Why the ISMNI and the Utah paradigm? Their role in skeletal and extraskeletal disorders

Besides bringing problems, aging can let the mind's eye see more clearly than before, and it can let us express ourselves better. As age, experience and common sense examine today's skeletal medicine and surgery two questions keep popping up: A) How did we fail?; B) How to make it better? The Utah paradigm of skeletal physiology and the seminal ISMNI offer some answers, but exploiting them faces problems. Problem #1: By 1960 all clinicians and physiologists 'knew' (as the ancients 'knew' this world is flat) that effector cells controlled solely by nonmechanical agents explain all skeletal physiology and disorders ('effector cells' include osteoblasts, osteoclasts, chondroblasts and fibro-blasts). Or, nonmechanical agents -->cell level -->organ and intact subject. Adding later-discovered information to that 1960 view led to the Utah paradigm, which reveals the formerly hidden tissue-level 'dimension' of skeletal physiology. It builds on this idea: (mechanical + nonmechanical agents) -->(tissue level + cell level) --> organ and intact subject. The paradigm assigns great influence of neuromuscular physiology and physical activities on skeletal architecture, strength and mechanical competence. It also exposes flaws in many older views so controversies arise. Problem #2: The Utah paradigm and Wegner's concept of plate tectonics in geology seem alike in that each is valid but came before its time, so others fought it. They differ in this: The fight about Wegner's idea is over, but for the Utah paradigm and the ISMNI it just began. Hence more controversies. Nevertheless: A growing minority realizes that paradigm provides a far better base to build on than its antecedents, and since it keeps evolving as more evidence comes in it could endure for some decades. Yet very few realize this: It and the ISMNI have important implications for fields besides biomechanics and orthopaedics. Examples include anatomy, cardiovascular disease, dentistry, endocrinology, family medicine, gastroenterology, general surgery, genetics, gerontology, gynecology, maxillofacial surgery, neurology, neurosurgery, nutrition, ophthalmology, pathology, pediatrics, physical medicine and rehabilitation, plastic surgery, radiology, rheumatology, space and sports medicine, and urology. Quite a list! For the italicized questions above this article offers answers, of which its conclusion distills an essence.     

The benefit of combining non-mechanical agents with mechanical loading: a perspective based on the Utah Paradigm of Skeletal Physiology

The Utah Paradigm of Skeletal Physiology with its key component, the mechanostat hypothesis, suggest plausible explanations of some of the tissue-level changes occurring from combining selected non-mechanical agents (anabolic and anti-resorptive/( re)modeling agents) with mechanical loading (osteogenic exercise) to increase bone mass and strength. The evidence for combining selected anabolic agents like parathyroid hormone, prostaglandin E(2), growth hormone, etc. with mechanical loading can increase bone mass is strong. Anabolic agents influence loading-related bone formation changes in a permissive manner and modulate (increase) the responsiveness of bone tissue to mechanical loading by changing thresholds for bone formation and resorption. However, any beneficial effect of combining selected anti-resorptive/(re)modeling agents like estrogen with loading is marginal, especially in adult skeletons. Postulated changes in modeling and remodeling thresholds (set points) and known direct effects on bone cells by non-mechanical agents may explain the observed tissue-level changes associated with large and minor increases in bone mass. Although the pharmaceutical industry has avoided considering osteogenic loading in the treatment of osteoporosis, a methodical dose-response study of anabolic agents combined with loading should: (1) provide opportunities for therapeutic intervention to imitate or enhance the osteogenic response to loading in order to correct osteopenias; (2) provide the potential to diminish the dosage of drugs required to induce bone formation in ways that enhanced efficacy and reduced any side effects; and (3) improve the quality of life and reduce the risk of falls by improving balance, gait speed and muscle strength with a non-mechanical agent like GH that could improve both muscle and bone mass and strength. Lastly, more studies are needed which determine bone strength instead of only "mass" in aged skeletons so one can assess how effective such treatments would reduce the risk of fracture in the clinic.     

