This document discusses adhesins and receptors involved in dental plaque formation. It describes the composition of dental plaque and the types of plaque. The mechanism of plaque formation involves 5 steps: 1) formation of the acquired pellicle on the tooth surface, 2) bacterial adherence via adhesins binding to receptors in the pellicle, 3) formation of an inter-microbial matrix, 4) bacterial colonization and plaque maturation, and 5) dispersion. Specific adhesins and receptors that facilitate plaque formation are also outlined.
Periodontal diseases are caused by a complex interplay between multiple local and systemic factors that influence the host response to the bacterial biofilm (plaque) that forms on the teeth. The plaque is composed of hundreds of bacterial species organized in a matrix on the tooth surface. As plaque matures, the proportion of gram-negative anaerobic bacteria increases, enhancing its pathogenicity. Subgingival plaque is more pathogenic than supragingival plaque due to its protected location below the gumline. The composition and virulence of the plaque, as well as the host immune response, determine the severity and progression of periodontal disease.
This document summarizes a seminar presentation on dental plaque as an oral biofilm. It defines plaque, describes its structure and composition, and explains the process of plaque formation. Plaque is defined as a bacterial biofilm that adheres to tooth surfaces. It has a stratified organization and is composed of bacteria, water, extracellular matrix, and host cells. Plaque formation begins with the development of an acquired pellicle on the tooth surface, which bacteria then attach to initially through non-specific interactions. This leads to the development of dental biofilm.
A complete detailed lecture on antiplaque Shani herbal mouthwash PDF.
You'll read all details about semi herbal mouthwash.
From introduction to refrence we write all for you.
Have a good study good luck
The document discusses dental plaque, which represents a biofilm that forms on teeth. It begins by describing how plaque formation starts after birth as microorganisms colonize the oral cavity. Plaque is defined as a structural entity resulting from the colonization of microorganisms on tooth surfaces. Over time it can calcify to form calculus. Plaque formation involves an initial phase where a pellicle layer forms, followed by the adhesion and colonization of bacteria. As plaque matures it develops a complex structure and composition. Certain bacterial complexes like the red complex are associated with periodontal disease. The document also discusses the nonspecific and specific plaque hypotheses for the causes of periodontal disease.
This document discusses dental plaque (biofilm) formation and its role in health and disease. It defines dental plaque as a structured microbial community that forms on tooth surfaces. Key points: plaque forms in distinct stages, from initial bacterial adhesion to the acquired pellicle to maturation of the biofilm; the biofilm has a complex architecture and composition that allows a diverse microbial community to thrive; and dental biofilms play an important role in oral health by protecting teeth but can also cause disease if pathogens overgrow.
The document discusses biofilms, also known as dental plaque. It defines biofilms as clusters of microorganisms embedded in a self-produced matrix on surfaces. In the oral cavity, biofilms form on teeth and gums. They begin forming within hours of birth as pioneer bacteria like Streptococcus adhere. Over days and years, the biofilm becomes more complex as more species colonize. Mature dental plaque biofilms have a layered structure and are embedded in an extracellular matrix that is resistant to removal.
Periodontal diseases are caused by a complex interplay between multiple local and systemic factors that influence the host response to the bacterial biofilm (plaque) that forms on the teeth. The plaque is composed of hundreds of bacterial species organized in a matrix on the tooth surface. As plaque matures, the proportion of gram-negative anaerobic bacteria increases, enhancing its pathogenicity. Subgingival plaque is more pathogenic than supragingival plaque due to its protected location below the gumline. The composition and virulence of the plaque, as well as the host immune response, determine the severity and progression of periodontal disease.
This document summarizes a seminar presentation on dental plaque as an oral biofilm. It defines plaque, describes its structure and composition, and explains the process of plaque formation. Plaque is defined as a bacterial biofilm that adheres to tooth surfaces. It has a stratified organization and is composed of bacteria, water, extracellular matrix, and host cells. Plaque formation begins with the development of an acquired pellicle on the tooth surface, which bacteria then attach to initially through non-specific interactions. This leads to the development of dental biofilm.
A complete detailed lecture on antiplaque Shani herbal mouthwash PDF.
You'll read all details about semi herbal mouthwash.
From introduction to refrence we write all for you.
Have a good study good luck
The document discusses dental plaque, which represents a biofilm that forms on teeth. It begins by describing how plaque formation starts after birth as microorganisms colonize the oral cavity. Plaque is defined as a structural entity resulting from the colonization of microorganisms on tooth surfaces. Over time it can calcify to form calculus. Plaque formation involves an initial phase where a pellicle layer forms, followed by the adhesion and colonization of bacteria. As plaque matures it develops a complex structure and composition. Certain bacterial complexes like the red complex are associated with periodontal disease. The document also discusses the nonspecific and specific plaque hypotheses for the causes of periodontal disease.
This document discusses dental plaque (biofilm) formation and its role in health and disease. It defines dental plaque as a structured microbial community that forms on tooth surfaces. Key points: plaque forms in distinct stages, from initial bacterial adhesion to the acquired pellicle to maturation of the biofilm; the biofilm has a complex architecture and composition that allows a diverse microbial community to thrive; and dental biofilms play an important role in oral health by protecting teeth but can also cause disease if pathogens overgrow.
The document discusses biofilms, also known as dental plaque. It defines biofilms as clusters of microorganisms embedded in a self-produced matrix on surfaces. In the oral cavity, biofilms form on teeth and gums. They begin forming within hours of birth as pioneer bacteria like Streptococcus adhere. Over days and years, the biofilm becomes more complex as more species colonize. Mature dental plaque biofilms have a layered structure and are embedded in an extracellular matrix that is resistant to removal.
This document discusses the immunology of dental caries. It begins by describing how the oral flora develops from birth and the role of bacteria like Streptococcus mutans in dental caries. Dental caries is considered a biofilm-induced disease. Key points include that S. mutans is a significant pathogen in enamel caries and lactobacillus is predominant in dentinal caries. The document also discusses potential caries vaccines and notes their development has focused on subunit vaccines to avoid potential heart-reactive antibodies induced by whole cell vaccines. In conclusion, while current prevention methods are not sufficient, a successful caries vaccine could make a significant contribution to disease control.
