Gingival Inflammation

Gingival Inflammation

1. Development

   • initial
     • 2-4d after plaque accumulation
     • subclinical; only seen histological
     • streptococcus form dental plaque
     • edema due to vascular change, inc. GCF, PMN (polymorphonuclear leukocyte) accum. (major host), 5-10% CT involvement
   • Early
     • 4-7 days
     • inc. vascular , permeability, proliferation of capillary loops, retepege formation in epi. leads to visible edema & erythema in gingival margin & BOP
     • PMN-->lymphocytes (70%)
     • no attachment loss, no permanent damage if plaque removed
   • Established
     • 7-21 days, end stage of gingivitis
     • B lymphocyte and plasma cell (IgG1 & IgG3) are predominant
     • T cell is stable compared to B/plasma cells which leads to perio pocket
     • inc epi permeability allow microbial products to continuously produce inflammatory cytokines, IL-1, TNF-α, PGE2
   • Advanced
     • same cellular make up as established
     • clinically/histologically attachment loss
     • host susceptibility concept
       • tissue destruction due to immune response
     • apical migration of JE= periodontal pocket forms
     • gingival fibroblast
       • favor destruction of CT and perio ligament
     • osteoclasts stimulated=bone loss

2. inflammation around implants

   • peri-implant disease
     • imbalance bet. bacteria and host response following implantation of endosseus implant
     • peri-implant mucositis
       • Presence of inflammation around a mucosa with no signs of bone loss
     • peri-implantitis
       • inflammation of mucosa & bone loss
   • Biofilm formation (3 wks)
     • no diff in biofilm formation & host response
     • similar clinical response and similar# of B lymphocytes/plasma cells
   • Established biofilm ( 3 mo.)
     • inflam. extending apical to JE; BOP on mild exploration
     • collagen loss; apical inflammation and size is 3X greater on peri-implant tissue
   • Advanced infection
     • once established it continues to progress
     • lack fibrous band surrounding inflamm. lesion

3. Cells in Gingival Inflammation

   • PMN
     • Component of non specific immunity Generally first line of defense Contains enzyme containing granules
   • B lymphocytes, plasma cells
     • Stem cells from bone marrow Maturation in bone marrow B memory cells Component of humoral immunity Responsible for Ig synthesis
   • T lymphocytes
     • Stem cells from bone marrow, maturation in thymus Component of cell mediated immunity Antigen recognition T-helper cells assist antibody production and cytotoxic T cell response Release of cytokines
   • host defense cells
     • lymphocytes, leukocytes, phagocytes, helper vells

4. chemokines

   • Hormone like small molecular weight peptides. Chemokines regulate cell functions such as proliferation, inflammation, immunity, repair

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