Etiology Flashcards
Periodontal Pathogenesis
Environment factors:
Microbial factors:
Host factors:
smoking
plaque/biofilm
susceptibility
Materia Alba
(4)
*White cheeselike
accumulation
*A soft accumulation of
salivary proteins,
bacteria, desquamated
epithelial cells, and food
debris
*No organized structure
*Easily displaced with a
water spray
Dental Plaque
(4)
*Resilient clear to yellow-
grayish substance
*Primarily composed of
bacteria in a matrix of
salivary glycoproteins
and bacterial products
*Considered to be a
biofilm
*Impossible to remove by
rinsing or spraying
Calculus
(2)
*Mineralized dental
plaque forms the hard
deposit
*Generally covered by a
layer of unmineralized
dental plaque
What is
Dental Plaque?
The structurally and
functionally organized,
species-rich
microbial biofilms
that form on teeth
Main etiology for
Periodontal diseases
Dental caries
Dental Plaque
Composition (3)
Water 70%
Microorganisms 70% (dry weight)
Intracellular Matrix 30% (dry weight)
Dental Plaque
Intracellular Matrix
Organic component
(4)
Polysaccharides
Proteins
Glycoproteins
Lipids
Dental Plaque
Intracellular Matrix
Inorganic component
(4)
Calcium
Phosphorous
Other minerals
Sodium
Potassium
Fluoride
1 gram of plaque contains approximately
— bacteria
(And human body has approximately 1012 bacteria)
10^11
More than — distinct microbial species
can be identified with highly sensitive
molecular techniques
500
What is dental plaque?
B. It is the structurally and functionally organized, species‐rich
microbial biofilm that form on teeth.
Sites of Accumulation
(4)
Gingival thirds
Cracks, pits and fissures
Under overhanging restorations
Around malaligned teeth
Classification
based on the position on the
tooth surface toward the
gingival margin (3)
Supragingival plaque
Marginal plaque
Subgingival plaque
Subgingival plaque
(3)
*Tooth attached
plaque
*Unattached plaque
*Epithelial associated
plaque
Supragingival plaque
Gram+ cocci and short rods
Aerobic environment
Slight diversity
Subgingival plaque
Gram- rods and spirochete
Anaerobic environment
Great diversity
Supragingival plaque
result
Calculus formation and root caries
Marginal plaque
result
Direct contact with gingival margin
Initiation and development of gingivitis
Subgingival plaque
result
Tissue destruction
Supragingival plaque
Subgingival plaque
Disruption of both is critical during
periodontal treatment.
why?
No supragingival plaque control
following disruption of subgingival
microflora allows rapid repopulation of
microorganisms that could lead to
periodontitis.
Formation of Dental Plaque
(3)
Step 1:
Formation of the pellicle
Step 2:
Initial colonization of bacteria
Step 3:
Secondary colonization and plaque
maturation
Acquired pellicle:
Adsorption of a conditioning film
- An organic material layer coated on all surfaces in
the oral cavity, including hard and soft tissues.
Acquired pellicle
Components derived from
saliva and crevicular
fluid.
Acquired pellicle
bacteria
Gram+ facultative microorganisms are involved
Initial stage of the development of the plaque
acquired pellicle
Formation of the Pellicle
*Reversible adhesion between the microbial cell
surface (adhesins) and the conditioning film
(receptors)
- Alters the charge and the free energy of the
surface which increases efficiency of the bacterial
adhesion
Pellicle serves as a
protective barrier
Initial Colonization
*Adherence - Coadhesion
(3)
- Primary colonizers - secondary colonizers
- Bacterial mass continue to grow
- Alteration in the oxygen gradient, anaerobic
conditions emerge in the deeper layers of the deposits
SKIPPED
Primary colonizers
(5)
*Streptococcus spp.
*Hemophilus spp.
*Neisseria spp.
*Actinomyces spp.
*Veillonella spp.
SKIPPED
Secondary colonizers
(4)
*Prevotella intermidia.
*Capnocytophaga spp.
*Fusobacterium nucleatum
*Porphyromonas gingivalis
Colonization and Maturation
Coaggregation
(2)
- Secondary colonizers adhere to the bacteria that
are already in the plaque mass - A significant feature can be seen by naked eye
Maturation
(2)
- Through further colonization and growth of
additional species - Quorum sensing: cell-cell signaling
- Quorum sensing: cell-cell signaling
(2)
- Environment modification
- metabolic interaction
Structure of Dental Plaque
— running through plaque mass
Distinct — produced by matrix
Steep —
— results in bacterial resistance
Open fluid-filled channels
microenvironment
Chemical gradients (oxygen, pH)
Quorum sensing
Periodontal Microbiology
Corn-cob formation
Coccal‐shaped cells attach along the tip of gram negative filamentous organisms
An example of inter-bacterial adherence or coaggregation
Dental calculus is
calcified dental plaque,
composed primarily of calcium phosphate
mineral salts.
