DENTAL PLAQUE

Learning outcomes:
Describe the development and characteristics of plaque biofilm
(C1)
Analyze and identify the role of plaque microbiota in the
etiopathogenesis of periodontal diseases (C4)
Definitions:
Materia Alba:

➢ Soft accumulations of bacteria and tissue cells, lack the

organized structure of dental plaque and easily displaced with
a water spray
Dental plaque is defined as specific but highly variable structural
entity resulting from sequential colonization of micro-organisms
o the tooth surfaces, restorations and other parts of the oral
cavity and consists of mucin, desquamated epithelial cells, debris
and micro-organisms all embedded in the gelatinous extra
cellular matrix. (WHO)
Calculus :

➢ Hard deposit, mineralization of dental plaque, generally

covered by a layer of unmineralized plaque
Intraoral surfaces for bacterial adhesion
5 major ecosystems(niches):

Teeth, implants, restorations, and prostheses

Periodontal / peri-implant pocket

Buccal , palatal, epithelium of floor of mouth

Dorsum of tongue

Tonsils
 At or above
gingival margin
Supra gingival
Marginal
plaque→
gingival margin
Plaque

Below gingival
Sub gingival margin

B/W tooth &

gingival / pocket
epithelium
Classification of
Dental Plaque Tissue Tooth associated
associated
Subgingival plaque bacteria
associated with tooth
surface and PDL tissues
Marginal plaque:
Initiation and development of gingivitis

Supragingival plaque & tooth associated subgingival plaque:

Calculus and root caries

Tissue associated plaque:

Tissue destruction , Periodontitis
 Dental plaque as a biofilm
Biofilm:

 Organized structure, micro colonies of bacterial cells are

non randomly distributed in a shaped matrix or glycocalyx.

Structure of biofilm:

 Heterogenous in structure, with open fluid channels through

plaque mass

 Passage of nutrients → “circulatory system”

 Substances produced by bacteria within biofilm are retained

and concentrated
 Intercellular matrix:

Organic constituents:
Inorganic components:
• Polysaccharides, proteins,
• Calcium
glycoproteins, lipids, albumin (GCF),
• Phosphorus
lipids(membranes)
• Traces of sodium, potassium, fluoride
• Glycoproteins (saliva)→ initial pellicle
Source →
• Polysaccharides→
• Supragingival → saliva
• Dextrans
• Subgingival → crevicular fluid
• Integrity of biofilm
Plaque Formation at the
Ultra structural Level
 Initial
Formation of adhesion and
pellicle on attachment of
tooth surface bacteria
3 major phases:

Colonization and
plaque maturation
1) Formation of pellicle:
Acquired pellicle:

➢ After vigorous polishing, thin layer of Glycoprotein (mucins)

➢ Proline rich proteins

➢ Phosphoproteins (statherin)

➢ Histidine rich proteins

➢ α- amylases
2) Initial adhesion and attachment of bacteria

Phase 1: Transport of bacterium to tooth surface via:

Random contacts, Sedimentation, Liquid flow , Chemotactic activity
Phase 2: Initial adhesion
➢ Reversible

➢ Interaction of bacterium and surface from a distance of 50nm

➢ Van der Waals attractive and electrostatic repulsive forces

 Phase 3: Attachment

Electrostatic Bacterial attachment Bacterial attachment via

interactions via specific lectin like hydrophobic interactions
interactions
Adhesions:
 Mediate bonding between bacteria and pellicle

 Specific extracellular proteinaceous components present on

surface of organism
Complementary receptors:
 Proteins , glycoproteins, polysaccharides

 Present on the surface like “Pellicle”

S. sanguis (early colonizer)→

 Bind to acidic proline-rich proteins and receptors in pellicle

like α-amylase and sialic acid

Actinomyces viscosus→

 Early colonizer

 Possess fimbriae that contains adhesins

 Bind to proline rich proteins

3) Colonization of surface and Plaque maturation

Co-aggregation-

Cell to cell recognition of genetically distinct partner cell types

Highly specific stereochemical interaction of protein and

carbohydrate molecules located on bacterial cell surfaces
Types of co-aggregation

Corncorb formation:

 Eg Streptococci which adhere along surface of rod-shaped cells

 Interaction of Fusobacterium nucleatum and coccal cells,

Test tube brush:

 Filamentous bacteria to which gram-negative rods adhere.

 Growth of plaque biofilm

via adhesion via multiplication

Mature plaque
Interactions Among Different Plaque Bacteria
➢ Transition of gram +ve to gram –ve organisms.

➢ Early colonizers use oxygen and lower the reduction-oxidation potential of

environment which favors the growth of anaerobic species.

