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La seminar

  1. 1. LOCAL ANESTHESIA IN DENTISTRY 1
  2. 2. CONTENTS • Definition • History • Classification • Properties of L.A • Nerve physiology • Mechanism of action • Specific local anesthetics • Local anesthetic techniques • Maxillary • Mandibular • Complications • Local • Systemic • Post operative 2
  3. 3. Definition of L.A Local anaesthesia has been defined as a “Loss of sensation in a circumscribed area of the body caused by a depression of excitation in nerve endings or an inhibition of the conduction process in peripheral nerves”. (According to Moheims) 3
  4. 4. HISTORY 4
  5. 5. Early History of Regional Anaesthesia  Koller and Gartner report local anesthesia (1884).  In 1884,Koller was the first, to use cocaine for topical anaesthesia in ophthalmological surgery. Carl Koller 1857 -1944 5
  6. 6. Early History Of Regional Anaesthesia  1885 Halsted injects cocaine directly into mandibular nerve and brachial plexus William S. Halsted 6
  7. 7. Common Uses Of Local Anesthetic : Excision Dermatology Spinal Anaesthesia Dentistry 7
  8. 8. CLASSIFICATION 8
  9. 9. BASED ON SITE Topical Cocaine, Prilocaine, Lignocaine Injectable Lignocaine, Mepivacaine 9
  10. 10. BASED ON CHEMICAL STRUCTURE ESTERS • Cocaine • Procaine • Benzocaine • Tetracaine AMIDES • Articaine • Bupivacaine • Lidocaine • Mepivacaine • Prilocaine • Ropivacaine 10
  11. 11. BASED ON DURATION OF ACTION Ultra Short • 2% lignocane without vasoconstrictor Duration Short duration Intermediate duration Long duration • Procaine, • 2 % Lignocaine with 1:1,00,000 Epinephrine • • • • Articaine Mepivacaine Prilocaine 2 % Lignocaine with 1:2,00,000 Epinephrine • Bupivacaine • Etidocaine • 5 % Lignocaine with 1:2,00,000 Epinephrine 11
  12. 12. DIFFERENCES AMIDES • longer lasting analgesia. • Produce more intense analgesia. • Rarely cause hypersensitivity reactions- no cross reactivity with ESTER L A s. • Not hydrolyzed by Plasma Cholinesterase, more slowly destroyed by liver microsomal P450 enzymes. ESTERS • Short duration of action • Less intense analgesia • Higher risk of hypersensitivity ESTER linked LA s are rarely used. • Hydrolyzed by Plasma Cholinesterase in blood. • Rarely used for Infiltration anesthesia • But useful for topical anaesthesia on mucous membranes. 12
  13. 13. Properties of L.A • It should not be irritating to the tissue to which it is applied. • It should not cause any permanent alteration of nerve structure. • Its systemic toxicity should be low. • The time of onset of anaesthesia should be as short as possible. • The duration of action must be long enough to permit completion of the procedure yet not so long as to require an extended recovery.
  14. 14. According to Beneett an ideal properties of local anaesthesia • It should have potency sufficient to give complete anaesthesia without the use of harmful concentrated solutions. • Its should be relatively free from producing allergic reactions. • It should be stable in solution &readily undergo biotransformation in the body. • It should either be sterile or capable of being sterilized by heat without deterioration.
