PATHOGENESIS OF PERIODONTAL DISEASE
PERIODONTOLOGY
Mechanism of disease
production
Direct damages cause by bacteria
Indirect damages triggered by host as a
protective response
Mechanism of disease
production
Disease Disease
Type of bacteria & their Nature of host
virulence response
Health Health
Disease
Disease
Aetiology
Diet & nutrition Diabetes mellitus
Psychosocial behavior
Smoking
Medications
Oral health care
Specific microorganism
Bacterial plaque Host susceptibility
Systemic disease Genetic
Ethnicity
Oral environment
Habits
Mechanism of disease
production
Dynamic equilibrium exists between dental
plaque bacteria & the innate host defense
system.
This is highly evolved interaction between
bacteria & host.
Dental plaque bacteria have adapted survival
strategies that favor growth in this
environment and host limits growth by a
combination of innate & adaptive immune
responses.
Mechanism of disease
production
Bacteria release antigens that host
recognizes as foreign & responds accordingly.
In health, they challenge the host to maintain
an effective defense.
Under disease condition such as acquisition of
certain species, combination of species or less
optimal host defense cause destructive
inflammation occur.
Direct Effect of Bacteria
1. Colonize the gingival sulcus – evading host
defense
2. Damage the epithelial barrier
3. Produce substances that can either directly
or indirectly cause tissue damage
Activation of Endothelial cells
DIRECT INDIRECT
LPS
IL – 2
Vesicle
LPS
Protein
PGE2
LPS Leukocyte
Bacteria
MMP
Protein
Bacterial shedding & host response : adapted from Periodontology 2000
Direct Effect of Bacteria
1. Colonize the gingival sulcus – evading host
response
- Direct damage to PMN’s
(polymorphonucleocytes)
- Reduced PMN chemotaxis
- Modulation of cytokines function
- Degradation of fibrin
- Altered lymphocyte function
Direct Effect of Bacteria
2. Damage to epithelial barrier
- Production of sulphur volatile compounds
- Porphyromonas gingivalis, P intermedia,
Treponema pallidum, T denticola, Fusobacterium
nucleatum
- Putrifactive & leads to oxygen deprivation
- Increase permeability of oral & sulcular
epithelium
- Induce disaggregation/breaking bonds of
preteoglycans & glycoprotein in the
extracellular matrix (ECM).
Direct Effect of Bacteria
3. Produce substances that can either directly
or indirectly cause tissue damage
- Degradation of tissue by enzymes
(hydrolytic/ proteolytic)
- Degradation of tissues/cells by toxins (by
leucotoxins & lipopolysaccharides - LPS)
- Other bacterial metabolites/ products
Direct Effect of Bacteria
Hydrolytic enzymes Proteolytic enzymes
Hyalurunidases Proteases
Chondroitinases Trypsin-like proteinases
Neuraminidases Collagenases
Phospholipases Cysteine proteinases
Alkaline phosphatase Gelatinases
Indirect Tissue Damage
Stimulation of inflammation & activate immune reactions
- Activation of complement systems
- Mechanisms of soft tissue destruction:
a. Lysosomes
b. ROS – produces via metabolic pathways of respiratory burst
c. Collagen & ECM degradation
- Mechanism of bone destruction:
a. Regulation of bone activation & resorption
b. Osteoclastic function in bone resorption
Indirect Tissue Damage
First:
a.Plaque intrusion
b.Monocyte activation
Then:
c.Ligament destruction
a d.Bone destruction
Steps in tissue destruction in periodontitis
b a. Pocket develops antigens from plaque
stimulate monocyte activation.
b. In the tissue to produce locally high
c concentration of cytokines. Then these bring
about the loss of ligament attachment.
d
c. By stimulation of metalloproteinases &
alveolar bone destruction.
d. By stimulation of osteoclastic activity.
Tissue destruction in periodontitis
Relationship between bacteria, inflammatory cells &
bone formation during periodontal disease.
Plaque -bacteria release LPS which activates inflammatory
bacteria cells resulting in the release of cytokines & local
factors.
-These factors can acts directly on osteoclasts to
stimulate their activity as well on pre- osteoclasts,
Inflammatory increased the pool of bone- resorbing cells.
cells
-The bacterial components and inflammatory may act
directly on osteoblasts or their progenitors, resulting
in decreased numbers of functional cells.
- the net result is loss of attachment including bone &
connective tissue.
Mechanism of Disease
Production
Initial lesions (1 – 2 weeks after initial plaque accumulation)
• vascular changes
-Dilation of arterioles, capillaries & venules
-Increase hydrostatic pressure
-Increase intracellular gap between endothelial cells – increase permeability of vessels
-Fluid & proteins exudates into tissues
-Increase gingival crevicular fluid
• inflammatory reaction
-Leukocytes migration from vessels
-Neutrophils increased in gingival sulcus, junctional epithelium & connective tissues
• tissue changes
-Features of acute inflammation
-Red & bleeds
Mechanism of Disease
Production
Early lesion (7 days – 2 weeks of plaque accumulation)
• vascular changes
-More vessels involved & remains dilated
-Enhancement of local effects
• inflammatory reaction
-Neutrophils & lymphocytes predominant
-Shift of the cells population with increase in numbers of lymphocytes & macrophages
-Plasma cell notes
-More features of chronic inflammation, with features of acute persists
• tissue changes
-Red, swollen & bleeds
-Increase rete-pegs formation in junctional epithelium
-Fibroblast degenerate
Mechanism of Disease
Production
Established lesion (3 – 4 weeks following plaque accumulation)
• vascular changes
-Further enhancements & extension of effects
• inflammatory reaction
-Features of chronic inflammation with lymphocytes dominates
-B cells have matures into plasma cells
-More collagen loss
-Epithelial rete-pegs extend deeper
• tissue changes
-Chronic gingivitis – red, swollen
-Lesion may become stable as chronic gingivitis
-Certain individuals may show progression
Mechanism of Disease
Production
Advanced lesion (periodontitis)
• vascular changes
-Further enhancements & extension of effects
• inflammatory reaction
-Features of chronic inflammation
-Inflammation further spread laterally & apically
-Loss of collagen
-Marked bone & attachment loss
-May become stable as advanced lesion or may progress even further – mobility &
tooth loss
-Some have certain complication such as abscesses formation
-Evidence of bone loss will appear radiographically
