Chondrocyte activity is increased in psoriatic arthritis and axial spondyloarthritis
Psoriatic arthritis (PsA) and axial spondyloarthritis (axSpA) are chronic inflammatory rheumatic diseases with complex origins. Both are characterized by altered extracellular matrix remodeling in joints and entheses that results in destructive and osteochondral proliferative lesions. There is a nee...
Saved in:
Published in | Arthritis research & therapy Vol. 18; no. 1; p. 141 |
---|---|
Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
BioMed Central Ltd
16.06.2016
BioMed Central |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | Psoriatic arthritis (PsA) and axial spondyloarthritis (axSpA) are chronic inflammatory rheumatic diseases with complex origins. Both are characterized by altered extracellular matrix remodeling in joints and entheses that results in destructive and osteochondral proliferative lesions. There is a need for biomarkers reflecting core disease pathways for diagnosis and disease mapping. Pro-C2 reflects mature cartilage collagen type IIB formation, while C-Col10 represents turnover of type X collagen, which is exclusively expressed by hypertrophic chondrocytes. The objectives of this study were to study cartilage metabolism in axSpA and PsA by assessing Pro-C2 and C-Col10 and to evaluate their diagnostic utility against a healthy reference population.
Patients with PsA (n = 101) or axSpA (n = 110) were recruited consecutively from three rheumatology outpatient clinics. Demographic and clinical disease measures were recorded. Pro-C2 and C-Col10 were quantified in serum by using newly developed and specific competitive enzyme-linked immunosorbent assays based on monoclonal antibodies. One-way analysis of variance and Tukey's multiple comparison tests were performed on log-transformed data. ROC curve analysis was carried out to evaluate their discriminative power.
Pro-C2 levels in serum were significantly increased in both axSpA (median concentration 1.11 ng/ml, 0.67-1.64) and PsA (median concentration 1.03 ng/ml, 0.53-1.47) compared with healthy controls (median concentration 0.30 ng/ml, 0.16-0.41) (p < 0.0001). Pro-C2 did not differ according to treatment. C-Col10 was slightly but equally elevated in the PsA and axSpA groups vs. the control group, but it was significantly lower in patients with axSpA undergoing tumor necrosis factor-α inhibitor (TNFi) treatment. ROC curve analysis revealed AUCs of 0.85 (95 % CI 0.79-0.89) for axSpA and 0.81 (95 % CI 0.75-0.86) for PsA.
These findings indicate that cartilage collagen metabolism was enhanced in the axSpA and PsA groups compared with the healthy control group. The lower C-Col10 level in patients with axSpA undergoing TNFi treatment may reflect that hypertrophic chondrocytes in axSpA are targeted by TNFi. ROC curve analysis showed a diagnostic potential for Pro-C2 in axSpA and PsA. |
---|---|
AbstractList | BACKGROUNDPsoriatic arthritis (PsA) and axial spondyloarthritis (axSpA) are chronic inflammatory rheumatic diseases with complex origins. Both are characterized by altered extracellular matrix remodeling in joints and entheses that results in destructive and osteochondral proliferative lesions. There is a need for biomarkers reflecting core disease pathways for diagnosis and disease mapping. Pro-C2 reflects mature cartilage collagen type IIB formation, while C-Col10 represents turnover of type X collagen, which is exclusively expressed by hypertrophic chondrocytes. The objectives of this study were to study cartilage metabolism in axSpA and PsA by assessing Pro-C2 and C-Col10 and to evaluate their diagnostic utility against a healthy reference population.METHODSPatients with PsA (n = 101) or axSpA (n = 110) were recruited consecutively from three rheumatology outpatient clinics. Demographic and clinical disease measures were recorded. Pro-C2 and C-Col10 were quantified in serum by using newly developed and specific competitive enzyme-linked immunosorbent assays based on monoclonal antibodies. One-way analysis of variance and Tukey's multiple comparison tests were performed on log-transformed data. ROC curve analysis was carried out to evaluate their discriminative power.RESULTSPro-C2 levels in serum were significantly increased in both axSpA (median concentration 1.11 ng/ml, 0.67-1.64) and PsA (median concentration 1.03 ng/ml, 0.53-1.47) compared with healthy controls (median concentration 0.30 ng/ml, 0.16-0.41) (p < 0.0001). Pro-C2 did not differ according to treatment. C-Col10 was slightly but equally elevated in the PsA and axSpA groups vs. the control group, but it was significantly lower in