Dental plaque forms through sequential colonization of microorganisms on tooth surfaces. It is made up of bacteria, epithelial cells, and extracellular matrix. Plaque formation involves acquired pellicle formation, reversible bacterial attachment, irreversible attachment through adhesins, microbial succession through coaggregation, and maturation of the biofilm and matrix. The microbial composition of plaque varies by oral site and influences diseases like periodontitis and dental caries. Periodontitis results from an imbalance in homeostasis allowing pathogenic bacteria to overgrow. Dental caries occurs when frequent sugar consumption in plaque favors acid-tolerant bacteria like mutans streptococci, changing the microbiota and predisposing to demineralization.
This document discusses dental biofilms, also known as dental plaque. It explains that dental biofilms are three-dimensional, multispecies microbial communities that form on teeth and other oral surfaces. The key points covered include:
- Dental biofilms provide benefits to microorganisms like increased habitat range and stress tolerance.
- They form through the adsorption of a conditioning film, followed by reversible and then permanent bacterial attachment and colonization.
- As biofilms mature, they develop complex architecture, metabolic gradients, cell signaling pathways, and interspecies interactions between diverse microbes.
- While associated with diseases like caries and periodontitis, the oral microbiome also benefits the host through commensalism
Role of dental biofilm in pathogenesis of periodontalManoj Paradhi
This document discusses the role of dental biofilm in the pathogenesis of periodontal disease. It begins by defining biofilm and dental plaque, and describing the formation of dental plaque. Key points include that plaque is a heterogeneous structure composed of bacteria, organic and inorganic materials. As plaque accumulates, certain bacteria can overwhelm the host's defenses and cause inflammation (gingivitis) or tissue destruction (periodontitis). The document then examines different periodontal diseases and associates each with certain pathogenic bacteria commonly found in the subgingival biofilm of affected individuals. It concludes that dental plaque is the main causative factor of periodontal diseases, so its removal through oral hygiene is important for periodontal health.
Dental plaque is a biofilm that forms on teeth and consists of a complex community of over 700 bacterial species. It is composed of 60-70% bacteria embedded in a matrix of 30-40% extracellular polymers, proteins and carbohydrates. Plaque forms in stages, beginning with the pellicle layer coating the tooth surface within hours, followed by colonization of primary colonizers like Streptococcus and Actinomyces. Secondary colonizers like Prevotella, Fusobacterium and Porphyromonas then adhere, forming the mature biofilm structure with stratified layers of cocci and rods. Plaque morphology demonstrates specific coaggregation of bacteria into corncob formations that contribute to pathogenesis of dental diseases.
1. The infant mouth is initially sterile at birth but is quickly colonized by bacteria from the mother or environment, usually streptococci that bind to oral surfaces.
2. As more bacteria colonize and their metabolic activity increases, the environment changes to allow colonization by other genera and species in a dynamic ecological system.
3. By age one, the normal oral flora includes streptococci, staphylococci, neisseriae, lactobacilli, and some anaerobes, with composition changing as teeth erupt and providing new niches for colonization.
Dental plaque is a biofilm that forms on teeth and consists of bacteria embedded in an intermicrobial matrix. Plaque can be classified as supragingival or subgingival depending on its location relative to the gingival margin. Plaque forms in stages beginning with the deposition of salivary proteins to form an enamel pellicle, which bacteria then attach to. Over time, plaque matures as more bacteria colonize the surface and interact with each other. The composition and microbial population of plaque can influence the development and progression of periodontal disease.
This document discusses dental plaque/biofilm, including its definition, classification, composition, properties, and factors that affect its composition. It begins by defining dental plaque as a host-associated biofilm that adheres tenaciously to intraoral hard surfaces. Plaque is classified as supragingival or subgingival based on its location relative to the gingival margin. The composition of plaque includes water, organic constituents like bacteria and carbohydrates, and inorganic constituents like calcium and phosphorus. Properties include its structure, exopolysaccharides that form its backbone, physiological heterogeneity, quorum sensing, and increased antibiotic resistance of bacteria within it. Factors like periodontal disease status, the local environment, transmission from other individuals,
Dental plaque is a biofilm that forms on teeth and consists of bacteria, salivary components, and food debris embedded in an extracellular matrix. As plaque matures it develops a complex structure resembling a corn cob. Bacteria in plaque exist in diverse microenvironments and communicate through quorum sensing. Certain pathogens in plaque below the gumline can cause periodontal disease by triggering an inflammatory host response. Plaque plays a key role in periodontal diseases according to various plaque hypotheses that have been proposed over time.
This document provides an overview of the microbiological and immunological aspects of the microbial-host interaction in periodontal disease. It discusses the various bacterial species involved, including the "red complex" bacteria Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. It describes the virulence factors of these bacteria and how they evade host defenses. It also summarizes the innate and adaptive immune response phases, focusing on the acute inflammatory response and roles of neutrophils in controlling bacterial challenge through opsonization and phagocytosis.
Bacteria of periodontits Powerpoint PresentationTaylor Goode
Periodontitis is a severe form of periodontal disease that involves the destruction of the tissues that support the teeth, including the gums, periodontal ligament, and alveolar bone. It is caused by bacterial plaque that accumulates at and below the gumline. If left untreated, periodontitis can result in tooth loss. The document discusses the differences between periodontal disease and periodontitis, signs and symptoms, contributing bacteria, and the multi-stage biofilm formation process that underlies the condition.
Periodontitis is a severe form of periodontal disease that involves the destruction of the tissues that support the teeth, including the gums, periodontal ligament, and alveolar bone. It is caused by bacterial plaque that accumulates at and below the gumline. If left untreated, periodontitis can result in tooth loss. The document discusses the differences between periodontal disease and periodontitis, signs and symptoms, contributing bacteria, and the multi-stage biofilm formation process that underlies periodontitis pathogenesis.
This document discusses plaque as a biofilm and the microbiology of periodontal diseases. It begins by introducing the complex microbial flora that inhabits the oral cavity. A key point is that while most of these microbes coexist harmlessly with the host, a subset of organisms can lead to periodontal diseases either through overgrowth or new pathogenic properties. The document then examines historical and modern evidence that supports the infectious nature of periodontal diseases. It discusses the unique features of periodontal infections as biofilms outside of the body on tooth surfaces. Finally, it reviews the current understanding of suspected periodontal pathogens and their role in destructive periodontal disease.
