The document discusses the components, pathways, and management of dental pain, including local anesthesia techniques. It covers topics such as the fast and slow pain pathways, gate control theory of pain, assessment of dental pain, and pharmacological and non-pharmacological pain management methods. The pharmacokinetics of common local anesthetics are also reviewed, including absorption, distribution, metabolism, excretion, and calculations for determining appropriate dosages in pediatric patients.

1. MANAGEMENT OF
DENTAL PAIN
KARISHMA.S
III MDS

2. CONTENTS:
 Introduction
 Components of pain
 Pain pathway
 Management of dental pain
 Local anesthesia
 Local anesthesia techniques
 Newer drug delivery systems for dental local anesthesia
 Conclusion
 References

3. INTRODUCTION
What is Pain??
“An unpleasant sensory and emotional response associated with
actual or potential tissue damage or described in terms of such
damage.”
( International Association for the Study of Pain)

4. BENEFITS OF PAIN SENSATION
• Pain is an important sensory symptom.
1. Pain gives warning signal about the existence of a problem or
threat. It also creates awareness of injury.
2. Pain prevents further damage by causing reflex withdrawal of the
body from the source of injury
3. Pain forces the person to rest or to minimize the activities thus
enabling rapid healing of injured part
4. Pain urges the person to take required treatment to prevent major
damage.

5. COMPONENTS OF PAIN
• Fast pain is due to activity of myelinated A  fibres
and it is appreciated as sharp bright and localized
sensation.
• Slow pain is due to activity of unmyelinated C fibres
and it is appreciated as dull aching and more diffuse.
Slow pain follows fast pain.
Peripheral
Nerve
C-FiberA-delta Fiber

6. Fast pain Slow pain
Felt within about 0.1 second after a
painful stimulus.
Begins after 1 second or more and
then increases slowly over many
sec. or min.
“Bright," sharp, localized
sensation
Dull, intense, diffuse, and
unpleasant feeling
sharp pain, pricking pain, acute
pain, and electric pain
slow burning pain, aching pain,
throbbing pain, nauseous pain,
and chronic pain
Felt mainly in skin. Not felt in most
deeper tissues of the body
It can occur both in the skin and in
almost any deep tissue or organ

7. Fast pain Slow pain
Pin prick, cutting or burning of skin Associated with tissue destruction.
Caused by mechanical or thermal
stimuli.
Caused mainly by chemical stimuli
Transmitted by Aδ fibers
(velocity 6-30 m/sec)
NT- Glutamate
Transmitted by C fibers
(velocity 0.5-2 m/sec)
NT- Substance P
Neo-spinothalamic tract Paleo-spinothalamic tract

8. NERVE FIBRES INVOLVED IN PAIN TRANSMISSION
A FIBRES C FIBRES
A – BETA
FIBRES
A – DELTA
FIBRES
 Large
 Myelinated
 Fast conducting
 Low stimulation
threshold
 Respond to light
touch
 Small
 Lightly Myelinated
 Slow conducting
 Respond to heat,
pressure, cooling &
chemicals
 sharp sensation of
pain
 Small & unmyelinated
 Very slow conducting
 Respond to all types of
noxious stimuli
 Transmit prolonged
dull pain
 Require high intensity
stimuli to trigger a
response

9. PATHWAYS OF PAIN SENSATION
 The pathways of pain sensation are as follows
 Pathway from skin & deeper tissues
 Pathway from face – pain sensation is carried by trigeminal nerve
 Pathway from viscera – pain sensation from thoracic & abdominal
viscera are transmitted by sympathetic nerves & from oesophagus,
trachea & pharynx by glossopharyngeal nerves
 Pathway from pelvic region – conveyed by sacral parasympathetic
nerves

10. PAIN RECEPTORS
• NOCICEPTORS or PAIN RECEPTORS are sensory receptors that are activated
by noxious insults to peripheral tissues
 The receptive endings of the peripheral pain fibres are free nerve endings
 These receptive endings are widely distributed in the
 Skin
 Dental pulp
 Periosteum
 Meninges

