Skeletal muscle and pediatric bone development

Kindler, Joseph M.; Lewis, Richard D.; Hamrick, Mark W.

doi:10.1097/med.0000000000000201

Cited by 30 publications

(21 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Unlike results showing greater radius and tibia cortical bone geometry and estimated bending strength in overweight versus normal-weight subjects [32], our data corroborate reports in younger children showing that cortical bone did not differ between OB and NW despite OB having nearly 10 kg greater FFST [12]. Lean body mass is among the strongest determinants of cortical bone development during the adolescent years, and is often greater in obese versus normal-weight individuals [8, 12, 15, 16]. Our group has shown upwards to 13% greater cortical bone measures acquired via pQCT in children with normal versus higher %BF after controlling for lean mass [7, 8].…”

Section: Discussionsupporting

confidence: 86%

Obese Versus Normal-Weight Late-Adolescent Females have Inferior Trabecular Bone Microarchitecture: A Pilot Case-Control Study

et al. 2017

Self Cite

View full text Add to dashboard Cite

Though still a topic of debate, the position that skeletal health is compromised with obesity has received support in the pediatric and adult literature. The limited data relating specifically to trabecular bone microarchitecture, however, have been relatively inconsistent. The aim of this pilot cross-sectional case-control study was to compare trabecular bone microarchitecture between obese (OB) and normal-weight (NW) late-adolescent females. A secondary aim was to compare diaphyseal cortical bone outcomes between these two groups. Twenty-four non-Hispanic white females, ages 18–19 years, were recruited into OB (n = 12) or NW (n = 12) groups based on pre-specified criteria for percent body fat (≥32 vs. <30, respectively), body mass index (>90th vs. 20th–79th, respectively), and waist circumference (≥90th vs. 25th–75th, respectively). Participants were also individually matched on age, height, and oral contraceptive use. Using magnetic resonance imaging, trabecular bone microarchitecture was assessed at the distal radius and proximal tibia metaphysis, and cortical bone architecture was assessed at the mid-radius and mid-tibia diaphysis. OB versus NW had lower apparent trabecular thickness (radius and tibia), higher apparent trabecular separation (radius), and lower apparent bone volume to total volume (radius; all P < 0.050). Some differences in radius and tibia trabecular bone microarchitecture were retained after adjusting for insulin resistance or age at menarche. Mid-radius and mid-tibia cortical bone volume and estimated strength were lower in the OB compared to NW after adjusting for fat-free soft tissue mass (all P <0.050). These trabecular and cortical bone deficits might contribute to the increased fracture risk in obese youth.

show abstract

Section: Discussionsupporting

confidence: 86%

Obese Versus Normal-Weight Late-Adolescent Females have Inferior Trabecular Bone Microarchitecture: A Pilot Case-Control Study

et al. 2017

Self Cite

View full text Add to dashboard Cite

show abstract

“…The human skeleton undergoes several changes in size and shape during the different stages of life. Childhood and adolescence are characterized by rapid and significant longitudinal bone growth, areal bone expansion, and bone mineral accrual (19). Ninety percent of the peak bone mass is achieved in late teenage and the amount of bone mass reached by this age predicts BMD in adulthood (20, 21) (see glossary in Table 1).…”

