A six years longitudinal cohort study on the changes in bone density and bone quality up to peak bone mass in adolescent idiopathic scoliosis (AIS) with and without 2 years of Calcium and Vit-D supplementation

Author(s):  
TP Lam ◽  
G Yang ◽  
H Pang ◽  
BHK Yip ◽  
WYW Lee ◽  
...  

Adolescent idiopathic scoliosis (AIS) is associated with osteopenia which could persist into adulthood affecting attainment of Peak Bone Mass thus resulting in osteoporosis in late adulthood. We previously reported a randomized double-blinded placebo-controlled trial(the Cal study) showing significant bone health improvement with 2-year calcium(Ca)+Vit-D supplementation for AIS girls. This study addressed the important issue whether bone health improvement from the initial 2-year Ca+Vit-D supplementation could persist as subjects approached towards Peak Bone Mass at 6-year ie after 4-year of supplement discontinuation. This was an extension of the Cal study on AIS girls (11–14 years old, mean age=12.9 years, Tanner stage<IV) with femoral neck aBMD Z-score<0 and Cobb angle≥15∘. 330 subjects were randomized to Group1(placebo), Group2(600mgCa+400-IU-Vit-D3/day) or Group3(600mgCa+800-IU-Vit-D3/day) for 2-year supplementation after which supplementation was stopped. Investigations at baseline, 2-year and 6-year included High-resolution Peripheral Quantitative Computed Tomography(HR-pQCT) at distal radius and Dual Energy X-ray Absorptiometry(DXA) at both hips. 270(81.8%) subjects completed 2-year supplementation when changes in left femoral neck aBMD, trabecular vBMD, Trabecular BV/TV, Trabecular Number and Trabecular Separation indicated significant bone health improvement with Ca+Vit-D supplementation(p<0.05). At 6-year(mean age=19.2 years), no between-group difference on bone parameters was noted except increase in Cortical Thickness being greater only in Group3 than in Group1. After 4-year supplement discontinuation, the treatment effect from the initial 2-year supplementation mostly dissipated indicating the need of continued supplementation in AIS girls to sustain therapeutic improvement on bone health as subjects approach towards Peak Bone Mass.

Scoliosis ◽  
2015 ◽  
Vol 10 (1) ◽  
Author(s):  
Nasreen Akseer ◽  
Kimberly Kish ◽  
W Alan Rigby ◽  
Matthew Greenway ◽  
Panagiota Klentrou ◽  
...  

Author(s):  
KL Cheng ◽  
QQ Li ◽  
Y Wang ◽  
J Zhang ◽  
TP Lam ◽  
...  

Adolescent Idiopathic Scoliosis (AIS) occurs during pubertal rapid growth period and is closely associated with low bone mass. The underlying mechanisms for systemic low bone mass in AIS remains unclear. Wnt signalling pathway is one of the important pathways regulating bone metabolism and influencing bone strength, its family member Wnt16 associates with lower bone mineral density (BMD) in late adulthood, and plays key regulatory role in determining cortical bone quality in adult mice. Our randomized control trial have reported vitamin D (VitD) supplementation significantly improved bone mass and reduced the risk of curve progression in AIS. A case-control study and animal study were employed to answer if WNT16 is associated with the abnormal bone quality in AIS and if the effect of VitD supplementation is associated with Wnt16, respectively. A cohort of 161 AIS and control female subjects were recruited for measurement of anthropometric parameters, bone qualities, and circulating Wnt16 level. In animal study, WT and Wnt16 gKO mice were both subjected to special VitD diet from week 4 and terminated at week 7 and 10 for samples harvesting. AIS showed significantly lower BMD, circulating WNT16 level, and elevated serum level of type I procollagen N-terminal propeptide. Wnt16 gKO mice demonstrated lower cortical bone density compared with WT mice from week 7 of age and Wnt16 gKO were less prone to cortical bone loss induced by high dosage VitD diet. Further study on the biological role of WNT16 and crosstalk with VitD metabolism on bone qualities is warranted which might shed light on prognostic gene of osteopenia and new perspectives for potential target to prevent curve progression.


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