Gingival Inflammation PDF
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Elrazi College of Medical & Technological Sciences
Nawal Khalifa Babikir
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This document presents a lecture or presentation about the stages of gingival inflammation. It discusses different stages, from the initial lesion to the advanced lesion, covering clinical and microscopic presentations, and the associated changes in the blood vessels, tissues, and immune cells. The document also includes an introduction and discussion on the types of organisms and related factors causing inflammation.
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GINGIVAL INFLAMMATION Dr. Nawal Khalifa Babikir BDS,PG.D.Res. M.,MD. Pridontics 1 LectureObjectives: Discussion about the different stages of gingival inflammation under clinical and microscopic presentation LectureOutline: STAGE I GINGIVITIS: THE INITIAL...
GINGIVAL INFLAMMATION Dr. Nawal Khalifa Babikir BDS,PG.D.Res. M.,MD. Pridontics 1 LectureObjectives: Discussion about the different stages of gingival inflammation under clinical and microscopic presentation LectureOutline: STAGE I GINGIVITIS: THE INITIALLESION STAGE IIGINGIVITIS: THE EARLYLESION STAGE IIIGINGIVITIS:THEESTABLISHEDLESION STAGE IVGINGIVITIS:THEADVANCED LESION 2 INTRODUCTION Pathologic changes in gingivitis are associated with the presence of oral microorganisms attached to tooth and in gingival sulcus. These organisms produce collagenase, hyaluronidase, protease, Chondroitin sulfatase, endotoxin that cause damage to epithelial and connective tissue cells and inter cellular constituents. 3 The microbial products activate Monocytes/Macrophages to produce vasoactive substances such as……. PROSTAGLANDIN E2 INTERFERON, TUMOR NECROSIS FACTOR (TNF)AND INTERLEUKIN-1 4 Inflammation of Gingiva 5 Despite extensive research, we still cannot distinguish definitively between normal gingival tissue and the initial stage of gingivitis. Most biopsies of clinically normal human gingiva contain inflammatory cells Under normal conditions, neutrophils are migrating from the vessels into the gingival sulcus and the oral cavity. 6 STAGES OF GINGIVITIS: I. Stage I Gingivitis: The Initial Lesion ii. Stage II Gingivitis: The Early Lesion iii. Stage III Gingivitis: The Established Lesion iv. Stage IV Gingivitis: The Advanced Lesion 7 STAGE I GINGIVITIS : THE INITIAL LESION 1. The first manifestations of gingival inflammation are vascular changes consisting of ……. Dilated capillaries and Increase blood flow. 2. These inflammatory changes occur in response to microbial activation of resident leucocytes and subsequent stimulation of endothelial cells. 3. Clinically this initial response of the gingiva to bacterial plaque is not apparent (subclinical gingivitis) 8 Microscopically, some classic features of acute inflammation can be seen in the connective tissue beneath the junctional epithelium. Leukocytes—mainly polymorphonuclear neutrophils (PMNs)—leave the capillaries by migrating through the walls via diapedesis and emigration Human biopsy sample, experimental gingivitis This happens within 1 week and sometimes as early as 2 days after plaque has been allowed to accumulate. Leukocyte traversing the vessel to enter connective tissue. 9 STAGE II GINGIVITIS :THE EARLY LESION The early lesion evolves from the initial lesion with in about one week after the beginning of plaque accumulation. Clinical signs of early lesion is Erythema which appear because of proliferation of capillaries and increased formation of Capillary Loops between Rete Pegs or Ridges. Bleeding on Probing 10 Microscopic examination shows leukocyte infiltration in the connective tissue beneath the junctional epithelium, consists mainly of lymphocytes (75%, with the majority being T Cells). The amount of collagen destruction alsoincreases. The main fiber groups that are affected appear to be the circular and dentogingival fiber assemblies. The junctional epithelium becomes densely infiltrated with neutrophils. 11 STAGE III GINGIVITIS:THE ESTABLISHED LESION It is characterized by a predominance of plasma cells and B Lymphocytes with creation of small gingival pocket lined with a pocket epithelium. The B cells found are Immunoglobulin G1- & G3 (IG3). Chronic gingivitis occurs 2 to 3 weeks after the beginning of plaque accumulation. 12 The Blood vessels become Engorged and Congested Venous return is impaired and blood flow becomes sluggish results in Localized Gingival Anoxemia Which super imposes a Bluish Hue on the reddened gingiva The established lesion can be described as moderately to severely inflamed gingiva. An inverse relationship appears to exist between the numberof intact collagen bundles and the number of inflammatory cells. 13 In histologic sections, a key feature that differentiates the established lesion is the increased number of plasma Cells. The junctional epithelium reveals widened intercellular Spaces. The basal lamina is destroyed in some areas. In the connective tissue, collagen fibers Advanced gingivitis in a human subject. are destroyed 14 Established lesion are of two types: a.Some remain stable and do not progress for months / years. b.Some become more active and to convert to progressively destructive lesion 15 STAGE IV GINGIVITIS : THE ADVANCED LESION Extension of lesion in to alveolar bone. This phase is also called as “the phase of periodontal breakdown” Gingivitis will progress to periodontitis only in individualswho are susceptible. Patients with experimental gingivitis hadsignificantly more……. Plaque accumulation, Higher interleukin-1β levels, Lower interleukin-8 concentrations at 28 days. 16 Microscopically, fibrosis of the gingiva is present, and there are widespread manifestations of inflammatory and immunopathologic tissue damage. At the advanced stage, the presence of plasma cells dominates the connective tissue. Neutrophils continue dominating the junctional epithelium. 17 STAGES OF GINGIVITIS junctional Blood Predominant Clinical and Sulcular Stage Time (days) vessels immune cells Collagen findings epithelium Vascular Infiltration by Perivasular Ginigival fluid dilation I. Initial lesion 2-4 PMNS PMNS loss flow vasculitis Same as stage Increased loss Erythema Vascular I Retepegs around Bleeding on II. Early lesion 4-7 proliferation Lymphocytes Atrophic areas infiltrate probing Same as state Same as stage Change in III. Established II plus blood II but more color size 14-21 Plasma cells Continued loss lesion stasis advanced texture 18 TANK YOU 19