Decline In Bone Strength Research Articles

Identify the Risk Factors of Osteoporosis Knowledge and Practices Regarding Prevention of Osteoporosis among Postmenopausal and Postmenopausal With Breast Cancer Women in Selected Tertiary Care Hospital

Background: Osteoporosis is defined as a decline in bone strength that raises the risk of fracture.Because the number of people in this area is so much higher than those in the osteoporosis range. Morethan 50% of the all the fractures among postmenopausal women, including hip fractures, occur in thisgroup with low density. Due to the lack of awareness about osteoporosis, many post - menopausalwomen do not take preventative actions to protect the osteoporosis.Materials and Methods: The study was conducted using an evaluative method and a non-probabilitypurposive sampling technique. The study was conducted as a descriptive one. A tertiary care hospitalwas chosen for the investigation. 50 postmenopausal women 25 postmenopausal women and 25 postmenopausalwomen with breast cancer), they were included in the study.Result : 14 (28.0%) were between the ages of 46 and 50 years. The high risk was 4 (16.0 %) and themoderate risk was 21(84.0 %) in women with breast cancer. The high risk is 1 (4.0 %) in women withoutca – breast cancer, and the moderate risk is 4 (96.0 %). The majority of postmenopausal women withbreast cancer had average knowledge, with 12 (48.0 %) having an average knowledge, 14 (56.0 %) hadaverage knowledge, and 10 (40.0%) had poor knowledge.The knowledge for postmenopausal womenwithout breast cancer (36.0%) were poor. 3 (12.0%) had good knowledge, whereas 2 (8.0%) had goodknowledge. The overall mean percentage is (40.1%). The majority of postmenopausal women withbreast cancer 18 (72.0%) and 20 (80.0%) had moderate practises for osteoporosis prevention, whereaspostmenopausal women without breast cancer had moderate practises. The overall mean percentage is(58.1%)Conclusion:The findings suggest that an awareness campaign should be conducted among womenduring the post-menopausal period to prevent complications arising due to osteoporosis.

Understanding and Managing Corticosteroid-Induced Osteoporosis.

Glucocorticoids are effective immunosuppressants used in a wide variety of diseases. Their use results in secondary osteoporosis in about 30–50% of chronic glucocorticoid users. Glucocorticoids cause a rapid decline in bone strength within the first 3–6 months mostly due to increased bone resorption by osteoclasts. This is followed by a more gradual loss of bone partly due to decreased osteoblastogenesis and osteoblast and osteocyte apoptosis. The loss of bone strength induced by glucocorticoids is not fully captured by bone mineral density measurements. Other tools such as the trabecular bone score and advanced imaging techniques give insight into bone quality; however, these are not used widely in clinical practice. Glucocorticoid-induced osteoporosis should be seen as a widely preventable disease. Currently, only about 15% of chronic glucocorticoid users are receiving optimal care. Glucocorticoids should be prescribed at the lowest dose and shortest duration. All patients should be counselled on lifestyle measures to maintain bone strength including nutrition and weight-bearing exercise. Pharmacological therapy should be considered for all patients at moderate to high risk of fracture as there is evidence for the prevention of bone loss and fractures with a favourable safety profile. Oral bisphosphonates are the current mainstay of therapy, whereas osteoanabolic agents may be considered for those at highest risk of fracture.

Association of ambient PM2·5 exposure with maternal bone strength in pregnant women from Mexico City: a longitudinal cohort study

