Intermittent administration of PTH for the treatment of inflammatory bone loss does not enhance entheseal pathological new bone formation
To investigate the effect of intermittent parathyroid hormone (iPTH) administration on pathological new bone formation during treatment of ankylosing spondylitis-related osteoporosis. Animal models with pathological bone formation caused by hypothetical AS pathogenesis received treatment with iPTH....
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| Veröffentlicht in: | Biochemical and biophysical research communications 2024-06, Vol.711, p.149888, Article 149888 |
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| container_title | Biochemical and biophysical research communications |
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| creator | Zhang, Shuai Hao, Wenjun Chen, Dongying Chen, Siwen Li, Zihao Zhong, Fangling Wang, Haitao Wang, Jianru Zheng, Zhaomin Zhan, Zhongping Dai, Guo Liu, Hui |
| description | To investigate the effect of intermittent parathyroid hormone (iPTH) administration on pathological new bone formation during treatment of ankylosing spondylitis-related osteoporosis.
Animal models with pathological bone formation caused by hypothetical AS pathogenesis received treatment with iPTH. We determined the effects of iPTH on bone loss and the formation of pathological new bone with micro-computed tomography (micro-CT) and histological examination. In addition, the tamoxifen-inducible conditional knockout mice (CAGGCre-ERTM; PTHflox/flox, PTH−/−) was established to delete PTH and investigate the effect of endogenous PTH on pathological new bone formation.
iPTH treatment significantly improved trabecular bone mass in the modified collagen-induced arthritis (m-CIA) model and unbalanced mechanical loading models. Meanwhile, iPTH treatment did not enhance pathological new bone formation in all types of animal models. Endogenous PTH deficiency had no effects on pathological new bone formation in unbalanced mechanical loading models.
Experimental animal models of AS treated with iPTH show improvement in trabecular bone density, but not entheseal pathological bone formation，indicating it may be a potential treatment for inflammatory bone loss does in AS.
•iPTH ameliorates osteoporosis in different animal models.•iPTH treatment didn't enhance PNB formation in different animal models.•iPTH deficiency had no effects PNB formation in unbalanced mechanical loading models. |
| doi_str_mv | 10.1016/j.bbrc.2024.149888 |
| format | Article |
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Animal models with pathological bone formation caused by hypothetical AS pathogenesis received treatment with iPTH. We determined the effects of iPTH on bone loss and the formation of pathological new bone with micro-computed tomography (micro-CT) and histological examination. In addition, the tamoxifen-inducible conditional knockout mice (CAGGCre-ERTM; PTHflox/flox, PTH−/−) was established to delete PTH and investigate the effect of endogenous PTH on pathological new bone formation.
iPTH treatment significantly improved trabecular bone mass in the modified collagen-induced arthritis (m-CIA) model and unbalanced mechanical loading models. Meanwhile, iPTH treatment did not enhance pathological new bone formation in all types of animal models. Endogenous PTH deficiency had no effects on pathological new bone formation in unbalanced mechanical loading models.
Experimental animal models of AS treated with iPTH show improvement in trabecular bone density, but not entheseal pathological bone formation，indicating it may be a potential treatment for inflammatory bone loss does in AS.
