口微03 oral microbial colonization-2 [相容模式] - tmu
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Microsoft PowerPoint - 03 Oral Microbial Colonization-2 [] Oral
microbiology & immunology
• 1. Contemporary oral microbiology and immunology. Slots Jorgen and Martin A Taubman. Mosby.
• 2. Oral microbiology and immunology. gy gy Michael G Newman and Russel Nisengard. Saunders.
• 3. .. • 4.
• Plaque maturation is associated with an increase in filamentous organisms.
l il i• A central filamentous organism surrounded by cocci can be observed and called corncob.
2
CORNCOB Corncob
• The central filament of corncobs was composed of i) Bacterionema matruchotii,) ,
a gram-positive, rod organism • ii) Fusobacterium nucleatum
presumably associated with subgingival plaque.
• The cocci were usually S. sanguis that contained tufts of fimbriae at one pole.
Corncob
p • An outer envelope of protein in the
Fusobacteria has been identified as a receptor for the streptococcal adhesion.
• The ability of F. nucleatum to form corncob with Streptococci represent a mechanism both for infecting the oral
Corncob
mechanism both for infecting the oral cavity and for maintaining it presence in the face of forces such as gingival fluid (wash corncob away).
Bridging of Bacterial Aggregation
• One organism acts as a bridging organism between two other bacteria which do not th l i t tthemselves interact.
• S. sanguis aggregate with both A. naeslundii and Rothia dentocariosus.
3
Plaque Maturation • As the plaque ages, the flora changes from
gram-positive cocci and actinomyces to gram-negative organisms.
Plaque Maturation The maturation of plaque have many characteristics of the coaggregation reactions.
5
• At approximately 3 weeks, the flora change to a more filamentous(G-) types.
• The first evidence of gingival
Plaque Maturation
g g inflammation is edema or swelling of the gingival margins.
• If unchecked , the swelling alters the relationship of some of the supragingival plaque so that, in effect, it is
Plaque Maturation
p q , , now ’subgingival “.
• Pseudopocket - The earlisest sign of periodontal disease. Its formation is due to the swelling of tissue rather than to apical
i ti f th tt h t t
Plaque Maturation
Plaque Maturation
Subgingival Plaque Formation
• Porphyromonas gingivalis is transmitted by a parent with periodontal disease to an adolescent.
• The Porphyromonas interact withThe Porphyromonas interact with Actinomyces, which is itself attached to a streptococccus adhering to the tooth surface (a bridge).
Actinomyces P. gingivalis Streptococcus
• The adolescent had become careless in home carehome care.
• The gingival is slightly inflamed and swollen and some hemin, a blood protein that is necessary for P. gingivalis, is present in the area.
Subgingival Plaque Formation
• When P. gingivalis was transmitted, F. nucleatum was also carried over and attached to a group of S. sanguis, forming a corncob.
• F. nucleatumis , a potential pathogen, can use both sugar and proteins for food.
Subgingival Plaque Formation
Subgingival Plaque Formation
• The products of proteolytic metabolism from F. nucleatumis are d b l t d i id ll ddecarboxylated amino acids called ptomaines, which can be used as food supplies for spirochetes.
Subgingival Plaque Formation
• A combination of adhesion, coaggregation, and bridging of organisms l d h f i f h i bi lleads to the formation of the microbial community called subgingival plaque.
• These communities can contain as many as 400-500 species of bacteria or more.
7
• Test-tube-brush or bristle-brush formations are commonly observed in subgingival plaque .
• The coaggregates consist of a central• The coaggregates consist of a central axis composed of filamentous bacteria; the bristles consist of G- rods.
• Spirochetes and G- bacteria (possible Selenomonas sputigena) are commonly observed.
Plaque Metabolism
• Subgingival plaque
• Supragingival plaque
Metabolism of Host Metabolite
• The use of the host metabolite, hemin, by Porphyromonas and Prevotella.
• The ptomaines (spermine , spermidine, and putrescine) produced by the Fusobacteria are used as food supplies for Spirochetes.
Metabolism of Bacteria Metabolite
• Bacteriocins produced by A.a. may inhibit S. sanguis.
8
• Steroid hormones produced during puberty, pregnancy, and
i i fl bmenstruation influence numbers and kinds of bacteria found in the subgingival plaque.
Metabolism of Supragingival PlaqueSupragingival Plaque
Stephan Curves
• Use Stephan curves to estimate the metabolic activity of in situ plaque by
i th H f l ithmeasuring the pH of plaque with a microelectrode after feedings of various substrates.