Dental plaque is a biofilm that forms on teeth and consists of bacteria, salivary and host cells embedded in an extracellular matrix. It develops in stages - initially the tooth pellicle forms, then bacteria attach reversibly before irreversible attachment. As more bacteria colonize, the plaque matures into a complex structure. Dental plaque is classified as supragingival or subgingival depending on location. Various hypotheses have been proposed to describe plaque's role in periodontal diseases, from early non-specific hypotheses to more modern theories highlighting specific pathogenic bacteria and microbial dysbiosis. Maintaining adequate plaque control remains important for periodontal health.
Dental plaque is a biofilm that forms on teeth and other oral surfaces. It is composed of bacteria embedded in an extracellular matrix. As plaque develops over time, the bacterial composition changes from primarily aerobic gram-positive bacteria to include more gram-negative and anaerobic bacteria. Plaque forms in distinct phases - initially with reversible bacterial adhesion to the acquired pellicle on the tooth surface, followed by irreversible adhesion and growth of microcolonies within the matrix. Mature plaque has a complex structure as a biofilm with water channels and bacterial clusters. Dental plaque is the primary cause of dental caries and periodontal disease.
Dental plaque is a microbial biofilm that forms on teeth. It is composed of bacteria, salivary components, food debris and other substances. As plaque matures over time, initially harmless streptococci are replaced with more pathogenic gram-negative bacteria and anaerobes. Mature plaque near the gums can cause inflammation and is associated with conditions like gingivitis and periodontitis. Plaque is assessed visually using disclosing agents or tactilely with probes, and proper removal through brushing and flossing is important for oral health.
This document provides information on periodontal diseases including their etiology, plaque, calculus, and periodontal abscesses. It discusses how plaque biofilm builds up in 4 stages and leads to gingivitis. It then explains how the inflammatory response creates an environment for more bacteria to colonize and cause periodontitis. It details the formation of supragingival and subgingival calculus from mineralization of plaque. Finally, it provides information on diagnosing and treating periodontal abscesses.
Dental plaque is a biofilm that forms on teeth and consists of bacteria embedded in an extracellular matrix. It develops in stages, beginning with the formation of a protein pellicle layer on the tooth surface within seconds of cleaning. Initial colonizers like streptococci then adhere to the pellicle. Secondary colonization involves more species adhering directly or co-aggregating with initial colonizers. Co-aggregation involves specific adhesins on bacteria binding together different species in complex biofilms. The plaque matures into distinct supragingival and subgingival biofilms as the environment changes below the gumline.
This document discusses biofilms and dental plaque. It begins by defining biofilms as self-produced extracellular matrices composed of biopolymers that allow microorganisms to stick to surfaces. Biofilms are found in various environments and contain diverse microbial communities embedded in a protective glycocalyx layer. As more microbes colonize the surface, mushroom-shaped structures called microcolonies form within the biofilm. Fluid channels also develop to transport nutrients and waste. Dental plaque is a specific oral biofilm that forms on teeth and other surfaces. It has both supragingival and subgingival components composed primarily of streptococci and other bacteria. Coaggregation and coadhesion between early and late colonizers aid in plaque maturation over time
The mandible is the only movable bone of the skull. It is formed by a body and two rami, and is connected to other bones via four ligaments. Two nerves - the inferior alveolar nerve and mental nerve - are related to foramina of the mandible. Two other nerves - the nerve to mylohyoid and lingual nerve - run in grooves of the mandible. The mandible has relationships to various arteries, nerves, and salivary glands.
The document discusses the anatomy of the human skull by presenting different views or "normas" including the frontal, vertical, lateral, external basal, and internal basal views. Each view provides a different orientation to examine the bones that make up the skull, including the mandible.
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Semelhante a adhesins and receptors[1]periodontal .pptx
This document discusses the immunology of dental caries. It begins by describing how the oral flora develops from birth and the role of bacteria like Streptococcus mutans in dental caries. Dental caries is considered a biofilm-induced disease. Key points include that S. mutans is a significant pathogen in enamel caries and lactobacillus is predominant in dentinal caries. The document also discusses potential caries vaccines and notes their development has focused on subunit vaccines to avoid potential heart-reactive antibodies induced by whole cell vaccines. In conclusion, while current prevention methods are not sufficient, a successful caries vaccine could make a significant contribution to disease control.
Dental plaque forms through sequential colonization of microorganisms on tooth surfaces. It is made up of bacteria, epithelial cells, and extracellular matrix. Plaque formation involves acquired pellicle formation, reversible bacterial attachment, irreversible attachment through adhesins, microbial succession through coaggregation, and maturation of the biofilm and matrix. The microbial composition of plaque varies by oral site and influences diseases like periodontitis and dental caries. Periodontitis results from an imbalance in homeostasis allowing pathogenic bacteria to overgrow. Dental caries occurs when frequent sugar consumption in plaque favors acid-tolerant bacteria like mutans streptococci, changing the microbiota and predisposing to demineralization.
This document discusses dental biofilms, also known as dental plaque. It explains that dental biofilms are three-dimensional, multispecies microbial communities that form on teeth and other oral surfaces. The key points covered include:
- Dental biofilms provide benefits to microorganisms like increased habitat range and stress tolerance.
- They form through the adsorption of a conditioning film, followed by reversible and then permanent bacterial attachment and colonization.
- As biofilms mature, they develop complex architecture, metabolic gradients, cell signaling pathways, and interspecies interactions between diverse microbes.
- While associated with diseases like caries and periodontitis, the oral microbiome also benefits the host through commensalism
Role of dental biofilm in pathogenesis of periodontalManoj Paradhi
This document discusses the role of dental biofilm in the pathogenesis of periodontal disease. It begins by defining biofilm and dental plaque, and describing the formation of dental plaque. Key points include that plaque is a heterogeneous structure composed of bacteria, organic and inorganic materials. As plaque accumulates, certain bacteria can overwhelm the host's defenses and cause inflammation (gingivitis) or tissue destruction (periodontitis). The document then examines different periodontal diseases and associates each with certain pathogenic bacteria commonly found in the subgingival biofilm of affected individuals. It concludes that dental plaque is the main causative factor of periodontal diseases, so its removal through oral hygiene is important for periodontal health.
Dental plaque is a biofilm that forms on teeth and consists of a complex community of over 700 bacterial species. It is composed of 60-70% bacteria embedded in a matrix of 30-40% extracellular polymers, proteins and carbohydrates. Plaque forms in stages, beginning with the pellicle layer coating the tooth surface within hours, followed by colonization of primary colonizers like Streptococcus and Actinomyces. Secondary colonizers like Prevotella, Fusobacterium and Porphyromonas then adhere, forming the mature biofilm structure with stratified layers of cocci and rods. Plaque morphology demonstrates specific coaggregation of bacteria into corncob formations that contribute to pathogenesis of dental diseases.
