Evidence of a direct relationship between neutrophil collagenase activity and periodontal tissue destruction in vivo: role of active enzyme in human periodontitis
To assess the temporal relationship between periodontal tissue destruction and the activity of collagenase, exudate from inflamed periodontal tissues was collected and latent and active collagenase activities were measured by a functional assay in a longitudinal cohort study. Comparisons were made b...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Lee, W. [verfasserIn] Aitken, S. [verfasserIn] Sodek, J. [verfasserIn] |
|---|
| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Publishing Ltd ; 1995 |
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| Schlagwörter: |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2006 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Journal of periodontal research - Oxford [u.a.] : Wiley-Blackwell, 1966, 30(1995), 1, Seite 0 |
| Übergeordnetes Werk: |
volume:30 ; year:1995 ; number:1 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1111/j.1600-0765.1995.tb01249.x |
|---|
| Katalog-ID: |
NLEJ239993365 |
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| 520 | |a To assess the temporal relationship between periodontal tissue destruction and the activity of collagenase, exudate from inflamed periodontal tissues was collected and latent and active collagenase activities were measured by a functional assay in a longitudinal cohort study. Comparisons were made between human subjects with either: 1) inflammation with a previous history of progressive loss of connective tissue and bone support (n=14); 2) inflammation and previous history of bone loss but now clinically stable (n=27); or 3) inflammation and no loss of bone support (n=17). Experiments using specific enzyme inhibitors, blocking antibodies and SDS-PAGE fluorograph to identify the pattern of collagen substrate degradation demonstrated that the collagenase activity was derived from neutrophils and not from bacteria or other host cells. Active collagenase activity pooled from 6 sites per subject was respectively 5 and 6-fold higher in the group with progressive loss of connective tissue compared to the groups with either inflamed tissues alone or with inflammation and previous bone loss. In contrast, latent collagenase was increased up to 2 fold higher in the group with inflammation but no bone loss compared to the group with progressive lesions. Moreover, the ratio of active to total collagenase activity was 50% higher in the group with progressive lesions. Although in all subjects successive measurements of site-specific active collagenase 1 month apart demonstrated wide variation (r<0.50), only in sites with progressive periodontal destruction was there significant increase of active collagenase with time (1.28×l0−4 collagenase units per day). There were also sharp elevations in active enzyme level at the time of detection of loss of connective tissue attachment in specific sites of 8 subjects. At the time of detection of connective tissue attachment loss, there was an overall 40% increase of pooled active collagenase activity in all subjects with progressive loss of connective tissue compared to pre-breakdown sampling times. These data provide strong in vivo evidence for a direct role of active neutrophil collagenase in the pathological destruction of periodontal connective tissue. | ||
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10.1111/j.1600-0765.1995.tb01249.x doi (DE-627)NLEJ239993365 DE-627 ger DE-627 rakwb Lee, W. verfasserin aut Evidence of a direct relationship between neutrophil collagenase activity and periodontal tissue destruction in vivo: role of active enzyme in human periodontitis Oxford, UK Blackwell Publishing Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To assess the temporal relationship between periodontal tissue destruction and the activity of collagenase, exudate from inflamed periodontal tissues was collected and latent and active collagenase activities were measured by a functional assay in a longitudinal cohort study. Comparisons were made between human subjects with either: 1) inflammation with a previous history of progressive loss of connective tissue and bone support (n=14); 2) inflammation and previous history of bone loss but now clinically stable (n=27); or 3) inflammation and no loss of bone support (n=17). Experiments using specific enzyme inhibitors, blocking antibodies and SDS-PAGE fluorograph to identify the pattern of collagen substrate degradation demonstrated that the collagenase activity was derived from neutrophils and not from bacteria or other host cells. Active collagenase activity pooled from 6 sites per subject was respectively 5 and 6-fold higher in the group with progressive loss of connective tissue compared to the groups with either inflamed tissues alone or with inflammation and previous bone loss. In contrast, latent collagenase was increased up to 2 fold higher in the group with inflammation but no bone loss compared to the group with progressive lesions. Moreover, the ratio of active to total collagenase activity was 50% higher in the group with progressive lesions. Although in all subjects successive measurements of site-specific active collagenase 1 month apart demonstrated wide variation (r<0.50), only in sites with progressive periodontal destruction was there significant increase of active collagenase with time (1.28×l0−4 collagenase units per day). There were also sharp elevations in active enzyme level at the time of detection of loss of connective tissue attachment in specific sites of 8 subjects. At the time of detection of connective tissue attachment loss, there was an overall 40% increase of pooled active collagenase activity in all subjects with progressive loss of connective tissue compared to pre-breakdown sampling times. These data provide strong in vivo evidence for a direct role of active neutrophil collagenase in the pathological destruction of periodontal connective tissue. