 Hello everyone, welcome back to another session in dentistry and more. So topic for today is trauma from occlusion in periodontology. So as we all know occlusion force is a critical factor which affects the condition and structure of the periodontia. Actually the periodontal ligament and alveolar bone require mechanical stimulation from the occlusion forces in order to remain structurally sound. So that is a essential force. But when this function is insufficient what happens is this tissues undergoes atrophy and when occlusion forces exceed the physiologic adaptive capacity of the tissues they cause damage. Such damage is referred to as trauma from occlusion. So normally the bone and periodontal ligament has a capacity to withstand a level of force. But beyond that level this force will result in injuring the tissues and the bone. So that is known as trauma from occlusion. So trauma from occlusion or TFO is also known as traumatizing occlusion, occlusion periodontal trauma, traumatogenic occlusion, periodontal traumatism or overload. So the adaptive capacity of the periodontium to occlusion forces varies in different persons and in the same person at different times and is influenced by the magnitude, direction, duration and frequency of the force. So regarding magnitude there will be change in periodontal ligament space that is widening happens and there will be increase in width of periodontal fibres and also an increase in density of alveolar bone will be seen with respect to the magnitude. Whereas the direction, the changing the direction of occlusion forces causes reorientation of stresses within the periodontium. So these fibres are arranged so that they best accommodate the occlusion forces. So compared to the vertical forces the lateral forces and torque are more likely to injure the periodontium and regarding the duration and frequency of force the constant pressure on the bone is more injurious than intermittent forces but also more frequent the application of intermittent force the more injurious is a force to periodontium. So the definition of trauma from occlusion by Karanta 11th edition when occlusion forces exceed the adaptive capacity of the tissues tissue injury results the resultant injury is termed as trauma from occlusion and many types of definitions given by various textbooks still man WHO glossary of periodontal term that is AAP 1986 sling fifth edition but this is the simplest definition that is the occlusion forces exceed adaptive capacity of the tissue which causes injury. Now types of trauma from occlusion so basically we can classify it as acute or chronic or primary or secondary trauma from occlusion. So the acute trauma from occlusion it develops from a prepped occlusion impact this is acute in nature such as biting on a hard food or restorations or prosthetic appliances that interfere with or alter the direction of occlusion forces that results in acute TFO. So clinical features it can vary from person to person tooth pain sensitivity to percation and increased tooth mobility. So it can result in shift in tooth position wearing of tooth structure correction of restoration sometimes it heals and subsides but sometimes in some persons it results in periodontal injury that is necrosis and abscess or a cementum tear happens whereas a chronic TFO which is more common and significant which happens in a slow manner over a period of time that is a gradual changes by tooth wearing, drifting movement and extrusion or by the para functional habits. Malocclusion is not necessarily a trauma from occlusion that is chronic and acute in nature whereas a primary and secondary TFO trauma from occlusion may be caused by alteration in occlusion forces or reduced capacity of the periodontium to withstand occlusion forces or both. So when trauma from occlusion is a result of alteration in occlusion forces okay alteration in occlusion forces. So occlusion force itself is altered which is known as primary trauma from occlusion but when it results from reduced ability of the tissue to resist the occlusion forces which is known as secondary okay this is primary whereas the occlusion forces is altered but in secondary what happens is the tissue is not having the normal capacity to withstand the forces it has compromised tissue structure. So that is resulting in secondary trauma from occlusion that is reduced ability of the tissue to resist the occlusion forces here the structure is normal in primary structure is normal whereas a secondary the structure is not normal it is compromised. So primary TFO which includes a tissue reaction that is a damage which is elicited around a tooth with normal height of periodontium it occurs if the trauma from occlusion is considered the primary etiological factor in periodontal destruction and occlusion results in only local alteration of teeth and para functional habits can also result in primary TFO. So common example for primary TFO is the periodontal injury happens around the teeth with previously healthy periodontium after a filling or insertion of a prosthetic replacement which creates excessive force on abutment and antagonist teeth or drifting movement or extension of teeth into space created by unreplaced missing teeth or orthodontic movement of teeth into functionally unacceptable positions. So changes produced by the primary trauma do not alter