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Analyses of muscular mass and function: The impact on bone mineral density and peak muscle mass
Abstract
Bone density and bone mass are commonly regarded as the essential parameters to describe fracture risk in osteology. Because fractures primarily depend on bone strength and secondarily on bone mass and density, bone strength should be the main parameter to describe fracture risk. The quantitative description of bone strength has the prerequisite that bone geometry is assessed despite bone density. Thus, volumetric osteodensitometric methods should be preferred, which enable the physician to evaluate parameters primarily associated with bone modeling or remodeling. Modeling describes the adaptation of bone geometry to applied muscular forces in contrast to remodeling representing bone turnover. The adaptation of bone geometry to muscle forces led to the term functional muscle-bone unit, which enables the physician to differentiate between primary and secondary bone diseases. Primary bone diseases are characterized by a defective adaptation of bone to muscle forces in contrast to secondary bone diseases, which are primary diseases of the neuromuscular system. Because muscle forces are essential in the feedback loop of bone adaptation to forces (mechanostat), the assessment of muscle function has become an essential part of osteologic diagnostics in pediatrics. Dynamometric and mechanographic methods have been introduced to properly characterize kinetic aspects of muscle function in children and adolescents. Therefore, emphasis should be put on the assessment of muscle function despite the evaluation of osteodensitometric parameters in pediatric osteology.
... The jumping exercise succeeded to retain cancellous bone mass and to improve the trabecular thickness in distal femur of growing rats [12]. Progressive and intensive treadmill running protected hindlimb muscles from atrophy secondary to 4 weeks tail suspension period [13]. A comparison between the treadmill running and jumping exercise was made to test their capability to restore bone loss secondary to tail suspension. ...
... The maximum protection against muscle atrophy was observed in histochemical type I (slow twitch, oxidative metabolic) muscle (soleus vastus intermedius, and adductor longus). The great improvement of soleus muscle mass in the suspended and exercised rats was further investigated for myofibril protein content which was found to be significantly lower than that of the control group [13], [21]. Similar results were obtained by a recent study compared between jumping and running exercises developed similar improvements in the trabecular width of the distal femur of the growing rats. ...
Exercises are important issue in the treatment of osteopenia and osteoporosis with elimination of several side
effects of drugs. Therefore, the aim of the current work is to compare between running and jumping exercise
effects on the trabecular bone architecture of both femur and tibiae in adult rats. Furthermore, to quantify the
appropriate dose of exercise to treat bone loss and osteopenia developed secondary to hindlimb unloading.
Forty Wister rats (20 males and 20 females) divided into four groups (each group n=10): Basal control (BCON),
Control (CON), Jumping (JUMP), and Running (RUN). All rats were tail suspended for two weeks to develop
osteopenia in their hindlimb femur and tibiae. The BCON group was sacrificed to represent the osteopenic bone
architecture. The CON group was left 6 weeks without any intervention while, the JUMP, and RUN groups were
treated by exercises for the same period. Histomorphometric assessment including the following parameters:
Tissue area (T.Ar): (in µm2), Marrow area (Ma.Ar.) (in µm2), Trabecular area (Tr.Ar) (in µm2), Trabecular width
(Tb Wi) (in µm), Cortical width (Ct Wi) (in µm), Trabecular separation (Tb Sp) (in µm), Trabecular bone volume:
normalized by tissue volume (BV%TV), Trabecular number (/mm), and Porosity (%). Both Jumping and running
improved bone architecture in the left femur by about 25 to 50% respectively, but only jumping exercise
improved right but not left tibial architecture by more than 50%. The effect of exercise developed was site
specific and type dependent. High impact exercise improved trabecular architecture greater than low impact
exercise.
... The impact of physical activity patterns on bone loss is mainly seen in the strong positive association between bone mass as well as bone density and skeletal muscle mass [36][37][38][39][40]. Skeletal muscle mass is one of the most powerful determinants of bone strength and bone density [41]. The strong relationship between bone and skeletal muscle was postulated and mainly viewed in the context of the mechanostat theory [42,43] and the theory of the functional muscle bone unit [44][45][46]. According to these theories bones respond to varying mechanical strains modulated by systemic effects such as hormones. ...
... There is a growing body of evidence that nutritional factors but also physical activity patterns, especially regular exercise, influence bone mass during childhood and adolescence growth [18,20,21]. Especially high impact and weight bearing activity in early childhood and prepuberty appear to be most beneficial in improving bone mass [16,19,20] and support the theory of a functional muscle bone unit during subadult life stage [44][45][46]53]. During adolescence after pubertal growth spurt, the growth rate declines, the consolidation of skeletal mass however, continues. ...
Increased life expectancy on the one hand and dramatically reduced physical activity in daily life on the other hand are characteristic features of postmodern life. Consequently Homo sapiens in Industrialized countries but also in threshold countries, is increasingly confronted with the problems associated with accelerated bone loss, osteoporosis and osteoporosis related fractures. On major risk factor of osteoporosis and low bone mass is physical inactivity. Bone loss and osteoporosis however are mainly focused on from clinical viewpoint. In the present review a bioanthropological perspective of the phenomenon physical inactivity and osteoporosis is provided. The problem is discussed from the viewpoint of life history theory, but also from the viewpoint of evolutionary biology, especially evolutionary medicine and paleopathology.
... In the current study, DXA was used to measure BMD and soft tissue composition in patients with the late onset form of Pompe disease. Although this technique has some limitations, such as the inability to measure cortical area and a real volumetric bone density (17), it remains a common and reliable method to evaluate bone mineral status and is used to diagnose osteoporosis and to predict fracture risk (18). The results reconfirmed that osteopenia may be present at diagnosis time in bones which are adjacent to the insertion of affected muscles, such as femur and lumbar spine. ...
... The results reconfirmed that osteopenia may be present at diagnosis time in bones which are adjacent to the insertion of affected muscles, such as femur and lumbar spine. Muscle weakness reduces the application of mechanical forces on the skeleton, which are essential for bone remodelling and adaptation to keep high bone strength (17). Similarly, BMD in the proximal femur but not the lumbar spine is severely diminished in boys with Duchenne muscular dystrophy early in the disease course before ambulation is significantly affected (19). ...
Pompe disease is an inherited metabolic disorder characterized by α-glycosidase deficiency, which leads to lysosomal glycogen accumulation in many different tissues. The infantile form is the most severe with a rapidly fatal outcome, while the late onset form has a greater phenotypic variability, characterized by skeletal muscle dysfunction and early respiratory involvement. Bone mineral density (BMD) has been recently reported to be reduced in many patients with both forms of the disease. Enzyme replacement therapy (ERT) is now available with an undefined, impact on BMD in patients with late onset disease.
The present study aimed to investigate BMD in patients with late onset form of Pompe disease before and after ERT initiation.
Dual x-ray absorptiometry (DEXA) was examined in four newly diagnosed patients with late onset Pompe disease and in four adults under ERT before and after ERT initiation with a treatment duration of 18 to 36 months.
The initial DEXA showed normal total body BMD z-score in all the patients, while L2-L4 and femoral neck BMD was reduced in three and two patients, respectively. After ERT administration, two patients had an improvement in L2-L4 lumbar spine and one patient in femoral neck BMD z-score with values within normal range.
The results suggested that regional BMD may moderately reduce in some patients with the late onset form of Pompe disease, although profound osteopenia was not observed. The improvement of measurements in L2-L4 and femoral neck BMD z-score in some patients with low pre-treatment values after ERT administration needs to be confirmed in larger scale studies.
... Furthermore, both components are regulated and controlled by the same hormones and genes (Matsuoka et al. 2005). The functional muscle bone unit was mainly described for children, adolescents and young adults (Schoenau 2005;Fricke and Schoenau 2007;Fricke et al. 2010) and its integrity during the ageing process is not well characterized. Only a few studies focused on the muscle-bone unit during adulthood and especially older age (Ferretti et al. 1998(Ferretti et al. , 2003Sumnik et al. 2006;Bleicher et al. 2011) and the effect of soft tissue body composition on bone mass and density during old age remains controversial. ...
... According to Lang (2011) the skeletal muscle is one of the most powerful determinants of bone strength and bone density and, therefore, sex differences in the bone -muscle relationship are of key interest in understanding sex differences in age-related bone loss and bone fracture risk. Sex differences in the bone -muscle relationship are mainly viewed in the context of the mechanostat theory (Frost 1987(Frost , 2000 and the theory of the functional muscle bone unit (Schoenau 2005;Fricke and Schoenau 2007;Fricke et al. 2010). According to this theory bones respond to varying mechanical strains modulated by systemic effects such as hormones. ...
This paper examines sex specific associations between soft tissue body composition (lean and fat mass) and bone mineral density among older adults.
Two hundred and eighty-two subjects (152 females and 130 males) aged 60-92 years ((x))= 71.9 ± 7.9) were enrolled. Body composition of the whole body and bone density (BMD) of the whole body and the femoral neckwere measured by dual energy x-ray absorptiometry. Body mass index (BMI), relative appendicular skeletal muscle mass (RASM) and relative total muscle mass (RTSM) were calculated. Subjects were categorized based on sarcopenia, i.e. reduced appendicular skeletal muscle mass, osteopenia and osteoporosis. BMD of the femoral neck was used to categorize osteopenia and osteoporosis.
Sex-specific correlation patterns between soft tissue body composition and bone density were observed. Lean body mass (RASM and RTSM) correlated significantly with total and femoral neck bone density in men, absolute and relative fat mass were significantly related to whole and femoral neck bone density among women only. Sarcopenic men suffered significantly more frequently from osteopenia and osteoporosis than their non-sarcopenic counterparts. Among females sarcopenia was not related to reduced bone density.
The impact of soft tissue body composition on bone density is different among men and women at older ages. A significant relation between muscle mass and bone density is found among elderly males only.
... By stabilizing the bones and joints, muscle mass enhances overall stability and reduces the likelihood of falls and fractures. 66 In addition to mechanical loading, muscle mass influences bone density through hormonal and metabolic pathways. Muscle contractions during physical activity trigger the release of growth factors and hormones that affect bone metabolism and remodeling processes. ...
... Age and other factors. The PBM is reached at ~30 years of age, and after 30 years, BMD and muscle mass begin to decrease (134). For this reason, both the incidence of sarcopenia and osteoporosis will increase with age (135). ...
Osteosarcopenia is a burgeoning geriatric syndrome and a familiar disease among older individuals. It is characterized by reduced skeletal muscle mass and bone mineral density due to osteoporosis and sarcopenia. Its clinical manifestations include reduced physical performance and individuals becoming prone to falls during the aging process resulting in fractures and hospitalization, which seriously affects the quality of life of patients and increases the risk of death. Due to the aging social structure of the global population, the morbidity of osteosarcopenia is expected to continue to increase. Both muscle and bone belong to the motor system and originate from the mesoderm; therefore, sarcopenia and osteoporosis also share similar pathogenical factors, which influence and regulate each other. Studying the pathogenesis and treatment of osteosarcopenia is of great significance to improve the quality of life of patients. Therefore, the present study reviewed the research progress on sarcopenia and osteoporosis in osteosarcopenia from the standpoints of its definition, epidemiology, clinical manifestations and diagnosis, prevention and treatment.
... The activity of the muscle-bone interface is closely related to the normal development of the growing skeleton, while it has been also shown that bone geometry can be affected by applied muscular forces [1,2]. However, the muscle-bone interaction is altered in neuromuscular diseases (NMD), resulting in several changes in bone geometry and bone quality [3]. ...