Growth hormone and osteoporosis: an overview of endocrinological and pharmacological insights from the Utah paradigm of skeletal physiology

Multidisciplinary advances in skeletal physiology offer a new paradigm for the effects of growth hormone (GH) and other agents on bone and osteoporosis. The still-evolving Utah paradigm of skeletal physiology supplements earlier ideas with later discovered roles of the skeleton's tissue-level 'nephron equivalents' and muscle strength in skeletal development, physiology and disorders. This article summarizes how these factors could influence the effects of GH on bone strength and bone 'mass', and the use of GH in the treatment of osteoporoses. Although the cellular and molecular biological mechanisms involved remain obscure, the associated cascades of cellular, genetic and biochemical processes and molecules should offer many opportunities to find or design agents that have medically useful effects on bone and muscle without giving rise to unwanted side-effects.     

Bone mass increase in puberty: what makes it happen?

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 strength of bone must be adapted to muscle strength (the functional muscle-bone unit). The Utah paradigm of skeletal physiology [J Hum Biol 1998;10:599-605] provides a model of bone development that describes how bone structure is regulated by local mechanical effects that can be adjusted by the effects of hormones. The DONALD (Dortmund Nutritional and Anthropometric Longitudinally Designed) study analysed the interaction between the muscle and bone systems in males and females before and during puberty. This study found that differences between the genders in bone adaptation during puberty are at least partly driven by the influence of oestrogen in females. Testosterone seems to have no direct relevant effect on bone during puberty, but may be implicated in the greater amount of muscle mass achieved in boys compared with girls.     

Why should many skeletal scientists and clinicians learn the Utah paradigm of skeletal physiology?

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.     

Coming changes in accepted wisdom about "osteoporosis"

Here a voice from the past suggests 28 changes that will affect how people study, manage, classify and think about "osteoporoses" today. Those changes depend mainly on two things: (i) "Connecting the dots" between diverse evidence and ideas from many fields and sources in order to find larger "messages" hidden in mountains of often poorly-organized lesser details, (ii) and features of the still-evolving Utah paradigm of skeletal physiology. That paradigm sums contributions from many people who worked in many fields for over 100 years. In one view it is the most important development in skeletal physiology since Rudolf Virchow and others realized approximately 150 years ago that cells provide the basis for human physiology and diseases. This article emphasizes the above messages instead of the details. The messages affect ideas about the nature, pathogenesis, diagnosis, classification, study and management of osteopenias and osteoporoses, as well as some roles of muscle, drugs, hormones, other agents and fatigue damage, in those disorders. Those larger messages also concern how to classify "osteoporosis fractures", how to define bone health, the choice of absorptiometric methods for noninvasive evaluations of bones, osteopenias and muscle strength, and new criteria for selecting patient cohorts for "risk-of-fracture" analyses and in searches for genetic roles in "osteoporoses". Finally, those larger messages identify many new targets for research that should prove unusually useful in clinical and pharmaceutical domains and work.     

On the strength-safety factor (SSF) for load-bearing skeletal organs

The strength of healthy postnatal mammalian load-bearing bones, growth plates, joints, fascia, ligaments and tendons exceeds the minimum strength needed to keep voluntary mechanical usage from breaking or rupturing them or from causing arthroses. Thus, they have a strength-safety factor (SSF). Some general features of the physiology in the Utah paradigm of skeletal physiology can explain two things: (i) Why load-bearing bones should have an SSF, (ii) and why its numerical value should approximately 6 in healthy young adult mammals. The number and kinds of studies and facts that revealed those two things for load-bearing bones do not yet exist for the extraosseous load-bearing organs that are made with cartilage and collagenous tissue. However, clinical-pathologic observations suggest the latter organs' SSFs should depend on features analogous to those that create SSFs for load-bearing bones. If so, the physiology on which bone's SSF depends could suggest directions for future studies of the SSF determinants of load-bearing extraosseous organs. Biomechanicians currently favor strain above stress when discussing biomechanical roles in the functional adaptations of bones to mechanical loading. However, an SSF is best expressed in stress terms, so a Table in this article provides corresponding strain/stress/unit-load values for bone's three important thresholds, and for its ultimate strength.     

