.pregnancy
ADVANTAGES DISADVANTAGES

1.No need for injection. 1.High cost of unit.

2.Anaesthetic effect only for the 2.Learning curve.

required time; does not last
longer.
3.Intraoral electrodes are a
3.Residual analgesic effect last weak link in the system.
for several hours.
 Transcutaneous electrical nerve stimulation (acronym
TENS) is the use of electric current produced by a device to
stimulate the nerves for therapeutic purposes.
 The unit is usually connected to the skin using two or more
electrodes.
 A typical battery-operated TENS unit is able to modulate
pulse width, frequency and intensity. Generally TENS is
applied at high frequency (>50 Hz) with an intensity below
motor contraction (sensory intensity) or low frequency (<10
Hz) with an intensity that produces motor contraction.[2
 Scientific studies show that high and low
frequency TENS produce their effects by
activation of opioid receptors in the central
nervous system.
 Specifically, high frequency TENS activates delta-
opioid receptors both in the spinal cord and
supraspinally (in the medulla) while low frequency
TENS activates beta-opioid receptors both in the
spinal cord and supraspinally.

Local anesthetic delivery system-j of Americal dental association

Vol133: no 8:page108-133
 HIGH FREQUENCY TENS

Reduces exitation of central neurons that transmits

nociceptive information

Increases releases of inhibitory nurotransmitters(GABA)

Activates muscarinic receptors

ANALGESIA
 LOW FREQUENCY TENS

Activates serotonin receptors

Releases serotonin in spinal card

Releases GABA

Activates muscarinic receptors

ANALGESIA
 FUTURE TRENDS IN PAIN CONTROL
 NEWER ARMAMENTARIUM
1) Safety syringes:
a) Ultra safe aspirating syringe system.
Two handed guarding technique
 Safety plus
 New needle free delivery systems
 Intra-osseous syringes
 Jet injections- Panjet, Mizzy syrijet
 Xylocard syringe
 NEWER BETTER ACTING LOCAL
ANESTHESIA:
 EMLA-which allows profound local topical
anesthesia& ph alterations to make
administration more comfortable.
  Computerized Delivery of Local
anesthesia (WAND)
 Consists of microprocessor combined with an
electronically controlled motor that enables to deliver a
small volume of anesthetic solution under a controlled
low pressure.
 The Wand is a lightweight probe attached to a
computer controlled injection device by a thin
plastic tube that carries the solution to the wand. A
foot pedal controls the device.
It takes a few injections to get accustomed to the
foot pedal.
This device allows two speeds of injection only the
slow speed was used.
It is also possible to aspirate by taking your foot off
the foot peddle.
 The VibraJect was clipped to the syringe body and
requires little if any change from the normal injection
technique. The body of the vibrator should be
oriented so it does not rest on the patient's teeth.
 ACUPUNCTURE
∆ Acupuncture could supplement conventional treatment
modalities.
∆ Its value in the treatment of temporomandibular dysfunction
syndrome and facial pain has been well documented.
∆ Although it may be useful in the control of post-operative pain,
its use as sole analgesia for operative care is questionable.
 ALTERNATIVE TOOTH
PREPARATIONS:
 Air abrasion
 Lasers
 Ultrasonics
 Chemomechanical means
 AIR ABRASION-utilizes micron sized particles to
remove tooth structure.
Advantage-more comfortable
Disadvantage-lack of control
not caught the popular imagination
LASERS-hard & soft tissue lasing
painless, noice less ,highly patient friendly.
still in research& high cost
 Chemo-mechanical caries removal involves the
chemical softening of carious dentine followed by
its removal by gentle excavation.

 The reagent involved is generated by mixing

amino acids with sodium hypochlorite; N-
monochloroamino acids are formed which
selectively degrade demineralised collagen in
carious dentine.
 It is well suited to the treatment of deciduous teeth, dental phobics
and medically compromised patients.

A new system, Carisolv- This comes as a gel, requires volumes of 0.2-

1.0 ml and is accompanied by specially designed instruments

[Chemo-mechanical caries removal: a review of the techniques and latest

developments
j of conservative dentistry 2001 Jul;108(7):277-81.
 CARE DURING OPERATIVE PROCEDURES:

 1.Use mouth mirrors to provide proper retraction of

tongue, cheeks, lips.
 2.Application of rubber dam to ensure protection of
gingiva & adjacent hard & soft tissues.
 Avoiding the use of slow speed drill for gross removal of
tooth structure, as it can be time consuming, and produces
heat & vibrations which may be traumatic to the patient.
 4.Use of coolant for the initial cavity preparation
stage. Intermittent cutting with light strokes is
most comfortable to the patient.
This avoids excessive cutting of tooth structure.
5.While treating deep carious lesions use of slow
speed, round steel burs or spoon excavators to
remove soft caries will provide a better tactile
feel& prevents pulp exposure& pain associated
with it.
 Mastery over proper instrument grasps, rests &
guards is necessary to prevent accidental damage
to adjacent hard & soft tissues.
 Avoiding desiccation of cavity preparations by
blowing air from the air – water syringe. a paid
blast of air from the air-water syringe can produce
a painful response & in deep caries produce pulpal
inflammation.
 Use of gingival retraction cords while working
close to the gingiva will protect the gingival tissue.

