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--- home:diseases:periodontal [01.25.2019] – [Notes and comments] sallieq
+++ home:diseases:periodontal [09.14.2022] (current) – external edit 127.0.0.1
@@ Line 6: / Line 6: @@
-The tooth provides a surface for the colonization of a diverse array of bacterial species. Bacteria may attach to the tooth itself, to the epithelial surfaces (surface-lining tissue) of the gingiva or periodontal pocket, to underlying connective tissues, if exposed, and to other bacteria attached to these surfaces. In contrast to the outer surface of most parts of the body, the outer layers of the tooth do not shed, and thus microbial colonization (accumulation) is facilitated.(({{pubmed>long:9673160}}))
+The tooth provides a surface for the colonization of a diverse array of bacterial species. Bacteria may attach to the tooth itself, to the epithelial surfaces (surface-lining tissue) of the gingiva or periodontal pocket, to underlying connective tissues, if exposed, and to other bacteria attached to these surfaces. In contrast to the outer surface of most parts of the body, the outer layers of the tooth do not shed, and thus microbial colonization (accumulation) is facilitated.(({{pmid>long:9673160}}))
-Periodontal disease is broadly classified as either gingivitis (inflammation of the gums) or periodontitis (inflammation of the ligaments and bones). Periodontitis is an ancient disease — fossil evidence demonstrates that our early ancestors experienced the localized alveolar bone loss around tooth root surfaces that is a hallmark of the disease. The loss of this bone, which supports the root structure of the tooth, leads to the eventual loss of the tooth.(({{pubmed>long:20514045}}))
+Periodontal disease is broadly classified as either gingivitis (inflammation of the gums) or periodontitis (inflammation of the ligaments and bones). Periodontitis is an ancient disease — fossil evidence demonstrates that our early ancestors experienced the localized alveolar bone loss around tooth root surfaces that is a hallmark of the disease. The loss of this bone, which supports the root structure of the tooth, leads to the eventual loss of the tooth.(({{pmid>long:20514045}}))
 While gingivitis is a reversible condition, affecting only the gingival tissue, it is a precursor to periodontitis. The transition from gingivitis to periodontitis may vary from weeks to years. Periodontitis is associated with attachment loss (teeth falling out) or alveolar bone loss.
@@ Line 16: / Line 16: @@
 <blockquote>Periodontal diseases are polymicrobial and reflect sequential colonization by a broad array of bacteria in the transition from a healthy subgingival biofilm to a diseased subgingival biofilm. While periodontal diseases are polymicrobial and reflect sequential colonization by a broad array of bacteria in the transition from a healthy subgingival biofilm to a diseased subgingival biofilm, the molecular mechanisms and synergism among the genera and species in the disease are not well understood.
-//**Lakshmyya Kesavalu** et al.//(({{pubmed>long:17210663}}))
+//**Lakshmyya Kesavalu** et al.//(({{pmid>long:17210663}}))
 </blockquote>
@@ Line 24: / Line 24: @@
   * **periodontal disease** –  disease that affect one or more of the periodontal tissues; broadly classified as either gingivitis or periodontitis
   * **periodontitis** – inflammation and infection of the ligaments and bones that support the teeth (alveolar bone)
-  * **gingivitis** – inflammation of the gums (gingiva); gingivitis always precedes periodontitis;(({{pubmed>long:765622}})) characterized by gingival redness, swelling, and bleeding provoked by a periodontal probe, brushing, or flossing
+  * **gingivitis** – inflammation of the gums (gingiva); gingivitis always precedes periodontitis;(({{pmid>long:765622}})) characterized by gingival redness, swelling, and bleeding provoked by a periodontal probe, brushing, or flossing
-Periodontitis is a major cause of tooth loss in adults. Almost 15 percent of the population in the United States (50 million) suffer from significant periodontal disease.(({{pubmed>long:2066519}})) A second study estimates that 116 million Americans suffer from periodontal disease.(({{pubmed>long:10965470}})) Moreover, approximately 50 percent of adults have gingivitis around more than six teeth.(({{pubmed>long:9526927}})) The prevalence of periodontal disease is closely associated with the level of oral hygiene.
+Periodontitis is a major cause of tooth loss in adults. Almost 15 percent of the population in the United States (50 million) suffer from significant periodontal disease.(({{pmid>long:2066519}})) A second study estimates that 116 million Americans suffer from periodontal disease.(({{pmid>long:10965470}})) Moreover, approximately 50 percent of adults have gingivitis around more than six teeth.(({{pmid>long:9526927}})) The prevalence of periodontal disease is closely associated with the level of oral hygiene.