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| collagenase Aitken, S. verfasserin aut Sodek, J. verfasserin aut McCulloch, C. A. G. oth In Journal of periodontal research Oxford [u.a.] : Wiley-Blackwell, 1966 30(1995), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927452 (DE-600)2025633-4 1600-0765 nnns volume:30 year:1995 number:1 pages:0 http://dx.doi.org/10.1111/j.1600-0765.1995.tb01249.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 30 1995 1 0 |
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10.1111/j.1600-0765.1995.tb01249.x doi (DE-627)NLEJ239993365 DE-627 ger DE-627 rakwb Lee, W. verfasserin aut Evidence of a direct relationship between neutrophil collagenase activity and periodontal tissue destruction in vivo: role of active enzyme in human periodontitis Oxford, UK Blackwell Publishing Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To assess the temporal relationship between periodontal tissue destruction and the activity of collagenase, exudate from inflamed periodontal tissues was collected and latent and active collagenase activities were measured by a functional assay in a longitudinal cohort study. Comparisons were made between human subjects with either: 1) inflammation with a previous history of progressive loss of connective tissue and bone support (n=14); 2) inflammation and previous history of bone loss but now clinically stable (n=27); or 3) inflammation and no loss of bone support (n=17). Experiments using specific enzyme inhibitors, blocking antibodies and SDS-PAGE fluorograph to identify the pattern of collagen substrate degradation demonstrated that the collagenase activity was derived from neutrophils and not from bacteria or other host cells. Active collagenase activity pooled from 6 sites per subject was respectively 5 and 6-fold higher in the group with progressive loss of connective tissue compared to the groups with either inflamed tissues alone or with inflammation and previous bone loss. In contrast, latent collagenase was increased up to 2 fold higher in the group with inflammation but no bone loss compared to the group with progressive lesions. Moreover, the ratio of active to total collagenase activity was 50% higher in the group with progressive lesions. Although in all subjects successive measurements of site-specific active collagenase 1 month apart demonstrated wide variation (r<0.50), only in sites with progressive periodontal destruction was there significant increase of active collagenase with time (1.28×l0−4 collagenase units per day). There were also sharp elevations in active enzyme level at the time of detection of loss of connective tissue attachment in specific sites of 8 subjects. At the time of detection of connective tissue attachment loss, there was an overall 40% increase of pooled active collagenase activity in all subjects with progressive loss of connective tissue compared to pre-breakdown sampling times. These data provide strong in vivo evidence for a direct role of active neutrophil collagenase in the pathological destruction of periodontal connective tissue. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| collagenase Aitken, S. verfasserin aut Sodek, J. verfasserin aut McCulloch, C. A. G. oth In Journal of periodontal research Oxford [u.a.] : Wiley-Blackwell, 1966 30(1995), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927452 (DE-600)2025633-4 1600-0765 nnns volume:30 year:1995 number:1 pages:0 http://dx.doi.org/10.1111/j.1600-0765.1995.tb01249.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 30 1995 1 0 |
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10.1111/j.1600-0765.1995.tb01249.x doi (DE-627)NLEJ239993365 DE-627 ger DE-627 rakwb Lee, W. verfasserin aut Evidence of a direct relationship between neutrophil collagenase activity and periodontal tissue destruction in vivo: role of active enzyme in human periodontitis Oxford, UK Blackwell Publishing Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To assess the temporal relationship between periodontal tissue destruction and the activity of collagenase, exudate from inflamed periodontal tissues was collected and latent and active collagenase activities were measured by a functional assay in a longitudinal cohort study. Comparisons were made between human subjects with either: 1) inflammation with a previous history of progressive loss of connective tissue and bone support (n=14); 2) inflammation and previous history of bone loss but now