➢ Various bacteria utilize sugars as energy source

➢ They release lactate and formate →utilized in metabolism of plaque m.organisms

➢ Nutritional interdependencies are critical for growth and survival of m.org in

plaque.
Host as a source of nutrients Bacterial enzymes

Degrade host proteins

Ammonia

Used by bacteria as source of

nitrogen

Hemin from hemoglobin

Metabolism of P.gingivalis
Microbial Complex:
The composition of different complexes is based on the frequency with which the
micro-organisms were recovered together

Early colonizers
 Found to be either independent of defined complexes or belonged to yellow or
purple complex.

Secondary colonizers
 Found in the green, orange and red complexes
 Green and orange complex → incl pathogens in pdl and non-pdl infections
 Red complex→ associated with Bleeding on Probing.
 Early colonizers

Secondary colonizers

•13000 plaque samples

•40 subgingival
microorganisms
•DNA hybridization

•Bleeding on probing
 Microbial specificity of periodontal disease
Non-specific plaque hypothesis
First proposed by W.D.Miller,1890 later by Walter Loesche, 1976

Periodontal disease results from the “ elaboration of noxious products by

the entire plaque flora”. According to this, all plaque bacteria are
thought to have some of the various virulence factors causing gingival
inflammation & periodontal destruction.

Thus, total plaque control is considered necessary in treatment & prevention

of periodontal disease.
Specific plaque hypothesis (Loesche 1976)

According to this hypothesis, only certain plaque is pathogenic, and its pathogenicity
depends on the presence of or increase in specific micro-organisms.

Plaque harbors specific pathogens→ Periodontal destruction

These organisms produce substances that mediate the destruction of host tissues.

Eg. Aggregati bacter actinomycetem comitans in the etiology of LJP.

Most accepted hypothesis, Ecologic/ unifying plaque hypothesis
Proposed by P.D.Marsh 1994

This hypothesis proposes that a change in a key environmental factor triggers a

shift in the balance of the resident flora.
Micro-organisms associated with specific Periodontal disease.
Periodontal Health
Primarily gram-positive facultative species and species like
Streptococcous and Actinomyces (e.g S.sanguis, S.mitis, A.viscosus and
A. naeslundi)

Small proportions of gram-negative species are also found especially

P.intermedia, F. nucleatum, Capnocytophaga.

Certain species have found to be protective or beneficial to the host, eg

S. sanguis, V.parvula—found in large numbers in periodontally inactive
sites, and in low numbers in sites where active pdl destruction occurs.
Chronic gingivitis
Gram positive rods, cocci and gram-negative cocci.
S. mitis, S.mitis, A.viscosus etc
Gram Negative organisms like F.nucleatum, P.intermedia

Pregnancy gingivitis
P. Intermedia

Acute necrotizing gingivitis

Spirochetes
P.intermedia
Adult Periodontitis
P.gingivalis, P.Intermedia, F.nucleatum, T.intermedia

Localized juvenile Periodontitis / generalized juvenile periodontitis

A.a, P.gingivalis, F.nucleatum, Capnocytophaga

Refractory Periodontitis
A.a, P.gingivalis, P.intermedia, Bacteroides forsythus

Abscess of Periodontium
F.nucleatum, P.intermedia, P.gingivalis, Peptostreptococcus micros
Hallmark of Periodontitis - loss of connective tissue attachment

Different forms of periodontitis are characterized by different rates of

progression and different responses to therapy.

Burst model

Continuous burst model

Some sites show progressive loss of attachment over time. The time of
onset and the extent of destruction vary among site.
Random burst model
Activity occurs at random at any site. Some sites show no activity,
whereas others show one or several bursts of activity
Cumulative extent of destruction varies among sites

Asynchronous multiple burst model

Several sites show bursts of activity over a finite period followed by
prolonged period of inactivity.
Occasional bursts may occur infrequently at certain sites at later period.
Other sites show no periodontal disease activity at any time.
 Criteria for identification of Periodontal Pathogens
KOCH, 1870, developed a criteria by which morg can be judged as
causative for infections

1.Be routinely isolated from diseased individuals

2.Be grown in pure culture in the lab.
3.Produce a similar disease when inoculated into susceptible laboratory
animals.
4.Be recovered from lesions in a diseased laboratory animal
SOCRANSKY, proposed criteria by which periodontal m-organism may be judged to
be a potential pathogen

According to this criteria, pdl pathogen must:

1.Be associated with disease, as evident by increases the number of organisms at
diseased sites.
2.Be eliminated or decreased in sites that demonstrate clinical resolution of disease
with treatment.
3.Demonstrate host response, in the form of alteration in the host cellular or humoral
immune response
4.Be capable of causing disease in experimental animal models.
5.Demonstrate virulence factors responsible for enabling the micro-organism to cause
destruction of the periodontal tissues