patients with axSpA undergoing tumor necrosis factor-α inhibitor (TNFi) treatment. ROC curve analysis revealed AUCs of 0.85 (95 % CI 0.79-0.89) for axSpA and 0.81 (95 % CI 0.75-0.86) for PsA.CONCLUSIONSThese findings indicate that cartilage collagen metabolism was enhanced in the axSpA and PsA groups compared with the healthy control group. The lower C-Col10 level in patients with axSpA undergoing TNFi treatment may reflect that hypertrophic chondrocytes in axSpA are targeted by TNFi. ROC curve analysis showed a diagnostic potential for Pro-C2 in axSpA and PsA. Background Psoriatic arthritis (PsA) and axial spondyloarthritis (axSpA) are chronic inflammatory rheumatic diseases with complex origins. Both are characterized by altered extracellular matrix remodeling in joints and entheses that results in destructive and osteochondral proliferative lesions. There is a need for biomarkers reflecting core disease pathways for diagnosis and disease mapping. Pro-C2 reflects mature cartilage collagen type IIB formation, while C-Col10 represents turnover of type X collagen, which is exclusively expressed by hypertrophic chondrocytes. The objectives of this study were to study cartilage metabolism in axSpA and PsA by assessing Pro-C2 and C-Col10 and to evaluate their diagnostic utility against a healthy reference population. Methods Patients with PsA (n = 101) or axSpA (n = 110) were recruited consecutively from three rheumatology outpatient clinics. Demographic and clinical disease measures were recorded. Pro-C2 and C-Col10 were quantified in serum by using newly developed and specific competitive enzyme-linked immunosorbent assays based on monoclonal antibodies. One-way analysis of variance and Tukey's multiple comparison tests were performed on log-transformed data. ROC curve analysis was carried out to evaluate their discriminative power. Results Pro-C2 levels in serum were significantly increased in both axSpA (median concentration 1.11 ng/ml, 0.67-1.64) and PsA (median concentration 1.03 ng/ml, 0.53-1.47) compared with healthy controls (median concentration 0.30 ng/ml, 0.16-0.41) (p < 0.0001). Pro-C2 did not differ according to treatment. C-Col10 was slightly but equally elevated in the PsA and axSpA groups vs. the control group, but it was significantly lower in patients with axSpA undergoing tumor necrosis factor-α inhibitor (TNFi) treatment. ROC curve analysis revealed AUCs of 0.85 (95 % CI 0.79-0.89) for axSpA and 0.81 (95 % CI 0.75-0.86) for PsA. Conclusions These findings indicate that cartilage collagen metabolism was enhanced in the axSpA and PsA groups compared with the healthy control group. The lower C-Col10 level in patients with axSpA undergoing TNFi treatment may reflect that hypertrophic chondrocytes in axSpA are targeted by TNFi. ROC curve analysis showed a diagnostic potential for Pro-C2 in axSpA and PsA. Background Psoriatic arthritis (PsA) and axial spondyloarthritis (axSpA) are chronic inflammatory rheumatic diseases with complex origins. Both are characterized by altered extracellular matrix remodeling in joints and entheses that results in destructive and osteochondral proliferative lesions. There is a need for biomarkers reflecting core disease pathways for diagnosis and disease mapping. Pro-C2 reflects mature cartilage collagen type IIB formation, while C-Col10 represents turnover of type X collagen, which is exclusively expressed by hypertrophic chondrocytes. The objectives of this study were to study cartilage metabolism in axSpA and PsA by assessing Pro-C2 and C-Col10 and to evaluate their diagnostic utility against a healthy reference population. Methods Patients with PsA (n = 101) or axSpA (n = 110) were recruited consecutively from three rheumatology outpatient clinics. Demographic and clinical disease measures were recorded. Pro-C2 and C-Col10 were quantified in serum by using newly developed and specific competitive enzyme-linked immunosorbent assays based on monoclonal antibodies. One-way analysis of variance and Tukey's multiple comparison tests were performed on log-transformed data. ROC curve analysis was carried out to evaluate their discriminative power. Results Pro-C2 levels in serum were significantly increased in both axSpA (median concentration 1.11 ng/ml, 0.67-1.64) and PsA (median concentration 1.03 ng/ml, 0.53-1.47) compared with healthy controls (median concentration 0.30 ng/ml, 0.16-0.41) (p < 0.0001). Pro-C2 did not differ according to treatment. C-Col10 was slightly but equally elevated in the PsA and axSpA groups vs. the control group, but it was significantly lower in patients with axSpA undergoing tumor necrosis