1) Dental plaque is a biofilm made up of many microbial species that normally exists in a stable state. Disruptions to factors like diet, saliva flow, or host defenses can cause shifts in the microbial population toward species associated with diseases.
2) Studies using defined microbial communities found that allowing pH to drop after sugar pulses selected for acid-tolerant, cariogenic species over time. Maintaining neutral pH did not cause such shifts. Low pH, rather than sugar alone, drives changes in microbial population linked to dental caries.
3) Controlling factors that lower plaque pH, like limiting sugar intake or boosting saliva, may help maintain a healthy microbial composition and reduce disease risk.
Bds 3 rd year lecture Dental plaque as a biofilmDr. Mamta Singh
1. Dental plaque is a biofilm that forms on teeth and consists of bacterial cells embedded in a glycocalyx matrix.
2. Biofilms provide bacteria advantages like attachment to surfaces, genetic exchange, quorum sensing, and antibiotic resistance that make them difficult to treat.
3. Factors like nutrient availability, environmental conditions, and microbial community composition influence biofilm development and structure.
The document discusses dental plaque formation and ecology. It begins by defining dental plaque and describing its bacterial composition. It then discusses the stages of plaque formation from pellicle formation to mature plaque development. The document also covers plaque retention sites, plaque disclosure methods, and classifications. It describes the hypotheses concerning plaque pathogenicity, including the non-specific, specific, and ecological plaque hypotheses. The strategies for caries prevention and control based on the ecological plaque hypothesis are preventing shifts in the microbial ecology through dietary and oral hygiene interventions. In healthy circumstances, the resident oral flora are generally not disease-causing, but environmental changes can trigger shifts to more cariogenic microbial compositions.
This document provides an overview of dental plaque, including its definition, structure, composition, formation process, and role in periodontal diseases. It discusses how plaque begins as a biofilm that forms on teeth, consisting primarily of bacteria embedded in an extracellular matrix. Over time, the plaque matures as early colonizing bacteria prepare the surface for secondary colonizers, causing the biofilm to shift from aerobic to anaerobic organisms. Mature plaque is associated with periodontal diseases as it grows below the gingival margin. The document outlines the key stages and microbial changes involved in dental plaque formation and maturation.
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.
Dental plaque biofilm cannot be eliminated permanently.
However, the pathogenic nature of the dental plaque biofilm can be reduced by reducing the bio burden (total microbial load and different pathogenic isolates within that dental plaque biofilm) and maintaining a normal flora with appropriate oral hygiene methods that include daily brushing, flossing and rinsing with antimicrobial mouth rinses.
This can result in the prevention or management of the associated squeal, including the development of periodontal diseases and possibly the impact of periodontal diseases on specific systemic disorders.
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
This document discusses the microbiology of periodontal diseases. It describes the typical microbiota found in healthy sites, gingivitis sites, and chronic or aggressive periodontitis sites. The microbiota shifts from mostly gram-positive facultative bacteria in health to include more gram-negative anaerobic bacteria in disease. Key pathogenic bacteria associated with periodontitis include Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Aggregatibacter actinomycetemcomitans, and Prevotella intermedia. These bacteria produce virulence factors like proteases, lipopolysaccharides, and leukotoxins that promote tissue destruction.
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.
Bds 3 rd year lecture Dental plaque as a biofilmDr. Mamta Singh
1. Dental plaque is a biofilm that forms on teeth and consists of bacterial cells embedded in a glycocalyx matrix.
2. Biofilms provide bacteria advantages like attachment to surfaces, genetic exchange, quorum sensing, and antibiotic resistance that make them difficult to treat.
3. Factors like nutrient availability, environmental conditions, and microbial community composition influence biofilm development and structure.
The document discusses dental plaque formation and ecology. It begins by defining dental plaque and describing its bacterial composition. It then discusses the stages of plaque formation from pellicle formation to mature plaque development. The document also covers plaque retention sites, plaque disclosure methods, and classifications. It describes the hypotheses concerning plaque pathogenicity, including the non-specific, specific, and ecological plaque hypotheses. The strategies for caries prevention and control based on the ecological plaque hypothesis are preventing shifts in the microbial ecology through dietary and oral hygiene interventions. In healthy circumstances, the resident oral flora are generally not disease-causing, but environmental changes can trigger shifts to more cariogenic microbial compositions.
This document provides an overview of dental plaque, including its definition, structure, composition, formation process, and role in periodontal diseases. It discusses how plaque begins as a biofilm that forms on teeth, consisting primarily of bacteria embedded in an extracellular matrix. Over time, the plaque matures as early colonizing bacteria prepare the surface for secondary colonizers, causing the biofilm to shift from aerobic to anaerobic organisms. Mature plaque is associated with periodontal diseases as it grows below the gingival margin. The document outlines the key stages and microbial changes involved in dental plaque formation and maturation.
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.
Dental plaque biofilm cannot be eliminated permanently.
However, the pathogenic nature of the dental plaque biofilm can be reduced by reducing the bio burden (total microbial load and different pathogenic isolates within that dental plaque biofilm) and maintaining a normal flora with appropriate oral hygiene methods that include daily brushing, flossing and rinsing with antimicrobial mouth rinses.
This can result in the prevention or management of the associated squeal, including the development of periodontal diseases and possibly the impact of periodontal diseases on specific systemic disorders.
Various Plaque Hypothesis are proposed to prove how plaque becomes pathogenic and cause periodontitis. Helpful in understanding pathogenesis of periodontitis especially how Gingivitis change to Periodontitis. All the details have been added and made in easy language to understand.
Useful for BDS and MDS students
This document discusses the microbiology of periodontal diseases. It describes the typical microbiota found in healthy sites, gingivitis sites, and chronic or aggressive periodontitis sites. The microbiota shifts from mostly gram-positive facultative bacteria in health to include more gram-negative anaerobic bacteria in disease. Key pathogenic bacteria associated with periodontitis include Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Aggregatibacter actinomycetemcomitans, and Prevotella intermedia. These bacteria produce virulence factors like proteases, lipopolysaccharides, and leukotoxins that promote tissue destruction.
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. Dental plaque is a biofilm that forms on teeth and consists of bacteria, host cells, and an extracellular matrix. It begins forming within minutes on teeth as the salivary pellicle.
2. Primary colonizers like streptococci initially adhere to the pellicle via electrostatic or hydrophobic interactions. They facilitate the adherence of secondary colonizers as plaque matures.
3. Coaggregation and coadhesion allow later colonizers like Porphyromonas gingivalis and Tannerella forsythia to join the biofilm through protein-carbohydrate interactions between species. Bacteria like Fusobacterium nucleatum act as bridges between early and late colonizers.
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 hundreds of microbial species embedded in an extracellular matrix. It contains bacteria, epithelial cells, macrophages, and leukocytes as well as organic and inorganic compounds. Plaque exists as either supragingival or subgingival plaque. Subgingival plaque is associated with periodontal disease and contains pathogens like Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola that make up the "red complex". The development of plaque involves initial pellicle formation, bacterial adhesion and colonization, and the accumulation of early colonizers from the yellow, purple, and green complexes that are later joined by orange complex bacteria which
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,
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.
