Transcribed by Leslie Afable Basic Tissues Lecture 16 Gingivitis by Dr.

Robert Davidson

January 30, 2014

Slide 1 Clinical Case Presentation: Chronic Gingivitis Dr. Harvey Wishe This is Dr. Robert Davidson, hes a member of the perio department and we are going to talk about gingivitis. Dr. Robert Davidson Good morning, today I am going to talk to you about gingivitis. Slide 2 Today Dr. Robert Davidson Gingivitis is by definition, an inflammation, an inflammatory process in the GINGIVAL tissues. Ok, youve had some dental anatomy already Im sure. Soft tissue, hard tissue, ok. Uh.. And what I will do is review the clinical features of gingivitis if its something you are not familiar with. And then look at a link/the connection between a couple of aspects of cell physiology and what manifests clinically when we see a patient with gingivitis. A very typical clinical manifestation. If you have any questions, dont hesitate, raise your hand. I think I have material that will fill up 45-46 minutes so theres little time in the lecture to answer questions. Slide 3 What is Gingivitis?.. Dr. Robert Davidson Uh, do you all have the printout or not? Because its been posted. Ok so what is gingivitis? Tell me what gingivitis is, a definition. Gingivitis is an inflammatory process in the gingival tissues. What causes gingivitis? Any idea? What causes infection? Bacteria. Slide 4 What is Gingivitis? Dr. Robert Davidson Clinically, what does gingivitis look like? Probably all of us have had some manifestation of gingivitis during our lifetimes and it ranges from very mild to almost imperceptibly detectable clinically, to much more severe. I will show you some pictures of typical gingivitis. But again, the definition is inflammation of the soft tissue surrounding the teeth and specifically that aspect of the soft tissue referred to as GINGIVAL TISSUE -- its typically KERATINIZED and it is characteristic of what we see clinically. Slide 5 Mild Gingivitis Dr. Robert Davidson So this is what mild gingivitis looks like. Does anything look a little abnormal? Anything a little abnormal or very abnormal? Can you see anything here? Any changes in what you would expect to see in a healthy individual? Anyone? Can you point me to something that looks abnormal? Does this look normal to you? This is probably fairly normal. This is what is abnormal in this picture. There is a little bit of puffiness/swelling and theres also what is referred to as ERYTHEMA -- a change in the color of whats typically seen in normal healthy tissue. Theres a change towards REDNESS. OK. Slide 6 Severe Gingivitis Dr. Robert Davidson This is much more severe gingivitis. It is the same phenomenon. In this case, it is actually associated with a reaction to a drug, and I 1

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will talk about that in a little bit more detail in a moment. But that drug induces enlargement of normal gingival tissue and predisposes patients to a form of gingivitis, more severe inflammatory gingivitis. This can also occur in patients that are NOT taking medication. Slide 7 Risk Assessment, Diagnosis and Prognosis Dr. Robert Davidson But before I start talking about gingivitis, I want to talk about risk assessment, diagnosis, and prognosis because it turns out that.. Slide 8 Patients Are Not Equally Susceptible to Periodontitis.. Dr. Robert Davidson .. the same bacteria which gingivitis in one patient has no effect on another patient. Whats the difference between these 2 patients? If the bugs are the same, and theres disease in one case, inflammatory periodontal disease in the form of gingivitis, and another case we cant detect any changes clinically, whats different here? So when you think about the immune response, we have to ID the host as the variable. So in one case, the host is susceptible and in the other case the host is not susceptible. Slide 9 Not Everyone Appears Equally Susceptible to Periodontal Diseases Dr. Robert Davidson Because everyones susceptibility is NOT the same. Ok. Slide 10 For Many Chronic Inflammatory Diseases There Exist Risk Factors.. Dr. Robert Davidson And here you see, for many chronic inflammatory diseases, there is something that is called RISK FACTORS. Is this something you are familiar with? Has anyone talked to you about that before? OK. So its intuitive, they dont directly cause disease. A risk factor is NOT something that is etiological/causative but it changes the manifestation of the disease. So a patient who is more susceptible to a disease may end up with a more severe condition than a patient who is not as susceptible. Can anyone tell me what a risk factor for gingivitis might be? Anything, just pick a number. (someone says: diabetes) diabetes? Not exactly, but a little bit. Umm uhh it.. What causes gingivitis? Bacteria/plaque. So PLAQUE IS A RISK FACTOR FOR GINGIVITIS. And we will talk about that in a minute in more detail. Slide 11 For Periodontal Disease, While Bacteria are Still Required to.. Dr. Robert Davidson So for periodontal diseases, including gingival diseases, again while bacteria still are required to initiate the patients response, certain risk factors again modulate or amplify that response which manifests in clinical disease. Slide 12 Because Risk Factors Put Certain Patients at Higher Risk.. Dr. Robert Davidson And here you see because they put patients at a higher risk for increased severity, they should be an integral part of our diagnostic workup. When you think about it, patients present with a profile, a specific profile. The best doctors are the ones that can predict the future. When you go to a doctor youre really not as much interested in whats wrong with you on that day but whats going to happen to you a week from now, a year from now, 10 years from now. In other words, the risk for future disease. And the best doctors are the doctors that can predict the future. 2

