Components Of Bone Strength Research Articles

Unique Effects of Energy versus Estrogen Deficiency on Components of Bone Strength in Exercising Women

Exercising women with menstrual disturbances are at risk for poor bone health due to hypoestrogenism. Energy deficiency often instigates menstrual dysfunction resulting in metabolic adaptations that independently threaten bone. Women experiencing both an energy and estrogen deficiency face an exacerbated risk to bone health. PURPOSE: To describe volumetric bone mineral density (vBMD), bone geometry, and estimated bone strength in exercising women (n=50) grouped by energy status (energy replete (EnR: n=25); energy deficient (EnD: n=25)) and estrogen status (estrogen replete (E2R: n=24); estrogen deficient (E2D: n=26)) resulting in four groups: EnR+E2R (n=12), EnR+E2D (n=13), EnD+E2R (n=12), EnD+E2D (n=13). METHODS: Energy status was defined by the ratio of measured to predicted resting energy expenditure (mREE/pREE). Estrogen status was defined by self-reported menstrual status and confirmed by assessment of urinary metabolites of reproductive hormones over one menstrual cycle or 28 day monitoring period. Peripheral quantitative computed tomography assessed vBMD, bone geometry, and estimated bone strength at the radius and tibia. RESULTS: The groups were similar in age (21 ± 0.4 years), gynecological age (8 ± 0.5 years), height (165.7 ± 0.9 cm), and weight (57.7 ± 1.2 kg). At the proximal tibia, EnD women exhibited significantly lower total vBMD, cortical area, and cortical thickness and greater endosteal circumference than EnR women (p≤0.020). E2D women exhibited significantly lower total and cortical vBMD and bone strength index (BSI) and greater total and trabecular area (p≤0.040) at the distal radius and lower cortical vBMD and thickness (p≤0.019) at the proximal radius compared to E2R women. EnD+E2D women had significantly lower total and trabecular vBMD at the distal tibia and radius and total vBMD and cortical thickness at the proximal tibia compared to EnR+E2D women (p≤0.048). CONCLUSION: Energy versus estrogen status affected bone differently and effects were site-specific. Women with both an energy and estrogen deficiency experienced the most adverse bone adaptations. Treating energy deficiency in exercising women may improve reproductive health, in turn addressing the unique contributions of energy status versus estrogen status to bone health. Supported by US DoD (PR054531).

Technology Insight: noninvasive assessment of bone strength in osteoporosis

Fractures that result from osteoporosis are an enormous and growing concern for public health systems; as the population ages, the number of fractures worldwide will double or triple in the next 50 years. The ability of a bone to resist fracture depends not only on the amount of bone present, but also on the spatial distribution of the bone mass, the cortical and trabecular microarchitecture, and the intrinsic properties of the materials that comprise the bone. Although low bone mineral density is one of the strongest risk factors for fracture, a number of clinical studies have demonstrated the limitations of using measurements of areal bone mineral density by dual-energy X-ray absorptiometry to assess fracture risk and to monitor responses to therapy. As a result, new, noninvasive imaging techniques that are capable of assessing various components of bone strength are being developed. These techniques include three-dimensional assessments of bone density, geometry and microarchitecture, as well as integrated measurements of bone strength by engineering analyses. Although they show strong potential, further development and validation of these techniques is needed to define their role in the clinical management of individuals with osteoporosis.

Schizophrenia, Osteoporosis, and an Examination of the Risk of Fractures in Patients Receiving ECT

