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PubMed2005

Severe bone alterations under beta2 agonist treatments: bone mass, microarchitecture and strength analyses in female rats.

AIMS: Beta2 adrenergic agonists are widely used in therapeutics and as doping agents by athletes. However, their effects on bone tissue, especially bone microarchitecture, remain poorly understood. Using three-dimensional (3D) microtomography, dual-energy X-ray absorptiometry, biomechanical testing and enzyme-linked immunosorbent assay, we evaluated the effects of two beta2 agonists, clenbuterol and salbutamol, on bone in growing rats. METHODS: Twelve-week-old Wistar female rats (N = 39), divided in 3 groups, received during 6 weeks either salbutamol (4 mg/kg/day), clenbuterol (2 mg/kg/day) or normal saline (0.5 ml/kg/day) by subcutaneous injections. RESULTS: After 6 weeks, the salbutamol and clenbuterol groups displayed lower bone mineral content (BMC), femoral length and cortical width than controls. Clenbuterol treatment further reduced bone mineral density. Bone microarchitecture was clearly altered by clenbuterol, as evidenced by lower trabecular number (-40.40%; P < 0.001), connectivity and trabecular bone volume (-42.85%; P < 0.001), leading to lower ultimate force. Clenbuterol significantly increased muscle mass (P < 0.01) and reduced fat mass when compared to controls. Salbutamol did not seem to have any effect on bone microarchitecture or body composition. Both beta2 agonists increased the bone resorption marker (C-terminal collagen crosslinks) without any change of a bone formation marker. At the end of the treatment, a drop in leptin was seen in the clenbuterol group only. Leptin levels were correlated with BMC (r = 0.69, P = 0.003). CONCLUSION: These results confirm the deleterious effect of beta2 agonists on bone mass and show the negative effects of clenbuterol on trabecular bone microarchitecture. Bone loss occurred independently from muscle mass but was related to fat mass. A leptin-mediated effect on bone tissue seems likely. These pathophysiological effects may have important consequences in human therapeutics and doping.

Adrenergic beta-Agonists↗
PubMed2000

Activin release from bone coupled to bone resorption in organ culture of neonatal mouse calvaria.

Activin, a member of the transforming growth factor-beta (TGF-beta) superfamily, is present in the bone matrix and assumed to be involved in the regulation of bone formation. In the present study, we investigated whether the release of activin from bone is coupled with bone resorption. Neonatal mouse calvaria were cultured in the presence of various stimulators of bone resorption (parathyroid hormone [PTH], interleukin-1beta, prostaglandin E2) for up to 72 h, and the activin activity in the medium was measured using a specific bioassay for activin. Activin activity was accumulated in proportion to the time- and dose-dependent increase in calcium release from bone into the medium (bone resorption). An inhibition of PTH-dependent bone resorption by a bisphosphonate, disodium dichlormethane-1,1-bisphosphonic acid (Cl2MBP), completely blocked release of activin activity from bone into the medium. In primary culture of calvarial cells, however, neither PTH nor Cl2MBP affected activin production. These findings indicate that release of activin activity from bone tissue is strongly coupled to bone resorption. Because activin possesses osteogenic activities, activin released locally from bone might be involved in the regulation of bone formation in the physiological process of bone remodeling, as has been suggested for TGF-beta.

Activins↗
PubMed2000

Recombinant human bone morphogenetic protein-7 in maxillary sinus floor elevation surgery in 3 patients compared to autogenous bone grafts. A clinical pilot study.