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The best way to predict the future is to understand the risk factors that are inherent in the patient that you are treating and then that way you can in a way, anticipate the risk for future disease and, ideally, prevent it from happening.. Take measures to prevent those risk factors from manifesting. Does that make sense to everyone? Its as much an issue for gingival disease as it is for caries, for cardiac disease, for lung disease or anything we see clinically. Slide 13 Untitled Slide

Dr. Robert Davidson This is a diagram that shows the relationships between the risk factors . There are genetic modifiers that are inherent. Can we change these? Typically NOT. There are also environmental modifiers. What is one really important environmental/acquired risk factor that can cause disease or modulate the manifestation of disease? So people who smoke typically are sicker than people who dont smoke. People with uncontrolled or poorly controlled diabetes are at higher risk for infection than people who have well controlled diabetes. So those are inherent/acquired risk factors. There are genetic risk factors for certain diseases that we really cant alter. But basically we ID a causative agent, we understand the risk factors that are acting on those or modulating the relationship between the causative agent and the host and we end up with a degree of severity of disease and also a type and that really represents a diagnosis. We really cant diagnose properly without understanding the risks involved. Slide 15 Untitled Slide

Dr. Robert Davidson It turns out that not only does risk affect the diagnosis but it also affects the outcome of therapy. So if were treating a patient who is a heavy smoker, do you think that that patient will respond as well as a patient who doesnt

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smoke, to the same therapy? Of course NOT. Whats the major target of smoking? What system do you think is affected most profoundly by smoking? Is it a local effect or systemic effect first? SYSTEMIC. So when you smoke theres local effects like VASOCONSTRICTION, of course, but theres also a profound effect on the IMMUNE SYSTEM and thats basically what puts people at risk who smoke. Its in the same way that poorly controlled diabetes puts people at risk. The affect is basically on the immune system and the immune system is what really represents the major response to infection in the host. Anything that compromises that puts the host at a more susceptible state. Slide 16 Risk Factors for Gingivitis Dr. Robert Davidson Ok so here are the risk factors for gingivitis. Bacterial plaque are the microbes/bacteria/bugs that we have identified that cause BOTH gingivitis & periodontitis, but Im not going to talk about that specifically today. Local factors, what do you think is a local factor is? What is a local factor? What am I talking about? You have.. Well I will show you in a minute, I dont want to spend too much time. Certain drugs put patients at higher risk for gingival disease. Each of these drugs, the Ca channel blocking agents which are treating hypertension among the most widely prescribed drugs on earth, anticonvulsants that treat epilepsy and also immunosuppressant drugs that permit solid organ transplants by suppressing the immune response and preventing rejection. In each case these drugs induce in some patients, gingival enlargement, the overgrowth of gingiva which predisposes patients to bacteria, no sorry, to INFLAMMATION. Finally, there are certain endocrine related conditions like pregnancy or changes in hormonal cycle that predispose patients again to gingivitis. Slide 17 Endocrine-related Risk for Gingivitis Dr. Robert Davidson You can see here these are endocrine related risks for gingivitis during pregnancy, mild, and severe. There are changes that take place. The more bacteria, the worse the condition. These patients, in the sense that the hormonal changes are NOT causative but they are RISK FACTORS that predispose patients for these conditions. And puberty, you can see in this graph that the incidence of gingivitis spikes at around AGE 13 and then as adults, everyone is more or less susceptible. Slide 18 Risk Factor: Bacterial Plaque Dr. Robert Davidson So heres a case. The risk factor in this case is simply bacterial plaque. A patient who fails to maintain proper adequate plaque control ends up with gingivitis. Its a causative agent AND a risk factor. Slide 19 Risk Factors: Bacterial Plaque, Local Factors Dr. Robert Davidson Here is a case where there is bacterial plaque associated with a local factor. This is a periodontal probe. Is that something you are familiar with? Whats the local factor here? What is a local factor? It could be one of a number of factors, it could be a poorly contoured restoration that traps bacteria. It could be an OPEN MARGIN between a crown and a tooth. It could be RECURRENT CARIES, 4