Introduction: Neuromuscular Diseases (NMD) are associated with decreased bone strength due to altered muscle–bone interaction. However, the evaluation of bone quality remains a certain challenge in these patients. The purpose of this scoping review is to investigate the recent literature regarding the assessment of Bone Mineral Density (BMD) in this population. Methods: An electronic search of the PubMed and Scopus database was performed considering studies published in the English literature after 2007 that evaluated BMD in pediatric and adolescent patients with NMD. We excluded studies that evaluated patients > 20 years, studies not involving humans, and studies investigating bone mineral density in various pediatric conditions, but without specific data on NMD. Results: Overall, 19 studies were included that evaluated BMD in 1983 patients with NMD. Duchenne Muscular Dystrophy was the most widely studied disease (n = 11 studies). Dual energy X-ray absorptiometry (DEXA) was the most common diagnostic modality for BMD evaluation, while the most frequent site for BMD measurement was the lumbar spine (89.4%, n = 17 studies), followed by total body BMD (68.4%, n = 13 studies). Low BMD in children with NMD was demonstrated in all studies, especially after loss of ambulation. Moreover, a positive correlation between lower BMD and older age was shown. Conclusions: BMD evaluation in NMD remains a clinical challenge, as indicated by the high heterogeneity regarding the optimal site and technique for the evaluation of bone quality in these patients. Although DXA is currently the diagnostic modality of choice, a consensus regarding the optimal site for BMD measurement, and the adjustment method for its obtained measurements for parameters such as age and height is needed.
... This may be because high muscle mass increases muscle strength and power exertion, and because increased muscle mass is generally associated with high bone mass and BMD. [37][38][39] Although some reports indicate that MAnP is associated with BMD, a study reported a positive Table 4 Relationship between maximum anaerobic power and bone mineral density in each sport type. Values are presented as mean ± standard deviation. ...
The aim of this study was to clarify the relationships between muscle power and bone mineral density (BMD) and the α-actinin-3 (ACTN3) R577X polymorphism in Japanese female collegiate athletes participating in sports with various mechanical-load characteristics. This study included 260 female collegiate athletes involved in 10 competitive sports and 26 controls (mean ages, 19.2 ± 1.2 and 19.7 ± 1.3 years, respectively). The sports were classified into 3 categories (low-impact, multidirectional, and high-impact) based on the exercise load characteristics. Data on sports participation and competition experience were obtained through a questionnaire-type survey. The maximum anaerobic power (MAnP) test was performed to measure muscle power. The total body BMD was measured using dual-energy X-ray absorptiometry. The ACTN3 R577X polymorphism (rs1815739) was analyzed using a TaqMan® assay. The multidirectional sports participants with the RR genotype of the ACTN3 R577X polymorphism had a higher BMD than those with the RX and RX + XX genotypes (P = .018 and P = .003, respectively). The RR genotype was also associated with a higher MAnP than those with the RX + XX genotypes (P = .035). No other variables related to BMD and MAnP were significantly different. Our results suggests that the RR genotype may confer high trainability for BMD and muscle power in Japanese female collegiate athletes participating in multidirectional sport types. However, these associations were not found in the athletes participating in the low- and high-impact sport types.
... Muscle and bone form a functional unit, with mechanical stimulation through muscle activity driving bone development. 28 Consequently, impaired muscle function, F I G U R E 2 Active rachitic bone disease on X-ray of both legs. ...
Cystinosis is an autosomal recessive storage disease due to impaired transport of cystine out of lysosomes. Since the accumulation of intracellular cystine affects all organs and tissues, the management of cystinosis requires a specialized multi‐disciplinary team consisting of pediatricians, nephrologists, nutritionists, ophthalmologists, endocrinologists, neurologists’ geneticists and orthopedic surgeons. Treatment with cysteamine can delay or prevent most clinical manifestations of cystinosis, except the renal Fanconi syndrome. Virtually all individuals with classical, nephropathic cystinosis suffer from Cystinosis Metabolic Bone Disease (CMBD), related to the renal Fanconi syndrome in infancy and progressive chronic kidney disease (CKD) later in life. Manifestations of CMBD include hypophosphatemic rickets in infancy, and renal osteodystrophy associated with CKD resulting in bone deformities, osteomalacia, osteoporosis, fractures, and short stature. Assessment of CMBD involves monitoring growth, leg deformities, blood levels of phosphate, electrolytes, bicarbonate, calcium, and alkaline phosphatase, periodically obtaining bone radiographs, determining levels of critical hormones and vitamins, such as thyroid hormone, parathyroid hormone, 25(OH) vitamin D, and testosterone in males, and surveillance for non‐renal complications of cystinosis such as myopathy. Treatment includes replacement of urinary losses, cystine depletion with oral cysteamine, vitamin D, hormone replacement, physical therapy, and corrective orthopedic surgery. The recommendations in this article came from an expert meeting on CMBD that took place in Salzburg, Austria, in December 2016. This article is protected by copyright. All rights reserved.
... Taking a life-course approach to understanding the development of osteoporosis and vascular disease would point to auxiliary factors that influence both bone heath and vascular health potentially earlier in life that may help explain their co-existence in older age. During ageing, and particularly in the growth phase of life, muscle mass and function are a crucial determinant of bone mass and strength and are also associated with a more favourable cardiovascular health profile [31]. Thus, understanding the relationship between the musculature and the vasculature may help unlock critical new pathways to further our knowledge of the bone-vascular axis (Table 1). ...
Vascular diseases account for a significant proportion of preventable deaths, particularly in developed countries. Our understanding of diseases that alter the structure and function of blood vessels such as vascular calcification and vascular stiffness has grown enormously such that we now appreciate them to be active processes that can be modified. Interest has also grown in examining the links between other diseases of ageing such as the loss of bone (osteoporosis) and muscle (sarcopenia) with the development and progression of vascular disease as these three disease states commonly co-occur in older age. Cardiovascular disease (including calcification and arterial stiffness) is highly prevalent in older populations and it appears that its progression is accelerated in patients with osteoporosis, fracture, sarcopenia and in those who are functionally impaired. Biological and clinical evidence supports a view that vascular disease (calcification/stiffness) may be both a cause and consequence of diseases of ageing including musculoskeletal decline. This review provides an overview of the development of vascular calcification and stiffness and explores the molecular and physiological mechanisms linking osteoporosis and sarcopenia to vascular disease development. This review also examines clinical evidence supporting the association of muscle and bone loss with vascular disease and concludes by reviewing the interventional and therapeutic potential of bone-active minerals and hormones (calcium and vitamin D) on cardiovascular disease biology, given that these represent potential interventions to target multiple body systems. Overall, this review will aim to highlight the underappreciated burden of cardiovascular disease in individuals in the context of musculoskeletal diseases.
... This may be a possible explanation for girls having a more bone per unit of lean body mass compared to boys (11,28). We do not know to what extent this better adaptation of the bone to the muscular forces in female sex with extra storage of calcium is a factor preventing the need for gestation and lactation (29). In practice, these findings provide an additional intervention avenue, focus on physical activities that increase muscle mass. ...
Purpose:
This study analyzed prospective associations between distinct trajectories of objectively measured physical activity (PA) and late adolescent bone parameters and explored the mediating effects of lean soft tissue (LST), a surrogate of muscle mass to associations.
Methods:
PA was measured by accelerometry starting at age 5 and continuing at 8, 11, 13, 15 and 17 years in approximately 524 participants from the Iowa Bone Development Study. Gender-specific group-based trajectory modeling was used to construct developmental trajectories of moderate-and-vigorous intensity PA (MVPA) from childhood to late adolescence. At age 17, proximal femur bone mineral density (aBMD) was assessed by dual X-ray energy absorptiometry, and its distribution was calculated by aBMD ratios. Specific geometric measures of the proximal femur were assessed using Hip Structural Analysis.
Results:
A significant portion of the total effect of MVPA from age 5 to 17 yr on bone parameters at age 17 was explained by an increase in leg LST in both sexes. For males and females, indirect effects were observed on the total and all regional proximal femur aBMDs, and on the ratio between the inferomedial and superolateral neck aBMD. The effect on the ratio between the trochanter and the total proximal femur was specific to females, while the effect on the hip axis length was specific to males. Direct effects of MVPA on aBMDs were identified only in males.
Conclusions:
Using robust mediation analysis, this is the first study addressing the indirect effect (through muscle) of PA across childhood and adolescence on proximal femur bone parameters. To improve bone health at the proximal femur, the results suggest PA interventions during growth that increase muscle mass, particularly in females.
... This signaling pathway regulates the osteoclasts and osteoblasts activity as well as mediates the effects of the hormones on the skeleton (Ostrowska 2009). The concept of muscle -bone unit assumes that bones and muscles represent evolutional functional unit that is under the control of insulin-like growth factor 1 (IGF-1), gonadal hormones and vitamin D (Ashby et al. 2011, Fricke et al. 2010. The anabolic effect of IGF-1 on bone is well known and this is true during the puberty and adolescence (Mohan andBaylink 2005, Venken et al. 2005). ...
Here we analyzed associations between muscles mass, total bone mineral content (BMC), lumbar spine bone density (BMD L1-L4) and serum or urine hormones in healthy peripubertal girls. Total BMC and areal BMD L1-L4, muscle mass and fat were measured by dual-energy X-ray absorptiometry (DXA). Muscle force (N) was estimated by a dynamometer. Circulating estradiol, folliclestimulating hormone (FSH), luteinizing hormone (LH), 25-hydroxy vitamin D, parathyroid hormone (PTH), insulin-like growth factor 1 (IGF-1), leptin, osteocalcin, bone isoenzyme of alkaline phosphatase (bALP) and total calcium and phosphorus were quantified as the nocturnal melatonin and serotonin urinary excretion. Partial correlations adjusted for height, Tanner score and physical activity confirmed positive relationships between BMC or BMD L1-L4 (Z-score) and lean mass or fat. Furthermore, positive relationship was observed between BMC or BMD L1-L4 (Z-score) and serum leptin. After adjustment for Tanner score and physical activity, positive associations were observed between lean mass and IGF-1, leptin levels or muscle force. We proved positive relationships between bone mass and serum leptin in peripubertal girls. © 2017 Institute of Physiology of the Czech Academy of Sciences, Prague, Czech Republic.
... For the reason that there is a feedback loop of bone adaptation to muscle forces, the evaluation of muscle function is essential in the diagnosis of bone condition in pediatrics. 33,34 On the other hand, periods of inactivity, low muscle support, immobilization or conditions of weightlessness have a profound effect on the integrity of bone and can cause loss of skeletal density. 32,35,36 Increased osteoclastic activity and cytokine production cause skeletal mobilization of calcium in immobilized patients. ...
Bone modeling is a process that starts with fetal life and continues during adolescence. Complex factors such as hormones, nutritional and environmental factors affect this process. In addition to these factors, physical conditioning and medications that have toxic effects on bony tissue should be carefully considered in patient follow-up. Osteoporosis is a significant problem in pediatric population because of ongoing growth and development of skeletal system. Two types of osteoporosis are primary and secondary types and children with neuromuscular disabilities constitute a major group with secondary osteoporosis. Low bone mass in patients with cerebral palsy, spina bifida, and Duchenne muscular dystrophy cause increased bone fragility in even slight traumas. Maximizing peak bone mass and prevention of bone loss are very important to reduce the fracture risk in neuromuscular diseases. This article aims to review the determinants of bone physiology and bone loss in children with cerebral palsy, spina bifida, and Duchenne muscular dystrophy.
... However, lean mass is a surrogate for muscle forces, i. e., the force generated by a muscle is proportional to the muscle mass [36]. Because muscular fitness directly measures muscle forces and because it can be systematically assessed at schools as part of the physical education curricula, it is the logical parameter for non-invasively understanding bone strength [10]. Regrettably, the most widely administered physical fitness batteries in North America and Europe do not include a muscle power test [33] and in other cases, muscle power tests are administered but without healthrelated standards [5]. ...
