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17 Cards in this Set
- Front
- Back
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What is meant by fibrosis?
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Clinical - harder connective tissue, less cellular.
Histologic - high density of fibers, low density of cells. Biochemical - high collagen content, high microfibril, high ECM |
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What is meant by inflammation?
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Softer in appearance, could be bloody due to bacterial load. Puffy, not firm like fibrotic tissue.
Histologic - lots of cells, lymphocytes biochemical - lot of connective tissue, collagen, GAGs, proteoglycans, ground substance. not much ECM due to MMPs - proteases degrade proteins and the matrix. TNF-alpha, PGs |
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Phenytoin induced gingival overgrowth - clinical and histologic
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Tissues almost completely cover the teeth by at least half.
Characterized by fibrosis! Cells in stroma are fibroblasts but you also see small dark stained cells. inflammatory cells - lymphocytes. Only occurs in the oral tissues, not in any others. |
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Human gingival fibromatosis
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Most amount of gingival growth that is not drug induced. Very firm gingiva, and overgrowth actually pushes teeth around.
-lots of collagen fibers, not many cells. |
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Where is most inflammation present in the gingiva?
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Sulcular epithelium and subepithelial connective tissue. More bacteria in this area than any others.
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Features of gingival overgrowth tissues
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-Varying degrees of inflammation and fibrosis
-Thickened epithelium -Thickened CT Consequences: -Poor oral hygiene -Increase bacterial load -Systemic consequences are likely |
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Cyclosporin induced gingival overgrowth
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There is more inflmmation in most areas especially in the sulcus than in the others. High inflammation characterizes this.
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Is CCN2 elevated in inducted gingival overgrowth
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Yes this is. Classic driver of fibromatosis is TGF beta. CT growth factor will sustain fibrosis over a long period of time.
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More information about CTGF (CCN2)?
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-Matricellular protein
-Strongly upregulated by TGF-beta, and promotes fibrosis =in lung and kidney cells it is strongly down regulated by inflammatory mediators TGF-alpha and PGE2 |
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Is is surprising that CTGF is found at high levels in some forms of gingival overgrowth?
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Yes and No. Not surprising since its known to sustain fibrosis but in oral tissues, thre's going to be an appreciable level of inflammation in oral tissues since its the only place wehre you have mineralized tissues next to soft ones that induce inflammation, even in the cleanest hygeine you can imagine.
Gingival tissues seem likely to resist the effects of inflamatory mediators to reduce CCN2/CTGF expression. -gingival overgrowth occurs in gingiva and not in other tissues! |
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What is PGE2? What happens when this is added along with TGF in gingiva, lung, and kidney cells?
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PGE2 is another growth factor that doesn't block TGFBeta 1 in fibroblasts. Major upregulator of CTGF is TGF beta. PGE2 and TGF beta together effect isn't diminishe, and you get same level of CT growth factor in gingiva.
In kidney cells and lung fibroblasts, PGE2 and TGF together leads to diminished activity of CTGF. |
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Signal tranduction for PGE2 and TGFB 1?
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Uses JNK as a signal transducer. TGFbeta invovles the MAP kinases. JNK is the active MAP kinase. When PGE2 comes along, it causes upregulation of cAMP that inhibits JNK. In gingiva, this response is small and that's why theres very little cAMP. PKA activation usually inhibits JNK but this is weak, so JNK is not inhibited. Therefore, CTGF expression does occur.
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Role of small G proteins
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COntribute significantly to CTGF expression. Another signal transducer. Need HMG CoA reductase, farnesyl transferase and geranyl-geranyl transferase to convert them eventually into Rho GTPases.
Statins will reduce production of these Rho GTPases by inhibiting cholesterol biosynthesis and acting on HMG CoA reductase. Statins inhibit HMGCo reductase. This also ultimately inhibits CCN2/CTGF production in the presence of TGF-b in gingival fibroblasts. |
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What is forskolin?
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Activates AC without prostaglandin. Add this to gingival cells, increase cAMP and increase inhibitory aspect of JNK
Forskolin can increase cAMP which ultimately inhibits CCN2/CTGF production in the presence of TGF-b in gingival fibroblasts. . |
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Epthelial and mesenchymal transition in gingival overgrowth
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Epthelim role is primarly protection. In cancer, there's inappropriate communication between epithelium and CT. This happens in gingival overgrwoth.
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What does disruption of epithelial cell contacts lead to?
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-Increase motitly of epithelial cells
-Increase proliferation of epi cells |
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E cadherin. What do we see in phenytoin induced overgrwoth? Cyclosporin induced?
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Expression normally occurs in epithelium and high along border between epi and CT area. In phenytoin induced overgrowth, you dont see that. There's no E cadherin expression.
Fcn is to help epithelium stick together. Same case in cyclosporin. Breaks in basement membrane. |
