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At least 451 records · Page 25Linked to original sources
PubMed2001

Parameters of high bone-turnover predict bone loss in renal transplant patients: a longitudinal study.

BACKGROUND: Osteoporosis is a serious complication of kidney transplantation. Various factors have been postulated to contribute to posttransplant bone loss, among them treatment with corticosteroids, the use of cyclosporine and cyclosporine-like agents, and persistent hyperparathyroidism. In a previous cross-sectional study of long-term renal transplant recipients, we observed that osteoporosis or osteopenia was present in 88% of patients. Because biochemical markers of bone formation (serum osteocalcin) and bone resorption (urine pyridinoline, PYD, and deoxypyridinoline, DPD) were elevated in the majority of study subjects, we hypothesized that elevated rates of bone-turnover contribute to posttransplant bone loss in long-term renal transplant patients. This study was performed to examine this hypothesis. METHODS: The study population was composed of 62 patients who were more than 1-year postrenal transplantation and who had preserved renal function. They were followed prospectively for 1 year. Biochemical markers of bone-turnover were measured at study entry, and patients were classified as having high bone-turnover based on elevated urinary levels of at least one marker of bone resorption (i.e., PYD or DPD) and/or serum osteocalcin (group 1). If none of these were present, they were classified as having normal bone-turnover (group 2). Bone mineral density (BMD) was measured by dual energy x-ray absorptiometry (DEXA) at time of entry into the study and again after 1 year of follow-up. The changes in BMD at the lumbar spine, hip, and wrist over the period of the study were compared between the high and normal bone-turnover groups. RESULTS: Forty-three patients (69%) were classified as having high bone-turnover (Group 1), and 19 patients (31%) were classified as having normal bone-turnover (Group 2). There was a statistically significant difference in change in BMD between the two groups at the lumbar spine (-1.11+/-0.42%, high bone-turnover, vs. 0.64+/-0.54%, normal bone-turnover; P=0.02) and the hip (-0.69+/-0.38%, high bone-turnover, vs. 1.36+/-0.66%, normal bone-turnover; P=0.006). Whereas group 2 had stable bone mass, group 1 exhibited bone loss at these skeletal sites. CONCLUSIONS: Our results indicate that bone loss is greater in renal transplant recipients with elevated biochemical markers of bone-turnover, suggesting that these markers may be useful in identifying patients at risk for continued bone loss. These data support the hypothesis that continued bone loss in long-term renal transplant recipients is associated with high bone-turnover. If accelerated bone resorption does play a role in posttransplant bone loss, this would provide a strong rationale for use of antiresorptive therapy for the prevention and treatment of this complication.

Amino Acids↗
PubMed2003

Reduced bone formation and increased bone resorption: rational targets for the treatment of osteoporosis.

The net amount of bone lost during aging is determined by the difference between the amount of bone removed from the endocortical, trabecular and intracortical components of its endosteal (inner) envelope and formed beneath its periosteal (outer) envelope. Endosteal bone loss is determined by the remodeling rate (number of basic multicellular units, BMUs) and the negative balance (the difference between the volumes of bone resorbed and formed in each BMU). Bone loss already occurs in young adult women and men and is probably due to a decline in the volume of bone formed in each BMU. The rate of loss is slow because the remodeling rate is low in young adulthood. Bone loss accelerates in women at menopause because remodeling intensity increases and BMU balance becomes more negative as estrogen deficiency reduces osteoblast lifespan and increases osteoclast lifespan. The high remodeling rate also reduces the mineral content of bone tissue. The negative BMU balance results in trabecular thinning, disappearance and loss of connectivity, cortical thinning and increased intracortical porosity. These changes compromise the material and structural properties of bone while concurrent age-related subperiosteal bone formation increases the cross-sectional area (CSA) of bone partly offsetting endosteal bone loss and the loss of structural and material strength. Thus, treatments aimed at reducing the progression of bone fragility, and reversing it, should reduce activation frequency and so reduce the number of remodeling sites, reduce osteoclastic resorption in the BMU, and so reduce the volume of bone resorbed on each of the three components of the endosteal surface thereby reducing the progression of trabecular thinning, loss of connectivity, cortical thinning and porosity. If treatment also increases periosteal bone formation, the CSA of the whole bone and its cortical area will increase. If treatment also increases endosteal bone formation in the BMU, bone balance will be less negative, especially if resorption depth is reduced. This may produce thickening of trabeculae provided activation frequency is not too low. If treatment can increase de novo bone formation at quiescent endosteal surfaces, this will increase cortical and trabecular thickness, and reduce intracortical porosity. In this way, drugs directed at both the resorptive and formative aspects of remodeling, and bone modeling may (i) increase compressive and bending strength of cortical bone by increasing the diameter of the whole bone, its CSA and the distance the cortical mass is placed from the neutral long bone axis; (ii) maintain or increase peak compressive stress and peak strain in trabecular bone, preventing microcracks and buckling; and (iii) increase the material density of bone tissue, an effect that probably should not be permitted to reach a level which reduces resistance to microdamage accumulation and progression (toughness).

