PathoGenesis of Periodontal Disease

PERIODONTOLOGY

PATHOGENESIS OF PERIODONTAL DISEASE

Mechanism of disease production

Direct damages cause by bacteria Indirect damages triggered by host

as a protective response

Mechanism of disease production

Nature of host response

Type of bacteria & their virulence

Disease

Disease

Health

Disease Diseas

e

Health

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

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.

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

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

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

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

Direct Effect of BacteriaHydrolytic enzymes Proteolytic enzymes

Hyalurunidases Chondroitinases Neuraminidases Phospholipases Alkaline phosphatase

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 burstc. Collagen & ECM degradation

- Mechanism of bone destruction:a. Regulation of bone activation & resorptionb. Osteoclastic function in bone resorption

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

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

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

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

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

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