Metabolism of Sugars by Supragingival Plaque
• When supragingival plaques were fed sugars, the pH decrease significantly.
• Stephan curves showed that plaque in patients with high caries activity shows a greater decrease in pH than found in plaque of patients with low or no caries activity.
9
Metabolism of Urea by Supragingival Plaque
• Feeding supragingival plaque which is rich in S.sanguis with urea resulted in an increase in pH, it was associated with the arginine dihydrolyase pathway .
• The ammoniated tooth pastes containing urea were developed.
Control of Plaque Metabolism
Anticariogenic Agent
• Sialin found in saliva, a tetrapeptide that is composed of glycene, lysine and argining,
has been synthesized as an anticariogenic agent.
• The sugarless gums, which contain mammitol and sorbitol didn’t reduce the pH as sugars did.
Calculus Formation
• Dental calculus result from the deposition of calcium salts, particularly phosphates, in organic debris form dead and dying microorganisms attached to other surface (the oldest layer of plaque).
• Saliva is supersaturated with calcium and phosphate ions.
Calculus Formation
• Calcium phosphates are very insoluble and readily precipitate in the matrix of dead cells lysing close to the tooth surface.lysing close to the tooth surface.
• Calculus is usually associated with deepest layers of plaque, and it tenaciously adheres to the tooth surface.
10
Calculus Formation
• In living plaque, some organisms produce phosphates that are secreted or released as a result of cell lysis; this also results in high concentration of phosphate ion in plaqueconcentration of phosphate ion in plaque.
• Certain viable bacteria in plaque can calcify themselves in the matrix.
Calculus Formation
• Removal of the calculus deposits has the practical value of removing a rough nidus that provides a large surface area for the attachment of the pathogenic soft tissues.
From Plaque to Disease.
• The plaque enriched with the Streptococci mutans lead to dental caries.
• Periodontal disease appears to be associated ith G bi dwith G- anaerobic rods.
• P. gingivalis and A. actinocmycetemcomitans are associated with adult types of periodontitis and juvenile periodontitis respectively.
Possible Strategies to Control Oral Biofilm
Control of nutrients • addition of base-generating
nutrients (arginine)
• reduction of GCF flow through antiinflammatory agents
• inhibition of key microbal enzymes
Control of redox potential • redox agents • oxygenating agents
fluoride stimulate base productio
• 1. Contemporary oral microbiology and immunology. Slots Jorgen and Martin A Taubman. Mosby.
• 2. Oral microbiology and immunology. gy gy Michael G Newman and Russel Nisengard. Saunders.
• 3. .. • 4.
• Plaque maturation is associated with an increase in filamentous organisms.
l il i• A central filamentous organism surrounded by cocci can be observed and called corncob.
2
CORNCOB Corncob
• The central filament of corncobs was composed of i) Bacterionema matruchotii,) ,
a gram-positive, rod organism • ii) Fusobacterium nucleatum
presumably associated with subgingival plaque.
• The cocci were usually S. sanguis that contained tufts of fimbriae at one pole.
Corncob
p • An outer envelope of protein in the
Fusobacteria has been identified as a receptor for the streptococcal adhesion.
• The ability of F. nucleatum to form corncob with Streptococci represent a mechanism both for infecting the oral
Corncob
mechanism both for infecting the oral cavity and for maintaining it presence in the face of forces such as gingival fluid (wash corncob away).
Bridging of Bacterial Aggregation
• One organism acts as a bridging organism between two other bacteria which do not th l i t tthemselves interact.
• S. sanguis aggregate with both A. naeslundii and Rothia dentocariosus.
3
Plaque Maturation • As the plaque ages, the flora changes from
gram-positive cocci and actinomyces to gram-negative organisms.
Plaque Maturation The maturation of plaque have many characteristics of the coaggregation reactions.
5
• At approximately 3 weeks, the flora change to a more filamentous(G-) types.
• The first evidence of gingival
Plaque Maturation
g g inflammation is edema or swelling of the gingival margins.
• If unchecked , the swelling alters the relationship of some of the supragingival plaque so that, in effect, it is
Plaque Maturation
p q , , now ’subgingival “.
• Pseudopocket - The earlisest sign of periodontal disease. Its formation is due to the swelling of tissue rather than to apical
i ti f th tt h t t
Plaque Maturation
Plaque Maturation
Subgingival Plaque Formation
• Porphyromonas gingivalis is transmitted by a parent with periodontal disease to an adolescent.
