Title
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 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
Author
Faculty/Department
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences . Biomedical Sciences
Publication type
article
Publication
New York, N.Y. ,
Subject
Human medicine
Source (journal)
Journal of bone and mineral research. - New York, N.Y.
Volume/pages
26(2011) :8 , p. 1721-1728
ISSN
0884-0431
ISI
000293382600005
Carrier
E
Target language
English (eng)
Full text (Publishers DOI)
Affiliation
University of Antwerp
Abstract
Patients with an activation mutation of the Lrp5 gene exhibit high bone mass (HBM). Limited information is available regarding compartment-specific changes in bone. The relationship between the phenotype and serum serotonin is not well documented. To evaluate bone, serotonin, and bone turnover markers (BTM) in Lrp5-HBM patients, we studied 19 Lrp5-HBM patients (T253I) and 19 age- and sex-matched controls. DXA and HR-pQCT were used to assess BMD and bone structure. Serum serotonin, sclerostin, dickkopf-related protein 1 (DKK1), and BTM were evaluated. Z-scores for the forearm, total hip, lumbar spine, forearm, and whole body were significantly increased (mean ± SD) between 4.94 ± 1.45 and 7.52 ± 1.99 in cases versus −0.19 ± 1.19 to 0.58 ± 0.84 in controls. Tibial and radial cortical areas, thicknesses, and BMD were significantly higher in cases. In cases, BMD at the lumbar spine and forearm and cortical thickness were positively associated and trabecular area negatively associated with age (r = 0.49, 0.57, 0.74, and −0.61, respectively, p < .05). Serotonin was lowest in cases (69.5 [29.9110.4] ng/mL versus 119.4 [62.3231.0] ng/mL, p < .001) and inversely associated with tibial cortical density (r = −0.49, p < .05) and directly with osteocalcin (OC), bone-specific alkaline phosphatase (B-ALP), and procollagen type 1 amino-terminal propeptide (PINP) (r = 0.520.65, p < .05) in controls only. OC and S-CTX were lower and sclerostin higher in cases, whereas B-ALP, PINP, tartrate-resistant acid phosphatase (TRAP), and dickkopf-related protein 1 (DKK1) were similar in cases and controls. In conclusion, increased bone mass in Lrp5-HBM patients seems to be caused primarily by changes in trabecular and cortical bone mass and structure. The phenotype appeared to progress with age, but BTM did not suggest increased bone formation
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