factor-[alpha] inhibitor (TNFi) treatment. ROC curve analysis revealed AUCs of 0.85 (95 % CI 0.79-0.89) for axSpA and 0.81 (95 % CI 0.75-0.86) for PsA. Conclusions These findings indicate that cartilage collagen metabolism was enhanced in the axSpA and PsA groups compared with the healthy control group. The lower C-Col10 level in patients with axSpA undergoing TNFi treatment may reflect that hypertrophic chondrocytes in axSpA are targeted by TNFi. ROC curve analysis showed a diagnostic potential for Pro-C2 in axSpA and PsA. Keywords: Spondyloarthritis, Psoriatic arthritis, Type II collagen, Type X collagen, Pro-C2, C-Col10 Psoriatic arthritis (PsA) and axial spondyloarthritis (axSpA) are chronic inflammatory rheumatic diseases with complex origins. Both are characterized by altered extracellular matrix remodeling in joints and entheses that results in destructive and osteochondral proliferative lesions. There is a need for biomarkers reflecting core disease pathways for diagnosis and disease mapping. Pro-C2 reflects mature cartilage collagen type IIB formation, while C-Col10 represents turnover of type X collagen, which is exclusively expressed by hypertrophic chondrocytes. The objectives of this study were to study cartilage metabolism in axSpA and PsA by assessing Pro-C2 and C-Col10 and to evaluate their diagnostic utility against a healthy reference population. Pro-C2 levels in serum were significantly increased in both axSpA (median concentration 1.11 ng/ml, 0.67-1.64) and PsA (median concentration 1.03 ng/ml, 0.53-1.47) compared with healthy controls (median concentration 0.30 ng/ml, 0.16-0.41) (p < 0.0001). Pro-C2 did not differ according to treatment. C-Col10 was slightly but equally elevated in the PsA and axSpA groups vs. the control group, but it was significantly lower in patients with axSpA undergoing tumor necrosis factor-[alpha] inhibitor (TNFi) treatment. ROC curve analysis revealed AUCs of 0.85 (95 % CI 0.79-0.89) for axSpA and 0.81 (95 % CI 0.75-0.86) for PsA. These findings indicate that cartilage collagen metabolism was enhanced in the axSpA and PsA groups compared with the healthy control group. The lower C-Col10 level in patients with axSpA undergoing TNFi treatment may reflect that hypertrophic chondrocytes in axSpA are targeted by TNFi. ROC curve analysis showed a diagnostic potential for Pro-C2 in axSpA and PsA. Psoriatic arthritis (PsA) and axial spondyloarthritis (axSpA) are chronic inflammatory rheumatic diseases with complex origins. Both are characterized by altered extracellular matrix remodeling in joints and entheses that results in destructive and osteochondral proliferative lesions. There is a need for biomarkers reflecting core disease pathways for diagnosis and disease mapping. Pro-C2 reflects mature cartilage collagen type IIB formation, while C-Col10 represents turnover of type X collagen, which is exclusively expressed by hypertrophic chondrocytes. The objectives of this study were to study cartilage metabolism in axSpA and PsA by assessing Pro-C2 and C-Col10 and to evaluate their diagnostic utility against a healthy reference population. Patients with PsA (n = 101) or axSpA (n = 110) were recruited consecutively from three rheumatology outpatient clinics. Demographic and clinical disease measures were recorded. Pro-C2 and C-Col10 were quantified in serum by using newly developed and specific competitive enzyme-linked immunosorbent assays based on monoclonal antibodies. One-way analysis of variance and Tukey's multiple comparison tests were performed on log-transformed data. ROC curve analysis was carried out to evaluate their discriminative power. Pro-C2 levels in serum were significantly increased in both axSpA (median concentration 1.11 ng/ml, 0.67-1.64) and PsA (median concentration 1.03 ng/ml, 0.53-1.47) compared with healthy controls (median concentration 0.30 ng/ml, 0.16-0.41) (p < 0.0001). Pro-C2 did not differ according to treatment. C-Col10 was slightly but equally elevated in the PsA and axSpA groups vs. the control group, but it was significantly lower in patients with axSpA undergoing tumor necrosis factor-α inhibitor (TNFi) treatment. ROC curve analysis revealed AUCs of 0.85 (95 % CI 0.79-0.89) for axSpA and 0.81 (95 % CI 0.75-0.86) for PsA. These findings indicate that cartilage collagen metabolism was enhanced in the axSpA and PsA groups compared with the healthy control group. The lower C-Col10 level in patients with axSpA undergoing TNFi treatment may reflect that hypertrophic chondrocytes in axSpA are targeted by TNFi. ROC curve analysis showed a diagnostic potential for Pro-C2 in axSpA and PsA. |