 Proper use of pulp protective agents like

varnishes, sealants, liners & bases during
restorative procedures will help to preserve pulp
vitality & prevent post operative pain.
 CONCLUSION
 NO PAIN-NO GAIN goes the old axiom:however it can be
modified in the modern dentistry to state
NO PAIN- ALL GAIN.
 The application of ideal techniques &procedures with
expertise& an attitude of empathy & understanding will help
the clinician-control & eliminate this highly unwelcome
stimulus to achieve greater efficiency &highly contended
individuals.
 Remember -“To the whole world you might just be one man,
but one man you might just be the whole world” that one man is
the individual who comes to us for relief- OUR PATIENT.
 Bibliography
 Textbook of medical physiology- Guyton—8th edition
 Local anesthesia—Mohneim’s 3rd edition
 Bell’s orafacial pain—2nd edition
 Textbook of Oral medicine—Burkits—10th edition
 Text book on periodontology—Carranza—9th edition
 Medical physiology—Ganong—18th edition
 Text book of oral surgery—Kruger 10th edition
 Operative dentistry –Sturdvants
 Pathways of pulp-Cohen
 Text book of endodontics- Ingle
 Conclusion

•Pt. Associate with pain because pain was a hall mark of early
endodontic treatment & partly because media portray endodontic
treatment in this light.
• Pt. Anticipating pain – prescription drug is only means of
effective management.
• Consider clinical diagnosis – to determine best means of
managing pain.
• Integration of these principles of pain mechanism & management
along with clinical assessment allows a clinician to devise an
effective approach to manage pain
of local anesthesia. This study was
performed in a general dental
practice. Nineteen injections were
done with the Wand handpiece of
the CompuDent ™ system by
Milestone and seventeen with the
VibraJect by VibraJect LLC.
Twenty-four were maxillary
infiltrations twelve were
mandibular blocks. Patients
reported the level of pain for the
needle piercing their tissue, the
injection of solution, and their
overall evaluation of the injection.
No difference was seen for piercing
the tissue, injecting the solution or
overall report of pain.
DISCUSSION
Two different techniques were used to control the pain of local
anesthetic injections. No difference could be shown between the two.
When the practitioner compared the two different techniques, the Wand
is a lightweight probe attached to a computer controlled injection
device by a thin plastic tube that carries the solution to the wand. A foot
pedal controls the device. It takes a few injections to get accustomed to
the foot pedal. This device allows two speeds of injection only the slow
speed was used. It is also possible to aspirate by taking your foot off the
foot peddle. The VibraJect was clipped to the syringe body and requires
little if any change from the normal injection technique. The body of
the vibrator should be oriented so it does not rest on the patient's teeth.
CONCLUSION
This study tends to indicate there is little difference in the pain
perceived by a dental patient when injected using the Vibraject as
opposed to injecting with the wand
Transcutaneous electrical nerve stimulation
(acronym TENS) is the use of electric current
produced by a device to stimulate the nerves
for therapeutic purposes. TENS by definition
covers the complete range of transcutaneously
applied currents used for nerve excitation
although the term is often used with a more
restrictive intent, namely to describe the kind
of pulses produced by portable stimulators used
to treat pain.[1] The unit is usually connected to
the skin using two or more electrodes. A
typical battery-operated TENS unit is able to
modulate pulse width, frequency and intensity.
Generally TENS is applied at high frequency
(>50 Hz) with an intensity below motor
contraction (sensory intensity) or low
frequency (<10 Hz) with an intensity that
produces motor contraction.[2
Scientific studies show that high
and low frequency TENS produce
their effects by activation of opioid
receptors in the central nervous
system[citation needed]. Specifically, high
frequency TENS activates delta-
opioid receptors both in the spinal
cord and supraspinally (in the
medulla) while low frequency
TENS activates beta-opioid
receptors both in the spinal cord
and supraspinally[citation needed].
Further high frequency TENS
reduces excitation of central
neurons[citation needed] that transmit
 • Article Links
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•P Rosted
•Palle Rosted

ould supplement conventional treatment modalities. Its value in the treatment of temporomandibular dysfunction syndrome and facial pain has been well documented and supported by randomised controlled trials.
Acupuncture: Introduction to acupuncture in dentistry
P Although
Rostedit may
& Palle
1
Rosted
be useful
1
in the control of post-operative pain, its use as sole analgesia for operative care is questionable. The mode of action of acupuncture can be explained with reference to modern neurophysiology. A short training course can allow the technique to be an effective tool in every dentist's hands.
In brief
• Acupuncture is not a miracle cure and is not going to replace the drill. However, the technique can be a supplement to conventional treatments in TMDs, facial pain, pain management Sjøegrens syndrome, and in phobias and anxiety.
• Acupuncture does have a scientific background and the efficacy has been tested in a number of clinical trials including pain management, facial pain, TMD and increasing of the pain threshold.
• Acupuncture is not without adverse effect and therefore proper training is essential.
• The technique can be achieved by any dentist after a short training programme
 • Article Links

in the light of current research. It is concluded that acupuncture could supplement conventional trea
•Figures and tables

