Mechanism of disease production 
Direct damages cause by bacteria  Indirect damages triggered by host as a

protective response

Mechanism of disease production

Disease Type of bacteria & their virulence Nature of host response






Diet & nutrition Psychosocial behavior Smoking Oral health care Medications Specific microorganism Host susceptibility Genetic Diabetes mellitus

Bacterial plaque Systemic disease

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


INDIRECT LPS Vesicle IL 2 LPS PGE2 LPS Protein Leukocyte MMP



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 
Hyalurunidases  Chondroitinases  Neuraminidases  Phospholipases  Alkaline phosphatase

Proteolytic enzymes 
Proteases  Trypsin-like proteinases  Collagenases  Cysteine proteinases  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 a. b.

Mechanism of bone destruction: Regulation of bone activation & resorption Osteoclastic function in bone resorption

Indirect Tissue Damage
First: a. Plaque intrusion b. Monocyte activation Then: c. Ligament destruction d. Bone destruction

a b 

Steps in tissue destruction in periodontitis a. Pocket develops antigens from plaque

c d

c. d.

stimulate monocyte activation. In the tissue to produce locally high concentration of cytokines. Then these bring about the loss of ligament attachment. By stimulation of metalloproteinases & alveolar bone destruction. By stimulation of osteoclastic activity.

Tissue destruction in periodontitis

Relationship between bacteria, inflammatory cells & bone formation during periodontal disease.
-bacteria release LPS which activates inflammatory

Plaque bacteria

cells resulting in the release of cytokines & local factors.
-These factors can acts directly on osteoclasts to

Inflammatory cells

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.

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


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