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PubMed2005

Effect of bone mineral density and amorphous diamond coatings on insertion torque of bone screws.

In this study, the potential of high-quality amorphous diamond (AD) coatings in reducing the torque and failures of bone screws was studied. Torque values were recorded for 32 stainless steel screws, 2.7 or 3.5 mm in diameter and 60 mm in length. Half of the screw sets were coated with the AD coating before installing in predrilled holes of human cadaveric femoral bone samples. The bone samples were selected from two groups of four persons with mean ages of 34 years (range 25-41 years) and 75 years (range 73-77 years), respectively. The bone mineral density (BMD) values of the samples were determined exactly at the screw insertion site by peripheral quantitative computed tomography (pQCT). In the mechanical tests, insertion and removal torques were measured. BMD had a significant effect on insertion torque; the maximum torque (adjusted with respect to the screw diameter) was significantly higher for the young bone than for the old bone (p < 0.05). By using a polished AD coating, insertion torque was decreased even up to 50% in comparison with the screws without coating. The results suggest that AD coating provides a stable, smooth surface and reduces the risk of screw failures.

Adult↗
PubMed2004

Biological laser printing of genetically modified Escherichia coli for biosensor applications.

One of the primary requirements of cell- or tissue-based sensors is the placement of cells and cellular material at or near the sensing elements of the device. The ability to achieve precise, reproducible and rapid placement of cells is the focus of this study. We have developed a technique, biological laser printing or BioLP, which satisfies these requirements and has advantages over current technologies. BioLP is capable of rapidly depositing patterns of active biomolecules and living cells onto a variety of material surfaces. Unlike ink jet or manual spotting techniques, this process delivers small volume (nl to fl) aliquots of biomaterials without the use of an orifice, thus eliminating potential clogging issues and enabling diverse classes of biomaterials to be deposited. This report describes the use of this laser-based printing method to transfer genetically-modified bacteria capable of responding to various chemical stressors onto agar-coated slides and into microtiter plates. The BioLP technology enables smaller spot sizes, increased resolution, and improved reproducibility compared to related technologies.

Biological Assay↗
PubMed2005

An amperometric glucose biosensor prototype fabricated by thermal inkjet printing.

The prototype of an amperometric glucose biosensor was realized by thermal inkjet printing using biological and electronic water-based inks, containing a glucose oxidase (GOD) from Aspergillus niger and the conducting polymer blend poly(3,4-ethylenedioxythiophene/polystyrene sulfonic acid) (PEDOT/PSS), respectively. The biosensor was fabricated microdepositing PEDOT/PSS and GOD, in sequence, on ITO-glass, by a commercial inkjet printer, with the help of a commercial software. High density microdots matrices were so-realized, with a calculated resolution of about 221 x 221 dpi (dot per inch). By means of a rapid and easy assay it was demonstrated that no activity loss occurred upon the printing of GOD, despite of the use of a thermal printhead. The device was encapsulated in a semipermeable membrane of cellulose acetate, applied by dip-coating, in order to prevent dissolution of the enzyme and/or PEDOT/PSS in water. The preliminary response of the electrode was measured in an aqueous glucose solution in the presence of ferrocenemethanol (FeMeOH) as a mediator, and resulted linear up to 60 mM in glucose. The best sensitivity value achieved was 6.43 microAM(-1) cm(-2) (447 nAM(-1) U(-1) cm(-2)). The characteristics of the device, and the possible performance improvements have been analyzed and discussed. The reported findings indicate that inkjet printing could be a viable instrument for the easy construction of a working biosensor via direct digital design using biological and conductive polymer based inks. Such an approach may be seen as an example of "biopolytronics".

Aspergillus niger↗
PubMed2005

Fabricating optical fiber imaging sensors using ink jet printing technology: a pH sensor proof-of-concept.

We demonstrate the feasibility of using Drop-on-Demand microjet printing technology for fabricating imaging sensors by reproducibly printing an array of photo-polymerizable sensing elements, containing a pH sensitive indicator, on the surface of an optical fiber image guide. The reproducibility of the microjet printing process is excellent for microdot (i.e. micrometer-sized polymer) sensor diameter (92.2+/-2.2 microm), height (35.0+/-1.0 microm), and roundness (0.00072+/-0.00023). pH sensors were evaluated in terms of pH sensing ability (< or =2% sensor variation), response time, and hysteresis using a custom fluorescence imaging system. In addition, the microjet technique has distinct advantages over other fabrication methods, which are discussed in detail.