The objective of this investigation was to evaluate the accuracy of peak vertical jump power (VJP) to identify children with bone mineral density (BMD) below average, defined as BMD measured by DXA and adjusted for body height at the whole body less head≤- 1.0 standard deviation (SD). The sample included 114 boys and girls aged 8.5±0.4 years old. VJP was estimated from a countermovement jump performed on a contact mat using the measured flight time to calculate the height of rise of the center of gravity. Logistic regression analysis revealed that the odds ratio of having BMD≤1.0 SD decreased 1.2% per watt of power and the probability of BMD below average was 75.6% higher in boys than in girls with the same peak power jump. Receiver operating characteristic analysis showed that the best trade-off between sensitivity and specificity to identify children with BMD<- 1.0 SD was 635 watts in boys (sensitivity=63.3%; specificity=69.2%; AUC=0.816, 95% CI: 0.681-0.95; p<0.001) and 515 watts in girls (sensitivity=75.0%; specificity=77.0%; AUC=0.849, 95% CI: 0.698-0.999; p=0.002). These cut-off values correspond to a vertical jump of 19.9 cm and 20.5 cm in 8-year-old boys and girls, respectively. The VJP showed a reasonable sensitivity and specificity as well good discriminant ability to identify children with BMD below average.
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... When compared, the muscle fatigue in boys (mean age 10 years) was lower and they had a faster recovery rate than adult men (mean age 26 years) [40]. Furthermore, bone mass is positively correlated with age, while the relationship between bone strength and age is primarily explained by the increase in muscle force in children and adolescents [41]. Due to the demanding nature of fast bowling in cricket, fast bowlers are not immune to age-related changes and there will be neuromuscular differences in players of different ages. ...
Background
The high prevalence of injury amongst cricket fast bowlers exposes a great need for research into the risk factors associated with injury. Both extrinsic (environment-related) and intrinsic (person-related) risk factors are likely to be implicated within the high prevalence of non-contact injury amongst fast bowlers in cricket. Identifying and defining the relative importance of these risk factors is necessary in order to optimize injury prevention efforts.
Objective
The objective of this review was to assess and summarize the scientific literature related to the extrinsic and intrinsic factors associated with non-contact injury inherent to adult cricket fast bowlers.
Method
A systematic review was performed in compliance with the PRISMA guidelines. This review considered both experimental and epidemiological study designs. Studies that included male cricket fast bowlers aged 18 years or above, from all levels of play, evaluating the association between extrinsic/intrinsic factors and injury in fast bowlers were considered for inclusion. The three-step search strategy aimed at finding both published and unpublished studies from all languages. The searched databases included MEDLINE via PubMed, Cumulative Index to Nursing and Allied Health Literature (CINAHL), the Cochrane Controlled Trials Register in the Cochrane Library, Physiotherapy Evidence Database (PEDro), ProQuest 5000 International, ProQuest Health and Medical Complete, EBSCO MegaFile Premier, Science Direct, SPORTDiscus with Full Text and SCOPUS (prior to 28 April 2015). Initial keywords used were ‘cricket’, ‘pace’, ‘fast’, ‘bowler’, and ‘injury’. Papers which fitted the inclusion criteria were assessed by two independent reviewers for methodological validity prior to inclusion in the review using standardized critical appraisal instruments from the Joanna Briggs Institute Meta Analysis of Statistics Assessment and Review Instrument (JBI-MAStARI).
Results
A total of 16 studies were determined to be suitable for inclusion in this systematic review. The mean critical appraisal score of the papers included in this study was 6.88 (SD 1.15) out of a maximum of 9. The following factors were found to be associated with injury: bowling shoulder internal rotation strength deficit, compromised dynamic balance and lumbar proprioception (joint position sense), the appearance of lumbar posterior element bone stress, degeneration of the lumbar disc on magnetic resonance imaging (MRI), and previous injury. Conflicting results were found for the association of quadratus lumborum (QL) muscle asymmetry with injury. Technique-related factors associated with injury included shoulder–pelvis flexion–extension angle, shoulder counter-rotation, knee angle, and the proportion of side-flexion during bowling. Bowling workload was the only extrinsic factor associated with injury in adult cricket fast bowlers. A high bowling workload (particularly if it represented a sudden upgrade from a lower workload) increased the subsequent risk to sustaining an injury 1, 3 or 4 weeks later.
Conclusion
Identifying the factors associated with injury is a crucial step which should precede the development of, and research into, the effectiveness of injury prevention programs. Once identified, risk factors may be included in pre-participation screening tools and injury prevention programs, and may also be incorporated in future research projects. Overall, the current review highlights the clear lack of research on factors associated with non-contact injury, specifically in adult cricket fast bowlers.
Systematic review registration number Johanna Briggs Institute Database of Systematic Reviews and Implementation Reports 1387 (Olivier et al., JBI Database Syst Rev Implement Rep 13(1):3–13. doi:10. 11124/ jbisrir-2015-1387, 2015).
... When compared, the muscle fatigue in boys (mean age 10 years) was lower and they had a faster recovery rate than adult men (mean age 26 years) [40]. Furthermore, bone mass is positively correlated with age, while the relationship between bone strength and age is primarily explained by the increase in muscle force in children and adolescents [41]. Due to the demanding nature of fast bowling in cricket, fast bowlers are not immune to age-related changes and there will be neuromuscular differences in players of different ages. ...
Review question/objective
Review question: which extrinsic and intrinsic factors are associated with non-contact injury in adult cricket pace bowlers?
Review objective: the objective of this review is to determine the extrinsic and intrinsic factors associated with non-contact injury in adult pace bowlers.
Inclusion criteria
Types of participants
This review will consider studies that include male cricket pace bowlers over the age of 18 years from all levels of play.
Types of intervention(s)/phenomena of interest
This review will consider studies evaluating the association between extrinsic and intrinsic factors, and lower quarter injury in pace bowlers. Intrinsic factors may include, but will not be limited to, muscle strength, flexibility, balance and biomechanics, while extrinsic factors may include bowling, but will not be limited to, workload, player position and time of play.
Types of outcomes
This review will consider studies that include any of the following outcome measures: non-contact injury. A non-contact injury is defined as an injury which is significant enough to cause an inability to fully or partially participate in training or matches and which was caused by an overuse mechanism rather than collision-type injuries.
... In support of a critical role for skeletal muscle-induced mechanical stimuli in the regulation of bone mass, studies have shown that a lack of muscle function in utero results in impaired fetal bone and joint development [17][18][19][20][21]. Furthermore, during post-natal skeletal growth (2-20 yr), there is a very strong positive correlation between muscle mass and bone mass, with gains in muscle mass preceding those in bone mass [22]. In fact, the associations between muscle/strength and bone mass in children are strong enough that clinical techniques for disease diagnosis can be founded upon them [23,24]. For instance, deficiencies in the amount of bone per unit muscle strength versus deficiencies in both factors allow for classification of diagnoses into primary (true or intrinsic) and secondary (physiologic) bone disorders. ...
The development and maintenance of skeletal muscle and bone mass is critical for movement, health and issues associated with the quality of life. Skeletal muscle and bone mass are regulated by a variety of factors that include changes in mechanical loading. Moreover, bone mass is, in large part, regulated by muscle-derived mechanical forces and thus by changes in muscle mass/strength. A thorough understanding of the cellular mechanism(s) responsible for mechanotransduction in bone and skeletal muscle is essential for the development of effective exercise and pharmaceutical strategies aimed at increasing, and/or preventing the loss of, mass in these tissues. Thus, in this review we will attempt to summarize the current evidence for the major molecular mechanisms involved in mechanotransduction in skeletal muscle and bone. By examining the differences and similarities in mechanotransduction between these two tissues, it is hoped that this review will stimulate new insights and ideas for future research and promote collaboration between bone and muscle biologists.
... Skeletal muscle mass and bone mass, as well as bone density, are interrelated. This bone-muscle relationship is mainly viewed in the context of the mechanostat theory [43,44], and the theory of the functional muscle bone unit [27,29,30]. These theories imply that bones and skeletal muscle respond to varying mechanical strains modulated by systemic effects, such as hormones. ...
Age Typical Associations between Skeletal Muscle Mass and Bone Mass among Healthy Women
Human body composition changes through the process of ageing. Beside a well documented increase in fat mass, bone mass and muscle mass decline progressively, resulting in pathologically deceased skeletal muscle mass, i.e. sarcopenia and osteoporosis, in the worst case. Both reduced bone density and reduced muscle mass have dramatic consequences, such as impaired functional performance, increased risk of falls, and consequently, an increased risk of fragility fractures.
... (35) However, a synergy has been demonstrated between muscle and bone mass and strength. (36,37) We observed a significant negative correlation between the percentage BMD change and the initial value. This finding also has been reported for antiresorptive therapy. ...
Disuse osteoporosis in children is a progressive disease that can affect quality of life. High-frequency, low-magnitude vibration (HFLMV) acts as an anabolic signal for bone and muscle. We undertook a prospective, randomized, double-blind, placebo-controlled clinical trial to assess the efficacy and safety of regional HFLMV in disabled children. Sixty-five children 6 to 9 year of age were randomized into three groups: placebo, 60 Hz, and 90 Hz. In the two active groups, a 0.3-g mechanical vibration was delivered to the radii and femurs for 5 minutes each day. After 6 months, the main endpoint was bone mineral density (BMD) at the ultradistal radius (UDR), 33% radii (33%R), and femoral necks (FN). Secondary endpoints were area and bone mineral content (BMC) at the UDR, 33%R, and FN; grip force of the upper and lower limbs; motor function; and PedsQL evaluation. An intention-to-treat analysis was used. Fifty-seven children (88%) completed the protocol. A significant increase was observed in the 60-Hz group relative to the other groups in BMD at the UDR (p = .011), in grip force of the upper limbs (p = .035), and in the "daily activities item" (p = .035). A mixed model to evaluate the response to intervention showed a stronger effect of 60 Hz on patients with cerebral palsy on the UDR and that between-subject variability significantly affected the response. There were no reported side effects of the intervention. This work provides evidence that regional HFLMV is an effective and safe strategy to improve bone mass, muscle strength, and possibly independence in children with motor disabilities.
... with measures of physical activity. Given the relationship of muscle power to bone mass in boys, it is likely that muscle force accounts for this association [31]. Similar findings were reported by Macdonald and colleagues [28] who found that geometric measures of the tibia (using pQCT) in preand early pubertal children (aged 9−11) were significantly and positively correlated with physical activity in boys, but not girls, and with maturity in girls, but not boys. ...
This study examines the relationships between bone mass, physical activity, and maturational status in healthy adolescent boys and girls. Methods. Ninety-nine early high-school (Year 9) students were recruited. Physical activity and other lifestyle habits were recorded via questionnaire. Anthropometrics, muscle power, calcaneal broadband ultrasound attenuation (BUA), bone mineral content (BMC), and lean tissue mass were measured. Maturity was determined by Tanner stage and estimated age of peak height velocity (APHV). Results. Boys had greater APHV, weight, height, muscle power, and dietary calcium than girls (P < .05). Boys exhibited greater femoral neck BMC and trochanteric BMC while girls had higher BUA and spine BMAD (P < .05). Physical activity and vertical jump predicted BMAD and BUA most strongly for boys whereas years from APHV were the strongest predictor for girls. Conclusion. Sex-specific relationships exist between physical activity, maturity and bone mass during adolescence.