Schizophrenic patients may be at increased risk of osteoporosis for several reasons: they may smoke and drink in excess, exercise little, consume insufficient calcium and vitamin D in their diet, get insufficient exposure to sunlight, receive antipsychotic medications that raise serum prolactin, and/or lose calcium through polydipsia and polyuria. 1,2 Hummer et al 3 reported femoral and lumbar spine osteoporosis in 4% and 11% (respectively) of young schizophrenic men (mean age, 35 years); interestingly, women were unaffected. Reviewing the literature, Meyer and Lehman 2 found 8 studies which provided data on bone mineral density (BMD) in men with schizophrenia. In every study in which information was provided, patients with schizophrenia had significantly lower BMD than nonschizophrenic controls or population norms, with the prevalence of osteopenia ranging from 40%Y72%. Osteoporosis is a marker for adverse orthopedic outcomes such as chronic low back pain or fractures. However, BMD, the standard technique used to diagnose osteoporosis, only provides data about the quantity of mineral in bone, which is only one component of bone strength; BMD provides no information about bone microarchitecture and bone turnover, which can also influence the fracture risk. 4 This may be why BMD is a weak marker of fracture risk. 5 Of note, BMD norms to define osteoporosis in men may underestimate the true magnitude of osteoporosis and hence the orthopedic risk. 6 Is there evidence for an increased risk of adverse orthopedic outcomes in schizophrenic men? A PubMed search conducted on May 23, 2007, using the search terms ‘schizophrenia’ and ‘fracture’, yielded 49 publications of which only two were distantly relevant: one 7 found an increased incidence of fractures in polydipsic schizophrenics relative to nonpolydipsic controls; the other 8 found poorer orthopedic outcomes after hip fracture in schizophrenics as compared with nonpsychiatric controls. There were no epidemiological studies at all. We however separately identified a study in which 25% of 141 nondemented elderly psychotic inpatients in a geriatric unit had records of at least one nontraumatic osteoporotic fracture; two-thirds of this sample was diagnosed with schizophrenia. 9 The study, unfortunately, did not present a diagnosis-wise break-up of the fracture rate. Does the lack of literature imply that, osteopenia and osteoporosis notwithstanding, schizophrenic patients are not at increased risk of orthopedic morbidity? Or are schizophrenic patients indeed at increased risk, and has the subject has been neglected in research? 10 It is hard to say. However, the subject may have some relevance to practitioners of ECT. In many parts of the world, schizophrenia is an important indication for ECT 11Y13 ; yet, there are no reports or warnings from these geographical zones to suggest a higher risk of fractures in schizophrenic patients. And, there is a reasonably large body of literature on ECT in patients with schizophrenia 14Y16 ; yet, there is no mention of fracture as an adverse effect of ECT in any of the studies. Perhaps the risks associated with osteopenia and osteoporosis are diminished by seizure modification; if so, the possibility remains that schizophrenic patients are especially COMMENTARY

Severity of vertebral fracture reflects deterioration of bone microarchitecture

Bone microarchitecture, a component of bone strength, is generally measured on transiliac bone biopsy samples. The objective of this study was to determine whether assessment of four grades of vertebral fracture severity could serve as a noninvasive surrogate marker for trabecular bone volume and microarchitecture. Baseline vertebral fracture severity was determined by semiquantitative assessment of spine radiographs from 190 postmenopausal women with osteoporosis. Bone-structure indices were obtained by 2D histomorphometry and 3D microcomputed tomography (CT) analyses. Significance of differences was determined after adjusting for age, height, and lumbar spine bone mineral density. There were significant (P < 0.05) trends in decreasing bone volume, trabecular number, and connectivity, and increasing trabecular separation with greater vertebral fracture severity. Histomorphometric bone volume was 25 and 36% lower (P < 0.05) in women with moderate and severe fractures than in women with no fractures, respectively. Compared with women without fractures, women with mild, moderate, and severe fractures had lower (P < 0.05) microCT bone volume (23, 30, and 51%, respectively). Microarchitectural deterioration was progressively worse in women with increasing severity of vertebral fractures. We conclude that assessment of vertebral fracture severity is an important clinical tool to evaluate the severity of postmenopausal osteoporosis.

The Effects of Antifracture Therapies on the Components of Bone Strength: Assessment of Fracture Risk Today and in the Future

To summarize the current knowledge regarding the impact of the most common antifracture medications on the various determinants of bone strength. Relevant English-language articles acquired from Medline from 1966 to January 2005 were reviewed. Searches included the keywords bone AND 1 of the following: strength, remodeling, microcrack, structure, mineralization, collagen, organic, crystallinity, osteocyte, porosity, diameter, anisotropy, stress risers, or connectivity AND alendronate, estrogen, etidronate, hormone replacement therapy, parathyroid hormone, risedronate, OR teriparatide. Abstracts from relevant conference proceedings were also reviewed for pertinent information. Antiresorptive therapies increase bone strength through decreasing bone turnover. This lower bone turnover results in a higher mean mineralization and decreases the number of active resorption pits within bone at any given time. These resorption pits are speculated to be areas of focal weakness and a higher number of them would, if all other things were equal, result in greater fragility. Parathyroid hormone therapy increases the rate of bone remodeling, which introduces many resorption pits, but this source of strength loss is thought to be compensated by rapid increases in bone mass. Both the antiresorptives, particularly bisphosphonates, and the parathyroid hormone therapy increase bone strength; however, the changes that are elicited to achieve this differ significantly.

