Serum markers of type I collagen formation and degradation in metabolic bone disease: Correlation with bone histomorphometry

2009 ◽  
Vol 8 (2) ◽  
pp. 127-132 ◽  
Author(s):  
Erik F. Eriksen ◽  
Peder Charles ◽  
Flemming Melsen ◽  
Leif Mosekilde ◽  
Leila Risteli ◽  
...  
2021 ◽  
Vol 42 (1) ◽  
pp. 3-10
Author(s):  
Melissa Gillet ◽  
Samuel Vasikaran ◽  
Charles Inderjeeth

Abstract Serum procollagen type I N-propeptide (PINP) is designated the reference marker of bone formation in osteoporosis; the reference marker for resorption is C-terminal telopeptide of type I collagen (CTX). PINP has very low circadian and biological variation, is not affected by food intake, and is very stable in serum after venepuncture. The two automated commercial assays for PINP provide similar results in subjects with normal renal function, allowing reference intervals to be used interchangeably. Bone turnover markers (BTM) are currently not recommended for fracture risk assessment and therefore not included in fracture risk calculators. In the management of osteoporosis, the main utility of BTM including PINP is for monitoring therapy, both antiresorptive as well as anabolic agents; monitoring is thought to help improve adherence. PINP as well as CTX may also be used in assessing offset of drug action following a pause in bisphosphonate therapy, to help decide when to re-instate therapy, or following cessation of denosumab therapy to assess efficacy of follow-on bisphosphonate therapy. PINP may also be used in the diagnosis of Paget’s disease of bone as well as in monitoring response to therapy and for recurrence. Although BTM other than bone alkaline phosphatase are currently not recommended for use in metabolic bone disease of chronic kidney disease, PINP measured by assays specific to the intact molecule has potential in this condition. Further studies are needed to examine this area, as well as in malignant bone disease.


2008 ◽  
Vol 94 (1) ◽  
pp. 105-111 ◽  
Author(s):  
Nicola Brunetti-Pierri ◽  
Stephen B. Doty ◽  
John Hicks ◽  
Kelly Phan ◽  
Roberto Mendoza-Londono ◽  
...  

2013 ◽  
Author(s):  
Adodra Annika ◽  
Kouklinos Andreas ◽  
Julies Priscilla ◽  
Shaw Mathew ◽  
Jacobs Benjamin

2001 ◽  
Vol 15 (3) ◽  
pp. 181-185 ◽  
Author(s):  
Michael P. Muldoon ◽  
Douglas E. Padgett ◽  
Donald E. Sweet ◽  
Patricia A. Deuster ◽  
Gregory R. Mack

2021 ◽  
Vol 10 (14) ◽  
pp. 3141
Author(s):  
Hyerin Jung ◽  
Yeri Alice Rim ◽  
Narae Park ◽  
Yoojun Nam ◽  
Ji Hyeon Ju

Osteogenesis imperfecta (OI) is a genetic disease characterized by bone fragility and repeated fractures. The bone fragility associated with OI is caused by a defect in collagen formation due to mutation of COL1A1 or COL1A2. Current strategies for treating OI are not curative. In this study, we generated induced pluripotent stem cells (iPSCs) from OI patient-derived blood cells harboring a mutation in the COL1A1 gene. Osteoblast (OB) differentiated from OI-iPSCs showed abnormally decreased levels of type I collagen and osteogenic differentiation ability. Gene correction of the COL1A1 gene using CRISPR/Cas9 recovered the decreased type I collagen expression in OBs differentiated from OI-iPSCs. The osteogenic potential of OI-iPSCs was also recovered by the gene correction. This study suggests a new possibility of treatment and in vitro disease modeling using patient-derived iPSCs and gene editing with CRISPR/Cas9.


Author(s):  
Mubashshar Ahmad ◽  
Gavin De Kiewiet

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