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At least 91 records · Page 5Linked to original sources
PubMed2002

Intramuscular bone induction by human recombinant bone morphogenetic protein-2 with beta-tricalcium phosphate as a carrier: in vivo bone banking for muscle-pedicle autograft.

An ideal replacement for bone defects is auto-bone tissue, of which there is an ample supply with the required form and with vascularity. Our strategy for generating such bone tissue is as follows. First, bone tissue is induced in muscle by bone morphogenetic protein-2 (BMP-2) with beta-tricalcium phosphate as a carrier to maintain its form in the muscle. Second, the induced bone in the muscle pedicle is grafted to the bone defect to maintain vascularity. In the first experiment, 50 microg of recombinant human BMP-2 (rhBMP-2) was inoculated into the hip abductor muscle of rabbits with beta-tricalcium phosphate under anesthesia. Five weeks after the operation, intramuscular bone formation was observed in all of the samples, and the form and size of the induced bone tissue were identical to those of the carrier. Ten weeks after the operation, the induced bone was partly absorbed. In the second experiment, 50 microg of rhBMP-2 was inoculated in the same manner as previously. Five weeks after the operation, the muscle tissue around the induced bone was incised, leaving just the proximal part as a pedicle. Two or four weeks after the second operation, the induced bone tissue had rich vascularity and no empty lacunae. This indicates the possibility of in vivo bone banking to enable morphologically controlled and vascularized auto-bone grafts.

Animals↗
PubMed1998

Concentration of transforming growth factor beta in human bone tissue: relationship to age, menopause, bone turnover, and bone volume.

Transforming growth factor beta (TGF-beta) is thought to play an important role in bone metabolism, but its relationship to human bone turnover and bone mass has not been examined yet. In this study, we measured the concentration of TGF-beta in 811 samples of male and female bone from four representative sites of the human skeleton and in the supernatants of 72 short-term human bone marrow cultures from the iliac crest. The concentrations of TGF-beta1 and TGF-beta2 in the bone matrix were positively correlated with histomorphometric indices of bone resorption and bone formation and with serum levels of osteocalcin and bone-specific alkaline phosphatase. We also observed a positive association between the release of TGF-beta in the bone marrow cultures and serum osteocalcin. Changes in the rate of cancellous or cortical bone remodeling with age or menopause were accompanied by corresponding changes in skeletal TGF-beta. In contrast, there was no significant relationship between the concentration of TGF-beta and bone volume at any skeletal site. In conclusion, our study supports the hypothesis that TGF-beta plays an important role in human bone remodeling, but fails to demonstrate an association between the skeletal concentration of TGF-beta and human bone mass.

Aging↗
PubMed2000

[Graft of AAA bone combined with autologous red bone marrow for treatment of bone defects].

To evaluate the effect of autolyzed antigen-extracted allogenic bone ("AAA" bone) graft combined with autogenic red bone marrow on bone defects, 58 cases with benign bone tumor(66 long bones) were treated with curettage operation, and the post-curettage bone defects were filled with the complex of "AAA" bone combined with autogenic red bone marrow. Forty two cases(49 bones) were followed up by taking X-ray radiography every 2 months in a period of 1-3 years. The result showed that 49 bones all got bony healing within 9 months(6 months in average). It is suggested that "AAA" bone combined with autogenic red bone marrow may be an ideal material for bone defect repairing.

Adolescent↗
PubMedDate not supplied

Bone augmentation of the inferior floor of the maxillary sinus with autogenous bone or composite bone grafts: a histologic-histomorphometric preliminary report.

Thirteen patients were treated for elevation of the maxillary sinus floor with autogenous or composite (autogenous bone + hydroxyapatite granules) bone grafts and endosseous implants. Bone biopsies were taken both at graft positioning and at implant placement. Histologic and histomorphometric results suggest that graft architecture, conformation, and composition may influence the mean bone content at the end of the healing. Iliac bone grafts contained 53% bone, while chin bone grafts contained 66% bone. Composite bone grafts had the smallest percentage of bone: 44.3%. Chin block bone grafts had the largest percentage of bone content (69.3%), while chin particulate bone graft conformation had 62.6%. Although particulate grafts healed in only 4 months, bone quality and quantity allowed earlier implant placement.