SummaryBackgroundPregnancy is associated with deteriorations in maternal bone strength and heightened susceptibility to bone fractures. We aimed to investigate whether ambient particulate matter (PM)2·5 concentrations were associated with bone strength during pregnancy.MethodsIn this longitudinal cohort study, we analysed longitudinal data from women participating in the Programming Research in Obesity, Growth, Environment and Social Stressors (PROGRESS) cohort in Mexico City, Mexico. Eligible women were aged 18 years or older, at less than 20 weeks’ gestation at the time of recruitment, planning to stay in Mexico City for the next 3 years, without heart or kidney disease, did not use steroids or anti-epileptic drugs, were not daily consumers of alcohol, and had access to a telephone. Daily ambient PM2·5 concentrations were estimated from a spatio-temporal model that was based on the individual’s address. Trabecular bone strength was measured using quantitative ultrasound from the radius of the middle finger and cortical bone strength from the proximal phalanx of the middle finger, during the second trimester, third trimester, and 1 and 6 months post partum. Bone strength T scores were modelled with PM2·5 concentrations using linear mixed models and distributed lag models.FindingsAdjusting for multiple exposure windows, each 10 ug/m³ increase in PM2·5 exposure concentrations in the first trimester was associated with a 0·18 SD decrease (95% CI −0·35 to −0·01; p=0·033) in ultrasound speed-of-sound (SOS) T score of trabecular bone strength from the second trimester until 6 months post partum. Similarly, each 10 μg/m³ increase in third trimester PM2·5 exposure was associated with a 0·18 SD decrease (−0·36 to −0·01; p=0·044) in the SOS T score of trabecular bone strength from the third trimester until 6 months post partum. PM2·5 exposure in the first month post partum was associated with a 0·20 SD decline (−0·39 to −0·01; p=0·043) in cortical bone strength until 6 months post partum.InterpretationAmbient PM2·5 exposure during and after pregnancy was associated with diminished trabecular and cortical bone strength. Early pregnancy PM2·5 exposure was associated with a greater decline in bone strength later during pregnancy. Late pregnancy and early post-partum exposures adversely affected the post-partum bone strength recovery. Technological and policy solutions to reduce PM2·5 pollution could improve public health by reducing bone fracture risk.

Fall Prevention and Anti-Osteoporosis in Osteopenia Patients of 80 Years of Age and Older: A Randomized Controlled Study.

ObjectiveTo evaluate the effects of two fall‐prevention and anti‐osteoporotic protocols in elderly patients with osteopenia (OPA).MethodsThe present randomized controlled study included patients with OPA (n =123). The age of these patients was ≥80 years old, with the mean age of 83.54 ± 2.99 years, and the male‐to‐female ratio was 2.97:1.00. Fall‐prevention guidance was given to all patients. Patients in the experiment group (n = 62) orally received 600 mg/d of calcium carbonate, 0.5 μg/d of alfacalcidol, and 70 mg/week of alendronate, while patients in the control group (n = 61) orally received 600 mg/d of calcium carbonate and 0.5 μg/d of alfacalcidol for 18 months. The grip strength, gait speed, bone turnover markers, serum calcium, serum phosphorus, parathyroid hormone (PTH), and bone mineral density were measured, and the Timed Up and Go (TUG) test and the chair rising test (CRT) were performed. Falls, fragility fractures, medication compliance, and side effects of the drugs were recorded.ResultsThe serum levels of bone turnover markers (type I procollagen amino‐terminal peptide [P1NP], type I collagen carboxyl terminal peptide [β‐CTx], and osteocalcin [OC]) decreased, while the bone mineral density of the lumbar spine and bilateral femoral neck increased after treatment in the experiment group (P < 0.05, P < 0.01). The rate of change in bone mineral density of the bilateral femoral neck was higher in the experiment group than the control group (3.43% vs 0.03%, P < 0.05; 2.86% vs −0.02%, P < 0.01). After treatment, the proportion of patients with increased hip T scores in the experiment group (66.1%, 41/62) was significantly higher than the proportion (35.0%, 21/60) in the control group (P = 0.001). The incidence of fall decreased in both groups after treatment compared to that before treatment (54.8% vs 33.9% and 54.1% vs 36.7%, respectively; P < 0.05). The incidence of fragility fractures was lower in the experiment group than the control group (8.1% vs 20.0%, P = 0.057). During the intervention period, the incidence of fragility fractures in patients who did not fall (3.8%, 3/79) was significantly lower than that in patients who fell (32.6%, 14/43) (P = 0.000). The risk of fragility fractures was significantly lower in patients who did not fall compared to patients who fell (relative risk: 0.117, 95% confidence interval: 0.035–0.384).ConclusionThe combination of alendronate sodium with alfacalcidol and calcium can significantly improve the bone mineral density of the lumbar spine and femoral neck. For older patients with OPA, subjectively paying attention to avoiding falls can significantly reduce the risk of fragility fractures.

Pro-inflammatory Cytokines: Cellular and Molecular Drug Targets for Glucocorticoid-induced-osteoporosis via Osteocyte.

