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Running Time: 68 min

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Review the rationale for NSPT Discuss the diagnosis criteria for Periodontal Disease Explain the clinical phenomena and the underlying mucosal changes Release: 9/26/2014 | Expires: 9/26/2017

Release Date: September 30, 2014

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Welcome. Over the last two decades or so, I’ve had an amazing privilege and an honor to travel to different parts of the world, meet with the different dental teams, and really work on the training modules with different people. And one thing that comes up again and again is the topic of nonsurgical periodontal therapy. I always have questions about what’s new, what’s the latest, what’s the best. And really, with all the new advances in biofilm, is nonsurgical periodontal therapy even valid in today’s day, with the evidence that we have? Welcome. My name is Karima Bapoo-Mohamed. I’m a dental hygienist with a clinical practice in Edmonton, Alberta, in Canada. And I’ve also been an associate professor with the University of Alberta in Edmonton for the last two decades or so. And I’m here actually to share with you my clinical and my teaching experiences on nonsurgical periodontal therapy. What I thought we would start out with was just review what is the rationale for nonsurgical periodontal therapy based on biofilm research. We did dedicate a separate module on dental biochemistry, and we discussed the features and characteristics of biofilm in that module. So quickly review the key points, and really spend a lot of the time in this module on the diagnosis criteria for periodontal disease, as well as what is that clinical phenomena that we are witnessing in the mouth of our patients. We do have a second module on nonsurgical periodontal therapy, too, in which we’re actually going to get into the scaling, [INAUDIBLE] and I guess therapeutic aspects of periodontal disease. So moving on with our first objective, what is that rationale? Periodontal disease absolutely is biofilm-mediated disease. Inherently, it’s difficult to treat, because it behaves very much like an opportunistic infection. One of the greatest challenges we learned from that biofilm module is that treatment is hard, because there’s no way really to eliminate the bacteria from the oral cavity. The bacteria is always present in that periodontal milieu. In addition, the bacteria within the biofilm is protected by that matrix. So it’s very resistant to antimicrobial agents. So in actually the second module of nonsurgical periodontal therapy, we’re going to talk about antimicrobial agents and host modulation therapies, as well. So they are some of the most virulent species in the biofilm, and that makes it very difficult, actually, to remove them. And they do cause very extensive periodontal destruction. We understand that plaque is essential in the disease progression, and really dictates the severity and the pattern of this disease. But we also know that the bone resorption is very dependent on some of these cytokines that are released as part of the biofilm reaction. Nonsurgical periodontal therapy, however, despite all these biofilm evidence that we have, still remains the most cornerstone therapy for treatment of periodontal disease. Patient compliance, of course, as we’ve mentioned in other modules. Proper selection of what kind of antimicrobial agents are we going to use for this patient, to really maintain and sustain their plaque control, becomes a really key factor in the long-term success of this result. Aside from the daily home care regimen, frequent recall appointments to intervene that disease process is also very critical, in addition to that meticulous nonsurgical periodontal therapy that we give in the office. So with the context of that rationale for yes, we still need to do that nonsurgical periodontal therapy. Let’s dive into the diagnosis criteria for periodontal disease. And I have some subobjectives that I have put out there. And let’s start with the first one there as what is the patient’s chief complaint? Now, a lot of times– you’ve probably noticed this in your private practices, as well– patients say, oh, my teeth were fine. But a week ago or a month ago, they’ve gotten a little sensitive. Some patients may say they started bleeding, and they never used to bleed before. Or some of them may say it’s quite sore. For some reason, this one area’s gotten really sore. A lot of patients will mention bad breath, actually. My breath doesn’t taste good or smell good. Very occasionally, I’ll have patients that say, my teeth feel a little loose. What’s going on? But the majority, actually I’d say 90% of my patients, have no complaints, as far as their mouth goes. So they’re here for their recall appointment. How does everything fill in the mouth? Everything feels great. No problems at all. So from a patient perspective, they may have no problems. However as clinicians, when we go in the mouth and do our comprehensive clinical exam, absolutely we’re finding evidence of gingivitis and periodontitis. That will be evidenced by bleeding, recession, deep pockets, of course. And we’re also keen on seeing the deposit, and doing an assessment on the deposits of these teeth. Sometimes, there may be infection, exudate. What about decay, demineralization? We’re constantly monitoring that with our radiograph and checking for bone loss there, as well as any mobility issues that the patient may be having. So it’s quite interesting that the patient may not have any symptomatic concerns about their mouth. But upon investigation intraorally, we find a whole slew of things. And now, the question becomes how do we communicate that to our patient? We’re doing the risk assessment for a patient. This is still the whole data gathering component of our treatment plan. And with the medical history, absolutely we want to check the systemic conditions. Is there any history of heart murmur or joint replacement, because that might indicate the prophylactic antibiotic regimen that we may have to follow. Patients’ systemic diseases, such as diabetes or any kind of blood disorders definitely merits attention prior to commencement of dental hygiene therapy. What about prescription pills? Are they on any NSAIDs or statins? That we do want to know about, because it will have oral manifestations. Allergic reactions, of course, is part of our medical-history-taking routine. And when was their most recent doctor’s visit is also important to find out. We have another module dedicated to actually periodontal links with systemic diseases. And we’ve talked about diabetes there. But just as to refresh our memories and to summarize, diabetes does have a bidirectional link. There is large evidence that suggests that diabetes is associated with an increased prevalence, extent, and severity of gingivitis and periodontitis. So inflammation is the common underpinning factor here. It plays an obvious role in periodontal disease. But evidence in the medical literature shows and supports that the role of inflammation– really, it’s a major component in the pathogenesis of diabetes, and actually how severe or complicated diabetes is going to get. So research shows that if we can control the infectious process in the mouth, we can maybe control