Lesson 27, 28, 29, 30

Dental plaque, caries, periodontal disease

and others
Microbiology

PhD. Begoña Alburquerque González

Bachelor in Dentistry
 Lesson 27
Dental Plaque
Microbiology

PhD. Begoña Alburquerque González

Bachelor in Dentistry
Plaque biofilm formation

Ecological succession

Composition

Distribution

Microbial adherence

Calculus formation

Further notes on biofilms

The dental plaque

Dental plaque is a general term for the complex microbial community

that develops on the tooth surface, embedded in a matrix of polymers of
bacterial and salivary origin.

Plaque biofilm formation

The dental plaque
Plaque biofilm formation

1. Pellicle formation- oral bacteria initially attach to the pellicle and not directly to
enamel (i.e. hydroxyapatite)

2. Transport of microorganisms- natural salivary flow, Brownian motion or

chemotaxis.

3. Long-range interactions- van der Waals forces and electrostatic repulsion produces
a reversible phase of net adhesion.

4. Short-range interactions- stereochemical reactions between adhesins on the

microbial cell surface and receptors on the acquired pellicle

5. Coaggregation or coadhesion- microbial succession and “corn-cob”

6. Biofilm formation- climax community
Detachment- planktonic phase
The dental plaque
Plaque biofilm formation

Corn-cob structure
stage number 5
The dental plaque
Ecological succession

gram + selectively colonise the surface of the

tooth (early colonizers)
Dental plaque biofilm
In summary

Tenacious microbial community

On the soft and hard-tissue surfaces of the mouth
Comprising:
Living, dead and dying bacteria
Extracellular products
Host compounds mainly derived from the saliva
Dental plaque biofilm
Composition

Organisms are surrounded by an organic matrix (30%

volume): products of both the host and biofilm constituents
In the gingival area, proteins from the crevicular exudate
become incorporated
Matrix acts as a food reserve and as a cement
Composition can vary widely between
individuals and location:
At different sites on the same tooth
At the same site on different teeth
At different times on the same
tooth site
Dental plaque biofilm
Distribution

Found on dental surfaces and appliances

Especially in the absence of oral hygiene
Anatomical areas protected from host
defences Supragingival:
Fissure plaque – mainly in molar fissures
Approximal plaque – at contact points of teeth
Smooth surface – e.g. buccal and palatal surfaces
Subgingival, or appliance-associated:
Full and partial dentures (denture plaque)
Orthodontic appliance-related plaque

The presence of plaque in the mouth can readily be

demonstrated by rinsing with a disclosing solution
such as erythrosin
Dental plaque biofilm
Microbial adherence

Adherence of a microbe to an oral surface is a prerequisite

Initial step to subsequent infection or invasion of tissues

Factors affecting microbial colonization of the oral mucosa

Dental plaque biofilm
Calculus formation

Calcium and phosphate ions derived from saliva deposit

within deeper layers of dental plaque
Accelerated by bacterial phosphatases and proteases that
degrade calcification inhibitors in saliva (statherin and
proline-rich proteins)
Formation of insoluble calcium phosphate crystals
that coalesce to form a calcified mass of plaque
Toothpastes now contain pyrophosphate compounds that
adsorb excess calcium ions

Dental calculus
Dental plaque biofilm plankton- microoganisms that live in water

Further notes on biofilms

65% of human infections are caused by biofilms

Preponderance of biofilms in nature (stagnant
water or water pipes)
In clinical terms, it is more resistant to antibiotics and
chemotherapeutic agents than their planktonic counterparts
Drug resistant not a major concern in dental plaque
biofilms- Mechanical cleansing measures (e.g., mouth)
But it is a major therapeutic problem in other
diseased states (e.g., airways infection by Pseudomonas
aeruginosa in cystic fibrosis)
 Lesson 28
Microbiology of Dental Caries
Microbiology

PhD. Begoña Alburquerque González

Bachelor in Dentistry
TOC

Dental caries

Aetiology

Plaque hypotheses

Ecological plaque

hypothesis Prevention
Dental caries
Tooth decay

Dental caries is a chronic endogenous infection caused by the

normal oral commensal flora
Result between de and re-mineralization of enamel
By acids produced by plaque microorganisms
After the surface layer of enamel, the infection
progress to dentine
Pulp becoming inflamed and necrotic

Caries is defined as localized destruction of the tissues of the

tooth by bacterial fermentation of dietary carbohydrates
 Dental caries
Tooth decay

m / p membrane
Classification Clinical presentation

cementum
or dentin

Nomenclature of dental caries. D, dentine; E,

enamel; P, pulp. *Also termed occlusal caries
Primary lesion: Chalkywhite or “white-spot” lesion that
can heal or remineralize- reversible
Dental caries
Aetiology