-[{{ :home:diseases:proalchengduchina2009revised.007.png?400|**The mouth is filled with hundreds of species, many of them known pathogens as Nasidzie showed in this [[http://www.ncbi.nlm.nih.gov/pubmed/19251737|2009 metagenomic analysis]].**}}]
+[{{ :home:diseases:proalchengduchina2009revised.007.png?400|**The mouth is filled with hundreds of species, many of them known pathogens as Nasidzie showed in this [[https://www.ncbi.nlm.nih.gov/pubmed/19251737|2009 metagenomic analysis]].**}}]
 ===== Detecting bacteria =====
 <relatedarticle> [[home:pathogenesis:microbiota:detecting|Detecting bacteria]]</article>
-Given its accessibility, the oral microbiome can easily be measured. Unlike, say, the kidney microbiome, institutional review boards rarely have reservations about researchers taking salivary samples. As a result, the microbial consortiums in dental plaque has become, according to a 2010 assessment, the most highly characterized in humans.(({{pubmed>long:20514045}})) This ease of detection may account for why evidence of the role of microbes in periodontal disease has been stronger than other diseases to date.
+Given its accessibility, the oral microbiome can easily be measured. Unlike, say, the kidney microbiome, institutional review boards rarely have reservations about researchers taking salivary samples. As a result, the microbial consortiums in dental plaque has become, according to a 2010 assessment, the most highly characterized in humans.(({{pmid>long:20514045}})) This ease of detection may account for why evidence of the role of microbes in periodontal disease has been stronger than other diseases to date.
 ==== Culture-based studies ====
-Culture-based studies have long identified substantial and diverse groups of bacteria living in the oral cavity. For example, in a 1971 analysis of the gingival crevice of healthy adults, the total microscopic counts averaged 2.7 x 10<sup>11</sup> microorganisms per gram of wet weight.(({{pubmed>long:4935491}})) The total cultivatable anaerobic bacteria averaged 1.8 x 10<sup>11</sup> microorganisms per gram, whereas facultative bacteria averaged 2.2 x 10<sup>10</sup> microorganisms per gram, which is an eightfold difference. Overall, //Streptococcus, Peptostreptococcus, Veillonella, Lactobacillus, Corynebacterium,// and //Actinomyces// accounted for more than 80% of the total cultivatable oral flora.
+Culture-based studies have long identified substantial and diverse groups of bacteria living in the oral cavity. For example, in a 1971 analysis of the gingival crevice of healthy adults, the total microscopic counts averaged 2.7 x 10<sup>11</sup> microorganisms per gram of wet weight.(({{pmid>long:4935491}})) The total cultivatable anaerobic bacteria averaged 1.8 x 10<sup>11</sup> microorganisms per gram, whereas facultative bacteria averaged 2.2 x 10<sup>10</sup> microorganisms per gram, which is an eightfold difference. Overall, //Streptococcus, Peptostreptococcus, Veillonella, Lactobacillus, Corynebacterium,// and //Actinomyces// accounted for more than 80% of the total cultivatable oral flora.
 ==== Molecular analyses ====
-However, results of surveys with molecular tools indicate a level of diversity in the human subgingival microflora that cannot be recognized by conventional culture techniques.(({{pubmed>long:10588742}})) More than 700 bacterial species from the oral cavity have been identified.(({{pubmed>long:11371542}})) In most instances, the cultivatable microflora probably represent less than 1% of the total extant population, as estimated by microscopy or other means.(({{pubmed>long:12620860}}))
+However, results of surveys with molecular tools indicate a level of diversity in the human subgingival microflora that cannot be recognized by conventional culture techniques.(({{pmid>long:10588742}})) More than 700 bacterial species from the oral cavity have been identified.(({{pmid>long:11371542}})) In most instances, the cultivatable microflora probably represent less than 1% of the total extant population, as estimated by microscopy or other means.(({{pmid>long:12620860}}))
-In 2009, Nasidze //et al.// used 16S ribosomal RNA (rRNA) sequences from saliva samples from 120 healthy individuals (10 individuals from each of 12 worldwide locations).(({{pubmed>long:19251737}})) The sequences found could be assigned to 101 known bacterial genera, of which 39 were not previously reported from the human oral cavity. The team found there is high diversity in the salivary microbiome within and between individuals, but little geographic structure.