clinically stable (n=27); or 3) inflammation and no loss of bone support (n=17). Experiments using specific enzyme inhibitors, blocking antibodies and SDS-PAGE fluorograph to identify the pattern of collagen substrate degradation demonstrated that the collagenase activity was derived from neutrophils and not from bacteria or other host cells. Active collagenase activity pooled from 6 sites per subject was respectively 5 and 6-fold higher in the group with progressive loss of connective tissue compared to the groups with either inflamed tissues alone or with inflammation and previous bone loss. In contrast, latent collagenase was increased up to 2 fold higher in the group with inflammation but no bone loss compared to the group with progressive lesions. Moreover, the ratio of active to total collagenase activity was 50% higher in the group with progressive lesions. Although in all subjects successive measurements of site-specific active collagenase 1 month apart demonstrated wide variation (r<0.50), only in sites with progressive periodontal destruction was there significant increase of active collagenase with time (1.28×l0−4 collagenase units per day). There were also sharp elevations in active enzyme level at the time of detection of loss of connective tissue attachment in specific sites of 8 subjects. At the time of detection of connective tissue attachment loss, there was an overall 40% increase of pooled active collagenase activity in all subjects with progressive loss of connective tissue compared to pre-breakdown sampling times. These data provide strong in vivo evidence for a direct role of active neutrophil collagenase in the pathological destruction of periodontal connective tissue. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| collagenase Aitken, S. verfasserin aut Sodek, J. verfasserin aut McCulloch, C. A. G. oth In Journal of periodontal research Oxford [u.a.] : Wiley-Blackwell, 1966 30(1995), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927452 (DE-600)2025633-4 1600-0765 nnns volume:30 year:1995 number:1 pages:0 http://dx.doi.org/10.1111/j.1600-0765.1995.tb01249.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 30 1995 1 0 |
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10.1111/j.1600-0765.1995.tb01249.x doi (DE-627)NLEJ239993365 DE-627 ger DE-627 rakwb Lee, W. verfasserin aut Evidence of a direct relationship between neutrophil collagenase activity and periodontal tissue destruction in vivo: role of active enzyme in human periodontitis Oxford, UK Blackwell Publishing Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To assess the temporal relationship between periodontal tissue destruction and the activity of collagenase, exudate from inflamed periodontal tissues was collected and latent and active collagenase activities were measured by a functional assay in a longitudinal cohort study. Comparisons were made between human subjects with either: 1) inflammation with a previous history of progressive loss of connective tissue and bone support (n=14); 2) inflammation and previous history of bone loss but now clinically stable (n=27); or 3) inflammation and no loss of bone support (n=17). Experiments using specific enzyme inhibitors, blocking antibodies and SDS-PAGE fluorograph to identify the pattern of collagen substrate degradation demonstrated that the collagenase activity was derived from neutrophils and not from bacteria or other host cells. Active collagenase activity pooled from 6 sites per subject was respectively 5 and 6-fold higher in the group with progressive loss of connective tissue compared to the groups with either inflamed tissues alone or with inflammation and previous bone loss. In contrast, latent collagenase was increased up to 2 fold higher in the group with inflammation but no bone loss compared to the group with progressive lesions. Moreover, the ratio of active to total collagenase activity was 50% higher in the group with progressive lesions. Although in all subjects successive measurements of site-specific active collagenase 1 month apart demonstrated wide variation (r<0.50), only in sites with progressive periodontal destruction was there significant increase of active collagenase with time (1.28×l0−4 collagenase units per day). There were also sharp elevations in active enzyme level at the time of detection of loss of connective tissue attachment in specific sites of 8 subjects. At the time of detection of connective tissue attachment loss, there was an overall 40% increase of pooled active collagenase activity in all subjects with progressive loss of connective tissue compared to pre-breakdown sampling times. These data provide strong in vivo evidence for a direct role of active neutrophil collagenase in the pathological destruction of periodontal connective tissue. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| collagenase Aitken, S. verfasserin aut Sodek, J. verfasserin aut McCulloch, C. A. G. oth In Journal of periodontal research Oxford [u.a.] : Wiley-Blackwell, 1966 30(1995), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927452 (DE-600)2025633-4 1600-0765 nnns volume:30 year:1995 number:1 pages:0 http://dx.doi.org/10.1111/j.1600-0765.1995.tb01249.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 30 1995 1 0 |