Adult↗
PubMed2005

A comparative qualitative histological analysis of tissue-engineered bone using bone marrow mesenchymal stem cells, alveolar bone cells, and periosteal cells.

For tissue-engineered bone formation, autogenous osteogenic cells are of paramount importance for successful bone formation. In order to investigate the donor cell-related differences in tissue-engineered bone, cultured bone marrow mesenchymal stem cells, cultured alveolar bone cells, and cultured periosteal cells were examined for their in vivo potential to form bone. These cells were isolated from dogs, expanded in vitro, mixed with autologous fibrin glue and BMP-2, and then injected into the subcutaneous space on the dorsum of nude mice. Bone formation was evaluated at 12 weeks. Histomorphometric analysis demonstrated that the subcutaneous nodules formed in nude mice contained 26.9% newly formed bone when using the bone marrow mesenchymal stem cells, 41.1% newly formed bone when using the alveolar bone cells, and 58.2% newly formed bone when using the periosteal cells. The results suggest that periosteal cells are the best choice for enhancing bone formation in tissue engineering of bone regeneration.

Alveolar Process↗
PubMed2004

[Long-term effects of 7-year growth hormone substitution on bone metabolism, bone density, and bone quality in growth hormone-deficient adults].

BACKGROUND AND PURPOSE: Subnormal bone mineral density (BMD) and increased fracture risk are described in patients with growth hormone deficiency (GHD). Growth hormone (GH) has been reported to have beneficial effects on bone in GHD. The aim of this study was to investigate the long-term effects of GH replacement therapy on bone metabolism, BMD, and bone quality in patients with GHD. PATIENTS AND METHODS: 20 adult patients with GHD (eleven male, nine female, mean age 42.5 years) were included in the study and randomized to either GH or placebo in a dose of 0.25 U/kg body weight/week. After 6 months all patients received GH. After a 1-year double-blind, placebo-controlled study the patients were followed for another 72 months in an open study. The patients were compared to 20 age- und sex-matched healthy controls. Bone turnover was determined by ICTP (type I collagen carboxyterminal cross-linked telopeptide) as parameter of bone resorption and PICP (carboxyterminal propeptide of type I procollagen) as marker of bone formation. BMD was measured at the lumbar spine by dual-photon absorptiometry (DPA) and at the forearm by single-photon absorptiometry (SPA). Apparent phalangeal ultrasound transmission velocity (APU) was assessed as parameter of bone quality independent of BMD. RESULTS: At the beginning of the study BMD at both measuring sites was lower in patients with GHD than in healthy controls. During the 1st year of GH replacement therapy BMD decreased, followed by a continuous increase in BMD (about 12%) up to 60 months which remained unchanged thereafter, building up a plateau. After 72 months no significant difference between the patients and the healthy controls could be detected. Concerning parameters of bone turnover, first ICTP as marker of bone resorption showed a significant increase, later on the marker of bone formation increased as well. APU decreased during the first 6 months of treatment, but had returned to its baseline value after 24 months and remained unchanged throughout the rest of the study. CONCLUSION: BMD is subnormal in adults with GHD. GH replacement therapy stimulates bone turnover in patients with GHD and in the long term such stimulation results in an increased BMD. Thereby, GH shows a triphasic action on BMD: an initial decrease in BMD during the 1st year, followed by a continuous increase in BMD with buildup of a stable plateau after 60 months. The newly formed bone seems to have normal bone elasticity.

Absorptiometry, Photon↗
PubMed2005

Genetic regulation of bone mass: from bone density to bone strength.

Osteoporosis is a common disease characterized in adults by diminished bone density. Bone is an organ that evolves and grows throughout life, and establishing optimal bone density in childhood and adolescence serves to buffer bone loss later in life. Bone density, a measurable entity, is the clinical substitute for bone strength, or the ability to defend against fracture. Chronic diseases may adversely affect optimal peak bone density. Bone density is under genetic control, as revealed by three lines of investigations. These include (1) the finding of quantitative trait loci for bone density, (2) the finding that specific mutations in genes that are important in the development of osteoblast or osteoclast lineages alter bone density, and (3) the linkeage of known polymorphisms for genes involved in mineral homeostasis to bone density and/or fracture. Future therapeutics for improving peak bone density or delaying bone loss later in life may take advantage of the genetic nature of bone density development.