the prevalence and the complications that go with the diabetes. And conversely, if we can take care of the health of the patient. Or the patient is better equipped as far as their maintenance of diabetes, chances of the extent of periodontal disease could be reduced greatly, as well. Smoking is absolutely another part of the patient history we want to gather. Is there any other social habits that are going on? And also, perceived historical data from the patient, aside from any chief complaints that we spoke about earlier on. Family history, as well, is an important factor on that slide. Dental history– we’re all good with this. We are capturing all the decayed, missing, and filled surfaces on the teeth. We’re checking for tooth mobility, and of course, any previous periodontal procedures that they may have had. And really, this is just data gathering for us to create a very customized, individualized treatment plan for our patients. Extraoral, intraoral exams absolutely a critical component of our assessment criteria, where we’re checking all those lymph nodes, as well as the salivary glands, which are extraorally located in the head and neck region. We are also checking for the TMJ and any dysfunction or any pain or limited range of motion, or actually any abnormal sounds that the patient may be experiencing with the opening and closing, as we do our assessment for the TMJ. Headaches can also be a symptom of a TMD issue going on there. Intraoral exam– we absolutely want to check the buccal and labial mucosa. We’re doing the digital palpation. Now, the tongue is, of course, a primary source for a lot of the issues that the patient may have, clinically or systematically. This is actually a case from about a month ago. Now, this patient is coming to see me on a routine basis. I believe Donna’s a four-month recall patient. This little elevation on the dorsal surface of her tongue has been there for a long time. However at the last recall last month, she’s presented with this little lesion here on the lateral border of her tongue. So this I am very curious about, because a, it wasn’t there the last time. It’s not symptomatic for this patient. However, we have sent it for a biopsy and get a second opinion, and understand what this leukoplakia-like manifestation is. So intraoral exams are really critical in helping us assess what the condition is, and more importantly, what the changes are in the dental condition of the patient. We want to talk about the dental diagnostic tests that we may do. And those pretty much start or range from full-mouth probing. We are capturing six-point readings on every single tooth. And as we’re measuring the pocket depth, we’re also measuring, documenting, calling out the bleeding response of our tissue. We are using our periodontal probe for recession areas, as well. Furcation invasions– absolutely we want to capture that information and look out for changes. Tooth mobility, as well as really looking for any mucogingival involvement. So this is all part of the dental diagnostic testing that we are constantly doing. And this is, again, to help us with the formulation of a customized treatment plan. So let’s go over some clinical slides of what that tissue could look like. As we can see and just for our review, the gingival margin is this little linear scalloped border just at the junction of the tooth and the gum. The gingival groove is actually this little, almost lifesaver roll or a look that I tell my students. And just where it stops is where that groove is. And anything below that is the mucogingival junction on the alveolar bone crest. So this patient’s manifesting stippled gingivae. This is something that gets us excited, when we see healthy, firm, tight tissue that’s pink in color, and probably manifesting very small pocket depth in this area. Comparing it to something like this, which is very bulbous, red, swollen, shiny, and absolutely looks like it’s endematous. It looks like it’s fluid-filled to me. And you can see the distension of the gums there, and slight loss of the interdental papilla there, as well. So that’s a big contrast from coral pink tissue. So as far as our gingival assessment, we were really focusing on the color of the tissue. What does the contour look like? And is there a texture to this tissue? Is it firm or is it fibrotic? What about the tone and consistency? Is there stippling or lack of stippling, a loss of stippling? So that gives us a good view of what healthy should look like. This is a nice contrast of healthy versus disease. And you can see this is a coral pink stippled knife-edge firm margin, compared to something that’s, again, very shiny and red, and possibly loaded with exudate. This is showing, again, just marginal generalized gingivitis. As you can see, the rolled margin of the gingival groove is quite accented here, based on this gingivitis condition that’s manifesting. And as we look at this lower slide here, we can see the evidence of what could be causing some of that gingivitis, as we see the hard deposits right along the gum line. So my home care recommendation for this patient will be really customized, based on this clinical finding. We talked about pocket depths and probe readings earlier. Why do we need to do that? Well, those are really essential for a few factors. We’re using our periodontal pocket for measurement of that recession. So that’s the distance away from the gingival margin to the cementoenamel junction. And the pocket death is, of course, we’re placing our probe into the sulcus. And it’s really the apical resistance of our probe, which is the junctional epithelium, that’s giving us the reading in millimeters. So by capturing that, it’s really giving us the severity of what that clinical attachment loss is. We all understand the clinical attachment loss to be a combination of the recession amount and the pocket depth amount. So you could have recession of about maybe one or two millimeters. But if the pocket depth is about five, then five and the two millimeters of recession will make it a clinical attachment loss of seven millimeters. This is critical, because a lot of categories and classification of periodontal disease is not based purely on pocket reading. It’s based on clinical attachment loss. So we need to capture both of those important readings of recession, as well as the pocket depth. This is that slide of a lady I showed you earlier, with that really puffy bulbous tissue. Sure enough, when I inserted my probe in there, we have an eight-millimeter pocket depth in this area. And a lot of times extraorally, here, I’m trying to press to see the reaction of the tissue. And it’s getting blanched and ischemic. That’s telling me that it’s probably loaded with some exudate in here. But a lot of times, I will actually give the patient a mouth mirror, like you would, and show them this is the kind of bony defect that’s happening underneath the gun that you can’t see, but my probe is picking up on. And that’s substantial, when you visualize that for the patient. You get them motivated about, oh my goodness, what do I need to do? Now, this slide that I just showed you with the deep eight-millimeter probe reading is actually a very young female patient of mine. In contrast to my star patient, she’s 75 years old. She comes in to see me every six months, and look at the