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10.1111/j.1600-0765.1995.tb01249.x doi (DE-627)NLEJ239993365 DE-627 ger DE-627 rakwb Lee, W. verfasserin aut Evidence of a direct relationship between neutrophil collagenase activity and periodontal tissue destruction in vivo: role of active enzyme in human periodontitis Oxford, UK Blackwell Publishing Ltd 1995 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To assess the temporal relationship between periodontal tissue destruction and the activity of collagenase, exudate from inflamed periodontal tissues was collected and latent and active collagenase activities were measured by a functional assay in a longitudinal cohort study. Comparisons were made between human subjects with either: 1) inflammation with a previous history of progressive loss of connective tissue and bone support (n=14); 2) inflammation and previous history of bone loss but now clinically stable (n=27); or 3) inflammation and no loss of bone support (n=17). Experiments using specific enzyme inhibitors, blocking antibodies and SDS-PAGE fluorograph to identify the pattern of collagen substrate degradation demonstrated that the collagenase activity was derived from neutrophils and not from bacteria or other host cells. Active collagenase activity pooled from 6 sites per subject was respectively 5 and 6-fold higher in the group with progressive loss of connective tissue compared to the groups with either inflamed tissues alone or with inflammation and previous bone loss. In contrast, latent collagenase was increased up to 2 fold higher in the group with inflammation but no bone loss compared to the group with progressive lesions. Moreover, the ratio of active to total collagenase activity was 50% higher in the group with progressive lesions. Although in all subjects successive measurements of site-specific active collagenase 1 month apart demonstrated wide variation (r<0.50), only in sites with progressive periodontal destruction was there significant increase of active collagenase with time (1.28×l0−4 collagenase units per day). There were also sharp elevations in active enzyme level at the time of detection of loss of connective tissue attachment in specific sites of 8 subjects. At the time of detection of connective tissue attachment loss, there was an overall 40% increase of pooled active collagenase activity in all subjects with progressive loss of connective tissue compared to pre-breakdown sampling times. These data provide strong in vivo evidence for a direct role of active neutrophil collagenase in the pathological destruction of periodontal connective tissue. 2006 Blackwell Publishing Journal Backfiles 1879-2005 |2006|||||||||| collagenase Aitken, S. verfasserin aut Sodek, J. verfasserin aut McCulloch, C. A. G. oth In Journal of periodontal research Oxford [u.a.] : Wiley-Blackwell, 1966 30(1995), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927452 (DE-600)2025633-4 1600-0765 nnns volume:30 year:1995 number:1 pages:0 http://dx.doi.org/10.1111/j.1600-0765.1995.tb01249.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 30 1995 1 0 |
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evidence of a direct relationship between neutrophil collagenase activity and periodontal tissue destruction in vivo: role of active enzyme in human periodontitis |
| title_auth |
Evidence of a direct relationship between neutrophil collagenase activity and periodontal tissue destruction in vivo: role of active enzyme in human periodontitis |
| abstract |
To assess the temporal relationship between periodontal tissue destruction and the activity of collagenase, exudate from inflamed periodontal tissues was collected and latent and active collagenase activities were measured by a functional assay in a longitudinal cohort study. Comparisons were made between human subjects with either: 1) inflammation with a previous history of progressive loss of connective tissue and bone support (n=14); 2) inflammation and previous history of bone loss but now clinically stable (n=27); or 3) inflammation and no loss of bone support (n=17). Experiments using specific enzyme inhibitors, blocking antibodies and SDS-PAGE fluorograph to identify the pattern of collagen substrate degradation demonstrated that the collagenase activity was derived from neutrophils and not from bacteria or other host cells. Active collagenase activity pooled from 6 sites per subject was respectively 5 and 6-fold higher in the group with progressive loss of connective tissue compared to the groups with either inflamed tissues alone or with inflammation and previous bone loss. In contrast, latent collagenase was increased up to 2 fold higher in the group with inflammation but no bone loss compared to the group with progressive lesions. Moreover, the ratio of active to total collagenase activity was 50% higher in the group with progressive lesions. Although in all subjects successive measurements of site-specific active collagenase 1 month apart demonstrated wide variation (r<0.50), only in sites with progressive periodontal destruction was there significant increase of active collagenase with time (1.28×l0−4 collagenase units per day). There were also sharp elevations in active enzyme level at the time of detection of loss of connective tissue attachment in specific sites of 8 subjects. At the time of detection of connective tissue attachment loss, there was an overall 40% increase of pooled active collagenase activity in all subjects with progressive loss of connective tissue compared to pre-breakdown sampling times. These data provide strong in vivo evidence for a direct role of active neutrophil collagenase in the pathological destruction of periodontal connective tissue. |