Calcium and phosphate homeostasis is maintained by the interaction of parathyroid hormone (PTH), calcitriol—the primary bioactive metabolite of vitamin D, the phosphatonin—fibroblast growth factor-23 (FGF23), and the thyroid gland product—calcitonin—acting in a coordinated manner upon the intestinal absorption of these ions, the proximal renal tubular reabsorption of filtered calcium and its excretion of phosphate, the deposition of these analytes into bone by the osteoblast, and their reabsorption from this site by the osteoclast. Calcium is essential for intracellular signal transduction, nerve conduction, blood clotting, and the strength and structural integrity of bone hydroxyapatite. Phosphate, second to calcium in abundance, is present in DNA and RNA nucleotides, requisite for energy generation, and a component of cell membranes, signal transduction pathways, and the bone mineral—hydroxyapatite. Phosphate is absorbed by the intestinal duodenum and jejunum, filtered through the renal glomerulus, reabsorbed by the proximal renal tubule or excreted in urine, and deposited into bone linked to calcium as hydroxyapatite from which site it may be reabsorbed by PTH and calcitriol. Under usual circumstances, the serum concentrations of calcium and phosphate are reciprocally related. Intact PTH is an 84-amino-acids (AA) peptide that is released from the parathyroid glands in response to declining serum concentrations of Ca2 + detected by the calcium sensing receptor expressed on the plasma membrane of the parathyroid gland chief cell whose message is transmitted through the seven transmembrane-heterotrimeric guanine nucleotide-binding PTH receptor that inhibits renal tubular reabsorption of filtered phosphate; increases synthesis of calcitriol, which enhances intestinal absorption of calcium; and activates osteoclastogenesis, thereby mobilizing calcium from bone . FGF23 inhibits renal tubular reabsorption of phosphate and decreases renal synthesis of calcitriol, thereby depressing intestinal absorption of calcium and phosphate; FGF23 increases the synthesis of water-soluble 1,24,25-trihydroxyvitamin D and thus its urinary excretion. Calcitonin, a 32 AA product of the parafollicular “C” cells of the thyroid gland, depresses serum calcium concentrations by inhibiting osteoclast function, thereby impairing its release from bone, and increasing its urinary excretion.
The purpose of this chapter is to provide an approach to the diagnosis and treatment of pediatric osteoporosis. Osteoporosis is defined in adults as low bone mineral mass and deterioration of bone micro architecture, with an increased risk of fragility (a traumatic) fractures. It is preceded by a less severe condition named osteopenia (scarcity of bone), the simple reduction of bone mass for gender and age. Osteoporosis is the most common metabolic bone disorder in adults, and remains a major health problem worldwide. There is increasing awareness that osteoporosis may also affect children and adolescents, either because of intrinsic skeletal defects (primary osteoporosis) or as a complication of other diseases or their treatment (secondary osteoporosis). Various methods have been employed to assess bone health in children and adolescents. Evaluation of bone pain and mobility, and x-ray confirmation of fractures are often the first diagnostic step. Low bone mass or osteoporosis are detected by bone densitometry, quantitative computed tomography, peripheral quantitative computed tomography, quantitative ultrasound and, in special cases, bone histology/histomorphometry. The assessment of the basic bone metabolism parameters, such as serum/ urinary levels of calcium, phosphate, vitamin D, parathyroid hormone, is a useful diagnostic complement, while that of bone turnover markers can be useful in special conditions.
As one of the major hard tissue in humans and most vertebrates, the skeleton, generally referring to bone, provides the essential frame to support the body and to thus permit locomotion. Considering the functional requirements of bones across different species, e.g. from rats to dinosaurs, or during different growth periods, e.g. from embryo to old age, it is not difficult to conceive that bones adapt to the experienced mechanical environment. In fact, mechanically regulated bone modeling and remodeling is one of the major means to maintain regular bone metabolism. The findings on the bone adaptation to the mechanical environment have been well theorized by Julius Wolff in 1890s [1] as ‘Wolff’s law’ and refined later by Harold Frost as ‘mechanostat’ [2-4]. Evidence from numerous animal studies in the past revealed the adaptation process of the bones to the well-defined artificial mechanical environment and suggested certain relationship between the adaptation in relation to the types of loading, e.g. loading amplitude, loading cycle, loading frequency and so on [5-8]. Conversely, bone degradation was generally observed during disuse, e.g. prolonged bed rest [9], or in the microgravity environment during space flight [10]. Indeed, the best way to further our understanding in this adaptation process is to quantitatively study the mechanical loading on bone during daily locomotor activities. However, this is still rather challenging due to technical difficulties. More importantly, the mechanical load on bones can vary greatly across individuals or species, as the variance between the body size, locomotor pattern and speed.
Little is known about interactions between muscle and bone during the removal and application of mechanical signals. Here, we applied 3wk of hindlimb unloading followed by 3wk of reambulation to a genetically heterogeneous population of 352 adult mice and tested the hypothesis that changes in muscle are associated with changes in bone at the level of the tissue and the genome. During unloading and relative to normally ambulating control mice, most mice lost muscle and cortical bone with large variability across the population. During reambulation, individual mice regained bone and muscle at different rates. Across mice, changes in muscle and trabecular/cortical bone were not correlated to each other during unloading or reambulation. For unloading, we found one significant quantitative trait locus (QTL) for muscle area and five QTLs for cortical bone without overlap between mechano-sensitive muscle and cortical bone QTLs (but some overlap between muscle and trabecular QTLs). The low correlations between morphological changes in muscle and bone, together with the largely distinct genetic regulation of the response indicate that the premise of a muscle-bone unit that co-adjusts its size during (un)loading may need to be reassessed. © 2016, International Society of Musculoskeletal and Neuronal Interactions. All rights reserved.
Background: The muscle-bone unit represents an evolutionary system, in which both of its components are under the common control of the insulin-like growth factor I (IGF-I), sex hormones, and vitamin D. The mutual interactions between these hormones maintain integrity, growth and maturation of pubertal bone mass. Thus, insufficiency of any of these hormones will negatively influence development of the skeleton during puberty. Objectives: The aim of the study as to analyse the correlation between muscle mass, total bone mineral content (BMC), bone mineral density (BMD) of the lumbar spine (BMD L 1-L 4), and serum or urine hormones. Materials and Methods: Total BMC (g) and areal BMD L 1-L 4 (g/cm 2and Z-score) as well as muscle mass and fat mass (g) were assessed by means of dual-energy X-ray absorptiometry (DXA). The Z-score is the number of standard deviations a patient's BMD which differs from the average BMD of their age, sex, and ethnicity. This Parameter is used in children. Muscle force (N) was measured using a dynamometer. Results: The simple correlations showed strong positive associations between BMC or BMD L 1-L 4 (g/cm 2) and serum phosphate, estradiol, insulin-like growth factor (IGF-I), leptin and fat masses, and muscle force (P < 0.001 for all parameters). Positive correlations were also observed between BMD and serum phosphate (P < 0.01), IGF-I (P < 0.01), estradiol (P < 0.001), leptin (P < 0.01), fat and lean mass (P < 0.001 and P < 0.001, respectively) and muscle force (P < 0.001). The partial correlations, after eliminating the impact of height, Tanner stage, and physical activity level, confirmed positive relationships between either BMC or BMD L 1-L 4 and lean mass (P < 0.001 and P < 0.001, respectively) and fat mass (P < 0.001 for BMC and BMD). Furthermore, a positive relationship was observed between serum leptin and both BMC and BMD (Z score) (P < 0.05 and P < 0.05, respectively). After removing the effects of height, Tanner stage, and physical activity, positive associations were observed between lean mass and IGF-I (P < 0.01), leptin levels (P < 0.05), and muscle force (P < 0.01). Conclusions: On the basis of the study results, it can be expected that low values of lean or fat mass, and insufficient production of IGF-I or leptin, could negatively influence bone development in pubertal girls.
Muscle and bone are anatomically and functionally closely connected. The traditional concept that skeletal muscles serve to load bone and transform skeletal segments into a system of levers has been further refined into the mechanostat theory, according to which striated muscle is essential for bone development and maintenance, modelling and remodelling. Besides biomechanical function, skeletal muscle and bone are endocrine organs able to secrete factors capable of modulating biological function within their microenvironment, in nearby tissues or in distant organs. The endocrine properties of muscle and bone may serve to sense and transduce biomechanical signals such as loading, unloading or exercise, or systemic hormonal stimuli into biochemical signals. Nonetheless, given the close anatomical relationship between skeletal muscle and bone, paracrine interactions particularly at the periosteal interface can be hypothesized. These mechanisms can assume particular importance during bone and muscle healing after musculoskeletal injury. Basic studies in vitro and in rodents have helped to dissect the multiple influences of skeletal muscle on bone and/or expression of inside-organ metabolism and have served to explain clinical observations linking muscle-to-bone quality. Recent evidences pinpoint that also bone tissue is able to modulate directly or indirectly skeletal muscle metabolism, thus empowering the crosstalk hypothesis to be further tested in humans in vivo.
Objectives:
To present gender-specific pediatric normative data on the main parameters of muscle function assessed using jumping mechanography.
Methods:
The study population included 796 non-selected Caucasian children and adolescents (432 girls and 364 boys) aged 6-19 years recruited from 6 primary schools and 3 high schools. Maximum peak power (Pmax) was examined by a single two-legged jump, and maximum force (Fmax) was examined by a multiple one-legged hopping. All measurements were performed using a portable force platform (Leonardo Mechanograph, Novotec). Pmax, Pmax/mass, Fmax and Fmax/body weight were analyzed as the main outcome parameters. LMS method was used to generate age- and weight-specific reference smooth curves.
Results:
Both Pmax and Fmax were strongly dependent on age and weight in both genders (all p<0.001). In prepubertal children, there was no intergender difference in Pmax or Fmax. Both parameters steadily increased in boys and plateaued in girls aged >13 years. Whereas Pmax/mass was more dependent on anthropometric parameters, Fmax/BW remained nearly constant with respect to age and weight.
Conclusions:
These reference data are intended to assist clinicians in the assessment of muscle function by jumping mechanography in pediatric patients.
Mechanical load activates bone modeling and increases bone strength. Thus physical activity is extremely important for overall bone health. Muscle volume and muscle contraction are closely related to bone mineral density in men and women, although these relationships are more significat in men. The muscle-bone unit has been defined as a functional system, in which both components are under control of the somatotropin-IGF-I system, androgens and D hormone. These endocrine systems play, via the muscle-bone unit, an important role in development of the skeleton and its stability in adulthood. That is why deficiency of any of these hormonal systems, or reduced physical activity (mainly in childhood) could seriously affect bone density and quality. Bone is also under control of adipose tissue, which modulates its metabolism via mechanical load and more importantly via adipocytokines (leptin, adiponectin and rezistin). Leptin increases bone formation by activation of osteoblasts. This direct effect of leptin is amplified by stimulation of the β-1 adrenergic system, which inhibits the negative osteotropic effects of neuropeptide Y. On the other hand, leptin also activates β-2 adrenergic receptors, which increase bone resorption. In humans, the overall osteo-anabolic effect of leptin tends to be dominant. Furthermore, leptin has a principal role in the start of puberty in girls and maturation, remodeling and development of the female skeleton. Adiponectin (and probably rezistin) has an unambiguous deteriorating effect on the skeleton. Further studies are needed to confirm the clinical importance of soft tissues relative to the integrity of the skeleton.
If height-limiting treatment is being considered for a child with tall stature, skeletal maturity is invaluable in the selection of appropriate patients for treatment, determining appropriate age of treatment commencement, monitoring progress of treatment, and determining the expected treatment effect on adult height. In precocious puberty, bone maturation can be usefully assessed at initial diagnosis and start of treatment and at regular intervals thereafter during treatment monitoring. Together with height, bone maturation is an essential parameter for long-term treatment monitoring in congenital adrenal hyperplasia. Bone age (BA) determination in children with skeletal dysplasia is only feasible in a few disorders and estimations should be treated with caution. Radiographs of the left hand and wrist are, however, essential in the diagnosis of many skeletal disorders. Bone mineralization and measures of bone lengths, width, thickness and cortical thickness should always be evaluated in relation to a child's height and BA, especially around puberty. The use of skeletal maturity, assessed on a radiograph alone to estimate chronological age for immigration authorities or criminal courts is not recommended.