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.
Oral microbiology:normal oram microflora and Dental plaqueKarishma Sirimulla
This document discusses oral microbiology and dental plaque. It begins by introducing the types of microorganisms found in the oral cavity, including bacteria, fungi, and protozoa. It then discusses the normal oral microflora, including indigenous, supplemental, and transient flora. Key topics covered include the various types of oral bacteria; factors that affect bacterial growth such as temperature, pH, nutrients, and host defenses; bacterial metabolism of carbohydrates, proteins, oxygen, and nitrogen; and the definition and formation of dental plaque.
Introduction……
Uterus……..Sterile
After birth……… few facultative & aerobic microorganisms
Second day……... anaerobic
2 weeks …….. Nearly mature microbiota
> 2 years …….. 400 different spp (10 14 )
After tooth eruption …… > 500 spp.
Any individual contains ≥150 spp.
6 Ecological niches
Or
Microbial habitats within the mouth
EARLYCOLONIZERS
Dental plaque
Formation
2. Specific Plaque Hypothesis
Only certain plaque is pathogenic, and its pathogenicity depends on the presence of or increase in specific microorganisms.
This concept predicts that plaque harboring specific bacterial pathogens results in periodontal disease because these organisms produce substances that mediate the destruction of host tissues.
3. Ecological plaque hypothesis
In 1990, PD Marsh et al developed the ecologic plaque hypothesis
According to this, both the total no. of dental plaque and the specific microbial composition of plaque may contribute to the transition from health to disease.
A change in the nutrient status of a pocket or chemical and physical changes to the habitat are thus considered the primary cause for overgrowth by pathogens.
Dental plaque begins as a conditioning film that forms on teeth within minutes of cleaning. Bacteria then adhere through reversible and irreversible binding. As bacteria multiply, they synthesize extracellular polymeric substances to form a biofilm matrix. Co-adhesion and co-aggregation allow more bacteria to attach, leading to microcolony formation. Over time, this results in a mature dental plaque biofilm embedded within the matrix on the tooth surface.
This document provides an overview of dental plaque, including its:
1) Classification, composition, structure and formation as a biofilm on teeth. Dental plaque is made up of bacteria and an intercellular matrix that accumulates on teeth.
2) Role in dental diseases like caries and periodontitis. The specific bacteria present in plaque influence which diseases may develop.
3) Methods of detection and removal, which are important for oral health maintenance and disease prevention. Effective plaque removal is needed to prevent its buildup and the diseases it can cause.
This document provides an overview of periodontal microbiology. It discusses the various bacteria that are associated with dental plaque and periodontal diseases. Key points include:
- Over 700 bacterial species can colonize the oral cavity, with plaque being the primary cause of periodontal disease.
- Periodontal diseases result from a mixed bacterial infection that produces inflammation and destruction of tissues around the teeth.
- Important pathogens associated with periodontal diseases include Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia, and Treponema denticola.
- Dental plaque develops through initial bacterial adhesion to the acquired pell
Dental plaque is a biofilm that forms on teeth. It consists of microbial communities embedded in an extracellular matrix. Bacteria in plaque interact through quorum sensing, metabolic cooperation, and horizontal gene transfer. As plaque matures, physiological heterogeneity develops within the biofilm as bacteria occupy different microenvironments. Plaque is resistant to antibiotics due to slow growth and matrix protection. Factors like saliva, nutrients, and surface properties influence plaque development and behavior. Effective strategies are needed to control the oral biofilm and prevent dental diseases.
Dental Plaque
Soft deposits that form the biofilm adhering to the tooth surface or other hard surfaces in the oral cavity, including removable & fixed restorations”
Bowen , 1976
Bacterial aggregations on the teeth or other solid oral structures
Lindhe, 2003
This document summarizes the microbiology of dental caries. It defines caries as a chronic infection caused by normal oral bacteria metabolizing dietary carbohydrates. The main causative microbes are Streptococcus mutans and lactobacilli. Caries develops when acids produced by these bacteria in dental plaque demineralize enamel. Prevention focuses on reducing sugars, increasing fluoride, sealing pits/fissures, and controlling cariogenic bacteria through antimicrobials like chlorhexidine or replacement with probiotics.
This document provides an overview of the microbiology of periodontal diseases. It discusses the colonization of bacteria in the oral cavity from birth and the hundreds of bacterial species that can colonize the adult mouth. It describes the classification of bacteria based on morphology, staining characteristics, and culturing characteristics. The document discusses the biofilm formation on tooth surfaces and how it protects colonizing bacteria. It also reviews the historical perspectives on periodontal disease-causing bacteria from the 1880s to 1930s and the return to the concept of specific microbial etiology in the 1960s.
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
“Introducing the All New Dentaid Channel on Slideshare! Just click to find our presentation of the Oral Biofilm study where you can find and download any information you would like!”
Este documento presenta una guía clínica sobre el diagnóstico, prevención y tratamiento de la caries dental desarrollada por la Facultad de Odontología de la Universidad Nacional de Colombia. La guía fue creada para mejorar la calidad de la atención odontológica en Bogotá y garantizar el acceso equitativo a los servicios de salud oral. Incluye información sobre la epidemiología de la caries dental, metas globales de salud oral, procedimientos de diagnóstico y manejo clínico, fundamentos teóricos
Diversity and Activity of Bacterial Biofilm Communities Growing on Hexachloro...Ahmed Shawky
This document summarizes a study on the diversity of bacterial biofilms and isolates able to degrade the pesticide γ-hexachlorocyclohexane (γ-HCH). Soil samples were collected around pesticide factories in Egypt. Highly diverse microbes were isolated from the soils that could grow using γ-HCH as their sole carbon source. The same soils were also used to inoculate γ-HCH microcrystals in microcosms, forming multispecies biofilms. While many Bacillus species were isolated, they were largely absent from the biofilm communities. Biofilm cells stained for hydrophobicity, suggesting an important role in degrading the hydrophobic substrate. Differences in species composition between isolates and biofilm communities
1. Dental plaque is a biofilm that forms on teeth and consists of bacteria, host cells, and an extracellular matrix. It begins forming within minutes on teeth as the salivary pellicle.
2. Primary colonizers like streptococci initially adhere to the pellicle via electrostatic or hydrophobic interactions. They facilitate the adherence of secondary colonizers as plaque matures.
3. Coaggregation and coadhesion allow later colonizers like Porphyromonas gingivalis and Tannerella forsythia to join the biofilm through protein-carbohydrate interactions between species. Bacteria like Fusobacterium nucleatum act as bridges between early and late colonizers.
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 hundreds of microbial species embedded in an extracellular matrix. It contains bacteria, epithelial cells, macrophages, and leukocytes as well as organic and inorganic compounds. Plaque exists as either supragingival or subgingival plaque. Subgingival plaque is associated with periodontal disease and contains pathogens like Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola that make up the "red complex". The development of plaque involves initial pellicle formation, bacterial adhesion and colonization, and the accumulation of early colonizers from the yellow, purple, and green complexes that are later joined by orange complex bacteria which
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,
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.
