Periodontology

Dr. Rawand Samy Mohamed Abu Nahla

Oral Medicine, periodontology&oral Radiology
Department.
Dr. Haydar.A.Shafy Faculty Of Dentistry.
El Azhar University.
Etiology Of Periodontal Diseases
Lecture 4
 Dental Disease As An Infectious Disease
• Understanding microbial etiology

• Pathogenicity (virulence) of pathogens

• Virulence factors

• Understanding microbial pathogenesis

• Genetic and Molecular Basis for Virulence

• Understanding host response

• Outcome of disease

• Applying to diagnosis, treatment, prevention

Dental Caries
Demineralization of the tooth surface caused by bacteria
Periodontal Disease
 Virulence Factors
• Gene products that enhance a microorganism’s potential to cause disease

• Involved in all steps of pathogenicity

• Attach to or enter host tissue

• Evade host responses

• Proliferate

• Damage the host

• Transmit itself to new hosts

• Encoded by virulence genes

 Identifying Virulence Factors

• Microbiological and biochemical studies

• In vitro isolation and characterization
• In vivo systems

• Genetic studies
• Study of genes involved in virulence
• Genetic transmission system
• Recombinant DNA technology
• Isogenic mutants
• A molecular form of Koch’s postulates.
 Specific Virulence Factors
• Adherence and Colonization Factors
• Invasion Factors
• Capsules and Other Surface Components
• Endotoxins
• Exotoxins
Etiological Factors For The Periodontal
Diseases
Initiating factors:
•Plaque
• Calculus

Predisposing factors:
Local Risk Factors:
•Anatomic factors
• Occlusal factors
• Restorative factors or iatrogenic
•Mouth breathing
• Habits as bruxism, tongue thrusting.
• Malocclusion
• Food impaction

Systemic predisposing factors:

• Endocrine Diseases.
• Nutritional Influence.
• Hematological Diseases.
• Immunodeficiency Disorders.
• Drugs And Metal Intoxications.
• Congenital And Hereditary Disorders.
• Psychosomatic Disorders.
Dental Plaque
What Is Plaque?
• An invisible layer of microorganisms growing in a colony on the
teeth

• Specific bacteria in the colony are the etiology of dental caries and
periodontal diseases.

• Plaque begins to form immediately on a freshly polished tooth, but

it takes approximately 21 days for plaque to completely mature.

• If plaque is disturbed (brushed away) when it begins to form, it

does not mature.
Removal Of Plaque And Calculus
Is This Plaque?
Arrow points to visible material so its not plaque, it’s materia
alba
Materia alba is food debris, dead cells, bacteria
plaque is underneath materia alba

Plaque requires stain to be

seen because it is invisible
Materia Alba
a soft white deposit around the necks of the teeth,  usually 
associated with poor oral hygiene;  composed of food
debris, dead tissue elements, and purulent matter; serves as

 a medium for bacterial growth.
Pellicle
acquired pellicle a colorless acellular bacteria-
free film composed of salivary glycoproteins, 
deposited on the
 teeth within minutes after eruption or cleaning.
Dental Calculus 
a hard, stone
like concretion, varying in color from creamy yellow to
 black, that forms on the teeth or dental prostheses through
 calcification of dental PLAQUE; it begins as a yellowish
film formed of calcium phosphate and carbonate, food
particles, and other organic matter that is deposited on the 
teeth by the saliva. Called also tartar.
Dental Stain
•A discoloration accumulating on the surface of teeth, dentures, o
r denture base material, most often attributed to the use of
tea, coffee, or tobacco. 
•Many stains contain calcium, carbon, copper, iron, nitrogen, 
oxygen, and sulfur. Stains may be intrinsic or extrinsic. 
•Extrinsic stains of teeth can be removed, e.g, , by brushing,
 rinsing, or sonication.
• Intrinsic stains cannot be removed by these methods.
What Is Plaque’s Composition?
Plaque is composed of:
• Components of saliva (glycoproteins)
• Various bacterium including gram + and gram -;
aerobic, facultative, and anaerobic; saccharolytic
(metabolize sugars) and asaccharolytic (don’t
require sugars)
• Bacteria metabolism products
• Minerals and their ions (ca+, PO4¯, F ¯)
DENTAL PLAQUE AS A BIOFILM
 Definition Of Biofilm
• Matrix-enclosed bacterial populations adherent
to each other and/or to surfaces or interfaces
• May form on a wide variety of surfaces, living tissues,
indwelling medical devices, water system piping.