11. FIRST ORDER NEURONS
 These are the cells in the posterior nerve root ganglia, receive
impulses from pain receptors through dendrites
 These impulses are transmitted through the axons to spinal cord
 Impulses are transmitted by Aδ fibre or C fibres
SECOND ORDER NEURONS
 The neurons of marginal nucleus & substantia gelatinosa form the
II order neurons
 Fibres from these neurons ascend in the form of the lateral
spinothalamic tract
 Fibres of fast pain arise from neurons of the marginal nucleus and
those of slow pain arise from neurons of substantia gelatinosa

12. THIRD ORDER NEURONS
 The neurons of pain pathway are the
neurons in Thalamic nucleus, reticular
formation, gray matter around the
aqueduct of sylvius
 Axons from these neurons reach the
sensory area of cerebral cortex or
hypothalamus

13. PAIN PATHWAY
DESCENDING/ANALGESIC PATHWAY: Analgesic pathway
that interferes with pain transmission is often considered as
descending pain pathway, the ascending pain pathway being the
afferent fibers that transmit pain sensation to the brain.
1).Fibers of analgesic pathway arise from frontal lobe of cerebral
cortex and hypothalamus
2).These fibers terminate in the gray matter surrounding the third
ventricle and aqueduct of Sylvius (periaqueductal gray matter)
3).Fibers from here descend down to brainstem and terminate on:
i. Nucleus raphe magnus, situated in reticular
formation of lower pons and upper medulla
ii. Nucleus reticularis, paragigantocellularis situated
in medulla

14. At synaptic level, analgesic fibers release neurotransmitters and inhibit the
pain transmission before being relayed to brain.
Neurotransmitters: serotonin and opiate receptor substances-enkephalin,
dynorphin and endorphin.

15. ROLE OF BRAIN IN GATE CONTROL MECHANISM
Gates in spinal cord are open
Pain signals reach the thalamus through lateral spinothalamic tract
Signals are processed in thalamus
Signal are sent to sensory cortex & perception of pain occurs in
cortex
Signals are sent from cortex back to spinal cord and the gate is
closed by releasing pain relievers such as opioid peptides
Minimizing the severity & extent of pain

16.  Proposed by MELZACK & WALL IN 1965
 According to this theory, the pain stimuli transmitted by afferent pain fibres are
blocked by GATE MECHANISM located at the posterior gray horn of the spinal
cord
 If the gate is open pain is felt, and if the gate is closed pain is suppressed
 Impulses in A – δ & C – fibres can be blocked by modulated activity that can
selectively block impulses from being transmitted to the transmission cells in the spinal
cord and then to CNS resulting in no pain
GATE CONTROL THEORY

17. GATE CONTROL THEORY-
MECHANISM
1.When pain stimulus is applied on any part of body, besides pain receptors, the receptors of
other sensations such as touch are also stimulated.
2.When all these impulses reach the spinal cord through posterior nerve root, the fibers of touch
sensation (posterior column fibers) send collaterals to the neurons of pain pathway, i.e. cells of
marginal nucleus and substantia gelatinosa.
3.Impulses of touch sensation passing through these collaterals inhibit the release of glutamate
and substance P from the pain fibers
4.This closes the gate and the pain transmission is blocked

19. PAIN
MANAGEMENT

20. ASSESSMENT OF PAIN
METHOD OF PAIN ASSESSMENT
 Comprehensive history intake
 Medical history
 Physical history
 Family history
 Physical exam
Questioning on characteristic of pain – onset, duration, location, quality, severity &
intensity
 Evaluation of psychological status

22. MANAGEMENT OF PAIN
GOALS OF THERAPY
 To decrease the subjective intensity
 To reduce the duration of the pain complaints
 To decrease the potential for conversion of acute pain to chronic persistent pain
syndromes
 To decrease the physiological, psychological, & socioeconomic sequelae associated
with under treatment of pain
 Improving the patients quality of life and the ability to perform activities of daily living

23. APPROACHES TO PAIN CONTROL

24. NON – PHARMACOLOGICAL
MANAGEMENT
 The non – pharmacological management involves the following approaches
 Physiotherapy
 Psychological techniques
 Stimulation therapies – Acupuncture & Transcutaneous Electrical Nerve
Stimulation (TENS)
 Palliative care – involves the alleviation of symptoms but does not cure the
disease