•iPTH ameliorates osteoporosis in different animal models.•iPTH treatment didn't enhance PNB formation in different animal models.•iPTH deficiency had no effects PNB formation in unbalanced mechanical loading models.</description><identifier>ISSN: 0006-291X</identifier><identifier>ISSN: 1090-2104</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2024.149888</identifier><identifier>PMID: 38603833</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Ankylosing spondylitis ; Endochondral ossification ; Osteoporosis ; Parathyroid hormone ; Pathological new bone formation</subject><ispartof>Biochemical and biophysical research communications, 2024-06, Vol.711, p.149888, Article 149888</ispartof><rights>2024 The Authors</rights><rights>Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c351t-7f73028830d1bf616216939a4c96d85ce7f1d8704b5ce047930ba0d4287b5b033</cites><orcidid>0000-0001-5851-9161</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006291X24004248$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38603833$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Shuai</creatorcontrib><creatorcontrib>Hao, Wenjun</creatorcontrib><creatorcontrib>Chen, Dongying</creatorcontrib><creatorcontrib>Chen, Siwen</creatorcontrib><creatorcontrib>Li, Zihao</creatorcontrib><creatorcontrib>Zhong, Fangling</creatorcontrib><creatorcontrib>Wang, Haitao</creatorcontrib><creatorcontrib>Wang, Jianru</creatorcontrib><creatorcontrib>Zheng, Zhaomin</creatorcontrib><creatorcontrib>Zhan, Zhongping</creatorcontrib><creatorcontrib>Dai, Guo</creatorcontrib><creatorcontrib>Liu, Hui</creatorcontrib><title>Intermittent administration of PTH for the treatment of inflammatory bone loss does not enhance entheseal pathological new bone formation</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>To investigate the effect of intermittent parathyroid hormone (iPTH) administration on pathological new bone formation during treatment of ankylosing spondylitis-related osteoporosis.
Animal models with pathological bone formation caused by hypothetical AS pathogenesis received treatment with iPTH. We determined the effects of iPTH on bone loss and the formation of pathological new bone with micro-computed tomography (micro-CT) and histological examination. In addition, the tamoxifen-inducible conditional knockout mice (CAGGCre-ERTM; PTHflox/flox, PTH−/−) was established to delete PTH and investigate the effect of endogenous PTH on pathological new bone formation.
iPTH treatment significantly improved trabecular bone mass in the modified collagen-induced arthritis (m-CIA) model and unbalanced mechanical loading models. Meanwhile, iPTH treatment did not enhance pathological new bone formation in all types of animal models. Endogenous PTH deficiency had no effects on pathological new bone formation in unbalanced mechanical loading models.
Experimental animal models of AS treated with iPTH show improvement in trabecular bone density, but not entheseal pathological bone formation，indicating it may be a potential treatment for inflammatory bone loss does in AS.
•iPTH ameliorates osteoporosis in different animal models.•iPTH treatment didn't enhance PNB formation in different animal models.•iPTH deficiency had no effects PNB formation in unbalanced mechanical loading models.</description><subject>Ankylosing spondylitis</subject><subject>Endochondral ossification</subject><subject>Osteoporosis</subject><subject>Parathyroid hormone</subject><subject>Pathological new bone formation</subject><issn>0006-291X</issn><issn>1090-2104</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kc2KFDEUhYMoTjv6Ai4kSzfV3vx0VQrcyKDOwIAuRnAX8nPLTlOVtElamUfwrU1bo0tXNyHfOeGeQ8hLBlsGrH9z2Fqb3ZYDl1smR6XUI7JhMELHGcjHZAMAfcdH9vWCPCvlAMCY7Men5EKoHoQSYkN-3cSKeQm1YqzU-CXEUGo2NaRI00Q_313TKWVa90hrRlOXM9ceQpxmsyympnxPbYpI51QK9QkLjalSjHsTHbbZpAXNTI-m7tOcvgXXLhF_rqpmvvz57Tl5Mpm54IuHeUm-fHh_d3Xd3X76eHP17rZzYsdqN0yDAK6UAM_s1LOes34Uo5Fu7L3aORwm5tUA0rYzyGEUYA14ydVgdxaEuCSvV99jTt9PWKpeQnE4zyZiOhUtWjJS8lFCQ_mKutx2yzjpYw6LyfeagT5XoA_6XIE-V6DXCpro1YP_yS7o_0n-Zt6AtyuAbcsfAbMuLmDLyoeMrmqfwv_8fwPnb5mX</recordid><startdate>20240604</startdate><enddate>20240604</enddate><creator>Zhang, Shuai</creator><creator>Hao, Wenjun</creator><creator>Chen, Dongying</creator><creator>Chen, Siwen</creator><creator>Li, Zihao</creator><creator>Zhong, Fangling</creator><creator>Wang, Haitao</creator><creator>Wang, Jianru</creator><creator>Zheng, Zhaomin</creator><creator>Zhan, Zhongping</creator><creator>Dai, Guo</creator><creator>Liu, Hui</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-5851-9161</orcidid></search><sort><creationdate>20240604</creationdate><title>Intermittent