Aging↗
PubMed2002

Impact of cortical perforations of contiguous donor bone in a guided bone augmentation procedure: an experimental study in the rabbit skull.

BACKGROUND: It has been shown that bone can be augmented beyond the original skeletal envelope by using space-making barriers. Further, it has been suggested that perforation of the contiguous donor bone enhances bone formation in guided bone augmentation procedures. PURPOSE: The goal of the present investigation was to evaluate whether perforations into the donor bone marrow through the cortical plate, located contiguous to an extracalvarial experimental space, influence bone generation into this space with regard to augmented bone tissue volume and bone density 3 months postoperatively. MATERIALS AND METHODS: Two titanium cylinders, each with a titanium lid, were subcutaneously placed with their open ends facing the parietal bones of eight rabbits and secured with miniscrews. The cortical bone plate on the test side was perforated with seven evenly distributed holes, each with a diameter of 1.2 mm, using carbon-steel burs. Together, these perforations corresponded to about one-third of the total experimental bone area. The bone on the control side was left intact, and no bleeding occurred during the placement of the titanium lid. The perforation procedure (test side) resulted in various degrees of blood fill. After 3 months, the animals were sacrificed to obtain ground sections for histology and histomorphometry. RESULTS: The cylinders were found to be partly filled with tissue containing slender bone trabeculae and marrow spaces in abundance. The bone consistently reached a higher level at the inner wall compared with the central part of the cylinders (p = .001). Hollow connections between the experimental space and the skull bone marrow were found in the contiguous outer cortical plate in four of the seven control sites. No statistically significant differences could be demonstrated between the perforated test sites and the control sites regarding augmented tissue volume (64.4 +/- 18.9% vs. 64.9 +/- 22.2%) or bone density, although there was a tendency toward denser bone in the test sites (21.5 +/- 11.1%) versus control sites (14.7 +/- 5.4%). There was no statistical difference regarding relative bone-to-titanium wall contact (27.4 +/- 14.7% for test; 38.6 +/- 25.9% for control). Thickness (height) and density of the skull bone vault were measured in the area beneath and lateral to the cylinders. No significant differences could be observed regarding these parameters between the test and control side. There were no correlations between thickness (height) or density of donor bone versus amount or density of augmented bone. The degree of immediate blood fill could not be shown to correlate with augmented tissue volume or augmented bone density. CONCLUSIONS: In the present model, as observed 3 months postoperatively, cortical perforations of contiguous donor bone or degree of immediate blood fill of an extracalvarial experimental space were not found to enhance augmented tissue volume beyond the skeletal envelope. Although there was a much higher mean value for bone density of augmented bone in the test sites, the large variations failed to show significant intergroup differences.

Animals↗
PubMed1999

The effect of regional gene therapy with bone morphogenetic protein-2-producing bone-marrow cells on the repair of segmental femoral defects in rats.