BACKGROUND/AIMS: This pilot study was designed to determine the clinical bone formation ability of a human recombinant DNA bone morphogenetic protein-7, also referred to as Osteogenic Protein-1 [OP-1] combined with a collagen carrier, implanted in the maxillary sinus of 3 patients. The results were compared with a group of 3 patients treated with sinus floor elevation and autogenous bone grafts. METHODS: 6 consecutive patients, 4 female and 2 male, between 48 and 57 years of age were treated by means of sinus floor elevation for insufficient bone height in the posterior maxilla for implant surgery. 3 patients, 2 female and 1 male, were treated with OP-1 attached to a collagen device. In these patients, 4 maxillary sinus grafting procedures according to Tatum's method were carried out. 1 g of collagen carrier containing 2.5 mg rhOP-1 mixed with 3 ml of saline was placed between the bony floor and the elevated mucosal lining of the most caudal part of the maxillary sinus, in order to increase the vertical bone dimension to place dental implants of a sufficient length. The 3 other patients, also 2 female and 1 male, with a total of 5 sinus sites, were treated with sinus floor elevation and autogenous iliac crest bone grafts. After 6 months, during dental implant preparation, bone cores were taken for histology. Thus, clinical, radiological and histological results of the 2 groups of 3 patients were compared. RESULTS: 6 months after sinus grafting with OP-1, in 1 male, well-vascularized bone-like tissue of good quality was observed clinically. This could be confirmed by histology. In the second, female, patient no bone formation was observed at all. A cyst-like granular tissue mass, without purulent content, was removed. In the 3rd, female, patient, who received bilateral sinus grafts, some bone-like formation was seen, however it showed flexible tissue which led to the decision that at 6 months after the sinus grafting, the implant placement had to be postponed. In all 5 autogenous grafted sinuses a bone appearance similar to normal maxillary bone was observed clinically as well as histologically and dental implants could be placed six months after sinus floor elevation surgery. CONCLUSIONS: These findings indicate that the OP-1 device has the potential for initiating bone formation in the human maxillary sinus within 6 months after a sinus floor elevation operation. However, the various findings in these 3 patients indicate that the behaviour of the material is at this moment insufficiently predictable, in this indication area. Further investigation is indicated before OP-1 can be successfully used instead of the "gold standard" autogenous bone graft.

Biopsy↗
PubMed1996

Biochemical evaluation of bone turnover in cancer patients with bone metastases: relationship with radiograph appearances and disease extension.

Serum bone alkaline phosphatase (BALP), serum carboxy-terminal propeptide of type I procollagen (PICP) and serum bone gla protein (BGP) as markers of bone formation, serum carboxy-terminal telopeptide of type I collagen (ICTP) as a marker of collagen resorption and fasting molar ratio of urinary calcium to creatinine (CaCr) and serum parathyroid hormone (PTH) were determined in two groups of cancer patients: 48 with advanced or metastatic disease with negative bone scan and 174 with bone metastases categorised as having lytic, mixed or blastic lesions and with more or fewer than or equal to three sites involved. In patients without apparent bone involvement, bone formation markers were rarely elevated. Conversely, serum ICTP was frequently found to be supranormal, showing it to be a non-specific marker for early detection of bone metastases. As expected, values of bone formation markers progressively increased in patients with lytic, mixed and blastic lesions, but ICTP levels did not show any differences according to the types of bone appearances, confirming previous reports of elevated osteoclast activity also in patients with apparent blastic lesions. Serum PTH increased significantly in patients with lytic compared with patients with mixed and blastic appearances, paralleling the bone formation markers, but CaCr showed the opposite pattern. These data are compatible with calcium entrapment in the bone in patients with increased osteoblast activity. This so called 'bone hunger syndrome' is further confirmed by the finding that in the subgroup of blastic appearances CaCr diminished whereas both ICTP and PTH increased according to the extent of tumour load in the bone.

Adult↗
PubMed2004

Bone mineral assessment by dual energy X-ray absorptiometry in children with inflammatory bowel disease: evaluation by age or bone area.

