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Periapical lesion progression and cytokine expression in an LPS hyporesponsive model
Aim The purpose of this study was to compare periapical lesion progression and the expression of the bone modulating cytokines IL‐1α, TNF‐α, IL‐4, IL‐6 and IL‐11 in periapical lesions of normal and C3H/HeJ (LPS hyporesponsive) mice. Methodology Pulps of both mandibular first molars from C3H/HeJ and...
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Published in: | International endodontic journal 2001-10, Vol.34 (7), p.506-513 |
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container_title | International endodontic journal |
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creator | Fouad, A. F. Acosta, A. W. |
description | Aim
The purpose of this study was to compare periapical lesion progression and the expression of the bone modulating cytokines IL‐1α, TNF‐α, IL‐4, IL‐6 and IL‐11 in periapical lesions of normal and C3H/HeJ (LPS hyporesponsive) mice.
Methodology
Pulps of both mandibular first molars from C3H/HeJ and BALB/c (normal) mice were exposed and inoculated with normal mouse oral microorganisms for 2, 4, 6, and 8 weeks. After euthanasia, specimens were prepared for histological examination. A quantitative evaluation of the lesional area and immunohistochemical stain counts was performed.
Results
There were no statistically significant differences in progression of periapical lesions for both mouse strains with time (two‐factor anova, P > 0.05). The immunohistochemical staining revealed no overall differences between the two strains in levels of expression of the cytokines (P > 0.05). IL‐11 expression did not change from control levels in BALB/c mice, but correlated with the expression of IL‐6 and IL‐4 in C3H/HeJ mice.
Conclusion
Responsiveness to LPS may not be significant in the pathogenesis of periapical lesions and in cytokine expression within the lesions, when the lesions are induced by non‐specific oral flora. |
doi_str_mv | 10.1046/j.1365-2591.2001.00423.x |
format | article |
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The purpose of this study was to compare periapical lesion progression and the expression of the bone modulating cytokines IL‐1α, TNF‐α, IL‐4, IL‐6 and IL‐11 in periapical lesions of normal and C3H/HeJ (LPS hyporesponsive) mice.
Methodology
Pulps of both mandibular first molars from C3H/HeJ and BALB/c (normal) mice were exposed and inoculated with normal mouse oral microorganisms for 2, 4, 6, and 8 weeks. After euthanasia, specimens were prepared for histological examination. A quantitative evaluation of the lesional area and immunohistochemical stain counts was performed.
Results
There were no statistically significant differences in progression of periapical lesions for both mouse strains with time (two‐factor anova, P > 0.05). The immunohistochemical staining revealed no overall differences between the two strains in levels of expression of the cytokines (P > 0.05). IL‐11 expression did not change from control levels in BALB/c mice, but correlated with the expression of IL‐6 and IL‐4 in C3H/HeJ mice.
Conclusion
Responsiveness to LPS may not be significant in the pathogenesis of periapical lesions and in cytokine expression within the lesions, when the lesions are induced by non‐specific oral flora.</description><identifier>ISSN: 0143-2885</identifier><identifier>EISSN: 1365-2591</identifier><identifier>DOI: 10.1046/j.1365-2591.2001.00423.x</identifier><identifier>PMID: 11601767</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Analysis of Variance ; Animals ; bone resorption ; Coloring Agents ; cytokines ; Cytokines - immunology ; Cytokines - physiology ; Dental Pulp - microbiology ; Dental Pulp Exposure - microbiology ; Dental Pulp Necrosis - microbiology ; Dentistry ; Disease Models, Animal ; Disease Progression ; Immunohistochemistry ; Interleukin-1 - immunology ; Interleukin-11 - immunology ; Interleukin-4 - immunology ; Interleukin-6 - immunology ; lipopolysaccharides ; Lipopolysaccharides - immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred Strains ; Periapical Diseases - immunology ; Periapical Diseases - microbiology ; Periapical Diseases - physiopathology ; periapical lesions ; Time Factors ; Tumor Necrosis Factor-alpha - immunology</subject><ispartof>International endodontic journal, 2001-10, Vol.34 (7), p.506-513</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11601767$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fouad, A. F.</creatorcontrib><creatorcontrib>Acosta, A. W.</creatorcontrib><title>Periapical lesion progression and cytokine expression in an LPS hyporesponsive model</title><title>International endodontic journal</title><addtitle>Int Endod J</addtitle><description>Aim
The purpose of this study was to compare periapical lesion progression and the expression of the bone modulating cytokines IL‐1α, TNF‐α, IL‐4, IL‐6 and IL‐11 in periapical lesions of normal and C3H/HeJ (LPS hyporesponsive) mice.
