Gingival inflammation-Stages of Gingivitis.pptx

gingival inflammation

1. GINGIVAL INFLAMMATION DR ANJHANA DEPT OF PERIODONTICS

2. CONTENTS Definition Cardinal signs of inflammation Stages of gingival inflammation Initial lesion Early lesion Established lesion Advanced lesion Conclusion

3. Inflammation is defined as the observable alteration in tissues associated with changes in vascular permeability and dilation,often with the infiltration of leucocytes into affected tissues. Cardinal signs of inflammation Rubor Calor Tumor Dolor Functio laesa[loss of function] Inflammation of gingiva is termed as Gingivitis .

4. STAGES OF GINGIVAL INFLAMMATION Stage 1 Gingival Inflammation: The initial lesion Stage 2 Gingival inflammation: The Early lesion Stage 3 Gingival Inflammation: The Established lesion Stage 4 gingival inflammation: The Advanced lesion

5. Stage 1 Gingival Inflammation:The Initial lesion 2-4 days after plaque accumulation. The first manifestation of gingival inflammation are vascular changes- dilated capillaries and increased blood flow These initial inflammatory changes occur in response to microbial activation of resident leukocytes and the subsequent stimulation of endothelial cells. Initial response of gingiva to bacterial plaque is not apparent. Subtle changes can also be detected in the junctional epithelium and perivascular connective tissue-for e.g. the perivascular connective tissue matrix becomes altered and there is exudation and deposition of fibrin in the affected area.

6. Lymphocytes begin to accumulate. An increase in the migration of leukocytes and their accumulation within the gingival sulcus may be correlated with an increase in the flow of gingival fluid into the sulcus. The character and intensity of host response determine whether this initial lesion resolves rapidly with restoration of tissue to a normal state;alternatively it may evolve into a chronic inflammatory lesion. If latter occurs an infiltrate of macrophages and lymphoid cells appear within a few days.

7. Microscopic features Changes in blood vessel morphologic features[widening of small capillaries and venules]and the adherence of neutrophils to vessel walls[ margination ]occur within 1 week and sometimes as early as 2days after plaque accumulation Leukocytes mainly polymorphonuclear neutrophils leave the capillaries by migrating through the walls via diapedesis and emigration. They can be seen in increased quantities in connective tissues,the junctional epithelium and the gingival sulcus. The exudation of fluid from the gingival sulcus and the extravascular proteins are present.

8. Stage 2 Gingival Inflammation:The Early Lesion The early lesion evolves from the initial lesion within 1 week after the beginning of plaque accumulation. Clinically early lesion appear as early gingivitis. clinical signs of erythema may appear, mainly because of proliferation of capillaries and increased formation of capillary loops between rete pegs or ridges. Bleeding on probing may also be evident. Gingival fluid flow and the number of transmitting leukocytes reach their maximum between 6 and 12 days after the onset of clinical gingivitis. The amount of collagen destruction increases -70% destroyed around cellular infiltrate The main fibre group that are affected appear to be circular and dentogingival fibre assemblies.

9. PMNs travel to epithelium and cross the basement membrane; they are found in the epithelium, emerging in the pocket area. PMNs are attracted to bacteria and engulf them during the process of phagocytosis. Microscopic features Leukocyte infiltration in the connective tissue beneath the junctional epithelium,which mainly consists of lymphocytes(70%with the majority being T lymphocytes),neutrophils,macrophages,plasma cells and mast cells. The junctional epithelium and gingival sulcus becomes densely infiltrated with neutrophils and junctional epithelium may show development of rete pegs or ridges.

10. Stage 3 Gingival inflammation:The Established Lesion Characterized by a predominance of plasma cell and b lymphocytes. In conjunction with creation of a small gingival pocket lined with a pocket epithelium. B cells are predominantly of immunoglobulin G1and G3 classes. With chronic gingivitis which occurs 2-3 weeks after the beginning of plaque accumulation, the blood vessel become engorged and congested ,venous return is impaired and blood flow become sluggish. This results in a localised gingival anoxemia-super imposes a bluish hue on the reddened gingiva. The extravasation of erythrocytes into the connective tissue and the breakdown of hemoglobin into its component pigments can deepen the colour of chronically inflamed gingiva.

11. Microscopic features Intense and chronic inflammatory reaction. Increased number of plasma cells. Plasma cells invade the connective tissue around the bloodvessels and between bundles of collagen fibres. Junctional epithelium reveals widened intercellular spaces that are filled with granular cellular debris including lysosomes derived from disrupted neutrophils,lymphocytes and monocytes. The junctional epithelium develops rete pegs that protrudes into connective tissue Basal lamina is destroyed in some areas.

12. Stage 4 Gingival inflammation:The Advanced lesion The extension of lesion into alveolar bone-advanced lesion or phase of periodontal breakdown. Microscopic features Fibrosis of gingiva The junctional epithelium migrates apically from the cementoenameljunction. Pocket epithelium is permeable to passage of substances into and out of the underlying connective tissue and temporarily ulcerated in many places. At advanced the presence of plasma cells dominates the connective tissue and neutrophils continue dominating the junctional epithelium.

13. STAGE VASCULAR CHANGES MICROSCOPIC CHANGES CLINICAL CHANGES 1.Initial lesion(2-4 days) Change in blood vessel morphologic features Presence of leukocytes,loss of perivascular collagen,changes in coronal most portion of junctional epithelium. Exudation of fluid from gingival sulcus 2.Early lesion(4-7days) Vascular proliferation, capillary loop Rete peg formation in junctional epithelium,presence of T- lymphocytes,loss of collagen,fibroblast show cytoplasmic alteration. Erythematous,gingival bleeding on probing 3.Established lesion(14-21 days) Engorged capillary B- lympho and plasma cells, junctional epithelium – rete peg extension into connective tissue,atrophic areas,further loss of collagen Changes in consistency and surface texture.Bluish hue around the reddened gingiva. 4.Advanced lesion Same as early and advanced lesions Persistence of features of established lesion,extension of inflammation into deeper structures,presence of all types of inflammatory cells. Formation of periodontal pocket, alveolar bone loss.