Biosensing Techniques↗
PubMed2004

Discrimination between cases of hip fracture and controls is improved by hip structural analysis compared to areal bone mineral density. An ex vivo study of the femoral neck.

In vivo bone densitometry is affected by measurement inaccuracies arising from the assumptions made about soft tissue and marrow composition. This study tested the hypothesis that section modulus (SM, a measure of bending resistance) when measured ex vivo, would discriminate cases of hip fracture from controls better than areal bone mineral density (aBMD). The biopsies were from (n = 22, female) subjects that had suffered an intracapsular hip fracture. The control material (n = 24, female) was from post-mortem subjects. Serial peripheral quantitative computed tomography (pQCT) 1-mm thick cross-sectional images of femoral neck previously embedded in methacrylate were obtained with the Densiscan 1000 pQCT densitometer and matched for lateral location. The image voxels were converted to units of bone mass, which were then used to derive the section modulus. The data were used to derive means from which receiver operating characteristic (ROC) curves could be generated. The area under the curves (AUC) showed that discrimination between the fracture cases and controls was better for SM than aBMD [SM: AUC = 0.83 (95% confidence interval: 0.71, 0.96), aBMD: AUC = 0.70 (0.54, 0.85); P = 0.034]. To simulate the forces experienced during a sideways fall, the model's neutral axis was rotated by 210 degrees. The results for section modulus were predictable from those at 0 degrees (r(2) = 0.97). We conclude that biomechanical analysis of the distribution of bone within the femoral neck may offer a marked improvement in the ability to discriminate patients with an increased risk of intracapsular fracture. Progress towards implementing this form of analysis in clinical densitometry should improve its diagnostic value, but may depend in part on better image resolution and more accurate corrections for the variability between subjects in regional soft tissue composition.

Absorptiometry, Photon↗
PubMed2004

Gene therapy with human recombinant osteoprotegerin reverses established osteopenia in ovariectomized mice.

Osteoporosis is a chronic condition that is typically treated by the long-term repeated administration of antiresorptive agents. Gene therapy has the potential to deliver protein-based antiresorptive agents without the need for repeated administration. Osteoprotegerin (OPG) is a naturally occuring protein that prevents bone resorption by inhibiting osteoclast formation, function and survival. We tested whether adeno-associated virus (AAV) could deliver OPG at levels that are sufficient to reverse established osteopenia in ovariectomized (OVX) mice without causing liver toxicity. Tibial bone mineral density (BMD) was measured by peripheral quantitative computed tomography (pQCT) in 12-week-old CDF1 mice prior to OVX or sham surgery. Six weeks later, BMD was significantly reduced in OVX mice compared to sham controls or pre-surgery values. Sham and OVX mice were then injected once IV with an AAV vector carrying cDNA for recombinant hOPG (AAV-OPG) or beta-galactosidase (AAV-betaGal). BMD and bone histomorphometry were assessed 10 weeks after treatment. A single injection of AAV-OPG led to the appearance of human OPG (hOPG) in the serum of mice within 7 days, and high serum levels of hOPG were maintained for the duration of the 10-week study. At the end of the study, OVX mice given AAV-OPG had significantly greater tibial BMD compared to age-matched OVX animals given AAV-betaGal. In sham-operated mice, AAV-OPG also significantly increased tibial BMD compared to AAV-betaGal. The increased BMD in AAV-OPG animals was accompanied by significantly increased bone volume and significantly reduced osteoclast surfaces in the proximal tibial metaphysis. Liver histology was normal, and circulating activities of hepatocyte cytosolic enzymes were unaffected by AAV exposure. In an accompanying experiment, young (3-4 weeks) C57BL/6 mice treated once IV with AAV-OPG maintained pharmacologically active levels of OPG in serum for at least 16 months. In summary, a single AAV-OPG treatment reversed established osteopenia in OVX mice without evidence of liver toxicity. AAV delivery appears to be a safe and effective method for producing sustained systemic exposure to OPG.

Animals↗
PubMed2004

Relationship between the duration of paralysis and bone structure: a pQCT study of spinal cord injured individuals.