• Like a complex, highly differentiated, multicultural community

of single or multi-species
 The Nature Of Biofilms
• Natural method of growth for microorganisms
Provides advantages for colonizing species
1-Protection from
• Competing microorganisms
• Environmental factors, host defense
• Toxic substances, such as lethal chemicals, antibiotics
2-Facilitate processing and uptake of nutrients, cross-
feeding, removal of harmful metabolic products
3-Development of an appropriate physico-chemical
environment.
Formation Of Dental Plaque
Acquired pellicle formation
• Adherence of salivary glycoprotein on tooth
surface
 Rapid colonization by pioneer species (Gram (+)
cocci and rods)
• S. sanguis, S. oralis, S. mitis, A. viscosus can
adhere to pellicle by specificity
• Resisting shear force (saliva) and electrostatic
repulsion
Predominance by Gram (-) filaments (in 5
days)
• Microbial interaction, replacing Gram (+)
cocci and rods
• Emergence of Gram (-) filamentous
bacteria
• Matrix of microorganisms and a ground
substance
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

Dental pellicle
Structure Of Biofilms

• Composed of microcolonies (15-20% by volume)

disctributed in a shaped matrix or glycocalyx (75-
80% volume)

• Presence of voids or water channels

• Permit the passage of nutrients and other agents, acting as

“circulatory” system
• Exopolysaccharides (EPS) – the backbone of the
biofilm
• 50-95% of the dry weight of the biofilm
• Maintain the integrity of the biofilm
• Act as a buffer and a substrate for resident bacteria
• Physiological heterogeneity within biofilms
• PH can vary quite remarkably within a biofilm
• Different chemical and physical microhabitats
Supragingival Dental Plaque Biofilm
Dental Plaque In Health And Disease

• Pattern of colonization (microbial succession) in dental

plaque formation
• Difference in predominant species
• Health-associated dental plaque
• Disease-associated dental plaque
• Dental plaque hypotheses
• Specific plaque hypothesis
• Non-specific plaque hypothesis
MICROBIOTA ASSOCIATED WITH PERIODONTAL
HEALTH, GINGIVITIS, AND ADVANCED
PERIODONTAL DISEASE

100% Gram-negative rods

80% Gram-positive rods

60%
Gram-negative
cocci
40%
Gram-positive cocci
20%

0%
Healthy - Gingivitis
supragingival crevicluar
Dental Plaque Hypothesis
• Specific plaque hypothesis
• A single or limited numbers of specific pathogen
within dental plaque
• Specific forms of periodontal disease have specific
bacterial etiologies, i.e. LJP
• Non-specific plaque hypothesis
• Overgrowth of dental plaque will lead to disease
• Plaque as a relatively homogeneous bacterial mass
• Gingivitis
• Intermediate
• Qualitatively distinct bacterial
composition: healthy vs. disease (subjects,
sites)
• Pathogenic shift; disturbed equilibrium
• A small group of bacteria: Gram (-),
anaerobic
Understanding Dental Diseases
From Ecological Perspective

• The mouth - a unique microhabitat

• Multi-species biofilm
• “Selection” of “pathogenic” bacteria among microbial
community
• Selection pressure coupled to environmental changes
• Therapeutic and preventive measures - by interfering with
the selection pressures responsible for their enrichment
Ecological
Plaque
Hypothesis
Dental Plaque Biofilm Infection
• Ecological point of view
• Ecological community evolved for survival as a whole
• Complex community
• Over 400 bacterial species
• Adherence, aggregation