Host factors
Tooth structure: some areas are much more susceptible -
differences in mineral content
Saliva (mechanical washing action, buffering capacity,
presence of calcium and phosphorus ions)
Diet (mainly the intake of fermentable carbohydrates):
sucrose
Plaque microorganisms (i.e. supragingival plaque).
Dental caries
Plaque hypotheses

Specific plaque hypothesis

one or more specific groups of bacteria are principally
involved in caries
S. mutans a collection of 7 different species

Non-specific hypothesis
Heterogeneous mixture of non-specific bacteria
S. mutans initiates almost all lesions
Not essential
Plaque hypotheses
The role of mutans streptococci

Seven different species:

S. mutans
S. sobrinus
S. criceti
S. ferus
S. ratti
S. macacae
S. downei
Eight serotypes (a-h)
S. mutans serotypes c, e,
antigens
f
S. sobrinus serotypes d, g
Plaque hypotheses
The role of mutans streptococci

Correlations of mutans streptococci counts in saliva and plaque with

the prevalence and incidence of caries

Positive correlation between the progression of carious lesions and

‘S. mutans’ counts

Production of extracellular polysaccharides from sucrose (which

help to cement the plaque organisms together and to the tooth
surface)

Ability to initiate and maintain microbial growth and to continue

acid production at low pH values

Rapid metabolism of sugars to lactic and other organic acids

Ability to attain the critical pH for enamel demineralization more

rapidly than other common plaque bacteria
Plaque hypotheses
The role of lactobacilli

Previously believed causative agents of caries but

Rarely isolated before the development of caries

Often absent from incipient lesions
Although the role of lactobacilli in the carious process is not well
defined, it is believed that:

Involved more in the progression of the deep enamel lesion

Pioneer organisms in advancing front (dentine)
first one is s. mutans lactobacilli have a later role
Plaque hypotheses
The role of Actinomyces spp.

Associated with the development of root surface

caries Especially A. viscosus
Role is still not clear.
Plaque hypotheses
The role of Veillonella spp.

there are 2 different theories

- s. mutans is the ONLY one involved but we can find 7 other
- lactobacilli and actinomyces and veillonella have an important role later on

In most supragingival plaque samples

Require lactate for growth
Unable to metabolize normal dietary carbohydrates
Produce less cariogenic organic acids
May have a beneficial effect
Dental caries
Ecological plaque hypotheses

Key features:
Absence of mutans streptococci at caries sites in some studies
and
Presence in high numbers, but no demineralization
Proposal:
Cariogenic flora in natural plaque:
Weakly competitive
Only a minority
Dental caries
Ecological plaque hypotheses

With conventional diet :

levels of potential cariogenic bacteria are clinically insignificant
remineralization and demineralization are in equilibrium.
If the frequency of intake of fermentable carbohydrates increases:
plaque pH level falls – promoting the growth of aciduric bacteria
prolonged low pH conditions – initiate demineralitation
balance in the plaque community in favour of mutans streptococci
and lactobacilli.
Dental caries
Prevention of dental caries

Management: remove and replace diseased tissue with an inert

restoration
Microbiological test: establish the numbers of S. mutans and
Lactobacillus spp. in the oral cavity.
not necessarily mean an increased risk of developing dental caries
Prevention:
1. Sugar substitutes
avoid 2. Fluorides- formation of fluoroapatite
3. Sealants
4. Reducing cariogenic flora
5. Probiotic therapy
 Lesson 29
Microbiology of Periodontal Disease
Microbiology

PhD. Begoña Alburquerque González

Bachelor in Dentistry
Periodontal disease

The specific plaque hypothesis

The non-specific plaque

hypothesis The ecological plaque

hypothesis
Periodontal disease
Disorders

Defined as disorders of supporting structures of the teeth

Including gingivae, periodontal ligament and
supporting alveolar bone
One of the major diseases afflicting humankind
In most people, can be controlled by mechanical
cleansing techniques and good oral hygiene
Periodontal disease
Classification

Progression (gingivitis and periodontitis)

The rate of disease progress (e.g. chronic,
aggressive) Lesion distribution (e.g. localized,
generalized)
Age group of the person (e.g. prepubertal, juvenile,
adult) Association with systemic or developmental
disorders.
Periodontal disease
Ecology

Gingival crevice: mineralized structure, the tooth, part embedded in the

connective tissue and part exposed to the oral environment.
more anaerobic than most locales of mouth
bathed by the gingival crevicular fluid (GCF)

Periodontal pocket
oxygen tension falls becoming highly anaerobic and
the flow of GCF increases.
proteolytic bacteria living in the periodontal pocket
raise the pH to alkaline levels – promotes growth of
Porphyromonas gingivalis.

Pioneer dwellers, streptococci and Actinomyces spp.