The aim of the present study was to describe bone loss of the separate compartments of trabecular and cortical bone, as well as changes in bone geometry of a large number of spinal cord injured (SCI) individuals. Eighty-nine motor complete spinal cord injured men (24 tetraplegics and 65 paraplegics) with a duration of paralysis of between 2 months and 50 years were included in the study. Distal epiphyses and midshafts of the femur, tibia, and radius were measured by peripheral quantitative computed tomography. The same measurements were performed in a reference group of 21 healthy able-bodied men of the same age range. In the femur and tibia, bone mass, total and trabecular bone mineral density (BMDtot and BMDtrab, respectively) of the epiphyses, as well as bone mass and cortical cross-sectional area of the diaphyses, showed an exponential decrease with time after injury in the spinal cord injured subjects. The decreasing bone parameters reached new steady states after 3-8 years, depending on the parameter. Bone mass loss in the epiphyses was approximately 50% in the femur and 60% in the tibia, while the shafts lost only approximately 35% in the femur and 25% in the tibia. In the epiphyses, bone mass was lost by reducing BMD, while in the shaft bone mass was lost by reducing cortical wall thickness, a process achieved by endosteal resorption advancing at a rate of about 0.25 mm/year within the first 5-7 years after injury. Except for a slight transient decrease in cortical BMD of the femoral and tibial shaft during the first 5 years after the spinal cord lesion, cortical BMD of the spinal cord injured subjects was found to be at reference values. Bone parameters of the radial epiphysis in paraplegic subjects showed no deficits compared to the reference group. Furthermore, a trend for an increased radial shaft diameter suggests periosteal apposition as a consequence of increased loading of the arms.

Adult↗
PubMed2004

Determinants and heterogeneity of mechanical competence throughout the thoracolumbar spine of elderly women and men.

Vertebral fractures represent the hallmark of osteoporosis. Here, we test the hypotheses that (sub)cortical bone strength and density predict failure better than trabecular core strength and density, and that elderly women display lower failure stress of thoracic vertebrae than men. We examined the vertebral bodies T3 to L5 in 39 spines from elderly donors (23 women; 16 men; age 79 +/- 11 years). Peripheral quantitative computed tomography was used to measure total, trabecular, and (sub)cortical bone density. Mechanical tests were performed in functional spinal units, planoparallel sections of vertebrae, trabecular cores, and (sub)cortical ring specimens. The failure stress decreased with descending vertebral level. Failure stress was highest for the (sub)cortical rings and planoparallel sections and lowest for the trabecular core. The failure stress did not differ significantly between men and women. Mechanical strength of the functional unit was more strongly correlated with the strength of the (sub)cortical ring (r = 0.78) than with that of the trabecular core (r = 0.62). However, total density was more highly correlated with mechanical strength of the same and remote vertebrae (r = 0.63) than trabecular (r = 0.50) or (sub)cortical density (r = 0.36), respectively. The results show that vertebral strength is similar in elderly women and men. Strength of (sub)cortical bone provides significantly better prediction of strength of functional spinal units than that of the trabecular core. However, total density predicts functional segment failure stress with higher accuracy than (sub)cortical or trabecular density and is thus recommended for predicting fracture strength clinically.

Aged↗
PubMed2004

The deficiency of immunoregulatory receptor PD-1 causes mild osteopetrosis.

Recently, the involvement of immune responses in metabolic bone disease and/or local bone destruction has received much attention. Cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), a member of the immunoglobulin (Ig) superfamily, negatively regulates T cell activation. The deficiency of CTLA-4 induces profound osteopenia with an increase in osteoclastogenesis, suggesting the important role of activated T cells in osteoclastogenesis. Programmed death-1 (PD-1) is the newly identified immunoregulatory receptor, which also belongs to the Ig superfamily. Both CTLA-4 and PD-1 are induced on activated T cells, however, there are no reports linking PD-1 with osteoclasts. In the present study, we have examined the bone phenotype in PD-1-deficient mice PD-1-/- and the role of PD-1 in osteoclastogenesis and osteoclast function. Both trabecular and cortical bone mineral densities of tibia were significantly increased, as observed in peripheral quantitative computed tomography (pQCT), at 12 weeks of age in PD-1-/- mice. Histomorphometric analysis of the PD-1-/- mice and the age-matched controls at 12 weeks of age showed a 2-fold increase in bone volume (BV/TV) with a 55% decrease in osteoclast number (N.Oc/BS). Bone formation indices were similar in both groups. The number of soluble receptor activator of nuclear factor kappaB ligand (sRANKL)-induced osteoclast-like cells (OCLs) derived from the PD-1-deficient splenocytes was significantly decreased (by 25%). On the other hand, PD-1 deficiency did not affect the bone-resorbing activity of mature osteoclasts. Our results suggest that PD-1 deficiency reduces osteoclastogenesis resulting in an osteopetrotic phenotype. Identical members of the Ig superfamily, CTLA-4 and PD-1, which negatively regulate immune responses, may differentially affect osteoclastogenesis and bone remodeling.