1. The infant mouth is initially sterile at birth but is quickly colonized by bacteria from the mother or environment, usually streptococci that bind to oral surfaces.
2. As more bacteria colonize and their metabolic activity increases, the environment changes to allow colonization by other genera and species in a dynamic ecological system.
3. By age one, the normal oral flora includes streptococci, staphylococci, neisseriae, lactobacilli, and some anaerobes, with composition changing as teeth erupt and providing new niches for colonization.
Dental plaque is a biofilm that forms on teeth and consists of bacteria embedded in an intermicrobial matrix. Plaque can be classified as supragingival or subgingival depending on its location relative to the gingival margin. Plaque forms in stages beginning with the deposition of salivary proteins to form an enamel pellicle, which bacteria then attach to. Over time, plaque matures as more bacteria colonize the surface and interact with each other. The composition and microbial population of plaque can influence the development and progression of periodontal disease.
This document discusses dental plaque/biofilm, including its definition, classification, composition, properties, and factors that affect its composition. It begins by defining dental plaque as a host-associated biofilm that adheres tenaciously to intraoral hard surfaces. Plaque is classified as supragingival or subgingival based on its location relative to the gingival margin. The composition of plaque includes water, organic constituents like bacteria and carbohydrates, and inorganic constituents like calcium and phosphorus. Properties include its structure, exopolysaccharides that form its backbone, physiological heterogeneity, quorum sensing, and increased antibiotic resistance of bacteria within it. Factors like periodontal disease status, the local environment, transmission from other individuals,
Dental plaque is a biofilm that forms on teeth and consists of bacteria, salivary components, and food debris embedded in an extracellular matrix. As plaque matures it develops a complex structure resembling a corn cob. Bacteria in plaque exist in diverse microenvironments and communicate through quorum sensing. Certain pathogens in plaque below the gumline can cause periodontal disease by triggering an inflammatory host response. Plaque plays a key role in periodontal diseases according to various plaque hypotheses that have been proposed over time.
This document provides an overview of the microbiological and immunological aspects of the microbial-host interaction in periodontal disease. It discusses the various bacterial species involved, including the "red complex" bacteria Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. It describes the virulence factors of these bacteria and how they evade host defenses. It also summarizes the innate and adaptive immune response phases, focusing on the acute inflammatory response and roles of neutrophils in controlling bacterial challenge through opsonization and phagocytosis.
Bacteria of periodontits Powerpoint PresentationTaylor Goode
Periodontitis is a severe form of periodontal disease that involves the destruction of the tissues that support the teeth, including the gums, periodontal ligament, and alveolar bone. It is caused by bacterial plaque that accumulates at and below the gumline. If left untreated, periodontitis can result in tooth loss. The document discusses the differences between periodontal disease and periodontitis, signs and symptoms, contributing bacteria, and the multi-stage biofilm formation process that underlies the condition.
Periodontitis is a severe form of periodontal disease that involves the destruction of the tissues that support the teeth, including the gums, periodontal ligament, and alveolar bone. It is caused by bacterial plaque that accumulates at and below the gumline. If left untreated, periodontitis can result in tooth loss. The document discusses the differences between periodontal disease and periodontitis, signs and symptoms, contributing bacteria, and the multi-stage biofilm formation process that underlies periodontitis pathogenesis.
This document discusses plaque as a biofilm and the microbiology of periodontal diseases. It begins by introducing the complex microbial flora that inhabits the oral cavity. A key point is that while most of these microbes coexist harmlessly with the host, a subset of organisms can lead to periodontal diseases either through overgrowth or new pathogenic properties. The document then examines historical and modern evidence that supports the infectious nature of periodontal diseases. It discusses the unique features of periodontal infections as biofilms outside of the body on tooth surfaces. Finally, it reviews the current understanding of suspected periodontal pathogens and their role in destructive periodontal disease.
Dental plaque is a biofilm that forms on teeth and consists of bacteria, salivary and host cells embedded in an extracellular matrix. It develops in stages - initially the tooth pellicle forms, then bacteria attach reversibly before irreversible attachment. As more bacteria colonize, the plaque matures into a complex structure. Dental plaque is classified as supragingival or subgingival depending on location. Various hypotheses have been proposed to describe plaque's role in periodontal diseases, from early non-specific hypotheses to more modern theories highlighting specific pathogenic bacteria and microbial dysbiosis. Maintaining adequate plaque control remains important for periodontal health.
Dental plaque is a biofilm that forms on teeth and other oral surfaces. It is composed of bacteria embedded in an extracellular matrix. As plaque develops over time, the bacterial composition changes from primarily aerobic gram-positive bacteria to include more gram-negative and anaerobic bacteria. Plaque forms in distinct phases - initially with reversible bacterial adhesion to the acquired pellicle on the tooth surface, followed by irreversible adhesion and growth of microcolonies within the matrix. Mature plaque has a complex structure as a biofilm with water channels and bacterial clusters. Dental plaque is the primary cause of dental caries and periodontal disease.
Dental plaque is a microbial biofilm that forms on teeth. It is composed of bacteria, salivary components, food debris and other substances. As plaque matures over time, initially harmless streptococci are replaced with more pathogenic gram-negative bacteria and anaerobes. Mature plaque near the gums can cause inflammation and is associated with conditions like gingivitis and periodontitis. Plaque is assessed visually using disclosing agents or tactilely with probes, and proper removal through brushing and flossing is important for oral health.
This document provides information on periodontal diseases including their etiology, plaque, calculus, and periodontal abscesses. It discusses how plaque biofilm builds up in 4 stages and leads to gingivitis. It then explains how the inflammatory response creates an environment for more bacteria to colonize and cause periodontitis. It details the formation of supragingival and subgingival calculus from mineralization of plaque. Finally, it provides information on diagnosing and treating periodontal abscesses.
Dental plaque is a biofilm that forms on teeth and consists of bacteria embedded in an extracellular matrix. It develops in stages, beginning with the formation of a protein pellicle layer on the tooth surface within seconds of cleaning. Initial colonizers like streptococci then adhere to the pellicle. Secondary colonization involves more species adhering directly or co-aggregating with initial colonizers. Co-aggregation involves specific adhesins on bacteria binding together different species in complex biofilms. The plaque matures into distinct supragingival and subgingival biofilms as the environment changes below the gumline.