• Article Tools
•Send to a friend
•Export citation
•Export references
•Rights and permissions
•Order commercial reprints
•Bookmark in Connotea

• Search Pubmed for

Its value in the treatment of temporomandibular dysfunction syndrome and facial pain has been
•P Rosted
•Palle Rosted

well documented and supported by randomised

Acupuncture: Introduction
P Rosted1 & Palle Rosted1
In brief
•
controlledintrials.
to acupuncture dentistry
Although it may be useful in the control of post-operative pain,
Acupuncture is not a miracle cure and is not going to replace the drill. However, the technique can be a supplement to conventional treatments in TMDs, facial pain, pain management Sjøegrens syndrome, and in phobias and anxiety.
• Acupuncture does have a scientific background and the efficacy has been tested in a number of clinical trials including pain management, facial pain, TMD and increasing of the pain threshold.
• Acupuncture is not without adverse effect and therefore proper training is essential.
• The technique can be achieved by any dentist after a short training programme

its use as sole analgesia for operative care is questionable. The mode of action of acupuncture
can be explained with reference to modern neurophysiology. A short training course can allow the t
to be an effective tool in every dentist's hands.
 The WAND is effective for all injections that can be
performed using a standard aspirating syringe with some
automation. The WAND is held like a pen, which may be
less cumbersome than a traditional syringe. A foot pedal
controls aspiration and injection of the anesthetic. Injections
may take more time because of the reduced anesthetic flow
rate. The controlled flow of anesthetic is thought to reduce
pain and, thus, patient fear and anxiety.

Am Dent Assoc, Vol 133, No

1, 106-107.
DENTAL
© 2002 American
PRODUCT Dental
SPOTLIGHT
Association
urfaces for bonding procedures or sealants.

arm soft mouth tissue and operates very quietly. Because air abrasion cuts tooth surfaces with the utmost precision, it removes less tooth than the drill and it reduces
2003 Jan;20(1):23-9, 78.
[Carisolv, a change in the perception of caries
treatment--a chemo-mechanical removal of caries]
[Article in Hebrew]
Beyth N, Mass A, Ziskind D.
Dept. of Prosthodontics, Hebrew University-Hadassah
School of Dental Medicine, Jerusalem.
Abstract
This paper reviews the chemo-mechanical method (Carisolv)
for caries removal. The mechanism of action and some
treatment choices are described. Modern dentistry aims to
preserve tooth structure by minimal invasive procedures.
Chemo-mechanical removal of caries is a new method with
the advantage of selective removal of severely demineralized
dentin. This enhances the caries diagnostic ability of the
clinician. Ensuring chair side caries diagnosis and removal,
based on a biological principle, helps to preserve as much
healthy tissue as possible. This method is most comfortable
for the patient. On the other hand treatment time is
prolonged. In most cases, the method has to be used in
combination with a conventional bur. Caries lesions in
which removal of enamel or a restoration is needed cannot
be treated exclusively by the chemo-mechanical method.
However, the chemo-mechanical caries treatment can be
used as the first choice of treatment in specific cases in the
prosthodontic and pediatric field.
PMID: 12674921 [PubMed - indexed for MEDLINE]
2001 Jul;108(7):277-81.
[Chemo-mechanical caries removal: a review of the
techniques and latest developments]
[Article in Dutch]
Beeley JA, Yip HK, Stevenson AG.
Department of Oral Biochemistry, University of Glasgow
Dental School te Glasgow, Engeland.
Abstract
Chemo-mechanical caries removal involves the chemical
softening of carious dentine followed by its removal by
gentle excavation. The reagent involved is generated by
mixing amino acids with sodium hypochlorite; N-
monochloroamino acids are formed which selectively
degrade demineralised collagen in carious dentine. The
procedure requires 5-15 minutes but avoids the painful
removal of sound dentine thereby reducing the need for local
anaesthesia. It is well suited to the treatment of deciduous
teeth, dental phobics and medically compromised patients.
The dentine surface formed is highly irregular and well
suited to bonding with composite resin or glass ionomer.
When complete caries removal is achieved, the dentine
remaining is sound and properly mineralised. The system
was originally marketed in the USA in the 1980's as Caridex.
Large volumes of solution and a special applicator system
were required. A new system, Carisolv, has recently been
launched on to the market. This comes as a gel, requires
volumes of 0.2-1.0 ml and is accompanied by specially
designed instruments
 a more thorough job in less time. Thi
decreased scaling time and healthier,
Hand scalers require repetitive scrapp
to adaptation of only one or two sides
all four sides of a power scaler can be
in an elliptical motion. This comes in
to cool the cavitron then helps to rinse