  15. 15. NERVE PHYSIOLOGY AND MECHANISM OF ACTION 15
  16. 16. Electrophysiology of nerve conduction • Electrical events that occurs within a nerve during the conduction of an impulse. • A nerve possesses a resting potential. This is a negative electrical potential of -70 mV that exists across the nerve membrane, produced by differing concentrations of ions on either side of the membrane. • A stimulus excites the nerve, in following sequence of event – 16
  17. 17. Step 1a – an initial phase of slow depolarization. The electrical potential within the nerve becomes slightly less negative. 1b –falling electrical potential reaches a critical level, it give result of rapid phase of depolarization. This is termed threshold potential, or firing threshold. 1c –this phase of rapid depolarization results in a reversal of electrical potential across the nerve membrane. electrical potential 0f+40 mV exists on the interior of the nerve cell. 17
  18. 18. Membrane excitation • Depolarization – Excitation of nerve segment leads to an increase in permeability of the cell membrane to sodium ions. The rapid influx of sodium ions to the interior of the nerve cell causes depolarization of the nerve membrane from its resting level to its firing threshold of approx. -50 to -60 mV. Exposure of the nerve to local anesthetic raises its firing threshold. 18
  19. 19. Repolarization • The action potential is terminated when the membrane repolarizes. This is caused by the inactivation of increased permeability to sodium. In many cells potassium also increases, resulting in the reflex of K+, and leading to more rapid membrane repolarization and return to its resting potential. 19
  20. 20. Mechanism of action A. 1. 2. 3. 4. 5. Theories for mechanism of action of L.A are : The Acetylcholine theory. The calcium displacement theory. The surface charge theory. Membrane expansion theory. Specific receptor theory. 20
  21. 21. THE ACETYLCHOLINE THEORY • Started that acetylcholine was involved in nerve conduction in addition to its role as a neurotransmitter at nerve synapses . THE CALCIUM DISPLACEMENT THEORY • L.A nerve block was produced by the displacement of calcium from some membrane site that controlled permeability to sodium. That varying the concentration of calcium ion bathing a nerve does not affect local anesthetic potency has diminished the credibility of this theory. 21
  22. 22. Membrane expansion theory • Stated that L.A molecules diffuse to hydrophobic regions of excitable membranes, producing a general disturbance if the bulk membrane structure, expending some critical regions in the membrane & preventing an increase in the permeability to sodium ions. 22
  23. 23. Specific receptor theory by strichartz 1987  Drug molecules bind to specific receptors present on the external or internal axoplasmic surface of sodium channels & by acting directly on them, decrease or eliminate permeability to Na2+ leading to interruption of nerve conduction. 23
  24. 24. B. Local anaesthesia act in following ways: Displacement of calcium ions from the sodium channel receptor site, which permits Binding of the L.A molecules to the receptor site, which thus produce Blockade of the sodium channel , 24
  25. 25. Decrease in sodium conductance, which lead to Depression of the rate of electrical depolarization Failure to achieve the threshold potential level, along with Lack of development of propagated action potentials, which is called Conduction blockade 25
  26. 26. CLINICAL PROPERTIES OF LOCAL ANESTHETICS 26
  27. 27. pKa • ONSET = pKa • pKa = pH at which 50% of drug is ionized • LA’s <50% exists in the lipid soluble in non ionized form • Only the non ionized form crosses into the nerve cell 27
  28. 28. pH influence • Usually at range 7.4 -8.5 • Decrease in pH shifts equilibrium toward the ionized form, delaying the onset action. • Lower pH, solution more acidic, gives slower onset of action. Presence of Pus and inflammation will retard the action of LA. ( probably low acidic pH) therefore • LA are more ionized - don’t penetrate very well. • Decreased ability of LA to produce effects. 28
  29. 29. VASODILATOR ACTIVITY • Affects Anesthetic potency and duration • Greater vasodilator activity = increased blood flow to region =rapid removal of anesthetic molecule from injection site ; thus decreased anesthetic potency and duration. 29
  30. 30. Composition Local Anesthetics solution contains : 1. Local anaesthetic agents – Ester linkage – procaine, cocaine, tetracaine. Amide linkage – lignocaine , prilocaine , mepivacaine, bupivacaine . 2. Vasoconstrictors – Adrenaline – a synthesis substance similar to that secreted in human body. 30