This document discusses biofilms and dental plaque. It begins by defining biofilms as self-produced extracellular matrices composed of biopolymers that allow microorganisms to stick to surfaces. Biofilms are found in various environments and contain diverse microbial communities embedded in a protective glycocalyx layer. As more microbes colonize the surface, mushroom-shaped structures called microcolonies form within the biofilm. Fluid channels also develop to transport nutrients and waste. Dental plaque is a specific oral biofilm that forms on teeth and other surfaces. It has both supragingival and subgingival components composed primarily of streptococci and other bacteria. Coaggregation and coadhesion between early and late colonizers aid in plaque maturation over time
Semelhante a adhesins and receptors[1]periodontal .pptx (20)
The mandible is the only movable bone of the skull. It is formed by a body and two rami, and is connected to other bones via four ligaments. Two nerves - the inferior alveolar nerve and mental nerve - are related to foramina of the mandible. Two other nerves - the nerve to mylohyoid and lingual nerve - run in grooves of the mandible. The mandible has relationships to various arteries, nerves, and salivary glands.
The document discusses the anatomy of the human skull by presenting different views or "normas" including the frontal, vertical, lateral, external basal, and internal basal views. Each view provides a different orientation to examine the bones that make up the skull, including the mandible.
The trigeminal nerve is the 5th cranial nerve and is a mixed nerve, mainly sensory and motor. It has three main branches: the ophthalmic, maxillary, and mandibular nerves. The maxillary nerve originates from the trigeminal ganglion and courses through the cranial cavity, pterygo-palatine fossa, floor of the orbit, and face, where it terminates and provides branches. The mandibular nerve is also a mixed nerve that originates from the trigeminal ganglion and courses through the cranium, middle ear, and face, where it terminates and provides several sensory and motor branches to structures in the face and oral cavity.
The document discusses the anatomy of the human skull by outlining four different views or "normas" - the frontal, vertical, lateral, and basal views. It also mentions that the skull is composed of multiple bones and references both the external and internal basal views.
This document provides information on human anatomy terms and concepts. It defines three planes of the body used to describe positions (sagittal, coronal, transverse), and anatomical terms like medial, lateral, superior and inferior. It also outlines types of joints (fibrous, cartilaginous, synovial), muscles (skeletal, cardiac, smooth) and movement terms like flexion, extension, and circumduction. Key facts about tissues, bones, and cartilage are summarized.
This document discusses the relationship between psychosomatic disorders and periodontal diseases. It outlines several factors that can affect periodontal health, including age, sex, genetics, stress, smoking, diet, parafunctional habits, medication side effects, and oral hygiene. Stress in particular is linked to conditions like necrotizing ulcerative gingivitis. The document also covers ways that psychosomatic disorders may induce oral issues like harmful habits or effects on tissues through the autonomic nervous system. Proper patient evaluation, education, and referral are important for managing oral health issues with potential psychological influences.
This document discusses genetic polymorphism and its relationship to periodontal disease. It begins by defining key genetic terms and describes how periodontal disease can be caused by single gene mutations (monogenic disorders) or variations in multiple genes (polygenic disorders). Several specific gene polymorphisms are examined, including genes related to cytokines, receptors, metabolism, and innate immunity. The roles of the IL-1, TNF-α, IL-10 genes and others are summarized. The document also explores several genetic syndromes associated with early-onset periodontitis, such as Papillon-Lefevre syndrome. In conclusion, genetic testing is available to assess patient susceptibility to severe periodontal disease.
This document discusses furcation involvement in multi-rooted teeth. It begins with definitions of furcation involvement from 1950-1968. The primary cause is plaque accumulation leading to inflammation. Local anatomical factors like root trunk length, root form, and furcation anatomy affect the progression of furcation involvement. Clinical diagnosis involves probing the furcation and correlating with radiographs. Treatment depends on the grade of involvement and may include nonsurgical approaches like scaling and root planing or surgical therapies such as osseous resection or extraction.
This document discusses gingival enlargement, including its terminology, classifications, and etiological factors.
It defines gingival enlargement and explains that the terms gingival hyperplasia and hypertrophy are not precise descriptions as they refer to histological diagnoses. Gingival enlargement can be caused by inflammatory conditions, systemic diseases, medications, and other factors.
It classifies gingival enlargement based on its location and distribution in the mouth. It also discusses diagnosing and grading gingival enlargement. The document then examines various etiological factors and pathological changes that can cause gingival enlargement, including inflammatory, drug-induced, and enlargement associated with systemic diseases or
1) The document discusses the relationship between periodontal disease and cardiovascular disease (CVS) and diabetes. It explores the focal infection theory and possible pathways linking oral infections to secondary non-oral diseases.
2) Periodontal disease is associated with increased risk of CVS diseases like atherosclerosis, coronary heart disease, and stroke. It may increase susceptibility through inflammation, endothelial injury, lipid peroxidation, molecular mimicry, and elevated antibodies from oral bacteria.
3) Periodontal disease is also linked to increased risk of diabetes through shared risk factors and inflammation. Periodontal bacteria may enter the bloodstream and stimulate liver proteins that amplify systemic inflammation, worsening insulin resistance.
Hematologic disorders like neutropenia, leukemia, anemia, and thrombocytopenia can influence the periodontium. Neutropenia involves low levels of circulating neutrophils which are important for inflammatory reactions and defense against infection. This makes the tissues more susceptible to destruction from conditions like periodontitis. Leukemia is a cancer of the blood cells that can lead to infiltration of leukemic cells into the gingiva and increased risk of infection. Anemia reduces oxygen delivery and makes tissues more friable. Thrombocytopenia increases risk of bleeding from the gums. Antibody deficiency disorders like agammaglobulinemia compromise immune defenses and can result in early loss of teeth from period
Hyperparathyroidism and diabetes can influence periodontal health in several ways:
1. They can alter immune responses, such as impairing neutrophil function, which helps bacteria evade the immune system and worsen periodontal disease.
2. Chronic hyperglycemia and hyperparathyroidism can impair collagen structure and function, damaging the integrity of the periodontium.