• The Porphyromonas interact withThe Porphyromonas interact with Actinomyces, which is itself attached to a streptococccus adhering to the tooth surface (a bridge).
Actinomyces P. gingivalis Streptococcus
• The adolescent had become careless in home carehome care.
• The gingival is slightly inflamed and swollen and some hemin, a blood protein that is necessary for P. gingivalis, is present in the area.
Subgingival Plaque Formation
• When P. gingivalis was transmitted, F. nucleatum was also carried over and attached to a group of S. sanguis, forming a corncob.
• F. nucleatumis , a potential pathogen, can use both sugar and proteins for food.
Subgingival Plaque Formation
Subgingival Plaque Formation
• The products of proteolytic metabolism from F. nucleatumis are d b l t d i id ll ddecarboxylated amino acids called ptomaines, which can be used as food supplies for spirochetes.
Subgingival Plaque Formation
• A combination of adhesion, coaggregation, and bridging of organisms l d h f i f h i bi lleads to the formation of the microbial community called subgingival plaque.
• These communities can contain as many as 400-500 species of bacteria or more.
7
• Test-tube-brush or bristle-brush formations are commonly observed in subgingival plaque .
• The coaggregates consist of a central• The coaggregates consist of a central axis composed of filamentous bacteria; the bristles consist of G- rods.
• Spirochetes and G- bacteria (possible Selenomonas sputigena) are commonly observed.
Plaque Metabolism
• Subgingival plaque
• Supragingival plaque
Metabolism of Host Metabolite
• The use of the host metabolite, hemin, by Porphyromonas and Prevotella.
• The ptomaines (spermine , spermidine, and putrescine) produced by the Fusobacteria are used as food supplies for Spirochetes.
Metabolism of Bacteria Metabolite
• Bacteriocins produced by A.a. may inhibit S. sanguis.
8
• Steroid hormones produced during puberty, pregnancy, and
i i fl bmenstruation influence numbers and kinds of bacteria found in the subgingival plaque.
Metabolism of Supragingival PlaqueSupragingival Plaque
Stephan Curves
• Use Stephan curves to estimate the metabolic activity of in situ plaque by
i th H f l ithmeasuring the pH of plaque with a microelectrode after feedings of various substrates.
Metabolism of Sugars by Supragingival Plaque
• When supragingival plaques were fed sugars, the pH decrease significantly.
• Stephan curves showed that plaque in patients with high caries activity shows a greater decrease in pH than found in plaque of patients with low or no caries activity.
9
Metabolism of Urea by Supragingival Plaque
• Feeding supragingival plaque which is rich in S.sanguis with urea resulted in an increase in pH, it was associated with the arginine dihydrolyase pathway .
• The ammoniated tooth pastes containing urea were developed.
Control of Plaque Metabolism
Anticariogenic Agent
• Sialin found in saliva, a tetrapeptide that is composed of glycene, lysine and argining,
has been synthesized as an anticariogenic agent.
• The sugarless gums, which contain mammitol and sorbitol didn’t reduce the pH as sugars did.
Calculus Formation
• Dental calculus result from the deposition of calcium salts, particularly phosphates, in organic debris form dead and dying microorganisms attached to other surface (the oldest layer of plaque).
• Saliva is supersaturated with calcium and phosphate ions.
Calculus Formation
• Calcium phosphates are very insoluble and readily precipitate in the matrix of dead cells lysing close to the tooth surface.lysing close to the tooth surface.
• Calculus is usually associated with deepest layers of plaque, and it tenaciously adheres to the tooth surface.
10
Calculus Formation
• In living plaque, some organisms produce phosphates that are secreted or released as a result of cell lysis; this also results in high concentration of phosphate ion in plaqueconcentration of phosphate ion in plaque.
• Certain viable bacteria in plaque can calcify themselves in the matrix.
Calculus Formation
• Removal of the calculus deposits has the practical value of removing a rough nidus that provides a large surface area for the attachment of the pathogenic soft tissues.
From Plaque to Disease.
• The plaque enriched with the Streptococci mutans lead to dental caries.
• Periodontal disease appears to be associated ith G bi dwith G- anaerobic rods.
• P. gingivalis and A. actinocmycetemcomitans are associated with adult types of periodontitis and juvenile periodontitis respectively.
Possible Strategies to Control Oral Biofilm
Control of nutrients • addition of base-generating
nutrients (arginine)
• reduction of GCF flow through antiinflammatory agents
• inhibition of key microbal enzymes
Control of redox potential • redox agents • oxygenating agents
fluoride stimulate base productio