Pathogenicity: is the ability of pathogen to interfere with one or more of essential cell function.
The differences between periodontal infection and other body infections:
The anatomy of the periodontium. As the permeable junctional epithelium that has remarkable cell and fluid dynamics, with its prime purpose to preserve epithelial continuity across the hard and soft tissue interface.Defensive processes in the periodontal tissues occur in response to large numbers and varieties of microbes that reside on the tooth surface in a biofilm community, close to rather than within the gingiva.
Periodontal disease has sometimes been referred to as a “mixed bacterial infection” to denote that multiple microbial species contribute to the development of disease.
Sites with clinically healthy gingiva appear to deal with continuous microbial challenges without progressing to clinical gingivitis (redness, swelling, bleeding on probing), probably because of several defensive factors that include:
• The intact barrier provided by the junctional epithelium
• The regular shedding of epithelial cells into the oral cavity
• The positive flow of fluid to the gingival crevice which may wash away unattached microorganisms and noxious products
• The presence in GCF of antibodies to microbial products
• The phagocytic function of neutrophils and macrophages
• The detrimental effect of complement on the microbiota.
The classical phases of “acute” and “chronic” inflammation are not easily applied in periodontal disease, probably because in clinically healthy gingiva a small lesion similar to an acute inflammatory reaction is already present. Subsequently developing chronic inflammatory changes become superimposed so that both acute and chronic elements co-exist in most gingival lesions.
In 1976, Page and Schroeder divided the progressing lesion in the gingival/periodontal tissues into four phases: initial, early, established, and advanced stages or lesions.
Page and Shroeder classification
Histopathological classification
Pristine stage
Histological perfection
initial
Clinically healthy ginigiva
Early
Early stage gingivitis
Established
Chronic gingivitis
advance
periodontitis
The initial lesion:
More blood is brought to the area. Dilation of the arterioles, capillaries, and venules of the vascular network becomes a prominent feature.Hydrostatic pressure within the microcirculation increases and intercellular gaps form between adjacent endothelial cells in the capillaries. Thus, an increase in the permeability of the microvascular bed.
Proteins and fluids exude into the tissues.
The flow of GCF increases. Noxious substances released from the biofilm are diluted both inside the gingival tissue and in the crevice.
PMN cell migration is facilitated by the presence of various adhesion molecules. These molecules assist the binding of PMN cells to the venules and subsequently they help the cells to leave the blood vessel
Lymphocytes are retained in the connective tissues on contact with antigens, cytokines or adhesion molecules and are therefore not so readily lost through the junctional epithelium and into the oral cavity, as are PMNs.
The early lesion:
The vessels in the dentogingival plexus remain dilated, but their numbers increase due to the opening up of previously inactive capillary beds. The increased size and enhanced numbers of vascular units are reflected in increased redness of the marginal gingiva that is a characteristic clinical symptom during this phase.
Lymphocytes and PMNs are also the predominant leukocytes in the infiltrate at this stage of gingivitis and very few plasma cells are noted within the expanding lesion.
Several fibroblasts within the lesion exhibit signs of degeneration, this serves to remove fibroblasts from the area, thus permitting more leukocyte infiltration
Breakdown of collagen fibers occurs in the infiltrated area. This net loss of collagen fibers will provide space for the infiltrating cells.
The basal cells of the junctional and sulcular epithelium now proliferate. This represents an attempt by the body to enhance the “mechanical” barrier to plaque bacteria and their products.
Epithelial rete pegs can be seen invading the coronal portion of the lesion in the connective tissue
Tissue alterations involve the loss of the coronal portion of the junctional epithelium.
The established lesion:
The flow of GCF is increased.The connective tissue as well as the junctional epithelium is transmigrated by an increased number of leukocytes.
The lesionis dominated by plasma cells.
Collagen loss continues as the inflammatory cell infiltrate expands, resulting in collagen-depleted spaces extending deeper into the tissues, which then become available for infiltration and accumulation of leukocytes.
The junctional epithelium is substituted by a pocket epithelium that is not attached to the tooth surface. This allows for a further apical migration of the biofilm.
The pocket epithelium differ from original junctional epithelium in that:
It harbors large numbers of leukocytes, predominantly PMNs.
It is more permeable to the passage of substances into and out of the underlying connective tissue.
It may be ulcerated in places.
Two types of established lesion appear to exist: one remains stable and does not progress for months or years, while the second becomes more active and converts more rapidly to a progressive and destructive advanced lesion.
The advanced lesion:
The advanced lesion has many of the characteristics of the established lesion but differs importantly in that loss of connective tissue attachment and alveolar bone occurs.
The damage to the collagen fibers is extensive.
The pocket epithelium migrates apically from the cemento-enamel junction,
It is generally accepted that plasma cells are the dominant cell type in the advanced lesion.