25. • Behaviour Management Techniques for L.A.
• Warm up to your patient ¸ (fav. Cartoons, Activity etc.)
• Tell, show, do
• Euphemisms - “Sleepy juice” (x hurt/pain)
• Distraction and verbal communication
• Positive reinforcement ¸ Reward
• Breathe/count to 10
Psychological techniques

26. • Active total care of patients whose disease is not responding to curative treatment.
• Maintenance of oral hygiene; dental examination may identify and cure
opportunistic infections and dental disease like caries, periodontal disease, oral
mucosal problems or prosthetic requirement.
• Reduce not only the microbial load of the mouth but the risk for pain and oral
infection as well.
• May reduce the oral debilities that influence the patient's ability to speak, eat or
swallow.
Palliative Pain Care

27. LOCAL ANAESTHESIA

28. 28
CLASSIFICATION OF LOCALANESTHETICS
ESTERS OF
BENZOIC ACID
ESTERS OF
PARA-AMINO
BENZOIC ACID
AMIDES QUINOLINE
Butacaine
Cocaine
Benzocaine
Piperocaine
Tetracaine
Chloroprocain
Procaine
Propoxycaine
Articaine
Bupivacaine
Dibucaine
Etidocaine
Lidocaine
Mepivacaine
Prilocaine
Ropivacaine
Centbucridine

29. ACCORDING TO BIOLOGICAL SITE AND MODE OF ACTION
CLASS A: Agents acting at receptor site on external surface of nerve membrane. eg: Biotoxins
(e.g., tetrodotoxin and saxitoxin)
CLASS B: Agents acting on receptor sites on internal surface of nerve membrane. eg: Scorpion
venom
CLASS C: Agents acting by receptor independent of physiochemical mechanism. eg: Benzocaine
CLASS D: Agents acting by combination of receptors and receptor independent mechanism. eg:
most clinically useful anesthetic agents (e.g.,lidocaine, mepivacaine, prilocaine)

30. BASED ON THE SOURCE
• Natural
• Synthetic
• Others
BASED ON MODE OF APPLICATION
• Injectable
• Topical
30

32. 32
Commercially prepared local anesthesia consists of :
• Local anesthetic agent (xylocaine, lignocaine 2%)
• Vasoconstrictor (adrenaline 1: 80,000)
• Reducing agent (sodium metabisulphite)
• Preservative (methylparaben, capryl hydrocuprienotoxin)
• Fungicide (thymol)
• Vehicle (distilled water, NaCl)

33. PHARMACOKINETICS OF LOCAL ANESTHETICS
UPTAKE:
 When injected into soft tissue most local anesthetics produce
dilation of vascular bed.
 Cocaine is the only local anesthetic that produces
vasoconstriction, initially it produces vasodilation which is
followed by prolonged vasoconstriction.
 Vasodilation is due to increase in the rate of absorption of the
local anesthetic into the blood, thus decreasing the duration of
pain control while increasing the anesthetic blood level and
potential for over dose.
33

34. ORAL ROUTE:
• Except cocaine, local anesthetics are poorly absorbed from GIT
• Most local anesthetics undergo hepatic first-pass effect following
oral administration.
• 72% of dose is biotransformed into inactive metabolites
• TOCAINIDE HYDROCHLORIDE an analogue of lidocaine is
effective orally
34

35. TOPICAL ROUTE:
• Local anesthetics are absorbed at different rates after application
to mucous membranes, in the tracheal mucosa uptake is as rapid
as with intravenous administration.
• In pharyngeal mucosa uptake is slow
• In bladder mucosa uptake is even slower
• Eutectic mixture of local anesthesia (EMLA) has been developed
to provide surface anesthesia for intact skin.
35

36. ROUTE TIME TO PEAK LEVEL
(MIN)
INTRAVENOUS 1
TOPICAL 5
INTRAMUSCULAR 5-10
SUBCUTANEOUS 30 - 90
INJECTION:
• The rate of uptake of local anesthetics after injection is related to both
the vascularity of the injection site and the vasoactivity of the drug.
• IV administration of local anesthetics provide the most rapid elevation
of blood levels and is used for primary treatment of ventricular
dysrhythmias.
RATES AT WHICH LOCAL ANESTHETICS ARE ABSORBED AND REACH THEIR PEAK BLOOD
LEVEL