administration of PTH for the treatment of inflammatory bone loss does not enhance entheseal pathological new bone formation</title><author>Zhang, Shuai ; Hao, Wenjun ; Chen, Dongying ; Chen, Siwen ; Li, Zihao ; Zhong, Fangling ; Wang, Haitao ; Wang, Jianru ; Zheng, Zhaomin ; Zhan, Zhongping ; Dai, Guo ; Liu, Hui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c351t-7f73028830d1bf616216939a4c96d85ce7f1d8704b5ce047930ba0d4287b5b033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Ankylosing spondylitis</topic><topic>Endochondral ossification</topic><topic>Osteoporosis</topic><topic>Parathyroid hormone</topic><topic>Pathological new bone formation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Shuai</creatorcontrib><creatorcontrib>Hao, Wenjun</creatorcontrib><creatorcontrib>Chen, Dongying</creatorcontrib><creatorcontrib>Chen, Siwen</creatorcontrib><creatorcontrib>Li, Zihao</creatorcontrib><creatorcontrib>Zhong, Fangling</creatorcontrib><creatorcontrib>Wang, Haitao</creatorcontrib><creatorcontrib>Wang, Jianru</creatorcontrib><creatorcontrib>Zheng, Zhaomin</creatorcontrib><creatorcontrib>Zhan, Zhongping</creatorcontrib><creatorcontrib>Dai, Guo</creatorcontrib><creatorcontrib>Liu, Hui</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Shuai</au><au>Hao, Wenjun</au><au>Chen, Dongying</au><au>Chen, Siwen</au><au>Li, Zihao</au><au>Zhong, Fangling</au><au>Wang, Haitao</au><au>Wang, Jianru</au><au>Zheng, Zhaomin</au><au>Zhan, Zhongping</au><au>Dai, Guo</au><au>Liu, Hui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intermittent administration of PTH for the treatment of inflammatory bone loss does not enhance entheseal pathological new bone formation</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2024-06-04</date><risdate>2024</risdate><volume>711</volume><spage>149888</spage><pages>149888-</pages><artnum>149888</artnum><issn>0006-291X</issn><issn>1090-2104</issn><eissn>1090-2104</eissn><abstract>To investigate the effect of intermittent parathyroid hormone (iPTH) administration on pathological new bone formation during treatment of ankylosing spondylitis-related osteoporosis.
Animal models with pathological bone formation caused by hypothetical AS pathogenesis received treatment with iPTH. We determined the effects of iPTH on bone loss and the formation of pathological new bone with micro-computed tomography (micro-CT) and histological examination. In addition, the tamoxifen-inducible conditional knockout mice (CAGGCre-ERTM; PTHflox/flox, PTH−/−) was established to delete PTH and investigate the effect of endogenous PTH on pathological new bone formation.
iPTH treatment significantly improved trabecular bone mass in the modified collagen-induced arthritis (m-CIA) model and unbalanced mechanical loading models. Meanwhile, iPTH treatment did not enhance pathological new bone formation in all types of animal models. Endogenous PTH deficiency had no effects on pathological new bone formation in unbalanced mechanical loading models.
Experimental animal models of AS treated with iPTH show improvement in trabecular bone density, but not entheseal pathological bone formation，indicating it may be a potential treatment for inflammatory bone loss does in AS.
•iPTH ameliorates osteoporosis in different animal models.•iPTH treatment didn't enhance PNB formation in different animal models.•iPTH deficiency had no effects PNB formation in unbalanced mechanical loading models.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>38603833</pmid><doi>10.1016/j.bbrc.2024.149888</doi><orcidid>https://orcid.org/0000-0001-5851-9161</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Ankylosing spondylitis Endochondral ossification Osteoporosis Parathyroid hormone Pathological new bone formation |
| title | Intermittent administration of PTH for the treatment of inflammatory bone loss does not enhance entheseal pathological new bone formation |
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