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which in effect, is a risk factor for inflammatory gingival disease. But local factors are not really biological but they are factors which place patients at higher risks for a condition. Slide 20 Risk Factors: Bacterial Plaque, Antihypertensive Dr. Robert Davidson Here you have an anti-hypertensive, this is that patient that I showed you before, along with bacterial plaque. Slide 21 Patient: 25 Year-Old Female Dr. Robert Davidson So here is a patient, 25 year old who comes in with a chief complaint of bleeding gums. You are going to meet these patients every day of the week. Slide 22 History of Present Illness Dr. Robert Davidson Its gone on for a long time, 5 years. Its all over, a generalized condition. It happens every day after brushing or eating and there really arent any symptoms and she has had no treatment so far. Slide 23 Medical History Dr. Robert Davidson She is in good health, shes had an uncomplicated pregnancy and she really is not taking any medication other than multivitamins and oral contraceptives. Slide 24 Dental History Dr. Robert Davidson She had an exam a few years ago, well now its 10 years ago. Third molars were extracted, some routine fillings and occasional cleanings periodontally. So some RED FLAGS should go up right away. What is one red flag for this person? When she says Ive had OCCASIONAL cleanings. Is that as good as routine/periodic? This is the kind of patient that probably comes to the dentist when she perceives a problem. someone who is NOT proactive, sort of speak. If you think about it, its a behavioral issue. Its a risk factor for disease, people who really dont take care of themselves it represents a risk factor. Can that be changed? Sure. Slide 25 Clinical Status Dr. Robert Davidson Its something to think about. So clinical status, what is wrong with this picture? I think there are some things, surface texture, shape, color, size of the gingiva. All of these things we can ID as something OTHER than what we would consider to be normal clinical gingival tissue. Slide 26 Are There Clinical Signs of Periodontal Disease? Dr. Robert Davidson First step is are there signs of clinical periodontal disease? Were really talking about GINGIVITIS here and not periodontitis. I will explain that in a minute. Slide 27 Clinical Signs of Periodontal Diseases 5

