PHYSIOLOGY OF NERVE CONDUCTION

 Simple & predictable (GA vs LA)  Corner stone in dentistry  Normal people (not dentists) usually tend to judge dentists according to the local anesthesia.  .LOCAL ANASTHESIA Has been introduced to the clinical world for more than 100 years.

PAIN CONTROL 1. Interrupt pathway that carry information of the stimulus from periphery CNS   Stimulus = instrumentation during dental tt By definition. Removing the stimulus 2. can’t be stopped  Achived by application of LA to the sensory nv supplying the area of stimulation .

A. LOCAL NERVE CONDUCTION Physiology & pathophysiology of pain .

Motor (CNS  periphery/skeletal muscle) 2. Sensory (Stimulus at periphery  CNS) 3. Proprioception (the reception of stimuli produced within the organism) .CNS 1.

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effectively jumping from one node to another (saltatory conduction)  .NERVE ANATOMY  Myelin sheath   Insulates nerve Prevents current flow Nerve (axon)  Nodes of Ranvier (myelin sheath gap/esposed nerve)  Occurs at regular intervals between segments of myelin sheath along a nv axon  Unmyelinated  Allow rapid passage of excitatory impulse along the nerve.

 Propagation of an A-P  Passage of information as an impulse  Synapse Junction between one nerve & another  Coordinate nervous activity  Ensure unidirectional flow of A-P  Saltatory conduction: the propagation of action potentials along myelinated axons from one node of Ranvier to the next node. . increasing the conduction velocity of action potentials.CONT.

Basis of A-P: Balance of ions  Resting membrane potential (-70 mV) .

ELECTROGENIC PUMP Results in a distribution of ions that produces a membrane potentioal = 70mV .

DIAMETERS OF NERVE FIBERS .1.

2. ION CHANNEL Voltage gated Chemical gated .

K-gated is open Ionic imbalances/change Inflammation  K & H release  acidic Membrane potential alteration . short-lived 2. Rest (-70mV): Na/K ATPase Change reaches -55 mV (threshold)  Na-gated channel permits Na influx Reaches +30mV K-gated channel open  permits K outflow a. Stimulus Eg: trauma  inflammation Minimal change Na-K ATPase restore to resting value Can’t reach +60mV (eq potential of Na): 1.3. PASSAGE OF AN ACTION-POTENTIAL b. reversed electrcal gradient 3.

B. MOLECULAR BASIS OF PAIN .

lysosomal Nerve hyperexcitability activation .lysis Direct / cells indirect Potent vasoactive of . Thermal 3. Chemical Infection Histamine & serotonin (5-hydroxyIonic imbalances (K & H) Tissue Cytokines (IL & GF) Cytokines (IL.Lowering threshold inflammation Substance P PG & metabolites .[↑] AA metabolites Localized pain @ pain) Immobility . mild irritating . Physical 2.PGE: pain & inflammation . osteoblast Mast cell Histamine & seratonin K: .lymphocyte.NTM .Vasodilatation & amine . GF) damage tryptamine) [↑]  pain P Substance PG & related metabolites .PAIN SENSATION AT CELLULAR LEVEL Trauma 1.LKB4 ~ PG (WHY??) Ionic imbalances (H & K) Stimulate PG production  pruritus (itch. MO.

Stimulate PG production Ionic imbalances (K & H) . GF) .LKB4 ~ PG .[↑]  pain .Direct / indirect .Nerve hyperexcitability .PGE: pain & inflammation .AA metabolites .[↑]  pruritus (itch.lysis of cells (WHY??) . MO.MOLECULES & IONS IN INFLAMMATORY PROCESS Cytokines (IL. mild irritating pain @ pain) Substance P .K: . osteoblast .Mast cell .Potent vasoactive amine .Lowering threshold Histamine & serotonin (5-hydroxy-tryptamine) .lymphocyte.NTM .Vasodilatation & lysosomal activation PG & related metabolites .

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