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Dental plaque
- 1. DENTAL PLAQUE GUIDED BY:PRESENTED BY: DR. PARUL ANEJA (READER) DR. MARIYAM MOMIN II YEAR PG DEPARTMENT OF PERIODONTOLOGY & ORAL IMPLANTOLOGY.
- 2. CONTENTS • Biofilms • Quorumsensing • Horizontal gene transfer • Tooth accumulated deposits • Materia alba • Dental pellicle • Dental stains • Dental plaque • Classification of dental plaque • Composition of plaque • Plaque formation • Subgingival microbial complexes • Metabolism of dental plaque bacteria • Structure of dental plaque • Clinical assessment of plaque • Plaque hypothesis
- 3. BIOFILMS • Biofilm isdefined as matrix enclosed bacterial population adherent to each other and/or to surface or interfaces - Costerton
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- 6. General properties ofbiofilm & microbial communities S.No. General property Dental plaque example 1 Open architecture Presence of channel or pores 2 Broader habitat range Obligate anaerobes in an overtly aerobic environment 3 More efficient metabolism Complete catabolism of complete host macromolecule (mucins) by consortium of food webs 4 Enhanced virulence Pathogenic synergism in abscess & periodontal disease 5 Protection from host defense desiccation Production of extracellular matrix to form a functional matrix 6 Neutralization of inhibitors Beta lactamases production by neighboring cells to protect sensitive organism 7 Novel gene expression Synthesis of novel proteins upon attachment 8 Co-coordinated gene response Production of cell to cell signaling molecules 9 Cell to cell signaling Production of CSP, AI2 etc. cross talk with host epithelial cells 10 Spatial &environmental heterogenticity pH & oxygen gradients; co-adhesion.
- 7. TOOTH ACCUMULATED DEPOSITS • DEVELOPMENTALORIGIN 1. Dental cuticle 2. Coronal cementum 3. Sub-surface enamel matrix 4. Reduced enamel epithelium • ACQUIRED COATINGS 1. Salivary pellicle 2. Bacterial coating – plaque & materia alba 3. Sub-surface pellicle 4. Surface stains
- 8. MATERIA ALBA • Materiaalba refers to the soft accumulation of bacteria & tissue cells that lack the organized structure of dental plaque and are easily displaced with a water spray – Carranza • COMPOSITION - Food debris - Dead tissue elements - Purulent material - Mixture of salivary proteins & lipids • CONSISTENCY : soft & sticky • SIGNIFICANCE : ideal growth medium for bacteria which can induce gingival inflammation.
- 9. DENTAL PELLICLE • SYNONYM– Acquired pellicle • DEFINITION - Pellicle is defined as tooth or mucosal adherent salivary protein - PLR • TYPES 1. Unstained pellicle 2. Stained pellicle 3. Sub-surface pellicle • COMPOSITION 1. Glycoproteins 2. Phosphoproteins 3. Proline rich proteins 4. Histidine rich proteins 5. Enzymes - amylase • FORMATION Components of GCF & saliva (+ve) Hydroxyapatite on the enamel surface (-ve) Pellicle +
- 10. Difference between Food debris,Materia alba & Plaque S.No. Feature Food debris Materia alba Plaque 1 Structure No structure Amorphous Definite structure 2 Adherence None Loose Close 3 Effect of rinsing Dislodge readily Dislodge by forceful rinsing Do not dislodge Food debris Materia alba Plaque
- 11. DENTAL STAINS • Theyare the pigmented deposits on the tooth surface. Green stains: - Gingival 3rd of facial surface of maxillary anterior teeth. - Penicillium & aspergillus - Common in children (boys). Black stains: - Thin black line on the facial & lingual surfaces of teeth near gingival margin in people with good oral hygiene - Actinomyces species - Common in women. Brown stains: - Buccal surface of maxillary molars & lingual surface of mandibular incisors. - Presence of tanin - Thin & translucent Acquired pigmented pellicle which is free from bacteria. - Common in people with poor oral hygiene. Metallic stains: - Bismuth pigmentation : black line - Arsenic pigmenation: black line - Mercury pigmentation: black line - Lead pigmentation: bluish red, deep blue or grey (burtonian line) - Silver pigmentation : Violet marginal line Tobacco stains: - Lingual and palatal surfaces - Common in pits, fissures & other enamel irregularities - Tobacco stain is directly proprtional to no. of cigarettes smoked per day Chlorhexidine stains: - Frequent use of chlorhexidine leads to dark yellow to brownish stain - Artificial as well as natural teeth are affected - At higher concentrations stains are more severe. Orange stains: - Facial & lingual surfaces of anterior teeth - Serratia marcescens & Flavobacterium lutescens - Rare stain
- 12. DENTAL PLAQUE • SYNONYMS -Microcorm - Host associated biofilm • DEFINITION - Dental plaque is defined as a specific but highly variable structural entity resulting from sequential colonization and growth of microorganisms on the surfaces of teeth and restoration consisting of microorganisms of various strains and species embedded in the extracellular matrix, composed of bacterial metabolic products and substance from serum, saliva and blood. - WHO 1978 - Dental plaque is defined as a soft deposit that forms the biofilm adherent to the tooth surface or other hard surfaces in the oral cavity including removable and fixed restorations. - Carranza - Microbial dental plaque described as aggregations of bacteria that are tenaciously attached to the teeth and other surfaces. - Genco
- 13. PLAQUE RETENTIVE AREAS •NATURAL AREAS / FACTORS Supra-gingival 1. Carious lesions 2. Exposed cementum 3. Supra-gingival calculus Sub-gingival 1. sub-gingival calculus 2. Cavitated caries lesions 3. Furcation involvement 4. Cemento-enamel junction 5. Rough, unplaned cementum 6. Root grooved & enamel projections 7. Deep & narrow infrabony pockets. • IATROGENIC FACTORS 1. Orthodontic bands 2. Overhanging restorative margins 3. Overcontoured & inadequate crown margins 4. Portions of removable prosthesis that impinge on gingiva.