condition of her gingival tissue. It’s firm. It’s tight. There’s a little bit of recession. It’s marginal recession, fairly generalized. I’d say it’s about one millimeter all over. But the probe readings are actually around one or two pretty much consistently. Check the occlusion at her recall appointment. And there we have it. You see this little high spot there. So of course, I want her to get that looked at and examined, and make sure that it doesn’t get into any other complications, based on excessive occlusal force. Exudate on probing, we are checking that out with our probe, as well. This looks suspect to me, as far as the tissue goes. Sure enough, as we insert our periodontal probe, there it is. We see the exudate just oozing out of that periodontal sulcus. Radiographically, we see evidence of the bone loss. The crestal bone level is way down here, compared to the distal area, which is so much more closer to where it should be by the CEJ. And of course, the radiolucency around the root surface there. So we do use our periodontal probe for a lot of diagnostic purposes. This is a good review, actually, of the types of pockets. So we know that the pocket depth is measured from where we’re inserting our probe all the way to the junctional epithelium. And sometimes, it is laden with calculus. So we have to be careful, as far as the parallelism of our probe, and making sure we’re getting accurate readings there. So that’s a Type 1 pocket. Type 2 and 3 types of pockets are ones where there is apical migration of the junctional epithelium. But look what’s happening. There’s crestal bone loss, as well. So in parallel to that crestal bone loss, the gums have also moved apically, and now you’ve ended up with a deepened pocket reading. Compared to a Type 4 pocket reading, which we call the intrabony pocket, where actually there is no change in the crestal bone loss. It’s exactly where it should be. However, there is apical migration of the junctional epithelium. This is another slide showing the use of the periodontal probe for bleeding and exudate detection. And same thing again, you are using the probe on top of the gingival margin to show the patient the extent of periodontal damage that’s happening below the gum line. It’s almost like an iceberg. You just see the tip of it. The gums look slightly red, but there’s a whole big structure and pathogenesis happening underneath there. So the value of perio probing would be the full-mouth probe depth with the recession gives us a clinical attachment level. And it really provides us a good baseline data, doesn’t it? So we have a benchmark to compare it to. So if I’m finding a five-millimeter today, I want to be able to see well, what was it a year ago, six months ago, or five years ago? The bleeding points are also ascertained a lot of times on probing. Sometimes, it’s spontaneous. But a lot of times, it’ll be delayed bleeding. So even after you’ve left the site and you’re on the adjacent tooth, watch out for that delayed bleeding, and be sure to capture those bleeding points. That becomes an important parameter for inflammation status in the mouth. Documentation, of course, not just for legal purposes, but again, for benchmarking and for baseline data comparison for us. And what an amazing opportunity then to use our periodontal probing for educating our patients and giving them a status update on where things are going in their mouth. Are they getting better? Are they getting worse? And I feel that really helps. The patient can understand and visually see it helps with case acceptance. So if I have to have them come in three or four or five times to finish off this periodontal therapy, the nonsurgical periodontal therapy, that they will be amenable and actually motivated to accept my treatment plan for this case. This is again, showing gingival recession, fairly severe in this clinical manifestation. There is a CEJ. And we can see it has actually exposed a large chunk of that cementum root structure here. And so there is a huge indication for clinical attachment loss. The probe readings may not be very high. It may be one or two millimeters only. However, the CAL reading will be a lot higher because of the recession amounts there, compared to something like this, which is not quite as recessed. So I’m curious to see what the patient is doing, as far as the resultant effect of this excessive recession. And why is recession– what are some of the clinical signs, you may wonder? What’s the big deal about recession? So the teeth get a little long in the face. You get older. You get hairline recession. You get gum line recession. What’s the big deal? Well, we want to monitor it, because this is now enamel is not there anymore. It’s cementum exposure. And cementum is not very resistant to acidic pH level. So couple that with a patient who has a dry mouth. This could be an invitation to trouble, as far as demineralization goes. And the patient could end up with sensitivity over time. So educate the patient. I’m just seeing a change in here. We want to watch out. Perhaps you will put them on some fluoridation therapy or desensitization therapy. Recession may manifest itself differently, in terms of abrasion. As you can see on this slide here, really abraded tissue, almost horizontal notching of the cementum there. The hard tissue is just literally disappeared here. And this is an excessive manifestation of actually erosion. This is from a stomach acid erosion from regurgitation that has caused– in a bulimic anorexic patient. So recession abrasion are really important documents for us to have. This image is just showing actually how you can take the measurement of recession using the periodontal probe, and then combine it, of course, with the pocket depth to give us the clinical attachment loss. There is some discussion in the literature about true and surrogate endpoints. And really, a true endpoint of periodontal disease is over is when the tooth is lost, really. So that would be a true measure of periodontal disease. However, we want to avoid all of that. So we use a measure or a proxy to prevent that disease. And so anything like a probe reading is a surrogate endpoint that we use to actually manage and monitor the degree of disease process and progression of this disease. So anything that we’re checking with our bleeding on probing, probe reading changes, attachment level changes, alveolar bone support. Just to throw it out there, it’s more of a surrogate reading of what the true endpoint would have been, which is tooth loss. We are also, as part of our dental diagnostic data gathering, capturing the assessment, as far as soft and hard deposits go, as far as the plaque scores and calculus index. There may be other indices you may use, like Modified Gingival Index or the Gingival Bleeding Index. What about furcations? Let’s do a quick review on the different grades of furcations. This is showing an early or Grade One furcation manifestation, where the level of the bone loss actually allows the insertion of your probe into that little concavity or the bifurcation area of the roots. And this is just usually I use a Nabers probe for this measurement. And so this is what a Class One manifestation of furcation would look like. Compare this to Class Two, where the level of bone loss is a little bit severe. And it’ll allow you to