BACKGROUND: Abnormal linear growth and deficient bone mineral acquisition may coexist in children with inflammatory bowel disease (IBD). Traditionally, bone mineral assessment by dual energy x-ray absorptiometry (DXA) involves comparison to age- and gender-matched reference ranges, and these studies in children with IBD show a high prevalence of osteopenia. AIMS: To compare the prevalence of osteopenia using two methods of interpretation; one adjusted for age and gender and the other adjusted for bone size and gender. PATIENTS: Forty-seven patients with Crohn disease (CD) and 26 patients with ulcerative colitis (UC) with a median age of 13.5 years (range, 5.5-18.2 years) were evaluated. METHODS: Lumbar spine (LS) and total body (TB) bone mineral content (BMC) were measured by DXA and converted to bone mineral density (BMD, g/cm) corresponding to BMC divided by the bone area. Age and gender-matched BMD standard deviation scores (SDS) were based on reference data providing age- and gender-matched BMC and bone area. These data also allowed calculation of percentage of predicted bone area for age and gender (ppBone Area) and percentage of predicted BMC for Bone Area (ppBMC). RESULTS: Patients with CD were shorter than those with UC (median height, SDS, -0.9 v 0, P < 0.05). Median ppBone Area for LS and TB for the whole group was 85% (10th centile, 68; 90th centile 99) and 81% (10th centile 66; 90th centile, 97), respectively. The ppBone Area at both sites was directly related to height SDS and BMI SDS (r > 0.5; P < 0.005). Median BMD SDS for LS and TB was -1.6 (10th centile -3.6; 90th centile, -0.2) and -0.9 (10th centile, -2.4; 90th centile, 0.4), respectively. Median ppBMC for LS and TB was 98% (10th centile, 84%; 90th centile, 113%) and 101% (10th centile 94%; 90th centile, 107%), respectively. The ppBMC showed no relationship to ppBone Area (r = 0.1, NS). Failure to account for bone area led to a label of moderate or severe osteopenia in 65% of cases. After adjustment for bone area, the proportion of children with osteopenia fell to 22%. CONCLUSIONS: The data suggest that children with IBD often have small bones for age because they have growth retardation. When DXA data are interpreted with adjustment for bone size, most children were found to have adequate bone mass. Correct interpretation of DXA is important for identifying children who may be at a real risk of osteoporosis.

Absorptiometry, Photon↗
PubMed2005

Alcohol-induced bone loss and deficient bone repair.

BACKGROUND: Chronic consumption of excessive alcohol eventually results in an osteopenic skeleton and increased risk for osteoporosis. Alcoholics experience not only increased incidence of fractures from falls, but also delays in fracture healing compared with non-alcoholics. In this review the term "alcohol-induced bone disease" is used to refer to these skeletal abnormalities. Alcohol-induced osteopenia is distinct from osteoporoses such as postmenopausal osteoporosis and disuse osteoporosis. Gonadal insufficiency increases the rate of bone remodeling, whereas alcohol decreases this rate. Thus, histomorphometric studies show different characteristics for the bone loss that occurs in these two disease states. In particular, alcohol-induced osteopenia results mainly from decreased bone formation rather than increased bone resorption. Human, animal and cell culture studies of the effects of alcohol on bone strongly suggest alcohol has a dose-dependent toxic effect on osteoblast activity. The capacity of bone marrow stromal cells to differentiate into osteoblasts has a critical role in the cellular processes involved in the maintenance of the adult human skeleton by bone remodeling. Chronic alcohol consumption suppresses osteoblastic differentiation of bone marrow cells and promotes adipogenesis. In fracture healing, the effect of alcohol is to suppress synthesis of an ossifiable matrix, possibly due to inhibition of cell proliferation and maldifferentiation of mesenchymal cells in the repair tissue. This results in the deficient bone repair observed in animal studies, characterized by repair tissue of lower stiffness, strength and mineral content. Current knowledge of cellular effects and molecular mechanisms involved in alcohol-induced bone disease is insufficient to develop interventional strategies for its prevention and treatment. OBJECTIVES: The objectives of this review are 1) to identify the characteristics of alcohol-induced bone loss and deficient bone repair as revealed in human and animal studies, 2) to determine the current understanding of the cellular effects underlying both skeletal abnormalities, and 3) to suggest directions for future studies to resolve current ambiguities regarding the cellular basis of alcohol-induced bone disease.

Animals↗
PubMed2006

Cranial bone regeneration using a composite scaffold of Beta-tricalcium phosphate, collagen, and autologous bone fragments.