37. DISTRIBUTION
• Once absorbed in the blood stream local anesthetics are
distributed through out the body to all tissues.
• Highly perfused organs such as brain, head, liver, kidney, lungs
have higher blood levels of anesthetic than do less higher
perfused organs.
All local anesthetic agents readily cross the blood-brain barrier,
they also readily cross the placenta.
37

38. METABOLISM (BIOTRANSFORMATION)
ESTER LOCAL ANESTHETICS:
• Ester local anesthetics are hydrolyzed in the plasma by the enzyme
pseudocholinesterase.
• Chloroprocaine the most rapidly hydrolyzed, is the least toxic.
• Tertracaine hydrolyzed 16 times more slowly than Chloroprocaine,
hence it has the greatest potential toxicity.
• Atypical form of psuedocholinesterase
38

39. AMIDE LOCAL ANESTHETICS:
• The metabolism of amide local anesthetics is more complicated than
esters. The primary site of biotransformation of amide drugs is liver.
• Entire metabolic process occurs in the liver for lidocaine, articaine,
etidocaine, and bupivacaine.
• Prilocaine undergoes more rapid biotransformation than the other
amides.
• METHAEMOGLOBINAEMIA

40. EXCRETION
• Kidneys are the primary excretory organs for both the local
anesthetic and its metabolites
• A percentage of given dose of local anesthetic drug is excreted
unchanged in the urine.
• Esters appear in only very small concentration as the parent
compound in urine.
• Procaine appears in the urine as PABA (90%) and 2% unchanged.
• 10% of cocaine dose is found in the urine unchanged.
• Amides are present in the urine as a parent compound in a greater
percentage then are esters.
40

41.  The maximum dose of lidocaine and mepivacaine, without
vasoconstrictors, recommended for children is 4.4 mg/kg body
weight, and 7 mg/kg body weight for lidocaine with
vasoconstrictors.(AAPD,2015)
 The most commonly used local anesthetics for pediatric dentistry
are the amide type agents. Lidocaine hydrochloride (HCl) 2% with
1:100,000 epinephrine is preferred because of their low allergenic
characteristics and their greater potency at lower concentrations.
Local anesthetic calculation: amount of local anesthetic in
cartridges.
2% anesthetic = 2 grams/100 ml in volume = 2000 mg/100 ml = 20
mg/ml
3% anesthetic = 3 grams/100 ml in volume = 3000 mg/100 ml = 30
mg/ml
1 cartridge of local anesthetic is 1.8 ml in volume (exception: 4%
articaine has 1.7 ml) Therefore…
2% cartridge: 20 mg/ml x 1.8 ml/cartridge = 36 mg/cartridge
3% cartridge: 30 mg/ml x 1.8 ml/cartridge = 54 mg/cartridge

42. So, for a child weighing 25 kg, the maximum permissible dosage of LA
is 7 × 25 = 175 mg of LA.
As lidocaine is generally available as 2% solution, this is 2 gm in 100 ml
of solution or 100 ml of solution will have 2 gm of LA.
1 ml of solution has 2/ 100 = 20 mg of LA 1.8 ml of solution (1
cartridge) will have – 20 × 1.8 = 36 mg of LA
If a total of 175 mg can be safely administered to a child weighing 25
kg, it means 175/36 = 4.8 or 5 Cartridges of Lidocaine with adrenaline
(1.8 ml of solution) can be safely administered.

43. 43
Maximum Recommended Dosage MRD

44. Rule of 10:
There has been discussions whether to give a local infiltration or an inferior
alveolar nerve block to anesthetize the mandibular primary molars. Rule of
10 is a better approach to determine which injection is appropriate.
This number is added to the age of the child (in years), and if the number is
10 or less, then an infiltration is more appropriate; if greater than 10, then
an inferior alveolar nerve block is likely to be more effective. This simple
approach works well in most cases. The only instance where the rule would
be contraindicated is where quadrant dentistry involving pulp treatment of
both first and second molar. In this case local infiltration may not provide a
sufficient depth of pulpal analgesia and a mandibular block would be
preferred.