+In 2009, Nasidze //et al.// used 16S ribosomal RNA (rRNA) sequences from saliva samples from 120 healthy individuals (10 individuals from each of 12 worldwide locations).(({{pmid>long:19251737}})) The sequences found could be assigned to 101 known bacterial genera, of which 39 were not previously reported from the human oral cavity. The team found there is high diversity in the salivary microbiome within and between individuals, but little geographic structure.
 ===== Evidence of infectious cause =====
-Overwhelming data exist indicating that bacteria initiate the major mechanisms of destruction of the periodontium.(({{pubmed>long:9673160}}))
+Overwhelming data exist indicating that bacteria initiate the major mechanisms of destruction of the periodontium.(({{pmid>long:9673160}}))
-  * **Correlation between plaque and gingivitis** – There is a positive correlation between the amount of bacterial plaque and the severity of gingivitis and amount of bone loss in cross-sectional studies of human populations.(({{pubmed>long:9673160}}))
+  * **Correlation between plaque and gingivitis** – There is a positive correlation between the amount of bacterial plaque and the severity of gingivitis and amount of bone loss in cross-sectional studies of human populations.(({{pmid>long:9673160}}))
-  * **Antibody response to microbes** – Numerous studies indicate that subjects with destructive periodontal diseases show an elevated serum antibody response to specific subgingival organisms.(({{pubmed>long:9673160}}))
+  * **Antibody response to microbes** – Numerous studies indicate that subjects with destructive periodontal diseases show an elevated serum antibody response to specific subgingival organisms.(({{pmid>long:9673160}}))
-  * **Pathogenic potential of plaque bacteria** – Human bacterial plaque has demonstrated pathogenic potential when implanted into outside the mouth to sites such as subcutaneous destructive abscesses in humans or in experimental animals. A number of toxic products can be detected in dental plaque, including endotoxins, and cell wall mucopeptides. In addition, enzymes have been shown to be produced by whole plaque or individual microorganisms from plaque that can be demonstrated to hydrolyze a wide variety of tissue constituents. Finally, it must be pointed out that the bacterial masses that accumulate at or in the gingival sulcus possess an array of antigens and possibly polyclonal activators capable of triggering sequences of host-mediated events that have been postulated as mechanisms of tissue destruction.(({{pubmed>long:9673160}}))
+  * **Pathogenic potential of plaque bacteria** – Human bacterial plaque has demonstrated pathogenic potential when implanted into outside the mouth to sites such as subcutaneous destructive abscesses in humans or in experimental animals. A number of toxic products can be detected in dental plaque, including endotoxins, and cell wall mucopeptides. In addition, enzymes have been shown to be produced by whole plaque or individual microorganisms from plaque that can be demonstrated to hydrolyze a wide variety of tissue constituents. Finally, it must be pointed out that the bacterial masses that accumulate at or in the gingival sulcus possess an array of antigens and possibly polyclonal activators capable of triggering sequences of host-mediated events that have been postulated as mechanisms of tissue destruction.(({{pmid>long:9673160}}))
-  * **Experimental animal models** – Studies in experimental animals have added considerable support to the hypothesis of the significant role of microorganisms in the etiology of periodontal disease.  Germ-free animals are essentially free of periodontal destruction. Minimal observable inflammation or pocket formation and only minor.  The use of antibiotics or antiseptics in a variety of animal model systems controls the soft tissue pathology and most of the hard tissue destruction in these animals. Periodontal disease can be transmitted from an animal harboring the disease to one initially free of it by caging diseased and disease-free animals together or by the implantation of plaque or specific microorganisms derived from the plaque of diseased animals. In addition, certain microorganisms isolated from human periodontal pockets can initiate periodontal destruction in several animal model systems.(({{pubmed>long:9673160}}))
+  * **Experimental animal models** – Studies in experimental animals have added considerable support to the hypothesis of the significant role of microorganisms in the etiology of periodontal disease.  Germ-free animals are essentially free of periodontal destruction. Minimal observable inflammation or pocket formation and only minor.  The use of antibiotics or antiseptics in a variety of animal model systems controls the soft tissue pathology and most of the hard tissue destruction in these animals. Periodontal disease can be transmitted from an animal harboring the disease to one initially free of it by caging diseased and disease-free animals together or by the implantation of plaque or specific microorganisms derived from the plaque of diseased animals. In addition, certain microorganisms isolated from human periodontal pockets can initiate periodontal destruction in several animal model systems.(({{pmid>long:9673160}}))