3. They may qualitatively change the subgingival microbiome, promoting pathogens like Porphyromonas and Prevotella that are linked to periodontitis.
salivary old new dd.pppptx disease and healthMohamedYElZahar
1. Salivary biomarkers can provide non-invasive alternatives to clinical diagnostics for periodontal diseases by detecting bacterial, host, and inflammatory markers. A combination of biomarkers may provide a more accurate assessment than a single marker.
2. Specific salivary biomarkers for periodontal diseases include immunoglobulins directed against periodontal pathogens, salivary enzymes like lysozyme and peroxidase, and ions like calcium. Nonspecific biomarkers include lactoferrin, histatin, fibronectin, and platelet activating factor.
3. Emerging biomarkers include analysis of the salivary proteome, transcriptome, and host genomic factors that influence susceptibility. However, no single biomarker adequately diagnoses
- This document discusses mediators of bone loss, focusing on alveolar bone destruction in periodontal disease. It outlines the cellular mechanisms and local mediators involved in bone remodeling and resorption, including pro-inflammatory cytokines, prostaglandins, and RANKL.
- Diagnostic tools for detecting periodontal bone resorption are discussed, including indirect clinical measures like probing depth and radiographs, which have limitations. Systemic biochemical markers of bone resorption are mentioned as another potential diagnostic method.
- The key cellular players in bone remodeling - osteoblasts, osteoclasts, and osteocytes - are described. Homeostatic balance between bone formation and resorption is maintained through
A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
This document provides an overview of wound healing, its functions, stages, mechanisms, factors affecting it, and complications.
A wound is a break in the integrity of the skin or tissues, which may be associated with disruption of the structure and function.
Healing is the body’s response to injury in an attempt to restore normal structure and functions.
Healing can occur in two ways: Regeneration and Repair
There are 4 phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This document also describes the mechanism of wound healing. Factors that affect healing include infection, uncontrolled diabetes, poor nutrition, age, anemia, the presence of foreign bodies, etc.
Complications of wound healing like infection, hyperpigmentation of scar, contractures, and keloid formation.
This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
Beyond Degrees - Empowering the Workforce in the Context of Skills-First.pptxEduSkills OECD
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ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...PECB
Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
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Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
How to Setup Warehouse & Location in Odoo 17 InventoryCeline George
In this slide, we'll explore how to set up warehouses and locations in Odoo 17 Inventory. This will help us manage our stock effectively, track inventory levels, and streamline warehouse operations.
1. ADHESINS AND RECEPTORS
IN Dental Plaque
PRESENTED BY : RANEEM GAMAL
SUPERVISED BY : DR. YASMEEN FOUAD
2. OUTLINE
Introduction
Dental plaque definition
Dental plaque composition
Types of dental plaque
Mechanism of dental plaque formation
1. Formation of acquired pellicle.
2. Bacterial adherence (adhesins and receptors)
3. Formation of inter-microbial matrix
4. Bacterial colonization and plaque maturation (co-aggregation)
5. Dispersion
Innovations and future research.
3. Introduction
The classic presentation of periodontal disease is associated with
accumulation of plaque and calculus that harbors bacteria and
potent virulence factors which lead to destruction of periodontal
tissue and resorption of alveolar bone around teeth.
4. Dental Plaque
• Dental plaque is a complex microbial community (predominantly bacteria, but it may
contain yeast , protozoa and virus) found on the tooth surface, embedded in a matrix
of bacterial and salivary origin, so firmly adherent to tooth surface that they resist
wash off by salivary flow.
6. Types of Dental Plaque
Plaque is divided into 2 distinct types based on the relationship of the
plaque to the gingival margin:
• Supragingival plaque
• Subgingival plaque
7. Supragingival plaque dominant bacteria :
Facultative streptococci (90%)
Actinomyces species
Subgingival plaque dominant bacteria according to location :
1. Tooth associated gram positive rods and cocci such as;
Streptococcus mitis
Streptococcus sanguis
Actinomyces viscosus
Actinomyces naeslundii
8. 2. Tissue associated bacteria in these area are more loosely organized than the
very dense tooth associated region.
It contains gram negative rods and cocci as well as filaments, flagellated rods
and spirochetes.
Bacteria mostly predominate tissue associated flora include;
Prophyromonas gingivalis
Prevotella intermedia
Actinobacellus actinomycitimocometans
Capnocytophaga
9. The process of plaque formation can be divided into:
1. Formation of acquired pellicle.
2. Bacterial adherence
3. Formation of inter-microbial matrix
4. Bacterial colonization and plaque maturation
5. Dispersion
10.
11. 1.Formation of Acquired Pellicle
All surfaces of the oral cavity, including all tissue surfaces as well as surfaces of
teeth and fixed and removable prosthesis are covered with a glycoprotein
pellicle.
• Dental pellicle can be considered as the “skin” of the teeth. It is also called acquired
pellicle, salivary acquired pellicle, and enamel pellicle.
• They form in just few seconds after brushing the teeth. If left undisturbed will turn
into plaque which if left again will turn into caries and periodontal disease
12. • In addition to components originating from salivary glands, pellicles also contain
molecules that are not of salivary gland origin, including:
• Albumin originating from gingival crevicular fluid
• Bacterial products such as the glucosyltransferase of S. mutan
Among the salivary components that have been detected in enamel pellicle are :
• MUCINS • α-AMYLASE • S IgA • CYSTATINS • LYSOZYME. • PROLINE RICH
PROTEINS (PRPS).
13. The pellicle forms by selective adsorption of the environmental
macromolecules.
The mechanisms involved in enamel pellicle formation include
Electrostatic
Van der waal
Hydrophobic forces.
14. PROBABLE FUNCTIONS of The Acquired
Pellicle :
• Protect against acid attack (local buffering)
• Facilitate adhesion of gingiva to enamel surface
• Assist in remineralization
• Bind microorganisms
15. Initial colonization of the tooth surface:
The initial bacteria colonizing the pellicle coated tooth surface are predominantly
gram - positive facultative microorganisms such as actinomyces viscosus and
streptococcus sanguis.
The initial colonizers adhere to the pellicle through specific molecules termed
adhesins, on the bacterial surface that interact with receptors in the dental pellicle.
• They reduce oxygen tension to the low level required for growth and survival
of anaerobic secondary colonizers .
16.
17. 2.Bacterial Adherence
Plaque bacteria have developed adhesion mechanisms to colonize surfaces in the
mouth and to withstand cleansing actions, such as salivary flow.