Animals↗
PubMed2004

Three children with lower limb fractures and a mineralization defect: a novel bone fragility disorder?

In this report, we describe three unrelated children with an apparently novel bone fragility disorder that is associated with an idiopathic mineralization defect. Recurrent lower limb fractures started with weight bearing. The patients had none of the phenotypic, radiological, or histomorphometric features classically associated with known bone fragility disorders such as osteogenesis imperfecta (OI), idiopathic juvenile osteoporosis (IJO), or mild autosomal dominant osteopetrosis. Radiologically, there was increased metaphyseal trabeculation, normal to increased cortical thickness, and no evidence of rickets or osteomalacia. Areal and volumetric bone mineral density (BMD) of the lumbar spine did not show any major alteration. Peripheral quantitative computed tomography of the radius showed elevated cortical thickness and total and trabecular volumetric bone mineral density in one patient. Qualitative histology of iliac bone biopsy specimens showed a paucity of the birefringent pattern of normal lamellar bone. Quantitative histomorphometric analysis demonstrated osteomalacia with a prolonged mineralization lag time in the presence of a decreased mineral apposition rate. There was no biochemical evidence of abnormal calcium or phosphate metabolism. Type I collagen mutation analysis was negative. We conclude that this is a bone fragility disorder of moderate severity that tends to cause fractures in the lower extremities and is associated with the accumulation of osteoid due to an intrinsic mineralization defect. The pathogenetic basis for this disorder remains to be elucidated.

Adolescent↗
PubMed2004

Genetic variation in femur extrinsic strength in 29 different inbred strains of mice is dependent on variations in femur cross-sectional geometry and bone density.

The femurs from groups of mice from 29 different inbred strains were characterized to study the genetic variations in bone parameters. For these analyses, we used peripheral quantitative computed tomography to assess bone size and density in addition to three-point bend testing to assess bone mechanical properties. Highly significant differences between inbred strains were found for all size, density, and mechanical parameters measured (P < 0.0001). Correcting femoral cross-sectional geometry values or bone mechanical properties values for body weight or femur length reduced but did not eliminate the variations in bone geometry or bone mechanical properties. Mice of similar body size had as much as a 40% difference in the midshaft total area of the femur. Regression analysis suggested that 50.9% of the variation in maximum load among strains was related to variations in section modulus, i.e., cross-sectional geometry, 21.5% was related to variations in material bone density, and 27.7% to variations in quality. These components were further analyzed to show that 3.9-27.8% of the variation in maximum load was related to adaptation to mechanical stress. These findings indicate that there is a significant genetic variation in the femur cross-sectional area, density, and mechanical properties between inbred mouse strains. These studies identify inbred mouse strains suitable for future studies identifying genes regulating bone geometry and mechanical properties.

Animals↗
PubMed2004

Impaired bone resorption in cathepsin K-deficient mice is partially compensated for by enhanced osteoclastogenesis and increased expression of other proteases via an increased RANKL/OPG ratio.

Previous reports indicate that mice deficient for cathepsin K (Ctsk), a key protease in osteoclastic bone resorption, develop osteopetrosis due to their inability to properly degrade organic bone matrix. Some features of the phenotype of Ctsk knockout mice, however, suggest the presence of mechanisms by which Ctsk-deficient mice compensate for the lack of cathepsin K. To study these mechanisms in detail, we generated Ctsk-deficient (Ctsk-/-) mice and analyzed them at the age of 2, 7, and 12 months using peripheral quantitative computed tomography, histomorphometry, resorption marker measurements, osteoclast and osteoblast differentiation cultures, and gene expression analyses. The present study verified the previously published osteopetrotic features of Ctsk-deficient mice. However, these changes did not exacerbate during aging indicating the absence of Ctsk to have its most severe effects during the rapid growth period. Resorption markers ICTP and CTX were decreased in the media of Ctsk-/- osteoclasts cultured on bone slices indicating impaired bone resorption. Ctsk-/- mice exhibited several mechanisms attempting to compensate for Ctsk deficiency. The number of osteoclasts in trabecular bone was significantly increased in Ctsk-/- mice compared to controls, as was the number of osteoclast precursors in bone marrow. The mRNA levels for receptor activator of nuclear factor (kappa)B ligand (RANKL) in Ctsk-/- bones were increased resulting in increased RANKL/OPG ratio favoring osteoclastogenesis. In addition, expression of mRNAs of osteoclastic enzymes (MMP-9, TRACP) and for osteoblastic proteases (MMP-13, MMP-14) were increased in Ctsk-/- mice compared to controls. Impaired osteoclastic bone resorption in Ctsk-/- mice results in activation of osteoblastic cells to produce increased amounts of other proteolytic enzymes and RANKL in vivo. We suggest that increased RANKL expression mediates enhanced osteoclastogenesis and increased protease expression by osteoclasts. These observations underline the important role of osteoblastic cells in regulation of osteoclast activity and bone turnover.