Bone Density↗
PubMed2005

The nucleocytoplasmic shuttling protein CIZ reduces adult bone mass by inhibiting bone morphogenetic protein-induced bone formation.

Osteoporosis is a major health problem; however, the mechanisms regulating adult bone mass are poorly understood. Cas-interacting zinc finger protein (CIZ) is a nucleocytoplasmic shuttling protein that localizes at cell adhesion plaques that form where osteoblasts attach to substrate. To investigate the potential role of CIZ in regulating adult bone mass, we examined the bones in CIZ-deficient mice. Bone volume was increased and the rates of bone formation were increased in CIZ-deficient mice, whereas bone resorption was not altered. CIZ deficiency enhanced the levels of mRNA expression of genes encoding proteins related to osteoblastic phenotypes, such as alkaline phosphatase (ALP) as well as osterix mRNA expression in whole long bones. Bone marrow cells obtained from the femora of CIZ-deficient mice revealed higher ALP activity in culture and formed more mineralized nodules than wild-type cells. CIZ deficiency enhanced bone morphogenetic protein (BMP)-induced osteoblastic differentiation in bone marrow cells in cultures, indicating that BMP is the target of CIZ action. CIZ deficiency increased newly formed bone mass after femoral bone marrow ablation in vivo. Finally, BMP-2-induced bone formation on adult mouse calvariae in vivo was enhanced by CIZ deficiency. These results establish that CIZ suppresses the levels of adult bone mass through inhibition of BMP-induced activation of osteoblasts.

Alkaline Phosphatase↗
PubMed2002

Treatment of active unicameral bone cysts with percutaneous injection of demineralized bone matrix and autogenous bone marrow.

BACKGROUND: The treatment of unicameral bone cysts varies from open bone-grafting procedures to percutaneous injection of corticosteroids or bone marrow. The purpose of this study was to evaluate the feasibility and effectiveness of percutaneous injection of a mixture of demineralized bone matrix and autogenous bone marrow for the treatment of simple bone cysts. METHODS: Twenty-three patients with an active unicameral bone cyst were treated with trephination and injection of allogeneic demineralized bone matrix and autogenous bone marrow. The patients were followed for an average of fifty months (range, thirty to eighty-one months), at which time pain, function, and radiographic signs of resolution of the cyst were assessed. RESULTS: The average time until the patients had pain relief was five weeks, and the average time until the patients returned to full, unrestricted activities was six weeks. Bone-healing at the site of the injection was first seen radiographically at three to six months. No patient had a pathologic fracture during this early bone-healing stage. Cortical remodeling was seen radiographically by six to nine months, and after one year the response was usually complete, changing very little from then on. Five patients required a second injection because of recurrence of the cyst, and all five had a clinically and radiographically quiescent cyst after an average of thirty-six additional months of follow-up. Seven of the twenty-three patients had incomplete healing manifested by small, persistent radiolucent areas within the original cyst. None of these cysts increased in size or resulted in pain or fracture. CONCLUSIONS: Percutaneous injection of allogeneic demineralized bone matrix and autogenous bone marrow is an effective treatment for unicameral bone cysts.

Adolescent↗
PubMed2005

Does early PTH treatment compromise bone strength? The balance between remodeling, porosity, bone mineral, and bone size.