  31. 31. Advantages – • Reduces toxic effect by retarding the absorption of the constituents. • It increases the depth & duration of anaesthesia and produces bloodless field for surgical procedure. 3. Reducing agent- Sodium bimetasulphite. • small quantity in the solution to prevents oxidation of the vasoconstrictors as they are unstable in solution especially on exposure to sunlight. 31
  32. 32. 4. Preservative – Caprylhydrocupeinotoxin • it helps to maintain sterility of the solution & also increases its self life. 5. Fungicide – Thymol • to prevents proliferation of minute fungi which causes cloudiness of the solution. 6.Vehicle – Ringer’s solution. • In which all constituent dissolves to minimizes discomfort during injection of L.A. 32
  33. 33. DOSES AND DURATION OF BLOCK Drug Conc. Total dose(mg) Dose(mg/k g) Duration of block Procaine 1-2% 400 6 30-60 min. Lidocaine 0.5-2% 300 4.5 60-120 min. Bupivacaine 0.25-0.5% 90 1.4 180-360 min. Tetracaine 0.25-0.5% 80 1.3 180-480 min. 33
  34. 34. UNDESIRED EFFECTS OF LOCAL ANESTHETICS 34
  35. 35. CENTRAL NERVOUS SYSTEM • CNS Stimulation: (More sensitive than cardiac) • Dose-related spectrum of effects and all effects are due to depression of neurons. • First an apparent CNS stimulation (convulsions most serious) • Premonitory signs include: ringing in ears, metallic taste, numbness around lips • Followed by CNS depression (death due to respiratory depression) Cocaine - Euphoria Lidocaine - Sedation even at nontoxic doses. 35
  36. 36. CARDIOVASCULAR SYSTEM • ARRHYTHMIAS: • Decrease cardiac excitability and contractility • Decreased conduction rate • Increased refractory rate (bupivicaine) • ALL can cause arrhythmias if conc. is high enough Note: cocaine is exception......it stimulates heart • HYPOTENSION: Arteriolar dilation is a result of: • Direct effect (procaine and lidocaine have most effect) • Block of postganglionic sympathetic fiber function • CNS depression • Avoid by adding vasoconstrictor to the preparation • Cocaine is exception: produces vasoconstriction. 36
  37. 37. • Hypersensitivity: • Common with ester-linked LA • Rashes, angio-edema, dermatitis and rare anaphylaxis • Sometimes typical asthmatic attack • Neurotoxicity: • LA can cause concentration-dependent nerve damage to central and peripheral NS • Mechanism(s) not clear • Permanent neurological injury is rare • May account for transient neurological symptoms. 37
  38. 38. SPECIFIC LOCAL ANESTHETICS 38
  39. 39. PROCAINE (NOVOCAINE) • First synthetic injectable local anesthetic. • Produce the greatest vasodilation of all currently used local anesthetics. • Slower clinical onset (6-10 min.) Used for • Soft tissue anesthesia for 15- 30 min. • Systemic toxicity negligible because rapidly destroyed in plasma • Max. recommended dose for peripheral nerve block 1000mg 39
  40. 40. LIDOCAINE 1:200000 conc. is safest As well as potent • The most popular contains epinephrine 1:100,000 and provides good anesthesia for healthy patients. • Lidocaine with epinephrine 1:50,000 is used for hemostasis, but because of the rebound effect noted earlier, it should be used sparingly. 40
  41. 41. Lidocaine ( Xylocaine ) • Most widely used Amide linked LA and most versatile anaesthesia. • Has variety of applications like Local, nerve block, topical. • When used locally action starts within 3 min., more profound anesthesia, has longer duration of action and greater potency. • Overdose causes muscle twitching, convulsions, cardiac arrhythmias, fall in BP, coma, respiratory arrest. • Most popular anti arrhythmic drug 41
  42. 42. Maximum Dose of Lignocaine • Without Vasoconstrictor : 4.4 mg / kg of body wt = 300 mg in a 70 kg individual = 15 ml of solution • With Vasoconstrictor : 7.2 mg / kg of body wt = 500 mg in a 70 kg individual = 25 ml of solution • For children with VC 3.2 mg/kg 42
  43. 43. MEPIVACAINE • 3% Mepivacaine without a vasoconstrictor is used as anesthetic for patients who cannot take a vasoconstrictor or for short procedures. • It is appropriate for pedodontics and for use on geriatric patients. • 2% Mepivacaine with vasoconstrictor provides pulpal anesthesia that is similar to lidocaine with epinephrine, but hemostasis is not as intense. 43
  44. 44. PRILOCAINE • The action of prilocaine plain varies with the area injected (longer with a nerve block). • Prilocaine with vasoconstrictor gives good anesthetic effect and uses a 1:200,000 concentration of epinephrine. 44