Animals↗
PubMed2005

Regional differences in cortical bone mineral density in the weight-bearing long bone shaft--a pQCT study.

This study used a multislice peripheral quantitative computed tomography (pQCT) to measure volumetric BMD (vBMD) and cortical thickness for investigating regional adaptation in lower tibial shaft in 72 healthy postmenopausal women aged 47-60. Tomographic slices were analysed on four distinct cortical regions: the anterior, posterior, medial and lateral cortical wall. One-way analysis of variance (ANOVA) test was used to compare the vBMD in the four regions. The results showed that the posterior cortex had the highest vBMD (1923 +/- 135.3 mg/cm(3)), significantly (P < 0.001) higher than the anterior cortex (1805 +/- 110.6 mg/cm(3)), medial cortex (1863 +/- 103.6 mg/cm(3)) and lateral cortex (1815 +/- 111.6 mg/cm(3)); whereas there was no significant difference (P > 0.05) between the medial and lateral cortices located near the neutral plane of bending. The anterior cortex had the greatest thickness (2.56 +/- 0.47 mm), significantly (P < 0.001) greater than that of the posterior cortex (2.11 +/- 0.27 mm), medial cortex (2.20 +/- 0.39 mm) and lateral cortex (2.03 +/- 0.29 mm). The vBMD of the posterior cortex was a significant 6.5% higher than that of the anterior cortex (P < 0.001); whereas the anterior cortical thickness was a significant 21.3% greater than that of the posterior cortex (P < 0.001). There was no linear relationship found between cortical vBMD and cortical thickness measured at the four cortical regions (r = 0.086, P > 0.05). In conclusion, the regional differences, with higher vBMD found in posterior cortex, might be a result of mechanical adaptation, which caused the posterior cortex to sustain higher compressive loading than the anterior tensile cortex during the landing phase in the gait cycles of individuals. Nevertheless, regional geometric adaptation in anterior cortical thickness might be adapted to accommodate for the reduced vBMD and to reduce the bending stress in this region.

Bone Density↗
PubMed2005

Retinoid-induced bone thinning is caused by subperiosteal osteoclast activity in adult rodents.

Excess of Vitamin A (retinol) and related compounds (retinoids) induces bone fragility and is associated with increased hip fracture incidence in humans. Yet, their impact on the adult skeleton has been studied in relatively little detail. It is assumed that they induce generalized bone loss and decrease long-bone thickness due to reduction of radial bone growth. Here we characterized early skeletal responses of adult rodents to retinoid treatment, revealing novel aspects of retinoid action on the mature skeleton. The retinoid Ro 13-6298, given subcutaneously for 4 days, induced bone loss in the hind limbs of 12- and 56-week-old rats and of 15-week-old mice. In vivo monitoring of bone mass and geometry changes by peripheral quantitative computed tomography demonstrated that bone mass decline was due to subperiosteal cortical bone loss, which induced a shrinkage of bone diameter, whilst cancellous bone mass was preserved. We observed that the native retinoic acid isomer all-trans RA induced an identical pattern of bone loss. Histomorphometric evaluation revealed that increased subperiosteal osteoclastic bone resorption caused the cortical bone destruction. Interestingly, bone resorption was suppressed in cancellous bone, which was in agreement with reduced in vitro formation of osteoclasts from bone marrow cells that were derived from the proximity of cancellous bone. The retinoid-induced increase in subperiosteal bone resorption could be blocked by bisphosphonate as direct potent inhibitor of osteoclast action, but not by estradiol. Retinoid treatment induced a reduction of bone-forming surfaces at the subperiosteal site, but not in cancellous bone. In vitro osteoblast performance was also reduced or unchanged, depending on the cellular system used and assay type/duration. In conclusion, our studies revealed that the impact of retinoids on bone is highly bone-compartment-specific at early treatment phases. Furthermore, we showed that bone diameter shrinks in the adult skeleton after retinoid treatment due to subperiosteal osteoclastic bone resorption. Thus, retinoid-induced bone thinning is not only due to reduced radial bone growth as previously assumed. Our findings might explain why high intake of retinol is associated with increased hip fracture risk in the elderly and suggest a therapy to prevent such potential negative effects.

