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

Pediatric dental medicine – Forrester JD

• 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.

• 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 10 11 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 host2. Presence of pathogenic species3. 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 factorsEg : 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• H2O2 by S. sanguis- H2O2 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 10th 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