Probably the single most important phenomenon in the development of a biofilm
is the process of microbial adhesion either to the substratum or to other adhering
cells of the same or another species.
18. Adhesins
• Adhesins are minor fimbria-associated proteins and are presented on the cell
surface at or near the tip of thin fimbrial structures extending from the cells.
• The theoretical maximum number of adhesin molecules on a cell surface is 300
and 500 molecules per cell for the 43- and 75-kDa adhesins size, respectively .
• Studies of coaggregation-mediating adhesins among the Gram-positive oral
bacteria have been limited to only a few streptococci and actinomyces.
• The adhesins of Gram-negative bacteria can be divided into two classes: fimbrial
adhesins and nonfimbrial adhesins.
19. 1.Streptococcal antigen I ⁄ II family of
proteins
• They are Polypeptides expressed by commensal oral streptococci such as S. gordonii,
S. oralis and S. sanguinis.
• High affinity binding is made by short fimbriae of P gingivalis which engage antigen
I/II adhesion on streptococci. (Jakubovics et al, 2005)
• Active immunization against Ag I/II or to block adhesins (fimbriae) with specific
inhibitors such as peptides have been recently investigated for immunization against
dental caries and PD (Younson and Kelly, 2004), (Li et al, 2009).
20. • Streptococci have the ability to coaggregate with other streptococci
( intrageneric coaggregation) , which offers an extra advantage in allowing them to
bind to the nascent monolayer of already bound streptococci . In addition,
actinomyces, which are other primary colonizers, bind to the acquired pellicle and to
the streptococci.
21.
22.
23. 2. Galactose binding adhesins
• It is an outer membrane polypeptide on F. nucleatum
• Mediates not only coaggregation with P. gingivalis, but also the attachment of F.
nucleatum to a variety of mammalian cells including human gingival and periodontal
ligament fibroblasts, macrophages, and PMNs (Weiss EI, et al. 2000)
• F. nucleatum is sometimes thought of as a bridging bacterium in plaque, adhering to
primary colonizers
24.
25. 3. Galactosyl-binding adhesins
• The increased exposure of galactosyl residues promotes the interaction of
actinomyces with this salivary molecule in the early stages of biofilm formation.
• Several mechanisms have been identified for adherence of A.actinomycetemcomitans
to epithelial cells : extracellular amorphous material, fimbriae, and extracellular
vesicles may all be involved .
• Smooth variants invade more proficiently than rough variants. Fimbriae most
probably function in adherence of rough variants, whereas non-fimbrial components
(eg. vesicles) are probably involved in adherence of smooth, highly invasive strains .
26. • Type 1 fimbriae mediate binding to saliva coated hydroxyapatite(SHA) and
specifically to salivary proline-rich proteins. Type 2 fimbriae mediate lactose-
inhibitable binding to other oral bacteria and to mammalian cells. Some
actinomyces strains bear both types of fimbriae, and others bear only type 2
27. 4.Glucan-binding proteins
• These are essentially lectins that bind glucans inside plaque matrix
• GBPs are found on the cell surface of S. mutans, and some other streptococci.
28. 5. Arginin inhibitable adhesins:
• It is a cell-surface protein of F. nucleatum
• It mediates large numbers of S. cristatus to adhere to F. nucleatum,
resulting in formations known as corncobs coaggregation (Kaplan et al,
2009).
• It enables S. cristatus to passively invade human epithelial cells (Edwards
et al. 2007)
29.
30. 6. Hemagglutinin
• It is important adhesion molecule which allows P gingivalis to adhere to gingival
tissue cells and to attach and lyse erythrocyte in order to uptake (Fe) ions as essential
nutrition
• Can bind to host proteins, such as fibronectin, fibrinogen , laminin, and collagen
type V . that have been reported to coat epithelial, endothelial, and fibroblast cells.
(TezukaA , et al.2006 , Sakai E, et al. 2007)
• Hemagglutinins are expressed on the bacterial cell surface in association either
with filamentous structures such as fimbriae (fimbrial adhesins) or with nonfimbrial
surface components (nonfimbrial adhesins) and are frequently the adhesins
through which bacteria attach to mammalian cells. (Han.1996)
31. 7.Bacterial Lipopolysaccarides
• Probably facilitates coaggregation with the diverse variety of
grampositive (Streptococcus and Actinomyces species) and
gramnegative (Haemophilus, Prevotella, and Veillonella) species
32.
33.
34.
35.
36. 1- Statherin receptors
• Porphyromonas gingivalis long fimbriae (FimA) adhere to salivary statherin in
pellicle.
• Of all human salivary proteins, statherin exhibited the strongest ability to bind to F.
nucleatum cell surface protein . (Sekine S et al. 2004, NakagakiH, et al, 2010)
Receptors
37. 2. Sialic acid binding protein receptor
• One of the components of saliva incorporated in acquired pellicle and act as a
receptor provided by the host for the early colonizers S. sanguinis and S. gordonii.
• Both organisms express specific cell surface adhesin molecules called the sialic acid–
binding protein.
• Inhibited by sialidase enzyme
38. 3.Proline-rich proteins (PRPs)
• Actinomyces naeslundii type 1 fimbriae and Porphyromonas
gingivalis long fimbriae (FimA) adhere to PRPs.
• PRPs are not only receptors for binding bacteria , they are also a ready
nutrient source for early colonizers. S. gordonii They can bind to other
host receptors or to other bacteria while degrading the PRP nutrient.(Li T
et al. 2000)
39. 4-Salivary agglutinin or glycoprotien340
• When gp340 is integrated into the acquired enamel pellicle, it was found to
promotes adhesion of streptococci binding proteins. (Loimaranta et al., 2005)
40.
41. 3.Formation of intermicrobial matrix
Organic substances formed by bacterial enzymes from sucrose, they are mainly
polysaccharides of:
• Glucans • Levans.
• The glucan is mainly dextran which is a sticky adhesive material that plays a major
role in colonization of bacteria.
• Glucan synthesis allows the bacteria to firmly attach to the tooth surface and form a
biofilm.
• Levan function as storage of polysaccharide, providing a source of fermentable
carbohydrate when hydrolyzed.
42. 4.Bacterial colonization and plaque
maturation
• Secondary colonizers are the microorganisms that do not initially colonize
clean tooth surface.
• Secondary colonizers include: Fusobacterium nucleatum, • Prevotella
intermedia, and • Capnocytophaga species.
