Dental Plaque and its role in Periodontal diseases Presented by Deepti Awasthi

Contents Introduction Definitions Classification Composition Plaque as a biofilm Plaque formation Plaque hypothesis Conclusion References

Introduction

Definitions It is defined clinically as a structured, resilient, yellow-grayish substance that adheres tenaciously to the intraoral hard surfaces, including removable and fixed restorations. (Carranza) A specific but highly variable structure entity resulting from colonization and growth of micro- organisms of various species and strains of bacteria on the surface of teeth/restoration and embedded in a intercellular matrix (WHO definition)

Dental plaque is a tenacious microbial deposit which forms on the hard tissue surfaces of mouth, comprising living, dead, and dying bacteria and their products, together with host compound mainly derived from saliva. Essential Microbiology –Lakshman Samarnayake

Dental plaque is defined as a highly specific variable structural entity formed by sequential colonisation of microorganism on the tooth surface, epithelium and restorations. The natural physiologic forces that clean the oral cavity are in-efficient in removing dental plaque. Essentials of preventive and community dentistry : soben peter

Plaque is a microbial ecosystem composed of densely packed microbial structures, insoluble salivary glycoprotein, microbial extracellular products and to a lesser extent epithelial & dietary debris which adheres firmly to the tooth. Pediatric dental medicine – Forrester JD

Material Alba is referred to as soft accumulation of bacteria and tissue cells that lack the organized structures of dental plaque and are easily displaced with water spray. Calculus is hard deposit that forms by mineralization of dental plaque and is generally covered by unmineralized plaque Clinical periodontology- Carranza

Classification of Plaque supragingival subgingival Sub gingival plaque again classified Tooth associated Tissue associated

Composition 1. Microorganism >500 species 1 gms contains - 2 x bacteria 2. Intercellular matrix- Consists of organic and inorganic material derived from,saliva, gingival crevicular fluid and bacterial products Organic part- Polysaccharides, protein, Glycoprotein and lipids Inorganic part- Calcium, Phosphorus, traces of Na, Pottasium, Flouride

Plaque as a biofilm Matrix enclosed bacterial population adherent to each other and/to surfaces or interfaces ( costerton et al 1994 ) Heterogeneous structure. Open fluid filled channels Provide circulation within the plaque to facilitate movement of soluble molecules such as nutrient or waste product. Bacteria exist and proliferate within intercellular matrix. Diagnosis & risk predictors of periodontal disease- Axelsson.

Plaque matrix provide unique environment to the bacteria as it acts as a biofilm. The bacteria in biofilm behave in different way than a free floating bacteria in saliva and crevicular fluid. Biofilm matrix serves as a barrier and retains products of bacterial metabolism in itself which serves as metabolic interaction between different bacteria of plaque.

Plaque Formation Formation of pellicle Initial adhesion Attachment Colonization Plaque maturation

Formation of the pellicle All surface of the oral cavity Within nanoseconds Components – albumin, lysozyme, amylase, immunoglobulin A, proline-rich proteins, histidine rich protein, enzymes etc. mechanism– electrostatic, van der waal’s & hydrophobic forces Clinical periodontology- Carranza

Initial adhesion & attachment of bacteria 1. Transport to the surface Random contact may occur, through Brownian motion, sedimentation, liquid flow or through active bacterial movement. 2. Initial adhesion Occurs through short & long range forces – van der waal & electrostatic forces. Clinical periodontology- Carranza

3. Attachment Firm anchorage is established by specific interactions. – covalent, ionic or hydrogen bonding. Adhesions of the organism and receptors on the surface of pellicle Specie specific Aa – fimbriae with adhesins with proline rich protein of the pellicle. Clinical periodontology- Carranza

Colonization & plaque maturation Coaggregation Secondary with early colonizers : F.Nucleatum with S.Sanguis P.loescheii with A.viscosus C.ochraceus with A.viscosus

Initial colonizers- pre dominantly gram positive facultative micro organism such as. Streptococcus sanguis, Streptococcus mutans, and Actinomyces viscosus The secondary colonizers include Gram- negative species as Fusobacterium nucleatum, Prevotella intermedia, P. gingivalis and Capnocytophaga species Clinical periodontology- Carranza

"corn-cob" arrays adherence of cocci to filaments “Test tube” brush filamentous bacteria to which gram negative rods adhere

The composition of different complexes was based on the frequency with which different clusters were recovered. Primary colonizers : Independent of defined complexes – A. Naeslundi, A.viscosus Yellow- streptococcus spc. Purple – A.odontolyticus

Secondary colonizers : Green - Aa, Eikenella corrodens & capnocytophaga Orange - Fusobacterium nucleatum, Prevotella intermedia, and Capnocytophaga Red –P.gingivalis,T.denticola, Tannerella forsythia Clinical periodontology- Carranza

Physiologic properties of plaque Early colonizers use oxygen & lower the redox potential of the environment Favors growth of anaerobic species. Mature plaque- anaerobic & asaccharolytic and use amino acids and small peptides as energy source.