On the pathogenesis of osteogenesis imperfecta: some insights of the Utah paradigm of skeletal physiology

The pathogenesis of osteogenesis imperfecta (OI) baffled physiologists and physicians for over a century. Most past efforts to explain it depended heavily on cell and molecular biology and on changes in the material properties of affected bones (an old idea that OI patients could not make enough bone erred). To such views the still-evolving Utah paradigm of skeletal physiology can add a model for bone and bones that depends on errors in three genetically-determined features. The errors include, 1,2) elevated 'set points' of the strain-dependent thresholds that help to control how lamellar bone modeling and remodeling adapt bone strength, architecture and 'mass' to the voluntary loads on load-bearing bones; 3) and a reduced modeling-rate limit for the appositional rate of the lamellar bone formation drifts that can increase bone strength, outside bone diameters, cortical and trabecular thickness, and bone 'mass'. If only abnormalities #1,#2 occurred, that should limit the eventual strength, architecture and 'mass' of load-bearing bones, while if only #3 occurred that should prolong or delay how long it took to achieve the above limits, but without changing them. Equally, in driving from New York to Boston, stopping at New Haven would prevent reaching Boston no matter how rapidly one drove (a limited trip). But by not stopping one could reach Boston by driving very slowly (a prolonged but not a limited trip). This model concerns general features of bone and bones in OI that would need study and explanation at the tissue, cellular and molecular-biologic levels. Other places and people must discuss any devils in the details, as well as collagenous tissue, auditory, dental and other problems in OI, and the effects of treatment on the above features.     

Trabecular architecture can remain intact for both disuse and overload enhanced resorption characteristics

The paradigm that bone metabolic processes are controlled by osteocyte signals have been the subject of investigation in many recent studies. One hypothesis is that osteoblast formation is enhanced by these signals, and that osteoclast resorption is enhanced by the lack of them. Reduced, or absent, osteocyte signaling can be an effect of reduced mechanical loading (disuse) or of defects in the canalicular network, due to microcracks. This would mean that bone is resorbed precisely there where it is mostly needed. In our study, we addressed this apparent contradiction. The purpose was to investigate how alternative strain-based local stimuli for osteoclasts to resorb bone would affect remodeling and adaptation of the trabecular architecture. For this purpose, a computer-simulation model was used, which couples morphological and mechanical effects of local bone metabolism to changes in trabecular architecture and density at large. Six resorption characteristics were studied in the model: (I) resorption occurs spatially random, (II) resorption is enhanced or (III) strongly enhanced where there is disuse, (IV) resorption is enhanced or (V) strongly enhanced where there are high strains, i.e. overload, and (VI) resorption is enhanced where there is disuse and where there are high strains. Results showed that the rates of structural adaptation to alternative loading were higher for disuse-controlled resorption than for overload-controlled resorption. Architecture and mass remained stable for all cases except (V) in which the structure deteriorated as in osteoporotic bone. We conclude that, given the potential of osteoblasts to form bone in highly strained areas, based on signals from osteocytes, osteoclast resorption can normally be compensated for.     

The mechanism of transduction of mechanical strains into biological signals at the bone cellular level

As appears from the literature, the majority of bone researchers consider osteoblasts and osteoclasts the only very important bony cells. In the present report we provide evidence, based on personal morphofunctional investigations, that such a view is incorrect and misleading. Indeed osteoblasts and osteoclasts undoubtedly are the only bone forming and bone reabsorbing cells, but they are transient cells, thus they cannot be the first to be involved in sensing both mechanical and non-mechanical agents which control bone modeling and remodeling processes. Briefly, according to our view, osteoblasts and osteoclasts represent the arms of a worker; the actual operation center is constituted by the cells of the osteogenic lineage in the resting state. Such a resting phase is characterized by osteocytes, bone lining cells and stromal cells, all connected in a functional syncytium by gap junctions, which extends from the bone to the vessels. We named this syncytium the Bone Basic Cellular System (BBCS), because it represents the only permanent cellular background capable first of sensing mechanical strains and biochemical factors and then of triggering and driving both processes of bone formation and bone resorption. As shown by our studies, signalling throughout BBCS can occur by volume transmission (VT) and/or wiring transmission (WT). VT corresponds to the routes followed by soluble substances (hormones, cytokines etc.), whereas WT represents the diffusion of ionic currents along cytoplasmic processes in a neuron-like manner. It is likely that non-mechanical agents first affect stromal cells and diffuse by VT to reach the other cells of BBCS, whereas mechanical agents are first sensed by osteocytes and then issued throughout     

