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