Transcribed by Leslie Afable

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Dr. Robert Davidson These are the FOUR CLINICAL SIGNS OF GINGIVITIS!!! Edema is swelling. Erythema is redness. Bleeding, typically in response to a mechanical insult like a probe, or air, or a gauze pad rubbing against the gingiva you induce bleeding and ulceration. Were NOT talking about peritonitis here when I talk about attachment loss. Is that something that you understand yet? Do you know what attachment loss is? Anyone? Do you all know what attachment loss is? I will explain it in a minute. I dont want to review things. Slide 28 Edema, Erythema Dr. Robert Davidson So here edema is a change in shape, swelling. Erythema is a change in color. Slide 29 Bleeding Dr. Robert Davidson Here is bleeding on probing or in response to any other mechanical challenge like air, syringe, pressure, gauze pad. Anything that disturbs the gingival surface that induces bleeding is a CARDINAL SIGN OF INFLAMMATION. Its a direct reflection of the patients clinical status with respect to inflammatory gingival disease. The absence of bleeding on probing in patients who have no other risk factors, is a sign of gingival stability/health and the presence of gingival bleeding on probing, is a sign of inflammation. Whats one risk factor that might alter that response? A minute ago I talked about what smoking does locally. What does it do? It constricts the vessels peripherally so if you have a heavy smoker you will have a blood supply that is not nearly as animated or vigorous as a person who doesnt smoke. So you probe a smoker, and very often there is NO bleeding even though there is inflammation. Its just that the inflammation doesnt manifest in a normal way. Slide 30 Ulceration Dr. Robert Davidson Anyone have a question about that? I will talk about that or someone will talk about that when you meet pathogenesis next year. So here is ulceration and ulceration really specifically to the GINGIVAL CREVICE, I should identify. This is cross section of the periodontium. This is the enamel, the CEJ, cementum, dentin, this is the keratinized gingiva. The little blue dots represent the INFLAMMATORY RESPONSE and its an INFILTRATE. This is the epithelial attachment. Theres a little bit of a defect up here as a result of ulceration of the interior of the sulcus here. This is bone, this part and these are collagen fibers, fibroblasts, and a blood vessels. So who are the players? Theres bacteria, infiltrate, and whats called a gingival pocket. So when you put a perio probe in here it will go a little bit deeper than in a site that is healthy. Ok so thats it. Slide 31 Clinical Signs of Periodontal Diseases Dr. Robert Davidson So clinical signs of periodontal diseases. We talked about gingivitis, I will spend a moment talking about periodontitis and the distinction between the 2 which is simply ATTACHMENT LOSS!! Slide 32 Loss of Epithelial Attachment 6

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Dr. Robert Davidson Here is a patient whos gingiva looks healthy. This is a periodontal probe that is 10 mm into the sulcus, thats a periodontal pocket. That represents ATTACHMENT LOSS. Slide 33 Healthy Gingiva Dr. Robert Davidson You can see here , Im just going to go over the anatomy very quickly. Theres the tooth. Theres the gingival sulcus and the free gingival margin. This is the keratinized tissue and this is the mucosa in healthy gingiva. Slide 34 Loss of Attachment Dr. Robert Davidson Here is what loss of attachment looks like. So heres the probe in a healthy site. Ok now heres the probe in a site with perio disease on right. The difference is the level of the attachment of the epithelium. Here is the epithelial attachment, and here is the epithelial detachment right here. And its actually damaged by this infiltrate and undergoing sort an inflammatory response. But loss of attachment distinguishes gingivitis from periodontitis. This is in fact, and just as an aside, this is REVERSIBLE, inflammatory gingival disease. This is largely irreversible, you lose attachment and its GONE. Whats the structure between the connective tissue here, the bone, and the tooth? Whats this called? PERIODONTAL LIGAMENT. Thats the attachment, the periodontal ligament, and thats what gets damaged and thats when we talk about loss of attachment were talking about the loss of the attachment between the tooth and the periodontal ligament. If thats lost, its gone forever. If theres anything at all that periodontal research would like to do, its to figure out a way to reattach the PDL, periodontal ligament to the tooth. So far, it has not been successful. Slide 35 What Structural Components are Affected? Dr. Robert Davidson So what structural components are affected? Theres collagen, vascular cells, immune system cells and resident fibroblasts. Thats basically what we see in health. Slide 36 Whats the Sequence? Dr. Robert Davidson Whats the sequence? Theres a collection of plaque. So someone doesnt clean their teeth, plaque accumulates. You can see it visibly/clinically and you can DISCLOSE it. Have you done disclosing? You will get to that. Theres a chemical like a wash we use that is bright purple and attaches to plaque and shows you where the visible plaque is; if you cant see it clinically, you disclose it using disclosing solution. So then theres is MIGRATION of immune system cells, the first wave is typically NEUTROPHILS. As a result of this infiltrate theres damage done to collagen. Then fibroblast damage and finally changes in the vascular system. Thats what well concentrate on for the next 35 minutes or so. If you can think ahead, if the vascular system, the microvascular begins to change, what changes do you think will take place? Are the vessels going to constrict during inflammation or enlarge? ENLARGE. That means there will be more blood flow so you can start to think of the 2 clinical signs that I talked about before, EDEMA and ERYTHEMA. Thats where it comes from. The idea today to give you a little sense of 7