the level of connective tissue attachment and do not initiate pocket formation so there is no pocket. Until the secondary trauma from occlusion it occurs when the adaptive capacity of the tissues to withstand the occlusion forces is impaired. So the capacity of the normal periodontium is not there so it is impaired and it is happened because of bone loss which results from marginal inflammation and it is previously well tolerated occlusion forces now become traumatic because of the change in the bone pattern or periodontal structure. So how exactly this trauma causes problem to the periodontal tissues? The first thing is we need to learn about the gingival inflammation pathway to the alveolar bone. So gingival inflammation which leads to collagen, fiber, bundles, then the blood vessels, then the alveolar bone that is the pathway of gingival inflammation and interproximately through the vessels which perforates the crest of the interdental septum and directly into the periodontal ligament from there into the interdental septum. And also facially and lingually which spreads along the outer periosteal surface and penetrates into the marrow space. Ultimately it destroys the transceptile gingival fiber and once the bone is reached that is the gingival inflammation reaches the bone which spreads into marrow space and replaces the marrow with exudate. So bone resorption proceeds from within the marrow spaces. So it results in thinning of bony trabeculae and enlargement of the marrow spaces and ultimately bone destruction and reduction of bone height and fatty bone marrow replaced with fibrous marrow. So there are two concepts which was put forward the first one by Glickman. So Glickman said the pathway so the Glickman concept of inflammation there is a pathway of spread of plaque associated gingival lesion can be changed if forces of an abnormal magnitude are acting on teeth harboring sub-gingival plague. So Glickman said the force has an impact in changing the spread of inflammation that is a plaque associated gingival lesion. So it implies that the character of progressive tissue destruction of periodontium at a traumatized tooth is different from that in a non-traumatized tooth. So this trauma or this abnormal force has a significant role in spreading the lesion. So instead of an even destruction of the periodontium and alveolar bone that is the supra-bony pockets and horizontal bone loss according to Glickman that is occurs at sites with uncomplicated plaque associated lesion sites which are also exposed to abnormal occlusion force will develop ankylar-bony defect and infra-bony pocket. So normally without these forces it would have the horizontal bone loss and the normal supra-bony pockets but the presence of an abnormal occlusion force. With this plaque associated lesion will result in angular-bony defect and infra-bony pockets. So he explained in zone of irritation and zone of co-destruction with respect to this concept that is this part is zone of irritation and this is zone of destruction. So zone of irritation which includes a marginal and interdental gingiva that is a soft tissue of this zone is bordered by hard tissue that is a tooth on only on one side and is not affected by force of occlusion. So because the tooth is only on the one side this means that the gingiva inflammation cannot be induced by trauma from occlusion but is a result of irritation from microbial plaque. So the plaque associated lesion at a non-traumatized tooth propagates in the apical direction by first involving the alveolar bone and only later the periodontal ligament area and the progression of this lesion results in an E1 that is a horizontal bone destruction and the zone of co-destruction which includes the PDL, root, cementum and alveolar bone coronally which is demarcated by the transeptal and the dendo alveolar collagen fibers. The trauma from occlusion may cause a lesion here in the zone of co-destruction not in the zone of irritation. So this part the fiber bundles which separates zone of co-destruction from this irritation can be affected from two different directions that is from the inflammatory lesion maintained by the plaque of zone of irritation or from the trauma induced changes in the zone of co-destruction. So through this exposure from two different directions the fiber bundles may become dissolved and or oriented in a direction parallel to the root surface and the spread of an inflammatory lesion from the zone of irritation directly down in the periodontal ligament that is not via the intertental bone. So this alteration of normal pathway of spirit of plaque associated inflammatory lesion results in the development of angla bony defect that was a glickman concept. Whereas the werehawks concept in 1979 concept he refuted the hypothesis that trauma from occlusion played a role in the spirit of gingiva lesion into the zone of co-destruction which was highlighted by glickman he didn't accept it. He measured in addition the distance between the sub gingival plaque and the periphery of associated inflammatory cell infiltrate in the gingiva and the surface of the adjacent alveolar bone and he concluded that the angla defects and infrabony pockets occurs equally frequent in teeth with tfo and in teeth without tfo. So glickman said when there is a abnormal force it results in angla bony defects and infrabony