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Frontiers of Medicine

ISSN 2095-0217

ISSN 2095-0225(Online)

CN 11-5983/R

Postal Subscription Code 80-967

2018 Impact Factor: 1.847

Front. Med.    2021, Vol. 15 Issue (1) : 53-69    https://doi.org/10.1007/s11684-020-0748-y
REVIEW
Factors influencing peak bone mass gain
Xiaowei Zhu, Houfeng Zheng()
Disease & Population (DaP) Geninfo Lab, School of Life Sciences, Westlake University, Hangzhou 310024, China; Institute of Basic Medical Sciences, Westlake Institute for Advanced Study, Westlake University, Hangzhou 310024, China; School of Life Sciences, Fudan University, Shanghai 200433, China
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Abstract

Bone mass is a key determinant of osteoporosis and fragility fractures. Epidemiologic studies have shown that a 10% increase in peak bone mass (PBM) at the population level reduces the risk of fracture later in life by 50%. Low PBM is possibly due to the bone loss caused by various conditions or processes that occur during adolescence and young adulthood. Race, gender, and family history (genetics) are responsible for the majority of PBM, but other factors, such as physical activity, calcium and vitamin D intake, weight, smoking and alcohol consumption, socioeconomic status, age at menarche, and other secondary causes (diseases and medications), play important roles in PBM gain during childhood and adolescence. Hence, the optimization of lifestyle factors that affect PBM and bone strength is an important strategy to maximize PBM among adolescents and young people, and thus to reduce the low bone mass or osteoporosis risk in later life. This review aims to summarize the available evidence for the common but important factors that influence bone mass gain during growth and development and discuss the advances of developing high PBM.

Keywords peak bone mass      children      adolescents      genetic      risk factors     
Corresponding Author(s): Houfeng Zheng   
Just Accepted Date: 26 March 2020   Online First Date: 10 June 2020    Issue Date: 11 February 2021
 Cite this article:   
Xiaowei Zhu,Houfeng Zheng. Factors influencing peak bone mass gain[J]. Front. Med., 2021, 15(1): 53-69.
 URL:  
https://academic.hep.com.cn/fmd/EN/10.1007/s11684-020-0748-y
https://academic.hep.com.cn/fmd/EN/Y2021/V15/I1/53
Fig.1  Bone mass throughout the life span.
Site Population Chromosome Loci Samples References
LL-BMD Children 1p36.12 WNT4 8007 European; 1177 Other; 232 Greater Middle Eastern [43]
7q31.31 WNT16
9q34.11 FUBP3
12p11.22 KLHDC5/PTHLH
14q32.12 RIN3
SK-BMD Children 1p36.12 WNT4 8007 European; 1177 Other; 232 Greater Middle Eastern [43]
6q22.32 CENPW
6q23.2 EYA4
7q31.31 CPED1
8q24.12 TNFRSF11B (OPG)
11p14.1 LGR4
11q13.2 LRP5
18q21.33 TNFRSF11A (RANK)
TB-BMD Children 1p36.12 WNT4 8007 European; 1177 Other; 232 Greater Middle Eastern [43]
2q24.3 GALNT3
7q31.31 CPED1-WNT16-FAM3C 2660 children; 12 066 individuals [37]
9q34.11 FUBP3 8007 European; 1177 Other; 232 Greater Middle Eastern [43]
12p11.22 KLHDC5/PTHLH
13q14.11 TNFSF11 (RANKL)
14q32.12 RIN3
12Q13 SP7 1518 European [36]
UL-BMD Children 1p36.12 WNT4 8007 European; 1177 Other; 232 Greater Middle Eastern [43]
2q24.3 GALNT3
6q22.32 CENPW
7q31.31 CPED1-WNT16-FAM3C 8007 European; 1177 Other; 232 Greater Middle Eastern [43]
337 African American or Afro-Caribbean, 908 European, 126 Hispanic or Latin American, Other; 481 European [38]
933 European American; 486 European [50]
13q14.11 TNFSF11 (RANKL) 8007 European; 1177 Other; 232 Greater Middle Eastern [43]
14q23.3 SPTB 933 European American; 486 European [50]
C-vBMD Children and young adult 6q25.1 CCDC170 5878 European; followed by replication in 1052 European [51]
6q25.1 ESR1
8q24.12 TNFRSF11B (OPG)
Adolescent and young adult 13q14.11 TNFSF11 (RANKL) 1934 European; replication in 3835 European [39]
Children and young adult 5878 European; replication in 1052 European [51]
T-vBMD Children and young adult 1q43 FMN2/GREM2 2500 European; replication in 1022 European [51]
Hip-BMD Children 3p14.1 MAGI1 933 European American; 486 European [50]
FN-BMD Children 14q22.3 TBPL2 933 European American; 486 European [50]
LS-BMD Children 9p21.3 IZUMO3 933 European American; 486 European [50]
Tab.1  The bone-related loci identified by GWAS in children and/or young populations to date
Fig.2  Genes identified in GWAS studies using BMD in children and young population.
Chronic and inflammatory Malabsorption syndromes Iatrogenic causes Medications Neuromuscular and metabolic
Inflammatory bowel disease Endocrine Corticosteroids Glucocorticoids Duchenne
Celiac disease Diabetes type I Anticonvulsants PPIs (chronic use) Gaucher’s disease
Nephropathies Hypovitaminosis D Gonadotropin-releasing hormone analogue Anticonvulsants Hemochromatosis
Cystic fibrosis Hypogonadism (amenorrhea, Turner, anorexia nervosa) L-thyroxine (high dose) Aromatase inhibitors, depot MPA Galactosemia
(Juvenile) rheumatoid arthritis Cushing’s syndrome Antiretroviral drugs High-dose thyroxine Glycogen storage disease
Systemic mastocytosis Primary hyperparathyroidism Anticoagulants Cytotoxic chemotherapy Marfan syndrome
Malabsorption Primary hypoparathyroidism Chemotherapeutic drugs Glitazones Others
HIV Panhypopituitarism; GH deficiency Aromatase inhibitor Cyclosporine (tacrolimus) Immobilization/little use
Organ transplant McCune Albright syndrome Nutritional problems GnRH inhibitors Intense physical activity
Connective tissue diseases Hormonal causes Nervous anorexia Heparin (long-term) Post-transplant
Thalassemia Premature menopause or premature ovarian insufficiency Lactose intolerance HAART Paget’s disease of youth
Leukemia Athletic amenorrhea Deficiency of calcium and copper Malignancies Juvenile idiopathic osteoporosis
Alcohol-related liver diseases Pregnancy Vegetarian diets Leukemia Prematurity
Pancreatic insufficiency Estrogen deficiency Malnutrition Lymphoma
Gastrectomy Insensitivity syndrome of estrogen Total parenteral nutrition Solid tumors
Tab.2  Main conditions potentially causing an altered bone density in childhood and young people
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