Periodontal Pathology

by

Dr. Marcel Hallare

The gingival tissue is constantly subjected to mechanical and bacterial aggressions Resistance to these actions is provided by the saliva, the epithelial surface, and the initial stages of the inflammatory response The pathologic changes that accompany gingivitis are associated with the presence of oral microorganisms in the gingival sulcus

These microorganisms are capable of synthesizing harmful products that cause damage to epithelial and connective tissue cells, as well as to intercellular constituents, e.g., collagen, ground substance, and glycocalyx (cell coat) The resulting widening of the spaces between the junctional epithelium cells during early gingivitis may permit injurious agents derived from bacteria themselves, to gain access to the connective tissue

Stage I Gingivitis
Vascular changes have been described as the first response to initial gingival inflammation Histologically, Stage I gingivitis shows some classic features of acute inflammation in the connective tissue beneath the junctional epithelium

Changes in blood vessel morphologic features, such as widening of small capillaries or venules, and adherence of neutrophils to cell walls, occur within 1 week and sometimes as early as 2 days after plaque has been allowed to accumulate Leukocytes, mainly polymorphonuclear neutrophils (PMNs), leave the capillaries by migrating through the walls They can be seen in increased quantities in the connective tissue, the junctional epithelium, and the gingival sulcus

HOST RESPONSE VASCULAR ACUTE BACTERIAL CHALLENGE PHASE: EPITHELIUM AND

ELEMENTS RESPONDS TO CHALLENGE

Several microorganisms that have been associated with gingival inflammation and periodontitis, such as Treponema denticola, Actinomyces viscosus, and Bacteriodes melaninogenicus, have been shown to promote neutrophil chemotaxis and vascular exudation Subtle changes can also be detected in the junctional epithelium and perivascular connective tissue at this early stage Lymphocytes soon begin to accumulate

The increase in the migration of leukocytes and their accumulation within the gingival sulcus can be correlated with an increase in the flow of gingival fluid into the sulcus Page & Schroeder called this stage the initial lesion Classic vasculitis of vessels subjacent to the junctional epithelium and gingival sulcus; presence of serum proteins, especially fibrin, extracellularly; alteration of the most coronal portion of the junctional epithelium; and loss of perivascular collagen

The nature and character of the host response determines whether this initial lesion resolves rapidly, with the restoration of the tissue to a normal state, or evolve into a chronic inflammatory lesion If the latter occurs, an infiltrate of macrophages and lymphoid cells appear within a few days

Stage II Gingivitis
Clinical signs of erythema may appear, mainly owing to the proliferation of capillaries and increased formation of capillary loops between rete pegs or ridges Bleeding on probing may be evident

Page & Schroeder call this stage the early lesion

Histologic examination of the gingiva reveals a leukocyte infiltration in the connective tissue beneath the junctional epithelium, consisting of mainly lymphocytes (75%) but also composed of some migrating neutrophils, as well as macrophages, plasma cells, and mast cells There is an intensified overall inflammatory cell response compared with that in the Stage I (initial) lesion

The junctional epithelium becomes densely infiltrated with neutrophils, as does the gingival sulcus The junctional epithelium may begin to show development of rete pegs or ridges Increase in the amount of collagen destruction The main fiber groups that are affected appear to be the circular and Dentogingival fiber assemblies

PMNs that have left the blood vessels in response to chemotactic stimuli from plaque components travel to the epithelium, cross the basement lamina, and are found in the epithelium and emerging in the pocket area PMNs are attached to bacteria and engulf them in a process of phagocytosis PMNs release their lysosomes in association with the ingestion of bacteria

HOST RESPONSE

ACUTE INFLAMMATORY RESPONSE PHASE: TISSUES RESPOND TO EARLY SIGNALS

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Stage III Gingivitis

In chronic gingivitis (Stage III), blood vessels become engorged and congested, venous return is impaired, and the blood flow becomes sluggish The result is localized gingival anoxemia, which superimposes a somewhat bluish hue on the reddened gingiva

Extravasation of red blood cells into the connective tissue and breakdown of hemoglobin into its component pigments can also deepen the color of the chronically inflamed gingiva The Stage III lesion can be described as moderately to severely inflamed gingiva A key feature that differentiates this lesion from Stage II lesion is the increase in the number of plasma cells, which becomes the preponderant inflammatory cell type

HOST RESPONSE

IMMUNE RESPONSE PHASE

Plasma cells invade the connective tissue not only immediately below the junctional epithelium, but also deep into the connective tissue, around blood vessels, and between bundles of collagen fibers. The junctional epithelium reveals widened intercellular spaces filled with granular cellular debris, including lysosomes derived from disrupted neutrophils, lymphocytes and monocytes The lysosomes contain acid hydrolases that can destroy tissue components

The junctional epithelium develops rete pegs or ridges that protrude into the connective tissue, and the basal lamina is destroyed in some areas In the connective tissue, collagen fibers are destroyed around the infiltrate of intact and disrupted plasma cells, neutrophils, lymphocytes, monocytes, and mast cells

REGULATION & RESOLUTION PHASE: DETERMINANTS

HOST RESPONSE

Interleukins:
IL-1 Stimulates other cells to proliferate, activate, and chemotax Stimulates IL-2 secretion Pyogenic (fever inducing) IL-2 Produced by activated T cells Stimulates T cells ( helper, cytotoxic and natural killer cells Stimulates B cells

IL-3 Secreted by activated T cells Stimulates bone marrow stem cells IL-4 Secreted by activated helper cells and mast cells Stimulates B cells Increases IgG and IgE IL-5 Secreted by activated helper cells and mast cells Promotes IgA and increases synthesis of eosinophils Promotes B-cell proliferation

IL-6 Stimulates production of acute phase reactants Stimulates B-cells IL-7 Stimulates pre-B and pre-T cells IL-8 Stimulates chemotaxis and adhesion of neutrophils IL-10 Inhibits cytokine release from macrophages Inhibits interferon synthesis by Th1 cells

IL-12 Activates natural killer cells Induces Th Th1 Increases CTL and DTH cell numbers