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the physiology that underlies the clinical manifestation of probably the most common oral disease on earth. More common than caries, I think is the gingivitis Slide 37 Clinical Signs of Periodontal Diseases Dr. Robert Davidson So here we get edema, erythema, bleeding and ulceration. I will just go over that. Slide 39 Edema & Erythema Dr. Robert Davidson We will talk about again, where edema and erythema come from. Ok youve had some anatomy, right? The trigeminal nerve? Am I correct? Ok, so in inflammation, theres release of CGRP, calcitonin gene-related peptide, and that induces smooth muscles to activate adenylate cyclase. Ok. Slide 40 -- .. and CGRP-induced Activation Dr. Robert Davidson And CGRP-induced activation of adenylate cyclase leads to an increase in cAMP. At the expense of what? ATP. Slide 41 How Does This Happen? Dr. Robert Davidson Ok so why does this happen? Why is it important? Slide 42 Untitled

Dr. Robert Davidson Heres the sequence. The CGRP binds to the Gs receptor complex, here, and that liberates the Gs moiety right here and that induces GTP to go to GDP and then that activates ADENYLATE CYCLASE which changes ATP to cAMP and basically the end result is a reduction intracellularly of ATP. This is fairly typical of basically ALL CELLS. Slide 43 Smooth Muscle Cell at Rest Dr. Robert Davidson So in general, smooth muscle cells at rest, and this is now physiology. There is a lot of K in the cell and Na outside the cell. Very little Na inside and very little K outside. At resting levels, theres a very relatively high conc. of ATP which induces a change potential gradient between the inside and the outside of the cell. Is this familiar at all to anyone? Ok ok, so this is basic cell physiology. Slide 44 CGRP-Induced Potassium Current

Transcribed by Leslie Afable

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Dr. Robert Davidson When CGRP, which during inflammation there is CGRP in the system, with HIGH intracellular ATP. So in HIGH intracellular ATP, there is a LOW AMPLITUDE K+ current that is essentially AMBIENT. Here you can see the scale is 20 pico amps. This is 20. This represents a K-current. This is where the CGRP is introduced into the system. This is under HOMEOSTATIC conditions. I will show you that now. Slide 45 Smooth Muscle Cell At Rest Dr. Robert Davidson Under homeostatic conditions, there is still a lot of K+ inside, very little K+ outside, a lot of Na outside and a lot of ATP and a very low amplitude K current that is leaving the cell. Theres an ongoing K+ leaving the cell and its compensated by Na coming in -- theres an exchange and theres a lot of different mechanisms involved. It basically keeps the inside of the cell with respect to the outside, at about essentially a 0 mV gradient ,there is EQUILIBRIUM. This is a resting cell!. Ok so then what happens? Slide 46 CGRP-Induced Potassium Current Dr. Robert Davidson At LOW ATP, and remember there is LESS ATP INSIDE THE CELL because CGRP is induced, there is a reduction in ATP because cAMP has gone up. The same CGRP induces a very large K+ current. So here is very low ATP, a big K current. Here its 40 pico amps instead of 20 and there is a very large K+ current. Slide 47 Smooth Muscle Cell Dr. Robert Davidson And theres a very large K current which is that big arrow in green. So theres little ATP, big K current going out, so what happens to the inside of the cell? It gets more positive or negative? Negative. I dont know if you remember or if you know that the more negative the inside of a cell is, the less excitable it is. In effect, it relaxes. If a cell is a muscle cell around a blood vessel, if the muscle cell relaxes the blood vessel gets BIGGER. Thats one of the reasons why there is EDEMA. Slide 48 Untitled

Dr. Robert Davidson Here is very simply, this is an experiment, in-vitro experiment measuring the POTENTIAL electrophysiologically inside a cell. Here it is the difference between inside and outside is near 0, they then introduce CGRP into the bath and almost immediately there is a 10mV shift towards the NEGATIVE of the inside of the cell. So this is a cell that is less excitable and its not contracting as vigorously as a cell at rest. So it dilates and gets a little bigger. 9

