| A | B |
|---|
| bright red color | vasodilation |
| swelling/edema | permeability of blood vessel walls |
| slight bleeding on probing | loss of collagen around blood vessels, sulcus epithelium begins to thin |
| flow of gingival crevicular fluid | exudate leaks through sulcular epithelium |
| soft, spongy consistency | exudate leaves permeable blood vessels, CT & epithelium destroyed |
| blue color | vasostagnation |
| Moderate to severe bleeding on probing | thinning and ulceration of sulcular epithelium |
| firm, leathery consistency | increased cell division in epithelium and/or increased fibroblast activity in CT |
| White color | increased division epithelium and/or CT |
| Enlargement | exudate leaves permeable blood vessels and enters tissues or increased cell division in CT |
| smooth, shiny | destruction of collagen and stretching of epithelium |
| bulbous | exudate leaves permeable vessels or increased cell division in CT |
| gingival recession | JE detaches and moves apical |
| malodor/bad taste | release of volatile sulfur compounds |
| alveolar bone loss | osteoclasts destroy bone |
| cytokines released by injured cells | histamine, PGE-2, IL-1, TNF-alpha, collagenase |
| MMP | collagenase, CT destruction and bone loss |
| PGE-2 | bone loss |
| IL-1 | sticky blood vessel walls, vasodilation & permeability, bone loss |
| TNF-alpha | recruits PMNs, increases vascular permeability, stimulates PGE realease & CT destruction (including bone)bone loss |
| PMN | polymorphonuclear leukocyte |
| Monocyte | becomes macrophage in tissue |
| B-lymphocyte | antibody-mediated immunity (humoral) |
| T-lymphocyte | cell-mediated immunity |
| plasma cell | antibody production |
| IgG | protects in first few weeks of life |
| IgA | saliva & mucosal surfaces |
| IgM | first to respond |
| IgE | allergic reactions |
| pavementing | WBCs attachj to blood vessel walls |
| margination | WBCs move from center to periphery of blood vessel walls |
| chemotaxis | chemical trail to area of injury or invasion |
| opsonization | antigens become coated/enhances phaogocytosis |
| diapedesis | WBCs ooze though blood vessel walls |
| basophils | release histamine |
| phagocyte | surrounds,e ngulfs, & digests microorganisms |
| antigen | substances recognized as foreign |
| lipolysaccharide | endotoxin, part of cell wall of gram-neg. microorganisms |
| lysosomes | granules found in WBCs capable of killing microorganisms |
| complement | series of proteins that opsonize antigens |
| microcirculation | small blood vessels such as arterioles, capillaries, and venules |
| purulent exudate | contains pus |
| lymphadenopathy | enlargement of lymph nodes |
| pathogenic microorganisms | microorganism that causes disease |
| immune complex | a combination of antibody and antigen |
| IL-6 | activates lymphocytes resulting in increased antibody production, stimulates bone resorption & inhibits bone formation |
| biologic equilibrium | state of balance in the internal environment of the body |
| phagosome | phagocytic vesecle within the phagocyte |
| phagolysosome | fusion of a phagosome with lysosomal granules (enzymes), digests the microorganism |
| Health | JE at CEJ |
| Gingivitis | JE at CEJ, reversible tissue destruction |
| Periodontitis | JE apical to CEJ, permanent tissue destruction |
| subclinical disease | so mild that doesn't produce sysmptoms |
| periodontal pathogens | primarily gram negative anaerobes, facultative anaerobes, & spirochetes |
| exotoxins | harmful proteins released by microorganisms that cause damage |
| bacterial enzymes | harmful enzymes released by microorganisms that cause tissue damage |
| host response | the way that the body responds to periodontal pathogens |
| orange complex | potential periodontal pathogens usually present in low numbers in most oral cavities |
| red complex | periodontal pathogens strongly associated with destructive periodontal diseases; know names |
| Actinobacillus actinomycetemcomitans | virulent periodontal pathogen that produces leukotoxin |
| arachidonic acid cascade | results in release of PGE2 |
| major histocampatibility complex | host system that differentiates between "self" & "nonself" |
| membrane attack complex | end-product of complement system activation that forms holes in bacteria and kills them |
| risk factors | increase host susceptibility to perio disease |
| PMN defects | decreased diapedesis, chemotaxis, phaogcytosis,digestion, or numbers; associated with more severe perio disease |