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.
Oral microbiology:normal oram microflora and Dental plaqueKarishma Sirimulla
This document discusses oral microbiology and dental plaque. It begins by introducing the types of microorganisms found in the oral cavity, including bacteria, fungi, and protozoa. It then discusses the normal oral microflora, including indigenous, supplemental, and transient flora. Key topics covered include the various types of oral bacteria; factors that affect bacterial growth such as temperature, pH, nutrients, and host defenses; bacterial metabolism of carbohydrates, proteins, oxygen, and nitrogen; and the definition and formation of dental plaque.
Introduction……
Uterus……..Sterile
After birth……… few facultative & aerobic microorganisms
Second day……... anaerobic
2 weeks …….. Nearly mature microbiota
> 2 years …….. 400 different spp (10 14 )
After tooth eruption …… > 500 spp.
Any individual contains ≥150 spp.
6 Ecological niches
Or
Microbial habitats within the mouth
EARLYCOLONIZERS
Dental plaque
Formation
2. Specific Plaque Hypothesis
Only certain plaque is pathogenic, and its pathogenicity depends on the presence of or increase in specific microorganisms.
This concept predicts that plaque harboring specific bacterial pathogens results in periodontal disease because these organisms produce substances that mediate the destruction of host tissues.
3. Ecological plaque hypothesis
In 1990, PD Marsh et al developed the ecologic plaque hypothesis
According to this, both the total no. of dental plaque and the specific microbial composition of plaque may contribute to the transition from health to disease.
A change in the nutrient status of a pocket or chemical and physical changes to the habitat are thus considered the primary cause for overgrowth by pathogens.
Dental plaque begins as a conditioning film that forms on teeth within minutes of cleaning. Bacteria then adhere through reversible and irreversible binding. As bacteria multiply, they synthesize extracellular polymeric substances to form a biofilm matrix. Co-adhesion and co-aggregation allow more bacteria to attach, leading to microcolony formation. Over time, this results in a mature dental plaque biofilm embedded within the matrix on the tooth surface.
This document provides an overview of dental plaque, including its:
1) Classification, composition, structure and formation as a biofilm on teeth. Dental plaque is made up of bacteria and an intercellular matrix that accumulates on teeth.
2) Role in dental diseases like caries and periodontitis. The specific bacteria present in plaque influence which diseases may develop.
3) Methods of detection and removal, which are important for oral health maintenance and disease prevention. Effective plaque removal is needed to prevent its buildup and the diseases it can cause.
This document provides an overview of periodontal microbiology. It discusses the various bacteria that are associated with dental plaque and periodontal diseases. Key points include:
- Over 700 bacterial species can colonize the oral cavity, with plaque being the primary cause of periodontal disease.
- Periodontal diseases result from a mixed bacterial infection that produces inflammation and destruction of tissues around the teeth.
- Important pathogens associated with periodontal diseases include Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Tannerella forsythia, and Treponema denticola.
- Dental plaque develops through initial bacterial adhesion to the acquired pell
Dental plaque is a biofilm that forms on teeth. It consists of microbial communities embedded in an extracellular matrix. Bacteria in plaque interact through quorum sensing, metabolic cooperation, and horizontal gene transfer. As plaque matures, physiological heterogeneity develops within the biofilm as bacteria occupy different microenvironments. Plaque is resistant to antibiotics due to slow growth and matrix protection. Factors like saliva, nutrients, and surface properties influence plaque development and behavior. Effective strategies are needed to control the oral biofilm and prevent dental diseases.
Dental Plaque
Soft deposits that form the biofilm adhering to the tooth surface or other hard surfaces in the oral cavity, including removable & fixed restorations”
Bowen , 1976
Bacterial aggregations on the teeth or other solid oral structures
Lindhe, 2003
This document summarizes the microbiology of dental caries. It defines caries as a chronic infection caused by normal oral bacteria metabolizing dietary carbohydrates. The main causative microbes are Streptococcus mutans and lactobacilli. Caries develops when acids produced by these bacteria in dental plaque demineralize enamel. Prevention focuses on reducing sugars, increasing fluoride, sealing pits/fissures, and controlling cariogenic bacteria through antimicrobials like chlorhexidine or replacement with probiotics.
This document provides an overview of the microbiology of periodontal diseases. It discusses the colonization of bacteria in the oral cavity from birth and the hundreds of bacterial species that can colonize the adult mouth. It describes the classification of bacteria based on morphology, staining characteristics, and culturing characteristics. The document discusses the biofilm formation on tooth surfaces and how it protects colonizing bacteria. It also reviews the historical perspectives on periodontal disease-causing bacteria from the 1880s to 1930s and the return to the concept of specific microbial etiology in the 1960s.
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
“Introducing the All New Dentaid Channel on Slideshare! Just click to find our presentation of the Oral Biofilm study where you can find and download any information you would like!”
Este documento presenta una guía clínica sobre el diagnóstico, prevención y tratamiento de la caries dental desarrollada por la Facultad de Odontología de la Universidad Nacional de Colombia. La guía fue creada para mejorar la calidad de la atención odontológica en Bogotá y garantizar el acceso equitativo a los servicios de salud oral. Incluye información sobre la epidemiología de la caries dental, metas globales de salud oral, procedimientos de diagnóstico y manejo clínico, fundamentos teóricos
Diversity and Activity of Bacterial Biofilm Communities Growing on Hexachloro...Ahmed Shawky
This document summarizes a study on the diversity of bacterial biofilms and isolates able to degrade the pesticide γ-hexachlorocyclohexane (γ-HCH). Soil samples were collected around pesticide factories in Egypt. Highly diverse microbes were isolated from the soils that could grow using γ-HCH as their sole carbon source. The same soils were also used to inoculate γ-HCH microcrystals in microcosms, forming multispecies biofilms. While many Bacillus species were isolated, they were largely absent from the biofilm communities. Biofilm cells stained for hydrophobicity, suggesting an important role in degrading the hydrophobic substrate. Differences in species composition between isolates and biofilm communities
This document is a student paper that investigates whether selected sugar alcohols found in sugar-free chewing gum can effectively reduce the concentration of Streptococcus mutans bacteria in dental plaque. The student describes using an in vitro closed chamber system to model the oral cavity and test sugar alcohols on biofilms grown on ceramic discs. The experiment involves growing biofilms on discs using saliva solution, then testing sugar alcohol solutions in trials run through the closed chamber system. The results will determine if sugar alcohols can lower S. mutans concentrations compared to a sucrose control.
A PROPOSAL ON BIOFILM FORMATION AND ANTIBIOTIC SUSCEPTIBILITY PATTERN OF Stap...Shrezjana Mainali
This document presents a proposal to study biofilm formation and antibiotic susceptibility patterns of Staphylococcus aureus in clinical samples. It provides background on S. aureus as a common pathogen and discusses the emergence of antibiotic-resistant strains like MRSA. The proposal aims to determine the prevalence of biofilm formation among S. aureus isolates from clinical samples and identify associations between biofilm production and antibiotic resistance profiles. It justifies the study by noting the lack of research on biofilm-producing MRSA in Nepal and the potential for findings to improve treatment. The proposal acknowledges limitations from the short study period and lack of extensive prior research and optimal laboratory facilities in Nepal.