The treatment of osteoporotic women with recombinant human parathyroid hormone (rhPTH) increases bone mineral density and reduces fracture risk. However, there has been concern that the initiation of therapy in women with low bone mass may cause an early and transient increased fracture risk because PTH stimulates bone remodeling, which in its first phase is associated with bone resorption. Animal and human studies suggest, however, that the stimulation of remodeling caused by rhPTH(1-34) does not lead to a deterioration of bone's mechanical properties or to an increased fracture risk even early in the treatment. There are several reasons for this. Bone biomarkers associated with formation rise earlier than those associated with resorption, suggesting that there is an initial period prior to the stimulation of remodeling during which bone formation occurs on surfaces without prior resorption. This initial period of formation may protect the patient from the later small and transient losses that occur through remodeling. Moreover, the increased remodeling occurs on cancellous surfaces or close to the endosteal surface of bone, where its mechanical effect is minimal. Additionally, these transient losses may be compensated by periosteal apposition that maintains the overall strength of the bone. Thus, the early stimulation of bone formation without prior resorption, and the redistribution of bone from cancellous and endocortical surfaces to the periosteal surface combine to prevent the mechanical deterioration that could otherwise occur with a transient acceleration of bone remodeling in a patient with low bone mass.

Animals↗
PubMed1997

Recombinant transforming growth factor-beta1 induces endochondral bone in the baboon and synergizes with recombinant osteogenic protein-1 (bone morphogenetic protein-7) to initiate rapid bone formation.

Several members of the bone morphogenetic protein (BMP) and transforming growth factor-beta (TGF-beta) families are molecular regulators of cartilage and bone regeneration, although their actual roles and combined interactions in skeletal repair are poorly understood. The presence of several molecular forms suggests multiple functions in vivo as well as synergistic interactions during both embryonic bone development and regeneration of cartilage and bone in postfetal life. Here we show for the first time that recombinant human transforming growth factor-beta1 (TGF-beta1) induces endochondral bone formation in extraskeletal sites of adult baboons. We also show that TGF-beta1 and recombinant human osteogenic protein-1 (OP-1, bone morphogenetic protein-7) synergize in inducing large ossicles in extraskeletal sites of the primate as early as 15 days after implantation. A single application of OP-1, in conjunction with an insoluble collagenous matrix as carrier (5, 25, and 125 microg/100 mg of carrier matrix) induced bone differentiation in the rectus abdominis of the baboon. This level of tissue induction was raised several-fold by the simultaneous addition of comparatively low doses of TGF-beta1 (0.5, 1.5, and 5 microg), which by itself induces bone formation in the rectus abdominis at doses of 5 microg/100 mg of carrier matrix. Combinations of OP-1 and TGF-beta1 yielded a 2- to 3-fold increase in cross-sectional area of the newly generated ossicles, with markedly elevated key parameters of bone formation, and corticalization of the newly formed bone by day 15, culminating in bone marrow generation by day 30. The tissue generated by the combined application of OP-1 and TGF-beta1 showed distinct morphological differences when compared with OP-1-treated specimens, with large zones of endochondral development and extensive bone marrow formation. At the doses tested, synergy was optimal at a ratio of 1:20 by weight of TGF-beta1 and OP-1, respectively. These results provide evidence for a novel function of TGF-beta1 in the primate and the scientific basis for synergistic molecular therapeutics for the rapid regeneration of cartilage and bone.

Animals↗
PubMed1998

Addition of human recombinant bone morphogenetic protein-2 to inactive commercial human demineralized freeze-dried bone allograft makes an effective composite bone inductive implant material.

