Dental Plaque PDF

So let's start with the definition of the dental plaque. It's a general term for the complex microbial community that develops on the two surfaces. It's embedded in the matrix of proteins or polymers of bacteria and saliva origin, which is yellowish color. Of course, it's the primary cause of that c...

So let's start with the definition of the dental plaque. It's a general term for the complex microbial community that develops on the two surfaces. It's embedded in the matrix of proteins or polymers of bacteria and saliva origin, which is yellowish color. Of course, it's the primary cause of that caries and gingivitis and the parents and the parent plant infections that we know today. So what's your problem? It's the assembly of the cells enclosed in a matrix supply. Because the biofilm itself is the definition is a community adhere to each other and to the two surface that's non sharing. It provides circulation within the plaque to facilitate movement of the nutrients and the waste products. So we're going to go how the composition of the dental plaque is formed in natural setting. Of course, the biofilm generally takes the form of the polymer microbial communities attached to dental to surface as a surface, become colonized with individual cells. The bacteria from micro colonies, which is a minor part of 15 to 20% of gram positive and gram negative cells. That secrete sticky polymeric substance that forms a major part of the problem, which is inorganic part mostly calcium and phosphate only content includes protein, carbohydrates and lipids. It helps the bacteria to adhere to the surface and as well as to each other. So I think many of you see this on yourself, too, when you look in the mirror. But the material is different from plaque. It's a soft non minerals deposit on the surface of the teeth that is right in color. It's soft, invisible to the naked eye. The formation is because the poor hygiene, of course, and it contains the food that buries the tissue cells and microorganisms. It comprises of bacteria, leukocytes and epithelial cells and saliva proteins. If you left untreated, it leads to dental plaque. And thereby causes the disease. The soft accumulation of the dental film can be destroyed with water spray that it consists of poorly organized structure. So stains is different from the plaque that we know. So there's of course, the external stain and the intrinsic stain. External stains is mostly caused by the food that we eat. Sometimes the wines and drinks and tobacco. It causes a feeling of protein that covers the two surface so that this type is really easily removed with like profile and all these mechanical move that can be used. It's fairly easily removed. However, the intrinsic part is staining below the surface of the teeth. It can happen through the child taking tetracycline medication and fluoride use which has been associated with intrinsic stain. So calculus is a mineralized plaque that forms the two surface. In most people, it varies widely among individuals and populations or self care. Age health diet affects the formation. Calculus is contributing factor of the parent of disease. Due to the retention of the plaque, it's divided into supra genes of a part and sub ginger part where super gingival is the calculus is at or above or the substantive is below the central margin. So the composition of calculus is mostly inorganic. Inorganic content is usually cast in phosphate. Organic parts is made up of carbohydrates, proteins, lipids and traces of cells and leukocytes and microorganisms. So there can be different visualization of how the crystal formation of the calculus is formed. Mostly it's a it's usually first start from the Bruce side formation, usually on the interior, and then it becomes active calcium phosphate, which is the later part of the calculus. Then it becomes hydroxyapatite, which is more mature form of calculus forming on the Super Bowl calculus in the. And sometimes when it becomes more matured, it forms on the posterior part and sublingual, where it's a little bit more difficult to be moved. Am I going a little too fast or am I going, okay. Okay. It's simple, right? All right. Okay, now we're going to go over the stages of the plaque formation. We're going to go one by one. How the plot formation and sometimes detach and go back to the first stage. So let's go with the stage one, the formation of the condition insulin. So when we eat all it drinks something, the molecules are drove to the two surfaces within seconds, immediately after cleaning or following initial exposure of anything that you eat. So these molecules are derived from saliva, but in some gingival region, the gingival fluid is a is originating. What causes the condition of the film that we know today. So it alters the properties of the surface and bacteria interact directly with the molecules. So it can be even detected one minute after exposure and becomes in equilibrium after two hours. So you can see that there's a little two surface here and there's a lot of micro molecules that attach. So here's the part when the bacteria comes in. So first stage is the reversal of adhesion, which involves very weak interaction between the charge and the bacteria and the pellicle. So the bacteria is transported passively to the surface, to the flow flow of the saliva. And then there's the reverse adhesion. We're involved interaction between the specific molecule of the surface called adhesion and molecules called receptors that's present on the protocol. And then the cohesion happens where the secondary bacteria binds to the colonizers by the cell surface