Biofilms are highly structured communities of bacteria that attach to surfaces and secrete an extracellular matrix. Within biofilms, bacteria communicate chemically through quorum sensing and are much more resistant to antibiotics than individual bacteria. This makes biofilms a major cause of persistent infections associated with medical implants and devices. Researchers are working to develop new treatments that target biofilm formation and quorum sensing, with some looking at natural compounds that inhibit these processes. Proper testing models are still needed, as bacteria in biofilms may differ significantly from individual bacteria and assumptions that they are similar could lead to problems.
Bone quality and quantity are important factors for successful implant treatment. Poor bone quality is more prevalent in the posterior maxilla. Smoking and diabetes can negatively impact bone density and healing around implants. Complications of implants include surgical risks, implant loss, bone loss, soft tissue issues, mechanical problems, and esthetic concerns. Failure rates are higher for shorter implants, in lower quality bone, and for smokers and diabetics. Implants should be removed if they cause pain, mobility, uncontrolled bone loss, or cannot be restored. Maintaining good glycemic control is important for diabetics undergoing implant treatment.
Avance de la ponencia del Dr. Ignacio Sanz Sánchez, en el I Simposio SEPA-Dentaid, que se centrará en el tratamiento y prevención de la peri-implantitis.
Dental plaque is a sticky biofilm that forms on teeth daily. It is made up of bacteria and other microorganisms from saliva. If plaque is not removed regularly through brushing, it can build up and the bacteria nearest the teeth produce acids. These acids demineralize the enamel and cause cavities. Plaque also irritates gums and can lead to gingivitis or periodontitis if left unchecked. Dentists can identify plaque using instruments or dye tablets to check if brushing and flossing have effectively removed it.
Dental implant failure / /certified fixed orthodontic courses by Indian dent...Indian dental academy
Welcome to Indian Dental Academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Indian dental academy has a unique training program & curriculum that provides students with exceptional clinical skills and enabling them to return to their office with high level confidence and start treating patients
State of the art comprehensive training-Faculty of world wide repute &Very affordable.
The document discusses various factors that can contribute to dental implant failures, including host factors like poor medical health, smoking, bruxism, and poor oral hygiene; surgical factors like trauma during surgery; and implant selection factors like bone quality. It provides definitions for different types of implant failures and lists criteria for determining implant success. The classifications, predictors, warning signs, and ways to enhance outcomes with implants are also examined.
This document provides an overview of periimplantitis, including its definition, classification systems, epidemiology, etiology, pathogenesis, diagnosis, and treatment. Periimplantitis is defined as an inflammatory process involving both soft and hard tissues around a dental implant, resulting in loss of supporting bone. It is distinguished from peri-implant mucositis, which only involves inflammation of soft tissues. The document discusses various classification systems for periimplantitis and reviews potential etiologic factors such as plaque, biomechanical overload, genetic factors, and iatrogenic causes. Diagnosis involves clinical parameters like bleeding, probing depth, and radiographic bone loss. Treatment aims to eliminate infection and may include nonsurgical and surgical
1) El documento describe la morfología y enfermedades de los tejidos periimplantarios. 2) Explica que la periimplantitis comienza en la parte coronaria del implante y progresa hacia el hueso, causando pérdida de oseointegración. 3) El tratamiento de la periimplantitis incluye eliminación del biofilm, regeneración de la superficie del implante y tratamiento antiinfeccioso para prevenir la recolonización bacteriana.
The document discusses various types of implant failure in orthopedic surgery. It begins by introducing commonly used implant materials like stainless steel, cobalt-chromium alloys, and titanium alloys. It then discusses factors that can lead to failure, including issues with materials, surgical technique, patient non-compliance, and infection. Specific types of failures are explored for different implant devices, such as loosening or fracture of plates and screws in plating, bending or breakage of intramedullary nails, and aseptic loosening in arthroplasty. Prevention of implant failure requires consideration of material properties, surgical best practices, and post-operative patient management.
Peri-implantitis is an inflammatory reaction around dental implants that can lead to loss of supporting bone. It has two forms: peri-implant mucositis, which is reversible inflammation confined to soft tissues; and peri-implantitis, which involves progressive bone loss beyond initial remodeling. Risk factors include a history of periodontitis, smoking, residual cement, and implant position/design. Treatment includes non-surgical approaches like mechanical debridement and antibiotics, as well as surgical methods such as regenerative procedures and surface decontamination. The combination of systemic antibiotics, antiseptic mouthwash, and surgical debridement can improve outcomes, though no single surface decontamination method is superior.
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.
Dental plaque is a biofilm that forms on teeth. It is made up of bacteria, salivary components, and food debris embedded in an extracellular matrix. Plaque forms in stages - first, a protein pellicle forms on the tooth surface. Bacteria then attach to the pellicle and begin to colonize. As the bacteria multiply, they produce a matrix material between them made of carbohydrates, proteins, and lipids. Over time this leads to the development of a mature dental plaque biofilm.
This document discusses dental plaque formation at the ultrastructural level. It begins by describing how a saliva-derived acquired pellicle forms on the tooth surface within nanoseconds. Bacteria then initially adhere reversibly to this pellicle via molecular interactions. They can then irreversibly attach through specific adhesins. Once attached, the bacteria begin colonizing the surface and forming a biofilm through multiplication and sequential adsorption of organisms.
Peri-implantitis is a chronic inflammatory disease affecting the bone and gum tissue around implants. As the number of implants being placed increases and subjected to inflammatory and occlusal demands the incidence of problems associated with Peri-implantitis will also increase. It is essential for practitioners to understand the etiology of Peri-implantitis and their role in preventing, treating and maintaining this growing problem.
This document summarizes key points about dental plaque as a biofilm and microbial community. It discusses how plaque forms in an ordered way and maintains a diverse but relatively stable microbial composition (microbial homeostasis) in healthy sites. However, perturbations like frequent sugar consumption can disrupt homeostasis and select for acidogenic bacteria like mutans streptococci and lactobacilli, leading to dental caries. Maintaining homeostasis through approaches like inhibiting sugar metabolism, stimulating saliva flow, or interfering with factors that allow pathogenic bacteria to outcompete healthy bacteria could help control caries in a holistic way by appreciating the ecological principles involved.
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 provides an overview of the microbiology of periodontal diseases. It begins with an introduction to the complex microbial flora found in the oral cavity and periodontal diseases as polymicrobial infections. The document then covers the historical perspectives on periodontal disease pathogenesis including the non-specific plaque hypothesis, specific plaque hypothesis, and updated hypotheses. Key microbial complexes and pathogens associated with periodontal diseases are discussed. The rest of the document focuses on dental plaque as a microbial biofilm, including its formation, structure, properties that contribute to pathogenicity, and gene regulation within biofilms.