Glucocorticoids are widely used to treat varieties of allergic and autoimmune diseases, however, long-term application results in glucocorticoid-induced osteoporosis (GIOP). Inflammatory cytokines: tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) play important regulatory roles in bone metabolism, but their roles in GIOP remain largely unknown. Osteocytes can modulate the formation and function of both osteoblasts and osteoclasts, directly via gap junctions, or indirectly by transferring molecule signaling. Apoptotic osteocytes release RANKL, HMGB1 and pro-inflammatory cytokines to stimulate osteoclastogenesis. Moreover, osteocytes can secrete FGF23 to regulate bone metabolism. Exposure to high levels of GCs can drive osteocyte apoptosis and influence gap junctions, leading to bone loss. GCs treatment is regarded to produce more FGF23 to inhibit bone mineralization. GCs also disrupt the vascular to decrease osteocyte feasibility and mineral appositional rate, resulting in a decline in bone strength. Apoptotic bodies from osteocytes induced by GCs treatment can enhance production of TNF-α and IL-6. On the other hand, TNF-α and IL-6 show synergistic effects by altering osteocytes signaling towards osteoclasts and osteoblasts. In addition, TNF-α can induce osteocyte apoptosis and attribute to a worsened bone quality in GCs. IL-6 and osteocytes may interact with each other. Therefore, we hypothesize that GCs regulate osteocyteogenesis through TNF-α and IL-6, which are highly expressed around osteocyte undergoing apoptosis. In the present review, we summarized the roles of osteocytes in regulating osteoblasts and osteoclasts. Furthermore, the mechanism of GCs altered relationship between osteocytes and osteoblasts/osteoclasts. In addition, we discussed the roles of TNF-α and IL-6 in GIOP by modulating osteocytes. Lastly, we discussed the possibility of using pro-inflammatory signaling pathway as therapeutic targets to develop drugs for GIOP.

Transient peak-strain matching partially recovers the age-impaired mechanoadaptive cortical bone response

Mechanoadaptation maintains bone mass and architecture; its failure underlies age-related decline in bone strength. It is unclear whether this is due to failure of osteocytes to sense strain, osteoblasts to form bone or insufficient mechanical stimulus. Mechanoadaptation can be restored to aged bone by surgical neurectomy, suggesting that changes in loading history can rescue mechanoadaptation. We use non-biased, whole-bone tibial analyses, along with characterisation of surface strains and ensuing mechanoadaptive responses in mice at a range of ages, to explore whether sufficient load magnitude can activate mechanoadaptation in aged bone. We find that younger mice adapt when imposed strains are lower than in mature and aged bone. Intriguingly, imposition of short-term, high magnitude loading effectively primes cortical but not trabecular bone of aged mice to respond. This response was regionally-matched to highest strains measured by digital image correlation and to osteocytic mechanoactivation. These data indicate that aged bone’s loading response can be partially recovered, non-invasively by transient, focal high strain regions. Our results indicate that old murine bone does respond to load when the loading is of sufficient magnitude, and bones’ age-related adaptation failure may be due to insufficient mechanical stimulus to trigger mechanoadaptation.

Body weight and bone/calcium metabolism. Relationship between insulin/glucose metabolism and bone/calcium metabolism.

Recent advances demonstrated that osteoporosis is one of the major complications in diabetes. In Diabetic conditions, both bone material properties and bone microarchitecture are impaired, resulting in the decline in bone strength. Furthermore, bone-derived osteocalcin stimulates insulin secretion, thereby regulates the whole body glucose metabolism. Thus, it was revealed that bone metabolism and glucose metabolism are intimately involved.

Moving toward a prevention strategy for osteoporosis by giving a voice to a silent disease.

A major unmet challenge in developing preventative treatment programs for osteoporosis is that the optimal timing of treatment remains unknown. In this commentary we make the argument that the menopausal transition (MT) is a critical period in a woman’s life for bone health, and that efforts aimed at reducing fracture risk later in life may benefit greatly from strategies that treat women earlier with the intent of keeping bones strong as long as possible. Bone strength is an important parameter to monitor during the MT because engineering principles can be applied to differentiate those women that maintain bone strength from those women that lose bone strength and are in need of early treatment. It is critical to understand the underlying mechanistic causes for reduced strength to inform treatment strategies. Combining measures of strength with data on how bone structure changes during the MT may help differentiate whether a woman is losing strength because of excessive bone resorption, insufficient compensatory bone formation, trabeculae loss, or some combination of these factors. Each of these biomechanical mechanisms may require a different treatment strategy to keep bones strong. The technologies that enable physicians to differentially diagnose and treat women in a preventive manner, however, have lagged behind the development of prophylactic treatments for osteoporosis. To take advantage of these treatment options, advances in preventive treatment strategies for osteoporosis may require developing new technologies with imaging resolutions that match the pace by which bone changes during the MT and supplementing a woman's bone mineral density (BMD)-status with information from engineering-based analyses that reveal the structural and material changes responsible for the decline in bone strength during the menopausal transition.