actually insert your probe horizontally through the furcation area or that bifurcation area, that concavity area. You’re way below the concavity area. So in Stage One, you were here. But in Grade Two, you’re actually apical to that concavity area there. Grade Three furcation is definitely more advanced. And here, what we’ll notice is the probe is going right through– or through and through, as we call it– and it actually comes out at the other end. So if you’re on the buccal side, it’ll actually manifest on the other side, on the lingual aspect, of course. So that’s just a quick review of what a Class Three furcation looks like. Mucogingival involvement– I always get questions asked. What exactly does mucogingival involvement mean? And I think most of us do understand that if we do a quick review of where the gingival margin is, where the gingival groove is, this is the majority of the gingiva. That’s the pink gum that most patients see. Mucogingival involvement is when the gingival margin goes apically towards the apex of the root, but actually moves beyond the gingival margin. And it’s actually at the junction of the mucogingiva. So that’s a demarcation point. Clinically, I would say the mucogingival margin for this patient is around here somewhere. And as you can see, the recession is way into the alveolar bone area here. So this is definitely showing mucogingival involvement. How do we quantify or label it? Usually calling it “adequate” or “inadequate” is sufficient. So that’s how I document it in my chart. Mucogingival involvement– something to monitor, watch out for. Is there a recession? Because of this recession, is there sensitivity or symptoms I need to support the patient with and watch out for? Make sure the patient’s not doing a lot of aggressive brushing or hard-bristle brushing or horizontal kind of brushing. Perhaps power brushing can be avoided in that area, would be some of the strategies I’d be thinking of for this patient. But I would document it as “adequate” or “inadequate involvement.” All right. Moving down our list of the diagnosis data gathering, we’ve talked about periodontal probing. I now want to move on to role of radiograph. And of course, we’re looking for any anatomical changes. We’re checking the sinuses. We’re checking the alveolar bone ridge. We’re really checking for any missing, impacted, supernumerary teeth. Sometimes implants, as I showed in one of my other modules, looks like a clinical crown manifesting when you look intraorally, but it’s actually supported with a tooth replacement, like a dental implant. A radiograph would show that to us. Of course, we’re checking for caries. Interestingly for caries, you need to have 55% to almost 60%, some studies say, of demineralization for it to actually appear radiographically. So interesting to know that it’s almost too late by the time you’re finding it in the radiographs. Is there any inflammatory lesions, as far periapical access is going on there? What about the root? Does it look like it might be resorbing? Or some pathologies could be going on under there. I’m really curious to find that out. And of course, the overhang or any dentistry that may be an impediment for the patient to then maintain a dental hygiene. A lot of offices, including ours, actually do have a CBCT. And they’re wonderful for really comprehensive and closeup assessments. Caries risk assessment– we’re using it as a moderate, high, or severe. And again, the risk factors are exactly what we went over with the radiograph slide. It could be anatomical. It could be physiological, environmental, maybe behavioral. And with behavioral, it’s very linked with dietary. Is the patient having a lot of sugar exposures that could be making them high-risk for caries? And the way we would assess for caries is, of course, clinically, radiographically, and the dialogue history. Part of radiographic exam is also the type of bone loss. We are really monitoring the crestal ridge of that alveolar bone, and trying to understand. Is it adequate? What is the crown to root ratio? And those furcation classification images that we show would probably be evident in our radiographs, as well. So we want to complement, most definitely, our radiographic interpretations to supplement our clinical examinations and findings. This is just showing an example of horizontal bone loss, where you can see if the CEJ’s roughly around there, the crest of the bone is actually parallel to the CEJ. But it’s actually moved further apically and further away. I’m very curious to see what kind of support this bone is now providing the tooth, and educating the patient that, did you know you have some crestal bone loss? And it is horizontal in nature. And if this continues– the bone is what’s holding your teeth in your mouth. So we just don’t want to lose too much of that bone. And what could be some other positive factors for that? So really watching the crestal bone loss there. And anything that’s crater-like could be a defect, as well. We want to really examine and watch out for. Compare horizontal bone loss to vertical bone loss, where it is definitely more angular. And you can see it’s a dramatic dip on a radiograph. So a great way of educating the patient to really explain to them that maybe I would give them some inner dental cleaners here, to access the space a little more effectively, because those anaerobic pathogens are living and thriving and surviving in there. Aside from the bone loss, we’re looking at the condition of that alveolar crest. We talked about the furcation areas we want to watch out for. This is abominable. Look at the big overhang that’s causing the bony defect in this distal area of that molar. So really want to check how this is comparing, based on this pathology here, as well. Check the root length morphology. And as we mentioned earlier, the crown to root ratio is important, as well. As hygienists, we’re always looking for the subgingival spicules, which will become really evident. And we’re all very good at picking those up right away. Part of that radiographic examination is a bone support. And if there is bone loss, we’re absolutely going to find it in a clinical parameter of tooth mobility. And that could be even a hyperfunction or loss of attachment. In my practice, I use three classifications, ranging from one to three. And anything that moves labial-lingually or facial-lingually of one millimeter is Class One. And progressively changing that from two millimeters to over two millimeters as Class Two and Class Three. So we have just gone over the diagnostic data gathering for periodontal disease with all those parameters. The second outline– the last outline for this course is, of course, for this module is to go over the clinical phenomena. And just like I did for the diagnosis criteria, I have some subtopics I want to talk about with the clinical phenomena of the underlying mucogingival tissues. Categories of periodontal disease– what about the etiology of this disease, and the prevalence of it? Risk factors is something we’re going to talk about, as well as what is the range of this perio condition that will require treatment. As I mentioned earlier, we have a dedicated module for the treatment aspect of periodontal disease. But I think it’s important to understand the categories classification of it before we get in