@@ Line 69: / Line 69: @@
-  * **[[home:diseases:alzheimers_dementia|Dementia]]** – The immunosuppression caused by increased numbers of pathogens doesn't just affect the spread of microbes in the heart. For example, researchers at Vasant Hirani at University College London found that elderly people who have lost their teeth are at more than three-fold greater risk of memory problems and dementia.(({{pubmed>long:17767683}}))
+  * **[[home:diseases:alzheimers_dementia|Dementia]]** – The immunosuppression caused by increased numbers of pathogens doesn't just affect the spread of microbes in the heart. For example, researchers at Vasant Hirani at University College London found that elderly people who have lost their teeth are at more than three-fold greater risk of memory problems and dementia.(({{pmid>long:17767683}}))
-  * **[[home:diseases:diabetes2|Diabetes]]** – Poorly controlled diabetes may be a risk factor for increased severity of periodontitis and poor response to periodontal treatment. Some studies have shown that patients with poor control of diabetes and severe periodontitis show improvement in their A1c levels, as well as decrease in periodontal inflammation, with treatment of the periodontitis.(({{pubmed>long:11314885}})) (({{pubmed>long:15766369}}))
+  * **[[home:diseases:diabetes2|Diabetes]]** – Poorly controlled diabetes may be a risk factor for increased severity of periodontitis and poor response to periodontal treatment. Some studies have shown that patients with poor control of diabetes and severe periodontitis show improvement in their A1c levels, as well as decrease in periodontal inflammation, with treatment of the periodontitis.(({{pmid>long:11314885}})) (({{pmid>long:15766369}}))
-  * **Pancreatic cancer** – Particular types of mouth bacteria, some of which are found in gum disease, are associated with the development of pancreatic cancer, indicates a small study published online in the journal //Gut//.(({{pubmed>long:21994333}})) The authors base their findings on an initial comparison of the bacteria found in the spit of 10 patients with pancreatic cancer, which had not yet spread, and 10 healthy people, matched for age and sex. They found significant differences between the bacterial colonies in the two groups, with 31 additional species and 25 fewer species in the spit of the cancer patients. They then checked spit samples from a further 28 pancreatic cancer patients and 28 healthy people to verify their findings. And they checked tissue samples from 28 patients with chronic inflammation of the pancreas (chronic pancreatitis), which is associated with an increased risk of developing pancreatic cancer. Among six suspicious species, two -- //Neisseria elongata// and //Streptococcus mitis// -- showed up significantly less often in the mouths of the cancer patients than in those of their healthy peers, while levels of another species -- //Granulicatella adjacens// -- were significantly higher. The combination of //N. elongata// and //S. mitis// accurately differentiated between healthy patients and those with cancer in more than 80% cases. Furthermore, they found similar differences in the prevalence of //S. mitis// and //G. adjacens// between the chronic pancreatitis samples and the spit of healthy people.
+  * **Pancreatic cancer** – Particular types of mouth bacteria, some of which are found in gum disease, are associated with the development of pancreatic cancer, indicates a small study published online in the journal //Gut//.(({{pmid>long:21994333}})) The authors base their findings on an initial comparison of the bacteria found in the spit of 10 patients with pancreatic cancer, which had not yet spread, and 10 healthy people, matched for age and sex. They found significant differences between the bacterial colonies in the two groups, with 31 additional species and 25 fewer species in the spit of the cancer patients. They then checked spit samples from a further 28 pancreatic cancer patients and 28 healthy people to verify their findings. And they checked tissue samples from 28 patients with chronic inflammation of the pancreas (chronic pancreatitis), which is associated with an increased risk of developing pancreatic cancer. Among six suspicious species, two -- //Neisseria elongata// and //Streptococcus mitis// -- showed up significantly less often in the mouths of the cancer patients than in those of their healthy peers, while levels of another species -- //Granulicatella adjacens// -- were significantly higher. The combination of //N. elongata// and //S. mitis// accurately differentiated between healthy patients and those with cancer in more than 80% cases. Furthermore, they found similar differences in the prevalence of //S. mitis// and //G. adjacens// between the chronic pancreatitis samples and the spit of healthy people.