45. ANAESTHETIC AGENT SUITABLE FOR CHILDREN
1.Lidocaine hydrochloride 2% with epinephrine 1:100,000
2.mepivacaine hydrochloride 2% with levonordefin 1:20,000
3.prilocaine hydrochloride 4% with epinephrine 1:200,000

46. • Different theories have been given to explain mode of action of
local anesthetic agent:-
1. Acetylcholine theory by Dett barn in 1967.
2. Calcium displacement theory by Goldman in 1966.
3. Surface charge theory by Wei in 1969.
4. Membrane expansion by Lee in 1976
5. Specific receptor
THEORIES:
HOW DOES LA WORK??

47. • It says that the blocking of local anesthetic is due to the binding
of the drug to a specific site inside the nerve cell.
• This decreases the permeability of nerve membrane to sodium
ions thus preventing the influx of the sodium ions into nerve.
• Thus the threshold potential of the nerve is increased which
causes the decreased conduction of the impulse.

48. L.A TECHNIQUES

50. TOPICAL ANESTHESIA
• It is the method of obtaining anesthesia by the application of
suitable agent to an area of either the skin or mucous membrane
through which it penetrates to anesthetize superficial nerve
endings.
• It is commonly used to obtain anesthesia of the mucosa prior to
injection.

51. 3 Main Types of LA Injections:
1)Local Infiltration
2)Field Block
3)Nerve Block

52. Supplemental Injections
The following are used in both arches:
• Supraperiosteal Injection
• Intraligamentary (PDL) Injection
• Intraseptal Injection
• Intraosseous Injection

53. • A method of obtaining primary anesthesia for one or two teeth or as a supplement to
infiltration or block techniques.
• The technique’s primary advantage is that it provides pulpal anesthesia for 30 to 45
minutes without an extended period of soft tissue anesthesia.
• It is useful in pediatric or disabled patients when there is concern of postoperative
tissue trauma to the lip or tongue.
• However, its use should be avoided in primary teeth with a developing permanent tooth
bud as there have been reports of enamel hypoplasia in permanent teeth following PDL
injection.
• Can be used in patients with bleeding disorders.
Intra ligamentary

54. Anatomy

55. Anesthesia for the
maxillary tissues
• The needle penetration site is determined by two anatomic landmarks, the
mucobuccal fold and mucogingival junction (Sweet's line), a visible white
border between the fixed gingiva and the red alveolar mucosa.
• The penetration site is 2 to 3 mm apical to the mucogingival junction and
into the alveolar mucosa and 2 mm from the labial or buccal surface
• Needle penetration is quickly accomplished by pulling the loose alveolar
tissue of the lip or cheek over the positioned needle.
• Penetration is rapid and relatively pain free.

56. Posterior Superior Alveolar Nerve Block (PSA)
 Effective for permanent maxillary 1st, 2nd and 3rd molars and buccal periodontium;
Mesiobuccal root of the maxillary 1st molar is not consistently innervated by the PSA
nerve.
 28% of maxillary 1st molars’ mesiobuccal roots are innervated by the middle superior
alveolar nerve (MSA).
 When the risk of hemorrhage is too great as with a hemophiliac, you should use the
supraperiosteal or PDL injections
 No pain during injection due to absence of bony landmarks

57.  The are of insertion is at the height of the
mucobuccal fold above the maxillary second
molar.
 The needle is advanced slowly upward
,backward and inward.
 Half the length of the needle should be
inserted.
 The target is PSA and is located posterior
superior and medial to maxillary tuberosity

58. Modification:
• Less dense maxilla, so supraperiosteal injections are recommended.
• Puncture point is last erupted molar.
• Depth of penetration is restricted to ¾ inch.

59. Middle Superior Alveolar Nerve Block (MSA)
 Middle Superior Alveolar Nerve is not present in 28% of the population
 MSA provides anesthesia to 1st and 2nd premolars and mesiobuccal root of maxillary 1st molar;
anesthetizes buccal periodontium and bone.
Technique
1.Target is the maxillary bone above the apex of the 2nd maxillary premolar.
2.Penetrate tissues placing bevel of needle well above the apex of the 2nd maxillary premolar.
3.Aspirate and slowly deposit 0.9-1.2 ml of solution.

