Inhibition of Apoptosis in Periodontitis

This study investigated whether the prolonged survival of inflammatory cells in periodontal disease could be due to the inhibition of apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) decoy receptors and inhibition of the terminal stages of apoptosis signaling by inhibitor...

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Published in:Journal of dental research Vol. 89; no. 1; pp. 29 - 33
Main Authors: Lucas, H., Bartold, P.M., Dharmapatni, A.A.S.S.K., Holding, C.A., Haynes, D.R.
Format: Journal Article
Language:English
Published: Washington, DC SAGE Publications 01.01.2010
International Association for Dental Research
SAGE PUBLICATIONS, INC
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ISSN:0022-0345, 1544-0591, 1544-0591
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Abstract This study investigated whether the prolonged survival of inflammatory cells in periodontal disease could be due to the inhibition of apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) decoy receptors and inhibition of the terminal stages of apoptosis signaling by inhibitor of apoptosis (IAP) family members. Gingival tissue samples were taken from healthy individuals and those with chronic periodontitis. The expression of TRAIL, TRAIL receptors, TUNEL, cleaved caspase-3, xIAP, and survivin was determined immunohistologically and at the level of mRNA expression. Higher levels of TRAIL and the TRAIL decoy receptor, TRAIL R4, were expressed in the diseased periodontal tissues (p < 0.005). Statistically (p < 0.05) higher levels of cleaved caspase-3 and the cleaved caspase-3 inhibitors, xIAP and survivin, were seen. Similar changes were seen at the level of mRNA. The results indicate that apoptosis in periodontitis may be inhibited by elevated expression of TRAIL decoy receptors and cleaved caspase-3 inhibitors.
AbstractList This study investigated whether the prolonged survival of inflammatory cells in periodontal disease could be due to the inhibition of apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) decoy receptors and inhibition of the terminal stages of apoptosis signaling by inhibitor of apoptosis (IAP) family members. Gingival tissue samples were taken from healthy individuals and those with chronic periodontitis. The expression of TRAIL, TRAIL receptors, TUNEL, cleaved caspase-3, xIAP, and survivin was determined immunohistologically and at the level of mRNA expression. Higher levels of TRAIL and the TRAIL decoy receptor, TRAIL R4, were expressed in the diseased periodontal tissues (p < 0.005). Statistically (p < 0.05) higher levels of cleaved caspase-3 and the cleaved caspase-3 inhibitors, xIAP and survivin, were seen. Similar changes were seen at the level of mRNA. The results indicate that apoptosis in periodontitis may be inhibited by elevated expression of TRAIL decoy receptors and cleaved caspase-3 inhibitors.
This study investigated whether the prolonged survival of inflammatory cells in periodontal disease could be due to the inhibition of apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) decoy receptors and inhibition of the terminal stages of apoptosis signaling by inhibitor of apoptosis (IAP) family members. Gingival tissue samples were taken from healthy individuals and those with chronic periodontitis. The expression of TRAIL, TRAIL receptors, TUNEL, cleaved caspase-3, xIAP, and survivin was determined immunohistologically and at the level of mRNA expression. Higher levels of TRAIL and the TRAIL decoy receptor, TRAIL R4, were expressed in the diseased periodontal tissues (p < 0.005). Statistically (p < 0.05) higher levels of cleaved caspase-3 and the cleaved caspase-3 inhibitors, xIAP and survivin, were seen. Similar changes were seen at the level of mRNA. The results indicate that apoptosis in periodontitis may be inhibited by elevated expression of TRAIL decoy receptors and cleaved caspase-3 inhibitors.This study investigated whether the prolonged survival of inflammatory cells in periodontal disease could be due to the inhibition of apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) decoy receptors and inhibition of the terminal stages of apoptosis signaling by inhibitor of apoptosis (IAP) family members. Gingival tissue samples were taken from healthy individuals and those with chronic periodontitis. The expression of TRAIL, TRAIL receptors, TUNEL, cleaved caspase-3, xIAP, and survivin was determined immunohistologically and at the level of mRNA expression. Higher levels of TRAIL and the TRAIL decoy receptor, TRAIL R4, were expressed in the diseased periodontal tissues (p < 0.005). Statistically (p < 0.05) higher levels of cleaved caspase-3 and the cleaved caspase-3 inhibitors, xIAP and survivin, were seen. Similar changes were seen at the level of mRNA. The results indicate that apoptosis in periodontitis may be inhibited by elevated expression of TRAIL decoy receptors and cleaved caspase-3 inhibitors.
