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34 Cards in this Set
- Front
- Back
Name the Aggressive Pathogens (Invaders)
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Actinobacillus actinomycetemcomitans (Aa)
Porphyromonas gingivalis (Pg) Treponema denticola (Td) Fusobacterium nucleatum (Fn) |
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How do endotoxins affect the periodontium?
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When Gram negative bacteria die their outer membrane of LPS (endotoxin) stimulate the body to break down tissue by stimulating immune cells to attack the endotoxin, thereby destroying the tissue.
Indirect effect of endotoxins |
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How do exotoxins affect the periodontium?
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Undesired proteins from the bacterial cell wall are released and act on host cells ex) leukotoxin from Aa destroys leukocytes subgingivally.
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How to bacterial enzymes affect the periodontium?
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-Increase permeability of epithelium in sulcus
-increase collagen destruction (collagenase) -promote apical migration of JE -widen intracellular spaces -decrease Ig and other proteins that defend the host |
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Nonspecific Plaque Hypothesis
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Periodontal disease results from the "elaboration of noxious products by the entire plaque flora." When small amounts of plaque are present, the noxious products are neutralized by the host. Large amounts of plaque would produce large amounts of noxious products and overwhelm the host.
-Control of periodontal disease depends on the controls of THE AMOUNT OF PLAQUE. DEALS W/ QUANTITY. |
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Specific Plaque Hypothesis
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Only certain plaque is pathogenic.
-deals with quality, not quantity. This is why some people have tons of plaque and no disease. Others have little plaque and sever disease. |
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When does pellicle formation occur?
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within minutes after brushing teeth
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When does Attachment and Colonization occur?
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Within hours and up to 4 days
-early colonizers attach to the pellicle using molecules called ADHESINS and fibrous proteins called FIMBRIAE |
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What bacteria make up the early/initial colonizers?
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90% of the initial colonizers are gram positive, facultative Streptococci including:
-S. mutans (smooth surface caries not perio-related) -S. sanguis -S. mitis -S. salivarius -Peptostreptococcus micros |
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The remaining 10% of initial colonizers are
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Gram positive, facultative rods; filamentous forms:
-Actinomyces viscosus -Actinomyces naeslundii -Actinomyces israelii and SOME are gram negative species: Prevotella intermedia, Fusobacterium nucleatum, Veillonella alcalescens |
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When does Secondary Colonization occur?
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4-14 days consisting of mainly gram positive cocci and rods, but as the days progress, more gram negative bacteria from the saliva adhere to the existing early colonizers via coaggregation
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What gram negative bacteria are adhering during secondary colonization?
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Gram negative faculative rods:
-Aa (invader) -Capnocytophaga ochracea -Eikenella corrodens Gram negative anaerobic rods: -Pg (invader) -Prevotella intermedia -Tannerella forsynthesis -Fusobacterium nucleatum (invader) Gram negative anaerobic spirochetes (MOTILE) -Treponema denticola (invader) |
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When does plaque maturation occur?
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two-three weeks
-at this point the proportion of gram positive to gram negative species is about equal! -faculatative to anaerobic ratios are also about equal |
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Name the types of subgingival plaques
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-Tooth attached biofilm
-Epitheliam attached biofilm -Unattached plaque |
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What is the source of nutrients for subgingival plaque?
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gingival crevicular fluid (GCF)
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Describe Tooth-Attached Biofilm
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-extend from gingival margin almost to JE (apical edge of the plaque mass is separated by the JE by a layer of leukocytes)
-strongly adherent to tooth surface -mostly gram positive cocci and rods -the more apical you go the move gram negative rods -LEAST virulent of subgingival biofilms -removed by scaling -associated with CHRONIC PERIODONTAL DISEASE |
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What type of biofilm is associated with chronic periodontal disease?
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Tooth-Attached Biofilm
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Describe Epitheliam-attached Biofilm
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-Plaque extends along the pocket EPITHELIUM from gingival margin to the JE
-mostly gram negative rods; large number of filamentous forms -Some of these bacteria can invade into the CT and attach to PDL fibers and alveolar bone -Virulent -Cannot remove with scaling, must be surgically removed -Associated with AGGRESSIVE PERIODONTAL DISEASE |
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What type of biofilm is associated with aggressive periodontal disease?
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Epithelial-attached Biofilm
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Describe Unattached Plaque
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-Free-floating (not a biofilm)
-Mostly gram negative rods and motile spirochetes -Virulent (but can't activate disease until they land on something) -Easily removed with lavage (irrigation) |
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Define Gingivitis
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Inflammatory disease process that results in REVERSIBLE damage to the gingival tissues
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Characteristics of Acute gingivitis
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Time: < or = to 2 weeks
Pain: always painful Does the clien typically notice: yes Duration: once stop inflammation process it heals |
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Characteristics of Chronic Gingivitis
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time: >2weeks
Pain: rarely painful Does the client typically notice? No Duration: depends on immune system. Periods of remission/quieesence and activity/exacerbation |
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Define Sign
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Objective; the clinician can observe it (vitals, probe depth, color change)
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Define Symptom
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Something the CLIENT feels or experiences
-A symptom is subjective (pain) |
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Define Subclinical
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Stage of disease that produces no signs or symptoms
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Why does gingivitis result in a red or reddish-blue color?
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Red- increased blood flow bc blood vessels dialate due to inflammatory process
Reddish-blue: cyanotix due to loss of oxygen; blood becomes stagnant (slow moving) |
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Does a pseudopocket result in apical migration of the JE?
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No, swelling of the gingiva causes the tissue to enlarge resulting in a gingival margin slightly coronal to the CEJ
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What changes occur in CT in patients with gingivitis?
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-destruction of supragingival fiber bundles (reversible)
-decreased collagen content resulting in the body attempting to replace that lost collagen fibers, so ends up producing excess CT resulting in fibrotic (leathery, white) tissue. |
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Describe Stage I of gingivitis
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Stage I: Initial, transient, incipient, subclinical (2-4 days)
-increased blood flow, BV dilate -increased transmigration of PMN's into JE and sulcus -increased tissue permeability (edema) -CORONAL ZONE OF JE IS LOST -No visible/clinical symptoms |
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Describe Stage II of gingivitis
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Stage II: Early, Developing(4-7 day-->14 days)
-Increased # of leukocytes in JE and sulcus -lymphocytes are lining up in the CT near the JE** -exudate continues -Fibroblasts have been altered and a large # of collagen is destroyed -JE lengthens -clinically: slight red, swollen, stipplgin disappears-->shiny, BUP |
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Describe Stage III of gingivitis
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Stage III: Established, chronic (14-21 days)
-JE thickens and extends apically and into CT -beginning gingival pocket formation -Plasma cells preodminate** -Clinically: increased redness, increased probe depths possible due to pseudopockets |
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Is there radiographic evidence of gingivitis?
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No
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Describe the Advanced stage following Stage III gingivitis
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Advanced: progressing to periodontitis (NOT reversible)
-apical migration of JE, loss of PDL fibers and bone loss |