Subgingival biofilm as etiological factor of periodontal diseaseDr Heena Sharma
This document summarizes subgingival biofilms as etiological factors of periodontal disease. It defines biofilms and describes the stages of biofilm formation. It discusses how subgingival biofilms are associated with periodontitis, including their composition, structure, and role in pathogenesis. The document also covers what metagenomics has revealed about subgingival biofilm composition and how in vitro models are used to study subgingival biofilms.
The oral cavity hosts a complex ecology of microbial populations that compete for available nutrients. While most oral bacteria grow best at a narrow pH range, some aciduric bacteria can grow at low pH levels and are favored in acidic environments. Sugar is the main energy source, but some bacteria can use other substrates like carboxylic acids. Key bacterial adaptations include maintaining metabolism at low pH, rapidly transporting sugars, and producing extracellular and intracellular polysaccharides. Major cariogenic bacteria associated with dental caries include Streptococcus mutans, Lactobacillus, Actinomyces, and Veillonella. Dental caries results from the net acid production of the overall plaque microflora through multiple bacterial interactions, competitions,
- Dental plaque begins as a biofilm that forms on teeth in several stages: pellicle formation, initial bacterial adherence, aggregation, and maturation.
- Early colonizers like Streptococcus attach within minutes and allow later colonizers like Actinomyces to adhere in about 2 hours.
- As plaque thickness increases due to bacterial proliferation, the microenvironment shifts from aerobic to anaerobic, changing the bacterial composition. Certain bacteria are implicated in dental diseases like gingivitis and periodontitis.
t is estimated over 95% of bacteria existing in nature are in biofilms.[1] The slime layer that forms on rocks in streams is a classic example of a biofilm. Biofilms are ubiqui-tous; they form on virtually all surfaces immersed in natural aqueous environments. Biofilms form particu-larly fast in flow systems where a regular nutrient supply is provided to the bacteria. The reason for the existence of the biofilm is that it allows the micro-organisms to stick and to multiply on surfaces. Micro-organisms undergo a wide range of physiological and morphological adaptations in response to environmental changes. In biofilms, different gradients of chemicals, nutrients and oxygen create micro-environments to which micro-organisms must adapt to survive.
t is estimated over 95% of bacteria existing in nature are in biofilms.[1] The slime layer that forms on rocks in streams is a classic example of a biofilm. Biofilms are ubiqui-tous; they form on virtually all surfaces immersed in natural aqueous environments. Biofilms form particu-larly fast in flow systems where a regular nutrient supply is provided to the bacteria. The reason for the existence of the biofilm is that it allows the micro-organisms to stick and to multiply on surfaces. Micro-organisms undergo a wide range of physiological and morphological adaptations in response to environmental changes. In biofilms, different gradients of chemicals, nutrients and oxygen create micro-environments to which micro-organisms must adapt to survive.
Microbial biofilms pathogenicity and treatment strategiesPratyush Kumar Das
Microbial biofilms are complex structures wherein the planktonic cells change their growth mode to the sessile form. This kind of growth is assisted by the formation of a matrix of extracellular polymeric substances (EPS) which encapsulates the bacterial cells within it and thus, provides an additional protection. These biofilms are highly resistant to high concentration of antibiotics and poses a great threat towards public health. These biofilms are even beyond the access of a normal human immune system and are involved in infections of teeth, lungs and many other diseases. There lies an immediate need to replace the extensive use of antibiotics with new emerging strategies. The review intends to provide an insight on the various perspectives of microbial biofilms including their formation, composition, mechanism of communication (Quorum sensing) and pathogenicity. Recent emerging strategies have also been discussed that can be considered for successful eradication or inhibition of biofilms and related infections.
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
1) Bacteria have evolved a wide range of weapons to harm competitors, including chemicals, toxins, and viruses. The evolution of these weapons is shaped by factors like cell density, nutrients, and spatial arrangements.
2) Bacteria employ diverse combat behaviors like preemptive attacks, suicidal attacks, and tit-for-tat responses. However, the reasons bacteria carry so many weapons and often use them remains poorly understood.
3) Bacterial aggression can strongly impact communities through complex evolutionary dynamics that influence species over space and time. Understanding bacterial warfare is important for manipulating systems like the human microbiome.
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.
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.
The term probiotics is a relatievly new word meaning “for life” and is currently used to name bacteria associated with beneficial effects for humans and animals. The development of resistance to range of antibiotics by some important pathogen has raised a possibility of return to pre antibiotic dark ages. So there was need of new treatment paradigm to be introduced to treat periodontal diseases. This need was fulfilled by the introduction of probiotics. Probiotics are counterparts of antibiotics thus are free from concerns for developing resistance, further they are body’s own resident flora hence are most easily adapted to host. The buzz about probiotics has become a roar but despite great promises, probiotics work is limited to gut. Periodontal works are sparse and need validation by large randomized trials. It can be said probiotics are still in “infancy” in terms of periodontal health benefits, but surely have opened door for a new paradigm of treating disease on a nano molecular mode. Novel species are likely to be added in the future as research data
accumulate. In-depth understanding of the intrinsic microbial ecological control of commensal microbiota may introduce new putative species to this discussion.
Oral health is inextricably linked to general health, and vice versa.
The mouth is the gateway of the body to the external world and represents one of the most biologically complex sites in the body.
Antimicrobial Defense System in Saliva, Antioxidant Role of Saliva, Maintenance of pH, Maintenance of Mucous Membrane Integrity, Maintenance of Ecological Balance, Maintenance of Tooth Integrity, Debridement & Lavage, Soft Tissue Repair, Saliva & Dental Caries, As Diagnostic Marker.
,
Esoteric communique amid microbes in an oral biofilmShruti Maroo
The document summarizes communication between microorganisms in oral biofilms. It discusses how bacterial cells interact and communicate with each other and other species via chemical signaling molecules during biofilm formation and development. Bacteria use quorum sensing to regulate processes like virulence, biofilm formation, and compete or cooperate with other species. The interactions can be antagonistic through competition for nutrients or synergistic through metabolic cooperation. Understanding these microbial communications could help develop novel therapies to disrupt pathogenic biofilms.
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.
Porphyromonas gingivalis is a gram-negative, anaerobic bacteria implicated in periodontitis. It is a late colonizer that survives and proliferates in the subgingival biofilm through invasion of host cells and evasion of the immune system. P. gingivalis functions as a keystone pathogen in the polymicrobial synergy and dysbiosis model of periodontal disease, where it can elevate the virulence of the entire microbial community and impair host immune responses, leading to tissue destruction. Targeting the pathogenic microbial community as a whole, rather than P. gingivalis alone, may be a more effective therapeutic strategy for treating periodontitis.
This document summarizes a study that isolated three strains of Lactobacillus (L. plantarum, L. acidophilus, L. casei) from human intestinal samples. It evaluated the antibacterial activity of these strains against five strains of Staphylococcus aureus, including three methicillin-resistant S. aureus strains. L. casei showed the highest inhibitory activity. The study aimed to explore the potential of isolated intestinal Lactobacillus strains to control methicillin-resistant S. aureus infections.