Calculus
Location: Supragingival
Detection
Color/Texture
Source of
mineralization
Distribution
At or above the gingival margin
Visual
Creamy-whitish to dark yellow or even
brownish mass of moderate hardness
Saliva
Buccal Max. molars & Lingual Mand.
incisors
Calculus
Location: Subgingival
Detection
Color/Texture
Source of
mineralization
Distribution
Below the gingival margin
Tactile or Radiographic
Brownish to black calcified hard
mass
GCF
varies
Calculus
Composition
Organic component
(4)
Leukocytes
Microorganisms
Desquamated epithelial cells
Protein polysaccharide complexes
Calculus
Composition
Inorganic component
70 - 90% comprising of
(3)
Calcium phosphate
Calcium carbonate
Magnesium phosphate
Calculus
Mineralization
(2)
- The mineralization starts in centers which
arise intracellularly in bacterial colonies or
extracellularly from matrix with
crystallization nuclei - At least 2/3 of the inorganic component is
crystalline in structure.
Four main crystal forms:
- Hydroxyapatite (HA) 58% [Ca10(PO4)6(OH)2]
- Whitlockite (WHT) 21% [Ca10(HPO4)(PO4)6 ]
may contain some Magnesium - Octacalcium phosphate (OCP) 12%
[Ca8(PO4)4(HPO4)25HO] - Brushite 9% [CaHPO4-2H2O] only in early
stage
Supragingival calculus is deposited in layers;
Subgingival calculus is commonly deposited in
rings or ledges on root surfaces, but it may also
appear on veneers.
vPlaque mineralization varies between and within
individuals and different region of oral cavity.
Calcification has been reported as early as
4- 8
hours.
Some subjects may form supra- gingival calculus
in 2 weeks, at which time the deposit may already
contain approximately —% of the inorganic
material found in mature calculus.
80
Nevertheless, the formation of dental calculus with
the mature crystalline composition of old calculus
may require
months to years.
Evaluation of calculus by conventional radiography showed
- Low sensitivity:
- High positive predictive value -
radiographic deposits were detected on only
44% of surfaces that demonstrated calculus microscopically.
when you see radiographic
calculus, 92% of the surfaces do have calculus microscopically.
Four modes of calculus attachment
(4)
- Lock into areas of cementum resorption
- Attach to irregularities of the cementum surface
- By bacterial penetration into the cementum
- By an organic pellicle
Calculus is a contributing factor or —
etiologic factor
SECONDARY
Calculus is a contributing factor or SECONDARY
etiologic factor
- It is always covered by
unmineralized viable
bacterial plaque. It extends the sphere of influence
of bacterial plaque (keeps it in close contact with
tissues)
It hinders adequate — control
plaque
1900s
1960s
1990s
Nonspecific Plaque Hypothesis
Specific Plaque Hypothesis
Ecologic plaque Hypothesis
Nonspecific
Plaque
Hypothesis
(4)
- Direct relationship between the
total amount of plaque and the
amplitude of the pathogenic effect - Concept inherited: Control of
periodontal disease depends on
control of plaque accumulation - Standard of care: oral
hygiene measures, non-
surgical/ surgical
debridement - All plaque are not equally
pathogenic
- All plaque are not equally
pathogenic
(2)
- Not all Gingivitis develop into
destructive periodontitis - Site specificity in the pattern
of disease was demonstrated
in some individuals with
periodontitis
Specific Plaque Hypothesis
The pathogenicity depends on
the presence of or increase in
specific microorganisms
- A. Actinomicetemcomitans
in localized aggresive
periodontitis
Specific Plaque Hypothesis
- Targeted treatment strategies
aim to
control or eliminate the
particular pathogenic
organisms
Specific Plaque Hypothesis
are pathogens present or absent in disease?
!!!Pathogens may be present at the absence of disease!!!
microbes to know (3)
P. gingivalis
B. forsythus
T. denticola
microbes present without disease
***B. forsythus
->T. forsythensis
->T. forthysia
Ecologic
plaque
Hypothesis
Microbiologic Specificity
(3)
- Both the total amount of dental
plaque and the specific
microbial composition of plaque
may contribute
-Environmental factors drives the
selection and enrichment of
specific bacteria - Microbial homeostasis: the state
of the dynamic equilibrium
Polymicrobial Synergy and Disbiosis
Combines the concepts of “disrupted
homeostasis” and “keystone
pathogen” but questions the primary
importance of the red complex
Kochs Postulates
Criteria for Identification of Periodontopathogens
*Be routinely isolated from
*Be grown in
*Produce a similar disease
when
*Be recovered from lesions in a
diseased individuals
pure culture in lab
inoculated into susceptible lab animals
diseases lab animal
Socransky’s Criteria
*Be — with disease
*Be — or decreased in
sites that demonstrate clinical
resolution
*Demonstrate a alteration in
*Be capable of causing disease
in
*Demonstrate
associated
eliminated
host cellular or immune response
experimental models
virulence factors
A. Actinomycetemcomitans
Association
Increased in localized aggressive periodontitis
lesions. Some in chronic periodontitis
lesions.
