8 - Pathogenesis of Periodontal Diseases

PATHOGENESIS OF PERIODONTAL DISEASES ‫ وضاح عبد الناصر نعمان الحاج‬/‫د‬
PATHOGENESIS OF PERIODONTAL
DISEASES
Definition: Pathogenesis is the sequence of events leading to the occurrence of a
disease. In periodontology, the pathogenesis of gingivitis and periodontitis are
related but tend to be described separately.
Bacteria Chronicity Periodontal

Immune
and their
response (Time) diseases
toxins
Progression of the inflammatory periodontal lesion

- The inflammatory reaction within the gingival tissue serves to contain or stop a
local microbial attack, and prevents the spread of attacking organism.
- Inflammatory reaction may also result in the destruction of surrounding cells,
connective tissue matrix and eventually bone.
- Early visible inflammatory changes in the gingival margin occur within a few days
if plaque growth is undisturbed.
- Within 10 to 20 days the plaque mass changes composition from mostly gram
positive coccoid and filamentous bacteria to gram-negative rods and spirochetes.
- Gram positive plaque is usually associated with periodontal health, while a gram-
negative is associated with disease.
Pathogenesis of inflammatory periodontal disease

A- Phases of gingivitis
1- Initial Lesion (2-4 days)
• In response to microbial activation of resident leukocytes and the subsequent

stimulation of endothelial cells.
• Vascular changes (dilation of capillaries, increase capillary permeability and
increased blood flow)
• This initial response of the gingiva to bacterial plaque (subclinical gingivitis) is
not apparent
1
• Leukocytes, mainly (PMNs), leave the capillaries by migrating through the

walls, produce enzymes which destroy both bacteria and gingiva
• Exudation of fluid from the gingival Sulcus
• Lymphocytes and macrophages soon begin to accumulate in junctional epithelium.
• Initial lesion either resolves rapidly, with the restoration of the tissue to a normal
state, or evolves into a chronic inflammatory lesion.
2- Early Lesion (4-7 days)

• Clinical signs of erythema may appear, due to the proliferation of capillaries and
increased formation of capillary loops between rete pegs or ridges. Bleeding on
probing may also be evident.
• Leukocyte infiltration in the CT beneath the JE, consisting of mainly lymphocytes
(B and T) and some migrating neutrophils, as well as macrophages, plasma cells,
and mast cells.
• Increase in the amount of collagen destruction.
2
• PMNs that have left the blood vessels in response to chemotactic stimuli from
plaque components travel to the epithelium
• PMNs are attracted to bacteria and engulf them in the process of phagocytosis,
release their lysosomes. B-lymphocytes produce antibodies and T-lymphocyts
produce cytokines to destroy bacteria
• Clinically, there is erythema, Bleeding on probing.
3- Established Lesion (2- 3 weeks) - Chronic phase

• The blood vessels become engorged and congested and the blood flow becomes static,
result in bluish hue on the reddened gingiva.
• Extravasation of RBCs into the connective tissue and breakdown of hemoglobin into
its component pigments can also deepen the color of inflamed gingiva.
• Increase in the number of plasma cells in connective tissue.
• The junctional epithelium develops rete pegs or ridges that protrude into the
connective tissue, and the basal lamina is destroyed in some areas, due to
lysosomes derived from disrupted neutrophils, lymphocytes, and monocytes
• Collagenase is normally present in gingival tissues and is produced by some oral
bacteria and by PMNs.
3
Summary of pathogenesis of gingivitis

Epithelial, BM
Bacterial Epithelial
Bacterial toxin and CT
plaque ulceration
destruction
Bacterial toxin
PMNs and
Chronic stimulate More bacterial
Macrophages
inflammation acute toxin enter
appear
inflammation
Inflammation
Vascular spreads Epithelial
proliferation throughout proliferation
gingival tissue
4
B- Phase of periodontitis
Advanced Lesion (1- 2 months) - periodontitis
• Extension of the lesion into the periodontal
ligament and supporting bone.
• Persistence of plasma cells in connective
tissue.
• The resulting outcome is bone loss that is
exhibited as clinical attachment loss and
pocket formation
• The mediators of inflammation that have been
identified as playing a significant role in
alveolar bone resorption include interleukin- 1β,
interleukin-6, Tumor Necrosis Factor-α (TNFα),
and Prostaglandin E2.
Principles in pathogenesis of periodontitis

- Bacterial plaque is essential for the initiation of periodontitis.
- The principal clinical signs on disease are the result of activated inflammatory
and immune mechanisms rather than the direct effects of bacteria
- The quantity of bacterial plaque and the types of bacteria found in the plaque do
not by themselves appear to explain the severity of clinical disease.
5
* Periodontitis is differentiated clinically from gingivitis by the following:
Loss of the connective tissue attachment

Loss of the periodontal ligament and disruption of its attachment to
cementum
Alteration of cementum
Migration of epithelial attachment
Resorption of alveolar bone
Histopathology of periodontitis
The transition from established gingivitis to periodontitis, which is characterised by:
• Vascular proliferation and vasodilatation; vessels becoming engorged with blood
• Plasma cells and B lymphocytes persisit in the connective tissues
• The pocket epithelium being very thin, frequently ulcerated and permeable to
bacterial products, inflammatory mediators and defence cells.
Bone loss
6
• Connective tissues exhibiting signs of degeneration and foci of necrosis.

• Fibers of the periodontal ligament apical to the junctional epithelium being
destroyed by collagenases.
• The junctional epithelium proliferating in an apical direction.
• Exposed cementum adsorbing bacterial products and becoming soft and necrotic.
• Osteoclast cause bone resorption, driven by plaque and host-derived mediators such as endotoxin,
prostaglandins (PG), interleukins (IL) and tumor necrosis factor (TNF), becoming evident.
***************************

8 - Pathogenesis of Periodontal Diseases

Uploaded by

Copyright:

Available Formats

8 - Pathogenesis of Periodontal Diseases

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

8 - Pathogenesis of Periodontal Diseases

Uploaded by

Copyright:

Available Formats

PATHOGENESIS OF PERIODONTAL DISEASES ‫ وضاح عبد الناصر نعمان الحاج‬/‫د‬

Bacteria Chronicity Periodontal

Progression of the inflammatory periodontal lesion

Pathogenesis of inflammatory periodontal disease

• In response to microbial activation of resident leukocytes and the subsequent

• Leukocytes, mainly (PMNs), leave the capillaries by migrating through the

2- Early Lesion (4-7 days)

3- Established Lesion (2- 3 weeks) - Chronic phase

Summary of pathogenesis of gingivitis

Principles in pathogenesis of periodontitis

* Periodontitis is differentiated clinically from gingivitis by the following:

Loss of the connective tissue attachment

• Connective tissues exhibiting signs of degeneration and foci of necrosis.

You might also like