adhesions to receptors that's already attached to the bacteria. Then it becomes increasing diversity of the bacteria within the biofilm. So then the multiplication of the cells that's already attached to the surface happens that increase in biomass over time. So there is a synthesis of new auto membrane components to form the ultimately the the matrix. The matrix that's shown in the blue color is makes a significant contribution of the integrity and general tolerance of the biofilm to environmental factors such as desiccation and against the antimicrobial agents. The chemistry of the matrix may also exclude or restrict the penetration of other molecules, including some antimicrobial agents like Chlorhexidine. Now becomes more matured over time. So the close of the cells to one another. The biofilm facilitated numerous synergistic and antagonistic interactions between the neighboring species. The metabolism of the organism itself produces gradients over time. For example, the nutrients and fermentation products, the bacteria respond to these fluctuating changes in the conditions by altering the patterns of the gene expression. The gradients in plaque are not necessarily linear, as you see. It's like the regions in mosaic environments. These processes lead to the establishment of mature biofilm that's relatively now becomes stable composition over time. There can be a time where the bacteria doesn't like the environment, so they sense the changes to the environment. So if the condition does not, it's not right for them. Some species, like AA, respond by operating enzymes that cleave their adhesions to detach and colonize somewhere else. Okay. Okay, now we're going to go over the structural traits of bacteria. So there are two parts that we described, usually in arrangement and the shape. So when viewed on the light microscope, I'm sure you took like microbiology course in undergrad. So most bacteria appear in different shapes. Sometimes it can be spherical rot or a spiral shape so far or the arrangement is concerned. It can be paired. It can be grape like clusters or in chains. So when we name a bacteria, we do it by adding arrangement plus the shape of the bacteria. For example, the bacteria can exist in pairs known as duplicates or in chains or streptococcus or in clusters because they follow. Most rod shaped terror like vessel appear a single rod. But of course there can be appear in pairs after division strap to busily in chains or cells divide in one plane, spiral kits take a helical shape and flexible bodies. They move by means of axial filaments. Vibrio are the common shape of bacteria with less than one complete turn into cell. Of course, in terms of the environment, oxygen is probably the things that we need to be more concerned about because oxygen can be very toxic to some bacteria due to the formation of superoxide and hydrogen peroxide. So they can be harmful if there is no enzyme to eliminate them or the oxygen concentration is too high to survive them in the environment. So the enzymes that neutralize oxygen includes superoxide dismutase, catalase and peroxides. If the microbe does not produce any of these enzymes, they must live in the anaerobic environment. Bacteria that live in oxygen content environment have above enzymes to convert these toxic superoxide and hydrogen peroxide into oxygen and water. So I know it looks very long, but the based on the bacteria, the oxygen requirements into five main classification, the strict of the bacteria was grown in the environment with oxygen because that's how they make their ATP energy by using the aerobic respiration strict anaerobes. These bacteria live only in environments lacking oxygen. For these cells, oxygen can be lethal because they lack normal cellular defense against oxygen stress. Uh, facultative anaerobes. These bacteria typically have access to all the enzymes to protect cells from distress using oxygen, but they use the oxygen for most of the time for aerobic respiration as much as possible. Micro airflow. As the name implies, these bacteria prefer environment with oxygen, but lower level than normal environments. These bacteria make ATP by aerobic respiration, but also from sugars. Error tolerant anaerobes. These bacteria are not affected by accident by using the enzymes to neutralize it in which oxygen has no effect. I'm sure also that you may have done the screen staining for the bacteria in undergrad, so I'm just going to go over one by one what these are. The diagram illustrates the difference in structure of the gram positive and gram negative bacteria. The two key features that lead to the different visualization is of course, the is due to the thickness of the peptidoglycan layer and the presence or absence of the outer membrane. Grandfather bacteria have a thick peptidoglycan layer and have no outer lipid membrane gram negative bacteria have a thin peptidoglycan peptidoglycan layer have an outer membrane. So of course, like I said, the gram positive bacteria have distinctive purple appearance when observed on the light microscope due to the retention of the purple crystal violet. That staying in the thick layer to to the cell wall. And the gram negative, of course, is the opposite deposit because they don't have the thick layer to contain the crystal violet which appear as a red counter stain. So up to up to today. How do we characterize the biofilm, the oral cavity that we know today? Of course, there are a lot of challenges and it's difficult to characterize all of them. So right now, there are over 700 species that have been detected and or cavity over half of which was never cultivated. And