Section: Bone Development Growth and Pubertymentioning

confidence: 99%

The Bones of Children With Obesity

et al. 2020

View full text Add to dashboard Cite

Excess adiposity in childhood may affect bone development, ultimately leading to bone frailty. Previous reports showing an increased rate of extremity fractures in children with obesity support this fear. On the other hand, there is also evidence suggesting that bone mineral content is higher in obese children than in normal weight peers. Both adipocytes and osteoblasts derive from multipotent mesenchymal stem cells (MSCs) and obesity drives the differentiation of MSCs toward adipocytes at the expense of osteoblast differentiation. Furthermore, adipocytes in bone marrow microenvironment release a number of pro-inflammatory and immunomodulatory molecules that up-regulate formation and activation of osteoclasts, thus favoring bone frailty. On the other hand, body adiposity represents a mechanical load, which is beneficial for bone accrual. In this frame, bone quality, and structure result from the balance of inflammatory and mechanical stimuli. Diet, physical activity and the hormonal milieu at puberty play a pivotal role on this balance. In this review, we will address the question whether the bone of obese children and adolescents is unhealthy in comparison with normal-weight peers and discuss mechanisms underlying the differences in bone quality and structure. We anticipate that many biases and confounders affect the clinical studies conducted so far and preclude us from achieving robust conclusions. Sample-size, lack of adequate controls, heterogeneity of study designs are the major drawbacks of the existing reports. Due to the increased body size of children with obesity, dual energy absorptiometry might overestimate bone mineral density in these individuals. Magnetic resonance imaging, peripheral quantitative CT (pQCT) scanning and high-resolution pQCT are promising techniques for the accurate estimate of bone mineral content in obese children. Moreover, no longitudinal study on the risk of incident osteoporosis in early adulthood of children and adolescents with obesity is available. Finally, we will address emerging dietary issues (i.e., the likely benefits for the bone health of polyunsaturated fatty acids and polyphenols) since an healthy diet (i.e., the Mediterranean diet) with balanced intake of certain nutrients associated with physical activity remain the cornerstones for achieving an adequate bone accrual in young individuals regardless of their adiposity degree.

show abstract

“…Accompanying the moderated IGF‐I‐cortical bone relationship, the children with high HOMA‐IR also had lower FFST and MCSA relative to IGF‐I. Lean body mass and MCSA are strong predictors of cortical bone areal measures and are an integral link between IGF‐I and bone . Mouse and human studies have provided evidence supporting the facilitative role of lean body mass in the link between IGF‐I and bone.…”

Section: Discussionmentioning

confidence: 93%

Insulin Resistance and the IGF-I-Cortical Bone Relationship in Children Ages 9 to 13 Years

Kindler

Pollock

Laing

et al. 2017

Journal of Bone and Mineral Research

View full text Add to dashboard Cite

IGF-I is a pivotal hormone in pediatric musculoskeletal development. Though recent data suggest that the role of IGF-I in total body lean mass and total body bone mass accrual may be compromised in children with insulin resistance, cortical bone geometric outcomes have not been studied in this context. Therefore, we explored the influence of insulin resistance on the relationship between IGF-I and cortical bone in children. A secondary aim was to examine the influence of insulin resistance on the lean mass-dependent relationship between IGF-I and cortical bone. Children were otherwise healthy, early adolescent black and white boys and girls (ages 9–13 years) and were classified as having high (n=147) or normal (n=168) insulin resistance based on the homeostasis model assessment of insulin resistance (HOMA-IR). Cortical bone at the tibia diaphysis (66% site) and total body fat-free soft tissue mass (FFST) were measured by pQCT and DXA, respectively. IGF-I, insulin and glucose were measured in fasting sera and HOMA-IR was calculated. Children with high HOMA-IR had greater unadjusted IGF-I (p<0.001). HOMA-IR was a negative predictor of cortical bone mineral content, cortical bone area (Ct.Ar) and polar strength strain index (pSSI; all p≤0.01) after adjusting for race, sex, age, maturation, fat mass, and FFST. IGF-I was a positive predictor of most musculoskeletal endpoints (all p<0.05) after adjusting for race, sex, age, and maturation. However, these relationships were moderated by HOMA-IR (pInteraction<0.05). FFST positively correlated with most cortical bone outcomes (all p<0.05). Path analyses demonstrated a positive relationship between IGF-I and Ct.Ar via FFST in the total cohort (βIndirect Effect=0.321, p<0.001). However, this relationship was moderated in the children with high (βIndirect Effect=0.200, p<0.001) versus normal (βIndirect Effect=0.408, p<0.001) HOMA-IR. These data implicate insulin resistance as a potential suppressor of IGF-I-dependent cortical bone development, though prospective studies are needed.

show abstract

Skeletal muscle and pediatric bone development

Cited by 30 publications

References 70 publications

Obese Versus Normal-Weight Late-Adolescent Females have Inferior Trabecular Bone Microarchitecture: A Pilot Case-Control Study

Obese Versus Normal-Weight Late-Adolescent Females have Inferior Trabecular Bone Microarchitecture: A Pilot Case-Control Study

The Bones of Children With Obesity

Insulin Resistance and the IGF-I-Cortical Bone Relationship in Children Ages 9 to 13 Years

Contact Info

Product

Resources

About