ArticleNumber | 141 |
Audience | Academic |
Author | He, Yi Junker, Peter Gudmann, Natasja Stæhr Karsdal, Morten Asser Bay-Jensen, Anne-Christine Siebuhr, Anne Sofie Munk, Heidi Lausten Ejstrup, Leif Loft, Anne Gitte Christensen, Anne Friesgaard Sørensen, Grith Lykke |
Author_xml | – sequence: 1 givenname: Natasja Stæhr surname: Gudmann fullname: Gudmann, Natasja Stæhr email: nsg@nordicbioscience.com organization: Nordic Bioscience Biomarkers and Research, Herlev Hovedgade 207, Herlev, 2730, Denmark. nsg@nordicbioscience.com – sequence: 2 givenname: Heidi Lausten surname: Munk fullname: Munk, Heidi Lausten organization: Department of Rheumatology, Odense University Hospital, Odense, Denmark – sequence: 3 givenname: Anne Friesgaard surname: Christensen fullname: Christensen, Anne Friesgaard organization: Department of Rheumatology, Vejle Hospital, Vejle, Denmark – sequence: 4 givenname: Leif surname: Ejstrup fullname: Ejstrup, Leif organization: Department of Rheumatology, Esbjerg Hospital, Esbjerg, Denmark – sequence: 5 givenname: Grith Lykke surname: Sørensen fullname: Sørensen, Grith Lykke organization: Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark – sequence: 6 givenname: Anne Gitte surname: Loft fullname: Loft, Anne Gitte organization: Department of Rheumatology, Aarhus University Hospital, Aarhus, Denmark – sequence: 7 givenname: Morten Asser surname: Karsdal fullname: Karsdal, Morten Asser organization: Nordic Bioscience Biomarkers and Research, Herlev Hovedgade 207, Herlev, 2730, Denmark – sequence: 8 givenname: Anne-Christine surname: Bay-Jensen fullname: Bay-Jensen, Anne-Christine organization: Nordic Bioscience Biomarkers and Research, Herlev Hovedgade 207, Herlev, 2730, Denmark – sequence: 9 givenname: Yi surname: He fullname: He, Yi organization: Nordic Bioscience Biomarkers and Research, Herlev Hovedgade 207, Herlev, 2730, Denmark – sequence: 10 givenname: Anne Sofie surname: Siebuhr fullname: Siebuhr, Anne Sofie organization: Nordic Bioscience Biomarkers and Research, Herlev Hovedgade 207, Herlev, 2730, Denmark – sequence: 11 givenname: Peter surname: Junker fullname: Junker, Peter organization: Department of Rheumatology, Odense University Hospital, Odense, Denmark |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27306080$$D View this record in MEDLINE/PubMed |
BookMark | eNptUk1rGzEQFSGl-Wh_QC5loZdcNp2RZEl7KQTTpIVAL74LrVYbK6wlV5JDnV9fGSduUsocZtC898TMvDNyHGJwhFwgXCEq8SUjAzlrAUWLwKF9OiKnyKVqBRP0-FV9Qs5yfgCgtKP8PTmhkoEABadkMV_GMKRot8U1xhb_6Mu28bnxwSZnshtq1axzTN4UbxuTyjL5UgEmDI357c3U5HWV2E7x0PtA3o1myu7jcz4ni5tvi_n39u7n7Y_59V1recdLa0bsDbNSjTM3yJ5xNQ6yc5QjZUrMeiWVYAjYdxIGVCNlVBqHasYADaPsnHzdy643_coN1oWSzKTXya9M2upovH7bCX6p7-Oj5h0CFVAFLp8FUvy1cbnolc_WTZMJLm6yRtlJJUXdW4V-_gf6EDcp1Ok0KgBFQSj2F3VvJqd9GGP91-5E9TUXqCRyzivq6j-oGoNbeVtPPPr6_oaAe4JNMefkxsOMCHrnBL13gq5O0Dsn6KfK-fR6OQfGy-nZH4wUsDQ |
CitedBy_id | crossref_primary_10_1186_s12891_020_03804_2 crossref_primary_10_3899_jrheum_220142 crossref_primary_10_1016_j_autrev_2021_102760 crossref_primary_10_3389_fimmu_2022_1054539 crossref_primary_10_3389_fimmu_2022_964274 crossref_primary_10_1186_s13075_022_02967_8 crossref_primary_10_1136_rmdopen_2023_003769 crossref_primary_10_1080_14737159_2020_1814746 crossref_primary_10_1186_s13075_023_03132_5 crossref_primary_10_1111_jcmm_15742 crossref_primary_10_3389_fmed_2022_860813 crossref_primary_10_1186_s12865_019_0297_9 crossref_primary_10_1038_s41598_020_70327_0 crossref_primary_10_1016_j_joca_2019_01_001 crossref_primary_10_1007_s40744_022_00444_x crossref_primary_10_1016_j_arr_2019_100964 crossref_primary_10_1111_liv_14390 crossref_primary_10_1007_s13238_017_0377_7 crossref_primary_10_1186_s13075_022_02839_1 crossref_primary_10_3390_ijms21082740 crossref_primary_10_1007_s00393_018_0503_9 |
Cites_doi | 10.1136/annrheumdis-2013-203419 10.1016/j.berh.2014.10.007 10.1007/s00296-015-3397-8 10.1136/annrheumdis-2011-200350 10.1186/ar2166 10.1111/dgd.12203 10.1186/1471-2474-15-309 10.1007/s11926-011-0202-x 10.1002/art.20870 10.1136/ard.2010.138883 10.1186/ar2571 10.1002/dvdy.1115 10.1155/2012/176298 10.1016/j.clinbiochem.2011.01.001 10.1016/j.berh.2014.10.008 10.1186/ar2642 10.1016/j.jbspin.2009.09.011 10.1097/00002281-200307000-00005 10.3390/ijms151018789 10.1186/s13075-015-0675-5 10.1016/j.joca.2006.08.015 10.2217/bmm.13.144 10.1002/1529-0131(199907)42:7<1443::AID-ANR18>3.0.CO;2-A 10.1080/03009740701824613 10.1016/j.joca.2008.04.021 10.1136/bmjopen-2015-009092 10.1002/art.10576 10.7326/0003-4819-136-12-200206180-00011 10.1083/jcb.114.6.1307 10.1136/ard.2007.082172 10.1093/rheumatology/ket407 |
ContentType | Journal Article |