second, there was substantial diversity in the microflora between individuals and the same site of the same individual. And third, of course, when we age over time, the composition of the bacteria can change. And when we eat something different and when there's poor hygiene, there's a shift in composition of the bacteria over time. However, despite these challenges, there has been progress. Some studies have identified bacteria that appear to be associated with health. For example, a positive association has been observed between the health and the presence of gram positive around the world bacteria such as Streptococcus, Midas Vennela they can be also considered as commensal microbiota because they promote oral health by resistance to colonization of not allowing cells to integrate by the oxygen is pathogens. How about oral disease? Later, in more advanced disease states such as the periodontitis, the diversity of the bacteria increases further. If composed, it is composed of surprisingly of dense filament containing plaque. And substantively, there's more gram negative rods and filaments, followed by sprockets and motile microorganisms. So here's a little diagram that shows how it changes the composition over time, as you see in the early colonization. It's mainly composed of mainly gram gram positive arrows, composed of streptococcus species, which in turn becomes more suitable for secondary colonizers acting as a bridging species and through the co-creation that allows the region of the lake colonies, including the red complex bacteria, including pigeon, devil's tea, forsythia and teeth into color. This succession induced a change in the local habitat that allows the pathogens to colonize. This difference of the one that before is that the saliva contains the thousands of free floating bacteria that progressively deposit and adhere to the surface by physical chemical means and then by specific interactions over time. So again, I just wanted to emphasize that the initial colonization, the gram positive, the population that becomes more complex, shifting progressively into gram negative, appearing more rods and filamentous organisms like Berrios and spiral kids. So this maturation of the plaque is very important because it is associated with the clinical environment, developing of the Gingival inflammation over time. So to summarize the specific complex is really to interpret it in terms of condition of the present health, local characteristics and the system of background of host. I think maybe some of you looked into this. What? How? We are divided into six different groups by Socrates group. We're going to go a little bit briefly one by one. So initially the colonization involved a blue species called the minor species, yellow, green and purple complex. They are the early colonizers. The two surface. The orange and red complex becomes more dominant over time as the disease progresses. One of the fun things that we know is that red complex can't exist without the orange complex. However, the the one primary colonies are like blue, yellow, green and purple complex are often even without the orange red complex. So what this means is that the absence of beneficial organisms is important as the presence of the pathogenesis. So instead of being associated with one particular agents, many chronic diseases appear to be following this microbial shift hypothesis. So Microbiome Shift refers the concept that some disease are due to the decrease in number of the beneficial symbionts or increase the number of pathogens over time. So as the President develops, the overall microorganism shifts from one particular of gram positive Arabs to one consisting of more gram negative anaerobes. So as I talked before, the biofilm consists of different physiological differences in the biofilm. So as you can see in this small environment, the particular cells of same species can exhibit different stage involvement with once very small distance of one another. The microorganisms, as I said, is in close proximity of one distance in. So as a plaque develops over time, there's a gradient and these are affect the distribution of the bacteria. The gradients in, for example, the essential nutrients and products in metabolism will develop with difference in difference in oxygen, difference in cations. So such stratification will allow enable enabling the micro colonies with different requirements to grow and ensuring the coexistence of different species over time. So overall, there is a synergistic and there's antagonistic interaction among the bacteria. In terms of synergistic, the bacteria collaborate to catalyze the complex molecules like proteins. We can also take and also use a number of bacteria that can survive in aerobic environment if they cooperate with the oxygen consuming species. Sometimes there can be a tokenistic interaction involving the production of toxic, including hydrogen peroxide and acids inhibit the growth of neighboring cells. Of course. Then we need to talk about the quorum sensing the bacteria. They can communicate like we do, relying on the chemical signaling called the auto inducers, which regulate the gene expression over time. Since the bacteria reproducing there, the more cells producing orange juice, it really eventually hits the critical mass called the quorum. So once concentration increases over time, the auto inducers bind to the receptors, triggering the cascades that change the transcription factor activity. So the change in gene expression includes deregulation of the auto industry synthesis by a negative feedback loop. So you can occur with the same single species