   * **obesity** – A 2011 cross-sectional study of obese adolescents versus normal weight subjects collected saliva performed a metagenomic analysis on that saliva. The study found that obese subjects had //Campylobacter rectus// and //Neisseria mucosa// in sixfold higher amounts than controls.[cite needed]((Microbiota in the Oral Subgingival Biofilm))
-  * **joint failure** – In a study of 36 patients with hip or knee joint failure, bacterial DNA from the synovial fluid was found to match microbial DNA from periodontal tissue in five patients.(({{pubmed>long:22426587}}))
+  * **joint failure** – In a study of 36 patients with hip or knee joint failure, bacterial DNA from the synovial fluid was found to match microbial DNA from periodontal tissue in five patients.(({{pmid>long:22426587}}))
 ==== Cause vs. effect====
-The correlations seen between periodontal disease and cardiovascular disease could be related to the transmission of microbes from one infectious site to another. However, it seems more likely that when periodontal disease arises at the same time as other inflammatory conditions, these conditions are the result of the same underlying disease process. In this sense, periodontal disease does not necessarily cause cardiovascular disease, or vise versa. Rather, as the immune system in the entire body is weakened by an increasingly pathogenic microbiota, the body finds it more difficult to control microbial virulence in several body sites at once. Notably, //Porphyromonas gingivalis//, a periodontal pathogen associated with various forms of marginal periodontitis, is present in periodontal pockets undergoing destruction as well as in healthy gingival margins.(({{pubmed>long:20712638}}))
+The correlations seen between periodontal disease and cardiovascular disease could be related to the transmission of microbes from one infectious site to another. However, it seems more likely that when periodontal disease arises at the same time as other inflammatory conditions, these conditions are the result of the same underlying disease process. In this sense, periodontal disease does not necessarily cause cardiovascular disease, or vise versa. Rather, as the immune system in the entire body is weakened by an increasingly pathogenic microbiota, the body finds it more difficult to control microbial virulence in several body sites at once. Notably, //Porphyromonas gingivalis//, a periodontal pathogen associated with various forms of marginal periodontitis, is present in periodontal pockets undergoing destruction as well as in healthy gingival margins.(({{pmid>long:20712638}}))
 ===== Successive infection =====
@@ Line 90: / Line 90: @@
-Microorganisms were first considered as possible aetiological agents of periodontitis in the late 1800s, when the germ theory of disease changed our understanding of disease aetiologies. Failure to identify a specific pathogen in the polymicrobial community dampened the enthusiasm for a microbial aetiology, and other causes for perionditis, such as trauma or disuse atrophy, were proposed. Finally, however, the resolution of gingival inflammation after the physical removal of dental plaque during routine dental cleanings led to the "nonspecific plaque" hypothesis. The premise of this hypothesis is that the quantity of dental plaque is more important to disease pathogenesis than the identity of the individual bacterial species present.(({{pubmed>long:20514045}}))
+Microorganisms were first considered as possible aetiological agents of periodontitis in the late 1800s, when the germ theory of disease changed our understanding of disease aetiologies. Failure to identify a specific pathogen in the polymicrobial community dampened the enthusiasm for a microbial aetiology, and other causes for perionditis, such as trauma or disuse atrophy, were proposed. Finally, however, the resolution of gingival inflammation after the physical removal of dental plaque during routine dental cleanings led to the "nonspecific plaque" hypothesis. The premise of this hypothesis is that the quantity of dental plaque is more important to disease pathogenesis than the identity of the individual bacterial species present.(({{pmid>long:20514045}}))
-Today, periodontal disease may be the most widely accepted example of successive infection, an infectious cascade of pathogens in which initial infectious agents slow the immune response and make it easier for subsequent infections to proliferate. Consistent with successive infection, no single bacterial species has been shown to be responsible for triggering the inflammatory host responses seen in periodontal disease.(({{pubmed>long:17210663}})) The sequential colonization by a broad array of bacteria in periodontal disease has been described by several commentators((Brogden, K. A. 2002. Polymicrobial diseases of animals and humans, p. 3-20. In K. Brogden and J. Guthmiller (ed.), Polymicrobial diseases. ASM Press, Washington, DC.)) (({{pubmed>long:14530302}})) (({{pubmed>long:15330940}})) (({{pubmed>long:15853940}})) (({{pubmed>long:9495612}})) as well as Darveau:
+Today, periodontal disease may be the most widely accepted example of successive infection, an infectious cascade of pathogens in which initial infectious agents slow the immune response and make it easier for subsequent infections to proliferate. Consistent with successive infection, no single bacterial species has been shown to be responsible for triggering the inflammatory host responses seen in periodontal disease.(({{pmid>long:17210663}})) The sequential colonization by a broad array of bacteria in periodontal disease has been described by several commentators((Brogden, K. A. 2002. Polymicrobial diseases of animals and humans, p. 3-20. In K. Brogden and J. Guthmiller (ed.), Polymicrobial diseases. ASM Press, Washington, DC.)) (({{pmid>long:14530302}})) (({{pmid>long:15330940}})) (({{pmid>long:15853940}})) (({{pmid>long:9495612}})) as well as Darveau:
-<blockquote>Similarly to other polymicrobial diseases(({{pubmed>long:17699621}})) (({{pubmed>long:18487399}})) (({{pubmed>long:19394334}})), periodontitis has been characterized as a microbial-shift disease owing to a well-characterized shift in the microorganisms that are present (from mostly Gram-positive to mostly Gram-negative species(({{pubmed>long:9673160}}))) during the transition from periodontal health to periodontal disease.(({{pubmed>long:7865085}}))
+<blockquote>Similarly to other polymicrobial diseases(({{pmid>long:17699621}})) (({{pmid>long:18487399}})) (({{pmid>long:19394334}})), periodontitis has been characterized as a microbial-shift disease owing to a well-characterized shift in the microorganisms that are present (from mostly Gram-positive to mostly Gram-negative species(({{pmid>long:9673160}}))) during the transition from periodontal health to periodontal disease.(({{pmid>long:7865085}}))
-//**Richard P. Darveau**// (({{pubmed>long:20514045}}))</blockquote>
+//**Richard P. Darveau**// (({{pmid>long:20514045}}))</blockquote>
-Three of the periodontal pathogens, //Porphyromonas gingivalis, Treponema denticola,// and //Tannerella forsythia//, are commonly coisolated or identified in subgingival biofilm samples from adult periodontitis lesions.(({{pubmed>long:15853935}})) (({{pubmed>long:15853940}})) (({{pubmed>long:9495612}}))  Increased numbers of several other bacterial species, including //Campylobacter rectus, Eubacterium nodatum, Prevotella spp., Peptostreptococcus micros,// and //Streptococcus intermedius//, as well as //Fusobacterium nucleatum//, have also been observed in deep periodontal pockets, and the presence of these organisms is positively correlated with increased probing depth and progressive periodontal ligament attachment loss (({{pubmed>long:15330940}})) (({{pubmed>long:11018133}})) (({{pubmed>long:15853940}})) (({{pubmed>long:9495612}})) These bacteria generally represent commensal opportunistic pathogens found at low levels at healthy sites; however, under the appropriate microenvironmental conditions, currently not well defined, they contribute to triggering periodontal disease progression.(({{pubmed>long:15853940}})) (({{pubmed>long:9495612}}))
+Three of the periodontal pathogens, //Porphyromonas gingivalis, Treponema denticola,// and //Tannerella forsythia//, are commonly coisolated or identified in subgingival biofilm samples from adult periodontitis lesions.(({{pmid>long:15853935}})) (({{pmid>long:15853940}})) (({{pmid>long:9495612}}))  Increased numbers of several other bacterial species, including //Campylobacter rectus, Eubacterium nodatum, Prevotella spp., Peptostreptococcus micros,// and //Streptococcus intermedius//, as well as //Fusobacterium nucleatum//, have also been observed in deep periodontal pockets, and the presence of these organisms is positively correlated with increased probing depth and progressive periodontal ligament attachment loss (({{pmid>long:15330940}})) (({{pmid>long:11018133}})) (({{pmid>long:15853940}})) (({{pmid>long:9495612}})) These bacteria generally represent commensal opportunistic pathogens found at low levels at healthy sites; however, under the appropriate microenvironmental conditions, currently not well defined, they contribute to triggering periodontal disease progression.(({{pmid>long:15853940}})) (({{pmid>long:9495612}}))
 ==== Synergistic activity of periodontal microbiota ====