BACKGROUND: Recombinant human bone morphogenetic proteins (rhBMPs) can induce bone formation, but the inability to identify an ideal delivery system limits their clinical application. We used ex vivo adenoviral gene transfer to create BMP-2-producing bone-marrow cells, which allow delivery of the BMP-2 to a specific anatomical site. The autologous BMP-2-producing bone-marrow cells then were used to heal a critical-sized femoral segmental defect in syngeneic rats. METHODS: Femoral defects in five groups of rats were filled with 5 x 10(6) BMP-2-producing bone-marrow cells, created through adenoviral gene transfer (twenty-four femora, Group I); twenty micrograms of rhBMP-2 (sixteen femora, Group II); 5 x 10(6) beta-galactosidase-producing rat-bone-marrow cells, created through adenoviral gene transfer of the lacZ gene (twelve femora, Group III); 5 x 10(6) uninfected rat-bone-marrow cells (ten femora, Group IV); or guanidine hydrochloride-extracted demineralized bone matrix only (ten femora, Group V). Guanidine hydrochloride-extracted demineralized bone matrix served as a substrate in all experimental groups. Specimens that were removed two months postoperatively underwent histological and histomorphometric analysis as well as biomechanical testing. RESULTS: Twenty-two of the twenty-four defects in Group I (BMP-2-producing bone-marrow cells) and all sixteen defects in Group II (rhBMP-2) had healed radiographically at two months postoperatively compared with only one of the thirty-two defects in the three control groups (beta-galactosidase-producing rat-bone-marrow cells, uninfected rat-bone-marrow cells, and guanidine hydrochloride-extracted demineralized bone matrix alone). Histological analysis of the specimens revealed that defects that had received BMP-2-producing bone-marrow cells (Group I) were filled with coarse trabecular bone at two months postoperatively, whereas in those that had received rhBMP-2 (Group II) the bone was thin and lace-like. Defects that had been treated with bone-marrow cells producing beta-galactosidase (Group III), uninfected bone-marrow cells (Group IV), or guanidine hydrochloride-extracted demineralized bone matrix only (Group V) demonstrated little or no bone formation. Histomorphometric analysis revealed a significantly greater total area of bone formation in the defects treated with the BMP-2-producing bone-marrow cells than in those treated with the rhBMP-2 (p = 0.036). Biomechanical testing demonstrated no significant differences, with the numbers available, between the healed femora that had received BMP-2-producing bone-marrow cells and the untreated (control) femora with respect to ultimate torque to failure or energy to failure. CONCLUSIONS: This study demonstrated that BMP-2-producing bone-marrow cells created by means of adenoviral gene transfer produce sufficient protein to heal a segmental femoral defect. We also established the feasibility of ex vivo gene transfer with the use of biologically acute autologous short-term cultures of bone-marrow cells.

Animals↗
PubMed2004

Growth hormone can reverse glucocorticoid-induced low bone turnover on cortical but not on cancellous bone surfaces in adult Wistar rats.

UNLABELLED: We evaluated the effect of glucocorticoids (GC) and growth hormone (GH) on cortical and cancellous bone turnover in adult rats using random vertical sections giving valid measurements of bone surfaces and bone formation parameters. GH administration could reverse GC-induced osteopenia and low bone turnover of cortical bone. However, GH could not reverse the GC-induced low bone turnover of cancellous bone. METHODS: Seventy female Wistar rats, 7 months of age, were divided into five groups: (1) start control, (2) saline, (3) GC 9 mg/kg/day (Solu Medrol), (4) GH 5 mg/kg/day, and (5) GC 9 mg/kg/day + GH 5 mg/kg/day, and injected for 3 months. The vertebral body was examined using dynamic histomorphometry and biomechanical tests. Nonparametric methods were used. RESULTS: Glucocorticoid administration induced a low bone turnover state of both the cortical and cancellous bone of the vertebral body, without altering the absolute amount of bone or the biomechanical competence of the vertebral body. GH administration induced a small increase in longitudinal bone growth and ventral modeling drift. This growth increased the total amount of cortical, endocortical, and cancellous bone in the vertebra. The biomechanical competence of a 3.5-mm-high cylinder of the central vertebral body was also increased due to an increase in the amount of cortical bone, whereas the total amount of cancellous bone in the cylinder was unaltered. The cancellous bone density (CBV) was, however, increased due to thicker trabeculae probably induced by an accelerated mineral appositional rate (MAR) induced by GH. GH also increased longitudinal and ventral modeling drifts in the GC-injected animals. GH increased the amount of cortical bone and also the amount of cancellous bone close to the epiphyseal growth plate, whereas the cancellous bone volume of the central vertebral cylinder was unaffected by GH administration in GC-injected animals. GH could also increase parameters of bone formation (bone mineralizing surface (MS) and MAR) on cortical bone surfaces in GC-injected animals, whereas parameters of bone formation [MS and bone formation rates (BFR)] on cancellous bone surfaces were even lower than those of animals injected with GC alone. CONCLUSION: GH can reverse GC-induced low bone turnover on cortical but not on cancellous bone surfaces.

