If the pathogens have not been eliminated, the immune response will intensify. Hallmarks of the Initial Lesion will continue, but will be accentuated. Clinically, there may be more swelling (edema) along with increased redness (erythema). Microscopically, the area of inflammatory infiltrate will increase, occupying as much as 10-15% of the gingival connective tissue beneath the junctional and sulcular epithelium. Loss of extracellular collagen may be as great as 60-70%, with cytopathic changes seen in the gingival fibroblasts. In an attempt to wall-off the growing lesion, JE cells will begin to proliferate in numbers.
Although PMNs are still prominent in number, lymphoid cells can now be seen accumulating subjacent to the junctional epithelium. Many of the lymphocytes come directly from the circulating blood responding to specialized chemokines that signal them to home to the site of the lesion. Other lymphocytes will begin to arrive from surrounding lymphoid tissue. Several studies have shown these small lymphocytes to be primarily T cells. Once activated by Antigen Presenting Cells such as the macrophage or dendritic cell, T Cells may function as helper and / or cytotoxic cells that orchestrate an appropriate immune response. This is accomplished through the production of various cytokines, or by cell-to-cell interaction. In a gingivitis lesion, T helper Cells increase the ability of macrophages to kill intracellular and extracellular pathogens, activate PMNs independently of the cytokines produced, and enhance PMN and macrophage phagocytosis. This is probably why T Cells are linked to the “stable lesion” as in gingivitis, since they tend to keep the infection under control.
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