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Slide 49 CGRP-Gated K Channels Dr. Robert Davidson This is another way that CGRP induces negative potential inside a cell. Its simply a CGRP activated K channel, the CGRP comes along and opens this ion channel. Anyone not know what an ion channel is? Ok, opens an ion channel and because theres a lot of K inside the cell and very little outside the cell, the K rushes OUT and makes the inside of the cell more NEGATIVE. So this is a direct effect of CGRP. It doesnt have to do it all with ATP, it doesnt have to do it all with the stimulatory moiety but basically its a direct effect that induces a decrease in the potential making it more negative which is associated with closing K channels, so K goes down and the physiology of muscle cells is such that there is going to be a VASODILATION. This in a sense, amplifies the effect related to ATP reduction. Its kind of a double whammy of CGRP. CGRP again is a NEUROTRANSMITTER that is very typically associated with INFLAMMATION. Its released by nerve endings and has a very sort of widespread effect on many different structures. But specifically on smooth muscle, it relaxes smooth muscle. By the same token, in the absence of CGRP, channels are NOT open and there is more and more positive charge INSIDE the cell as these charges build up and the cell becomes more excitable. In other words it begins to CONSTRICT if its a muscle cell or its more predisposed to constriction if its a muscle cell which reduces the lumen which reduces the blood flow and there wont be edema or erythema. Slide 50 Untitled

Dr. Robert Davidson So here are the 2 ways this works. CGRP increases cAMP, ATP goes down and K current increases. Here is CGRP opening K channels and the K current increases. Membrane hyper-polarization meaning it is more negative with respect to the outside, its HYPERPOLARIZED. When a cell, when a muscle cell contracts, its the result of DEPOLARIZATION of the cell. Positive charges RUSH INTO the cell and its depolarized and becomes LESS polarized. Our country is polarized, there are RED states and BLUE states so when you get depolarization its like PURPLE , you know it depolarizes. Actually it goes towards blue if you want to think about it in those terms. Umm, decrease of smooth muscle excitability and vasodilation. Anyone have any questions about this? Im not sure if this is something you are familiar with physiologically but I hope I explained it in a logical way.

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Transcribed by Leslie Afable

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Slide 51 Within 24 Hours: Dr. Robert Davidson Within 1-2 days you will see the beginnings of in some patients, the clinical manifestation of gingivitis. These are tissues that are inflamed among many cytokines and molecules that are released during inflammation is CGRP which has a myriad of effects. I just explained 2 specific effects of CGRP that could explain, in part, the manifestation of erythema and edema. Slide 52 Are There Additional Effects of ATP Depletion? Dr. Robert Davidson Are there any other effects of ATP depletion? Slides 53 -- Untitled

Dr. Robert Davidson So heres healthy gingiva again and here is diseased gingiva. There is an incipient gingival pocket, the beginning of and this is terminology associated with periodontal disease. The formation, and I will go backwards one slide (Note -- the 2 slides he is referring to are superimposed on each other forming 1 single slide in our version of the lecture). Were looking here at a SULCUS, there is always a little bit of plaque and always 1-2 immune cells floating around. But this is healthy gingiva, the epithelial attachment basically allows the probe to go about 1-2 mm below the free gingival margin. That is fundamentally health. In inflammatory disease, you get the beginning of the breakdown of the epithelial attachment, it doesnt go away but its damaged. So the probe instead of 1 mm, it can sink in 2-3 mm depending on the patient. Thats called a GINGIVAL POCKET. an incipient pocket. The PMNs neutrophils go into junctional epithelium. The lymphocytes into sub-epithelial tissue. There are big changes in FIBROBLASTS and as the fibroblasts change, there is a loss of collagen. This explains what happens during gingivitis. What is one reason you might see collagen depletion during inflammation as the result of release of certain cytokines? What are some of the cytokines that may relate to collagen breakdown? (Student answers, cannot hear). Exactly, COLLAGINASE . So collagenase is one of the key factors that are released during inflammation and directly effects the stability and integrity of the resident collagen. But Im going to talk about something that is sort of opposite to that. Slide 54 Cytopathic Changes in Fibroblasts Dr. Robert Davidson Um you can see cytoplasmic changes in fibroblasts leads to loss of collagen. The fibroblasts themselves, can actually produce, during inflammation, can produce collagenases along with many other cells. Most immune system cells that are stimulated release some sort of enzyme that can affect collagen.