Secondary colonizers: Prevotella and Porphyromonas spp.
Others, such as Peptostreptococcus micros, can adhere to the crevicular
epithelium. Prof. Dra. Ana I. García Guillén / igarcia53@ucam.edu
Microbiology
Periodontal disease
Progression

1) healthy gingival sulcus with minimal supragingival plaque

2) established chronic gingivitis with minor inflammatory enlargement
3) long-standing chronic gingivitis with subgingival plaque extension into
the pocket
4) chronic periodontitis with destruction of the periodontal membrane,
alveolar bone loss and apical migration of the epithelial attachment
Periodontal disease
Aetiological factors

The main aetiological agent of periodontal disease is

microflora inhabiting subgingival plaque biofilms.

However, the host tissues and its specific and non-

specific host defence mechanisms play crucial
modulating roles
Periodontal disease
The specific plaque hypothesis

The specific plaque hypothesis

Certain states - necrotizing ulcerative gingivitis

fusobacteria and spirochaetes are the key aetiological
agents
Resolved by antibiotics active against anaerobes
Involvement of Aggregatibacter actinomycetemcomitans (aggressive
(juvenile) periodontitis)
Resolution with tetracycline.
Periodontal disease
The non-specific plaque hypothesis

The non-specific plaque

hypothesis
Collective groups or consortia of different bacteria
Plaque cause disease irrespective of its
composition
Supported by numerous bacterial species in diseased
periodontal pockets
Periodontal disease
The ecological plaque hypothesis

Causative process:
Inflammatory response in the crevice to a natural plaque
accumulation
Increased GCF flow provides complex host molecules (catabolized by
proteolytic Gram-negative anaerobes)
Suppression of growth of common species in healthy crevice-
population shift
Periodontopathic flora then produce virulence factors

The ecological plaque hypothesis. Eh, redox potential; GCF, gingival

crevicular fluid
Periodontal disease
Plaque bacterial morphotypes

’Red complex’: Treponema denticola, Tannerella forsythia and

Porphyromonas gingivalis

In active pockets, Porphyromonas, gingivalis, A. actinomycetemcomitans,

Prevotella intermedia and F. nucleatum may be present.
 Lesson 30
Other infections of dental interest
Microbiology

PhD. Begoña Alburquerque González

Bachelor in Dentistry
TOC

Dentoalveolar infections

Dentoalveolar

abscess Ludwig’s

angina Periodontal

abscess
Other infections
Overview

Pus producing or pyogenic infections

Associated with the teeth and surrounding supporting structures

Clinic depends on virulence, local and systemic defence

mechanisms of the host, and the anatomical features of the region

Infection may present as:

Abscess localized to the tooth that initiated the infection,
diffuse cellulitis that spreads along fascial planes, or mixture of
both

Prof. Dra. Ana I. García Guillén / igarcia53@ucam.edu

Microbiology
Other infections
Dentoalveolar abscess

Develops by the extension of the initial carious lesion into

dentine
Bacteria spread to the pulp via the dentinal tubules
The pulp responds by acute inflammation which quickly
becomes necrosed or developing a chronic localized abscess

the bacteria enters directly to the pulp

The pathways by which microorganisms may invade

the pulp and periapical tissues: (1) from the apical
foramen, (2) via the periodontal ligament and (3) via
the blood stream (anachoresis)

Prof. Dra. Ana I. García Guillén / igarcia53@ucam.edu

Microbiology
Other infections
Dentoalveolar
Microbiologyabscess
Usually polymicrobial (endogenous)
Unusual monomicrobial (endogenous)
Strict anaerobes are predominant organisms
viridans group streptococci less common tan thought
Common species: Prevotella, Porphyromonas and
Fusobacterium spp.
Facultative anaerobes (Streptococcus milleri) (second
largest group)
Other infections
Ludwig’s angina

Spreading, bilateral infection of the sublingual and

submandibular spaces
About 90%- Ludwig’s angina is precipitated by
dental or post-extraction infection
Essentially a cellulitis of the fascial spaces rather
than true abscess formation.

The infection of sublingual and

submandibular spaces raises the floor of
the mouth and tongue and causes the
tissues at the front of the neck to swell.
Other infections
Ludwig’s angina

Complications:

Airway obstruction due to either oedema of the glottis

or a swollen tongue

Spread of infection to the masticator and pharyngeal

spaces

Death due to asphyxiation

Other infections
Ludwig’s angina

Oral commensal bacteria are common agents

Porphyromonas and Prevotella spp.
Fusobacteria and anaerobic streptococci
Mixed endogenous infection
Because of the severity of the condition, samples for
microbiology assessment should always be obtained, if
possible
Other infections
Periodontal abscess

Result of destructive process in the periodontium

Pus communicating through the gingival sulcus
Endogenous, polymicrobial, subgingival plaque bacteria
Anaerobic Gram-negative rods (black-pigmented
Porphyromonas and Prevotella spp.)
Fuso-spirochaetal complex
Haemolytic and anaerobic streptococci
Capnocytophaga spp. and Actinomyces spp.