-In a 2007 study, groups of rats were infected with either //Porphyromonas gingivalis//, //Treponema denticola//, or //Tannerella forsythia// in monomicrobial infections or with all three species in polymicrobial oral infections with or without //Fusobacterium nucleatum//. Radiographic measurement of alveolar bone resorption showed that rats infected with the polymicrobial consortium with or without //F. nucleatum// exhibited significantly increased alveolar bone resorption compared to the resorption in uninfected control rats, as well as the resorption in rats infected with one of the microbes. Kesavalu //et al.// were able to conclude that these microbes acted synergystically resulting in the immunoinflammatory bone resorption characteristic of periodontitis.(({{pubmed>long:17210663}}))
+In a 2007 study, groups of rats were infected with either //Porphyromonas gingivalis//, //Treponema denticola//, or //Tannerella forsythia// in monomicrobial infections or with all three species in polymicrobial oral infections with or without //Fusobacterium nucleatum//. Radiographic measurement of alveolar bone resorption showed that rats infected with the polymicrobial consortium with or without //F. nucleatum// exhibited significantly increased alveolar bone resorption compared to the resorption in uninfected control rats, as well as the resorption in rats infected with one of the microbes. Kesavalu //et al.// were able to conclude that these microbes acted synergystically resulting in the immunoinflammatory bone resorption characteristic of periodontitis.(({{pmid>long:17210663}}))
@@ Line 116: / Line 116: @@
 ===== Periodontal microbes slow innate immune activity =====
-In healthy periodontal tissue, all microbes, even commensal bacteria, elicit a robust innate immune response.(({{pubmed>long:19161412}})) (({{pubmed>long:12960260}})) However, in tissue consistent with periodontal disease, innate immune activity is slowed by microbes. This is particularly well-documented in the pathogens known as the "red-complex organisms" – //Porphyromonas gingivalis, Tannerella forsythia,// and //Treponema denticola// – but virulence activity such as inhibition of IL-8 (see below) is present even in commensal microbes.(({{pubmed>long:20514045}}))
+In healthy periodontal tissue, all microbes, even commensal bacteria, elicit a robust innate immune response.(({{pmid>long:19161412}})) (({{pmid>long:12960260}})) However, in tissue consistent with periodontal disease, innate immune activity is slowed by microbes. This is particularly well-documented in the pathogens known as the "red-complex organisms" – //Porphyromonas gingivalis, Tannerella forsythia,// and //Treponema denticola// – but virulence activity such as inhibition of IL-8 (see below) is present even in commensal microbes.(({{pmid>long:20514045}}))
-  * **Inhibition of the chemokine IL-8** – IL-8 is an important chemokine responsible for recruiting neutrophils to phagocytose the antigen, which in triggers the antigen pattern toll-like receptors such as TLR4. //P. gingivalis//, the best characterized periopathogen, can inhibit host defense functions — including the gingival epithelial secretion of IL-8 that is induced by other oral bacteria — by several mechanisms. One way is through production of phosphoserine phosphatase SerB, which contributes to the inhibition of IL-8. Synthesis of SerB is induced on contact with gingival epithelial cells and may modify normal host cell functions to create a suitable intracellular environment for the bacteria. This  virulence mechanism, known as "local chemokine paralysis" impairs the production of IL-8 in clinically healthy tissue. Once the innate immune status of the periodontal pocket is compromised by the reduction in IL-8 secretion, neutrophil transit may be disrupted, resulting in an increase in the number and types of bacteria in the dental plaque.(({{pubmed>long:20514045}}))
+  * **Inhibition of the chemokine IL-8** – IL-8 is an important chemokine responsible for recruiting neutrophils to phagocytose the antigen, which in triggers the antigen pattern toll-like receptors such as TLR4. //P. gingivalis//, the best characterized periopathogen, can inhibit host defense functions — including the gingival epithelial secretion of IL-8 that is induced by other oral bacteria — by several mechanisms. One way is through production of phosphoserine phosphatase SerB, which contributes to the inhibition of IL-8. Synthesis of SerB is induced on contact with gingival epithelial cells and may modify normal host cell functions to create a suitable intracellular environment for the bacteria. This  virulence mechanism, known as "local chemokine paralysis" impairs the production of IL-8 in clinically healthy tissue. Once the innate immune status of the periodontal pocket is compromised by the reduction in IL-8 secretion, neutrophil transit may be disrupted, resulting in an increase in the number and types of bacteria in the dental plaque.(({{pmid>long:20514045}}))