Bone strains are the most important factors for osteogenic adaptive responses. During the past decades, scientists have been trying to describe the relationship between bone strain and bone osteogenic responses quantitatively. However, only a few studies have examined bone strains under physiological condition in humans, owing to technical difficulty and ethical restrictions. The present paper reviews previous work on in vivo bone strain measurements in humans, and the various methodologies adopted in these measurements are discussed. Several proposals are made for future work to improve our understanding of the human musculoskeletal system. Literature suggests that strains and strain patterns vary systematically in response to different locomotive activities, foot wear, and even different venues. The principal compressive, tension and engineering shear strain, compressive strain rate and shear strain rate in the tibia during running seem to be higher than those during walking. The high impact exercises, such as zig-zag hopping and basketball rebounding induced greater principal strains and strain rates in the tibia than normal activities. Also, evidence suggests an increase of tibia strain and strain rate after muscle fatigue, which strongly supports the opinion that muscle contractions play a role on the alteration of bone strain patterns.
The neck and shoulder region of vertebrates has undergone a complex evolutionary history. To identify its underlying mechanisms we map the destinations of embryonic neural crest and mesodermal stem cells using Cre-recombinase-mediated transgenesis. The single-cell resolution of this genetic labelling reveals cryptic cell boundaries traversing the seemingly homogeneous skeleton of the neck and shoulders. Within this assembly of bones and muscles we discern a precise code of connectivity that mesenchymal stem cells of both neural crest and mesodermal origin obey as they form muscle scaffolds. The neural crest anchors the head onto the anterior lining of the shoulder girdle, while a Hox-gene-controlled mesoderm links trunk muscles to the posterior neck and shoulder skeleton. The skeleton that we identify as neural crest-derived is specifically affected in human Klippel–Feil syndrome, Sprengel's deformity and Arnold–Chiari I/II malformation, providing insights into their likely aetiology. We identify genes involved in the cellular modularity of the neck and shoulder skeleton and propose a new method for determining skeletal homologies that is based on muscle attachments. This has allowed us to trace the whereabouts of the cleithrum, the major shoulder bone of extinct land vertebrate ancestors, which seems to survive as the scapular spine in living mammals.
Albright’s hereditary osteodystrophy is a rare inherited metabolic disorder characterized by a typical phenotype. It may be
associated with or without resistance to parathyroid hormone (pseudohypoparathyroidism). Both forms may co-exist in the same
family. Pseudohypoparathyroidism Type 1 and Pseudo-pseudohypoparathyroidism occur as a consequence of reduced erythrocyte
membrane coupled with Gs alpha activity. We report here the variable inheritance of hormone resistance in the presence of
characteristic phenotype and reduced Gs alpha activity in the same family.
The International Society for Clinical Densitometry (ISCD) conducts Position Development Conferences (PDCs) for the purpose of establishing standards and guidelines in the field of bone densitometry. Topics for consideration are selected according to clinical relevance, a perceived need for standardization, and the likelihood of achieving agreement. Questions regarding nomenclature, indications, acquisition, analysis, quality control, interpretation, and reporting of bone density tests for each topic area are assigned to task forces for a comprehensive review of the scientific literature. The findings of the review and recommendations are then presented to an international panel of experts at the PDC. The expert panel votes on potential Official Positions for appropriateness, necessity, quality of the evidence, strength of the recommendation, and applicability (worldwide or variable according to local requirements). Recommendations that are approved by the ISCD Board of Directors become Official Positions. The first Pediatric PDC was 20-21 June 2007 in Montreal, QC, Canada. The most recent Adult PDC was held 20-22 July 2007, in Lansdowne, VA, USA. This Special Report summarizes the methodology of the ISCD PDCs and presents selected Official Positions of general interest.
This review focuses on methodological concepts in the evaluation of skeletal muscle function and on adaptation. It is now thought that the critical property of bone is strength rather than weight, and that control of bone strength is mainly exercised through the effect of the mechanical loads brought to bear on bone. Muscle contraction places the greatest physiological load on bone, and so the stability of bone must be adapted to muscle strength (the functional muscle-bone unit). The described suggestions and recommendations outline a new concept: bone mass and strength should not be related to age. There is now more and more evidence that bone mass and strength should be related to muscle function. Thus analyzed, there is no such entity as 'peak bone mass'. Many studies are presently under way to evaluate whether these novel approaches increase the sensitivity and specificity of fracture prediction in an individual. Furthermore, the focus of many bone researchers is shifting away from bone mass to bone geometry or bone strength and their relationship with the driving muscle system.
Bone structure and muscular strength of 30 children with renal disease were investigated by peripheral computed tomography and grip strength. Sixteen children suffered from nephrotic syndrome (NS) and had previously been treated with corticosteroids. Fourteen children suffered from chronic renal failure (CRF) ranging from mild renal failure to end-stage renal disease. Six children had received kidney transplants and corticosteroids for immunosuppression. There was a significant decrease in grip strength of children with NS (SD -0.91+/-1.5; P=0.042) and children with CRF (SD -1.38+/-1.4; P<0.001) compared with normal children. Furthermore, there was a significant correlation between cortical area and grip strength in all children with renal disease (r=0.92; P<0.0001). Trabecular bone mineral density did not correlate well with grip strength. These findings resemble results found in healthy children. Trabecular bone mineral density was significantly elevated in children with CRF compared with normal children (SD 1.14+/-1.4; P=0.008). Grip strength as a marker of muscle mass and cortical area as a marker of bone strength correlate well in children with renal disease, similar to the correlation in healthy children. Grip strength is significantly lower in children with NS and CRF compared with normal children. These data suggest that muscular impairment could be involved in renal osteopathy.
Current investigations of bone development mostly focus on bone mass, but bone strength may be functionally more important than mass. Therefore, we compared the developmental changes in cortical bone mass (BMCcort) and parameters of cortical bone strength [polar moment of inertia, section modulus, and strength strain index (SSI)]. Analyses were performed at the 65% site of the proximal radius using peripheral quantitative computed tomography. The study population comprised 469 healthy subjects, 6-40 yr of age (273 females). Both in prepubertal children (pubertal stage 1) and after puberty (pubertal stage 5 and adults) all studied parameters were significantly higher in males. During puberty (pubertal stages 2-4) the gender-specific differences were generally somewhat smaller. All of the measured parameters increased significantly with age and pubertal stage. However, although the percent increase in BMCcort between the youngest children and adults was similar between the genders, the increases in polar moment of inertia, section modulus, and SSI were higher in males. The ratio between section modulus and BMCcort was consistently higher in males after the age of 11 yr and after pubertal stage 2. Similar results were found for ratios between polar moment of inertia or SSI and BMCcort. These results show that for a given bone mass, males have stronger bones than females after pubertal stage 2. This reflects the fact that in puberty males add bone mostly on the periosteal surface, where the effect on bone strength is highest, whereas females add bone on the endocortical surface, which has a small effect on bone stability. The purpose of the mechanically inefficient endocortical apposition in female puberty might be to create a reservoir of calcium for future pregnancy and lactation.
Peripheral quantitative computed tomography (pQCT) has the ability to improve the diagnostic utility of densitometry in children and adolescents, because bone size and volumetric bone mineral density (vBMD) can be measured independently. Nevertheless, detailed reference data are lacking. We therefore performed pQCT (XCT-2000 scanner, Stratec, Inc., Pforzheim, Germany) at the distal radius in 371 healthy children, adolescents, and young adults (185 males and 186 females, ages 6-23 years) and in 107 of their parents (19 men and 88 women, ages 29-40 years). Total vBMD, trabecular, and "cortical + subcortical" vBMD as well as cross-sectional area (CSA) were determined at the "4% site" of the distal radius. This location was defined as the site whose distance to the most distal portion of the growth plate or to the radial articular surface corresponded to 4% of the forearm length. In both genders, total vBMD remained stable between 6 and 15 years of age and then increased by 30% in girls and by 46% in boys. Regarding pubertal development, total vBMD remained almost constant throughout pubertal stages 1-4 and thereafter increased in both genders. Trabecular vBMD did not change with age in girls, whereas in boys an increase with age of about 10% was noted after 15 years of age. Males had higher trabecular vBMD than females. This gender difference increased from 6% in prepubertal children to 23% in adults. The variation with age and pubertal stage in "cortical + subcortical" vBMD-cort was similar to that of total vBMD. CSA roughly doubled between 6 and 15 years of age in both genders. In conclusion, the availability of this reference material will provide a basis for the use of pQCT in the assessment of pediatric bone diseases.
Skeletal muscle development is one of the key features of childhood and adolescence. Determining maximal isometric grip force (MIGF) using a hand-held Jamar dynamometer is a simple method to quantify one aspect of muscle function. Presently available reference data present MIGF as a function of chronological age. However, muscle force is largely determined by body size, and many children undergoing muscle performance tests in the clinical setting suffer from growth retardation secondary to a chronic disorder. Reference data were established from simple regressions between age or log height and log MIGF in a population of 315 healthy children and adolescents aged 6 to 19 y (157 girls). These data were used to calculate age- or height-dependent SD scores (SDS) for MIGF in three pediatric patient groups. In renal graft recipients (n = 14), the age-dependent MIGF SDS was markedly decreased (-2.5 +/- 1.9; mean +/- SD). However, these patients had short stature (height SDS, -2.5 +/- 1.2), and the height-dependent MIGF SDS was close to normal (-0.4 +/- 1.5). Similarly, in cystic fibrosis patients (n = 13) age-dependent MIGF SDS was -1.6 +/- 1.6, but height-dependent MIGF SDS was -0.5 +/- 1.1. Children with epilepsy who were taking anticonvulsant therapy (n = 34) had normal stature, and consequently age- and height-dependent MIGF SDS were similar (0.4 +/- 1.0 and 0.4 +/- 0.8, respectively). In conclusion, MIGF determination provides information on an important aspect of physical development. Height should be taken into account to avoid misinterpretation.
Bone densitometry is currently one of the mainstays in the evaluation of systemic bone diseases in adults and is also increasingly used to assess primary or secondary bone disorders in children and adolescents. The purpose of carrying out densitometric studies in such circumstances is to measure the densitometric indicators of bone stability. Following procedures which were established for diagnosing adult osteoporosis, a decrease in densitometric surrogates of bone stability is usually interpreted as indicating increased fracture risk. The most basic densitometric parameter is bone mineral content (BMC), which can be measured with most densitometric techniques. BMC is either defined as the mass of mineral contained in an entire bone or as the mass of mineral per unit bone length. While mineral mass can be expected to be a good surrogate for bone stability, BMC is obviously a size-dependent parameter, since small bones weigh less than big bones. This is a drawback in paediatric use, since many children and adolescents who are examined by densitometry suffer from chronic disorders and are small-for-age. Short children will have a lower BMC than their healthy age-matched peers, even if their (smaller) bones are otherwise completely normal.
A group of 25 female individuals, who had been admitted to the University Hospital with the diagnosis of anorexia nervosa (AN) 3 to 10 years before, was seen for a follow-up visit in the hospital. These women got a psychiatric exploration to detect a present eating disorder. Moreover, parameters of the muskuloskeletal interaction were determined on the non-dominant forearm. Bone mineral content (BMC) of the radius was measured by pQCT and maximal grip force was evaluated by the use of a dynamometer. Eating disorders were present in 12 females. The mean of BMC standard deviation (SD) score was significantly reduced in comparison with reference values. Furthermore, the mean of BMC SD score was also significantly lower than the mean of grip force in SD score. These results gave the suggestion that the adaptation of bone mass to biomechanical forces is disturbed in AN. The linear regression analyses between the parameters grip force and BMC were compared between the study and the reference group. The comparison delivered a significantly lower constant in the regression equation of the study group. This result can be interpreted on the background of the mechanostat theory. The affection with an eating disorder decreases the set point in the feedback loop of bone modeling. The results offer for the first time the possibility to analyse osteoporosis in anorexic females under the paradigm of muskuloskeletal interaction.