there and start treating the patient. So why do we need to classify? Well, it helps us with the framework of studying the etiology, the pathogenesis of it, and really, the treatment will really depend on what type of classification of periodontal disease exists. I think classification– especially when I travel all over, it’s nice to have an international standard that everybody in the dental health care industry understands as a common language for us to communicate. So really important to classify the type of periodontal disease. When I graduated actually, there was just five categories of periodontal disease. It was juvenile periodontitis, early-onset periodontitis, adult periodontitis. And then, we had the acute necrotizing ulcerative periodontitis. And then, the last category was refractory periodontitis. The AAP actually has a new classification of actually seven categories now. And these are some key changes which I think are so valid and very evidence-based. It’s because of the new body of evidence and data we have needed to classify periodontal disease into these seven categories. So gingival disease is now a category on its own. We also have the adult perio is now replaced by chronic periodontitis. Refractory disease category’s actually been removed. Early-onset is now replaced by aggressive periodontitis. And the comprehensive definition of actually periodontal disease is now linked in with systemic diseases. So there’s a category for that, as well. Necrotizing periomucositis diseases covers both. It was just perio before. It covers both gingivitis and periodontitis. And, now periodontal abscesses are actually categorized as periodontal and endodontic lesions. That has been added, as well as a category for development or acquired lesions is also introduced. So here we have it. This is the new category of periodontal diseases, and that’s what the seven categories look like. We’re going to spend time with some of these to understand really what and how the categories came to be, so that we can then implement an effective treatment plan for our patients. Starting with gingival disease, it’s actually subcategorized for dental plaque-induced gingival disease. Or is it non-plaque-induced gingival disease? Interesting category. Chronic periodontitis– this is where the clinical attachment loss comes into play. So really be measuring recession with your pocket depth. I think we’re so conditioned to just measure pocket depth. But the combination of the recession with the periodontal pockets will give us a CAL reading. And the CAL reading is what’s going to help us categorize and classify chronic periodontitis as mild, moderate, or severe. And again, just like the other categories, it would be either localized or generalized. The same CAL readings are also used in a category of aggressive periodontitis as localized or generalized. The fourth category of periodontitis as a manifestation of systemic diseases is actually– we’re subcategorizing it now to understand, is it part of a blood disorder, is it part of a genetic disorder, or is it something that’s not specified within that? So there’s always that C category that we can subclassify our periodontal disease in. The necrotizing periodontal disease is, like I mentioned earlier, it has the categories of both gingivitis and periodontitis as a subcategory. Abscesses of the periodontium– is it a gingival abscess? Is it a periodontal abscess? Is it a pericoronal abscess is a subcategory for the types of abscesses. There’s also abscesses associated with the endodontic lesion. So maybe a patient had a root canal done, or needing a root canal based on the pulp canal getting inflamed and infected. And of course, any acquired deformities or conditions that cause periodontal disease. And those are also subcategorized in this classification. So interesting to learn about the classification are now seven. Again for our purposes, gingival sulcus is a depth. And usually, about three millimeters around that depth of pocket space between the tooth and the gum line is the acceptable area as healthy, because a patient can actually self-manage and clean it quite effectively. Again, a qualifier is a pseudopocketing. Pseudopocketing is actually the junctional epithelium hasn’t necessarily moved apically. But the inflammatory status is such that it’s caused the gingiva to really extend itself coronally, which then ends up with a deeper pocket reading. So really if you have a pocket reading that’s beyond three millimeters, it’s a good idea to have in our back mind, is it a pseudopocket or is it actual migration of the junctional epithelium apically? And of course, a periodontal pocket– anything that’s over three millimeters that’s going below the CEJ usually, and the junctional epithelium has definitely moved apically, is a periodontal pocket as a classification. And periodontal pockets, as we know, are irreversible. Patients get shocked when I sometimes mention to them about this. Most patients know it. But there are patients that’ll be like oh, it can’t go back to normal? Because they think of gingivitis as something that’s reversible. So a great education criteria in motivating our patients. So again, looking at the types of periodontal disease with the seven classifications, we just want to categorize them as early, moderate, or advanced. And the next three slides are actually giving you a clinical manifestation of what that could possibly look like. So with just gingivitis, there’s really no attachment loss or any changes. Bleeding may or may not be present, but pseudopockets may be present. And the gingival tissue actually is really affected by the inflammatory process. And this part of the disease is actually reversible. Radiographically, there won’t be any evidence of actually bone loss, and the crestal bone is actually fairly healthy-looking and you see that the crestal lamina dura is present and very visible, as well, in this type of periodontal disease. Compare this to early periodontitis, where there will be bleeding on probing, because this is now getting into an active phase of the disease. Our pocket depths are definitely deeper, because we’re having that attachment loss happening there. There are localized, possibly generalized, areas of recession. May have furcation Class One involvement. There is horizontal type of bone loss. That may be fairly common. Not extremely evident– you almost have to go hunting for it. But clinically, you can see the manifestations change. And the tissue’s definitely more red, shiny, bulbous-looking. And the interdental papilla is not quite as pointy as we’ve seen it in the gingivitis. So this is early periodontitis compared to moderate periodontitis, where now the big defining moment is the pocket depth of the attachment levels are around four, six, or deeper millimeters of depth. There is most likely going to be bleeding in this area. Furcation involvement may be Grade Two even, by this stage. There might even be Class One mobility. So that’s a one-millimeter labial-lingual movement of the tooth. There may be both horizontal and vertical bone loss present in the radiographic interpretation of this type of periodontal disease. And the crown-root ratio, watch those really closely. You may have some loss of that supporting alveolar bone, in which the crown will absolutely dominate the ratio of