scholarly journals Levels of serotonin, sclerostin, bone turnover markers as well as bone density and microarchitecture in patients with high-bone-mass phenotype due to a mutation in Lrp5

2011 ◽  
Vol 26 (8) ◽  
pp. 1721-1728 ◽  
Author(s):  
Morten Frost ◽  
Tom Andersen ◽  
Fatma Gossiel ◽  
Stinus Hansen ◽  
Jens Bollerslev ◽  
...  
2009 ◽  
Vol 28 (3) ◽  
pp. 161-165 ◽  
Author(s):  
Jasmina Jovčevska ◽  
Slavica Stratrova ◽  
Icko Gjorgovski ◽  
Todor Gruev ◽  
Mimoza Kotevska ◽  
...  

Bone Turnover Markers Relations to Postmenopausal OsteoporosisOsteoporosis is a systemic disease characterized by low bone mass and high bone turnover markers in postmenopausal women (PM). The relationship between biochemical bone markers C-telopeptides of type 1 collagen (CTX) and osteocalcin (OC), and bone mineral density (BMD) in the postmenopausal period was examined in 104 PM women divided into three groups according to their BMD: group A - control PM with normal bone density, group B - osteopenic PM and group C - osteoporotic PM. Mean CTX values were highest in group C (0.54±0.24 ng/mL) compared to group B (0.44±0.21 ng/mL) (p<0.0001), and group A (0.33±0.13 ng/mL) (p<0.029). Mean OC levels in group C (26.83±9.91 ng/mL) were significantly higher compared to group A (20.47±7.03 ng/mL) (p<0.011) but not significantly higher compared to group B (24.11±8.38 ng/mL) (p>0.05). Postmenopause duration was longest in group C (13.1±8.31 yrs) compared to group B (9.6±6.24 yrs), and group A (8.15±6.86 yrs). Postmenopausal women developed osteoporosis with longer menopause duration. PM osteoporotic women were characterized by increased levels of bone turnover markers indicating increased rate of bone remodeling, which resulted in excessive bone resorption, and loss of bone mass. Long-term persistence of high bone resorption marker CTX, insufficiently compensated with bone formation marker OC, enabled osteoporosis development.


Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 2075
Author(s):  
Anne Daly ◽  
Wolfgang Högler ◽  
Nicola Crabtree ◽  
Nick Shaw ◽  
Sharon Evans ◽  
...  

In patients with phenylketonuria (PKU), treated by diet therapy only, evidence suggests that areal bone mineral density (BMDa) is within the normal clinical reference range but is below the population norm. Aims: To study longitudinal bone density, mass, and geometry over 36 months in children with PKU taking either amino acid (L-AA) or casein glycomacropeptide substitutes (CGMP-AA) as their main protein source. Methodology: A total of 48 subjects completed the study, 19 subjects in the L-AA group (median age 11.1, range 5–6 years) and 29 subjects in the CGMP-AA group (median age 8.3, range 5–16years). The CGMP-AA was further divided into two groups, CGMP100 (median age 9.2, range 5–16years) (n = 13), children taking CGMP-AA only and CGMP50 (median age 7.3, range 5–15years) (n = 16), children taking a combination of CGMP-AA and L-AA. Dual X-ray absorptiometry (DXA) was measured at enrolment and 36 months, peripheral quantitative computer tomography (pQCT) at 36 months only, and serum blood and urine bone turnover markers (BTM) and blood bone biochemistry at enrolment, 6, 12, and 36 months. Results: No statistically significant differences were found between the three groups for DXA outcome parameters, i.e., BMDa (L2–L4 BMDa g/cm2), bone mineral apparent density (L2–L4 BMAD g/cm3) and total body less head BMDa (TBLH g/cm2). All blood biochemistry markers were within the reference ranges, and BTM showed active bone turnover with a trend for BTM to decrease with increasing age. Conclusions: Bone density was clinically normal, although the median z scores were below the population mean. BTM showed active bone turnover and blood biochemistry was within the reference ranges. There appeared to be no advantage to bone density, mass, or geometry from taking a macropeptide-based protein substitute as compared with L-AAs.


2017 ◽  
Vol 59 (4) ◽  
pp. 351-363 ◽  
Author(s):  
Alexander Kot ◽  
Zhendong A Zhong ◽  
Hongliang Zhang ◽  
Yu-An Evan Lay ◽  
Nancy E Lane ◽  
...  

Increasing peak bone mass is a promising strategy to prevent osteoporosis. A mouse model of global progesterone receptor (PR) ablation showed increased bone mass through a sex-dependent mechanism. Cre-Lox recombination was used to generate a mouse model of osteoprogenitor-specific PR inactivation, which recapitulated the high bone mass phenotype seen in the PR global knockout mouse mode. In this work, we employed RNA sequencing analysis to evaluate sex-independent and sex-dependent differences in gene transcription of osteoprogenitors of wild-type and PR conditional knockout mice. PR deletion caused marked sex hormone-dependent changes in gene transcription in male mice as compared to wild-type controls. These transcriptional differences revealed dysregulation in pathways involving immunomodulation, osteoclasts, bone anabolism, extracellular matrix interaction and matrix interaction. These results identified many potential mechanisms that may explain our observed high bone mass phenotype with sex differences when PR was selectively deleted in the MSCs.


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