Animals↗
PubMed1999

Biochemical markers of bone turnover and the volume and the density of bone in children at different stages of sexual development.

Bone mass and biochemical markers of bone turnover increase significantly during puberty. We studied the possible relationships between markers of bone formation and bone resorption and increases in skeletal size, bone volume, and bone density in healthy children at different stages of sexual development. Serum concentrations of bone specific alkaline phosphatase (BALP) and osteocalcin (bone Gla protein, BGP), urinary levels of pyridinoline (Pyr) and deoxypyridinoline (Dpyr) and computed tomography (CT) measurements of the cross-sectional areas of the vertebrae and the femurs, the apparent density of cancellous bone in the vertebrae, and the volume and the material density of cortical bone in the femurs were determined in 126 boys and 143 girls, ages 7-18 years. Serum levels of BALP and BGP and urinary concentrations of Pyr and Dpyr peaked in early puberty and were lowest in the later stages of puberty. CT measurements for the cross-sectional areas of the vertebrae and the femurs, the femoral cortical bone areas, and the apparent density of cancellous bone increased in all children during puberty, while values for material bone density did not change significantly with the stage of sexual development. BALP and BGP showed significant inverse correlations with the material density of bone (r = -0.23 and -0.24, respectively), but no association with bone volume in the appendicular or axial skeleton. In contrast, Pyr and Dpyr correlated with femoral cross-sectional area (r = -0.24 and -0.33, respectively) and cortical bone area (r = -0.29 and -0.33, respectively), and with the apparent density of vertebral cancellous bone (r = -0.26 and -0.19, respectively), but not with the material density of bone. We conclude that, during puberty, there is a differential association between the two components of bone mass and the markers of bone formation and bone resorption; while markers of bone formation are related to the material density of bone, markers of bone resorption are related to the volume of bone.

Adolescent↗
PubMedDate not supplied

Variations in bone regeneration adjacent to implants augmented with barrier membranes alone or with demineralized freeze-dried bone or autologous grafts: a study in dogs.

A study was performed in two large hound dogs to evaluate the bone-induction potential of demineralized freeze-dried bone (DFDBA) placed into defects adjacent to implants that were placed into extraction sockets. Two implants were untreated controls, two implants received only Gore-Tex Augmentation Membrane (GTAM), two implants received GTAM and autologous bone, and six sites received GTAM and DFDBA. DFDBA was prepared from the long bones of a dog of the same breed as the experimental dogs. P2, P3, and P4 were extracted bilaterally, and buccal defects were created and measured. Twelve commercially pure titanium Brånemark implants were placed. At 12 weeks, clinical measurements were taken and the dogs were sacrificed. The untreated control defects had a mean clinical bone fill of 1.75 mm (37%). Sites treated with autologous bone had a mean of 5.0 mm (95%) of clinical bone fill within the original defects. Sites treated with DFDBA and barriers had 3.8 mm (75%) of bone fill, while sites treated with membranes alone had a mean of 4.2 mm (80%) of bone fill. Histologic evaluation revealed that DFDBA sites had retained nonviable bone chips in 45.4% of the bone matrix, and only 8.3% was lamellar bone. Autologous graft sites had 26.2% retained bone chips within the bone matrix, and 61% percent of the matrix consisted of lamellar bone. For GTAM-only sites, 70.2% of the matrix was lamellar bone and 29.8% was woven bone. Retained DFDBA bone chips were nonviable, occasionally surrounded by woven bone, and appeared to break up and then remineralize without the presence of osteoclastic or osteoblastic activity. Retained autologous bone chips were surrounded and incorporated by the host bone. The autologous bone grafts and DFDBA implants were considered to be osteoconductive. For the three treatment groups, within the defects there were sparse bone-implant contacts. The results indicate that GTAM barriers alone or with autologous bone grafts produced the best clinical and histologic results. DFDBA did not appear to induce bone formation in any of the evaluated specimens.