Copyright | COPYRIGHT 2016 BioMed Central Ltd. Copyright BioMed Central 2016 The Author(s). 2016 |
Copyright_xml | – notice: COPYRIGHT 2016 BioMed Central Ltd. – notice: Copyright BioMed Central 2016 – notice: The Author(s). 2016 |
DBID | CGR CUY CVF ECM EIF NPM AAYXX CITATION 3V. 7X7 7XB 88E 8FI 8FJ 8FK ABUWG AFKRA AZQEC BENPR CCPQU DWQXO FYUFA GHDGH K9. M0S M1P PIMPY PQEST PQQKQ PQUKI PRINS 7X8 5PM |
DOI | 10.1186/s13075-016-1040-z |
DatabaseName | Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed CrossRef ProQuest Central (Corporate) Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central ProQuest Central Essentials ProQuest Central ProQuest One Community College ProQuest Central Korea Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Health & Medical Complete (Alumni) Health & Medical Collection (Alumni Edition) Medical Database Publicly Available Content Database ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Academic ProQuest One Academic UKI Edition ProQuest Central China MEDLINE - Academic PubMed Central (Full Participant titles) |
DatabaseTitle | MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) CrossRef Publicly Available Content Database ProQuest Central Essentials ProQuest One Academic Eastern Edition ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) ProQuest One Community College ProQuest Hospital Collection Health Research Premium Collection (Alumni) ProQuest Central China ProQuest Hospital Collection (Alumni) ProQuest Central ProQuest Health & Medical Complete Health Research Premium Collection ProQuest Medical Library ProQuest One Academic UKI Edition Health and Medicine Complete (Alumni Edition) ProQuest Central Korea ProQuest One Academic ProQuest Medical Library (Alumni) ProQuest Central (Alumni) MEDLINE - Academic |
DatabaseTitleList | MEDLINE - Academic Publicly Available Content Database MEDLINE |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database – sequence: 3 dbid: 7X7 name: Health & Medical Collection url: https://search.proquest.com/healthcomplete sourceTypes: Aggregation Database |
DeliveryMethod | fulltext_linktorsrc |
Discipline | Medicine |
EISSN | 1478-6362 |
EndPage | 141 |
ExternalDocumentID | 4105837831 A461871444 10_1186_s13075_016_1040_z 27306080 |
Genre | Research Support, Non-U.S. Gov't Journal Article |
GeographicLocations | Denmark |
GeographicLocations_xml | – name: Denmark |
GrantInformation_xml | – fundername: ; – fundername: ; grantid: 305815 |
GroupedDBID | --- -5E -5G -A0 -BR .GJ 0R~ 23N 2WC 3V. 4.4 5GY 5VS 6J9 7X7 88E 8FI 8FJ AAFWJ AAJSJ ABUWG ACGFS ACJQM ACRMQ ADBBV ADINQ ADUKV AEGXH AENEX AFKRA AHBYD AHMBA AHSBF AHYZX ALIPV ALMA_UNASSIGNED_HOLDINGS AMKLP AMTXH AOIAM AOIJS BAPOH BAWUL BCNDV BENPR BFQNJ BMC BPHCQ BVXVI C24 C6C CCPQU CGR CS3 CUY CVF DIK E3Z EBD EBLON ECM EIF EJD EMOBN F5P FYUFA GROUPED_DOAJ GX1 H13 HMCUK HYE HZ~ IAO IHR INH INR ITC KQ8 M1P NPM O5R O5S O9- PGMZT PIMPY PQQKQ PROAC PSQYO RBZ ROL RPM RSV SMD SOJ SV3 TR2 U2A UKHRP WOQ Z7U AAYXX CITATION 7XB 8FK AZQEC DWQXO K9. PQEST PQUKI PRINS 7X8 5PM AFPKN |
ID | FETCH-LOGICAL-c494t-af1ba3c78f5ed7b348fd79e24123865b87863101b970d18f2327ae185301a323 |
IEDL.DBID | RPM |
ISSN | 1478-6362 1478-6354 |
IngestDate | Tue Sep 17 21:22:17 EDT 2024 Thu Oct 24 23:28:51 EDT 2024 Thu Oct 10 18:05:02 EDT 2024 Tue Nov 19 21:29:27 EST 2024 Tue Nov 12 23:34:42 EST 2024 Thu Nov 21 22:28:18 EST 2024 Wed Oct 16 00:58:38 EDT 2024 |
IsDoiOpenAccess | true |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 1 |
Keywords | Pro-C2 C-Col10 Type X collagen Type II collagen Spondyloarthritis Psoriatic arthritis |
Language | English |
License | Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
LinkModel | DirectLink |
MergedId | FETCHMERGED-LOGICAL-c494t-af1ba3c78f5ed7b348fd79e24123865b87863101b970d18f2327ae185301a323 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
OpenAccessLink | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4910260/ |
PMID | 27306080 |
PQID | 1800820683 |
PQPubID | 42876 |
PageCount | 1 |
ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_4910260 proquest_miscellaneous_1797876002 proquest_journals_1800820683 gale_infotracmisc_A461871444 gale_infotracacademiconefile_A461871444 crossref_primary_10_1186_s13075_016_1040_z pubmed_primary_27306080 |
PublicationCentury | 2000 |
PublicationDate | 2016-06-16 |
PublicationDateYYYYMMDD | 2016-06-16 |
PublicationDate_xml | – month: 06 year: 2016 text: 2016-06-16 day: 16 |
PublicationDecade | 2010 |
PublicationPlace | England |
PublicationPlace_xml | – name: England – name: London |
PublicationTitle | Arthritis research & therapy |
PublicationTitleAlternate | Arthritis Res Ther |