Formation of sub gingival plaque Bacteria moves – 1) non motile piggyback on motile 2) amoebic Bottle brushes Plaque free zones Diagnosis & risk predictors of periodontal disease- Axelsson

Special bacterial behavior in biofilm- Quorum sensing Play a role in expressing genes for antibiotic resistance and in encouraging the growth of beneficial species to the biofilm and discouraging the growth of competitors. Diagnosis & risk predictors of periodontal disease- Axelsson

Association of plaque microorganisms 3 groups of factors : 1. Susceptible host 2. Presence of pathogenic species 3. Absence of beneficial bacteria

1.The susceptibility is partially hereditary but can be influenced by environmental and behavioral factors – smoking, stress and diabetes 2. Presence of 1 or more pathogens of sufficient clonal type & in sufficient numbers Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and tanerrela forsythia as key pathogen because they are strongly associated with progression & unsuccessful therapy Clinical periodontology- Carranza

3. Beneficial species can affect disease progression in different ways By limiting pathogen’s ability to adhere By adversely affecting the growth of pathogens To produce virulence factors Degrading virulence factors Eg : S. Sanguis produces H2O2 which can kill Aa. Clinical periodontology- Carranza

The acquisition of the plaque flora At birth - sterile Within hours – S.Salivarius 1yr – streptococcus, staphylococcus, neisseria, lactobacillus and veillonella With the continued eruption of teeth-

Plaque Hypothesis Specific Plaque Hypothesis Non Specific Plaque Hypothesis Ecological Plaque hypothesis

Specific Plaque hypothesis Only certain plaque Presence of specific pathogen. Aa – localized aggressive periodontitis.

Non Specific Plaque Hypothesis Loesche, 1976 Elaboration of noxious products by the entire plaque flora. Contradictions : 1. considerable amount of plaque & calculus- never developed periodontitis 2. site specificity

Ecological Plaque Hypothesis

Socransky's criteria for periodontal pathogens ASSOCIATION ELIMINATION HOST RESPONSE VIRULENCE FACTORS ANIMAL STUDIES

Currently recognized key periodontopathogens  Porphyromonas gingivalis,  Prevotella intermedia,  Bacteroides forsythus,  Actinobaccilus actinomycetemcomitans,  Fusobacterium nucleatum,  Capnocytophaga species,  Campylobacter rectus

Microbial shift during disease; Gram positive gram negative Cocci rods Non-motile motile organisms Facultative obligate anaerobes Fermenting proteolytic species

Periodontal health grampositive facultative species - streptococcus and Actinomyces (S sanguis, S mitis, S viscosus and A naeslundi) gram negative species – P intermedia, F nucleatum and Capnocytophaga, Neisseria and Veillonella sp.

protective or beneficial - S sanguis, Veillonella parvula and C ochracea No attachment loss low number - active periodontal destruction occurs H 2 O 2 by S. sanguis- H 2 O 2 is known to be lethal to Aa C. ochracea and S sanguis - greater gain of attachment level after therapy

Pathobiology of periodontal disease Hyaluronidase, collagenase, proteases P. gingivalis – Arg- and Lys- gingipain cystein proteinases, key virulent factor Once the immune and inflammatory processes are initiated- protease, MMP, cytokines, prostaglandin from leukocytes and fibroblasts.

As disease progresses, epithelial cells proliferate apically CD4+T cells – increased RANKL Activated osteoclasts

References Clinical periodontology- Carranza 10 th ed Pediatric dental medicine – Forrester JD Diagnosis & risk predictors of periodontal disease- Axelsson. Vol 3 Essential Microbiology –Lakshman Samarnayake Essentials of preventive and community dentistry - soben peter Pediatric dental medicine – Forrester JD Preventive material, methods & programmes- Axelsson