pathogenesis of periodontal disease
TRANSCRIPT
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PERIODONTOLOGY
PATHOGENESIS OF PERIODONTAL DISEASE
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Mechanism of disease production
Direct damages cause by bacteria Indirect damages triggered by host
as a protective response
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Mechanism of disease production
Nature of host response
Type of bacteria & their virulence
Disease
Disease
Health
Disease Diseas
e
Health
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Aetiology
Bacterial plaque Host susceptibility
Psychosocial behavior
Diet & nutrition
Medications
Diabetes mellitus
Smoking
Specific microorganism
Genetic
Ethnicity
Habits
Systemic disease
Oral environment
Oral health care
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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.
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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.
Mechanism of disease production
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Direct Effect of Bacteria1. Colonize the gingival sulcus –
evading host defense2. Damage the epithelial barrier3. Produce substances that can either
directly or indirectly cause tissue damage
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Vesicle
LPS Leukocyte Bacteria
IL – 2
PGE2
MMP
INDIRECT
DIRECT
Bacterial shedding & host response : adapted from Periodontology 2000
Protein
Protein
LPS
LPS
Activation of Endothelial cells
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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
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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
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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
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Direct Effect of BacteriaHydrolytic enzymes Proteolytic enzymes
Hyalurunidases Chondroitinases Neuraminidases Phospholipases Alkaline phosphatase
Proteases Trypsin-like
proteinases Collagenases Cysteine proteinases Gelatinases
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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 burstc. Collagen & ECM degradation
- Mechanism of bone destruction:a. Regulation of bone activation & resorptionb. Osteoclastic function in bone resorption
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Indirect Tissue Damage
Steps in tissue destruction in periodontitis
a. Pocket develops antigens from plaque stimulate monocyte activation.
b. In the tissue to produce locally high concentration of cytokines. Then these bring about the loss of ligament attachment.
c. By stimulation of metalloproteinases & alveolar bone destruction.
d. By stimulation of osteoclastic activity.
a
b
cd
Tissue destruction in periodontitis
First:a.Plaque intrusionb.Monocyte activationThen:c.Ligament destructiond.Bone destruction
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Relationship between bacteria, inflammatory cells & bone formation during periodontal
disease.
-bacteria release LPS which activates inflammatory 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, increased the pool of bone- resorbing 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.
Plaque bacteria
Inflammatory cells
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Mechanism of Disease ProductionInitial 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
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Early lesion (7 days – 2 weeks of plaque accumulation)
Mechanism of Disease Production
• 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
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Established lesion (3 – 4 weeks following plaque accumulation)
Mechanism of Disease Production
• 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
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Advanced lesion (periodontitis)
Mechanism of Disease Production
• 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
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