CARIOLOGY
LESSON #2
TOPIC: DENTAL BIOFILMS
Dental Biofilm
• Dental researchers have attempted to
understand the microbial nature of oral
diseases over the past 130 years. Their
view of plaque and its constituent
microorganisms has shifted from a
specific plaque hypothesis to a non-
specific plaque hypothesis and again to
a theory of specific periodontal
pathogens in plaque. Changes in the
way plaque and its microorganisms are
viewed affect the strategies used to
prevent and control periodontal
diseases. In recent years, dental
researchers have begun to view plaque
as a biofilm. This shifting view of plaque
has important implications for future
efforts in research, treatment and
prevention.
• Despite the best efforts of dental health
professionals, oral infections are still
widespread.
• There is a universal recognition these
oral infections are multifactorial, with
specific bacteria residing in intraoral
plaques as a necessary, but not
sufficient cause of disease. Exactly how
these plaque-dwelling microorganisms
cause oral diseases is not completely
clear.
• How dental plaque and its resident
microorganisms are viewed is dictated
by the analytical tools used to study it.
• Mucous membranes and teeth are
constantly covered with a salivary film
whose proteins adhere to all surface in
the mouth.
• Saliva – highly complex proteinaceous
liquid that contains millions of
microorganisms.
• Different species have different surface
proteins compromising their cell wall,
which coat the surface of each cell –
they stick to the salivary proteins at the
surfaces of mucous membranes and
teeth.
• Metagenome – The recovery and
complete sequencing of genetic
material extracted directly from all
environmental samples.
• Eukaryotes – store their DNA in
membrane ‘sac’ (nucleus)
• Prokaryotes – live in a variety of
ecological niches. Traditional
bacteriological methods: ineffective in
isolating prokaryotes.
• Oral cavity has its own endogenous flora
• Microorganisms attach to all surfaces
that are covered with a proteinaceous
film and stick to them.
• Mucosal surfaces – do not allow growth
of a biofilm
• Tooth surfaces – stable
• Stagnation area – biofilm will form
What is a biofilm?
• Biofilm – a well-organized, cooperating
community of microorganisms.
• Dental biofilm – defined as a microbial
community growing on a tooth surface.
Positive examples of biofilms: detoxification
of waste water and sewage; Humans have a
symbiotic relationship with their
microbiome. Our resident microorganisms
can provide benefits.
Harmful Biofilms:
• The slime layer that forms in dental unit
water lines
• Biofilms are responsible for the majority
of infections in humans
• Legionnaire’s disease that killed 29
persons in Philadelphia in 1976
What is dental plaque?
A gelatinous (soft, translucent and
tenaciously adhering) mass of bacteria
adhering to the tooth surface.
Note: A mature biofilm
Dental biofilm and plaque
• Dental biofilm: easily disclosed when
the mouth is rinsed with a disclosing
solution.
Clean surface: cocci attach to the pellicle
(the proteinaceous saliva film) withing 12
hours -> Cells start to multiply and form
microcolonies within 24 hours -> If left
undisturbed, there is a microbial succession,
continued growth and an increases species
diversity.
• Mature biofilm within a week – Dental
plaque
Thickness and composition varies
extensively between and within individuals.
Some are rapid plaque formers-the dental
plaque in elderly people who ignore oral
hygiene can grow to a substantial thickness.
Changing views of plaque
• 1880 – 1930: Golden age of
microbiology, search for oral pathogens
using plaque samples.
• 1930 – 1960: Plaque control, Non-
specific hypothesis, Disease linked to
constitutional defects
• 1960 – present: Biofilm, Specific plaque
hypothesis, Treatment is aimed at
causative agent.
Hypothesis concerning etiology of caries
• Non-specific plaque hypothesis: all
plaque are pathogenic, heterogenous
groups of bacteria are involved in caries
initiation.
• Specific plaque hypothesis:
- Plaque is pathogenic only if associated
with clinical disease
- Different bacteria will have different
functions
- “The goal of therapy is to suppress the
cariogenic plaques and to replace them
with pathogen-free plaques”. – Walter
Loesche
Metabolism in the Dental Biofilm
Dental caries lesions are a result of an
imbalance in physiological equilibrium
between tooth mineral and biofilm fluid.
Oral Flora
1. Specific niche in the flora
2. Imbalance = favor one
type of bacteria over
another
3. Opportunistic bacteria
4. Remains unchecked =
imbalance will continue
5. Disease
 Properties of cariogenic bacteria Streptococcus MutansSerotypes Associated
• Acidogenicity: metabolize sugars to acid with Caries
• Acidurity: survival and growth
• Adherent: synthesize polysaccharides • Streptococcus mutans
• Streptococcus sobrinus
Different bacteria – different characteristics • Streptococcus rattus – rats
– different pathogenicity • Streptococcus cricetus – hamsters
• Streptococcus ferus – wild rats
Bacteria associated with caries • Streptococcus macacae – primates
• Streptococcus downei - primates
Mutas Lactobacilli Actinomycetes
streptococci Species Plaque
(streptococcus (actinomycetes
mutans) viscosus)
Dental plaque accumulation on teeth is
- Is the - Acidogenic, - Acidogenic,
highly organized and not haphazard
collective aciduric aciduric
term for all - Dentin caries - Root caries
the - Are present
stereotypes in high
- Acidogenic, number
aciduric, saliva,
adherent dorsum of
- Caries tongue hard
initiator – palate,
enamel mucous
caries membranes
- Absent in
incipient
lesions
- Better
criterion than Development of bacterial plaque
Streptococcu
s mutans 1. Pellicle covers all oral surfaces
when
evaluation
within 30 minutes to 1 hour after
carious risk brushing
2. It becomes colonized by bacteria
within 12-24 hours
3. High sucrose diet or frequent
ingestion of sucrose – favors
colonization of acidogenic bacteria
and exclusion of non-carcinogenic
bacteria (e.g S. sanguis, S. mitis)
4. Special receptors make it easy for
acidogenic bacteria to adhere and
extracellular matrix facilitates
cohesion
 5. Metabolism of sucrose results in
acid productions – lactic acid from
sucrose
6. Plaque below 5.5 – period of
demineralization
7. Plaque pH above 5.5 – period of
remineralization

The gelatinous nature of the plaque limits

outward diffusion of metabolic products
and thus serve to prolong the retention of
acids.