OBJECTIVE: The aim of our study was to examine the tissue response and new bone formation induced by beta-tricalcium phosphate (beta-TCP), collagen, and autologous bone fragments with fibrin glue implanted into a cranial bone defect. MATERIALS AND METHODS: Granulated beta-TCP and collagen from porcine skin were mixed and freeze-dried. The weight ratio of both materials was 98:2. The composite scaffold for bone regeneration was composed of this artificial material and autologous bone fragments. Five adult beagle dogs were used. A cranial bone defect (2 cmx2 cm) was created in each dog. The animals were divided into two groups. In group 1 (n=3), the cranial bone defect was closed by replacing the original free bone flap, and the residual fissure and burr holes were filled with the composite scaffold with fibrin glue. In group 2 (n=2), the bone defect was closed only by replacing the original free bone flap. Three months after the treatment, computed tomography and histologic examinations were done in all animals. RESULTS: In all dogs in group 1, the defects were almost closed by new bone; whereas in group 2, the defects were filled with fibrous tissues instead of bone. CONCLUSION: This study showed that the composite scaffold made of beta-TCP, collagen, and autologous bone fragments with fibrin glue enabled reconstruction of cranial bone defects without the usual fixation materials.

Animals↗
PubMed1991

Role of peak bone mass and bone loss in postmenopausal osteoporosis: 12 year study.

OBJECTIVE: To examine the role of peak bone mass and subsequent postmenopausal bone loss in the development of osteoporosis and the reliability of identifying women at risk from one bone mass measurement and one biochemical assessment of the future bone loss. DESIGN: Population based study. SETTING: Outpatient clinic for research into osteoporosis. SUBJECTS: 178 healthy early postmenopausal women who had participated in a two year study in 1977. 154 of the women underwent follow up examination in 1989, of whom 33 were excluded because of diseases or taking drugs known to affect calcium metabolism. MAIN OUTCOME MEASURES: Bone mineral content of the forearm and values of biochemical markers of bone turnover. RESULTS: The average reduction in bone mineral content during 1977-89 was 20%, but the fast losers had lost 10.0% more than had the slow loser group (mean loss 26.6% in fast losers and 16.6% in slow losers; p less than 0.001). Prediction of future bone mineral content using baseline bone mineral content and estimated rate of loss gave results almost identical with the actual bone mineral content measured in 1989. Seven women had had a Colles' fracture and 20 a spinal compression fracture. The group with Colles' fracture had low baseline bone mineral content (34.7 (95% confidence interval 31.3 to 38.1) units v 39.4 (38.1 to 40.8) units in women with no fracture) whereas the group with spinal fracture had a normal baseline bone mineral content (38.1 (35.0 to 41.1) units) but an increased rate of loss (-2.4 (-3.5 to -1.3)%/year v -1.8 (-2.1 to -1.5)%/year in women with no fracture). CONCLUSIONS: One baseline measurement of bone mass combined with a single estimation of the rate of bone loss can reliably identify the women at menopause who are at highest risk of developing osteoporosis later in life. The rate of loss may have an independent role in likelihood of vertebral fracture.

Age Factors↗
PubMed1997

Prostaglandin E2 (PGE2) and risedronate was superior to PGE2 alone in maintaining newly added bone in the cortical bone site after withdrawal in older intact rats.