  45. 45. ARTICAINE • Articaine is a newer anesthetic typically given in a 4% solution with 1:100,000 epinephrine. • However, concern has arisen about its potential for tissue necrosis and persistent nerve parasthesia. 45
  46. 46. BUPIVACAINE • Bupivacaine is used when pulpal anesthesia is desired for longer appointments and when postoperative pain is anticipated. • Bupivacaine is not recommended for children or handicapped patients because of the increased risk of postoperative injury (chewing on a numb lip). 46
  47. 47. • Available as 0.5% solu.1:2,00,000 (vc) • Indication- Pulpal anesthesia >90- min.  Full mouth reconstruction.  Extensive oral and maxillofacial surgery, periosurgery. • Duration –Pulpal - 90- 180 min. Soft tissue- 4-12 hrs. • Contra indication- Burning sensation at site of injection, in children anticipating self trauma . 47
  48. 48. POSTPROCEDURAL PAIN CONTROL • Prescribe nonsteroidal antiinflammatory agents prior to the appointment. • Use an intermediate duration anesthetic for the procedure. • Inject bupivacaine just prior to the patient's dismissal . • Direct the patient to take oral analgesics for a certain number of days following the procedure. 48
  49. 49. LOCAL ANAESTHESIA TECHNIQUE 49
  50. 50. TOPICAL • The local anesthetic solution is applied on the mucous membrane or skin, through which it penetrates to anesthetize superficial nerve endings. e.g. - Ointments containing 5%lignocaine -Viscous solution containing lignocaine hydrochloride -Ethyl chloride sprays 50
  51. 51. EMLA = Eutectic Mixture of Local Anesthetics • Eutectic = two solid substances mixed together in equal quantities by weight form a eutectic mixture • The melting point of the mixture is lower than the melting points of the individual components • EMLA = lidocaine and prilocaine becomes an oily mixture 51
  52. 52. INFILTRATION • Small terminal nerve endings in the area of dental treatment are flooded with local anesthetic. • The treatment is done in the same place where anesthetic is deposited. 52
  53. 53. FIELD BLOCK • Local anesthetic solution is deposited near the larger terminal branches so the anesthetized area is well circumscribed. • Incision or treatment is done at an area away from the site of injection of local anesthetic. 53
  54. 54. NERVE BLOCK • Local anesthetic solution is deposited close to the main nerve trunk, usually at a distance from the site of operative intervention 54
  55. 55. SUPRA PERIOSTEAL INJECTION 55
  56. 56. POSTERIOR SUPERIOR ALVEOLAR NERVE BLOCK Nerves anaesthetized – posterior superior alveolar and branches. Areas anaesthetized – Pulps of the maxillary third, second and first molars. Buccal periodontium and bone overlying these teeth. 56
  57. 57. Indications: • When treatment involves two or more maxillary molars. • When supraperiosteal injection has proved ineffective. Contraindication: • When the risk of hemorrhage is too high. 57
  58. 58. • Procedure – • Insert the needle slowly in upward, inward and backward direction. • Upward: superiorly at 45-degree angle to the occlusal plane. • Inward: medially toward the midline at a 45-degree angle to the occlusal plane. • Backward: posteriorly at a 45-degree angle to the long axis of the second molar. 58
  59. 59. Sign and symptoms: • Subjective: none • Objective: absence of pain during therapy. Complications: • Hematoma • Mandibular anesthesia 59
  60. 60. MIDDLE SUPERIOR ALVEOLAR NERVE BLOCK Nerves anaesthetized – middle superior alveolar and terminal branches. Areas anaesthetized – Pulps of the maxillary first and second premolars, mesiobuccal root of the first molar. Buccal periodontal tissues and bone over the same teeth. 60
  61. 61. Indications – • When infraorbital nerve block fails to provide pulpal anaesthesia distal to the maxillary canine. Indicated for both maxillary premolars only Contraindication: • Infection or inflammation in the areas of injection. Sign and symptoms: • Subjective: upper lip numb • Objective: no pain during treatment 61
  62. 62. INFRAORBITAL NERVE BLOCK Nerve anaesthetized – •Anterior superior alveolar •Middle superior alveolar •Infraorbital nerve a) inferior palpebral b) Lateral nasal c) Superior labial 62
  63. 63. Indications • Involving more than two maxillary teeth and their overlying buccal tissues • Infection or inflammation • When supraperiosteal injections have been ineffective because of dense cortical bone Contraindications – • Discrete treatment areas • Hemostasis of localized area 63
  64. 64. 64
  65. 65. Sign and symptoms – Subjective – tingling and numbness of the lower eyelid, side of the nose and upper lip Objective – no pain during procedure 65
