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PERIODONTICS- GINGIVAL INFLAMMATION-
- 2. GINGIVAL HEALTH LOCAL INNATE IMMUNITY SPECIFIC IMMUNITY Epithelial cells Mucins, lysozymes, lactoferrins & LPO Beta defensins, Histatins ©medicodontology
- 3. SEQUENCE OF EVENTS Micro-org attached to tooth surface/near gingival sulcus Capable of synthesizing products like collagenase, hyaluronidase, protease etc. cause damage to epi & CT cells and I/C constituents such as Collagen, Ground subs and glycocalyx resultant widening of junctional epithelial cells during early gingivitis may permit injurious agents derived from bacterial product or bacteria itself to gain access to CT Microbial products activates cells like monocytes and macrophages to produce vasoactive subs like TNF, IL-1, PGE2 Alters gingival FB by delaying their death by mechanism blocking apoptosis Stabilizes gingival FB population during inflammation PATHOLOGIC CHANGES à INITIATED BY A HOST RESPONSE TO ORAL MICRO-ORG. ©medicodontology
- 4. STAGES OF GINGIVITIS TABLE 17.1 Stages of Gingivitis ŠŽ ’–Ž ǻŠ¢œǼ •˜˜ ŽœœŽ•œ ž—Œ’˜—Š• Š—ȱž•Œž•Š› ™’‘Ž•’Š ›Ž˜–’—Š— ––ž—Ž Ž••œ ˜••ŠŽ— •’—’ŒŠ• ’—’—œ ǯȱ —’’Š• •Žœ’˜— Řȱ˜ȱŚ ŠœŒž•Š› ’•Š’˜— ŠœŒž•’’œ —’•›Š’˜—ȱ‹¢ œ œ Ž›’ŸŠœŒž•Š› •˜œœ ’—’ŸŠ• •ž’ȱ•˜ ǯȱŠ›•¢ •Žœ’˜— Śȱ˜ȱŝ ŠœŒž•Š› ™›˜•’Ž›Š’˜— Š–ŽȱŠœ œŠŽȱ ŽŽȱ™Žœ ›˜™‘’Œ Š›ŽŠœ ¢–™‘˜Œ¢Žœ —Œ›ŽŠœŽ •˜œœȱŠ›˜ž— ’—’•›ŠŽ ›¢‘Ž–Š •ŽŽ’— ˜— ™›˜‹’— ŗŚŝŘ ǯ œŠ‹•’œ‘Ž •Žœ’˜— ŗŚȱ˜ Řŗ Š–ŽȱŠœȱœŠŽ ǰȱ™•žœȱ‹•˜˜ œŠœ’œ Š–ŽȱŠœȱœŠŽ ȱ‹žȱ–˜›Ž ŠŸŠ—ŒŽ •Šœ–ŠȱŒŽ••œ ˜—’—žŽ •˜œœ ‘Š—Žœȱ’— Œ˜•˜›ǰȱœ’£Žǰ Ž¡ž›ŽǰȱŠ— œ˜ȱ˜— PMNs, Polymorphonuclear leukocytes (neutrophils). Žœ™’ŽȱŽ¡Ž—œ’ŸŽȱ›ŽœŽŠ›Œ‘ǰȱ Žȱœ’••ȱŒŠ——˜ȱŽ’—’’ŸŽ•¢ ©medicodontology
- 5. STAGE –1 : THE INITIAL LESION Characterized by VASCULAR CHANGES – Dilated capillaries Increased blood flow. Occur in response to the microbial activation of resident leukocytes and subsequent activation of endothelial cells. CLINICALLY, initial response à NOT EVIDENT. MICROSCOPICALLY, features of ACUTE INFLAMMATION seen in CT beneath junctional epithelium. • Changes in BV morphologic feature e.g., widening of capillaries and venules. • Margination i.e. adherence of Neutrophil to vessel wall occur within 1 week. • Neutrophils leave capillaries via DIAPEDESIS and present in increased quantity in CT, JE GS. Exudation of fluid from GS and Extravascular proteins à present. 1 2 3 4 ©medicodontology