pockets but werehawks says there is no difference in the presence of a abnormal occlusion force he says it happens both with and without the abnormal force that is the tfo has not much role in spreading the lesion or infection. So the loss of connective tissue attachment and the resorption of bone around teeth are exclusively the result of inflammatory lesion associated with sub gingival plaque there is no role for the tfo and he concluded that angla bony defects and these infrabony pockets occur when the sub gingival plaque of one tooth has reached a more apache level than the microbiota on the neighboring tooth and when the volume of the alveolar bone surrounding the roots is comparatively large. So when comparing two teeth at the same time when one happens at a more accelerated fashion there will be angla bony defect. So werehawks and glickmans concepts are entirely contradicting. So what are the stages of tissue response to increased occlusion force? So tissue response. So tissue response to increased occlusion force that is stage one is injury then stage two is repair then stage three is adaptive remodeling. So these are three changes when there is increased occlusion force happens injury repair and adaptive remodeling. So stage one injury which caused by the excessive occlusion force under the force of occlusion or the tooth rotates around a fulcrum which creates pressure and tension on opposite sides of fulcrum. So slight excessive pressure stimulates the resorption of alveolar bone with compression of PDL fibres and the excessive tension cause elongation of PDL fibres and apposition of alveolar bone. So in areas of increased pressure blood vessels are numerous and reduced in size and in increased tension they are enlarged. So when there is greater pressure there will be compression of fibres which produce hyalination and injury to fibroblasts and other connected tissue cells leads to necrosis. Then the vascular changes that is within 30 minutes there will be retardation and stasis of blood flow in 2 to 3 hours there will be blood vessels post with erythrocytes 1 to 7 days there will be disintegration of the blood vessel walls. When there is severe tension happens there will be widening of the PDL, thrombosis, hemorrhage, tearing of the PDL, ligament and resorption of alveolar bone. So the areas of periodontium most susceptible to injury from excessive occlusion forces are the furcation areas and injury to the periodontium produces a temporary depression in the mitotic activity and the rate of proliferation of fibroblasts, collagen and bone formation. So that was stage 1 now we have repair that is stage 2. So it is constantly occurring in normal periodontium and trauma from occlusion stimulates increased reparative capacity or the activity. The damaged tissues are removed and new connected tissue cell, fibre, bone, cementum are formed in an attempt to restore the injured periodontium that is a repairing part. So when bone is resolved by excessive occlusion forces the body attempts to reinforce a thin bone with new bone. This attempt to compensate for lost bone is called as buttressing bone that is a buttressing bone formation it is a compensation mechanism and that is an important feature of trauma from occlusion. So buttressing bone formation occurs within the jaw that is central buttressing on the surface it is known as peripheral buttressing. This is central or it can be peripheral. In central buttressing the endosteal cells deposit new bone which restores the bony trabeculae and reduces the size of the marrow spaces whereas peripheral buttressing occurs on the facial and lingual surfaces of the alveolar plate. So depending on its severity peripheral buttressing may produce a shelf like thickening of the alveolar margin which is referred to as lipping or a pronounced bulge in the contour of the facial and lingual bone. And finally we have the adaptive remodeling that is if the repair process cannot keep pace with the destruction the periodontium is remodeled in an effort to create a structured relationship in which the forces are no longer insurance to the tissues. This reserves in a thickened periodontal ligament which is funnel shaped at crest angular defects in the bone with no pocket formation and there will be increased mobility and increased vascularization. So what are the symptoms of TFO? The first symptom is pain that is periodontal pain. In severe trauma from occlusion there is localized sharp pain or so on as to the tooth. In chronic nature the pain will be little. Second can be pulpel pain. It is seen as sensitivity of teeth especially to cold. Then there will be food impaction. Food impaction the plencher cusp effect of occlusion interference may produce a functional opening of contact between the teeth which leads to food impaction. Then we can also have our TMG pain and there will be signs that is increased mobility. This is a hallmark of trauma from occlusion can be easily measured by blend ends of a two instrument which are placed approximately at buccal and lingual heights of contour then force applied to in the buccal and lingual direction or we can also use the millius mobility index mobility 1, 2 and 3. Then there will be migration of teeth the movement of teeth migration of teeth because of the loss of inter proximal contact. Then there will be a typical pattern of