Hierarchical relationship between bone traits and mechanical properties in inbred mice

Abstract Osteoporotic fracture incidence and underlying risk factors like low peak bone mass are heritable, but the genetic basis of osteoporosis remains poorly understood. Based on beam theory, stating that mechanical properties of a structure depend on both the amount and quality of the constituent materials, we investigated the relationship between whole bone mechanical properties and a set of morphological and compositional traits in femurs of eight inbred mouse strains. K-means cluster analysis revealed that individual femora could be classified reliably according to genotype based on the combination of bone area (tissue amount), moment of inertia (tissue distribution), and ash content (tissue quality). This trait combination explained 66–88% of the inter-strain variability in four whole-bone mechanical properties that describe all aspects of the failure process, including measures of brittleness. Stiffness and maximum load were functionally associated with cortical area, while measures of brittleness were associated with ash content. In contrast, work-to-failure was not directly related to a single trait but depended on a combination of trait magnitudes. From these findings, which were entirely consistent with established mechanical theory, we developed a hierarchical paradigm relating the mechanical properties that define bone fragility with readily measurable phenotypic traits that exhibit strong heritability. This paradigm will help guide the search for genes that underlie fracture susceptibility and osteoporosis. Moreover, because the traits we examined are measurable with non-invasive means, this approach may also prove directly applicable to osteoporosis risk assessment.     

Cellular and molecular aspects of muscle growth,adaptation and ageing

Although major advances have been made over the past few decades in prosthetic dentistry, deterioration in oral function and altered facial appearance are still common accompaniments of ageing. Molecular biology methods now allow us to understand these age-related changes at the level of gene expression. Muscle loss as well as bone loss still present major problems, the magnitude of which increases as the age profile of our society changes. Both muscle and bone tissue respond to mechanical signals for which bone depends on muscle and for muscle, stretch has been shown to be important as it induces protein synthesis and an increase in girth as well as length of the muscle fibres. The latter involves the production of more sarcomeres in series so that the jaw muscles adapt to a new functional length following changes in vertical dimension of occlusion. It also determines the postural position of the lower jaw. In our investigations into the control of muscle mass we have recently cloned a growth factor which is expressed in exercised and/or overloaded muscles. This comes in two forms: an autocrine or local form and a paracrine or systemic form. Both growth factors influence muscle growth markedly and it is probable that the systemic type is also involved in maintenance of bone. The discovery of these growth factors provides the mechanisms by which mechanical signals are transduced into chemical signals that in turn regulate gene expression and protein synthesis.     

Mechanisms of human osteopenia and some peculiarities of bone metabolism in weightlessness conditions

Systematically results and new analysis data on the investigation of human bone system in space flight, the orbital station Mir and International Space Station, are presented. The bone mineral density, bone mineral content, identified as bone mass and body composition using dual energy X-ray absorptiometry were measured. Theoretically, an expected bone mass loss in trabecular tissue of lower skeletal half may by described as a quickly developing but reversible osteopenia and considered as evidence of functional adaptation of bone tissue to the changing mechanical load. A hypothesis of main mechanisms of osteopenia in microgravity is presented. High individual variability of bone mass losses and stability of individual pattern of correlation between bone mass losses in different skeletal segments were found. It is not possible to identify the relationship between bone mass losses and duration of space missions. Therefore it is not a sufficient ground to calculate the probability of reaching the critical level of bone demineralization by prolonged space flight. The same relates to the probability of prognosis of bone quality changes. There is data about dual energy X-ray absorptiometry that is insufficient for this prognosis. The main direction of investigations is presented which might optimize the interplanetary mission from the point of view of skeletal mechanical functions preservation.     