COMMERCIAL PREPARATIONS OF HUMAN DEMINERALIZED freeze-dried bone allograft (DFDBA) vary in their ability to induce new bone formation. This study tested the hypothesis that inactive DFDBA can be used as an effective carrier of recombinant human bone morphogenetic protein-2 (rhBMP-2). Two batches of active DFDBA were used as controls. Two batches of DFDBA, previously shown to be inactive, were treated with vehicle or with 5 or 20 microg rhBMP-2 and implanted into the calf muscle of male Nu/Nu (nude) mice. Each mouse received one implant in each hind limb, both of which were of the same formulation, resulting in 8 groups of 4 mice per group: active DFDBA batch A, active DFDBA batch B, inactive DFDBA batch A, inactive DFDBA batch B, inactive DFDBA batch A plus 5 microg rhBMP-2, inactive DFDBA batch A plus 20 microg rhBMP-2, inactive DFDBA batch B plus 5 microg rhBMP-2, and inactive DFDBA batch B plus 20 microg rhBMP-2. After 56 days, the implants were removed and histologically examined. A semiquantitative bone induction index was calculated based on the amount of new bone covering each histological section. Histomorphometry was also used to evaluate the area of new bone formed and the area of residual implant material. The results showed that active DFDBA induces new bone formation, whereas inactive DFDBA does not. Addition of rhBMP-2 to inactive DFDBA results in new bone formation with a bone induction index comparable to that of active DFDBA. Histomorphometric analysis, however, revealed that the rhBMP-2-containing implants caused a dose-dependent increase in new bone area that exceeded that induced by active DFDBA. At the highest concentration of rhBMP-2, bone formation was exuberant. rhBMP-2 also caused the resorption of residual implant material to levels comparable to that seen in sites treated with active DFDBA, suggesting that this growth factor may regulate resorptive cells either directly or indirectly. This study shows that addition of rhBMP-2 to inactive DFDBA provides reproducible, consistent bone induction, and suggests that inactive commercial preparations may contain inadequate amounts of BMP to cause bone induction compared to active preparations.

Animals↗
PubMed2005

[Expression of vascular endothelial growth factor in repairing bone defect with vascularized bone graft- reconstituted bone xenograft].

OBJECTIVE: To study efficiency of vascularized bone graft combining with reconstituted bone xenograft (RBX) in repairing bone defect and the expression of the vascular endothelial growth factor (VEGF) in serum. METHODS: From January 1998 to December 2002, 27 cases of bones defects were treated and randomly divided into 3 groups according to different repair materials: group A (the vascularized bone graft- RBX group, n=9), group B (the vascularized bone graft group, n=10) and group C(the RBX group, n=8). The bone defect repair, the bone healing time and the bone graft resorption were observed by radiograph after 3 months, 6 months and 12 months of operation, and the expression of VEGF in serum was assayed with lumino-enzyme immunoassay before operation and after operative 2 weeks, 4 weeks, 6 weeks and 8 weeks respectively. RESULTS: The X-ray films showed that the bone healing was achieved in 8 cases of group A, in 6 cases of group B and in 3 cases of group C after 3 months; in 1 case of group A, respectively in 3 cases of both group B and group C after 6 months. The bone graft resorption was observed in 1 case of group B and in 2 cases of group C after 12 months. The serum VEGF values after operative 2 weeks and 4 weeks were higher than those before operation in all of 3 groups (P<0. 05), and the VEGF values of groups A and B were higher than that group C(P<0. 05) after 4 weeks. There were no significant differences (P>0. 05) in serum VEGF level between postoperative 6, 8 weeks and pre-operation in 3 groups. CONCLUSION: The expression of serum VEGF obviously increase in the early period of bone transplanting, it is value of clinical evaluation of reparative efficiency of bone defect.

Adolescent↗
PubMed2005

Recombinant human bone morphogenetic protein-7 and bone marrow as a substitute for bone graft in reconstruction defect of rabbit mandible.

OBJECTIVE: To obtain information on the feasibility of employing recombinant human bone morphogenetic protein-7 (rhBMP-7), mixed with bone marrow as a substitute for autologous bone graft. METHODS: We carried out the study in the University Clinic Center, Sarajevo, Bosnia and Herzegovina, from February 2002 to January 2004. Six New Zealand rabbits underwent hemiresection of the mandible. We placed rhBMP-7 in a concentration of 100 micrograms and collagen (ACS) as carrier mixed with bone marrow in the defects in 3 animals. In another group of 3, we restored the defect by placement of autologous bone graft harvested from the iliac crest. We evaluated the results by the activity of the alkaline phosphatase enzyme (ALP), CT assessment with bone mineral density (BMD) analysis, and clinical and histologic examinations. RESULTS: The ALP activity was significantly higher after 14 days, in the rhBMP7/ACS sites than the bone graft sites (30th day). Mean BMD of tissue induced by rhBMP-7/ACS on the 30th day was 510 mg/cm3 in caudal, and 553 mg/cm3 in sagittal plane, and bone graft tissue was 510 mg/cm3 in caudal and 530 mg/cm3 in sagittal plane. Clinical inspection and histologic examination on the 60th day showed complete bridged defects with abundant woven bone in 2 of 3 rhBMP-7/ACS sites (67%), and no incorporation of the autologous bone graft into the other groups treated sites. CONCLUSION: The rhBMP-7/ACS mixed with bone marrow was very effective in establishing complete bone regeneration into the defects, indicating that it could be an adequate alternative for autologous bone transplantation.