Animals↗
PubMed2005

Muscle atrophy and bone loss after 90 days' bed rest and the effects of flywheel resistive exercise and pamidronate: results from the LTBR study.

Muscle atrophy and bone loss pose substantial problems for long-term space flight and in clinical immobilization. We therefore tested the efficacy of flywheel resistive exercise and pamidronate to counteract such losses. Twenty five young healthy males underwent strict bed rest with -6 degrees head-down tilt for 90 days. Subjects were randomized into an exercise group that practiced resistive exercise with a 'flywheel' (FW) device every 2-3 days, a pamidronate group (Pam) that received 60 mg pamidronate i.v. 14 days prior to bed rest and a control group (Ctrl) that received none of these countermeasures. During the study, Ca(++) and protein intake were controlled. Peripheral quantitative computed tomography (pQCT) was used to assess bone mineral content (BMC) and muscle cross sectional area (mCSA) of calf and forearm. Measurements were taken twice during baseline data collection, after 28 and after 89 days bed rest, and after 14 days recovery. On the same days, urinary Pyridinoline excretion and serum levels of alkaline phosphatase, Ca(++) and PTH were measured. Pre-study exercise habits were assessed through the Freiburg questionnaire. Losses in calf mCSA were significantly reduced in FW (Ctrl: -25.6% +/- 2.5% Pam: -25.6% +/- 3.7%, FW: -17.3% +/- 2.7%), but not in the forearm mCSA (Ctrl: -6.4% +/- 4.33%, Pam: -7.7% +/- 4.1%, FW: -7.6% +/- 3.3%). Both diaphyseal and epiphyseal BMC losses of the tibia were mitigated in Pam and FW as compared to Ctrl, although this was significant only at the diaphysis. Inter-individual variability was significantly greater for changes in BMC than in mCSA, and correlation of BMC losses was poor among different locations of the tibia. A significant positive correlation was found between change in tibia epiphyseal BMC and serum cortisol levels. These findings suggest that both countermeasures are only partly effective to preserve BMC (FW and Pam) and mCSA (FW) of the lower leg during bed rest. The partial efficacy of flywheel exercise as well as the bones' response to unloading per se underlines the importance of mechanical stimuli. The huge variability of BMC changes, however, suggests that other factors affect changes in whole-bone strength following acute mechanical disuse.

Adult↗
PubMed2005

Maturity- and sex-related changes in tibial bone geometry, strength and bone-muscle strength indices during growth: a 20-month pQCT study.

During growth, bone strength is conferred through subtle adaptations in bone mass and geometry in response to muscle forces. Few studies have examined the changes in bone geometry, strength and the bone-muscle strength relationship across maturity in boys and girls. Our aims were to describe (i) 20-month changes in bone geometry and strength at the tibial midshaft across three maturity groups of boys and girls, (ii) differences in these adaptations between sexes at the same approximate level of maturity and (iii) the bone-muscle strength relationship across maturity groups of boys and girls and between sexes. We used peripheral quantitative computed tomography (pQCT, Stratec XCT-2000) to measure change in total bone cross-sectional area (ToA, mm(2)), cortical area (CoA, mm(2)), average cortical thickness (C.Th., mm), section modulus (mm(3)) and muscle cross-sectional area (mm(2)) at the tibial midshaft (50% site) in 128 EARLY-, PERI- and POST-pubertal girls (n = 69, 11.9 +/- 0.6 years) and boys (n = 59, 12.0 +/- 0.6 years) across 20 months. We also calculated two bone-muscle strength indices (BMSI) for compression (CoA/MCSA) and bending [strength index/MCSA; where strength index = Z / (tibial length / 2)]. EARLY boys and girls had smaller ToA at baseline than same sex PERI or POST participants. There were no sex differences in ToA or CoA at baseline; however, boys increased both parameters significantly more than girls in every maturity group (8.5-11.1%, P < 0.01). These changes in bone geometry conferred greater gains in bone strength for boys compared with girls in each maturity group (13.8-15.6%, P < 0.01). Baseline BMSIs did not differ between sexes for EARLY and PERI groups, whereas BMSIs were significantly higher for POST boys compared with POST girls (P < 0.05). BMSIs decreased for EARLY and PERI girls (-7.4-(-1.1%)) whereas the ratios remained stable for EARLY and PERI boys (-0.6-2.5%). This sex difference in BMSI change was due to a relatively greater increase in CoA among EARLY and PERI boys compared with same-maturity girls. BMSIs remained stable in POST girls and decreased in POST boys due to relatively greater gains in MCSA. This study provides novel longitudinal descriptions of the maturity- and sex-specific changes in bone geometry, strength and bone-muscle strength indices.