Methodology
Pulps of both mandibular first molars from C3H/HeJ and BALB/c (normal) mice were exposed and inoculated with normal mouse oral microorganisms for 2, 4, 6, and 8 weeks. After euthanasia, specimens were prepared for histological examination. A quantitative evaluation of the lesional area and immunohistochemical stain counts was performed.
Results
There were no statistically significant differences in progression of periapical lesions for both mouse strains with time (two‐factor anova, P > 0.05). The immunohistochemical staining revealed no overall differences between the two strains in levels of expression of the cytokines (P > 0.05). IL‐11 expression did not change from control levels in BALB/c mice, but correlated with the expression of IL‐6 and IL‐4 in C3H/HeJ mice.
Conclusion
Responsiveness to LPS may not be significant in the pathogenesis of periapical lesions and in cytokine expression within the lesions, when the lesions are induced by non‐specific oral flora.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>bone resorption</subject><subject>Coloring Agents</subject><subject>cytokines</subject><subject>Cytokines - immunology</subject><subject>Cytokines - physiology</subject><subject>Dental Pulp - microbiology</subject><subject>Dental Pulp Exposure - microbiology</subject><subject>Dental Pulp Necrosis - microbiology</subject><subject>Dentistry</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Immunohistochemistry</subject><subject>Interleukin-1 - immunology</subject><subject>Interleukin-11 - immunology</subject><subject>Interleukin-4 - immunology</subject><subject>Interleukin-6 - immunology</subject><subject>lipopolysaccharides</subject><subject>Lipopolysaccharides - immunology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C3H</subject><subject>Mice, Inbred Strains</subject><subject>Periapical Diseases - immunology</subject><subject>Periapical Diseases - microbiology</subject><subject>Periapical Diseases - physiopathology</subject><subject>periapical lesions</subject><subject>Time Factors</subject><subject>Tumor Necrosis Factor-alpha - immunology</subject><issn>0143-2885</issn><issn>1365-2591</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><recordid>eNpFkEtPwzAQhC0EoqXwF1BO3BK8fsSxxAVVBYoqUYlyttzYAZe8iFto_j1JH3BY7WhmtFp9CAWAI8Asvl1FQGMeEi4hIhhDhDEjNNqeoOFfcIqGGBgNSZLwAbrwfoUx5pjCORoAxBhELIZoMbeN07VLdR7k1ruqDOqmem-s32ldmiBt19WnK21gt_XRd30UzOavwUdbV51bV6V33zYoKmPzS3SW6dzbq8MeobeHyWL8FM5eHqfj-1lYgyQ0FFpmS6atSHBCQCfEGJ3IboSUlBNmWMoBmOQpJ5BlgqUiZmlGLTUGxJLQEbrZ3-1e_tpYv1aF86nNc13aauOVICAlJ7grXh-Km2VhjaobV-imVUcOXeFuX_hxuW3_c6x63mqleqyqx6p63mrHW23VdPLcCfoLMutzrw</recordid><startdate>200110</startdate><enddate>200110</enddate><creator>Fouad, A. F.</creator><creator>Acosta, A. W.</creator><general>Blackwell Science Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200110</creationdate><title>Periapical lesion progression and cytokine expression in an LPS hyporesponsive model</title><author>Fouad, A. F. ; Acosta, A. W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p1923-7a9fb4ae780821a82dda89da87993524d4c511495c521ff74c764cf3e3dd17b23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>bone resorption</topic><topic>Coloring Agents</topic><topic>cytokines</topic><topic>Cytokines - immunology</topic><topic>Cytokines - physiology</topic><topic>Dental Pulp - microbiology</topic><topic>Dental Pulp Exposure - microbiology</topic><topic>Dental Pulp Necrosis - microbiology</topic><topic>Dentistry</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Immunohistochemistry</topic><topic>Interleukin-1 - immunology</topic><topic>Interleukin-11 - immunology</topic><topic>Interleukin-4 - immunology</topic><topic>Interleukin-6 - immunology</topic><topic>lipopolysaccharides</topic><topic>Lipopolysaccharides - immunology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C3H</topic><topic>Mice, Inbred Strains</topic><topic>Periapical Diseases - immunology</topic><topic>Periapical Diseases - microbiology</topic><topic>Periapical Diseases - physiopathology</topic><topic>periapical lesions</topic><topic>Time Factors</topic><topic>Tumor Necrosis Factor-alpha - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fouad, A. F.</creatorcontrib><creatorcontrib>Acosta, A. W.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>International endodontic journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fouad, A. F.</au><au>Acosta, A. W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Periapical lesion progression and cytokine expression in an LPS hyporesponsive model</atitle><jtitle>International endodontic journal</jtitle><addtitle>Int Endod J</addtitle><date>2001-10</date><risdate>2001</risdate><volume>34</volume><issue>7</issue><spage>506</spage><epage>513</epage><pages>506-513</pages><issn>0143-2885</issn><eissn>1365-2591</eissn><abstract>Aim
The purpose of this study was to compare periapical lesion progression and the expression of the bone modulating cytokines IL‐1α, TNF‐α, IL‐4, IL‐6 and IL‐11 in periapical lesions of normal and C3H/HeJ (LPS hyporesponsive) mice.
Methodology
Pulps of both mandibular first molars from C3H/HeJ and BALB/c (normal) mice were exposed and inoculated with normal mouse oral microorganisms for 2, 4, 6, and 8 weeks. After euthanasia, specimens were prepared for histological examination. A quantitative evaluation of the lesional area and immunohistochemical stain counts was performed.
Results
There were no statistically significant differences in progression of periapical lesions for both mouse strains with time (two‐factor anova, P > 0.05). The immunohistochemical staining revealed no overall differences between the two strains in levels of expression of the cytokines (P > 0.05). IL‐11 expression did not change from control levels in BALB/c mice, but correlated with the expression of IL‐6 and IL‐4 in C3H/HeJ mice.
Conclusion
Responsiveness to LPS may not be significant in the pathogenesis of periapical lesions and in cytokine expression within the lesions, when the lesions are induced by non‐specific oral flora.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>11601767</pmid><doi>10.1046/j.1365-2591.2001.00423.x</doi><tpages>8</tpages></addata></record> |
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source | Wiley-Blackwell Read & Publish Collection |
subjects | Analysis of Variance Animals bone resorption Coloring Agents cytokines Cytokines - immunology Cytokines - physiology Dental Pulp - microbiology Dental Pulp Exposure - microbiology Dental Pulp Necrosis - microbiology Dentistry Disease Models, Animal Disease Progression Immunohistochemistry Interleukin-1 - immunology Interleukin-11 - immunology Interleukin-4 - immunology Interleukin-6 - immunology lipopolysaccharides Lipopolysaccharides - immunology Male Mice Mice, Inbred BALB C Mice, Inbred C3H Mice, Inbred Strains Periapical Diseases - immunology Periapical Diseases - microbiology Periapical Diseases - physiopathology periapical lesions Time Factors Tumor Necrosis Factor-alpha - immunology |
title | Periapical lesion progression and cytokine expression in an LPS hyporesponsive model |
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