The importance of mechanical loading in bone biology and medicine

This paper discusses the premise that the skeleton is primarily a mechanical organ, and reviews the reasons that mechanical factors play a major role in bone biology. It begins by considering three basic observations: (1) Galileo's observation that bone proportions become more robust as the species' overall size increases; (2) da Vinci's observation that larger structures are inherently weaker than smaller structures subjected to the same stress; and (3) the general observation that each unit of bone mass provides structural support for about 15 units of soft tissue organ mass. Together, these observations lead to the concept that it can be advantageous to minimize bone mass, consistent with constraints on other factors. This premise is discussed here in relation to the phenomenon of bone remodeling, which is seen to serve two purposes: the adjustment of bone mass and geometry to maintain peak bone strains at their maximum tolerable values, and the continual removal of fatigue damage produced at those strain levels. Finally, it is observed that bone remodeling apparently originated approximately 250 million years ago when the first vertebrates of substantial size became weight-bearing on land, suggesting that mechanical forces associated with weight-bearing were instrumental in the evolution of bone remodeling.     

Comparative analysis of changes in the skeleton of cosmonauts in long-term orbital flights and the possibilities of prediction for interplanetary missions

The results of long-term investigations of the bone system of humans during space flights (SFs) on board the Mir orbital station (OS) and international space station (ISS) using osteodensitometry are summarized. Comparative analysis of the results showed the absence of significant differences in changes in the bone mass (BM) in the crew members of both OSs. Theoretically, the expected bone mass losses in the trabecular bone structures of the lower part of the body in the process of a SF (five to seven months) are interpreted in some cases as quickly developing, but reversible, osteopenia and generally interpreted as the evidence of bone functional adaptation to altering mechanical loads on the skeleton. The high individual variability of changes and the stability of the individual character of the BM alteration ratio in different skeletal segments irrespective of the OS type are shown. Owing to the aforementioned individual features, it is not possible to establish a strict relationship between BM changes and the duration of space missions, and, therefore, there is no good reason for calculating the probability of achieving the critical demineralization level when the duration of an SF increases to 1.5–2 years. The probability of prediction of changes in the bone quality (structure) is still less, which, together with BM losses, determines the risk of fractures, and osteodensitometry for such an analysis is insufficient. The main directions of the studies, which could optimize the development of the interplanetary expedition project from the point of view of maintenance of the mechanical function of the skeleton, are considered.     

Analysis of bone architecture sensitivity for changes in mechanical loading, cellular activity, mechanotransduction, and tissue properties

Bone has an architecture which is optimized for its mechanical environment. In various conditions, this architecture is altered, and the underlying cause for this change is not always known. In the present paper, we investigated the sensitivity of the bone microarchitecture for four factors: changes in bone cellular activity, changes in mechanical loading, changes in mechanotransduction, and changes in mechanical tissue properties. The goal was to evaluate whether these factors can be the cause of typical bone structural changes seen in various pathologies. For this purpose, we used an established computational model for the simulation of bone adaptation. We performed two sensitivity analyses to evaluate the effect of the four factors on the trabecular structure, in both developing and adult bone. According to our simulations, alterations in mechanical load, bone cellular activities, mechanotransduction, and mechanical tissue properties may all result in bone structural changes similar to those observed in various pathologies. For example, our simulations confirmed that decreases in loading and increases in osteoclast number and activity may lead to osteoporotic changes. In addition, they showed that both increased loading and decreased bone matrix stiffness may lead to bone structural changes similar to those seen in osteoarthritis. Finally, we found that the model may help in gaining a better understanding of the contribution of individual disturbances to a complicated multi-factorial disease process, such as osteogenesis imperfecta.     