According to the Utah paradigm of skeletal physiology: (1) mechanical forces on skeletons generate signals in skeletal organs that control the biologic mechanisms that determine the architecture and strength of those organs, (2) these occur in ways that let the organs endure their voluntary mechanical usage for life without hurting or breaking, (3) to work properly, these mechanisms need nonmechanical factors (hormones, vitamins, calcium, genes, cytokines, etc.), (4) only mechanical factors can guide those mechanisms in time and anatomical space, (5) this arrangement determines skeletal health and disorders can cause or help to cause numerous disorders of skeletal and extraskeletal organs (the collagenous tissue in ligaments and tendons also forms a part of extraskeletal organs). Accumulated evidence now strongly supports these features of the Utah paradigm, which supplements a 1960 paradigm. It incites reassessment of some former ideas about skeletal physiology and disease. Some controversies ensue that will take time to resolve. After they are resolved, skeletal science, medicine, and surgery should be significantly better than before and different in unforeseeable respects as well. Am. J. Hum. Biol. 10:599–605, 1998. © 1998 Wiley-Liss, Inc.
To characterize the relationship between muscle function and auxology in preterm born children.
Forty-five preterm born children (birth weight < or =1,500 g with mean +/- SD: 1,069 +/- 281 g; median of gestational age: 29 weeks; 50% multiple births) were analyzed for auxological parameters (weight, height) and muscle function at the age of 7 years. Maximal isometric grip force (MIGF) and ground reaction forces of goal-directed counter-movement jumping were measured using the Preston dynamometer and the Leonardo force plate. MIGF, peak jump force (PJF), peak jump power (PJP) and the maximal velocity of take-off (V(max)) were analyzed for their relationship to perinatal risk factors and actual auxological parameters.
With reference to age, weight-standard deviation score (SDS) and height-SDS were lower than in the reference population. With reference to height, MIGF-SDS and PJP-SDS were lower than in reference individuals. Children with intraventricular hemorrhage (IVH) had lower PJP-SDS and V(max) than children without IVH. PJP-SDS was lower than PJF-SDS in children with IVH.
Analyses showed a discrepancy between maximal force and power due to a decline of V(max) in children with IVH.
The cumulative risk of fracture for a postmenopausal woman over the age of 50 can reach up to 60%. Exercise has the potential to modify fracture risk in postmenopausal women through its effects on bone mass and geometry; however, these effects are not well characterized. To determine the effects of exercise on bone mass and geometry in postmenopausal women, we conducted a systematic review of the literature. We included all randomized controlled trials, cross-sectional studies, and prospective studies that used peripheral quantitative computed tomography to assess the effects of exercise on bone mass and geometry in this population. Exercise effects appear to be modest, site-specific, and preferentially influence cortical rather than trabecular components of bone. Exercise type also plays a role, with the most prominent mass and geometric changes being observed in response to high-impact loading exercise. Exercise appears to positively influence bone mass and geometry in postmenopausal women. However, further research is needed to determine the types and amounts of exercise that are necessary to optimize improvements in bone mass and geometry in postmenopausal women and determine whether or not these improvements are capable of preventing fractures.
Distraction osteogenesis is an established method of treatment of non-unions and limb length discrepancies. Despite improvements in surgical techniques and fixation devices there is still a considerable possibility of failure of the regenerate bone after frame removal. The hypothesis of the present experimental study was that a noninvasive bone strength marker, the strength-strain index (SSI) measured by peripheral quantitative computerized tomography (pQCT), could be significantly correlated with a biomechanical bone strength index, the maximum load at bone failure (F(max)), assessed in a three-point bending test. The right tibias of fifteen male New Zealand White rabbits were subjected to gradual lengthening using an external fixator. At the end of the consolidation phase (55th day) the animals were sacrificed and the lengthened tibiae were collected free of soft tissue, after removal of the lengthener, for immediate scanning and mechanical testing. The values of cortical bone mineral density, cortical bone area, and the corresponding SSIy, as measured by pQCT, were assessed for statistically significant correlation relative to the values of the F(max) and stiffness as evaluated by the three-point bending test were assessed. SSIy showed a statistically significant positive correlation with the maximum load (F(max)) with a correlation value R=0.846 (p<0.001), and it was a good predictor of F(max) since it was able to describe the 71.6% of variability of F(max)(R2=0.716). Furthermore, cortical bone area appeared to be highly correlated with F(max) (p<0.005), but it was a less efficient predictor of F(max) (R2=0.471). There was, also, a statistically significant correlation between SSIy and bone stiffness as assessed in the 3-point bending test (p<0.005). In conclusion, the present study reveals that the SSI can be used as a sensitive index of adequate consolidation of the regenerate bone, possibly able to reduce mechanical failure due to premature frame removal. In clinical relevance, the aforementioned hypothesis should be applied in studies of human populations and possible confirmation of its validity would establish pQCT as a valuable diagnostic tool not only in distraction osteogenesis but also in other techniques of bone healing.
The growth of lean mass precedes that of bone mass, suggesting that muscle plays an important role in the growth of bone. However, to date, no study has directly followed the growth of bone and muscle size through puberty and into adulthood. This study aimed to test the hypothesis that the growth of muscle size precedes that of bone size (width and length) and mass during puberty. Bone and muscle properties were measured using pQCT and DXA in 258 healthy girls at baseline (mean age, 11.2 yr) and 1-, 2-, 3-4- and 7-yr follow-up. Growth trends as a function of time relative to menarche were determined from prepuberty to early adulthood for tibial length (TL), total cross-sectional area (tCSA), cortical CSA (cCSA), total BMC (tBMC), cortical volumetric BMD (cBMD), and muscle CSA (mCSA) in hierarchical models. The timings of the peak growth velocities for these variables were calculated. Seventy premenopausal adults, comprising a subset of the girl's mothers (mean age, 41.5 yr), were included for comparative purposes. In contrast to our hypothesis, the growth velocity of mCSA peaked 1 yr later than that of tibial outer dimensions (TL and tCSA) and slightly earlier than tBMC. Whereas TL ceased to increase 2 yr after menarche, tCSA, cCSA, tBMC, and mCSA continued to increase and were still significantly lower than adult values at the age of 18 yr (all p < 0.01). The results do not support the view that muscle force drives the growth of bone size during puberty.
Vitamin A deficiency has a plethora of clinical manifestations, ranging from xerophthalmia (practically pathognomonic) to disturbances in growth and susceptibility to severe infection (far more protean). Like other classical vitamin deficiency states (scurvy, rickets), some of the signs and symptoms of xerophthalmia were recognized long ago. Reports related to vitamin A and/or manifestations of deficiency might conveniently be divided into "ancient" accounts; eighteenth to nineteenth century clinical descriptions (and their purported etiologic associations); early twentieth century laboratory animal experiments and clinical and epidemiologic observations that identified the existence of this unique nutrient and manifestations of its deficiency; and, most recently, a flowering of carefully conducted clinical studies and field-based randomized trials that documented the full extent and impact of deficiency among the poor of low- and middle-income countries, which in turn changed global health policy.
Bone mineral density measurements using dual X-ray absorptiometry (DXA) are commonly expressed as areal density (g/cm2). However, areal BMD (BMDareal) is dependent on bone size and this can lead to erroneous interpretations of BMD values. We have previously presented a simple method for calculating apparent volumetric bone mineral density (BMDvol) using ancillary DXA-derived data. In the present study we tested the validity of our model using in vivo volumetric data obtained from magnetic resonance imaging (MRI) of lumbar vertebrae. BMDareal and BMDvol of L3 were measured from sixteen pairs of identical twins (24 men, 8 women), aged 25-69 years. The dimensions of the lumbar vertebra L3 were measured from MR images and BMD values were corrected for these dimensions. The DXA-derived apparent volumetric bone mineral density (BMDvol) correlated moderately with MRI-derived BMDs (r values from 0.665 to 0.822). In contrast to BMDareal, BMDvol and MRI-derived BMDs were not related to body size variables. All these volume-corrected BMDs diminished the erroneous effect of vertebral size on areal BMD. We conclude that the simple DXA-derived BMDvol can be used for normalization of bone mineral density values in subjects of different body sizes, and especially in growing children.
The largest voluntary loads on bones come from muscles. To adapt bone strength and mass to them, special strain threshold ranges determine where modeling adds and strengthens bone, and where remodeling conserves or removes it, just as different thermostat settings control the heating and cooling systems in a house. If estrogen lowers the remodeling threshold, two things should occur. First, at puberty in girls, bone mass should begin to increase more than in boys with similar muscle strengths, owing to reduced remodeling-dependent bone losses, while gains from longitudinal bone growth and bone modeling continue normally. That increase in bone mass in girls should plateau when their muscle strength stops increasing, since their stronger bones could then reduce bone strains enough to turn modeling off, but could let remodeling keep conserving existing bone. Second, decreased estrogen secretion [or a related factor(s)], as during menopause, should raise the remodeling threshold and make remodeling begin removing that extra bone. That removal should also tend to plateau after the remaining and weaker bone lets bone strains rise to the higher threshold. Postmenopausal bone loss shows the second effects. Previously unremarked relationships in the data of a 1995 Argentine study showed the first effects. This supports the idea that estrogen can affect human bone strength and mass by lowering the remodeling threshold, and loss of estrogen would raise the threshold and help cause postmenopausal bone loss even if other factors help to do it. The Argentine study also suggested ways to study those things and the roles of muscle strength and other factors in controlling bone strength and mass in children and adult humans. Those factors included, in part, hormones, vitamins, calcium, diet, sex, race, age, medications, cytokines, genetic errors, gene expression patterns, and disease.
The mineral, lean, and fat contents of the human body may be not only allometrically but also functionally associated. This report evaluates the influence of muscle mass on bone mass and its age-related changes by investigating these and other variables in both genders in the different stages of reproductive life. We have analyzed the dual-energy X-ray absorptiometry (DEXA)-determined whole-body mineral content (TBMC), lean body mass (LBM), and fat body mass data (FBM) of 778 children and adolescents of both genders, aged 2-20 years [previously reported in Bone 16(Suppl.): 393S-399S; 1995], and of 672 age-matched men and women, aged 20-87 years. Bone mass (as assessed by TBMC) was found to be closely and linearly associated with muscle mass (as reflected by LBM) throughout life. This relationship was similar in slope and intercept in prepubertal boys and girls. However, while keeping the same slope of that relationship (50-54 g increase in TBMC per kilogram LBM): (1) both men and women stored more mineral per unit of LBM within the reproductive period than before puberty (13%-29% and 33%-58%, respectively); (2) women stored more mineral than age-matched men with comparable LBM (17%-29%) until menopause; and (3) postmenopausal women had lower values of bone mineral than premenopausal women, similar to those of men with comparable LBM. Men showed no age effect on the TBMC/LBM relationship after puberty. Multiple regression analyses showed that not only the LBM, but also the FBM and body height (but not body weight), influenced the TBMC, in that decreasing order of determining power. However, neither the FBM nor body height could explain the pre/postpubertal and the gender-related differences in the TBMC/LBM relationship. Accordingly: (1) calculated TBMC/LBM and FBM-adjusted TBMC/LBM ratios were lower in girls and boys from 2-4 years of age until puberty; (2) thereafter, females rapidly reached significantly higher ratios than age-matched men until menopause; and (3) then, ratios for women and age-matched men tended to equalize. A biomechanical explanation of those differences is suggested. Sex hormones or related factors could affect the threshold of the feedback system that controls bone remodeling to adapt bone structure to the strains derived from customary mechanical usage in each region of the skeleton (bone "mechanostat"). Questions concerning whether the mineral accumulation in women during the reproductive period is related or not to an eventual role in pregnancy or lactation, or whether the new bone is stored in mechanically optimal or less optimal regions of the skeleton, are open to discussion.