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Slide 55 Collagen Production Decreases Dr. Robert Davidson Here you get collagen production decrease. In fact, the fibroblast number goes DOWN because theyre damaged so theres less synthesis of collagen by cells that are just no longer there. The collagen synthesis of the cells that are still alive DIMINISHES. And what I just mentioned a moment ago, collagenase activity increases. Thats during inflammation and these are BAD EFFECTS, they are not good effects, they disrupt the tissue. When you think of the 3rd cardinal sign, of gingivitis, do you remember what it is? There is erythema, edema and one other sign. BLEEDING. So what maintains the integrity of tissue, blood, collagen? As collagen begins to break down, tissue begins to get FRIABLE, it weakens and you stick a probe in it and you can induce bleeding. So here you have, in a way, an explanation in part of some of the clinical signs that we see during inflammation. Slide 56 Untitled

Dr. Robert Davidson On the other hand, If ATP increases, you get more collagen so you can see how a reduction in ATP very indirectly can ultimately increase or amplify the effect of inflammation in general. Along with the direct and indirect effects on collagen of fibroblast activity, there is also a sort of subtle effect on lowering ATP and ultimately effecting collagen synthesis. Does that make sense? I hope I make sense. Slide 57 What Other Factors In This Patients History Might.. Dr. Robert Davidson This is I think the last slide, so Im almost right on the money here. What are the other factors in the patients history that might explain the gingivitis? I mentioned it in passing when we started. Slide 58 Risk Factors for Gingival Diseases Dr. Robert Davidson So the patient risk factors, remember these are the risk factors for gingival disease. Theres plaque and certain endocrine related conditions. Slide 59 Medical History Dr. Robert Davidson This patient to begin with was probably not the greatest patient on earth in terms of what we call compliance. Anyone, what do I mean by compliance? Someone who comes when its a good idea for them to come to get checked. If they come every 3 months or 6 months, depending on the... what would be determinant on how often you should see a patient? This is the beginning of understanding the importance of risk assessments. So you have office full of patient 12

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and you have a staff that is overburden, does every patient have to come every 6 months? Maybe not. Maybe some should come 1x a year and what determines that cycle? How susceptible they are or how at risk are they for disease. Then there are other patients you probably see every 2 months because you perceive a high risk for ongoing disease and you want to make sure youre there to either prevent or mitigate this. This has a clear economic and psychological and psychosocial importance and significance . Understanding risk, how it translates into how you basically live life whether you are against it or in control. One of the ways, again, is understanding your patient so that your treatment is consistent with their susceptibility or resistance to disease. It also saves them money. Slide 60 Is There Also An Effect of Oral Contraceptives? Dr. Robert Davidson So here we are, the patient is on oral contraceptives. Now this could have an effect on hormones and it certainly does have an effect on hormones, but then again it could also have an effect on as a risk factor disease. It turns out that oral contraceptives are more 20-30 yrs. ago than now, but it has an effect on the permeability of the microvasculature which speaks to what? It speaks to edema. Not so much erythema but edema. Its going to be a lot of fluid or more fluid in the connective tissue and you might see some edema. When I talked about it before as a risk factor for gingivitis, it turns out that hormones change not the substrate, but the cells predilection for certain substrates. It turns out that theres a predilection for pathogenic bacteria as a result of oral contraceptives in some patients. That is a REAL risk factor for inflammatory disease. I think Im done. Does anyone have any questions? So Im going back to clinic now, I work in Dr. Shackmans clinic on Wednesday mornings so if youre in Dr. Shackmans group Ill see you. I work in Dr. Resnicks clinic.. Oh no today is Thursday, I work in Dr. Resnicks clinic this morning and on Wednesday afternoon I work in Dr. Berkowtizs clinic. I will certainly see you next year in D2 in lecture. If you have any questions that you think of when you go home, feel free to email me. Im really good at responding. Thank you, thank you, thank you.

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