Gingivitis and Periodontitis

Clinical features of gingivitis & gingival inflammation

Malik Hudieb, BDS, PhD (Implant), JDB(Perio)
Department of Preventive Dentistry Faculty of Dentistry Jordan University of Science and Technology
Healthy Gingiva Gingivitis Periodontitis

Pathogenesis..

Innate immunity
Inflammation is one of the first responses
Redness, swelling, heat and pain Chemical and cellular response During the acute phase of inflammation, particularly as a result of bacterial infection, neutrophils migrate toward the site of inflammation in a process called chemotaxis, and are usually the first cells to arrive at the scene of infection

Bacterial Plaque

Host response

Immune system

Inflammation

Clinical signs
4

Injury

INFLAMMATION

Acute inflammation Abscess Chronic inflammation

Resolution

Repair

Inflame to set fire. Inflammation is A dynamic response of vascularised tissue to injury. It is a protective response. It serves to bring defense & healing The

Inflammation
vascular & cellular responses of inflammation are mediated by chemical factors (derived from blood plasma or some cells) & triggered by inflammatory stimulus.

Tissue injury or death ---> Release mediators mechanisms to the site of injury.

Inflammation.. etiology
Microbial infections: bacterial, viral, fungal, etc. Physical agents: burns, trauma--like cuts, radiation Chemicals: drugs, toxins, or caustic substances Immunologic reactions: rheumatoid arthritis.

Cardinal Signs of Inflammation

Redness : Hyperaemia. Warm : Hyperaemia. Pain : Nerve, Chemical mediators. Swelling : Exudation Loss of Function: Pain

Periodontal Diseases are Acute or Chronic?

Acute inflammation: Neutrophils Chronic inflammation: Mononuclear cells

Inflammation
Injury
Chemical mediators

Increase blood flow (redness and warmth). Increase vascular permeability (swelling, pain & loss of function). Leukocytic Infiltration.

(Macrophages, Lymphocytes, Plasma cells).

Mechanism of Inflammation
1. Vaso dilatation 2. Exudation - Edema 3. Emigration of cells 4. Chemotaxis

Changes in vascular flow

Slowing of the circulation outpouring of albumin rich fluid into the extravascular tissues results in the concentration of RBCs in small vessels and increased viscosity of blood. Leukocyte margination Neutrophi become oriented at the periphery of vessels and start to stick.

Transudate:
An ultrafiltrate of blood plasma permeability of endothelium is usually normal. low protein content ( mostly albumin)

Exudate:
A filtrate of blood plasma mixed with inflammatory cells and cellular debris. permeability of endothelium is usually altered high protein content.

Leukocyte Exudate

Chemical Mediators:
Chemical substances synthesised or released and mediate the changes in inflammation.

Histamine by mast cells - vasodilatation. Prostaglandins Cause pain & fever. Bradykinin - Causes pain.

Saliva
Protective in nature. Mechanically cleanses the exposed oral surfaces. Buffers acids produced by bacteria. Antibacterial factors: inorganic and organic Lysozyme: hydrolytic enzyme of the bacterial cell wall. Salivary antibodies: IgA predominantly.

Significance of saliva in periodontal pathology

Influence on plaque initiation and maturation. Influence on calculus formation. Xerostomiaincreased incidence of dental caries, periodontal disease and delayed wound healing.

Clinically healthy gingiva

Stages of periodontal diseases

Copyright 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins

Stages of periodontal diseases

Stage 1: The Initial Lesion. Stage 2: The Early Lesion. Stage 3: The Established Lesion. Stage 4: The Advanced Lesion.

The Initial Lesion

Subclinical gingivitis (2-4 days) Changes in junctional epithelium and perivascular connective tissue. Increased migration of leukocytes (PMN).

The Initial Lesion

- Plaque formation on the cervical 3ed .. 24 hours dentogingival plexus (Hydrostatic pressure increased ) increased exudate The flow of GCF increases.

The Initial Lesion

PMN cells Migrate by the help of: Adhesion molecules (intercellular adhesion molecule-1 (ICAM-1), Endothelial leukocyte adhesion molecule-1 (ELAM-1), in the dentogingival vasculature (to leave the blood vessels) Other adhesion molecules uniquely present on the junctional epithelial cells The presence of microbial chemotactic factors

The Initial Lesion

The Early Lesion

Within several days of plaque accumulation

Lymphocytes Retained in the connective tissues (cytokines, antigens, adhesion molecules) Lymphocytes have the ability to produce CD44 (cluster determinant) binding to the connective tissue.

Dentogingival plexus dilated, increased in no. PMN migration to perio pocket and phagocytosis of bacteria. Redness of the marginal gingiva (erythema), BOP

The Early Lesion

Lymphocytes and PMNs are the predominate
(Listgarten & Ellegaard 1973; Payne et al. 1975; Seymour et al. 1983; Brecx et al. 1987).

The Early Lesion

Proliferation of basal cells (junctional and sulcular epithelium) mechanical barrier Epithelial rete pegs can be seen invading the coronal portion of the lesion in the connective tissue (Schroeder 1970;Schroeder et al. 1973). Loss of the coronal portion of the junctional epithelium.

Degeneration of fibroblasts and breakdown of collagen fibers (70%) (mainly circular and dentogingival fiber groups). leukocyte infiltration
(Page & Schroeder 1976; Takahashi et al. 1995)

The Established Lesion

Chronic gingivitis. Congested blood vessels. -Impaired venous return -Extravasation of RBCs GCF flow is increased.

The Established Lesion

Leukocyte exudate: - Dominated by plasma cells. (animal experiments) - Young human individuals: lymphocytes
(Brecx et al. 1988; Fransson et al. 1996).

- Old human individual, plasma cells

(Fransson et al. 1996).

Rete pegs extend deeper into the connective tissue

The Established Lesion

The pocket epithelium: Not attached to the tooth surface Harbors large numbers of leukocytes Allows for a further apical migration of the biofilm Compared to the junctional epithelium: --- more permeable. --- may be ulcerated.

The Established Lesion

Two types of established lesion: One remains stable for months or years, Second becomes more active and converts more rapidly to destructive advanced lesion.

(Lindhe et al. 1975; Page et al. 1975)

The Advanced Lesion

Loss of connective tissue attachment and alveolar bone Extensive damage to collagen fibers The pocket epithelium migrates apically from the cemento-enamel junction

The Advanced Lesion

It is generally accepted that plasma cells are the dominant cell type in the advanced lesion
(Garant & Mulvihill 1972; Berglundh & Donati 2005).