| abstractGer |
To assess the temporal relationship between periodontal tissue destruction and the activity of collagenase, exudate from inflamed periodontal tissues was collected and latent and active collagenase activities were measured by a functional assay in a longitudinal cohort study. Comparisons were made between human subjects with either: 1) inflammation with a previous history of progressive loss of connective tissue and bone support (n=14); 2) inflammation and previous history of bone loss but now clinically stable (n=27); or 3) inflammation and no loss of bone support (n=17). Experiments using specific enzyme inhibitors, blocking antibodies and SDS-PAGE fluorograph to identify the pattern of collagen substrate degradation demonstrated that the collagenase activity was derived from neutrophils and not from bacteria or other host cells. Active collagenase activity pooled from 6 sites per subject was respectively 5 and 6-fold higher in the group with progressive loss of connective tissue compared to the groups with either inflamed tissues alone or with inflammation and previous bone loss. In contrast, latent collagenase was increased up to 2 fold higher in the group with inflammation but no bone loss compared to the group with progressive lesions. Moreover, the ratio of active to total collagenase activity was 50% higher in the group with progressive lesions. Although in all subjects successive measurements of site-specific active collagenase 1 month apart demonstrated wide variation (r<0.50), only in sites with progressive periodontal destruction was there significant increase of active collagenase with time (1.28×l0−4 collagenase units per day). There were also sharp elevations in active enzyme level at the time of detection of loss of connective tissue attachment in specific sites of 8 subjects. At the time of detection of connective tissue attachment loss, there was an overall 40% increase of pooled active collagenase activity in all subjects with progressive loss of connective tissue compared to pre-breakdown sampling times. These data provide strong in vivo evidence for a direct role of active neutrophil collagenase in the pathological destruction of periodontal connective tissue. |
| abstract_unstemmed |
To assess the temporal relationship between periodontal tissue destruction and the activity of collagenase, exudate from inflamed periodontal tissues was collected and latent and active collagenase activities were measured by a functional assay in a longitudinal cohort study. Comparisons were made between human subjects with either: 1) inflammation with a previous history of progressive loss of connective tissue and bone support (n=14); 2) inflammation and previous history of bone loss but now clinically stable (n=27); or 3) inflammation and no loss of bone support (n=17). Experiments using specific enzyme inhibitors, blocking antibodies and SDS-PAGE fluorograph to identify the pattern of collagen substrate degradation demonstrated that the collagenase activity was derived from neutrophils and not from bacteria or other host cells. Active collagenase activity pooled from 6 sites per subject was respectively 5 and 6-fold higher in the group with progressive loss of connective tissue compared to the groups with either inflamed tissues alone or with inflammation and previous bone loss. In contrast, latent collagenase was increased up to 2 fold higher in the group with inflammation but no bone loss compared to the group with progressive lesions. Moreover, the ratio of active to total collagenase activity was 50% higher in the group with progressive lesions. Although in all subjects successive measurements of site-specific active collagenase 1 month apart demonstrated wide variation (r<0.50), only in sites with progressive periodontal destruction was there significant increase of active collagenase with time (1.28×l0−4 collagenase units per day). There were also sharp elevations in active enzyme level at the time of detection of loss of connective tissue attachment in specific sites of 8 subjects. At the time of detection of connective tissue attachment loss, there was an overall 40% increase of pooled active collagenase activity in all subjects with progressive loss of connective tissue compared to pre-breakdown sampling times. These data provide strong in vivo evidence for a direct role of active neutrophil collagenase in the pathological destruction of periodontal connective tissue. |
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Evidence of a direct relationship between neutrophil collagenase activity and periodontal tissue destruction in vivo: role of active enzyme in human periodontitis |
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