  66. 66. GREATER PALATINE NERVE BLOCK Nerves anaesthetized – Greater palatine Area anaesthetized – posterior portion of hard palate, anteriorly upto first premolar and medially to the midline 66
  67. 67. Indications – • For pain control during periodontal or oral surgical procedures involving the palatal soft and hard tissues. Contraindications – • Inflamation or infection at the injection site • Smaller area of therapy. 67
  68. 68. Sign and symptoms – • Subjective – numbness in the posterior portion of the palate • Objective – no pain during dental therapy. Complications – • Few of significance • Ischemia and necrosis of soft tissues when highly conc. vasoconstructing solution used for homeostasis over a prolonged period. • Hematoma is possible but rarely occur. 68
  69. 69. NASOPALATINE NERVE BLOCK Nerves anaesthetized – nasopalatine nerves bilaterally. Area anaesthetized – anterior portion of the hard palate from the mesial of the right first premolar to the mesial of the left first premolar. 69
  70. 70. Indications – • For pain control during periodontal or oral surgical procedures involving palatal soft and hard tissues. • For subgingival restoration and insertion of matrix bands (subgingivally). Contraindications – • Inflammation or infection at the injection site • Smaller area of treatment i.e. one or two teeth • Alternatives • Local infiltration into specific regions • Maxillary nerve block. 70
  71. 71. Techniques – • Target area – incisive foramen, beneath the incisive papilla. • Landmarks – central incisor and incisive papilla. 71
  72. 72. Signs and Symptoms – • Subjective – numbness in the anterior portion of the palate. • Objective – no pain during dental treatment. Complications – • Necrosis of soft tissue occurs when highly concentrated vasoconstriction solutions (norepinephrine). • Interdental papilla tenderness are present sometimes after few days of injection. 72
  73. 73. ANTERIOR MIDDLE SUPERIOR ALVEOLAR NERVE BLOCK Nerves anaesthetized – •Anterior superior nerve •Superior alveolar nerve, when present Sub neural dental nerve plexus of the anterior and middle superior alveolar nerves. Areas anaesthetized – •Pulpal anaesthesia of the max. Incisors, canines, and premolars. •Buccal attached gingival of the same teeth. •Attached palatal tissues from midline to free gingival margin on the associated teeth. 73
  74. 74. Indications – • Is easier performed with a CCLAD system. • When maxillary anterior teeth involves any dental procedure. • When supraperiosteal injection is failed because of dense cortical bone. Contraindications – • Patients with usually thin palatal tissues. • Procedures requiring more than 90 min. 74
  75. 75. Signs and Symptoms – Subjective • A sensation of firmness and numbness is immediately on palatal tissue. • Numbness of the teeth and associated soft tissues Objectives – • Blanching of the soft tissues of the palatal and facial attached gingival from central incisor to premolar region. • No pain during dental procedure. Complications – • Palatal ulcer at injection site after 1 to 2 days postoperative. • Density of injection site causing squirt – back of anaesthetic and bitter taste. 75
  76. 76. MAXILLARY NERVE BLOCK Nerves anaesthetized – • Maxillary division of the trigeminal nerve 76
  77. 77. Indications – • Pain control during extensive oral surgical, periodontal, or restorative procedures. • When tissue inflammation or infection precludes the use of other regional nerve blocks. Contraindications – • Inexperienced administrator • Paediatric patients • Uncooperative patients • Inflammation or infection of tissues overlying the injection site. 77
  78. 78. Procedure – • Locate the greater palatine foramen at the region of the second molar. • It mostly located at the distal aspect of the second molar. 78
  79. 79. Signs and symptoms – Subjective – • Sensation of numbness in the teeth and buccal and palatal soft tissues on the side of injection. Objectives – • No pain during dental therapy. Complications – • Hematoma develops rapidly if the maxillary artery is punctured during maxillary nerve block. 79
  80. 80. INFERIOR ALVEOLAR NERVE BLOCK Nerves anaesthetized – • Inferior alveolar, a branch of the posterior division of he mandible • Incisive • lingual 80
  81. 81. Indication – 1. Multiple mandibular teeth in one quadrant. 2. When buccal soft tissue anaesthesia is necessary. 3. When lingual soft tissue anaesthesiais necessary. Contraindication – 1. Infection or acute inflammation in the area of injection. 2. Physically or handicapped adult or child. 81