PublicationYear | 2016 |
Publisher | BioMed Central Ltd BioMed Central |
Publisher_xml | – name: BioMed Central Ltd – name: BioMed Central |
References | 19232069 - Arthritis Res Ther. 2009;11(1):210 15299208 - Methods Mol Med. 2004;101:25-37 25329619 - Int J Mol Sci. 2014 Oct 17;15(10):18789-803 23749611 - Ann Rheum Dis. 2014 Jan;73(1):6-16 24369419 - Rheumatology (Oxford). 2014 Sep;53(9):1547-59 25488783 - Best Pract Res Clin Rheumatol. 2014 Oct;28(5):765-77 19439035 - Arthritis Res Ther. 2009;11(2):221 18415769 - Scand J Rheumatol. 2008 Mar-Apr;37(2):120-6 21953336 - Ann Rheum Dis. 2012 Jan;71(1):4-12 25123039 - Biomark Med. 2014;8(5):713-31 22216409 - Arthritis. 2011;2011:205904 25488776 - Best Pract Res Clin Rheumatol. 2014 Oct;28(5):663-72 26123554 - Arthritis Res Ther. 2015 Jul 17;17:170 11307168 - Dev Dyn. 2001 Apr;220(4):350-62 10403272 - Arthritis Rheum. 1999 Jul;42(7):1443-50 26560062 - BMJ Open. 2015 Nov 11;5(11):e009092 21833700 - Curr Rheumatol Rep. 2011 Oct;13(5):416-20 21223960 - Clin Biochem. 2011 Apr;44(5-6):423-9 18556223 - Osteoarthritis Cartilage. 2008 Dec;16(12):1494-500 25785119 - Int J Clin Exp Med. 2015 Jan 15;8(1):1241-6 25245039 - BMC Musculoskelet Disord. 2014 Sep 22;15:309 12384919 - Arthritis Rheum. 2002 Oct;46(10):2613-24 23209897 - Arthritis. 2012;2012:176298 20409741 - Joint Bone Spine. 2010 May;77(3):206-11 1894696 - J Cell Biol. 1991 Sep;114(6):1307-19 17045814 - Osteoarthritis Cartilage. 2007 Mar;15(3):335-42 15751093 - Arthritis Rheum. 2005 Mar;52(3):885-91 12819466 - Curr Opin Rheumatol. 2003 Jul;15(4):394-407 18208866 - Ann Rheum Dis. 2008 Oct;67(10):1422-6 21551511 - Ann Rheum Dis. 2011 Aug;70(8):1375-81 24217097 - Aust Fam Physician. 2013 Nov;42(11):780-4 26620690 - Rheumatol Int. 2016 Apr;36(4):541-9 17634141 - Arthritis Res Ther. 2007;9 Suppl 1:S2 25714187 - Dev Growth Differ. 2015 Feb;57(2):179-92 12069564 - Ann Intern Med. 2002 Jun 18;136(12):896-907 OB Pedersen (1040_CR5) 2008; 67 M Resorlu (1040_CR24) 2015; 8 L Gossec (1040_CR26) 2012; 71 Y He (1040_CR19) 2014; 15 LJ Sandell (1040_CR17) 1991; 114 T Aigner (1040_CR16) 1999; 42 OB Pedersen (1040_CR4) 2008; 37 KY Tsang (1040_CR34) 2015; 57 AS Siebuhr (1040_CR10) 2014; 8 AK Olsen (1040_CR15) 2007; 15 RJ Lories (1040_CR35) 2014; 28 TH Kim (1040_CR11) 2005; 52 AC Bay-Jensen (1040_CR30) 2011; 44 JC Rousseau (1040_CR31) 2004; 101 AT Masi (1040_CR33) 2011; 2011 J Braun (1040_CR8) 2003; 15 HL Munk (1040_CR13) 2016; 36 OV Nemirovskiy (1040_CR14) 2008; 16 G Schett (1040_CR28) 2007; 9 MA Khan (1040_CR3) 2002; 136 RJ Lories (1040_CR22) 2009; 11 M Ronneberger (1040_CR21) 2011; 13 JE Paramarta (1040_CR1) 2014; 53 Y Zhu (1040_CR32) 2001; 220 SJ Pedersen (1040_CR12) 2011; 70 AL Tan (1040_CR25) 2010; 77 P Lloyd (1040_CR9) 2012; 2012 P Garnero (1040_CR18) 2002; 46 J Bleil (1040_CR23) 2015; 17 N Garg (1040_CR7) 2014; 28 J Londono (1040_CR6) 2015; 5 NS Gudmann (1040_CR20) 2014; 15 JS Smolen (1040_CR27) 2014; 73 G Schett (1040_CR29) 2009; 11 V Golder (1040_CR2) 2013; 42 |
References_xml | – volume: 73 start-page: 6 year: 2014 ident: 1040_CR27 publication-title: Ann Rheum Dis. doi: 10.1136/annrheumdis-2013-203419 contributor: fullname: JS Smolen – volume: 28 start-page: 663 year: 2014 ident: 1040_CR7 publication-title: Best Pract Res Clin Rheumatol. doi: 10.1016/j.berh.2014.10.007 contributor: fullname: N Garg – volume: 36 start-page: 541 year: 2016 ident: 1040_CR13 publication-title: Rheumatol Int. doi: 10.1007/s00296-015-3397-8 contributor: fullname: HL Munk – volume: 71 start-page: 4 year: 2012 ident: 1040_CR26 publication-title: Ann Rheum Dis. doi: 10.1136/annrheumdis-2011-200350 contributor: fullname: L Gossec – volume: 9 start-page: S2 issue: Suppl 1 year: 2007 ident: 1040_CR28 publication-title: Arthritis Res Ther doi: 10.1186/ar2166 contributor: fullname: G Schett – volume: 57 start-page: 179 year: 2015 ident: 1040_CR34 publication-title: Dev Growth Differ. doi: 10.1111/dgd.12203 contributor: fullname: KY Tsang – volume: 15 start-page: 309 year: 2014 ident: 1040_CR19 publication-title: BMC Musculoskelet Disord. doi: 10.1186/1471-2474-15-309 contributor: fullname: Y He – volume: 13 start-page: 416 year: 2011 ident: 1040_CR21 publication-title: Curr Rheumatol Rep. doi: 10.1007/s11926-011-0202-x contributor: fullname: M Ronneberger – volume: 52 start-page: 885 year: 2005 ident: 1040_CR11 publication-title: Arthritis Rheum. doi: 10.1002/art.20870 contributor: fullname: TH Kim – volume: 70 start-page: 1375 year: 2011 ident: 1040_CR12 publication-title: Ann Rheum Dis. doi: 10.1136/ard.2010.138883 contributor: fullname: SJ Pedersen – volume: 11 start-page: 210 year: 2009 ident: 1040_CR29 