or as well as different diverse species. So what eventually this does is that encourages the growth of bacteria of species in the biofilm, or it can sometimes discourage the growth of competing species. So you can modulate the expression of genes for antibiotic resistance, encourage the growth of very beneficial bacterial species while discouraging the growth of competing species. Okay, So now we're going to talk about how we came up with different hypothesis over time. The first hypothesis was the work based on Miller in 1988, 1890, it was thought that was the quantity of the plaque that determined the pathogenicity without discriminating between the levels of variance of bacteria. So between the believing this, the host would have the threshold capacity to detoxify the bacteria, products and disease that will eventually develop if the threshold this threshold was surpassed. The conclusion was that if any plaque has equal potential to cause disease, the best way to prevent is, of course, removal of the plaque. However, of course, as we know, all bacteria does not have the potential to cause disease. They have a different virulence factors and the improvement of technique of isolating and identifying the bacteria in the later century led to the abandoning of this hypothesis. Solos developed a specific plague hypothesis stating that only certain plaque is pathogenic, and that depends on the specific microorganisms. So development of the culture based technique and aerobic hood evolved allow the cultivation of the gram negative and anaerobic species. This proposed that inflammation can cause by specific perio pathogens and antibiotic treatment could be effective. The finding of different species lead to the disease led to the idea that all disease could be initiated by the specific disease like AA that causes locally localized, aggressive Titus. However, of course, the plague does not live alone. We need to also consider about the environmental factors that play around the microorganisms. Then in 1994, Marsh proposed a hypothesis that combined the key concepts of the early hypothesis. So in his ecological play carp hypothesis, disease is a resulting imbalance of the microflora due to the ecological stress resulting in enrichment of the some or all pathogens or disease related microorganisms. So he expanded theory that the change in microbial composition is due to the environment. For example, let's, for example, the frequent exposure of the low PH, for instance, to sugar fermentation leads to the increase in acid tolerant species. So disease can be prevented not only by inhibiting the pathogens but also interfering with the environment factors that drives the selection and growth of the selected bacteria. However, this theory does not address the important of the genetic factors that that plays a really important role causing the disease. Then later they came up with the Keystone Hypothesis. The concept is that low abundance of the pathogens can cause inflammatory disease by increasing the quantity of the normal microflora into this biotic one by controlling the host immune system by doing it. So it was known that it does not only facilitate its own survival and multiplication, but entire community. In contrast to the dominant species that can influence the inflammation by the abundant presence. So let's go with an example. So the colonization of the Keystone pathogens indicated here the poor, the pitch alters the host response that triggers the interactions that result changes in symbiotic microbiota into this biotic one. The extra base inflammation by activating the complement system. And inflammation not only promotes the prolonged Titus. But also fuze further bacterial growth by providing nutrients in the form of tissue breakdown products. So increase dysbiosis results in even greater inflammation by continuing the cycle, thereby reinforcing the cycle of inflammation tissue breakdown products from this small amount of keystone pathogen. Okay. The Cook's postulates. So this is published in 1890. This is a set of criteria that establish whether a particular organism is a cause of a particular disease. First one, of course, is that the bacterium must be isolated from the disease individual. They must be grown in pure culture and provide a similar disease when it's inoculated into susceptible animals and later it should be recovered from the disease. Lab animals that we know today. So, for example, like here we have a disease rabbit. We isolate the pathogen from the sick rabbit and we should be able to culture them. And then when we inoculate healthy one, the pathogen should be causing the same disease symptoms and we must be able to isolate them from the second sick animals. But this was too simple. Of course, in reality, it doesn't work this way. Some of the exceptions are it does not apply to every situations. For example, the microorganisms are there are some bacteria that cannot be cultured in the media like viruses. And sometimes there could be mixed infection. Two or more organisms they work work together to cause a disease. And of course, some pathogens can cause several different diseases, not only single disease and only single pathogens can cause disease. And humans only like HIV. So what they did was that they modify it by using the theory into molecular level, by application of the PCR revealed a great deal about association of the highly uncomfortable viruses that are found associated with tissues even without development of disease. So, for example, by using the molecular level, the nucleic acid sequence should be found in the disease and the sequence should