the whole crown root. And then the last type is, of course, the advanced periodontitis. Clinically, it just doesn’t look right. Very much bleeding on probing. Pocket depths are over six millimeters. You have a furcation of Grade Two, Grade Three, mobility of Class Two, Class Three, definite horizontal, vertical bone loss areas happening there, and the level will change. Radiographically, you will see some changes. Aside from the horizontal, vertical bone loss, the furcation involvement will also become evident. Patients probably clinically experiencing some halitosis or a bad taste, as well. And again, the crown-root ratio will be significantly different from the other one. So again, with those seven categories, I should mention– and I think the next slide talks about it– is “localized” is defined as something which is 30% of the site. So if there is plaque, for example, up to 30% of the site, we are qualifying or classifying that as localized, as opposed to anything over 30 is now a generalized type of situation. Just to review, our severity is qualified as slight, moderate, and severe, based on our CAL readings of one to two, three to four, or greater than four. And so chronic periodontitis is very prevalent in adults. And that destruction is very consistent with the local risk factors. So subgingival removal and frequent removal of the deposit really helps with the progression of this disease. This disease is also very much modified by any systemic diseases that may be going on. So watch out and do a comprehensive assessment in your data-gathering phase. Aggressive periodontitis actually usually starts around puberty. You’ll probably be able to notice this very easily in that first molar region and the incisor region of our adolescent patients. And there’s actual increase serum antibodies in there. And it’s really responding to the periodontal pathogens that are present in there. So that’s when it’s localized. When it’s generalized, it’s just poor antibody response. And it may be episodic for a lot of these patients. From one recall to the other, it may change very easily. And now, it’s going to affect more than just the molars and the incisors. It’s going to affect more than 30% of the mouth. Periodontitis as a manifestation of systemic disease– that’s the third category. Again, the subclassifications is what is it induced by? Is it plaque-induced? And if it’s plaque-induced, guess what? We want to understand, is it endocrinal in origin? So it would be hormonal changes during puberty or menstrual cycles. Or pregnancy would qualify as endocrinal. Diabetes, of course, is associated with the endocrine, and so would be qualified in this category, as well. Systemic diseases of any kind of blood disorders, like leukemia, would also fall under this category. The necrotizing periodontal disease– the fourth category. What kind of abscess is it? Is it gingival? Is it periodontal? Is it periapical? And just moving through these categories very quickly. They’re fairly self-explanatory. The last category at the bottom there is relating to endodontic lesions relating to periodontitis. So really, the considerations for periodontal disease. It has been developed, and it’s important that we control it. There are irreversible stages of periodontal disease, and it is a permanent destruction of that connective tissue and the alveolar bone. Early intervention is totally the key to a better outcome, to really help rebuild those gums and create that connectivity between the teeth and gums. And advanced periodontal disease really increases the inflammation. And that inflammation can then– we now learned– can spread through the other parts of your body, too. So as I mentioned to our patients, I can’t get to your other organs like lungs and heart and what have you. However, we can certainly work on what’s in your mouth, and try and control this. And so we really, by controlling periodontal disease, we’re reducing the risk of developing other exacerbating diseases in other parts of the body. So that covered the categories of periodontal disease. I feel it’s an important topic, and I’m glad we took the time to get a clear understanding of what the categories are. Let’s talk about the etiology of periodontal diseases. It’s multi-factorial, as we know. Oral environment plays a key role. And let’s go over, actually, each one of these very quickly, to refresh our memories and get validation of the knowledge base that we are operating from. Lack of oral hygiene, of course, encourages the bacterial buildup, the plaque formation. And not only will the plaque form, but it will be uninhibited in maturing and progressing in its complexity. The oral environment– actually, the sugars and the acid has a huge effect on the oral environment. So we want to make sure that we don’t allow that environment, because that makes periodontal disease thrive. And limiting the types of food and the acidic environment in the mouth. Dentistry that has poor contours will have an effect on the oral environment and capturing of the plaque bacteria in there, as well. Any kind of anatomical tooth abnormality– and it may have been genetic– is something that merits attention and take a look at. Wisdom teeth, of course. It can be a breeding ground for bacteria, depending on how it’s positioned and what the pericoronal tissue looks like, that perhaps removal of them might help with the oral environment and maintenance of periodontal disease. Moving on with the patient age as part of the etiology of periodontal disease. We have evidence that show that children and adolescents, especially with the hormonal changes we talked about, it is a universal finding that they may end up with more of the gingivitis condition. The two bacteria really responsible for that are the P. gingivalis and the T. denticola. And so it’s not uncommon for healthy children really to have gingivitis there. Educating them on that oral environment becomes really critical. Adults actually can also pose a risk of periodontal disease. And really, half of American adults have gingivitis around three or four teeth. And 30% of them have significant periodontal disease. So this study also shows that 70-year-olds have about 86% moderate periodontitis. And a lot of them have lost their teeth because of periodontitis. So really watching that adult population becomes really important, as well. What about female hormones? We talked about that having an effect on periodontal disease. And it’s interesting statistics I learned, that 3/4 of the visits at the periodontal office are made by women. And although there’s statistics that show women take better care of their teeth than men do. And some of these hormonal changes is actually the progesterone might be the culprit, because during menstruation, for example, the progesterone levels are quite high. And gum inflammation will maybe occur during ovulation, as well. As we know, progesterone actually dilates the blood vessels, causing inflammation and bleeding, and actually blocks the repair of collagen. And, of course, we want collagen for repairing of periodontal disease. So when you have too much progesterone, it creates havoc in the mouth, as well. Pregnancy hormonal changes can definitely have an effect on gingivitis. Just a proviso– pregnancy doesn’t cause gingivitis or periodontal disease, but it can exacerbate