A. Actinomycetemcomitans
Elimination
Suppressed or eliminated in successful
therapy, can be found in recurrent lesions
A. Actinomycetemcomitans
Host response
Increased serum and local antibody levels
A. Actinomycetemcomitans
Animal studies
Capable of inducing disease in gnotobiotic
rats
A. Actinomycetemcomitans
Virulence factors
Host tissue cell adherence and invasion,
leukotoxin, protease, collagenase,
epitheliotoxin, FIF, bone resorption inducing
factors
P. Gingivalis
Association
Increased in periodontitis lesions, found
associated with the crevicular epithelium
P. Gingivalis
Elimination
Suppressed or eliminated in successful
therapy, can be found in recurrent lesions
P. Gingivalis
Host response
Increased systemic and local antibody levels
P. Gingivalis
Animal studies
Important in experimental mixed infections
P. Gingivalis
Virulence factors
Host tissue cell adherence and invasion,
trypsin-like enzyme, collagenase, fibrinolysis,
phospholipase A, endotoxin, gingipains,
factors that affect PMN function
P. gingivalis is known as a
notorious periodontal
pathogen. Which complex
of color does it belong to?
A. Yellow complex
B. Green complex
C. Orange complex
D. Red complex
D. Red complex
Toxins and enzymes
- Bacterial products that promote tissue destruction:
lipopolysaccharides(LPS), leukotoxin, gingipains,
collagenase, protease
Adhesins
- Factors that promote
colonization: fimbria,
gingipains
Evading mechanisms
* The production of an extracellular —
* Proteolytic degradation of host immunity components:
* Modulate host response:
* Invasion of gingival epithelial cells:
capsule
gingipains
bind serum components on bacterial cell surface
lipopolysaccharides(LPS)
Bacteria of Gingivitis
(8)
Actinomyces spp.
Capnocytophaga spp.
Campylobacter spp.
Streptococcus spp.
Parvimonas micra
Fusobacterium nucleatum
Prevotella intermedia
Treponema spp.
Bacteria of Periodontitis
Specific Bacteria in Disease
(8)
Aggregatibacter actinomycetemcomitans (Type b)
Porphyromonas gingivalis
Prevotella intermedia
Parvimonas micra
Fusobacterium nucleatum
Tannerella forsythia
Treponema denticola
Spirochetes
Bacteria of Necrotizing Periodontal DIsease
(4)
Fusobacterium nucleatum
Prevotella intermedia
Treponema spp.
Spirochetes
Bacteria Associated with Pregnancy and Puberty
(2)
Prevotella intermedia
Capnocytophaga spp.
Bacteria in Abscess of the Periodontium
(5)
Fusobacterium nucleatum
Parvimonas micra
Prevotella intermedia
Porphyromonas gingivalis
Spirochetes
Health
(5)
Gram +ve
Cocci
Nonmotile
Facultative anaerobes
Fermenting
Disease
(5)
Gram -ve
Rod
Motile
Obligate anaerobes
Proteolytic
Choose correct answer for the
specific bacteria observed in
correlated periodontal disease
A. In diseased sites, more gram positive, nonmotile cocci are
observed
B. In healthy sites, more orange and red complex bacteria are
observed
C. A. actinomycetemcomitans and P. gingivalis are highly related to periodontitis
D. Capnocytophaga spp. is usually found in periodontal abscess
C. A. actinomycetemcomitans and P. gingivalis are highly related to periodontitis
Transmission of Periodontal Pathogens
Source: Saliva
Bacteria involved:
Donor-recipient:
A. actinomycetemcomitans & P. gingivalis
Parent to child & Spouse to spouse
A —% chance of transmission between spouses
20-30
Does not always result in periodontal disease in the recipient spouse.
Stronger bacterial transmission was found from
parent to child
!!!Periodontal pathogens are — but not readily —!!!
communicable
transmissible
Goals of
Plaque Control
(4)
Disrupt ecological
succession
Reduce degree of
organization
“Healthy” plaque (G+, aerobic, indigenous flora)
Shift in flora compatible
with health
Future Advances
Modulating —
—
Target proteins that are essential for —
Limitation of the identifying the —
host response (i.e. Resolvins)
Antibiotics
the maintenance of Biofilm
microbial risk markers