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Dental plaque as a biofilm and a microbial community
1. Dental plaque as a biofilm and a microbial community – implications for health and
disease
Abstract
Dental plaque is a structurally- and functionally-organized biofilm. Plaque forms in an ordered
way and has a diverse microbial composition that, in health, remains relatively stable over time
(microbial homeostasis). The predominant species from diseased sites are different from those
found in healthy sites, although the putative pathogens can often be detected in low numbers at
normal sites. In dental caries, there is a shift toward community dominance by acidogenic and
acid-tolerating species such as mutans streptococci and lactobacilli, although other species with
relevant traits may be involved. Strategies to control caries could include inhibition of biofilm
development (e.g. prevention of attachment of cariogenic bacteria, manipulation of cell signaling
mechanisms, delivery of effective antimicrobials, etc.), or enhancement of the host defenses.
Additionally, these more conventional approaches could be augmented by interference with the
factors that enable the cariogenic bacteria to escape from the normal homeostatic mechanisms
that restrict their growth in plaque and out compete the organisms associated with health.
Evidence suggests that regular conditions of low pH in plaque select for mutans streptococci and
lactobacilli. Therefore, the suppression of sugar catabolism and acid production by the use of
metabolic inhibitors and non-fermentable artificial sweeteners in snacks, or the stimulation of
saliva flow, could assist in the maintenance of homeostasis in plaque. Arguments will be
presented that an appreciation of ecological principles will enable a more holistic approach to be
taken in caries control.
Introduction
Dental plaque is the community of microorganisms found on a tooth surface as a biofilm,
embedded in a matrix of polymers of host and bacterial origin [1,2]. Of clinical relevance is the
fact that biofilms are less susceptible to antimicrobial agents, while microbial communities can
display enhanced pathogenicity (pathogenic synergism) [3]. The structure of the plaque biofilm
might restrict the penetration of antimicrobial agents, while bacteria growing on a surface grow
slowly and display a novel phenotype, one consequence of which is a reduced sensitivity to
inhibitors [4]. Plaque is natural and contributes (like the resident microflora of all other sites in
the body) to the normal development of the physiology and defenses of the host [5].
Development of dental plaque biofilms
Dental plaque forms via an ordered sequence of events, resulting in a structurally- and
functionally-organized, species-rich microbial community [2]. Distinct stages in plaque
formation include: acquired pellicle formation; reversible adhesion involving weak long-range
physico-chemical interactions between the cell surface and the pellicle, which can lead to
stronger adhesin-receptor mediated attachment; co-adhesion resulting in attachment of secondary
colonizers to already attached cells (Cisar – this symposium)[6]; multiplication and biofilm
formation (including the synthesis of exopolysaccharides) and, on occasion, detachment. The
increase in knowledge of the mechanisms of bacterial attachment and co-adhesion could lead to
strategies to control or influence the pattern of biofilm formation (Cisar – this symposium).
2. Analogs could be synthesized to block adhesin-receptor attachment or co-adhesion, and the
properties of the colonizing surfaces could be chemically modified to make them less conducive
to microbial colonization. However, cells can express multiple types of adhesin [7,8], so that
even if a major adhesin is blocked, other mechanisms of attachment may be invoked.
Furthermore, although adhesion is necessary for colonization, the final proportions of a species
within a mixed culture biofilm such as dental plaque will depend ultimately on the ability of an
organism to grow and outcompete neighboring cells.
Once formed, the overall composition of the climax community of plaque is diverse, with many
species being detected at individual sites. Molecular ecology approaches, in which 16S rRNA
genes are amplified from plaque samples, have identified >600 bacterial and Archae taxa, of
which approximately 50% are currently unculturable [9]. Once plaque forms, its species
composition at a site is characterized by a degree of stability or balance among the component
species, in spite of regular minor environmental stresses, e.g., from dietary components, oral
hygiene, host defenses, diurnal changes in saliva flow, etc. This stability (termed microbial
homeostasis) is not due to any biological indifference among the resident organisms, but is due
to a balance imposed by numerous microbial interactions, including examples of both synergism
and antagonism [10]. These include conventional biochemical interactions such as those
necessary to catabolize complex host glycoproteins and to develop food chains, but in addition,
more subtle cell-cell signalling can occur. This signalling can lead to coordinated gene
expression within the microbial community, and these signalling strategies are currently being
viewed as potential targets for novel therapeutics [11,12].
Perturbations to dental plaque
In any ecosystem, microbial homeostasis can break down on occasion due to a substantial
change in a parameter that is critical to maintaining ecological stability at a site, resulting in the
outgrowth of previously minor components of the community. A clinical consequence of this
breakdown in the mouth can be disease.
Significant parameters regulating homeostasis in the mouth include the integrity of the host
defenses (including saliva flow) and the composition of the diet [13]. Subjects who regularly
consume dietary components with a high fermentable sugar content have greater proportions of
mutans streptococci and lactobacilli in plaque, while impairment of neutrophil function is a risk
factor for periodontal diseases. Much less is known about the significance of particular
antimicrobial peptides in regulating the resident microflora at sites in the body, but a reduction in
some of their activities may increase the risk of caries (Dale – this symposium). Certainly,
antimicrobial peptides are being recognized as important components in controlling microbial
populations in the mouth, although their role is complex because they are multi-functional and
have more than a mere antimicrobial action; for example, by linking the innate and adaptive arms
of the immune response [14].
In addition, identification of factors that regulate the natural homeostasis present in plaque
during health but, when perturbed, drive the enrichment of putative oral pathogens could open up
novel ways to control plaque composition. Manipulation of these ecological influences could
help maintain the beneficial microbial composition and normal metabolic activity of plaque
biofilms, and augment more conventional approaches to control caries. These concepts will be
explored throughout the remainder of this paper.
3. Dental plaque and disease
Numerous studies have been undertaken to determine the composition of the plaque microflora
from diseased sites in order to try and identify those species directly implicated in causing
pathology. Interpretation of the data from such studies is difficult because plaque-mediated
diseases occur at sites with a pre-existing diverse resident microflora, and the traits associated
with cariogenicity (acid production, acid tolerance, intracellular and extracellular polysaccharide
production) are not restricted to a single species. A comparison of the properties of strains
representing several streptococcal species have shown considerable overlap in the expression of
these cariogenic traits [15] (see below). Microorganisms in biofilms such as plaque are in close
physical contact, and this can increase the probability of interactions, some of which can
modulate the pathogenic potential of cariogenic bacteria (for example, Kuramitsu and Wang –
this symposium). Similarly, the consequence of acid production by cariogenic species can be
ameliorated by the development of food chains with Veillonella spp., or due to base production
by neighboring organisms. Not surprisingly, therefore, there has been only limited success in
using the presence of specific species as diagnostic or prognostic indicators of disease. The
advent of microarrays, in which the presence of all of the possible groups of micro-organisms in
plaque can be determined, may enable particular microbial profiles (or molecular "signatures") to
be identified that correlate with caries or periodontal disease (Stahl, this symposium), although
markers of biochemical activity might also be needed.