Animals↗
PubMed1979

[An experimental study on the effects of the plating method for bone fractures--with reference to bone union and bone strength (author's transl)].

The plating method for bone fractures is in wide use. The author studied both new bone formation and bone atrophy of the cortex of fracture site after long periods of plating. This study is concerned with the bone strength of the fracture site as influenced by rigid plate fixation, and also with bone union after the removal of the plate. The experimental results, using mature rabbits as subjects, showed the following: X-rays of the bone union at the fracture site treated by the plating method confirmed evident union at 8 weeks after surgery. The bone strength at the region of this union, as tested by the bending method (an Instron Type Testing Machine was used), showed its highest values at 28 weeks after surgery. Yet, this was only 60% of the bone strength as measured at a non-fracture site; it then gradually declined in strength. On the other hand, in the case where the plate had been removed 8 weeks after surgery, bone strength was recovered to the same level as that of non-fracture sites 16 weeks after surgery. In conclusion, rigid plate fixation for a long period may result not only in progressive bone atrophy of the cortex but also in a delayed remodeling of the bone at the region of the bone union. It is, therefore, very important to remove the plate as early as possible once union has been achieved. Careful observation, however, is necessary during the short time between plate removal and the period when bone strength becomes again normal.

Animals↗
PubMedDate not supplied

Effects of bone block position and orientation within the tibial tunnel for posterior cruciate ligament graft reconstructions: a cyclic loading study of bone-patellar tendon-bone allografts.

BACKGROUND: Posterior laxity occurring after posterior cruciate ligament reconstruction with a tibial tunnel could be related to thinning and permanent elongation of the graft as it is cyclically loaded in vivo. HYPOTHESIS: The orientation and position of the bone block within the tibial tunnel will have a significant effect on thinning and elongation of the graft after cyclic loading. STUDY DESIGN: Controlled laboratory study. METHODS: In test series 1 (27 fresh-frozen graft pairs), all bone blocks were positioned flush with the posterior opening of the tibial tunnel; 1 graft was oriented with the bone block facing posteriorly, whereas its pair was tested with the bone block facing anteriorly. In test series 2 (20 graft pairs), all grafts were oriented with the bone block facing posteriorly; 1 graft had the bone block positioned flush with the posterior tunnel opening, whereas its pair was tested with the bone block recessed 1 cm from the posterior opening. RESULTS: In series 1, 3 of 27 grafts with posterior bone block orientations failed at the tunnel edge before 2000 cycles of testing could be completed; all specimens with anterior bone block placements survived the testing intact. In series 2, 3 of 20 grafts with recessed bone blocks failed at the tunnel edge, whereas all those with flush bone blocks survived. CONCLUSIONS: The best position for the bone block of a bone-patellar tendon-bone graft was flush with the posterior tunnel opening with the bone block facing anteriorly in the tibial tunnel.

Adult↗
PubMed1994

Reduced bone density in women with fractures: contribution of low peak bone density and rapid bone loss.

Osteoporosis is regarded as a disease of the elderly because fractures occur late in life. Although excessive bone loss during aging is likely to contribute to the deficit in bone density, patients with fractures do not consistently have more rapid bone loss, greater bone resorption or lower bone formation (measured using biochemical or histomorphometric markers of bone turnover). The pathogenesis of the low bone density and bone fragility that characterize osteoporosis may begin during the first two decades of life. There are differences in the hormonal regulation of regional growth and mineral accrual, differences in the age of onset, rate and duration of linear growth and mineral accrual of the axial and appendicular skeleton, of cortical and trabecular bone, and of proximal and distal limb segments. Illnesses, risk or protective factors, and disorders of hormonal deficiency or excess may affect longitudinal growth, mineral accrual, or both, depending on the timing of exposure. Quantitatively larger and qualitatively different effects on bone density may result when exposure occurs during growth rather than during adulthood. The magnitude of these deficits and their location are likely to establish the relevance of regional age-related and sex hormone dependent bone loss. Thus, any unifying hypothesis concerning the epidemiology and pathogenesis of osteoporosis must consider the relative contributions of low peak bone density and bone loss to the deficit in bone density in adulthood. A great deal of research is needed to examine the physiology of longitudinal growth and mineral accrual as the pathogenesis of osteoporosis is at least partly explained by events occurring during the first 20 years of life.