The objects of this study were (1) to determine the effects of risedronate (Ris) and prostaglandin E2 (PGE2) alone and in combination, on tibial diaphyses of older intact female rats; and (2) to observe the fate of any extra bone if formed after withdrawal of the treatment. Nine-month-old female Sprague-Dawley rats were treated with 6 mg of PGE2/kg/day, 1 or 5 micrograms of Ris/kg twice a week, or 6 mg of PGE2/kg/day plus 1 or 5 micrograms of Ris/kg twice a week for the first 60 days and followed by vehicle injections for another 60 days. Cross-sections of double fluorescent labeled, undecalcified tibial diaphyses proximal to the tibiofibular junction were processed for histomorphometry. We found that: (1) neither the 1 microgram nor the 5 micrograms of Ris treatment in the 60-day on/60-day off group showed any histomorphometric differences from age-related controls; (2) while the 60 days of PGE2 treatment added extra cortical bone (6%) on the tibial shaft (due to stimulation of periosteal, endocortical, and marrow trabecular bone formation), the new endocortical and most of the new marrow trabecular bone were lost when treatment was withdrawn; however, the new periosteal bone remained; (3) PGE2 with Ris added the same amount of new bone to tibial diaphysis as did PGE2 alone and upon withdrawal, new marrow trabecular bone was lost but new periosteal and endocortical bones were preserved in PGE2 + 1 microgram of Ris on/off group. In contrast, all the new bone was maintained in the PGE2 + 5 micrograms of Ris on/off group; (4) PGE2 + Ris cotreatment failed to block the increase in cortical bone porosity induced by PGE2; and (5) in the PGE2 alone and PGE2 + 1 microgram of Ris on/off groups bone turnover was higher than that in the PGE2 + 5 micrograms of Ris on/off group. These results indicate that on/off treatment with PGE2 and Ris is superior to PGE2 alone in that it forms the same amount of new bone during treatment, but preserves more cortical bone during withdrawal. Depression of bone resorption and turnover were the tissue mechanisms responsible for this protection.

Age Factors↗
PubMed2000

Immunosuppression with FK506 increases bone induction in demineralized isogeneic and xenogeneic bone matrix in the rat.

The aim of the present study was to investigate a systemic induction of bone formation in rats by immunosuppression with FK506 (1 mg/kg body weight intraperitoneally [ip]) in a model of osteoinduction of isogeneic and xenogeneic demineralized bone matrix (DBM) for a period of 28 days. In particular, alterations of in vitro cytokine synthesis and changes of lymphocyte subsets were studied. DBM was implanted intramuscularly in the abdominal wall of Lewis rats (seven per group). Blood was sampled on days -7, 0, 7, and 28 for determination of in vitro tumor necrosis factor a (TNF-alpha) synthesis and lymphocyte subsets by flow cytometry (CD3+, CD4+, CD8+, CD45+, ED9+, and Ia+ antibodies). Ossicles of de novo formed bone and the tibias were removed on day 28 after double tetracycline labeling for histomorphometric analysis. Immunosuppression with FK506 significantly decreased lipopolysaccharide (LPS)-stimulated in vitro cytokine synthesis after 7 days and 28 days (p < 0.05). Compared with control animals FK506 treatment significantly increased the volume of induced bone in isogeneic (2.1 +/- 0.3 mm3 vs. 10.8 +/- 0.9 mm3) and xenogeneic (O mm3 vs. 4.7 +/- 0.8 mm3) DBM. Bone histomorphometry of the tibias revealed that immunosuppression increased both bone formation and bone resorption, accompanied by a significant reduction in the relative trabecular area (Tb.Ar). FK506 caused a decrease in the counts of CD8+ T cells probably because of destruction or dislocation of these cells. This suggests that the amount of CD8+ cells and the degree of T cell activation in terms of mean fluorescence intensity (MFI) may be associated with bone metabolism. In support of this, statistical analysis revealed a significant positive correlation between parameters of bone formation as well as bone resorption and the CD4+/CD8+ ratio. There was a significant negative correlation between parameters of remodeling of the metaphysis of the tibia and induced bone volume (BV), respectively, and MFI values of CD3+/Ia+ cells. These findings suggest an important role of T lymphocytes in bone formation and bone resorption in vivo. FK506 caused a marked increase of bone formation in DBM. However, the conclusion that immunosuppression increases fracture healing warrants further investigation.

Alkaline Phosphatase↗
PubMed2006

Comparative effects of alendronate and alfacalcidol on cancellous and cortical bone mass and bone mechanical properties in ovariectomized rats.