Despite all of these issues, clinical studies have shown that caries is associated with increases in
the proportions of acidogenic and aciduric (acid-tolerating) bacteria, especially mutans
streptococci (such as S. mutans and S. sobrinus) and lactobacilli, which are capable of
demineralizing enamel [16-19]. These bacteria can rapidly metabolize dietary sugars to acid,
creating locally a low pH. These organisms grow and metabolize optimally at low pH. Under
such conditions they become more competitive, whereas most species associated with enamel
health are sensitive to acidic environmental conditions. However, although mutans
streptococci are strongly implicated with caries, the association is not unique; caries can occur in
the apparent absence of these species, while mutans streptococci can persist without evidence of
detectable demineralization [20,13]. Indeed, in such circumstances, some acidogenic, non-
mutans streptococci are implicated with disease [18,21,22]. Detailed studies of the glycolytic
activity of a large number of oral streptococci have shown that some strains of non-mutans
streptococci(e.g.S. mitis biovar 1 and S. oralis) can still metabolize sugars to acid at a moderately
low environmental pH at rates comparable to those achieved by mutans streptococci[15].
Source of cariogenic pathogens
The origin and role of oral pathogens has been the subject of much debate. Indeed, the resolution
to this debate is pivotal to the development of effective plaque control strategies. Early studies
using conventional culture techniques often failed to recover the putative pathogens from healthy
sites or, when pathogens were present, they comprised only a small proportion of the microflora.
However, the recent application of more sensitive molecular techniques has led to the frequent
detection of low levels of several pathogens (implicated in caries and periodontal diseases) at a
wide range of sites [23]. Bacterial typing schemes have shown that identical strains of putative
cariogenic bacteria can be found in the plaque of mother (or other close caregiver) and
infants[24], implying that transmission of such bacteria can occur. In either situation (i.e. natural
low levels of "pathogens" or low levels of exogenously-acquired "pathogens"), these species
4. would have to outcompete the already established residents of the microflora in order to achieve
an appropriate degree of numerical dominance to cause disease. As argued above, in order for
this to happen, the normal homeostatic mechanisms would need to be disrupted, and this is only
likely to occur if there is a major disturbance to the local habitat (Figure 1). This suggests that
plaque-mediated diseases result from imbalances in the resident microflora resulting from an
enrichment within the microbial community of the pathogens due to the imposition of strong
selective pressures. If so, interference with these driving forces could prevent pathogen selection
and reduce disease incidence.
Figure 1. Schematic representation of the relationship between the microbial
composition of dental plaque in health and disease. Potential pathogens (grey) may be present in
low numbers in plaque, or transmitted in low numbers to plaque; both situations may be
compatible with health. A major ecological pressure will be necessary for such pathogens to
outcompete other members of the resident microflora (white) and achieve the levels (numerical
dominance) needed for disease to occur. Possible ecological pressures for caries include a sugar-
rich diet, conditions of low pH, or low saliva flow. Disease could be prevented not only by
targeting the pathogen directly (e.g. with antimicrobial or anti-adhesion agents) but also
indirectly by interfering with the ecological pressure responsible for the selection of the
pathogen.
Factors responsible for the disruption of microbial homeostasis
Studies of a range of habitats have given clues as to the type of factors capable of disrupting the
intrinsic homeostasis that exists within microbial communities. A common feature is a
significant change in the nutrient status, such as the introduction of a novel substrate or a major
chemical perturbation to the site. For example, in environmental microbiology, it is recognized
that nitrogenous fertilizers washed off farmland into lakes and ponds can promote overgrowth by
algae. The algae can consume dissolved oxygen in the water, leading to the loss of aerobic
microbial, plant, and insect life (eutrophication). Similarly, atmospheric pollution with sulphur
dioxide and nitrogen oxides can result in acid rain, causing damage to plants and trees, and loss
of aquatic life.
The local environment is known to change in plaque during disease. Caries is associated with a
more regular intake of fermentable carbohydrates in the diet, and hence plaque is exposed more
frequently to low pH. The effect of such environmental changes in nutrient availability and pH
on gene expression by oral bacteria predominating in either health or disease has shown that
organisms such as mutans streptococci are better able to adapt to low pH, and they up-regulate a
number of genes that protect against acid stress. For example, cells of S. mutans up-regulate a
number of specific proteins and functions when exposed to sub-lethal pH values (approximately
5.5). This enhances survival under acidic conditions such as those encountered in caries
lesions[25-27]. These differences in phenotype will alter the competitiveness of bacteria in
plaque. Laboratory modeling studies involving diverse but defined communities of oral bacteria
have been performed to answer specific questions concerning the consequence of such changes
on the relative competitiveness of individual species and the impact on community stability.
Analysis of these studies led to the formulation of an alternative hypothesis relating the role of
5. oral bacteria to dental disease, and the identification of factors that disrupt the natural balance of
the resident plaque microflora.
Impact of environmental change – mixed culture modeling studies
As stated earlier, individuals who frequently consume sugar in their diet generally have elevated
levels of cariogenic bacteria such as mutans streptococci and lactobacilli in their plaque, and are
at greater risk of dental caries. In animal studies or epidemiological surveys of humans, it can
never be determined whether the rise in cariogenic bacteria is due to the sudden availability of
sugar per se (e.g. because of more efficient sugar transport systems in these bacteria), or is a
response to the inevitable conditions of low pH following sugar consumption. Exploitation of the
unique benefits of parameter control in the chemostat, coupled with the reproducibility of a
defined mixed culture inoculum, enabled these linked effects to be separated for the first
time[28]. Two mixed culture chemostats were inoculated with 9 or 10 species (representative of
those in health and disease) in a growth medium at pH 7.0 in which mucin was the main source
of carbohydrate; under these conditions, S. mutans and Lactobacillus rhamnosus were
noncompetitive and made up <1% of the total microflora (Table 1). Once the consortia were
stably established, both chemostats were pulsed daily for ten consecutive days with a
fermentable sugar (glucose). In one chemostat, the pH was maintained automatically throughout
the study at neutral pH (as is found in the healthy mouth) in order to determine the effect of the
addition of a fermentable sugar on culture stability, while in the other the pH was allowed to fall
by bacterial metabolism for six hours after each pulse (as occurs in vivo); the pH was then
returned to neutrality for 18 hours prior to the next pulse [28]. Daily pulses of glucose for 10
consecutive days at a constant pH 7.0 had little or no impact on the balance of the microbial
community, and the combined proportions of S. mutans and L. rhamnosus stayed at ca. 1% of the
total microflora (Table 1). In contrast, however, when the pH was allowed to change after each
pulse, there was a progressive selection of the cariogenic (and acid-tolerating) species at the
expense of bacteria associated with dental health. After the final glucose pulse, the community
was dominated by species implicated in caries (S. mutans and L. rhamnosus comprised ca. 55%
of the microflora) [28]. When this study was repeated, but the pH fall was restricted after each
glucose pulse to either pH 5.5, 5.0, or 4.5 in independent experiments [29], a similar enrichment
of cariogenic species at the expense of healthy species was observed, but their rise was directly
proportional to the extent of the pH fall (Table 1). Collectively, these studies showed
conclusively that it was the low pH generated from sugar metabolism rather than sugar
availability that led to the breakdown of microbial homeostasis in dental plaque. This finding has
important implications for caries control and prevention; the data suggest that the selection of
cariogenic bacteria could be prevented if the pH changes following sugar metabolism could be
reduced (see later).