Adolescent↗
PubMed2005

Human parathyroid hormone (1-34) accelerates the fracture healing process of woven to lamellar bone replacement and new cortical shell formation in rat femora.

This study aimed to test whether intermittent treatment of human parathyroid hormone [hPTH(1-34)] disturbs or accelerates the fracture healing process using rat surgical osteotomy model. One hundred five, 5-week-old SD rats were allocated to vehicle control (CNT) and four PTH groups; 10 and 30 microg/kg of hPTH(1-34) treatment before surgery (P10, P30), and treatment before and after surgery (C10, C30). All animals were given subcutaneous injections three times a week for 3 weeks. Then, fractures were produced by transversely cutting the midshaft of bilateral femora and fixing with intramedullary wire. Human PTH(1-34) treatment was continued in C10 and C30 groups until sacrifice at 3, 6, and 12 weeks after surgery. The femora were assessed by peripheral quantitative computed tomography, three-point bending mechanical test, and histomorphometry. Total cross-sectional area was not significantly different among all groups at any time point. At 3 weeks after surgery, the lamellar bone/callus area was significantly increased in C10 and C30 groups compared to the other groups. At 6 weeks, remodeling of woven bone to lamellar bone in the callus was almost complete in all groups. At 12 weeks, percent new cortical shell area was significantly higher in C10 and C30 groups compared to the other groups, and the ultimate load in mechanical testing was significantly higher in C30 group than in CNT, P10, and P30 groups. Intermittent PTH treatment at 30 microg/kg before and after osteotomy accelerated the healing process as evidenced by earlier replacement of woven bone to lamellar bone, increased new cortical shell formation, and increased the ultimate load up to 12 weeks after osteotomy.

Animals↗
PubMed2005

Differential turnover of cortical and trabecular bone in transgenic mice overexpressing cathepsin K.

Cathepsin K is a major osteoclastic protease. We have recently shown that overexpression of mouse cathepsin K gene in transgenic UTU17 mouse model results in high turnover osteopenia of metaphyseal trabecular bone at the age of 7 months. The present report extends these studies to a systematic analysis of cortical bone in growing and adult mice overexpressing cathepsin K. Mice homozygous for the transgene locus (UTU17+/+) and their control littermates were studied at the age of 1, 3, 7, and 12 months. Bone properties were analyzed using peripheral quantitative computed tomography (pQCT), histomorphometry, histochemistry, radiography, and biomechanical testing. In addition, the levels of biochemical markers of bone turnover were measured in the sera. Unexpectedly, cortical thickness and cortical bone mineral density were increased in the diaphyseal region of growing and adult UTU17+/+ mice. This was associated with an increased number of vascular canals leading to increased cortical porosity in UTU17+/+ mice without changes in the ultimate bending force or stiffness of the bone. In UTU17+/+ mice, osteopenia of metaphyseal trabecular bone was observed already at the age of 1 month. In sera of 1-month-old UTU17+/+ mice, the activity of tartrate-resistant acid phosphatase 5b was decreased and the levels of osteocalcin increased. Our results support the role of cathepsin K as a major proteinase in osteoclastic bone resorption. Excessive production of cathepsin K induced osteopenia of metaphyseal trabecular bone and increased the porosity of diaphyseal cortical bone. The increased cortical thickness and bone mineral density observed in diaphyses of UTU17+/+ mice demonstrate the different nature and reactivity of trabecular and cortical bone in mice. These results suggest that the biomechanical properties of cortical bone are preserved through adaptation as outlined in Wolff's law.

Animals↗