Alveolar Process↗
PubMed2005

Changes in bone mass and bone turnover following tibial shaft fracture.

INTRODUCTION: Bone loss occurs in the regional bone following tibial shaft fracture. An earlier cross-sectional study showed that measurements made at the metaphyseal region of the tibia using peripheral quantitative computed tomography (pQCT) and the ultradistal region of the tibia using dual-energy X-ray absorptiometry (DXA) were the most responsive at monitoring this bone loss. Biochemical markers of bone turnover enable us to assess the activity of bone formation and resorption during fracture healing. The aim of this longitudinal study was to determine the pattern and distribution of bone loss and bone turnover following a tibial shaft fracture treated with either plaster cast or intramedullary nail. METHODS: Eighteen subjects underwent bone mass measurements using DXA at the tibia and hip and quantitative ultrasound (QUS) at the tibia and calcaneus of both limbs at 2 weeks, 8 weeks, 12 weeks and 24 weeks following fracture, with hip and tibia DXA measurements also performed at 52 weeks. Nine of the patients treated with plaster cast had pQCT measurements at the tibia at 24 weeks. We measured three bone formation markers, bone alkaline phosphatase (bone ALP), osteocalcin (OC) and procollagen type 1 N-terminal peptide (PINP), a marker of bone resorption, serum C-telopeptides of type 1 collagen (beta-CTX) and a marker of collagen III turnover, procollagen type III N-terminal peptide (PIIINP) at 1 day, 3 days and 7 days and at 2, 4, 8, 12, 16 and 24 weeks following fracture. The greatest bone losses were observed at the ultradistal region of the tibia using DXA (28%, p <0.001) and the metaphyseal region of the tibia using pQCT (26-31%, p <0.001) at 24 weeks. In the hip, the greatest loss was in the trochanter region at 24 weeks (10%, p <0.001). The greatest loss at the calcaneus measured using QUS was for broadband ultrasound attenuation (BUA) measured using CUBA Clinical at 24 weeks (13%, p =0.01). RESULTS: At 1 year, there was a small recovery in bone loss (ultradistal tibia DXA, 20%, p <0.01; trochanter DXA 9%, p <0.001). Bone turnover increased following fracture (PINP +72+/-21%, p <0.0001, bone ALP +199+/-22%, p =0.004, beta-CTX +105+/-23%, p <0.0001, all at 24 weeks). There was a smaller +33+/-10% increase in osteocalcin at 24 weeks. PIIINP concentration peaked at week 8 (+57+/-9%, p <0.0001). The bone resorption marker beta-CTX showed an earlier rise (week 2, 139+/-33%) than the bone formation markers. CONCLUSIONS: We conclude that: (1) bone loss following tibial shaft fracture occurs both proximal and distal to the fracture; (2) the decreased BMD is largest for trabecular bone in the tibia with similar measurements using DXA and pQCT; (3) there is limited recovery of bone lost at the hip and tibia at 1 year; (4) tibial speed of sound (SOS) demonstrated a greater decrease than calcaneal SOS when comparing z -scores; (5) BUA is the QUS variable that shows the biggest decrease of bone mass at the calcaneus; (6) increase in bone turnover occurs following fracture with an earlier increase in bone resorption markers and a later rise in bone formation markers.

Absorptiometry, Photon↗
PubMed2004

Alfacalcidol prevents age-related bone loss and causes an atypical pattern of bone formation in aged male rats.