Table 1. The effect of glucose and low pH on the stability of a microbial community. A mixed
culture of 9 oral bacteria (representative of those found in health and disease) were grown in a
mucin-based medium at a constant pH 7.0. In independent experiments, the culture was pulsed
daily on 10 consecutive days with 28 mM glucose. In one culture the pH was maintained
throughout the pulsing at pH 7.0, while in other experiments the pH was allowed to fall by
bacterial metabolism for 6 hours to pre-set levels of pH 5.5, 5.0 or 4.5. In a final study, the pH
was allowed to fall without any pH control imposed [28,29]. Viable counts were determined on
selective and non-selective media; proportions are shown after the final glucose pulse for two
species implicated in caries and for two species associated with sound enamel
6. Current hypotheses to explain the role of plaque bacteria in the etiology of dental caries
There have been two main schools of thought on the role of plaque bacteria in the etiology of
caries and periodontal diseases. The "Specific Plaque Hypothesis" proposed that, out of the
diverse collection of organisms comprising the resident plaque microflora, only a few species are
actively involved in disease [30]. This proposal focused on controlling disease by targeting
preventive measures and treatment against a limited number of organisms. In contrast, the "Non-
Specific Plaque Hypothesis" considered that disease is the outcome of the overall activity of the
total plaque microflora [31]. In this way, a heterogeneous mixture of microorganisms could play
a role in disease. In some respects, the arguments about the relative merits of these hypotheses
may be about semantics, since plaque-mediated diseases are essentially mixed culture
(polymicrobial) infections, but in which only a limited (perhaps specific!) number of species are
able to predominate.
More recently, an alternative hypothesis has been proposed (the "Ecological Plaque Hypothesis")
that reconciles the key elements of the earlier two hypotheses [32]. The data from the mixed
cultures studies described above, and from other work, provide an argument for plaque-mediated
diseases being viewed as a consequence of imbalances in the resident microflora resulting from
an enrichment within the microbial community of these "oral pathogens.". Potentially cariogenic
bacteria may be found naturally in dental plaque, but these organisms are only weakly
competitive at neutral pH, and are present as a small proportion of the total plaque community.
In this situation, with a conventional diet, the levels of such potentially cariogenic bacteria are
clinically insignificant, and the processes of de- and re-mineralization are in equilibrium. If the
frequency of fermentable carbohydrate intake increases, then plaque spends more time below the
critical pH for enamel demineralization (approximately pH 5.5). The effect of this on the
microbial ecology of plaque is two-fold. Conditions of low pH favor the proliferation of acid-
tolerating (and acidogenic) bacteria (especially mutans streptococci and lactobacilli), while
tipping the balance towards demineralization (Figure 2). Greater numbers of bacteria such as
mutans streptococci and lactobacilli in plaque would result in more acid being produced at even
faster rates, thereby enhancing demineralization still further. Other bacteria could also make acid
under similar conditions, but at a slower rate [15]. These bacteria could be responsible for some
of the initial stages of demineralization or could cause lesions in the absence of other (more
overt) cariogenic species in a more susceptible host. If aciduric species were not present initially,
then the repeated conditions of low pH coupled with the inhibition of competing organisms
might increase the likelihood of successful colonization by mutans streptococci or lactobacilli.
This sequence of events would account for the lack of total specificity in the microbial etiology
of caries and explain the pattern of bacterial succession observed in many clinical studies.
Figure 2. The "ecological plaque hypothesis" and the prevention of dental caries.
Caries is a result of changes in the environment due to acid production from the fermentation of
dietary carbohydrates, which selects for acidogenic and acid-tolerating species such as mutans
streptococci and lactobacilli. Disease could be prevented not only by targeting the putative
pathogens directly, but also by interfering with the key environmental factors driving the
deleterious ecological shifts in the composition of the plaque biofilms [32].
Key features of this hypothesis are that (a) the selection of "pathogenic" bacteria is directly
coupled to changes in the environment (Figure 2), and (b) diseases need not have a specific
etiology; any species with relevant traits can contribute to the disease process. Thus, mutans
7. streptococci are among the best adapted organisms to the cariogenic environment (high
sugar/low pH), but such traits are not unique to these bacteria. Strains of other species, such as
members of the S. mitis-group, also share some of these properties and therefore will contribute
to enamel demineralization [15,21,22]. A key element of the ecological plaque hypothesis is that
disease can be prevented not only by targeting the putative pathogens directly, e.g. by
antimicrobial or anti-adhesive strategies, but also by interfering with the selection pressures
responsible for their enrichment [32].
In dental caries, regular conditions of sugar/low pH or reduction in saliva flow appear to be
primary mechanisms that disrupt microbial homeostasis. Strategies that are consistent with the
prevention of disease via the principles of the ecological plaque hypothesis include the
following:
(a) Inhibition of plaque acid production, e.g. by fluoride-containing products or other metabolic
inhibitors. Fluoride not only improves enamel chemistry but also inhibits several key enzymes,
especially those involved in glycolysis and in maintaining intracellular pH [33]. Fluoride can
reduce the pH fall following sugar metabolism in plaque biofilms, and in so doing, prevent the
establishment of conditions that favor growth of acid-tolerating cariogenic species [34].
(b) avoidance between main meals of foods and drinks containing fermentable sugars and/or the
consumption of foods/drinks that contain non-fermentable sugar substitutes such as aspartame or
polyols, thereby reducing repeated conditions of low pH in plaque.
(c) the stimulation of saliva flow after main meals, e.g. by sugar-free gum. Saliva will introduce
components of the host response, increase buffering capacity, remove fermentable substrates,
promote re-mineralization, and more quickly return the pH of plaque to resting levels.
Conclusion
The key to a more complete understanding of the role of microorganisms in dental diseases such
as caries may depend on a paradigm shift away from concepts that have evolved from studies of
classical medical infections with a simple and specific (e.g. single species) etiology to an
appreciation of ecological principles. The development of plaque-mediated disease at a site may
be viewed as a breakdown of the homeostatic mechanisms that normally maintain a beneficial
relationship between the resident oral microflora and the host. When assessing treatment options,
an appreciation of the ecology of the oral cavity will enable the enlightened clinician to take a
more holistic approach and consider the nutrition, physiology, host defenses, and general well-
being of the patient, as these will affect the balance and activity of the resident oral microflora.
Future episodes of disease will occur unless the cause of any breakdown in homeostasis is
recognized and remedied. For example, a side effect of many medications is a reduction in saliva
flow. This will deleteriously impact on sugar clearance and buffering ability, thereby favoring
the growth of acid-tolerating and potentially cariogenic bacteria. Identification of such critical
control points can lead to the selection of appropriate caries preventive strategies that are tailored
to the needs of individual patients. In this way, the clinician does not just treat the end result of
the caries process, but also attempts to identify and interfere with the factors that, if left
unaltered, will inevitably lead to more disease.
Competing interests
8. The author(s) declare that they have no competing interests.
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