Age Factors↗
PubMed2006

Spinal cord injury causes more damage to bone mass, bone structure, biomechanical properties and bone metabolism than sciatic neurectomy in young rats.

INTRODUCTION: Although both spinal cord injury (SCI) and sciatic neurectomy (NX) can cause osteopaenia in young rats, the effects of these two injuries on cortical and cancellous bone may differ. The objective of this study was to compare the effects of SCI and NX on bone weight, bone material property, bone mass, bone geometry, trabecular microarchitecture, mechanical strength and bone turnover in young rats. MATERIALS AND METHODS: Thirty six-week-old male Sprague-Dawley rats were randomised into three groups (10 per group): SCI, bilateral sciatic NX and untreated control (CON). All rats were killed on day 21. Bone mineral density (BMD) was studied using dual-energy X-ray absorptiometry (DXA). At death, the right proximal tibial metaphysis and the fourth lumbar vertebra were examined for bone structural geometric analysis by micro-computed tomography (CT) and then processed for histomorphometry to assess bone cell activity. Serum N-terminal telopeptide of type I collagen (NTX) and osteocalcin (OC) levels were analysed by enzyme-linked immunosorbent assay (ELISA). Biomechanical strength properties of the femur and humerus were measured by three-point bending, and the third lumbar vertebra and the proximal end of tibia were tested by compression. RESULTS: BMD in the sublesional areas of SCI rats was significantly lower than that of NX rats (proximal tibia, 0.176+/-0.018 g/cm(2) vs. 0.224+/-0.015 g/cm(2), P<0.001). Bone volume (BV/TV), trabecular number (Tb.N) and thickness (Tb.Th) in the tibial second spongiosa of SCI rats were significantly less than those in NX rats (BV/TV: 7.15+/-1.18% vs. 12.32+/-1.83%, P<0.001; Tb.N: 1.23+/-0.22 vs. 2.38+/-0.45, P<0.001; Tb.Th: 33.73+/-5.15 microm vs. 42.80+/-7.44 microm, P<0.01) and trabecular separation (Tb.Sp: 1,053.37+/-164.24 microm vs. 748.32+/-129.36 microm, P<0.01) was significantly greater than in NX rats. Furthermore, poorer trabecular connectivity was found in SCI rats than in NX rats (number of nodes, N.Nd/TV: 1.04+/-0.09 vs. 3.29+/-0.53; number of terminus, N.Tm/TV: 28.53+/-3.17 vs. 21.64+/-2.31, P<0.01). The bone formation rate of the tibial second spongiosa in SCI rats was significantly higher than in NX rats (2.06+/-0.13 vs. 1.53+/-0.09, P<0.001) and, also, the eroded surface in SCI rats was significantly higher than in NX rats (13.42+/-1.24 vs. 10.36+/-1.07, P<0.001). In addition, biomechanical tests showed that SCI rats had poorer biomechanical properties of the femur, proximal tibia and fourth lumbar vertebra than in NX rats. There were significantly higher levels of OC in SCI rats compared with NX rats (30.19+/-1.17 vs. 21.15+/-1.76, P<0.001). Also, serum NTX levels were significantly higher than in NX rats (51.60+/-2.61 vs. 33.85+/-1.93, P<0.001). CONCLUSION: SCI caused more damage to bone mass, bone structure, biomechanical properties and bone metabolism than NX in young rats. This suggests that different mechanisms may underlie osteopaenia following SCI and NX.

Absorptiometry, Photon↗