- 6. STAGE 2- THE EARLY LESION ‘ŽȱŽŠ›•¢ȱ•Žœ’˜—ȱŽŸ˜•ŸŽœȱ›˜–ȱ‘Žȱ’—’’Š•ȱ•Žœ’˜—ȱ ’‘’—ȱŠ‹˜žȱŗȱ ŽŽ” ŠŽ›ȱ‘Žȱ‹Ž’——’—ȱ˜ȱ™•ŠšžŽȱŠŒŒž–ž•Š’˜—ǯřśǰŚŗ ȱ•’—’ŒŠ••¢ǰȱ‘ŽȱŽŠ •Žœ’˜—ȱ–Š¢ȱŠ™™ŽŠ›ȱŠœȱŽŠ›•¢ȱ’—’Ÿ’’œǰȱŠ—ȱ’ȱ˜ŸŽ›•Š™œȱ ’‘ȱŠ— ŽŸ˜•ŸŽœȱ›˜–ȱ‘Žȱ’—’’Š•ȱ•Žœ’˜—ȱ ’‘ȱ—˜ȱŒ•ŽŠ›ȬŒžȱ’Ÿ’’—ȱ•’—Žǯȱœ ’–Žȱ˜Žœȱ˜—ǰȱŒ•’—’ŒŠ•ȱœ’—œȱ˜ȱŽ›¢‘Ž–Šȱ–Š¢ȱŠ™™ŽŠ›ǰȱ–Š’—•¢ ‹ŽŒŠžœŽȱ˜ȱ‘Žȱ™›˜•’Ž›Š’˜—ȱ˜ȱŒŠ™’••Š›’ŽœȱŠ—ȱ‘Žȱ’—Œ›ŽŠœŽ ˜›–Š’˜—ȱ˜ȱŒŠ™’••Š›¢ȱ•˜˜™œȱ‹Ž ŽŽ—ȱ›ŽŽȱ™Žœȱ˜›ȱ›’Žœȱǻ’ǯȱŗŝǯ •ŽŽ’—ȱ˜—ȱ™›˜‹’—ȱ–Š¢ȱŠ•œ˜ȱ‹ŽȱŽŸ’Ž—ǯŗ ȱ ’—’ŸŠ•ȱ•ž’ȱ•˜ ȱŠ— ‘Žȱ—ž–‹Ž›œȱ˜ȱ›Š—œ–’›Š’—ȱ•Žž”˜Œ¢Žœȱ›ŽŠŒ‘ȱ‘Ž’›ȱ–Š¡’–ž– ‹Ž ŽŽ—ȱŜȱŠ—ȱŗŘȱŠ¢œȱŠŽ›ȱ‘Žȱ˜—œŽȱ˜ȱŒ•’—’ŒŠ•ȱ’—’Ÿ’’œǯŘŜ FIG. 17.5 Marginal gingivitis and irregular gingival contour. ȱ ’Œ›˜œŒ˜™’ŒȱŽ¡Š–’—Š’˜—ȱ˜ȱ‘Žȱ’—’ŸŠȱ›ŽŸŽŠ•œȱ•Žž”˜Œ¢Ž ’—’•›Š’˜—ȱ’—ȱ‘ŽȱŒ˜——ŽŒ’ŸŽȱ’œœžŽȱ‹Ž—ŽŠ‘ȱ‘Žȱ“ž—Œ’˜—Š• Evolves from initial within about 1 week after the beginning of plaque accumulation. CLINICALLY Erythema b/c of proliferation of capillaries and formation of capillary loops b/w rete pegs. BOP- may be evident. Gingival fluid flow and no. of transmigrating leukocytes reach their max. b/w 6 12 days after onset of clinical gingivitis. ©medicodontology
- 7. MICROSCOPICALLY Leukocyte infilteration in CT beneath JE. Lymphocytes, T cells, macrophages, plasma cells mast cells are found. JE GS- densely infilterated with Neutrophils; Dev of rete pegs. Cytotoxic alteration in FB - Dec. capacity for collagen. STAGE II- THE EARLY LESION FIG. 17.4 Early human gingivitis lesion. There is an area of lamina propria subjacent to the crevicular epithelium that shows a capillary with several extravascular lymphocytes and one lymphocyte within the lumen. The specimen also exhibits a considerable loss of perivascular collagen density (magnification, ×2500). (Courtesy Dr. Charles Cobb, Kansas City, Missouri.) ˜ ŽŸŽ›ǰȱ‘ŽœŽȱ’—’—œȱŠ›Žȱ—˜ȱŠŒŒ˜–™Š—’Žȱ‹¢ȱ–Š—’ŽœŠ’˜—œ ȱ’œœžŽȱŠ–ŠŽȱ‘ŠȱŠ›Žȱ™Ž›ŒŽ™’‹•ŽȱŠȱ‘Žȱ•’‘ȱ–’Œ›˜œŒ˜™’Œȱ˜› •›Šœ›žŒž›Š•ȱ•ŽŸŽ•Dzȱ‘Ž¢ȱ˜ȱ—˜ȱ˜›–ȱŠ—ȱ’—’•›ŠŽǰȱŠ—ȱ‘Ž’› ›ŽœŽ—ŒŽȱ’œȱ—˜ȱŒ˜—œ’Ž›Žȱ˜ȱ’—’ŒŠŽȱ™Š‘˜•˜’ŒȱŒ‘Š—ŽǯřŜ ž‹•ŽȱŒ‘Š—ŽœȱŒŠ—ȱŠ•œ˜ȱ‹ŽȱŽŽŒŽȱ’—ȱ‘Žȱ“ž—Œ’˜—Š•ȱŽ™’‘Ž•’ž– ©medicodontology