• Dynamic equilibrium between bacteria and a host defense

• Adopted survival strategies favoring growth in plaque
• Disturbed equilibrium leading to pathology

• The dental plaque bacterial composition may result in a

destructive inflammatory response
Socransky Criteria’
‘

• Association with disease;

• Elimination or suppression of the organism results in disease
remission;
• Host response- detection of adaptive immune responses to
the organism;
• Demonstration that the organism is pathogenic in an
experimental animal
• The organism should possess an array of virulence factors
that can be linked to the pathogenesis of periodontal
inflammation.
Common Periodontal Pathogens
• Aggregatibacter actinomycetemcomitans
• Campylobacter rectus
• Eubacterium nodatum
• Fusobacterium nucleatum
• Herpesvirus
• Peptostreptococcus micros
• Prevotella intermedia/nigrescens
• Porphyromonas gingivalis*
• Streptococcus intermedius
• Tannerella forsythia (B. forsythus)*
• Treponema denticola*
*- late colonizers- “Red Complex
Concepts of Periodonto pathogens
• Lists of specific bugs.
• Sometimes use the eradication of a specific bacteria as a
primary study outcome- is this valid based on the poly
microbial nature of the infections?
• Problematic because the bacteria do not act in isolation.
• Still do not know EXACTLY which bacteria(s) and their
relationships initiate and cause progression of disease.
• Periodontal diseases are polymicrobial infections.
• This may be the reason that routine microbial
testing appears to have limited clinical utility.
• Pathogens may be found in low levels in clinically
healthy people. Concept of healthy biofilm and
pathogenic biofilm.
Pathobiology of periodontal disease
•P. gingivalis –, 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
•Activated osteoclasts
What is Calculus?
• Calculus is mineralized plaque

• Calculus is a contributing factor to dental diseases

• Calculus provides a rough surface on which bacterial plaque

can grow
Supragingival vs Subgingival Calculus
Supragingival
• Minerals come from saliva
• Usually whitish in color
• Found mainly near salivary ducts

Subgingival
• Minerals come from sulcular fluids
• Usually black in color
• Found everywhere
Calculus Composition
• Calcium
• Phosphorus
• Carbonate
• Na, Mg, K
• Hydroxyapatite (Ca5(PO4)3 x OH) is major crystal form in
mature calculus.
•Whitlockite is the most common form in subgingival calculus.
•Also has octacalcium phosphate (Ca4H(PO4)3 x 2H2O),
whitlockite (B-Ca3(PO4)2, and brushite (CaH(PO4) x 2H2O).
How Does Calculus Attach?

• Attaches three ways

– Irregularities

– Cohesion

– Acquired pellicle
Calculus Mechanisms of Attachment
• Secondary cuticle (organic pellicle that also calcifies).
• Mechanical locking into irregularities in cemental surface.
•Close adaptation of calculus undersurface depressions to
unaltered cementum surfaces.
• Bacterial penetration of cementum (not universally
accepted).
•“Subgingival calculus contributes significantly in the
chronicity and progression of the disease, even if it can no
longer be considered as responsible for initiation.”
Predisposing factors:
Local Risk Factors
Restorative Factors

1-Subgingival margins

•Overhangs.

•1 mm overhangs harbored black pigmented Bacteroides even with good plaque control.

•The more severe the periodontal disease, the greater the role of the overhang appeared.

•“The influence of a marginal overhang on pocket depth and attachment loss decreases
with increasing pocket depth.”
2-Inadequate embrasures

3-Open margins

4- Marginal ridge relationships

5-Root surface caries

6-Overhanging restorations
7-Subgingival margins and biologic width
8-Prostheses- Increased mobility,
inflammation, and pocketing around
abutments.
Local Tooth-related Factors
•Molars Furcation's.
•Root concavities.
•Cervical enamel projections.
• Crowding
• Vertical root fractures
• Mucogingival deformities
• Adjacent hopeless teeth
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