it. So if you have existing gingivitis and now you’re pregnant, the hormonal changes will give you this exaggerated response. So really good way of educating our female patients who are thinking of pregnancy or maybe pregnant. And as we learned from our dental anatomy module, that those primary dentition are starting to form in the fetal membrane at six weeks, between six and eight weeks. So great educational opportunity for our patients. There’s some studies that show oral contraceptives actually play havoc with hormonal changes, too. But there isn’t any conclusive evidence. Again, there’s suggestion that the progesterone levels might be interfering with a periodontal disease. Another hormonal change for women issues is, of course, menopause, where estrogen is not being produced anymore. And so that affects the bone mineral density. And of course, when there’s not density of the bone, you get bone loss. And bone loss is a clear symptom of periodontal disease. So really, if you have a patient who’s postmenopausal, going through hormone changes, really monitor their periodontal status, and maybe have frequently recalls for them. Moving down our list, we have family factors as part of the etiology of periodontal disease. And what do we mean by family factors? Well, genetics is definitely a critical role, because half the cases of periodontal disease, some studies show, is reliant on a genetic predisposition. 30% of the population may have that susceptibility to periodontal disease based on their genetics. There’s also evidence and some papers and publications on exchange of saliva between partners or spouses who are intimate that may be a risk of periodontal disease. And they’ve found that the P. gingivalis can be contagious and can infect another partner. Moving down our list, we also want to just put smoking also as a causative agent for periodontal disease. And with that, what we’re seeing is it does cause a lot of vasoconstriction. It can cause bone loss and gum recession really manifesting as periodontal disease. And what it is an overproduction of the cytokines, which is a real culprit at a biochemical level. And the P. gingivalis is a bacteria that’s so opportunistic. And it’ll produce even greater levels of cytokines and eventually lead to a connective tissue breakdown, which is manifested as periodontal disease. So really, smokers– there’s studies that show more than 10 times likely to harbor these pathogenic bacteria, which will cause periodontal disease. Don’t forget secondhand smoke, too, is a risk factor. And I put it under this slide as a reminder for our patients who may be exposing themselves to secondary smoke. There’s some research on marijuana and its effect, and couldn’t really find anything so conclusive linking it to periodontal disease. There is some very strong evidence that that may also cause issues, as far as etiology of periodontal disease. Vitamin C deficiencies– and before we get to vitamin C deficiencies, let’s talk about other diseases. And I just created a slide and bunched in all these other diseases. Diabetes, we talked about earlier on, because that will just actually affect the severity of periodontal disease, based on increased blood sugar levels. And really, it appears that time that the blood sugar levels elevated will have a direct effect on the periodontal disease impact. So they are a high-risk population, for sure. Osteoporosis– we talked a little bit about it during hormonal changes in female patients. But of course, it applies to any patient, male or female, that may be osteoporotic. And what it is is the change in the bone density, where– the way I explain it to patients is that it’s like an AERO chocolate bar. You’ve just got more holes in between your bone sandwiches. So what ends up happening is the bone isn’t as strong, because it’s not so dense, and it doesn’t have so much weight-bearing capacity. And aside from hormone changes, sometimes it’s just age, wear, tear– and really, weight-bearing exercises stimulate the bone, as far as the density goes. So regular exercising, vitamin, and mineral supplementation may be good advice we can have our patients think about. In the other category, I’ve also included the herpes-related gingivitis, which is, again, a common cause of gingivitis in children. And it is actually becoming increasingly common in adults. That’s when the tissue goes really cyanotic-looking, and it is quite boggy when you press on the gums. And it may have multiple blister manifestations, but usually, they resolve within seven to 14 days. HIV-associated gingivitis is a factor that’s been reported from 15% to 50% of patients with HIV. And they do tend to harbor a large number of periodontal pathogens. So that’s a category of patients we want to watch out and be on alert for progression of periodontal disease. And sometimes, there is pain that’s characterized with this disease. There may be some odor, spontaneous bleeding– of course, the ulcers would be another manifestation of very big, swollen, bright gums. In its worst form, I guess it’s almost necrotizing stomatitis is what it would look like. So watch out for patients with those HIV/AIDS medical histories. Autoimmune disease is, again, in the other category, as well. And within that is things like Crohn’s disease, multiple sclerosis, rheumatoid arthritis, and a whole bunch of other diseases that I’ve bunched in together that– anything that’s positive on our medical history, just have it on our background of my mind that I’m going to watch out for progression of periodontal disease, because it could come on very fast for these patients. Vitamin C deficiency– were going down our list here– is an area that research actually has indicated that that deficiency will contribute to periodontal disease. So really watching out for smoker patients, for example. Not a bad idea having a vitamin C supplementation. And ideally, we should be having fruits and vegetables that are high in vitamin C, and that actually helps patients with periodontitis progression. What about ethnic, socioeconomic, and geographic factors that may have an effect on periodontal disease. Dental disease is most likely, actually, to happen– there’s evidence that shows patients in that socioeconomic status, which is fairly lower in the demographics out there. Children and elderly are probably the most marginalized, and probably suffer the most for most of the studies in the literature we see. Lack of access is a key issue, and of course, the financial burden of treating disease. And it’s a catch-22. Because they don’t have access to care, the disease progression goes into the highest severity. And they’re the ones that actually need the most care and don’t have access or the financial means. So that’s an important factor for periodontal etiology. Drug-induced gingivitis– I have a slide here of Dilantin. We all know about the epileptic medication patients take, and it gives us this kind of exaggerated gingival manifestation. So this is a category now in our periodontal classification. And something like Dilantin would show this kind of manifestation there. And going down to our last category that I just put under “Other.” and it’s a potpourri of things that I wanted to just put out there and mention and watch out for when you’re doing your assessments for your patients. Is the patient a mouth