 Hello everyone, welcome back to another session in dentistry and more. So today's topic in oral surgery is local anesthesia. This is a huge topic, this will be dealt in 3 or 4 sessions. So today's session is about the mechanism, the repolarization, depolarization and action potential mechanism and the basic things of local anesthesia. So next session we have the theories of local anesthesia and then we have the properties, the local anesthetic solution and its classification. So all will be covered in future sessions. So today's session is about the mechanism, that is the action potential mechanism across the nerve membrane, how the polarization is happening, the resting potential and how it is getting changed and what is the role of local anesthetic in this polarization. So all this will be dealt into. So let's start learning local anesthesia. The loss of sensation in a circumscribed area of the body caused by depression of excitation in nerve endings or an inhibition of the conduction process in peripheral nerves. So it is going to act on the nerves, either on the nerve endings or the conduction process, okay. Either it depress the excitation of nerve endings or it inhibits the conduction process in peripheral nerves, that is how it is creating the anesthesia. So it is a loss of sensation without inducing loss of consciousness, there is no loss of consciousness like general anesthesia. So we have lots of method to produce this local anesthesia such as low temperature, mechanical trauma, anoxia, neurolytic agents such as alcohol or phenols and the chemical agents such as local anesthetics. So these are the other methods for producing local anesthesia. So not just local anesthetics does anesthesia. We have local low temperature, mechanical trauma, anoxia, neurolytic agents such as alcohol and phenols. So all can produce the effect of local anesthesia. So what are the properties of local anesthesia? So the properties we have instead synonym I4 non-irritating, okay, non-irritating because it should not be irritating due to use to which it is applied. Then it is related to nerve. It should not cause any permanent alteration of the nerve structure. Then the systemic effect should be very low because anyway it is going to enter in the blood circulation so it should not create any systemic toxicity. Then the time of onset should be short. Then it should be effective regardless of whether it is injected into the tissue or applied locally to mucus membranes. It should be effective and the duration of action. So it should be long enough to permit the completion of procedure that is the duration. So we need to have proper local anesthetic effect so that we can complete the surgical procedure. So it should be non-irritating, should not create any permanent damage to nerve structure. The systemic toxicity should be very low and it should be having very low or short time of onset and should be effective irrespective of if it is injecting or if we are applying it on the mucus membrane and we should have enough duration of action. And also it should have the potency sufficient to give complete anesthesia without the use of harmful concentration solutions and it should be free from producing allergic reactions and it should be free in solution and relatively undergo biotransformation in the body. It should be either sterile or capable of being sterilized by heat without deterioration. So these are the properties of local anesthesia. Now let's learn the electrophysiology of nerve conduction. So this is important part, electrophysiology. So what exactly is happening at the nerve membrane where the local anesthetic going to work? So we have a nerve membrane here, let this be the nerve membrane and this is inside the nerve membrane and this is outside the nerve membrane, this is outside, this is inside. So usually the outside the nerve membrane we have positive charges, okay so this is positively charged and inside we have usually negatively charged, we have negative charged inside. So this is our nerve membrane and there will be always a electric charge across the membrane. So that is known as membrane potential, okay membrane potential. So this membrane potential is also known as resting potential which is equal to minus 70 milliwatt that is the resting potential. So without any excitation, without any changes in the cell this will be the electric wall to which is existing between or the membrane surface. So we learned what is membrane potential. Now let's learn what is action potential, okay so action potential is nothing but when this membrane potential is going to change under stimulation or fiber excitation, okay so this is outside and this is inside, outside we have positively charged and this is negatively charged. So this minus 70 milliwatt is because of the gradient, okay so we have lots of positive charge and lots of negative charge. So the change in concentration gradient across the membrane is resulting minus 70 milliwatt. So when there is an action potential before we have all the channels or the sodium potassium channels are closed at resting potential. So when this nerve fiber is excited or stimulated what happens is the sodium channel will be opened, okay. So this is the inside area, this is the outside area. So from outside there will be influx of sodium ions. So lots of sodium ions will be entering, okay. So sodium ions will be entering into the cell membrane. So once this sodium ions enters from outside to inside this process will be takes place. This is known as depolarization, that is a polarity is going to changed. So the sodium channel closes once it enters and it reaches level the minus 70 will become plus 20 that is depolarization happened, okay. So this minus become positive because of the influx of sodium ions. So the sodium channel