61. Anterior Superior Alveolar Nerve Block (ASA)
• Provides profound pulpal and soft tissue anesthesia from the maxillary central
incisor distal to the premolars in 72% of patients
• Uses less anesthetic solution than the supraperiosteal injection
• Supraperiosteal  3.0 ml solution
• ASA  1.0 ml solution

62. Areas Anesthetized
1) Pulp of the maxillary central incisor through the canine
2) 72% of patients have premolars and mesiobuccal root of 1st molar
anesthetic
3) Buccal periodontium and bone of the above teeth
4) Lower eyelid, lateral aspects of the nose and upper lip

63. Modifications:
 Local infiltration / supra periosteal injection is used.
 Inject close to gingival margin.
 Solution deposited close to the bone diffuses easily and faster

64. Greater Palatine Nerve Block
• Anesthetizes palatal soft tissue distal and medially to the canine
• Tissues around the Greater Palatine Foramen are able to
accommodate a larger volume of solution than the tissue in the
vicinity of the Nasopalatine Foramen  less patient discomfort

65. Locate the Greater Palatine Foramen:
• Use cotton swab/mirror handle
• place a cotton swab at the junction of the maxillary
alveolar process and the hard palate
• press firmly into tissues moving posteriorly from the
maxillary 1st molar
• swab “falls” into the depression of the greater palatine
foramen

67. Modification:
• Location:
• In primary dentition only: approx 10mm posterior to distal surface of 2nd primary
molar.
• In mixed dentition: imaginary line drawn from gingival border of most posterior
molar that has erupted to the midline.
 Buccal infiltration of articaine minimizes the need for further palatal injections.

68. Nasopalatine Nerve Block
 Considered by many to be the most traumatic, painful injection of all the
dental injections
 Anesthetizes the anterior portion of the hard palate (soft and hard tissues) from
the mesial of the left premolar to the mesial of the right premolar
 Target area is the incisive foramen beneath the incisive papilla

69. Palatal Anesthesia
• Extremely painful procedures.
• Ramirez et al described methods to minimize this pain..
• Post buccal infiltration an interdental/interpapillary injection.
• Constant pressure before and during insertion.
• Slow deposition
• Control over the needle.

70. Mandibular Anesthesia
Lower success rate than Maxillary anesthesia - approx. 80- 85 %
 Related to bone density
 Less access to nerve trunks
MANDIBULAR NERVE BLOCKS
• Inferior alveolar
• Mental - Incisive
• Buccal
• Lingual
• Gow-Gates
• Akinosi

71. IANB
 Area of insertion: medial ramus, mid-coronoid notch,
 advance to bone (20-25 mm).
 Target Area: Inferior alveolar nerve, near mandibular foramen.
 Landmarks:
• Coronoid notch
• Pterygomandibular raphe
• Occlusal plane of mandibular posteriors
• Retromolar triangle area

72. • Greatest depth of anterior
border of the ramus of
mandible – coronioid
notch.
• Pterygo mandibular raphe.
• Needle is penetrated until
gentle contacting bone on
medial surface.

73. Precautions
Do not inject if bone not contacted
Avoid forceful bone contact
Failure of Anesthesia
Injection too low
Injection too anterior
Accessory innervation
-Contralateral Incisive nerve innervation
Complications
Hematoma
Trismus
Facial paralysis

74. MODIFICATION:
• Barrel of syringe is placed over opposite side primary molars.
• Depth of penetration is 15mm.
• Site of insertion in children is more inferior and distal.
Below occ.plane At occ.plane above occ.plane

75. GOW GATES TECHNIQUE
• Entire mandibular branch of
trigeminal
• Landmark-
• imaginary line from corner of mouth
to intertragic notch of ear and
anterior border of ramus
• Approach - Distal to the molar from
opposite side
• Needle is advanced until bone is
contacted at the neck of the condyle
and avg depth of penetration is
25mm

76. VAZIRONI AKINOSI
• The entire mandibular branch except the long buccal
• 25 gauge 38-40mm needle
• Land marks – occlusal plane,ant border of ramus of mandible,maxillary
tuberosity
• Target area- medial surface of the ramus of the mandible in the region
of inferior alveolar nerve as it travels toward the mandibular foramen
• Needle is penetrated medial to ramus and lateral to maxillary tuberosity