- 14. CLASSIFICATION OF PLAQUE Dental plaque Supra- gingival CoronalMarginal Sub-gingival Attached Tooth associated Tissue associated Peri-implant plaque Unattached
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- 16. Differencebetweentoothassociatedandtissue associatedsubgingivalplaque S.N o. Tooth associated subgingival plaque Tissueassociated subgingival plaque 1 Gram +ve bacteria predominates Gram +ve and gram –ve bacteria 2 Does not extend to junctional epithelium Extends to junctional epithelium 3 May penetrate cementum May penetrate epithelium & connective tissue 4 Microorganisms: S.sanguinis, S. mitis, A. naeslundii, A. viscosus, Eubacterium Microorganisms: Staphylococcus intermedius, S.oralis, P.micros, P. gingivalis, P. intermedia, F.nucleatum, T. forsythia. 5 Plays a role in calculus formation & root caries Plays a role in gingivitis & periodontitis.
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- 19. PLAQUE FORMATION Steps inplaque formation: 1. Formation of pellicle on the tooth surface 2. Initial adhesion/ attachment of bacteria 3. Colonization/ plaque maturation.
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- 22. METABOLISM OF DENTAL PLAQUEBACTERIA
- 23. STRUCTURE OF PLAQUE Supragingivalplaque Subgingival plaque Corncob formation Test tube-brush formation
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- 25. MICROBIAL SHIFT DURING PERIODONTALDISEASES S. No. Shift from Shift to 1 Gram positive Gram negative 2 Cocci Rods & spirochetes 3 Non-motile Motile 4 Facultative anaerobes Obligate anaerobes 5 Fermenting Proteolytic species
- 26. CLINICAL ASSESSMENT OF DENTALPLAQUE • Direct vision • Use of explorers • Disclosing solutions • Clinical records
- 27. Criteria for identificationof periodontopathogens Koch’spostulates (1870s) • It must be routinely isolated from diseased individuals. • It must be grown in pure culture in the laboratory. • It must produce a similar disease when inoculated into a susceptible host. • It must be recovered from lesions in a diseased laboratory animal. Limitations in periodontal microbiology • The inability to culture all the organisms associated with the disease. • The difficulties inherent in defining and culturing sites of the active disease. • Lack of good animal model system for the study of periodontitis.
- 28. SOCRANSKY’S POSTULATES • Mustbe associated with the disease, as evident by increase in the number of organisms at diseased sites. • Must be eliminated or decreased in sites that demonstrate clinical resolution of disease with the treatment. • Must demonstrate a host response, in the form of an alteration in the host cellular or humoral immune response. • Must be capable of causing disease in experimental animal models. • Must demonstrate virulence factors responsible for enabling the microorganism to cause destruction of the periodontal tissues.
- 29. CLINICAL SIGNIFICANCE OF PLAQUE PLAQUEIN INITIATION OF PERIODONTAL DISEASES Noxious products release from plaque bacteria Release of gingipains from P. gingivalis Destruction of host collagen Direct destruction of host soft tissue and hard tissues. Release of endotoxins from plaque bacteria Stimulation of host immune and inflammatory systems Stimulation of IL & TNF Destruction of host tissue. Direct effect of plaque Indirect effect of plaque
- 30. Role of bacteriain periodontal diseases / etiological significance of dental plaque • Plaque vs gingivitis • Plaque vs chronic periodontitis • Plaque vs LAP • Plaque Vs necrotizing periodontal diseases • Abscesses of periodontium • Periimplantitis
- 31. MICROBIAL FLORA INPERIODONTAL HEALTH & DISEASES PERIODONTAL HEALTH • S. sanguis • S. mitis • Veillonella • Streptococcus • Capnocytophaga GINGIVITIS • Gram +ve species - S. mitis - S. oralis - S. sanguis - A. viscosus - Peptostreptococcus micros • Gram –ve species - F. nucleatum - P. intermedia - Hemophilus - Capnocytophaga - Campylobacter species PREGNANCY ASSOCIATED GINGIVITIS Prevotella intermedia
- 32. CHRONIC PERIODONTITIS • P. gingivalis •B. forsythus • P. intermedia • C. rectus • E. corrodens • F. nucleatum • A. actinomycetum comitans REFRACTORY PERIODONTITIS • A. actinomycetum comitans • P. gingivalis • P. intermedia • Bacteroides forsythus NECROTIZING ULCERATIVE PERIODONTITIS - Spirochetes - P. intermedia Abscesses of the periodontium - P. intermedia - P. gingivalis - Bacteroides forsythus - Peptostreptococcus micros - Fusobacterium nucleatum
- 33. LOCALIZED AGGRESSIVE PERIODONTITIS • A. actinomycetum comitans •C. rectus • P. gingivalis • F. nucleatum • Capnocytophaga • E. corrodens • Bacteroides capillus GENERALIZED AGGRESSIVE PERIODONTITIS • P. gingivalis • A. actinomycetum comitans • P. intermedia • E. corrodens • Capnocytophaga • Nisseria
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- 36. References • Newman &Carranza’s Clinical Periodontology-(13th edition) • Textbook of Periodontics – (Shalu Bathla 2nd edition) • Essentials of Periodontology – (Sahitya Reddy S)