The purpose of the present study was to compare the effects of alendronate and alfacalcidol on cancellous and cortical bone mass and bone mechanical properties in ovariectomized rats. Twenty-six female Sprague-Dawley rats, 7 months of age, were randomized by the stratified weight method into four groups: the sham-operated control (Sham) group and the three ovariectomy (OVX) groups, namely, OVX + vehicle, OVX + alendronate (2.5 mg/kg, p.o., daily), and OVX + alfacalcidol (0.5 mug/kg, p.o., daily). At the end of the 8-week experimental period, bone histomorphometric analyses of cancellous bone at the proximal tibial metaphysis and cortical bone at the tibial diaphysis were performed, and the mechanical properties of the femoral distal metaphysis and femoral diaphysis were evaluated. OVX decreased cancellous bone volume per total tissue volume (BV/TV), and the maximum load of the femoral distal metaphysis, as a result of increases in serum osteocalcin (OC) levels, and also the number of osteoclasts (N.Oc), osteoclast surface (OcS) and bone formation rate (BFR) per bone surface (BS), and BFR/BV, without any effect on cortical area (Ct Ar), or maximum load of the femoral diaphysis. Alendronate prevented this decrease in cancellous BV/TV by suppressing increases in N.Oc/BS, OcS/BS, BFR/BS, and BFR/BV, without any apparent effect on Ct Ar, or maximum load of the femoral distal metaphysis and femoral diaphysis. On the other hand, alfacalcidol increased cancellous BV/TV, Ct Ar, and the maximum load of the femoral distal metaphysis and femoral diaphysis, by mildly decreasing trabecular BFR/BV, maintaining trabecular mineral apposition rate and osteoblast surface per BS, increasing periosteal and endocortical BFR/BS, and preventing an increase in endocortical eroded surface per BS. The present study clearly showed the differential skeletal effects of alendronate and alfacalcidol in ovariectomized rats. Alendronate prevented OVX-induced cancellous bone loss by suppressing bone turnover, while alfacalcidol improved cancellous and cortical bone mass and bone strength by suppressing bone resorption and maintaining or even increasing bone formation.

Alendronate↗
PubMed1999

Qualitative analysis of peripheral peri-implant bone and influence of alendronate sodium on early bone regeneration.

BACKGROUND: Alendronate sodium increases alveolar bone density with systemic use. It inhibits osteoclast activity and is thought to result in a net increase in osteoblastic activity. However, little is known about local in vivo use. The purpose of this study was to evaluate the effect of local delivery of alendronate on bone regeneration within peri-implant defects. Peri-implant bone was examined histomorphometrically to evaluate the amount of supporting bone peripheral to the bone-implant interface. METHODS: Six adult hound dogs were evenly divided into 2 groups, with one group receiving alendronate-coated dental implants and the other group serving as controls. Dental implants were placed immediately after extraction of right and left second, third, and fourth mandibular premolars. Forty-eight dental implants were placed (2 types in each dog: 24 hydroxyapatite [HA]-coated and 24 titanium machine-polished [TMP]), for a total of 4 variables. A bioabsorbable collagen membrane was secured over the implants and defects, and the flaps closed primarily. The dogs were sacrificed on day 28. Specimens were sectioned, mounted, and stained with Stevenel's blue and van Gieson's picric fuchsin. The amount of bone adjacent and 1 mm peripheral to the implant surface was recorded with a computerized microscopic digitizer. RESULTS: Locally applied alendronate resulted in significantly increased amounts of bone (P<0.0002, ANOVA) in the peripheral area with both HA and TMP implants. However, the most influential factor in the amount of peripheral bone was the type of implant surface (P<0.0001). CONCLUSIONS: Local application of alendronate is useful in increasing the amount of peripheral peri-implant bone. Also, the amount of supporting bone was not related to the bone-to-implant contact but to the surface characteristics of the implant. The findings of the present study indicate that the evaluation of dental implant-supporting bone should include peripheral bone as well as bone-to-implant interface.

Alendronate↗
PubMed1999

Magnesium deficiency-induced osteoporosis in the rat: uncoupling of bone formation and bone resorption.