77. Long Buccal Nerve Block
• Anterior branch of Mandibular nerve (V3)
• Provides buccal soft tissue anesthesia adjacent to mandibular
molars.
Alternatives
 Buccal infiltration
 Gow-Gates
 PDL
 Intraseptal

78. Technique
• Insertion distal and buccal to last molar
• Target - Long Buccal nerve as it passes anterior border of ramus
• Inject 0.3-0.5 ml of solution, slowly
• 25-27 gauge needle
• Area of insertion:- Mucosa adjacent to most distal molar.
Landmarks
Mandibular molars
Mucobuccal fold
Not much difference between children and adult technique.

79. Mental Nerve Block
• Terminal branch of IAN as it exits mental foramen
• Provides sensory innervation to buccal soft tissue anterior to
mental foramen, lip and chin
• 5-6 mm between the premolars
Modification:
 Mental foramen is located near the apex of the mesial
root of the primary first molar.

80. Incisive Nerve Block
• Terminal branch of IAN
• Originates in mental foramen and proceeds anteriorly
• Good for bilateral anterior anesthesia
• Not effective for anterior lingual anesthesia

82. A comparative evaluation of pain perception following topical application of benzocaine
gel, clove-papaya based anesthetic gel and precooling of the injection
site before intraoral injections in children A Anantharaj, Jiline Mary Sabu, Sudhir Ramakrishna, Ramya
Bangalore Jagdeesh, P Praveen, Prathibha Rani Shankarappa
Aim: To compare the topical anesthetic efficiency of precooling with ice, clove–papaya based topical gel and
benzocaine gel in pediatric patients.
Methodology: Sixty healthy children aged 9–10 years who required local anesthetic injections for dental procedures
were selected and divided into three groups with 20 patients each. In the first visit, written consent and intraoral
screening of the patients were performed. In the second visit, the topical anesthetic agents were applied in the
respective groups for 1 min and later local anesthetic injections were administered. Pain perception was evaluated
using Sound, Eye, Motor Scale (SEM scale) and Wong Baker Faces Pain Rating Scale (WBFPRS), tabulated, and
statistically analyzed.
Results: The test results demonstrated that benzocaine group has the highest mean WBFPRS score followed by
clove– papaya group and then ice cone group. The ice group showed the least mean SEM scale score, followed by
the benzocaine group and then clove–papaya group. However, the mean WBFPRS score and the mean SEM scale
score did not show any statistically significant difference.
Interpretation and Conclusion: All the three topical anesthetic agents provided similar surface anesthesia in
children. The newly introduced clove–papaya based topical anesthetic gel showed encouraging results, hence can
be used as a potent topical anesthetic agent.

83. Newer Drug Delivery Systems for
Dental Local Anesthesia

84. Topical anaesthetics reversibly block nerve conduction near the site of
administration. They act on the free nerve endings in the dermis or
mucosa producing temporary loss of sensation in a limited area. Nerve
impulse conduction is blocked by decreasing nerve cell membrane
permeability to sodium ions.
Types of topical anaesthetics According to the vehicle that used to
make them amenable to surface application, topical anaesthetics are
classified as:
A) Non aqueous or water insoluble
B) Aqueous or water soluble

85. Combinations of benzocaine :
1. Orabase- combination of benzocaine,gelatin, pectin & sodium
carboxymethylcellulose.
2. Cetacine: It contains 14% benzocaine, 2% butamen, 2% tetracaine Hcl
Combinations of tetracaine hydrochloride:
1. Tetracaine, adrenaline (epinephrine), and cocaine (TAC)
2. Lidocaine, epinephrine, and tetracaine (LET)
 S-caine patch™ and local anesthetic peel the
patch
 Eutectic mixture of local anaesthetics (EMLA)
 Betacaine-LA contains lignocaine, prilocaine and
phenylephrine

86. Recent Advances In Topical Anaesthesia
1)Precooling (Cryo Anaesthesia)
It is the application of cold to a localised part of body in order to block the
local nerve conduction of painful impulses
2) Iontophoresis :Iontophoresis is a method of enhancing the transport of
topically applied drugs using a mild electric current to increase the
permeability of charged drugs through the skin.