-  * **Modulation of signalling in "lipid rafts"** – //P. gingivalis// has also been shown to interfere with an innate host defence protection mechanism by inducing crosstalk between TLR2 and CXC-chemokine receptor 4 (CXCR4) after they are recruited to a lipid raft in response to //P. gingivalis fimbriae//. This crosstalk attenuates the protective and bactericidal response to P. gingivalis. These findings provide another example of how bacteria manipulate the intricate regulatory mechanisms of host cells to survive in the host.(({{pubmed>long:20514045}}))
+  * **Modulation of signalling in "lipid rafts"** – //P. gingivalis// has also been shown to interfere with an innate host defence protection mechanism by inducing crosstalk between TLR2 and CXC-chemokine receptor 4 (CXCR4) after they are recruited to a lipid raft in response to //P. gingivalis fimbriae//. This crosstalk attenuates the protective and bactericidal response to P. gingivalis. These findings provide another example of how bacteria manipulate the intricate regulatory mechanisms of host cells to survive in the host.(({{pmid>long:20514045}}))
-  * **Directly antagonizing TLR4 through production of Lipid A** – The red-complex bacteria have been shown to also inhibit innate host defense by producing a lipid A structure that acts as a TLR4 antagonist. One experiment showed that a TLR4 antagonist decreased beta-defensin expression, a key family of antimicrobial peptides.(({{pubmed>long:19675119}}))
+  * **Directly antagonizing TLR4 through production of Lipid A** – The red-complex bacteria have been shown to also inhibit innate host defense by producing a lipid A structure that acts as a TLR4 antagonist. One experiment showed that a TLR4 antagonist decreased beta-defensin expression, a key family of antimicrobial peptides.(({{pmid>long:19675119}}))
-The naturally occurring proteins in the human salivary proteins varies according to age.(({{pubmed>long:19591489}}))
+The naturally occurring proteins in the human salivary proteins varies according to age.(({{pmid>long:19591489}}))
 ===== Pathophysiology of alveolar bone and teeth resorption =====
@@ Line 131: / Line 131: @@
 ===== Microbes adhere to some root canal filling materials and sealers =====
-Certain microorganisms have a high affinity to some root canal filling materials and sealers, especially to one named "gutta-percha."(({{pubmed>long:21846541}})) Those microbes were //Enterococcus faecalis, Streptococcus mutans, Streptococcus sanguis,// and //Prevotella nigrescens.// Because of this high level of bacterial adhesion, subsequent biofilm formation on these materials could lead to the persistence of microorganisms in root canals.
+Certain microorganisms have a high affinity to some root canal filling materials and sealers, especially to one named "gutta-percha."(({{pmid>long:21846541}})) Those microbes were //Enterococcus faecalis, Streptococcus mutans, Streptococcus sanguis,// and //Prevotella nigrescens.// Because of this high level of bacterial adhesion, subsequent biofilm formation on these materials could lead to the persistence of microorganisms in root canals.
@@ Line 146: / Line 146: @@
 While human subgingival plaque harbors more than 500 bacterial species, considerable research has shown that Porphyromonas gingivalis, a Gram-negative anaerobic bacterium, is the major etiologic agent which contributes to chronic periodontitis. This black-pigmented bacterium produces a myriad of virulence factors that cause destruction to periodontal tissues either directly or indirectly by modulating the host inflammatory response.
-Various studies have shown that periodontitis occurs more often among patients with systemic diseases such as diabetes mellitus, AIDS, leukemia, and Down’s syndrome. (({{pubmed>long:26903954}}))</blockquote>
+Various studies have shown that periodontitis occurs more often among patients with systemic diseases such as diabetes mellitus, AIDS, leukemia, and Down’s syndrome. (({{pmid>long:26903954}}))</blockquote>
-Oil pulling is a traditional folk remedy practiced in ancient India. It is believed to cure more than thirty systemic diseases when practiced regularly and as directed.   (({{pubmed>long:28053895}}))
+Oil pulling is a traditional folk remedy practiced in ancient India. It is believed to cure more than thirty systemic diseases when practiced regularly and as directed.   (({{pmid>long:28053895}}))
 ===== Patients experiences =====
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 {{tag>disease}}
+<nodisp>
 ===== Notes and comments =====
@@ Line 283: / Line 284: @@
-  (({{pubmed>long:000}}))
+  (({{pmid>long:000}}))
@@ Line 323: / Line 324: @@
-===== References =====
+===== References =====</nodisp>

home/diseases/periodontal.1548456576.txt.gz · Last modified: 01.25.2019 by sallieq