Age-related changes in bone strength from HR-pQCT derived microarchitectural parameters with an emphasis on the role of cortical porosity

The high resolution peripheral computed tomography (HR-pQCT) technique has seen recent developments with regard to the assessment of cortical porosity. In this study, we investigated the role of cortical porosity on bone strength in a large cohort of women.The distal radius and distal tibia were scanned by HR-pQCT. We assessed bone strength by estimating the failure load by microfinite element analysis (μFEA), with isotropic and homogeneous material properties. We built a multivariate model to predict it, using a few microarchitecture variables including cortical porosity.Among 857 Caucasian women analyzed with μFEA, we found that cortical and trabecular properties, along with the failure load, impaired slightly with advancing age in premenopausal women, the correlations with age being modest, with |rage| ranging from 0.14 to 0.38. After the onset of the menopause, those relationships with age were stronger for most parameters at both sites, with |rage| ranging from 0.10 to 0.64, notably for cortical porosity and failure load, which were markedly deteriorated with increasing age. Our multivariate model using microarchitecture parameters revealed that cortical porosity played a significant role in bone strength prediction, with semipartial r2=0.22 only at the tibia in postmenopausal women.In conclusion, in our large cohort of women, we observed a small decline of bone strength at the tibia before the onset of menopause. We also found an age-related increase of cortical porosity at both scanned sites in premenopausal women. In postmenopausal women, the relatively high increase of cortical porosity accounted for the decline in bone strength only at the tibia.

Alterations in Different Indices of Skeletal Health after Prolonged Residency at High Altitude

The aim of this study was to evaluate the effect of prolonged residency at high altitude (HA) on different indices of bone health in sea level (SL) residents staying at an altitude of 3450 m for 4 months to 1 year. The assessment of bone health parameters included multisite quantitative bone speed of sound (SOS), and markers of bone metabolism such as serum alkaline phosphatase (ALP), bone specific alkaline phosphatase (BAP), urinary deoxypyridinoline (DPD), C-terminal propeptide of type I collagen (CICP), N-telopeptide of type I collagen (NTX), and hormonal regulators such as 25-hydroxy vitamin D3 (25Vit D), intact parathyroid hormone (i-PTH), and cortisol. The body weight in all the age groups was significantly lower at HA as compared to SL values. Prolonged residency at HA led to a significant decline in bone strength in terms of SOS, both at radius and phalanx. There was a significant increase in circulating Ca and ALP levels. Serum i-PTH and 25VitD levels decreased significantly. Significant decreases were also observed in CICP and BAP, bone formation markers, and serum NTX, DPD/Cr ratio, markers of bone resorption. These observations suggest that prolonged residency under hypoxic environment is associated with a decline in both bone formation and bone resorption markers, reflecting a lower bone turnover at HA.

Bone properties of the humeral head and resistance to screw cutout.

Surgical treatment of fractures involving the proximal humeral head is hampered by complications. Screw cutout is the major pitfall seen in connection with rigid plating. We have exploited a bony explanation for this phenomenon.Materials and Methods:We examined the convex surface of the humeral head looking at the density and the topographical strength of the subchondral bone using mechanical testing of bone cylinders harvested from the humeral head. We also studied the osseous architecture of the subchondral bone and thickness of the boneplate of the humeral head using a 3-dimensional serial sectioning technique.Results:The bone strength and bone density correlated well and revealed large regional variations across the humeral head. Bone strength and stiffness of the trabecular bone came to a maximum in the most medial anterior and central parts of the humeral head, where strong textural anisotropy was also found. We found in particular a lower bone strength and density in the posterior and inferior regions of the humeral head. A rapid decline in bone strength within a few mm below a relatively thin subchondral plate was also reported.Clinical Relevance:We have in this paper explored some of the most important factors connected with screw stability at the cancellous bone level. We discovered large variations in bone density and bone strength across the joint surface rendering certain areas of the humeral head less suitable for screw placement. The use of rigid plate constructs with divergent screw directions will predictably place screws in areas of the humeral head comprising low density and low strength cancellous bone. New concepts of plates and plating techniques for the surgical treatment of complex fractures of the proximal humerus should take bone distribution, strength, and architecture into account.