87. Injectable Local Anaesthetics
Recent advances in local anaesthetic solution
a) Phentolamine mesylate
1)Oraverse was found to be safely tolerated in children
between 4-11 years
2) Sodium bicarbonate - As we know, local
anaesthetics are weak bases. They are combined with
an acid to form hydrochloride salt, to render them
water soluble, creating a stable injectable anaesthetic
solution

88. Buffered versus unbuffered local anesthesia for inferior
alveolar nerve block injections in children: a systematic review
sunny priyatham tirupathi srinithya rajashekhar
The present study aimed to evaluate and compare the efficacy of buffered and unbuffered local
anesthesia solutions during inferior alveolar nerve block (IANB) administration in children.
Methods: PubMed, Ovid SP, and Cochrane databases were searched separately by two independent
reviewers for potential papers published between 1980 and April 2020 using relevant MeSH terms and
pre-specified inclusion and exclusion criteria.
Results: A total of five articles were included in a qualitative analysis; among them, four qualified for
quantitative analysis of the primary outcome and three for quantitative analysis of the secondary
outcome. A fixed-effects model was used to perform the meta-analysis.
Pain perception (child-reported pain): Significantly lower pain scores were reported with buffered local
anesthesia solution than with unbuffered solution (P = 0.006, MD: −0.32, 95% CI: −0.55 to −0.09).

89. Onset of anesthesia: A significantly lower duration of anesthesia onset was reported with
buffered local anesthesia solution than with unbuffered solution (P = 0.00001, MD: −12.38, 95%
CI: −17.64 to −7.13].
Pain reaction (observer-reported pain reaction in child): No significant difference was found
between buffered and unbuffered solution in terms of observer-reported pain behavior in the
child (P = 0.09, MD: −0.21, 95% CI: −0.46 to 0.04).
Conclusion:Buffering local anesthesia solution may reduce discomfort due to IANB injection
administration and lower the initial onset time of anesthesia. More randomized control trials with
adequate sample sizes should be carried out to validate the accuracy of these results.

90. Transcutaneous electric nerve stimulation ( TENS)/ electronic
dental anaesthesia
 It is a non- pharmacological method which is widely used for the
management of acute and chronic pain in a variety of conditions.
 Gate control theory
 By transcutaneous electric nerve stimulation large myelinated fibres(A
FIBERS) are stimulated and inhibits transmission of small unmyelinated
fibres.

91. Munshi et al in 2000 used TENS for the management of pain during
treatment procedures such as minor extractions, restorations and pulp
therapy in children between the age of 5-12 years and found significantly
favoured results .
Dhindsa et al 2011 compared efficacy of TENS with 2% lignocaine in
reducing pain during extraction, cavity preparation, pulpotomy and
pulpectomy of deciduous teeth and concluded that TENS can be a useful
adjunct in pediatric patients in achieving anaesthesia .

92. Jet injection
The basic principle of this injection is “if a high enough pressure
can be generated by a fluid in intimate contact with the skin, then
the liquid will punch a hole in to the skin and be delivered in to the
tissues in and under the skin”

93. Computer controlled local anaesthetic delivery system (C-CLAD)
Indications:
Trade names: Compudent, Comfort control syringe, Single tooth
anaesthesia, Quick sleeper, Sleeper one.
• Slow rate 0.5 mL/min
• Fast rate 1.8 mL/min

94. Vibrotactile devices
• C fibres -dull, slow, diffuse burning pain is carried by small unmyelineated
• A fibres - the sensation of light, touch is carried by large myelinated.
Transcutaneous electric nerve stimulation of large myelinated fibres is done and
inhibits transmission of small unmyelinated fibres. So in short, pain control can
be achieved by increasing large fiber input and decreasing small fiber input and
thus closing the gate.

95. Intraosseous anaesthetic system
 Stabident
 X-tip
 Intraflow

97. conclusion

98. references
1. Essential Medical Physiology – K Sembulingam
2. Fundamentals of pediatric dentistry – Richard j mathewson
3. Handbook of Local anesthesia – Stanley F. Malamed (4th
edition).
4. Textbook of medical physiology – Guyton and Hall (11th
edition).
5. Dentistry for the child and adolescent- McDonald and Avery’s
9th edition

99. Thank you