The effect of zinc and phytoestrogen supplementation on the changes in mineral content of the femur of rats with chemically induced mammary carcinogenesis

The aim of this study was to assess skeletal effects of zinc or zinc with phytoestrogen (resveratrol or genistein) supplementation in an animal model of rats with DMBA-induced mammary carcinogenesis. The changes in bone parameters such as the length and mass were examined, as well as the changes in concentrations of selected minerals: calcium, magnesium, zinc, iron and phosphorus. Moreover, the investigations focused on finding the differences between the levels of iron and zinc in other tissues: the liver, spleen and serum of the examined rats.Fifty-six female Sprague–Dawley rats, 40 days old, were divided into four groups, regardless of the diets: standard (77 mg Zn kg/food), zinc (4.6 mg/mL via gavage), zinc (4.6 mg/mL) plus resveratrol (0.2 mg/kg bw), and zinc (4.6 mg/mL) plus genistein (0.2 mg/kg bw) for a period from 40 days until 20 weeks of age. The study rats were also treated with 7,12-dimethyl-1,2-benz[a]anthracene (DMBA) to induce mammary carcinogenesis.The applied diet and the advanced mammary cancer did not affect macrometric parameters of the rats’ bones, but they strongly affected their mineral content. It was found that mammary cancer, irrespectively of the applied diet, significantly modified the iron level in the femur, liver, spleen and serum of the examined rats. In addition, zinc supplementation significantly lowered the levels of calcium, magnesium and phosphorus in the femur of rats with mammary cancer as compared with respective levels in the control group. So, it was found that additional supplementation with zinc, which is generally considered to be an antioxidant, with the co-existing mammary carcinoma, increased the unfavorable changes as concerns the stability of bone tissue. The appropriate combination of zinc and phytoestrogens (resveratrol or genistein) could help prevent or slow bone loss associated with a range of skeletal disorders in breast cancer.     

Contribution of postnatal collagen reorientation to depth-dependent mechanical properties of articular cartilage

The collagen fibril network is an important factor for the depth-dependent mechanical behaviour of adult articular cartilage (AC). Recent studies show that collagen orientation is parallel to the articular surface throughout the tissue depth in perinatal animals, and that the collagen orientations transform to a depth-dependent arcade-like structure in adult animals. Current understanding on the mechanobiology of postnatal AC development is incomplete. In the current paper, we investigate the contribution of collagen fibril orientation changes to the depth-dependent mechanical properties of AC. We use a composition-based finite element model to simulate in a 1-D confined compression geometry the effects of ten different collagen orientation patterns that were measured in developing sheep. In initial postnatal life, AC is mostly subject to growth and we observe only small changes in depth-dependent mechanical behaviour. Functional adaptation of depth-dependent mechanical behaviour of AC takes place in the second half of life before puberty. Changes in fibril orientation alone increase cartilage stiffness during development through the modulation of swelling strains and osmotic pressures. Changes in stiffness are most pronounced for small stresses and for cartilage adjacent to the bone. We hypothesize that postnatal changes in collagen fibril orientation induce mechanical effects that in turn promote these changes. We further hypothesize that a part of the depth-dependent postnatal increase in collagen content in literature is initiated by the depth-dependent postnatal increase in fibril strain due to collagen fibril reorientation.     

Anthropometric and biomechanical characteristics of body segments in persons with spinal cord injury

People with spinal cord injury (SCI) experience bone and muscle loss in their paralyzed limbs that is most rapid and severe in the first 3 years after injury. Restoration of mechanical loading through therapeutic physical activity may potentially slow or reverse post-SCI bone loss, however, therapeutic targets cannot be developed without accurate biomechanical models. Obesity is prevalent among SCI population, and it alters body composition and further affects parameters of these models. Here, clinical whole body dual-energy X-ray absorptiometry data from people with acute (n = 39) and chronic (n = 61) SCI were analyzed to obtain anthropometric parameters including segment masses, center of mass location, and radius of gyration for both obese and non-obese individuals. Chronic SCI was associated with higher normalized trunk mass of 3.2%BW and smaller normalized leg mass of 1.8%BW in males, but no significant changes in segment centers of mass or radius of gyration. People with chronic SCI had 58.6% lean mass in the trunk, compared to 66.6% lean mass in those with acute SCI (p = 0.01), with significant changes in all segments. Obesity was associated with an increase in trunk mass proportion of 3.1%BW, proximal shifts in thigh and upper arm center of mass, and changes to thigh and shank radius of gyration. The data presented here can be used to accurately represent the anthropometrics of SCI population in biomechanical studies, considering obesity and injury duration.