will be closed because it is depolarized, okay. So we have sodium channel closed. So after that what happens is the nerve membrane or the nerve tries to go back to its original position or original state that is a resting potential to maintain the equilibrium. So again one more channel will be opened that is not the sodium it is potassium, okay. So from inside there is out flex of potassium, okay until it reaches minus 70 millivolt, okay. So resting potential we have depolarization and this is known as repolarization because we revert the polarity, okay. Before it was depolarized now it is repolarized because we revert back. So that is minus 70 MP we went back to the resting potential. So once it is reached minus 70 what happens is this channel also will be closed. It is like resting potential where sodium and potassium channels are closed. So during depolarization sodium channel open and it enters it reaches plus 20 that is depolarization then potassium going outward and balancing to reach the minus 70 millivolt. So this voltage gradient along axon causing a current, okay. This causes configurational change in sodium channel in the next segment and the conduction process is happening. So this is how the electro reaction happening in nerve endings or in nerve membrane, okay. That is a depolarization and repolarization mechanism. So what exactly happening with respect to the two types of nerve membrane? So we have two types of nerve membrane one we know myelinated and the second one is unmyelinated. So it differs from myelinated and unmyelinated. So this impulse spread from one segment to another segment because a depolarized segment impulse will be spread to the next segment. So the propagated impulse travels along the nerve membrane towards the CNS, okay. The spread of impulse the rate of speed is differ in myelinated and unmyelinated. So first let's take unmyelinated nerve fibers. So unmyelinated nerve fiber it doesn't have a myelin sheath. So because of this it has high resistance cell membrane and extracellular media. It produce a rapid decrease in density of current within a short distance of depolarized segment. So it doesn't have a myelin sheath. So it will be producing a rapid decrease in density of current. So what happens is the spread of impulse is characterized as a slow forward creeping process. Slow forward creeping process it cannot propagate in a very fast manner. So the conduction rate is very slow 1.2 meter per second and it goes like this. So if we have a nerve membrane here we have this impulse. So just go like this okay. So the impulse moves forward by sequential depolarization of short adjoining membrane segments okay. But whereas on the myelinated nerve fiber. So in myelinated nerve fiber it's a different story. So the current leaps from nodes to nodes is happening not the sequential depolarization. So here the impulse goes like this from nodes to nodes. Here it was sequential depolarization. So the impulse moves forward by sequential depolarization of short adjoining membrane segments okay. But here it is impulse leaps forward from one node to another one. So the myelinated nerve fiber process the nerve impulse from nodes to nodes forward movement is known as saltatory conduction. So it is more rapid in thicker nerves because of increase in thickness of myelin sheath and increase in distance between the adjacent nodes of ran wear. So this is the nodes of ran wear. So if conduction of impulse is blocked at one node of node the local current will skip over that node and prove adequate to raise that membrane potential at next node to its firing potential and produce depolarization. So that the process will not be stopped if there is blockage at one node. So it will jump to the next one it will skip that particular node and jump to the next one. So the conduction here it was just 1.2 meter per second but here it is almost 120 meter per second almost 100 times faster in myelinated nerve fibers. And now we are going to learn the basic mechanism of local anesthesia. So so far we finished our electrophysiology of the nerve fiber how the repolarization depolarization is happening. Now the local anesthetic action. So this local anesthetic agent interferes with the excitation process. So it can be done in many ways. The first one is changing the resting potential of nerve membrane. So we know what is resting potential. So the first mechanism of this local anesthetic is changing the resting potential then changing the threshold potential. So this local anesthetic will increase the threshold potential so it will remain repolarized. So there will be less chances of depolarization. So ultimately local anesthetic is increasing the rate of repolarization. That is it is not allowing depolarization. So increasing the rate of repolarization and decreasing depolarization. So repolarization is the process happened when we apply local anesthesia because there is no depolarization or it prolongs the repolarization or decrease the depolarization. So that's all about local anesthesia. So we can say it as a part one where we discussed about the action potential, the membrane potential, the sequential depolarization, the solitary conduction and local anesthesia mechanism that is changing the resting potential, threshold potential or increasing the repolarization or decreasing the depolarization, the electrophysiology. So this is the introduction part of local anesthesia. So the next session is about various theories of local anesthesia. So we have many theories such as acetylcholine theory, calcium displacement theory, surface charge theory, membrane expansion theory, then specific receptor. So all these theories we are going to learn in next session. Okay. So I'll come back with the theories of local anesthesia in my next session. Thank you.