ONO-5334, a cathepsin K inhibitor, improves bone strength by preferentially increasing cortical bone mass in ovariectomized rats

This study compared the effects of ONO-5334, a cathepsin K inhibitor, with those of alendronate on bone mass and strength in ovariectomized rats. Ovariectomy resulted in significant elevation in urinary deoxypyridinoline and plasma C-terminal cross-linking telopeptide of type I collagen (CTX) 8 weeks after surgery. Peripheral quantitative computed tomography analysis showed that total, trabecular, and cortical bone mineral content (BMC) decreased in the proximal tibia, which was paralleled with a significant decline in bone strength. Treatment with ONO-5334 (0.12, 0.6, 3 or 15 mg/kg) once daily for 8 weeks dose-dependently restored the decrease in total BMC and bone mineral density (BMD) in the proximal tibia and suppressed urinary deoxypyridinoline and plasma CTX levels. Alendronate (1 mg/kg, once daily) also fully restored these bone mass parameters. Separate analysis of trabecular and cortical bones, however, showed that ONO-5334 only partially restored trabecular BMD and BMC at 15 mg/kg, whereas alendronate fully restored these parameters. On the other hand, ONO-5334 increased both cortical BMD and BMC with an effect more potent than that of alendronate. Bone geometric analysis indicated that ONO-5334 at 15 mg/kg decreased endosteal circumference without affecting periosteal circumference, resulting in marked increase in cortical thickness. Interestingly, the effects of ONO-5334 on bone strength parameters were more prominent than those of alendronate, although the two test compounds had a similar effect on total BMC. Taken together, our results indicate that ONO-5334 has pharmacological characteristics different from those of alendronate and may offer a unique therapy for patients with osteoporosis.

Early High Calcium and Phosphorus Intake by Parenteral Nutrition Prevents Short‐term Bone Strength Decline in Preterm Infants

Very premature newborns have an increased risk of low bone mass and metabolic bone disease. Most longitudinal studies report a significant decline in bone strength in the first weeks after birth. The aim of the study was to evaluate whether higher early calcium (Ca) and phosphorus (P) intake delivered by parenteral nutrition (PN) can prevent bone strength decline in preterm infants, within the first weeks after birth. This was a randomized controlled trial of consecutively admitted neonates born with ≤ 33 weeks of gestational age, assigned to receive either Ca 45 mg · kg⁻¹ · day⁻¹ (low dose [LD]) or Ca 75 mg · kg⁻¹ · day⁻¹ (high dose [HD]) by PN. P was added to the PN solutions at a fixed Ca:P ratio (mg) of 1.7:1. Bone strength was assessed by the speed of sound (SOS) using the quantitative ultrasound method. Measurements were performed weekly from birth until discharge. Low bone strength (SOS < 10th centile of reference values) was the main outcome. Eighty-six infants were enrolled, 40 assigned to LD group and 46 to HD group. Mean (standard error) gestational age was 29.6 weeks (2.1) and birth weight was 1262 g (0.356). In the HD group, the SOS values never fell below those recorded at birth and, up to the sixth week of life, low bone strength was significantly less frequent as compared with that in the LD group, in spite of progressive reduction in parenteral mineral intake and/or establishment of full enteral feeding. Early assigned parenteral intake of Ca 75 mg · kg⁻¹ · day⁻¹ and P 44 mg · kg⁻¹ · day⁻¹ significantly contributed to preventing short-term bone strength decline in preterm infants.

Mechanical contributions of the cortical and trabecular compartments contribute to differences in age-related changes in vertebral body strength in men and women assessed by QCT-based finite element analysis

The biomechanical mechanisms underlying sex-specific differences in age-related vertebral fracture rates are ill defined. To gain insight into this issue, we used finite element analysis of clinical computed tomography (CT) scans of the vertebral bodies of L3 and T10 of young and old men and women to assess age- and sex-related differences in the strength of the whole vertebra, the trabecular compartment, and the peripheral compartment (the outer 2 mm of vertebral bone, including the thin cortical shell). We sought to determine whether structural and geometric changes with age differ in men and women, making women more susceptible to vertebral fractures. As expected, we found that vertebral strength decreased with age 2-fold more in women than in men. The strength of the trabecular compartment declined significantly with age for both sexes, whereas the strength of the peripheral compartment decreased with age in women but was largely maintained in men. The proportion of mechanical strength attributable to the peripheral compartment increased with age in both sexes and at both vertebral levels. Taken together, these results indicate that men and women lose vertebral bone differently with age, particularly in the peripheral (cortical) compartment. This differential bone loss explains, in part, a greater decline in bone strength in women and may contribute to the higher incidence of vertebral fractures among women than men. © 2011 American Society for Bone and Mineral Research.

