Download as PDF, PPTX
More Related Content
Similar to Oral biofilm and calculus.pdf
Oral biofilm and calculus.pdf
- 1.
- 2. 1. Biofilm i) Formation & maturation ii) Composition • Supragingival & Subgingival iii) Concept of biofilm iv) Clinical implications 2. Plaque Theories i. Specific ii. Non specific iii. Ecological 3. Calculus i) Appearance and distribution ii) Structure of supra & subgingival iii) Clinical implications
- 4. Terminology Acquired pellicle The conditioning film that form from adsorption of hydrophobic and macromolecules onto hard, non- shedding surfaces immediately following immersion in the fluid environment of the oral cavity, or upon cleaning of a solid surface in the mouth Dental biofilm consists of well-organized bacteria community in a matrix composed mainly of extracellular bacterial polymers and salivary and/or gingival exudate products
- 5. Supragingival plaque Deposit is found at or above the gingival margin Subgingival plaque Deposit found below the gingival margin between the tooth and the gingival pocket epithelium
- 6. Immediately followingimmersion of hard, non-shedding surfaces into the fluid environment of the oral cavity, adsorption of macromolecules will lead to the formation of a biofilm. Bacterial adhesion to this glycoprotein layer will first involve primary plaque formers (Gram +ve facultative cocci and rods).
- 7. Subsequent colonization:Gram -ve, strictly anaerobic bacteria The primary plaque formers also multiply to form colonies. The heterogeneity of the complex biofilm increases with time, as the ecologic conditions gradually change.
- 8. Formation of dentalbiofilm
- 10. Phase I Formation of pellicle on the tooth surface Phase II Initial adhesion and attachment of bacteria Phase III Colonization and maturation
- 11. Formation of pellicleon the tooth surface Thin coat of salivary proteins and environmental macromolecules (seconds after cleaning) Glycoproteins, proline-rich-proteins, phosphoproteins, enzymes Mechanisms :electrostatic, van der Waals and hydrophobic forces Like double sided tape
- 12. Initial adhesion and attachmentof bacteria Transportation of bacteria to the pellicle Reversible adhesion Irreversible adhesion Firm anchorage between bacteria and surface by specific interactions (covalent, ionic or hydrogen bonding) Hair-like structures (fimbriae) facilitate Bacteria are better protected against sheer forces on rough surface Initial colonizer: Streptococcus and Actinomyces
- 13. Colonization and maturation Firmly attached bacteria start growing and the newly formed cluster remain attached- microcolonies form Co-aggregation- second wave of bacteria (second colonizer) adheres to the initial colonizer P. intermedia, Capnocytophaga spp, F. nucleatum, Porphyromonas gingivalis Cannot colonize tooth surface, but can adhere to bacteria already in the plaque mass
- 14. 1. Initial attachment 2.Irreversible attachment 3. Maturation 1 4. Maturation 2 5. Dispersal http://mathbio.colorado.edu/mediawiki/index.php/MBW:Role_of_Biofilm_M atrix_in_Structural_Development
- 16. Almost allbacteria has the ability to adhere to surfaces acquired pellicle- composed of a variety of salivary glycoproteins (mucins) and antibodies. This thin film alters the charge and free energy of the surface, which in turn increases the efficiency of bacterial adhesion Active cellular growth of previously starving bacteria and synthesis of new outer membrane components. The bacterial mass increases due to continued growth of the adhering organisms, adhesion of new bacteria and synthesis of extracellular polymers.
- 18. Subgingival plaque Deepeningof the gingival sulcus Microbial composition Predominantly Gram –ve anaerobic bacteria, 3-12 weeks after beginning of supragingival plaque formation Amount of plaque varies, influenced by: Diet Age Salivary factors OH Tooth alignment Systemic disease Host factors
- 20. With increasedthickness, poor diffusion of oxygen through the biofilm matrix, nutrients supply Major nutritional source for bacterial metabolism comes from the periodontal tissues and blood.