It was shown in a recent multivariate analysis of lumbar vertebral (L1-L3) CT scans of 171 women without fractures and 57 fractures somewhere in their skeletons, that regional assessment of the spinal mineral distribution can result in the discrimination of the above patient groups with an accuracy of about 90%. This level of discrimination was possible even in those cases with bone densities below the fracture threshold, where the overlap of patients with and without fractures is the greatest and clinically the most significant. In this region this new analytical technique could also identify a subgroup of patients who not yet had a fracture, but for whom all three lumbar vertebrae were classified as osteoporotic. From these results it follows that the osteoporosis model proposed by the World Health Organization (WHO), which assumes that fragility depends only on a single mean value of bone mineral density (BMD) for a patient, is overly simplistic and requires upgrading to include indices representing the distribution of bone mineral.
The aim of the current study is to analyze the interaction of the muscle and bone system (muscle-bone unit) during puberty in males and females by computed tomography of the nondominant forearm. The data presented here are the first results from 318 healthy children (159 boys and 159 girls), aged 6-22 yr, and 336 adults (parents) participating in the DONALD Study (Dortmund Nutritional and Anthropometric Longitudinally Designed Study). Cortical area (CA) of the radius representing bone strength and muscle area (MA) representing muscle strength were measured with peripheral quantitative computed tomography (XCT 2000; Stratec, Pforzheim, Germany). A single slice measurement at a site corresponding to 65% of the ulnar length proximal to the radial endplate was used. MA and CA of the radius have been determined by a built-in software algorithm using density differences. There was a strong correlation between MA (x) and CA (y) in all children, adolescents, and adults (y = 0.019x + 10.93; r2 = 0.77). Before puberty, boys and girls displayed a similar relation between MA and CA. CA in relation to MA was greater in girls than in boys during puberty. Analysis of covariance was performed investigating the dependency of CA on MA, five pubertal stages, sex, and interaction of sex and pubertal stages. MA representing muscle strength was the strongest predictor of CA (P < 0.001) representing bone mass. Pubertal stage (P < 0.001) and interaction of pubertal stage*sex (P = 0.002) also had a significant influence on CA. r2 of the model was 0.85. These data suggest that in pubertal girls and women rather than in pubertal boys and men an additional factor shifts the relationship between MA and CA to higher values of cortical area. The present data confirm previous studies of the influence of puberty and estrogens or related factors on the muscle-bone interaction.
In a 1960 paradigm of skeletal physiology, effector cells (chondroblasts, fibroblasts, osteoblasts, osteoclasts, etc.) regulated by nonmechanical agents wholly determined the architecture, strength, and health of bones, joints, fascia, ligaments, and tendons. Biomechanical and tissue-level phenomena had no roles in that paradigm. Subsequent studies and evidence slowly revealed skeletal tissue-level mechanisms and their functions, including biomechanical ones, as well as "game rules" that seem to govern them. That slow discovery process found that effector cells are only parts of tissue-level mechanisms, as kidney cells are only parts of nephrons and wheels are only parts of cars. Normally all those things help to determine skeletal architecture, strength, and health, and adding them to the 1960 paradigm led to the still-evolving Utah paradigm of skeletal physiology that concerns, in part, how load-bearing skeletal organs adapt to the voluntary mechanical loads on them. That caused controversies this article does not try to resolve; instead, it describes some issues they concern. In that regard, controversy can depend on how one assesses the relevance of facts to a problem more than on their accuracy. If a paradigm added new facts to a former one and the new one's advocates viewed all those facts as relevant, but the former's advocates questioned the relevance of some of the new facts, their views about a problem could differ even though each view depended on accurate facts. Readers would make their own judgments about the bearing of those ideas on this article's content.
A large number of molecular, cellular, and epidemiologic factors have been implicated in the regulation of bone development. A major unsolved problem is how to integrate these disparate findings into a concept that explains the development of bone as an organ. Often events on the organ level are simply presented as the cumulative effect of all factors that individually are known to influence bone development. In such a cumulative model it must be assumed that each bone cell carries the construction plan of the entire skeletal anatomy in its genes. This scenario is implausible, because it would require an astronomical amount of positional information. We therefore propose a functional model of bone development, which is based on Frost's mechanostat theory. In this model the genome only provides positional information for the basic outline of the skeleton as a cartilaginous template. Thereafter, bone cell action is coordinated by the mechanical requirements of the bone. When mechanical challenges exceed an acceptable level (the mechanostat set point), bone tissue is added at the location where it is mechanically necessary. The main mechanical challenges during growth result from increases in bone length and in muscle force. Hormones, nutrition, and environmental factors exert an effect on bone either directly by modifying the mechanostat system or indirectly by influencing longitudinal bone growth or muscle force. Predictions based on this model are in accordance with observations on prenatal, early postnatal, and pubertal bone development. We propose that future studies on bone development should address topics that can be derived from the mechanostat model.
Bone densitometric data often are difficult to interpret in children and adolescents because of large inter- and intraindividual variations in bone size. Here, we propose a functional approach to bone densitometry that addresses two questions: Is bone strength normally adapted to the largest physiological loads, that is, muscle force? Is muscle force adequate for body size? To implement this approach, forearm muscle cross-sectional area (CSA) and bone mineral content (BMC) of the radial diaphysis were measured in 349 healthy subjects from 6 to 19 years of age (183 girls), using peripheral quantitative computed tomography (pQCT). Reference data were established for height-dependent muscle CSA and for the variation with age in the BMC/muscle CSA ratio. These reference data were used to evaluate results from three pediatric patient groups: children who had sustained multiple fractures without adequate trauma (n = 11), children with preterminal chronic renal failure (n = 11), and renal transplant recipients (n = 15). In all three groups mean height, muscle CSA, and BMC were low for age, but muscle CSA was normal for height. In the multiple fracture group and in renal transplant recipients the BMC/muscle CSA ratio was decreased (p <. 0.05), suggesting that bone strength was not adapted adequately to muscle force. In contrast, chronic renal failure patients had a normal BMC/muscle CSA ratio, suggesting that their musculoskeletal system was adapted normally to their (decreased) body size. This functional approach to pediatric bone densitometric data should be adaptable to a variety of densitometric techniques.
The peak bone mass concept implies that optimal skeletal development during childhood and adolescence will prevent fractures in late adulthood. This concept is based on the observation that areal bone density increases with growth during childhood, is highest around 20 years of age and declines thereafter. However, it is now clear that strong bones in the youngster do not necessarily lead to a fracture-free old age. In the recent bone densitometric literature, the terms bone mass and bone density are typically used synonymously. In physics, density has been defined as the mass of a body divided by its volume. In clinical practice and science, "bone density" usually has a different meaning-the degree to which a radiation beam is attenuated by a bone, as judged from a two-dimensional projection image (areal bone density). The attenuation of a radiation beam does not only depend on physical density, but also on bone size. A small bone therefore has a lower areal bone density than a larger bone, even if the physical density is the same. Consequently, a low areal bone density value can simply reflect the small size of an otherwise normal bone. At present, bone mass analysis is very useful for epidemiological studies on factors that may have an impact on bone development. There is an ongoing discussion about whether the World Health Organization (WHO) definition of osteoporosis is over-simplistic and requires upgrading to include indices representing the distribution of bone and mineral (bone strength indices). The following suggestions and recommendations outline a new concept: bone mass should not be related to age. There is now more and more evidence that bone mass should be related to bone size or muscle function. Thus analyzed, there is no such entity as a "peak bone mass". Many studies are currently under way to evaluate whether these novel approaches increase sensitivity and specificity of fracture prediction in an individual. Furthermore, the focus of many bone researchers is shifting away from bone mass to bone geometry or bone strength. Bone mass is one surrogate marker of bone strength. Widely available techniques for measurement of bone mass, such as dual-energy X-ray absorptiometry, radiogrammetry, and computed tomography, can also be used to measure variables of bone geometry such as cortical thickness, cortical area, and moment of inertia.
Renal transplantation in children and adolescents is associated with various skeletal complications. The incidence of spontaneous fractures appears to be increased, but the reasons for this are not entirely clear. Our objective was therefore to evaluate macroscopic bone architecture, mass, and strength by peripheral quantitative computed tomography (pQCT), a method that is not influenced by size-related artifacts. In addition, we investigated the muscle-bone relationship in these patients because under physiologic conditions bone strength continually adapts to increasing mechanical loads, that is, muscle force.
In 55 patients (41 males) aged 15.8 +/- 4.1 years, we evaluated in a cross-sectional study 4.9 +/- 3.6 years after renal grafting bone mass, density, geometry, and strength of the radius, as well as forearm muscle size and strength, using pQCT at the proximal and distal radius, radiography of the second metacarpal shaft and hand dynamometry. Data were compared to a large cohort (N= 350) of healthy children.
Muscle mass and force were adequate for body size in pediatric renal transplant recipients. However, the radial bone was characterized by an inadequately thin cortex in relation to muscular force, as shown by a reduced height-adjusted cortical thickness both at the proximal (-0.83 +/- 1.12 SDS) and distal radius (-0.52 +/- 1.69 SDS), the metacarpal shaft (-0.54 +/- 1.35 SDS), and by a reduced relative cortical area (-0.90 +/- 1.13 SDS), while the mineralization of trabecular bone was unaltered. As a consequence of cortical thinning, the Strength-Strain Index that reflects the combined strength of trabecular and cortical bone was reduced in these patients.
While bone mineral density of the forearm is not decreased in pediatric renal transplant recipients, bone strength in relation to muscular force is reduced. This alteration may contribute to the increased propensity for fractures in these patients.
Osteoporosis is the main cause of bone fragility. The diagnosis is suspected in the presence of low-energy traumatic fracture and/or low bone mineral density. Vertebral fractures may be asymptomatic, and they are under-diagnosed. Dual energy X-ray absorptiometry is the gold standard of bone density measurement, at the lumbar spine, and hip. Providing quality control of the device and assessments, the measurements are accurate and precise; BMD is the basis of osteoporosis diagnostic and risk fracture evaluation. Osteoporosis may be related to malignant and metabolic diseases, which must be checked before any treatment.
Adding later facts and ideas to a universally accepted "1960 paradigm" of skeletal physiology led to the still-evolving "Utah paradigm". The ASBMR's William Neuman award in 2001 to one of the latter paradigm's architects (HMF) suggested that physiologists began to view it as a valid supplement to its predecessor. Nevertheless it diffused poorly among most SSCs (Skeletal Scientists and Clinicians, plus all others who work in any way on skeletal matters), even though success in the quest for knowledge and recognition by many of them could depend on learning that paradigm's insights. Those insights can help to minimize serious errors in some experimental designs and in interpreting some kinds of data. To explain how success in that quest could depend on the Utah paradigm requires explaining the nature of the above errors, some features of both paradigms, some implications of the newer one, and when that quest's success might not require knowing the Utah paradigm. A three-part message distilled from the past for present and future SSCs concludes the article. It took decades to understand such things and find effective ways to explain them, and both matters probably need improvement (to paraphrase Pogo, "We met the enemy and perhaps it was us more than them"). During those decades the author changed from an active SSC hunter-player to a spectator, known to some as a feisty eccentric old dinosaur (FEOD) (Note A). So here a voice from the past would speak to present and future SSCs.