Mechanical consequences of different scenarios for simulated bone atrophy and recovery in the distal radius

Metabolic bone diseases such as osteoporosis usually cause a decrease in bone mass and a deterioration of bone microarchitecture leading to a decline in bone strength. Methods to predict bone strength in patients are currently based on bone mass only. It has been suggested that an improved prediction of bone strength might be possible if structural changes are taken into account as well. In this study we evaluated which structural parameters (other than bone mass) are the best predictors for changes in bone mechanical properties of the human radius after different bone atrophy scenarios and whether the original strength of the affected bone can be recovered if bone loss is restored by thickening of the remaining structures. To answer these questions, a human radius was measured with a microcomputer tomography scanner to extract the full three-dimensional architecture of the distal radius at an isotropic resolution of 80 μm. Eight models with modified bone architecture were created and the mechanical variations due to these modifications were studied using microfinite element (micro-FE) simulations. In four models mass was lowered by 20%, either by reducing cortical thickness, trabecular thickness, or number of trabeculae or by overall thinning of structures. In the other four models bone mass was restored to the original value using a trabecular bone thickening procedure. The micro-FE analyses revealed that most load was carried by the cortical bone. For this reason, bone strength was affected most in the reduced cortical thickness model. For the same reason, the trabecular bone atrophy scenarios, all of which affected bone strength in a very similar way, resulted in less dramatic bone strength reduction. The restoration of bone mass did not recover the original bone strength. These findings demonstrate that the importance of different parameters for the prediction of bone strength also depends on the mechanical loading. This could explain why results of earlier studies on the importance of structural parameters can be inconsistent and site-dependent.

Vertebral structure and strength in vivo and in vitro.

The incidence of vertebral fragility fractures has increased 2-4-fold during the past 30 years and the rate of increase is the same for both men and women. To arrest or reverse this increase, thorough understanding of normal, age-related changes in bone structure and strength is crucial. The human vertebral body is constructed to provide maximum strength with minimum bone mass. The strength is the sum of bone size, cortical thickness, trabecular architecture, and bone mass. With age, all these factors change due to the remodeling process, but the decline in bone strength is much more pronounced than the decline in mass. In individuals with very low bone mass, this discrepancy between mass and strength is even more marked. Structural studies have all shown a disruption of the trabecular network with age--mainly caused by perforation of horizontal supporting struts. These changes begin in the vertebral center. Later, a decline in cortical thickness is disclosed. The biomechanical consequence of this is a 4-6-fold decrease in vertebral strength during normal aging. As the structural changes cannot be reversed, it is difficult to increase bone strength by therapeutic regimens. Focus should therefore be placed on prevention. Three avenues are suggested: (1) to use the vast amount of existing biological data in a computer model to increase the understanding of the relationship among bone structure, mass, and strength, and to help identify the intervention regimens offering the best prospects of success; (2) to investigate characteristics of load-bearing trabecular bone that does not fracture; and (3) to focus more on life-style factors.

Effect of husbandry system on broken bones and bone strength in hens

The effects of rearing system, forced moulting and three different layer housing systems on broken bones and bone strength, were examined in hens at the end of lay. Weak bones and broken bones were more common in battery hens which had been reared to point of lay on deep litter rather than in cages. The incidence of old breaks was greater in perchery birds (14 per cent) than in tiered terrace birds (5 per cent), and there was also a difference between their incidence in two types of perchery design (17 per cent and 11 per cent). Moulting was associated with a transient decline in bone strength, followed by an increase in strength during the second lay.

Trauma type, age, and gender as determinants of hip fracture.

We determined the trauma type of femoral neck and trochanteric fractures in men and women aged greater than or equal to 20 years in 19, 128 fractures reported to a computerized medical information register during 1972-1981. We found that the earlier known exponential increase of fracture incidence by age started in early adulthood rather than during middle age. An age-related increase was found for each type of injury as well, although the incidence of fractures resulting from severe trauma increased less than that of fractures associated with moderate trauma. The incidence of low-energy fractures in men as well as in women displayed a constant increase rate with age from young adulthood on, impugning the widely held belief that the menopause is a significant risk factor for fractures. The dominating risk factor for proximal femoral fracture in adults appears to be age, irrespective of the cause of injury, with a chronological decline in bone strength as the most likely cause of the exponential increase in the fracture incidence during adult life.