  82. 82. Sign and symptoms – Subjective – tingling or numbness of the lower lip. Objective – no pain . Complications – 1. Hematoma . 2. Trismus . 3. Facial paralysis . 82
  83. 83. BUCCINATOR / LONG BUCCAL NERVE BLOCK 83
  84. 84. MENTAL NERVE BLOCK 84
  85. 85. GOW GATES TECHNIQUE (MANDIBULAR N. BLOCK) Nerves anaesthetized – • Inferior alveolar • Mental • Incisive • Lingual • Mylohoyid • Auricotemporal • Buccal 85
  86. 86. Area anaesthetized – • Mandibular teeth to the midline • Buccal mucoperiosteum and mucous membranes on the side of injection • Anterior two thirds of the tongue and floor of the oral cavity • Lingual soft tissues and periosteum • Body of the mandible, inferior portion of the ramus 86
  87. 87. Indications – 1. multiple procedure on mandibular teeth 2. When buccal soft tissue anesthesia, from third molar to the midline 3. For lingual soft tissue anesthesia Contraindications – 1. Infection or acute inflammation in area of injection. 2. In children, physically or mentally handicapped patients 3. Patient who are unable to open their mouth wide 87
  88. 88. Target area – lateral side of the condylar neck, just below the insertion of the lateral pterygoid muscle Landmarks – Extraoral – • Lower border of tragus • Corner of the mouth 88
  89. 89. Intraoral – •Place the needle tip just below the mesiolingual cusp of the maxillary second molar •Penetrates soft tissues just distal to the maxillary second molar. 89
  90. 90. Sign and symptoms – Subjectives – tingling or numbness of the lower lip and tongue Objectives – no pain is felt during dental therapy. Complications – 1. Hematoma 2. Trismus 3. Temporary paralysis of cranial nerves III, IV AND VI. 90
  91. 91. COMPLICATIONS OF LOCAL ANESTHETICS 91
  92. 92. COMPLICATIONS – 1. LOCAL COMPLICATIONS. 2. SYSTEMIC COMPLICATIONS. 92
  93. 93. LOCAL COMPLICATIONS • Needle Breakage • Prolonged anesthesia • Facial nerve paralysis • Trismus • Soft- tissue injury • Hematoma • Pain on injection • Burning on injection • Infection • Edema • Sloughing of tissues 93
  94. 94. SYSTEMIC COMPLICATIONS Adverse Drug Reactions 1) Side effects 2) Overdose reactions 3) Local toxic effects (most common) 4) Allergic reactions 94
  95. 95. Signs and Symptoms – Toxic Reaction to Local Anesthesia •Talkativeness •Slurred speech •Dizziness •Nausea •Depression •Euphoria •Excitement •Convulsions 95
  96. 96. Overdose Reactions Clinical signs and symptoms that develop as a result of an over-administration of a drug. 96
  97. 97. Overdose Contributing Factors •Age •Weight •Sex •Presence of disease •Mental attitude 97
  98. 98. Drug Factors • Vasoactivity – All L.A currently used in dentistry have vasodilating properties. Injection into the soft tissues increases perfusion area which lead to an increases rate of drug absorption . • Dose – Larger the volume of L.A administered, greater the no. of milligram injected which result in increased circulating blood level. 98
  99. 99. • Concentration • Vascularity of the injection site • Presence of vasoconstrictors 99
  100. 100. Signs and Symptoms of Epinephrine Overdose • Fear, anxiety • Tenseness • Restlessness • Throbbing headache • Tremor • Weakness • Dizziness • Pallor • Respiratory difficulty • Palpitations 100
  101. 101. Management of Epinephrine Overdose • Terminate dental procedure • Sit patient upright in the dental chair • Reassure patient • Monitor blood pressure • Administer oxygen 101
  102. 102. Allergic Reactions to Local Anesthetic Agents •Hypersensitive state as a result of exposure to an allergen. •Re-exposure can heighten the initial reaction. 102
  103. 103. Clinical Manifestations of an Allergy • Fever • Angioedema • Urticaria • Dermatitis • Depression of blood-forming organs • Photosensitivity • Anaphylaxis 103
  104. 104. Post anaesthetic complications – Lip biting – commonly seen in children's. 104
  105. 105. Cheek biting Blanching due to vasoconstrictor 105
  106. 106. Hematoma due to local anaesthesia 106
  107. 107. Conclusion Local anaesthesia is considered as a backbone of pain control in dentistry. Research has continued in both medical and dental to seek new and better means of managing pain associated with mainly surgical treatment. 107
  108. 108. References 1. Monheim's Local Anesthesia and Pain Control in Dental Practice. 2. Handbook of local anesthesia Stanley F. Malamed , 6th edition,2004. 3. Essentials of pharmacology for dentistry,KDTriphati,1st edition,2005 4. Short textbook of anaesthesia, Ajay yadav,4th edition, 2009. 5. Millers anaesthesia, 7th edition, Ronald. D Miller, 2010. 108
  109. 109. Thank You 109

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