Bone densitometric data are often difficult to interpret in children and adolescents because of large inter- and intraindividual variations in bone size. Here, we propose a functional approach to bone densitometry that addresses two questions: is bone strength normally adapted to the largest physiological loads, that is, muscle force? Is muscle force adequate for body size? The theoretical background for this approach is provided by the mechanostat theory, which proposes that bones adapt their strength to keep the strain caused by physiological loads close to a set point. Because the largest physiological loads are caused by muscle contractions, there should be a close relationship between bone strength and muscle force or size. The proposed two-step diagnostic algorithm requires a measure of muscle force or size and a measure of bone mineral content (BMC) at a corresponding location. The results can be combined into four diagnostic groups. In the first situation, muscle force or size is adequate for height. If the skeleton is adapted normally to the muscle system, the result is interpreted as "normal". If it is lower than expected for muscle force or size, a "primary bone defect" is diagnosed. In the second situation, muscle force or size is too low for height. Even if the skeleton is adapted adequately to the decreased mechanical challenge, this means that bone mass and presumably strength are still too low for body height. Therefore, a "secondary bone defect" is diagnosed. It is hoped that the more detailed insights thus gained could help to devise targeted strategies for the prevention and treatment of pediatric bone diseases.
This review focuses on methodological concepts in the evaluation of skeletal muscle function, taking into account classical muscle physiology, the developing motor system in children and anthropometric parameters. Thereby, the classical concept of kinetic and thermodynamic description of muscle function is discussed in relation to data pertaining to human physiology. Emphasis is given to the specific problems that arise when assessing muscle function during development. Two important factors influencing muscle function are discussed in detail: changes in anthropometric characteristics and changes in co-ordinative skills in the developing individual. Finally, we discuss currently available methods for the evaluation of anaerobic muscle function in children and adolescents (maximal isometric grip force, peak jump force, peak jump power, Wingate test, Bosco test).
The development of the musculoskeletal system in children and adolescents became an important topic in the field of pediatric research when the connections between muscle force and bone diseases were revealed. The present study focused on reference values of ground reaction forces, which derive from muscle forces of the lower limbs. Specifically, the study investigated the relationship between anthropometric characteristics and peak jump force (PJF), and peak jump power (PJP). The parameters were assessed by jumping mechanography using the Leonardo Jumping Platform. The entire study group was comprised of 135 school boys (ages 7-21 y) and 177 girls (ages 6-19 y), who were enrolled in a German primary school and a German high school. The analysis of the parameters revealed that forces deriving from the motor performance of jumping follow an exponential relationship to body size parameters. Therefore, with consideration of anthropometric characteristics, the assessment of ground reaction forces might provide a novel, inexpensive, and accurate approach for the assessment motor performance in children and adolescents.
The objective of this article was to systematically review all published studies that investigated the association between bone density and fractures in children.
Potentially relevant articles were identified by searching electronic databases. Duplicates were removed, abstracts were inspected, and relevant articles were obtained. Studies were included in the systematic review if participants were <16.0 years old, were healthy, had extractable data on bone mass, and had fractures as the outcome.
Ten case-control studies were identified. No prospective studies were found. There was no evidence of heterogeneity between studies or of funnel-plot asymmetry. Eight of the studies were included in the meta-analysis, because they presented results as means and standard deviations of bone density in cases and controls. The pooled standardized mean difference for bone mass in children with and without fractures, from a fixed-effects model, was -0.32 (95% confidence interval: -0.43 to -0.21).
Evidence for an association between bone density and fractures in children is limited. The results from this meta-analysis suggest that there is an association between low bone density and fractures in children. Although there was no evidence of heterogeneity or publication bias, this meta-analysis is based on case-control studies that are prone to bias. Large, well-conducted prospective cohort studies are required to confirm the association between bone density and fractures in children.
The strong correlation between a bone's architectural properties and the mechanical forces that it experiences has long been attributed to the existence of a cell that not only detects mechanical load but also structurally adapts the bone matrix to counter it. One of the most likely cellular candidates for such a "mechanostat" is the osteocyte, which resides within the mineralized bone matrix and is perfectly situated to detect mechanically induced signals. However, as osteocytes can neither form nor resorb bone, it has been hypothesized that they orchestrate mechanically induced bone remodeling by coordinating the actions of cells residing on the bone surface, such as osteoblasts. To investigate this hypothesis, we developed a novel osteocyte-osteoblast coculture model that mimics in vivo systems by permitting us to expose osteocytes to physiological levels of fluid shear while shielding osteoblasts from it. Our results show that osteocytes exposed to a fluid shear rate of 4.4 dyn/cm(2) rapidly increase the alkaline phosphatase activity of the shielded osteoblasts and that osteocytic-osteoblastic physical contact is a prerequisite. Furthermore, both functional gap junctional intercellular communication and the mitogen-activated protein kinase, extracellular signal-regulated kinase 1/2 signaling pathway are essential components in the osteoblastic response to osteocyte communicated mechanical signals. By utilizing other nonosteocytic coculture models, we also show that the ability to mediate osteoblastic alkaline phosphatase levels in response to the application of fluid shear is a phenomena unique to osteocytes and is not reproduced by other mesenchymal cell types.
Unlabelled:
This is the first prospective cohort study of the association between bone mass and fracture risk in childhood. A total of 6213 children 9.9 years of age were followed for 24 months. Results showed an 89% increased risk of fracture per SD decrease in size-adjusted BMC.
Introduction:
Although previous case-control studies have reported that fracture risk in childhood is inversely related to bone mass, this has not been confirmed in prospective studies. Additionally, it remains unclear which constituent(s) of bone mass underlie this association. We carried out a prospective cohort study to examine the relationship between DXA measures in children 9.9 years of age and risk of fracture over the following 2 years.
Materials and methods:
Total body DXA scan results obtained at 9.9 years of age were linked to reported fractures over the following 2 years in children from a large birth cohort in southwest England. DXA measures consisted of total body less head (TBLH) BMD, bone area, and BMC, and results of subregional analysis of the humerus. Analyses were adjusted for age, sex, ethnicity, and social position.
Results:
Complete data were available on 6213 children. There was a weak inverse relationship between BMD at 9.9 years and subsequent fracture risk (OR per SD decrease = 1.12; 95% CI, 1.02-1.25). In analyses examining the relationship between fracture risk and volumetric BMD, fracture risk was inversely related to BMC adjusted for bone area, height, and weight (OR = 1.89; 95% CI, 1.18-3.04) and to estimated volumetric BMD of the humerus (OR = 1.29; 95% CI, 1.14-1.45). Fracture risk was unrelated to both TBLH and humeral bone area. However, in analyses of the relationship between fracture risk and bone size relative to body size, an inverse association was observed between fracture risk and TBLH area adjusted for height and weight (OR = 1.51; 95% CI, 1.17-1.95).
Conclusions:
Fracture risk in childhood is related to volumetric BMD, reflecting an influence of determinants of volumetric BMD such as cortical thickness on skeletal fragility. Although bone size per se was not related to fracture risk, we found that children who fracture tend to have a smaller skeleton relative to their overall body size.
The present study comprised 29 adolescents and young adults (15 females, 14 males; aged 14.1-23.9 years) with congenital heart disease (CHD) and focused on the interaction between the biomechanical system and CHD. Individuals were characterized by auxological (height, weight), dynamometric (MIGF, maximal isometric grip force) and mechanograpic parameters (Vmax, maximal velocity; PJF, peak jump force; PJP, peak jump power; time of five stand-ups in chair-rising test). PJF, PJP and MIGF were transformed into height-related SD-scores. MIGF-SDS and PJP-SDS were lower in the CHD patients than in reference individuals. PJP-SDS was lower than PJF-SDS. PJP-SDS was correlated to Vmax (r = 0.62) and to the time of five-stand-ups in chair-rising (r = -0.62). Transcutaneous oxygen saturation and NYHA classes were correlated to Vmax (r = 0.42 and r = -0.57, respectively) and to chair-rising performance (r = -0.60 and r = 0.50, respectively). To conclude, individuals with CHD are characterized by an impaired inter- and intramuscular coordination, which is characterized by a greater decrease in muscular power than muscle force.
In recent years, the issue of low bone density in children and adolescents has attracted much attention. The classical definition of osteoporosis should be valid at any age, yet its practical applicability to children and adolescents remains a matter of debate and there is no consensus on a diagnosis based solely on the BMD value. The clinical relevance of uncomplicated low bone density in the young and its long-term consequences remain difficult to evaluate and there is only preliminary evidence that the BMD value is a predictor of fracture risk in growing subjects. Moreover, the interpretation of densitometric data in the young is difficult because the "normal" BMD values to be used for comparison are continuously changing with age, and in addition, depend on several variables, such as gender, body size, pubertal stage, skeletal maturation and ethnicity. Although Z-score values below -2 are generally considered a serious warning, most bone specialists make a diagnosis of osteoporosis in children and adolescents only in the presence of low BMD and at least one fragility fracture. The scope of this review is limited to presenting a picture of the available knowledge. The literature on fractures will be presented in detail, since fractures are one of the key elements in the debate. There are countless papers on fractures in childhood and adolescence, but very few of them attempt to identify fragility fractures, and still fewer develop the concept of osteoporosis in the young in relation to fractures. The different forms of primary and secondary osteoporosis, the more technical aspects of bone densitometry in pediatrics, and the delicate issue of treatment will be discussed only briefly.
Peripheral quantitative computed tomography (pQCT) has been used in a number of pediatric studies. Reference data for children are primarily limited to the radius. The purpose of this study was to establish normal reference ranges for pQCT measurements of the tibia for children. A cross-sectional sample of healthy, white, non-Hispanic children aged 5-18 years (n=416; 197 boys) was measured at the distal tibia metaphysis and diaphysis by pQCT to assess trabecular and cortical bone, respectively. Differences were determined between and within genders by height for bone geometry, density, and strength. Height-specific normal ranges were calculated, and gender-specific centile curves were generated. A positive, linear relationship was found between tibia cortical bone geometry and strength parameters and height (r2 >or=0.58, p<0.001), with mean values greater for boys than girls (p <or=0.05). Trabecular volumetric bone mineral density values were relatively stable, but greater in boys than girls independent of height or age (p <or=0.01). The reference data for pQCT analyses of the tibia provide additional information on bone size, geometry, and strength in children. pQCT technology provides an additional tool for the evaluation of bone health in young subjects.
Abnormalities in mineral metabolism and changes in skeletal histology may contribute to growth impairment in children with chronic renal failure. Hyperphosphatemia, hypocalcemia, metabolic acidosis, alterations in vitamin D and IGF synthesis and parathyroid gland dysfunction play significant roles in the development of secondary hyperparathyroidism and subsequently, bone disease in renal failure. The recent KDIGO conference has made recommendations to consider this as a systemic disorder (chronic kidney disease-mineral bone disorder) and to standardize bone histomorphometry to include bone turnover, mineralization and volume (TMV). The use of DXA to assess bone mass is controversial in children with chronic renal failure. Questions arise regarding the accuracy of bone measurements and difficulty in data interpretation especially in children with renal failure who are not only growth retarded but often have pubertal delay and osteosclerosis. The validity and feasibility of new modalities of skeletal imaging which can detect changes in both trabecular and cortical bone are currently being investigated in children. The management of mineral abnormalities and bone disease in chronic renal failure is multifactorial. To manage hyperphosphatemia, dietary phosphate restriction accompanied by intake of calcium-free and metal-free phosphate binding agents are widely utilized. Vitamin D analogs remain the primary therapy for secondary hyperparathyroidism, although the use of the less hypercalcemic agents is preferred due to concerns of calciphylaxis and vascular calcification. Future clinical studies are needed to evaluate the long-term effects of calcimimetic agents and bisphosphonate therapy in children with chronic renal failure.