publication-title: Arthritis Res Ther. doi: 10.1186/ar2571 contributor: fullname: G Schett – volume: 220 start-page: 350 year: 2001 ident: 1040_CR32 publication-title: Dev Dyn. doi: 10.1002/dvdy.1115 contributor: fullname: Y Zhu – volume: 2012 start-page: 176298 year: 2012 ident: 1040_CR9 publication-title: Arthritis. doi: 10.1155/2012/176298 contributor: fullname: P Lloyd – volume: 44 start-page: 423 year: 2011 ident: 1040_CR30 publication-title: Clin Biochem. doi: 10.1016/j.clinbiochem.2011.01.001 contributor: fullname: AC Bay-Jensen – volume: 28 start-page: 765 year: 2014 ident: 1040_CR35 publication-title: Best Pract Res Clin Rheumatol. doi: 10.1016/j.berh.2014.10.008 contributor: fullname: RJ Lories – volume: 11 start-page: 221 year: 2009 ident: 1040_CR22 publication-title: Arthritis Res Ther doi: 10.1186/ar2642 contributor: fullname: RJ Lories – volume: 77 start-page: 206 year: 2010 ident: 1040_CR25 publication-title: Joint Bone Spine. doi: 10.1016/j.jbspin.2009.09.011 contributor: fullname: AL Tan – volume: 42 start-page: 780 year: 2013 ident: 1040_CR2 publication-title: Aust Fam Physician. contributor: fullname: V Golder – volume: 15 start-page: 394 year: 2003 ident: 1040_CR8 publication-title: Curr Opin Rheumatol. doi: 10.1097/00002281-200307000-00005 contributor: fullname: J Braun – volume: 15 start-page: 18789 year: 2014 ident: 1040_CR20 publication-title: Int J Mol Sci. doi: 10.3390/ijms151018789 contributor: fullname: NS Gudmann – volume: 17 start-page: 170 year: 2015 ident: 1040_CR23 publication-title: Arthritis Res Ther. doi: 10.1186/s13075-015-0675-5 contributor: fullname: J Bleil – volume: 2011 start-page: 205904 year: 2011 ident: 1040_CR33 publication-title: Arthritis. contributor: fullname: AT Masi – volume: 8 start-page: 1241 year: 2015 ident: 1040_CR24 publication-title: Int J Clin Exp Med. contributor: fullname: M Resorlu – volume: 15 start-page: 335 year: 2007 ident: 1040_CR15 publication-title: Osteoarthritis Cartilage. doi: 10.1016/j.joca.2006.08.015 contributor: fullname: AK Olsen – volume: 8 start-page: 713 year: 2014 ident: 1040_CR10 publication-title: Biomark Med. doi: 10.2217/bmm.13.144 contributor: fullname: AS Siebuhr – volume: 42 start-page: 1443 year: 1999 ident: 1040_CR16 publication-title: Arthritis Rheum. doi: 10.1002/1529-0131(199907)42:7<1443::AID-ANR18>3.0.CO;2-A contributor: fullname: T Aigner – volume: 37 start-page: 120 year: 2008 ident: 1040_CR4 publication-title: Scand J Rheumatol doi: 10.1080/03009740701824613 contributor: fullname: OB Pedersen – volume: 16 start-page: 1494 year: 2008 ident: 1040_CR14 publication-title: Osteoarthritis Cartilage doi: 10.1016/j.joca.2008.04.021 contributor: fullname: OV Nemirovskiy – volume: 5 start-page: e009092 year: 2015 ident: 1040_CR6 publication-title: BMJ Open. doi: 10.1136/bmjopen-2015-009092 contributor: fullname: J Londono – volume: 101 start-page: 25 year: 2004 ident: 1040_CR31 publication-title: Methods Mol Med. contributor: fullname: JC Rousseau – volume: 46 start-page: 2613 year: 2002 ident: 1040_CR18 publication-title: Arthritis Rheum. doi: 10.1002/art.10576 contributor: fullname: P Garnero – volume: 136 start-page: 896 year: 2002 ident: 1040_CR3 publication-title: Ann Intern Med. doi: 10.7326/0003-4819-136-12-200206180-00011 contributor: fullname: MA Khan – volume: 114 start-page: 1307 year: 1991 ident: 1040_CR17 publication-title: J Cell Biol. doi: 10.1083/jcb.114.6.1307 contributor: fullname: LJ Sandell – volume: 67 start-page: 1422 year: 2008 ident: 1040_CR5 publication-title: Ann Rheum Dis. doi: 10.1136/ard.2007.082172 contributor: fullname: OB Pedersen – volume: 53 start-page: 1547 year: 2014 ident: 1040_CR1 publication-title: Rheumatology (Oxford) doi: 10.1093/rheumatology/ket407 contributor: fullname: JE Paramarta |
SSID | ssj0022924 |
Score | 2.352316 |
Snippet | Psoriatic arthritis (PsA) and axial spondyloarthritis (axSpA) are chronic inflammatory rheumatic diseases with complex origins. Both are characterized by... Background Psoriatic arthritis (PsA) and axial spondyloarthritis (axSpA) are chronic inflammatory rheumatic diseases with complex origins. Both are... BACKGROUNDPsoriatic arthritis (PsA) and axial spondyloarthritis (axSpA) are chronic inflammatory rheumatic diseases with complex origins. Both are... |
SourceID | pubmedcentral proquest gale crossref pubmed |
SourceType | Open Access Repository Aggregation Database Index Database |
StartPage | 141 |