breather? Is there a lot of psychological stress? Because studies have shown that stress has a huge influence in the chronic inflammatory process, or any chronic inflammatory disease, periodontitis being one of them. What kind of alcohol use or abuse is happening with our patients is also– I didn’t know where to put it, so I put it under other etiology cause. Incidence of canker sores, that abscess ulcer? Is the patient seeing them quite often? And really, it’s stress-induced. It is a viral disease that lies dormant. But I’m curious to understand, is there any self-injury going on? Is there any genetics that might dictate it? And you really want to watch out for any allergic reactions that could be bringing out the onset of canker sores. A lot of times, it’s stress-related, as I mentioned. And just the idea or notion of going into a dental office can incite canker sores for a lot of patients. All right. So we have covered the categories of periodontal disease. We’ve discussed the etiology and then some, and created different categories to really get a broad scope of what could the possible causes of periodontal disease be. I would now like to move on to the prevalence of periodontal disease. And really, as we learned earlier on in the module, it is an opportunistic infection. And so it doesn’t behave like a classic infection. It is biofilm-mediated, and so the bacteria won’t be eliminated very easily in the oral cavity. And because of that protective matrix, it is resistant to the antimicrobial agents or antibiotic therapy, a lot of the time. So really, the severity and the pattern of this disease is very dependent on plaque management and periodontal disease progression management. It is the second most common disease in the world, periodontal disease is. And it is chronic, and it can be very progressive in nature. It’s usually painless, and it can go undetected for a very long time, as we know. But the destruction of the tissue once it gets to the periodontitis stage, as we know, is permanent. So why is it so prevalent? Partially because it is not painful, and so patients can easily discount it as I don’t have any disease activity going on. I think the other part is this statistic that shows it affects approximately 90% of the people of age 60 and over. I’d like you to meet Mr. A right here. He’s my patient who just turned 101 years old two months ago. Mr. A comes to see me every three months for his dental hygiene therapy. And he’s fully dentate. He has some tooth replacement based on implant. So the point I’m trying to make is we have longevity happening in our culture. And chances or incidence and prevalence of periodontal disease based on the longevity of our patients is also contributing to the higher statistics of the incidence of periodontal disease. Another statistic shows that 50% of the adults have gingivitis. Studies have also found that in early childhood, it’s definitely more prevalent and severe, in that the average number of bleeding sites– or bleeding points, as we capture them– is higher in older than younger men. 50% of the adults have been found to have gingivitis on at least three or four of the teeth. So some amazing stats on the incidence and prevalence of the diseases. Let’s move on to the risk factors associated with periodontal disease, as they go down our subobjectives for the module. The risk factors have been recognized in response, of course, to the therapy. And the big thing with risk factors is it varies from one patient to the other patient. And bacteria themselves are actually essential in initiating the disease, but it’s insufficient by themselves to cause the disease. So very important to examine the risk disease, the host factors on which these pathogens are proliferating and existing. So there is value in doing a risk assessment of all our patients, because really, it helps us with the communication piece to our patients, and convey to our patients, did you know you are at high-risk because of this? And now, this adds to your chances of getting advanced periodontal disease. By having a risk assessment, you’re actually getting some accurate diagnostic readings, which will then help you customize your treatment plan for the patient. And maybe your risk assessment might give you a clue to say, maybe I don’t want to proceed with treatment today, based on the risk assessment I’ve done for this patient. So there is definite value. It’s time-consuming, but there’s value to risk assessment. Once we have a risk assessment, we can actually modify the risk or minimize the risk and mitigate the risk by maybe having more frequent dental hygiene visits. Maybe we’ll counsel them on smoking cessation or nutrition counseling– the hormonal variations perhaps to make them more aware that these are the times you really need to watch out for. Risk assessment will also help us to reach out to our interdisciplinary approach, based on the systemic disease finding, and maybe consult with their physician for a whole bunch of the medical conditions that we have identified and talked about. It may just require corrective dental surgery, or it may just need occlusal adjustment, aside from an external referral for our patient. Stress management is huge. And I have known to actually refer patients to psychologists to help them with this time in their life. So here, we reviewed the rationale for nonsurgical periodontal therapy. We discussed the diagnostic criteria for periodontal disease, and we actually went on and explained the clinical phenomena, the prevalence, the incidence of periodontal disease, and what are some of the underlying mucosal changes. We learned a lot about the new categories of periodontal disease. And so this really prepares us and makes us well-equipped to now dive into the mouth and actually deal with the periodontal status of the disease. I’d like to end the module today with a quote from Michelangelo, which says– this is actually a picture of David at the Uffizi Gallery in Florence. And there’s a story with it. As you walk up to the statue of– it’s in a big huge atrium and the Uffizi Gallery, and there’s some unfinished work of Michelangelo on either side of this corridor as you walk up into this beautiful dome. And there’s David. And it’s a magnificent piece of art. And it was told that when– first of all, when Michelangelo started working on this piece of marble, it was discarded by another sculptor as not being a good piece and not workable. And Donatello says, no. I’ll take that piece and I will work with it and create a David from it, of course. But when he unveiled it in the piazza, when he completed David after months and months of laborious work, people asked him, my goodness. How did you manage to create David? It’s just absolutely magnificent. And it’s told that Michelangelo pauses and says, “I just remove the pieces of marble that don’t represent my image of David.” And I think in a lot of ways in our dental world, we have an image of how we want the gums to project from patient’s mouth. What does “healthy” look like? What do we want for our patients? So in our rights, I feel we are Michelangelo’s of our dental world, as well, helping our patients achieve optimum health and really reduce the risk of pathogenesis in their mouth. Thank you for joining us. Good bye.

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