• Interaction occurs among different gram positive species and gram
negative species.
• In the later stages of plaque formation , coaggregation between different
gram negative species predominates.
43.
44. • After one week of plaque accumulation, other gram-negative species may also be
present in plaque. These species represent what is considered to be the "tertiary
colonizers", and include:
• 1. Porphyromonas gingivalis (Pg)
• 2. Aggregatibacteractinomycetemcomitans
• 3. Campylobacter rectus
• 4. Eikenella corrodens
• 5. Spirochetes (Treponema species).
• Gram positive species use sugars as an energy source and saliva as a carbon source
• The bacteria that predominates in mature plaque are anaerobic and asaccharolytic,
and use amino acids and small peptides as energy sources
45. Colonization and adsorption to a surface are followed by the
matrix production and development of the water channels
46.
47. The initial attachment of primary colonizers to oral surfaces presents new receptors for
the subsequent adhesion of other bacteria.
The binding of bacterial cells to pre-adherent cells on a surface is important for the
recruitment of secondary colonizers to the oral biofilm. The adhesion of different
bacteria to one another in suspension is termed ‘co-aggregation’
(Cisar et al., 1979)
In many cases, co-aggregation involves the recognition of carbohydrate structures on
one organism by lectin-like protein adhesins on the compatible partner. The
identification of the key protein adhesins is still very much a work in progress.
Co-Aggregation and Co-adhesion
48. Conclusion
• Coaggregation is highly specific in that partners of one cell type may not be partners of a closely
related cell type.
• The recognition may be intrageneric, intergeneric or multigeneric in nature .
• All coaggregations occur between genetically distinct bacteria, including those that occur between
bacteria of the same genus.
• The latter intrageneric coaggregations seem to be limited to those among streptococci and a few
actinomyces; both of these groups of bacteria are initial colonizers and may use intrageneric
coaggregation as a critical function in adherence
49. • An interesting feature of the coaggregations is the bridging
between one cell type and its partners.
• One of the first examples of a coaggregation bridge was
Prevotella loescheii PK1295, which can serve as a bridge
between Streptococcus oralis and Actinomyces israelii PK14,
two gram-positive oral bacteria that are otherwise unable to
coaggregate
53. Carbohydrate receptors that mediate coaggregation have been
isolated and extensively characterized from five streptococci .
All five of the carbohydrate receptors are linear cell wall
polysaccharides, each having been removed from the cell wall
by the action of mutanolysin,
a mureinolytic enzyme.
54. Several structural features are common to these receptor
polysaccharides. All contain:
1- Galactopyranose and -galactofuranose
2- Hexasaccharides or heptasaccharides
3 - Phosphodiester linkages.
55.
56. The top four of the five polysaccharides are similar in structure and in
biological activity and will be discussed as a group.
- Two common features of these four polysaccharides are :
1) the oligosaccharide repeating units are linked by phosphodiester bonds to the
6-carbon of the nonreducing terminal sugar.
2) all contain N-acetylgalactosamine.
- The top two streptococcal polysaccharides
contain --Galfi 1-36)-f3-GalpNAc (1-*3)-a- Galp(1-*)
- The next two contain -J-GalJ(1--*6)-fr Galp( 1-i.3)-ct-GalpNAc (1-i).
They differ in the order of the two sugars near the reducing end (GalNAc-
Gal vs.
Gal-GalNAc), but the glycosidic linkages are the same.
This disaccharide region of the four oligosaccharides is considered to be the
active actinomyces-adhesin binding site. Abeygunawardana et al.
57. All four of these streptococci are partners of actinomyces and all exhibit lactose-
inhibitable coaggregalions with some of the actinomyces.
Yet the degree of coaggregation of the streptococcus-actinomyces coaggregation
varies with each streptococcus and any common- partner actinomyces.
For example,
S. sanguis C104 co-aggregates poorly with A. naeslundii T14V, whereas the other
three show strong coaggregation.
58.
59. The fifth streptococcal polysaccharide acts as a receptor for a
Gram-negative bacterium.
Of the five streptococci listed . only S. oralis ATCC 55229 coaggregates with
C. ochracea ATCC 33596.
S. oralis ATCC 55229 contains a quite different surface receptor that lacks N-
acetylated sugars.
- The repeating hexasaccharide is not linked by phosphodiester bonds, but
rather the phosphate is found as a glycerol phosphate substitution on an internal
galactose moiety .
- The coaggregation is sensitive to lactose and galactose, 16-fold more sensitive
to L-rhamnose, but insensitive to GalNAc.
60. 5. Dispersion
• Once biofilms are established, planktonic bacteria may periodically leave the biofilm
on their own. When they do, they can rapidly multiply and disperse.
• Biofilm bacteria can move in numerous ways: collectively, by
• Rippling or rolling across the surface
• Detaching in clumps.
• Individually, through a “swarming and seeding” dispersal.
61. • Dispersal of cells from the biofilm colony is an essential stage of
the biofilm lifecycle.
• Dispersal enables biofilms to spread and colonize new surfaces
62. INNOVATIONS AND FUTURE
RESEARCH
•Understanding these methods of bacterial-
bacterial interactions and bacterial-host
interaction develops new strategies to
inhibit bacterial adhesion as seen in the
diagram
63. • The principle of oral disease vaccines is to induce antigen specific antibodies against
the causative agent or agents that inhibit the infection process by one of 3 main
mechanisms:
1. Antibody-mediated clearance,
2. Blocking of essential receptors required for microbial attachment,
3. Inhibition of enzymes required for metabolism or colonization.
• For mutans streptococci, 3 proteins are promising vaccine candidates:
AgI/II family polypeptide SpaP, GTF, and GbpB (Taubman and Nash, 2006).
• However, dental caries is not associated just with S. mutans; therefore, vaccines
targeting only these organisms may not be 100% effective
64. • No clinical trials have been performed to date against periodontitis. Nonetheless,
animal models have shown that vaccines against fimbriae, gingipains, or OMPs can
successfully interfere with P. gingivalis colonization and reduce periodontal bone
resorption (Persson, 2005; Beevi et al., 2009).
• Molecular information about adherence mechanisms can also be exploited in the
design of replacement therapies, attachment-blocking peptides, and biomimetics or
signaling inhibitors to disrupt microbial community development. (Nobbs et al.,
2009; Chen and Wang, 2010).