This study investigated whether the prolonged survival of inflammatory cells in periodontal disease could be due to the inhibition of apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) decoy receptors and inhibition of the terminal stages of apoptosis signaling by inhibitor of apoptosis (IAP) family members. Gingival tissue samples were taken from healthy individuals and those with chronic periodontitis. The expression of TRAIL, TRAIL receptors, TUNEL, cleaved caspase-3, xIAP, and survivin was determined immunohistologically and at the level of mRNA expression. Higher levels of TRAIL and the TRAIL decoy receptor, TRAIL R4, were expressed in the diseased periodontal tissues ( p < 0.005). Statistically (p < 0.05) higher levels of cleaved caspase-3 and the cleaved caspase-3 inhibitors, xIAP and survivin, were seen. Similar changes were seen at the level of mRNA. The results indicate that apoptosis in periodontitis may be inhibited by elevated expression of TRAIL decoy receptors and cleaved caspase-3 inhibitors. [PUBLICATION ABSTRACT]
Author DHARMAPATNI A. A. S. S. K.
HOLDING C. A.
HAYNES D. R.
LUCAS H.
BARTOLD P. M.
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Issue 1
Keywords survivin
apoptosis
TRAIL
xIAP
caspase-3
Human
Immunohistochemistry
Pathophysiology
Stomatology
Survivin
X linked inhibitor of apoptosis protein
Anatomic pathology
Periodontal disease
Periodontitis
Apoptosis inhibitory protein
TNF related apoptosis inducing ligand
Inhibition
Gingiva
Apoptosis
Language English
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PublicationTitle Journal of dental research
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International Association for Dental Research
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Snippet This study investigated whether the prolonged survival of inflammatory cells in periodontal disease could be due to the inhibition of apoptosis by tumor...
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StartPage 29
SubjectTerms Adult
apoptosis
Apoptosis - physiology
Biological and medical sciences
Case-Control Studies
Caspase 3 - genetics
Caspase 3 - metabolism
caspase-3
Chronic Periodontitis - immunology
Chronic Periodontitis - metabolism
Chronic Periodontitis - pathology
Facial bones, jaws, teeth, parodontium: diseases, semeiology
Gingiva - cytology
Gingiva - immunology
Humans
Immunohistochemistry
In Situ Nick-End Labeling
Inhibitor of Apoptosis Proteins
Leukocytes - metabolism
Medical sciences
Microtubule-Associated Proteins - genetics
Microtubule-Associated Proteins - metabolism
Middle Aged
Non tumoral diseases
Otorhinolaryngology. Stomatology
Receptors, TNF-Related Apoptosis-Inducing Ligand - genetics
Receptors, TNF-Related Apoptosis-Inducing Ligand - metabolism
Reference Values
RNA, Messenger - analysis
survivin
TNF-Related Apoptosis-Inducing Ligand - genetics
TNF-Related Apoptosis-Inducing Ligand - metabolism
TRAIL
Tumor Necrosis Factor Decoy Receptors - genetics
Tumor Necrosis Factor Decoy Receptors - metabolism
X-Linked Inhibitor of Apoptosis Protein - genetics
X-Linked Inhibitor of Apoptosis Protein - metabolism
xIAP
Title Inhibition of Apoptosis in Periodontitis
URI https://cir.nii.ac.jp/crid/1573950400963818752
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https://www.ncbi.nlm.nih.gov/pubmed/19948942
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Volume 89
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