be absent in healthy individual. The resolution of disease should result in decreasing patterns of associated sequences and the path that the presence of the acid in healthy individuals should predict the development of disease, and then it should be consistent and the sequence should be reproducible. Now, how how would we transport that or trans translate that in terms of present titles? But of course, the three problems in parentheses that we can apply is that it's enabled to culture all organisms associated with the disease. And it's difficult to inherit inherent or in defining the culture insights. And we don't have a good animal model for the study of the parent. Titus. So what Socrates Kita was that as the disease was not the classical disease process caused by single organisms, they derived a new set of postulates that help us to understand the risk factor for the for the parental disease. Of course, it's very similar, but we just modify a little bit. So it must be associated with the disease by increasing number of pathogens in the site. It should be eliminated or we try to suppress the mountainsides to demonstrate clinical resolution of disease. It must demonstrate host response in the form of alteration of the immune response and must be capable of causing the disease in the animal model. And we must be able to demonstrate the virulence factor responsible for the destruction of the tissue. So now we're going to go in terms of clinical point of view, of course. How do we define the Gingival plaque is based on the location of the plaque. When the plaque is above the dental margin, we say the super principal and it's below the margin. We say it's substantive. So supra gingival plaque is the multi-layered accumulation of bacteria, while the substance of a plaque. It depends on the pocket depth. That's why. Um. Surprisingly, the plug has a gram positive round and more road shaped where the substantive plaque is primarily by the anaerobic environment inside the pocket depth, which is by growing in terms of availability of the blood products in super supply. There's a gram negative rods and filament spiral kits on the outer surface of the plaque. When the sub apical part is more dominated by the gram negative spiral rods, while more corner part is predominated by the filaments. So we can also differentiate them in terms of color. That's where the super essential plug is more white, where the substantial black is more dark brown because it can be because of the local blood products. The shape in terms of general plug is more bulky or the single plug is more flat because of the pocket wall. So potential is more hard compared to the subject plug, which is more brittle. Super gingival plaque is more easily detached, while the substantive part is there, are they a little bit more firmly attached than the supercharger plaque? So of course, because the super ginger black is above the ginger, Martin is more visible. The source of supercharger plug is from saliva, or the substance of the plug is from the GCF. Supercharger plug is distributed Multi-lingual service or the subject plug is more the heaviest on the approximate surface. So what are the factors that affect the plaque formation? And of course ourselves in the oral pharynx is an open ecosystem where the bacteria are always present. Um, factors. That includes the natural factors, estrogenic factors and local defectors. So for the natural factors, the formation of play can be enhanced by the natural factors making the oral hygiene more difficult, such as the calculus and the more productions, vacation fissures, grooves, carries and crowding of teeth. So let's look at this picture. The calculus, of course, is not pathogenic. However, its rough surface act as a niche for retaining the bacteria. Vacation entrances, of course. You can see the retentive niche for the plaque and crowding makes the oral hygiene more difficult. How about the factors that we contribute as a dentist as a result of dentistry from simple restorations to more full mouth reconstruction, it can do more harm than good if it's not done properly. Some of them are subs interval Margin overhang. Open margin. So like the fillings in crown that appear to be perfect, but sometimes there's deficiencies that can cause retention for the plaque over time. So when the margins are located more substantively, the present irritation for the tissues overhang over margins, of course they accumulate more plaque over time. How about the local diet factors? This is just an example. For example, if you intake sugars like sucrose, there's acid production of the plaque that causes the PS to be lowered in 5.5, inhibiting inhibiting the growth benefit of beneficial bacteria. That further lowers the PH promoting more tolerant bacteria, which allows more carious bacteria to be promoted over time. So in clinic, how do we detect the plaque? Well, first one simple thing is we can look directly. But the thin plaque, we cannot see them. But the thick plaque, we can see them by visible eyes. But you can also use the present explorer to scrape. And if you can see the plaque or not. One of the easier that we can use is the disclosing tablet. You allow the patients to chew and spit. This dye react with the plaque and you can see in the mirror and identify the location of the plaque. And you can also use this as a in terms of giving patients or hygiene instructions to see where the patients need to focus a little more. The measurement of the hygiene is measured by the low plaque index. Grade zero is no plaque. Grade one is the film that's not visible. Grade two is moderate accumulation