Important Determinants of Bone Strength

Osteoporosis is a systemic skeletal disorder characterized by compromised bone strength that predisposes individuals to increased fracture risk. Bone strength is determined by its material and structural properties. Bone mineral density (BMD) is a useful tool for diagnosis; however, this parameter provides information regarding only the quantity of mineral in bone, which is only one component of bone strength. Osteoporosis treatments have been shown to have beneficial effects on bone turnover, microarchitecture, and/or mineralization, all of which can help account for the reductions in fracture risk above and beyond changes in BMD. Newer noninvasive imaging methods are being developed that assess bone strength independent of BMD, and these methods should improve the assessment of fracture risk and response to treatment. These imaging methods are not currently available for routine clinical use, and therefore, clinicians need to continue for now to rely on surrogate markers of bone fragility, including BMD, prevalent fracture, and other important risk factors for fracture.

The use of bisphosphonates in the treatment of osteoporosis

The bisphosphonates alendronate and risedronate, given orally once weekly, are the cornerstone of treatment of postmenopausal osteoporosis, as well as of male and secondary osteoporosis. They reduce significantly the risk of vertebral and nonvertebral fractures; their effects appear early, within 6-12 months, and appear to be sustained. Several questions remain unanswered, however. In addition, data on a new bisphosphonate became available in 2004. The optimal duration of treatment has not been clearly established. Long-term data with alendronate are now available, indicating a persistence of alendronate effects on bone mineral density and bone turnover markers several years after stopping treatment given for 5 years. Whether these effects translate into sustained reduction of fractures needs to be further analyzed. Because of their efficacy, bisphosphonate use has been explored in other forms of osteoporosis, such as after androgen deprivation therapy for prostatic cancer. The challenge of long-term compliance with treatment of osteoporosis has triggered the use of intermittent bisphosphonate. The effects of intermittent oral and intravenous ibandronate on bone mineral density, bone turnover, and fractures have been recently reported. The mechanism by which bisphosphonates improve bone strength is not yet fully understood but probably involves complex effects on different components of bone strength, such as microarchitecture.

Vibration and Components of Bone Strength

Vibration and Components of Bone Strength

Vibration and Components of Bone Strength

Vibration and Components of Bone Strength

Genetics of osteoporosis.

Osteoporosis is a common multifactorial disorder of reduced bone mass. The disorder in its most common form is generalized, affecting the elderly, both sexes, and all racial groups. Multiple environmental factors are involved in the pathogenesis. Genes also play a major role as reflected by heritability of many components of bone strength. Quantitative phenotypes in bone strength in the normal population do not conform to a monogenetic mode of inheritance. The common form of osteoporosis is generally considered to be a polygenic disorder arising from the interaction of common polymorphic alleles at quantitative trait loci, with multiple environmental factors. Finding the susceptibility genes underlying osteoporosis requires identifying specific alleles that coinherit with key heritable phenotypes in bone strength. Because of the close correspondence among mammalian genomes, identification of the genes underlying bone strength in mammals such as the mouse is likely to be of major assistance in human studies. Identification of susceptibility genes for osteoporosis is one of several important approaches toward the long-term goal of understanding the molecular biology of the normal variation in bone strength and how it may be modified to prevent osteoporosis. As with all genetic studies in humans, these scientific advances will need to be made in an environment of legal and ethical safeguards that are acceptable to the general public.

Determinants and assessment of bone strength

Osteoporosis is a systemic skeletal disease characterised by low bone mass and micro-architectual deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture. Bone mineral density is a major component of bone strength and is predictive of future fracture risk. It is possible to measure BMD non-invasively at various skeletal sites using dual energy absorptiometry. Techniques such as quantitative ultrasound and magnetic resonance imaging also provide additional information on other facets of skeletal strength, although at present further research is required before they are incorporated into routine clinical practice. There is currently much interest in identifying factors involved in the determination of BMD and bone strength. Based on this knowledge, it may be possible to identify subjects who will have low BMD and will therefore be at risk of future fracture. Lifestyle interventions and drug treatments could therefore be targeted to "high risk" subjects to reduce the burden of osteoporotic fractures.