Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Neisseria meningitidis wikipedia , lookup
Bacterial taxonomy wikipedia , lookup
Bacteriophage wikipedia , lookup
Anaerobic infection wikipedia , lookup
Bacterial cell structure wikipedia , lookup
Small intestinal bacterial overgrowth wikipedia , lookup
What is a dental plaque? •A microbial deposit on the hard-tissue surface of the mouth comprising living and dying bacteria, their products and host compounds derived from saliva •Its role is to exclude exogenous often pathogenic microbes •However shift in the balance of the endogenous microflora of the plaque predisposes to dental and parodontal disease Maturation of dental plaque clean enamel early colonizer cocci – bacterial polysaccharides late colonizers – climax community with corn-cob fromation Tooth surfaces •non shedding surface (enamel) •pellicle (biofilm) formation form saliva and bacterial products salivary pellicle onto clean enamel Successive development of dental plaque I •Salivary pellicle comprises salivary glycoproteins and minerals •Saliva flow transports bacteria to the site •Oral streptococci and commensal Neisseriae can attach to the pellicle and not directly to the enamel (n.b. they have enhanced binding ability and increased resistance to oral defense mechansims) Successive development of dental plaque II •Long-range (distant) interactions of bacterial attachment –van der Waals’ forces – reversible (can washed off with water flush) •Short-range (close) interactions – bacterial adhesins to pellicle – irreversible! (cannot be washed off) Successive development of dental plaque III polysaccharide production •Coaggregation and coadhesion Fresh bacteria attach on the first generation of cells and their products Coaggregation and coadhesion late colonizers early colonizers Coaggregation and coadhesion Streptococcus - Streptococcus Mediated by lectins •Actinomyces – Actinomyces (carbohydrate binding protiens) •Streptococcus – Actinomyces and surface carbohydrates Corn-cob formation •Streptococcus - Corynebacterium matruchotii •Veillonella – Eubacterium Successive development of dental plaque III •Climax community forms a biofilm with high bacterial diversity and large amount of extracellular matrix •Detachment Bacteria are continuously shedding from the dental plaque Calculus (tartar) •Deposit of minerals into the plaque Risk of retaining cariogenic bacteria and conditions Smooth surface (supragingival) dental plaque Supragingival dental plaques II •Fissure plaque: mutans streptococci, Actinomyces, Veillonella, Propionibacterium, Lactobacillus •Approximal plaque: mutans streptococci, Actinomyces, (n.b. relative lack of anaerobes) Subgingival dental plaques •Gingival crevice plaque: Streptococcus mitis group, S anguinosus group, oral terponemes, Actinomyces, Rothia dentocariosa, Porphyromonas, Prevotella, Fusobacterium •Denture plaque: mutans streotococci, Veillonella, Staphylococcus aureus, Actinomyces Candida (yeast) species, Synergestic nutrional interactions in dental plaque I Collaborate breakdown of complex substrates (Host glycoproteins) •Streptococcus oralis utilizes carbohydrate sidechains •Prevotella intermedia, P.oralis, Fusobacterium nucleatum hydrolyses the protein core •Peptostreptococcus micros and Eubacterium brachy extensive amino acid fermentation Synergestic nutrional interactions in dental plaque II Utilization of bacterial polymers •Fructan of Streptococcus salivarius is hydrolized and fermented by: •mutans streptococci, Streptococcus mitis group, Actinomyces, Capnocytophaga, Fusobacterium Synergestic nutrional interactions in dental plaque III End product of primary feeder is utilized by a secondary feeder Antagonistic interactions in dental plaque •Competition for nutrients •Bacteriocin production (oral streptococci, Corynebacterium matruchotii, black pigmented anaerobes, A actinomycetemcomitans) •hydrogen peroxide production •low pH by organic acids Dental caries Localized destruction of tooth tissues by bacterial fermentation of dietary carcohydrates i.e. multifactorial plaque-related infection of enamel, cementum or dentin •Initial caries lesion – white spot still reversible •Caviation •Dentine infection •Pulpitis, inflammation of dental pulpa •Pulpal necrosis early enamel caries Multifactorial etiology of caries Plaque microbes Genetical background •shape of teeth •dentin/enamel structure •immunity caries duration of exposure nutritional factor e.g.saccharose Microbial etiology of caries •Streptococcus mutans – most acidogenic oral bacterium (rapid lactate producer) •Lactobacillus – able to grow at low pH (<5.0), produce lactic acid, involved in the progression of deep advancing carious process •Actinomyces – root surface caries after gingival recession •Veilonella – protective effect against dental caries due to secondary feeding on lactic acid and producing less cariogenic acetic and propionic acid Caries Prevention Eliminate as many cariogenic factor as possible! •Nutrition: •Cariogenic order of sugars and sugar derivatives: saccharose > glucose > fructose >> mannitol > sorbitol >> xylitol •Fluorid intake: remineralization (of fluoriapatit) inhibits bacterial glycolyis, polysaccharide synthesis •Time factor: •Regular elimination of plaques (see next slide!) A caries megelőzése •Plaque microbes: •Toothe brushing (mechanical effect) •Antimicrobial components: (chlorhexidine), fluorids, timol, triclosan, zinc compounds, enzymes: dextranase, glucanase •Probiotics? – antagonistic bacteria (non- mutans Str.) •Compenstaing host (genetic) factors: •fissure sealing •Immunization? – still at the stage of animal experiments