Pathogenesis Perio Disease 7

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What causes the transition from clinical gingival health to gingivitis?
presence of sufficient amounts of plaque.
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what would be a high and low susceptibility subject?
high- molar incisor pattern stage IV Grade C. Low- Localised stage1. Grade A
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What are the 3 theories of periodontitis progression?
continuous rate theory, random burst theory, asynchronous multiple burst theory
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Talk about the continuous rate theory
sites are either active or inactive. at active sites the periodontal destruction continues at a constant rate over time unless treatment is carried out. different active sites may be progressing at different rates
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describe the random burst theory
sites can be active or inactive. at active sites there random bursts of periodontal destruction followed by periods of no activity with possible periods of repair- these sites may become active again at a later time
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previous q continued answer
different sites active at diff time, progress at different rates and are active for different lengths of time
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describe the asynchronous multiple burst theory
similar to random burst theory except that multiple active breakdown within a short defined periods of time. activity followed by long periods of no activity
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what are the 2 different rates of disease progression (LOA)
RAL- rapid LOA: Extensive LOA detected in a short period of time (by manual periodontal probes). GAL: gradual: small amounts of LOA over time, in lots of mini bursts or slow continuous LOA (detectable by v sensitive electronic probes)
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where is RSD carried out?
in true pockets 4mm or greater with BOP. AND OR presence of sub gingival calculus and adequate oral hygiene
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what are some of the periodontal risk factors?
high genetic susceptibility, smoking, alcohol, stress, overhanging restorations/ fillings, immunodeficiency, uncontrolled diabetes
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what evidence increases the evidence of gingival inflammation
increased GCF. increase in inflammation and immune cellular infiltrate in the CT underlying Junctional epithelium. Fewer fibroblasts in the gingival ct underlying JE. Reduction in the collagen content of infiltrate ct under the JE
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What are the 4 phases of the. progression lesion?
initial, early, established and advanced
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what does each lesion mean
initial and early= early. stages of gingivitis. established= clinically apparent gingivitis. advanced= periodontitis
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Initial lesion: when does it occur? what bacteria it is made of? and what are the characteristics of it
occurs within 24-48 hrs of plaque accumulation. mainly gram +ve, aerobic and saccharolytic. characteristics: vasodilation, increased PMNs and GCF production
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how would you describe the tissue damage in initial lesion? where is the infiltrate and how are the bacterial factors described?
tissue damage- minimal. infiltrate confined to small area of CT below the JE. bacterial factors are antigenic thus immune response provoked
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when does the early lesion occur? what is produced and released? what happens to the inflammatory infiltrate?
occurs after 1 week. immunoglobulin produced and cytokine release. the inflammatory infiltrate increases in size- mainly PMNs and lymphocytes
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Loss of A and B in infiltrated area. C and rate peg formation in JE. Increased D. PMNs accumulate in E
A- Fibroblasts. B- collagen. C- proliferation. D- GCF. E- gingival crevice
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the established lesion stage corresponds to what? what is the gingival ct replaced by?what is the dominant cell type found in animal and human studies
corresponds to clinically diagnosis of gingivitis. gingival CT replaced by inflammatory infiltrate. in animal studies= plasma cells. in human studies: in older subjects: plasma. in older studies: lymphocytes
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what s the junctional epithelium replaced by int he established lesion stage?
by pocket epithelium which shows retentions peg growth and ulceration.
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how does the pocket epithelium allow apical migration of the crevice and the plaque biofilm
pocket epithelium is not attached to the tooth
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how do bacterial products cause damage in the established lesion stage
directly by enzymes. indirectly by triggering host response- cytokines, complement, enzymes
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what happens in the advanced lesion stage
inflammatory infiltrate extends apically and laterally comprises >50% plasma cells. continued loss of collagen. ulceration and migration of JE apically onto the root surface
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to what stage does the advanced lesion correspond to?
periodontitis
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what is 80% of the LOA/ bone loss in periodontitis due to?
due to the host response (inflammatory/ immune response) to the invading bacteria
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what are the 2 purposes of the host response to the plaque biofilm?
1.protection of the host against local microbial attack. 2. prevention of spread of micro organisms beyond the immediate target attack site
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how is the PDL damaged?
PDL fibres inserting into the bone and cementum destroyed. loss of ECM. fibroblast damage. loss of the surface cementoblast layer
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what is bone resorption mediated by? and what is. bone loss due to
mediated by: host derived and bacterial factors. bone loss due to release of factors proceeded by the host response such as cytokines(- interleukin 1 ) and prostaglandins, which lead to activation of osteoclasts
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what are the factors mentioned above secreted by?
PMNs, macrophages, fibroblasts, endothelial cells. and osteoclasts. during inflammatory and immune reactions
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what are the relevant bacterial factors, relevant host factors and. risk factors that can alter the balance between the host facts and bacterial factors?
bacterial factors: increase in. number, presence or overgrowth of specific pathogens indirect bacterial tissue invasion. relevant host factors: reduced effectiveness of host defences or release of host derived factors leading to tissue damage. r
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Other cards in this set

Card 2

Front

what would be a high and low susceptibility subject?

Back

high- molar incisor pattern stage IV Grade C. Low- Localised stage1. Grade A

Card 3

Front

What are the 3 theories of periodontitis progression?

Back

Preview of the front of card 3

Card 4

Front

Talk about the continuous rate theory

Back

Preview of the front of card 4

Card 5

Front

describe the random burst theory

Back

Preview of the front of card 5
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