The current study was designed to investigate the skeletal effects of alfacalcidol in aged rats. Eighteen-month-old male rats were treated with 0, 0.1, or 0.2 microg/kg/d of alfacalcidol by daily oral gavage, 5 days/week for 12 weeks. At the beginning of the treatments, one group of rats was euthanized to serve as a baseline control. At the end of the study, the second lumbar vertebrae and the right tibial diaphysess were processed for bone histomorphometric analysis. The fourth lumbar vertebrae were subjected to strength testing. The control group of rats at 21 months of age had decreased serum testosterone levels and decreased cancellous bone mass associated with increased bone turnover on the trabecular surface. The older rats had increased bone turnover on the endocortical surface and decreased bone formation on the periosteal surface compared with the 18-month group. In contrast, alfacalcidol treatment increased cancellous and cortical bone mass in aged male rats. Trabecular bone resorption was decreased whereas bone formation was maintained or increased in the rats treated with alfacalcidol. In addition, endocortical bone formation was decreased whereas periosteal bone formation was increased in the rats treated with alfacalcidol compared with vehicle-treated rats. Marrow trabecular bone area was increased by alfacalcidol treatment in tibial diaphyses. Furthermore, bone strength of the lumbar vertebral body was increased after alfacalcidol treatment. An atypical pattern of bone formation on endosteal bone surfaces was seen in the rats treated with alfacalcidol. The atypical bone formation is characterized by small, focal packets of newly formed bone on trabecular and endocortical bone surfaces. This gave the appearance of the formation of "bone buds" emanating from trabecular surfaces. These bony outgrowths were mineralized and demonstrated significant fluorochrome label indicating recent mineralization. Also, lamellae of the bony buds did not run parallel to those of the trabecular plate to which they are attached. Arrest lines presented in most of the "bone buds". In summary, alfacalcidol treatment increased cancellous and cortical bone mass and improved bone strength, resulting in the prevention of age-related bone loss in aged male rats. An atypical pattern of bone formation observed in this study may be a result of minimodeling based bone formation stimulated by alfacalcidol treatment.

Aging↗
PubMed2000

The influence of bone thickness on facial marginal bone response: stage 1 placement through stage 2 uncovering.

BACKGROUND: Various causes of facial bone loss around dental implants are reported in the literature; however, reports on the influence of residual facial bone thickness on the facial bone response (loss or gain) have not been published. This study measured changes in vertical dimension of facial bone between implant insertion and uncovering and compared these changes to facial bone thickness for more than 3,000 hydroxyapatite (HA)-coated and non-HA-coated root-form dental implants. METHODS: Subjects were predominantly white males, 18 to 80+ years of age (mean 62.9 years), who were patients at 30 Department of Veterans Affairs Medical Centers and two university dental clinics. Alveolar ridges ranged from normal to resorbed with intact basal bone. Following preparation of the osteotomy site, direct measurements with calipers were made of the residual facial bone thickness, approximately 0.5 mm below the crest of the bone. The distance from the top of the implants to the crest of the facial bone was also measured using periodontal probes. Implants were uncovered between 3 to 4 months in the mandible and 6 to 8 months in the maxilla after insertion. Facial bone response was the difference between the height of facial bone at Stage 1 (insertion) and Stage 2 (uncovering). RESULTS: The mean facial bone thickness after osteotomies were made was 1.7 +/- 1.13 mm. When a mean facial bone thickness of 1.8 +/- 1.41 mm or larger remained after site preparation, bone apposition was more likely to occur. The mean facial bone response for 2,685 implants was -0.7 +/- 1.70 mm. For implants integrated at uncovering, the mean bone response was -0.7 +/- 1.69 mm, and -2.8 +/- 1.57 mm for implants mobile at uncovering. Bone quality-4 had the least facial bone response, -0.5 +/- 2.11 mm. Bone responses were similar for both HA-coated and non-HA-coated implants. CONCLUSIONS: Significantly greater amounts of facial bone loss were associated with implants that failed to integrate. As the bone thickness approached 1.8 to 2 mm, bone loss decreased significantly and some evidence of bone gain was seen. There was no statistically or clinically significant difference in bone response between HA-coated and non-HA-coated implants.

Adolescent↗