- 21. Composition Supragingival Aerobicbacteria matrix composed mainly of extracellular bacterial polymers and salivary and/or gingival exudate products, dead and lysed bacteria Organic and inorganic solids form about 20%- remainder is water Bacteria constitutes 70-80% of the solid material
- 22. Organic content Polysaccharide protein complex- carbohydrates + protein (30% each) Lipids 15% Remainder- extracellular products of bacteria, cytoplasm, cell membrane remnants, undigested foodstuff, derivatives of salivary glycoprotein Carbohydrate : Dextran Levan, galactose, methylpentose Inorganic content Calcium, phosphorus, small amount of magnesium, potassium, sodium, Fluoride (from drinking water, toothpaste, floss and mouthwash)
- 23. Composition Subgingival Thebacteria comprise Gram +ve and Gram - ve cocci, rods, and filamentous organisms (fewer in deeper part of pocket). Spirochetes and various flagellated bacteria may also be encountered (apical extension of the plaque) Organisms have direct access to the nutrient and Ig present in sulcular fluid
- 24. 3 zonesin subgingival plaque biofilm Tooth attached Epithelial attached Unattached
- 25. leukocytes areregularly interposed between the plaque and the epithelial lining of the gingival sulcus The surface layers of microorganisms in the periodontal pocket facing the soft tissue are distinctly different from the adherent layer along the tooth surface, and no definite intermicrobial matrix is apparent
- 26. Properties of biofilms Structure Exopolysaccharides – the backbone of the biofilm Physiological heterogeneity within biofilms Quorum sensing and exchange of genetic information Attachment of bacteria Mechanisms of increased antibiotic resistance of organisms in biofilms Microbial complexes
- 27. The materialpresent between the bacteria in dental plaque is called the intermicrobial matrix accounts for approximately 25% of the plaque volume. Three sources may contribute to the intermicrobial matrix: the plaque microorganisms, the saliva, and the gingival exudate.
- 28. Clinical Implications Biofilmseffectively protect bacteria from antimicrobial agents. Protection From competing microorganisms, from environmental factors such as host defence mechanisms, and from potentially toxic substances Deposits need to be removed mechanically
- 29. facilitate processingand uptake of nutrients, cross-feeding (one species providing nutrients for another), removal of potentially harmful metabolic products (often by utilization by other bacteria), as well as the development of an appropriate physicochemical environment (e.g. a properly reduced oxidation reduction potential).
- 30. Clinical implications Removalof plaque leads to the disappearance of the clinical signs of this inflammation (Löe et al. 1965; Theilade et al. 1966). Similar cause and effect relationships have been demonstrated for plaque and peri-implant mucositis (Pontoriero et al. 1994).
- 31. Plaque theories Non-specific Specific Ecological- any change in the nutrient status in the pocket, i.e. physical and chemical change to the habitat are considered the primary cause for the overgrowth of the pathogens
- 32. Non-specific plaque theory Inflammatory periodontal disease develops when bacteria proliferation exceeds the threshold of host resistance, and is caused by the effects of the total plaque flora All plaque bacteria are thought to have some virulence factors, causing gingival inflammation and periodontal destruction Disease will occur regardless of its composition
- 33. Non-specific plaque theory (Theilade1986) a direct relationship was often assumed to exist between the total number of accumulated bacteria and the amplitude of the pathogenic effect; Biofilm is a microbial community, disease results from the outcome of interactions among all of the component species
- 34. Non- Specific plaquetheory According to this hypothesis, any accumulations of microorganisms at or below the gingival margin would produce irritants leading to inflammation. The inflammation in turn was responsible for the periodontal tissue destruction. The specific species of microorganisms that accumulated on the teeth was not considered to be particularly significant, providing that their numbers were sufficiently large to trigger a destructive process.
- 35. Specific plaque theory A single specific pathogen is the cause of inflammatory periodontal disease (eg: tuberculosis, syphilis) Loesche 1976: specific form of periodontal disease have specific bacterial etiologies
- 36. Specific plaque theory Out of the diverse collection of bacterial in biofilm, only a very limited number of species are involved in disease. These species can be regarded as specific pathogens that be targeted with specific antimicrobial therapy
- 37. Ecological plaque theory Disease result from shifts in the balance of the resident bacterial in the biofilm Potentially cariogenic/periopathogenic bacteria can be present in health, but at levels that are not clinically relevant. Disease can be controlled by targeting putative pathogens, and also by interfering with the factors responsible for driving the deleterious shifts in the bacterial community
- 38. Calculus Appearance anddistribution Structure of supra & subgingival Clinical implications
- 39. Supragingival plaquebecomes mineralized saliva and subgingival plaque in the presence of the inflammatory exudate in the pocket. The formation of dental calculus with the mature crystalline composition of old calculus may require months to years (Schroeder & Baumbauer 1966).
- 40. Mineralized bacterialplaque providing an ideal surface configuration conducive to further plaque accumulation and subsequent mineralization calculus is always covered by an unmineralized layer of viable bacterial plaque
- 43. keeping thebacterial deposits in close contact with the tissue surface, influencing both bacterial ecology and tissue response (Friskopp & Hammarström 1980). supragingival plaque is bacterial reservoir for subgingival recolonization.
- 44. Natural factors favouring plaqueretention
- 45.
- 46. References 5th editionClinical Periodontology and Implant Dentistry (Jan Lindhe) 10th edition Clinical Periodontology, Carranza Color atlas of dental medicine- Periodontology, Rateitschak KH, Wolf HF