that can be seen with naked. Eye grade three is abundance of plaque where it's easily be seen. And you can see that if the patient doesn't do proper hygiene, where the plaque everywhere is usually grade three. So the plaque formation occurs first in the lower teeth compared to the upper teeth. More on the posterior teeth on the crossovers and between the the teeth itself and into dental areas. Are we going a little bit, talk about the two components of the inflammation. Of course, is the acute phase where the response is more rapid and short. The bacteria products trigger the junction epithelium cells to produce cytokines that causes vessel dilation, edema and polymorphic nucleotides. When it becomes more chronic over time, then the adaptive immune system kicks in involving the acquired immunity, including macrophage plasma cells, T and B cells. Clinically, the stage is more moderate to severe gingivitis, including the gingival bleeding final stage, the transition to present Titus where there is an irreversible attachment loss. So how do we define gingivitis? Is that it's inflammation caused by the plaque and between the host immune system is contained within gingiva. It does not extend to present attachment and it is reversible, but retains the level of plaque over time. One of the important features of the gingivitis is redness. Boppy changes, contour, and there should be no evidence of bone loss, and it should be reversible by removing the cause of the biofilm. So how did we know it was the low study experiment that was done in 1965? He brought patients with clinical health gingiva, but they didn't allow the patients to proper hygiene from 10 to 20 days. So time to develop gingivitis was the imagine was from 10 to 21 days without any oral hygiene. Once the oral hygiene was resumed, the gingival inflammation was reduced within a week. Like the plaque index, gingivitis Gingival index. We classify them based on what we see clinically. Grade zero is normal. Grade one is mild, but grade two is time. It's the time when we see the BOP over time. Grade three is spontaneous, bleeding and probing. So even if you don't probe, there's a chance that the patient's bleeding. Then that becomes grade three. So how do we how do we really remove the plaque? Of course, it's limited by the physical physical removal. One of them is called proof and that sort of proof. And SRP has a non surgical approach to remove the plaque. But if they do not work, then we move into open slab deployment. Like including the auto surgery. The calculus itself is also associated with disease with the rough surface. So it's important some of that we use as the hand instruments, or you can use the ultrasonic scalers. And sometimes there's now that we have a erbium lasers that can be used to remove the super substantive calculus over time. If they do not work, sometimes we can use systemic antibiotics. As for the patients with who continues to have loss of attachment even with the conventional mechanical therapy. But the study shows that usually works the best with patients with aggressive status by taking maxilla and metronidazole together. You can also work together with their sirup for patients having necrotizing ulcerative gingivitis by taking metronidazole. Of course. But I just wanted to emphasize that. You cannot skip SRP. You need to do do with that XRP as an adjunct and the system antibodies should not be used alone. And instead of systemic, now we have a locally developed antibiotics. So these are placed in the pocket in the delivery system that's released over seven days after the SRP is performed. The study shows that by doing this, so there's a decrease in pocket depth, bleeding, improving and an improvement of the clinical attachment loss. There was one called active site, which is no longer available but which was tetracycline fiber. Dox is a doxycycline gel 10%, which is also a mixture in a syringe. It's placed below the transfer margin period. Chip is a 2.5mg chlorhexidine and we can also use the Reston, but it's a minocycline microspheres one milligram, but I'm sure. But next year we're going to go over more specifically how they work over time. Another one is the host modulation therapy. As I said before, we sometimes use the antibiotic called doxycycline. If you use it as a low dosage, like about 40mg, we can use this to modify the host immune response by suppressing it. What's it called? Matrix metal proteins. So the role of this enzyme here, matrix mirror proteins is the one that plays a role in tissue destruction by causing bone loss. But if you use in very low doses. Um, there is no antibacterial activity, but it blocks this enzyme involved in tissue destruction. And there's some studies show that there's a benefit in terms of patients going through the chronic prison. Titus. So my last slide, I just wanted to emphasize how do we assess that we have done it right? We can do it in terms of biologic Stem point of view. Of course, by looking at if there's a decrease in amount of bacteria over time or what we see in mostly the clinical point of view, we need to make sure that by doing proper hygiene, giving proper phase one side and profile, or sometimes we flip development, we want to see differences in reduction of pocket depth. We want to see the gain in clinical attachment. We want to see reducing pre-op and further, we want to maintain patient compliance by going through the same amount of recall with patients as history presenters want to keep them in three month recall to make sure that we want to keep them on the same level. So that's my intellectual. I hope you learned something today.