- 8. STAGE – III: THE ESTABLISHED LESION Charac. by predominance of PLASMA cells and B lymphocytes (Ig G1 , G3) small gingival pocket lined with pocket epithelium. BV- Engorged congested, impaired venous return sluggish blood flow. Localised gingival anoxemia (bluish hue on reddened gingiva). Extravasation of erythrocytes into CT Hb breakdownà deepens color of chronically inflamed gingiva. Collagenolytic activity increased. Elevated levels of acid and alkaline phosphatase, Beta-glucuronidase, esterase etc. Moderately to severely inflamed gingiva. 2 types: STABLE (do not progress for months) ACTIVE (convert progressively to destructive lesions) CLINICAL FEATURES ©medicodontology
- 9. HISTOLOGICAL FEATURES Increased Plasma cells Junctional epithelium Connective Tissue • Inflammatory type • Invade deep to the CT, around BV b/w collagen bundles. • Widened intercellular spaces filled with granular cellular debris inc. lysosomes and monocytes. • Rete pegs protrude to CT. • Collagen fibers are destroyed around the infilterate of intact disrupted plasma cells, neutrophils, lymphocytes , monocytes and mast cells. FIG. 17.8 Established gingivitis in a human subject. An area of crevicular epithelium exhibits enlarged intercellular spaces with numerous microvilli and desmosomal junctions. Several lymphocytes, both small and large, are seen migrating through the epithelial layer (magnification, ×3000). ©medicodontology
- 10. STAGE IV: THE ADVANCED LESION Extension of lesion into alveolar bone. “PHASE OF PERIODONTAL BREAKDOWN.” Fibrosis of gingiva and widespread manifestations of inflammatory and immunopathologic tissue damage. Plasma cells dominate CT Neutrophils dominate junctional epithelium and gingival crevice. HISTOLOGICAL FEATURES CLINICAL FEATURES FIG. 17.9 Advanced gingivitis in a human subject. This specimen from the lamina propria exhibits plasma cell degeneration, with abundant cellular debris visible (magnification, ×3000). (Courtesy Dr. Charles Cobb, Kansas City, Missouri.) ‘Žȱ™›Ž˜–’—Š—ŒŽȱ˜ȱ™•Šœ–ŠȱŒŽ••œȱ’œȱ‘˜ž‘ȱ˜ȱ‹ŽȱŠȱ™›’–Š›¢ ©medicodontology