The role of gingival epithelial cells in periodontal disease progression

Gingival epithelium provides the mechanical and biological protective integument of the periodontium. Inflammatory periodontal diseases are characterized by a pathological deepening of the gingival sulcus concomitant with an apical migration of the epithelial attachment and destruction of underlying connective tissue and alveolar bone. These changes result in the formation of a periodontal pocket, lined by pocket epithelium. Histological findings show that the initial inflammatory infiltrate is dominated polymorpho-nuclear leukocytes (PMNs) and T-cells situated immediately beneath the sulcular and junctional epithelia and, at a later stage, pocket epithelium. As the disease progresses, the number of PMNs and T-cells close to the epithelial cells increases. Although much is known concerning immunological mechanisms involved in periodontal disease, the contribution of the gingival epithelial cells to the disease process has not yet been extensively studied. The purpose of the present discussion is to highlight the potential contribution of the gingival epithelial cells to the pathogenesis of periodontal disease. Emphasis will be placed on the complementing a re-cent review on adhesive events between cells of immune system and gingival epithelial cells. The gingival epithelial cells have the capacity to secrete various pro-inflammatory cytokines, such as IL-1 and IL-8,responsible for the influx of PMNs and T-cells, as well as autocrine and paracrine growth and activating factors. Furthermore, activated gingival epithelial cells also have the capacity to act as antigen presenting cells and may thus initiate an immune response by presenting antigens to T-cells. The understanding of the role of the gingival epithelial cells in the pathogenesis of periodontal disease may allow to biological intervention to be part of an early therapeutic approach aimed at preventing disease progression