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This Concept Map, created with IHMC CmapTools, has information related to: GROUP 3 - ETIOLOGY AND PATHOGENESIS, EARLY LESION may progress to if oral hygiene is neglected, EARLY LESION Histologically, there is Basal cells of epithelium proliferate, Formation of pocket epithelium which is more permeable, Formation of pocket epithelium contains Large number of neutrophils, Neutrophils accumulate in the tissues releasing lysosomal contents extracellularly, EARLY LESION Histologically, there is Collagen destruction in infiltrated areas, 3 Mechanisms it interferes with the complement system of the immune system., 7 days of plaque accumulation progresses to EARLY LESION, EARLY LESION PROPER TREATMENT SUCH AS professional treatment check up, irreversible infectious disease characterized by predominance of gram negative microorganisms in subgingival film. Histologically, there is domination of plasma cells, EARLY LESION Cells that are present during immune response are: Proinflammatory cytokines, irreversible infectious disease characterized by predominance of gram negative microorganisms in subgingival film. Histologically, there is extension of the inflammatory infiltrate laterally and apically, gram-positive bacteria ???? Actinomyces species, Chronic Gingivitis Host response include Neutrophils accumulate in the tissues, Chronic Gingivitis Histologically, there is Marked proliferation of junctional epithelium into the CT spaces, irreversible infectious disease characterized by predominance of gram negative microorganisms in subgingival film. Cells that are present during immune response are Balance in Th1 and Th2 cells with a shift towards a Th2 profile., EARLY LESION Histologically, there is Very few plasma cells are present, Proinflammatory cytokines will trigger capillary action, PRISTINE GINGIVA Histologically, there is... No gingival sulcus, normal microflora . INITIAL LESION