occlusal wear occlusal wear will be there occlusal wear with a typical pattern that is a tooth where which appears to be greater than one might expect in a patient of that age and which cannot be attributed to any special diet or deficiency in tooth mineralization that is a atypical pattern and there will be also changes in the percation sound percation sound. The sound will be gives a dull sound whereas a normal teeth gives a sharp sound so there will be a dull sound on vocation. This difference could be due to the altered width and consistency of pyridontal membrane and partial resorption of lamina dura and also another sign is hyper tonicity of masticatory muscle hyper tonicity of masticatory muscle. So that is bruxism and hyper tonicity makes the predominance susceptible to trauma. So these are symptoms and sign. Now let's learn what is a Fremontes test. Fremontes test is the test to detect TFO. It is the measurement of vibratory pattern of the teeth when the teeth are placed in contacting position and movements. To measure the Fremontes a dampened index finger as you see the picture here finger is placed along the buccal and labial surface of the maxillary teeth and patient is asked to tap the teeth together in the maximum inter cuspal position and then grind systematically in the lateral protrusive and lateral protrusive contacting movements and position. So the teeth that are displaced by the patient in these jaw positions are then identified. That is a Fremontes test. So mantibular teeth assessed in edge to edge occlusion. So we were talking about maxillary, now the mantibular teeth. So the following classification that is a class 1 Fremontes, class 2 and class 3. Class 1 is mild vibration, class 2 is easily palpable vibration and class 3 is movement visible with naked eye. The Fremontes differs from mobility in that Fremontes is tooth displacement created by patients on occlusion force and it is a guide to the ability of the patient to displace and traumatize the teeth. So in posterior teeth the trauma from occlusion can be detected with the help of occlusion, registration strip or using an articulating paper. So the pressure points can be detected. So the radiographic change there will be a vertical bond loss rather than the horizontal destruction and root resorption will be there, widening of the PDL space at the crest and there will be funnel shaped appearance and angular defects. Now how do we plan the treatment? So the decision to treat the patient occlusion either by adjusting the occlusion surfaces or by the use of occlusion appliances will be influenced by the patient's symptoms because we need to go with the symptoms. Symptoms can be sensitivity, pain on chewing, mobility, presence of wave facets, extent of verodontal destruction or patient's ability to adequately function. So all these factors we should take into consideration and if the patient is symptomatic and does not have significant verodontal disease, treatment of occlusion may not be indicated even if significant occlusion discrepancies are present. If the patient has occlusion discrepancies in addition to parodontal disease occlusion treatment can be considered. So the decision to perform occlusion therapy should be made after reevaluation of the patient's response to non-surgical treatment such as oral hygiene instructions and root planning. Okay, oral hygiene instructions and root planning should be first planned. So mobility and parameters will often be greatly reduced by these procedures and the need for occlusion treatment may be diminished. So an exception to this treatment timing would be when the patient has difficulty chewing or tooth pain when chewing that appears directly related to occlusion trauma. So the occlusion treatment consists of basically two basic approaches that is the use of a bite appliances that is bite guard. First we should go for oral hygiene and root planning. So occlusion treatment is bite guard then adjusting the occlusion by altering the occlusion relationship between the teeth. So bite appliances we can give, it fits over the patient teeth and creates an artificial occlusion surfaces for the opposing condition to contact or occlusion adjustment we can do which is known as coronoplasty or selective grinding. So selective grinding or coronoplasty is a procedure by which the occlusion surfaces of the teeth are precisely altered to improve the overall contact pattern. The tooth structure is selectively removed until the reshaped teeth contact in such a manner as to fulfill the treatment goals. So that was all about trauma from occlusion and important topic in Paradondology. There will be lots of questions, short notes, short essays, need to write the classification, concepts, your treatment and the Fremont test test and the stages that is injury repair and the remodeling all those things will be asked. So occlusion trauma is an important risk factor which can increase the rate of progression of an existing paranormal disease. So there is a place for occlusion therapy in the management of paranormal disease especially when related to the patient's comfort and function and occlusion therapy is not a substitute for conventional methods of resolving plaque induced inflammation. So hope you understood the topic trauma from occlusion. So I will come up with another topic in Paradondology. Thank you.