SubjectTerms | Adult Area Under Curve Arthritis Arthritis, Psoriatic - metabolism Arthritis, Psoriatic - pathology Biomarkers - blood Cartilage cells Cartilage, Articular - metabolism Cartilage, Articular - pathology Chondrocytes - metabolism Chondrocytes - pathology Collagen Type II - analysis Collagen Type II - blood Collagen Type X - analysis Collagen Type X - blood Development and progression Enzyme-Linked Immunosorbent Assay Female Genetic aspects Humans Male Physiological aspects Psoriatic arthritis ROC Curve Sensitivity and Specificity Spondylarthritis - metabolism Spondylarthritis - pathology |
SummonAdditionalLinks | – databaseName: Health & Medical Collection dbid: 7X7 link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3da9wwDBdbB2MvY99L1w0PBoNBqB07tvM0Slkpg-7pBvdmHNvh7iV3W66w9a-vlPiuzR72FrBDHEnWT7JkCeBTaiSPES23VvuqVKGLpfU2lNamOmkpIu_oaODqh778qb4v62U-cBtyWuVeJ46KOm4CnZGfCjuilbby6_ZXSV2jKLqaW2g8hEeiQihHeTbLO4eraqamtgo9JQRWlaOawurTAXW3obQ1jYpI8fJmhkv_aud78DRPnbyHRRfP4Gk2ItnZxPXn8CD1L-DxVQ6Tv4TF-WpDhQjC311idHOBGkSw9cDWPRmJQ4r4xLYD_h8VbGUoPquxuBHzfWT-D8oko9TZiN78YewVLC6-Lc4vy9w-oQyqUbvSd6L1Mhjb1SmaVirbRdMkhOyKGn221lhkBhdtY3gUtkPbyvhE-M2Fl5V8DUf9pk9vgfGkVINgLkKyKtnacxWk7WQTeM2rzhTwZU87t52KZLjRubDaTYR2lEhGhHY3BXwm6jraQEjC4PM9APwUlaJyZ0oL9OKUUgWczGai4If58J4_Lm-8wd2JSQEfD8P0JiWT9WlzjXMMus5jQLKANxM7D8tGa45rtKILMDNGHyZQOe75SL9ejWW5FVpe6B0e_39Z7-BJRVJH7Y_0CRztfl-n92jX7NoPo_DeAvtK9ZY priority: 102 providerName: ProQuest |
Title | Chondrocyte activity is increased in psoriatic arthritis and axial spondyloarthritis |
URI | https://www.ncbi.nlm.nih.gov/pubmed/27306080 https://www.proquest.com/docview/1800820683 https://search.proquest.com/docview/1797876002 https://pubmed.ncbi.nlm.nih.gov/PMC4910260 |
Volume | 18 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV3fa9swED7aDsZexn7PXRc0GAwGbmRbluTHLLSUQUoZKeTNyJJMAqsTmhTW_vW7k-0Q73EvxiAZy3ef9N1ZpzuAr77IuHNouVXSpLGwtYu10TbW2udeZonjNf0amF3Lq1vxc5EvjiDvz8KEoH1brc6b33fnzWoZYis3d3bcx4mNb2ZTgRyHdvj4GI6RfnsXvfOy0qKtZCvQPUI2Fd1WZqLleIsLtqJYNYmrj-DxE6UCRojLkBXygJf-XZ0P6GkYOnnARZev4GVnRLJJO9jXcOSbN_B81m2Tv4X5dLmmRAT2cecZnVygAhFstWWrhozErXd4xzbb9T0pxjL86mVIbsRM45j5g5hkFDrr0Jvft72D-eXFfHoVd-UTYisKsYtNnVQms0rXuXeqyoSunSo8UnZKhT4rrTQqgydVobhLdI22lTKe-JsnJkuz93DSrBv_ERj3QhRI5on1WnidGy5spuussDznaa0i-N7Lrty0STLK4FxoWbYyLymQjGRePkXwjaRb0gRCEVrTnQPAV1EqqnIiZIJenBAigrNBTwS-HTb3-im7ibctEx2MGqmzCL7sm-lJCiZr_PoB-yh0ncOGZAQfWnXuh93DIQI1UPS-A6XjHrYgSkNa7g6Vp__95Cd4kRI2qTKSPIOT3f2D_4wmz64aIdAXagTPflxc3_wahR8HowB7vN6mk79fOgL0 |
link.rule.ids | 230,314,727,780,784,864,885,12056,21388,27924,27925,31719,31720,33744,33745,43310,43805,53791,53793 |
linkProvider | National Library of Medicine |
linkToHtml | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV3di9QwEB90D9QX8fOsnhpBEIRyaZsm6ZOcxx2r3i4iK9xbSJOU3ZfuavdA7693ps2uVx98KySl6cxkPjKT3wC8DVXBvUfPrZY2T4VrfKqtdqnWoQyyyDxv6GhgNpfT7-LzZXkZD9y6WFa504m9ovZrR2fkx5nurZXUxYfNj5S6RlF2NbbQuA0HhJxeTuDg49n867d9yJVXQ1tbgbESmlYR85qZlscdam9FhWsSVZHg6fXIMv2rn28YqHHx5A1rdP4A7kc3kp0MfH8It0L7CO7MYqL8MSxOl2uCInC_t4HR3QVqEcFWHVu15CZ2weMT23T4hwTZylCAlj28EbOtZ_YXSiWj4lmP8fx-7Akszs8Wp9M0NlBInajENrVNVtvCKd2Uwau6ELrxqgpotHNq9VlrpZEdPKsrxX2mG_SulA1kwXlmi7x4CpN23YZnwHgQokJznrmgRdCl5cIVuikqx0ueNyqB9zvamc0Ak2H68EJLMxDaUCkZEdpcJ_COqGtoCyEJnY03AfBTBEZlToTMMI4TQiRwNJqJou_Gwzv-mLj1OvNXUBJ4sx-mN6mcrA3rK5yjMHjuU5IJHA7s3C8b_Tku0Y9OQI0YvZ9AgNzjkXa17IG5BfpeGB8-__-yXsPd6WJ2YS4-zb-8gHs5SSA1Q5JHMNn-vAov0cvZ1q-iKP8B43X57A |
linkToPdf | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1La9wwEBZtCqGX0PQVt0mrQqFQcCxbsiQfw7ZL-tiQwxZyE7IkswuJd4k30OTXZ8aPZd1jbwZJWJ75pJmxPs0Q8jkUnHkPnlspbRYLV_lYW-1irUMeJE89q_DXwOxCnv8RP6_yq51SXy1p35XL0_r65rReLlpu5frGJQNPLLmcTQTYOPDDk7WvkqfkWc4BZEOg3sdaWdHVsxUQJIFNFf2BZqpl0sC2rZCxJmEPEix-wITAAHTZ5obcsU7_7tE7RmpMoNyxSNMX5KB3JelZN-VD8iTUL8n-rD8sf0Xmk8UK0xG4-02geH8By0TQZUOXNbqKTfDwRNfN6hbV4yh8-6JNcURt7an9C8ikSKD1ENNv216T-fT7fHIe90UUYicKsYltlZaWO6WrPHhVcqErr4oAhjvDcp-lVhpUwtKyUMynugIPS9mAVpyllmf8DdmrV3U4IpQFIQow6akLWgSdWyYc1xUvHMtZVqmIfB1kZ9ZdqgzThhhamk7mBulkKHPzEJEvKF2DywhE6Gx_GwBehQmpzJmQKcRyQoiIHI96AvzduHnQj-mXX2NS3bo2UvOIfNo240iklNVhdQd9FATQ7bFkRN526txOe4BDRNRI0dsOmJR73AJYbZNz99h8998jP5L9y29T8_vHxa_35HmGMMVSSfKY7G1u78IJ-ECb8kOL9keZWAL9 |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Chondrocyte+activity+is+increased+in+psoriatic+arthritis+and+axial+spondyloarthritis&rft.jtitle=Arthritis+research+%26+therapy&rft.au=Gudmann%2C+Natasja+Staehr&rft.au=Munk%2C+Heidi+Lausten&rft.au=Christensen%2C+Anne+Friesgaard&rft.au=Ejstrup%2C+Leif&rft.date=2016-06-16&rft.pub=BioMed+Central+Ltd&rft.issn=1478-6354&rft.volume=18&rft.issue=1&rft_id=info:doi/10.1186%2Fs13075-016-1040-z&rft.externalDocID=A461871444 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1478-6362&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1478-6362&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1478-6362&client=summon |