Magnesium (Mg) intake has been linked to bone mass and/or rate of bone loss in humans. Experimental Mg deficiency in animal models has resulted in impaired bone growth, osteopenia, and increased skeletal fragility. In order to assess changes in bone and mineral homeostasis that may be responsible, we induced dietary Mg deficiency in adult Simonsen albino rats for 16 weeks. Rats were fed either a low Mg diet (0.002 percent) or a normal control Mg diet (0.063 percent). Blood was obtained at baseline, 4 weeks, 8 weeks, 12 weeks and 16 weeks in both groups for serum Mg, calcium, PTH, and 1.25(OH)2-vitamin D determinations. Femora were harvested at 4 weeks and 16 weeks for mineral analysis and histomorphometry. Serum Mg fell in the Mg depleted group to 0.6 mg/dl (mean) by 16 weeks (controls = 2.0 mg/dl). The serum calcium (Ca) concentration was higher in the Mg depleted animals at 16 weeks, 10.8 mg/dl (controls = 8.9 mg/dl). Serum PTH concentration fell progressively in the Mg deficient rats to 30 pg/ml by week 16 (control = 96 pg/ml). Serum concentration of 1.25(OH)2-vitamin D also fell progressively in the Mg deficient animals by 16 weeks to 14 pg/ml (control = 30 pg/ml). While the percent ash weights of Ca and phosphorus in the femur were not different at any time point, the percent ash weight of Mg progressively fell to 0.54 percent vs control (0.74 percent) by 16 weeks. The percent ash weight of potassium also fell progressively in the Mg deficient group to approximately 30 percent of control by 16 weeks. Histomorphometric analyses showed a significant drop in trabecular bone volume in Mg deficient animals by 16 weeks (percent BV/TV = 13.2 percent vs 17.3 percent in controls). Evaluation of the endosteal bone surface features showed significantly greater bone resorption in the Mg depleted group as reflected in increased number of tartrate-resistant positive osteoclasts/mm bone surface (7.8 vs 4.0 in controls) and an elevated percent of bone surface occupied by osteoclasts (percent OcS/BS = 12.2 percent vs 6.7 percent in controls. This increased resorption occurred in the presence of an inappropriate lowered bone forming surface relative to controls; a decreased number of osteoblasts per mm bone surface (0.23 vs 0.94 in control) and a decrease in percent trabecular surface lined by osteoid (percent OS/BS = 0.41 vs 2.27 percent in controls) were also noted. Our findings demonstrate a Mg-deficiency induced uncoupling of bone formation and bone resorption resulting in a loss of bone mass. While the fall in PTH and/or 1.25(OH)2-D may explain a decrease in osteoblast activity, the mechanism for increased osteoclast activity is unclear. These data suggest that Mg deficiency may be a risk factor for osteoporosis.

Animals↗
PubMedDate not supplied

Titanium alloy osseointegration in cancellous and cortical bone of ovariectomized animals: histomorphometric and bone hardness measurements.

PURPOSE: Histomorphometry and microhardness measurements were performed after Ti6AI4V implantation in cancellous and cortical bone of healthy and ovariectomized animals to determine characterization of the bone-biomaterial interface in osteopenic bone. MATERIALS AND METHODS: Nine ovariectomized and 9 sham-aged rats were used. Four months later, nails were implanted in the distal femurs, and the animals were sacrificed after 8 weeks. Moreover, 3 ovariectomized and 3 sham-aged sheep were used. Twenty-four months later, screws were implanted in the tibial diaphyses and the animals were sacrificed after 12 weeks. RESULTS: Histomorphometry showed the development of osteopenia in both trabecular and cortical bone, and revealed a significant decrease in the osseointegration rate in osteopenic versus sham-aged animals for both trabecular (Affinity Index: -18.6%, P < .001) and cortical bone (Affinity Index: -23.5%, P < .005; Bone Ingrowth: -9%, P <.05). At the interfaces of the sham-aged animals in both trabecular and cortical bone, a decrease of bone microhardness was observed in comparison with preexisting bone (trabecular: -9.8%, P < .0005; cortical: -19.3%, P < .0005). In case of osteopenia, this decrease was even more extensive (trabecular: -15.5%, P < .0005; cortical: -24.7%, P < .0005). DISCUSSION: The present data suggest that bone formation around Ti6AI4V was not associated with complete bone maturation, even in healthy animals. In case of osteopenia, both bone formation and maturation were delayed. CONCLUSION: These results apparently demonstrate the utility of investigating biomaterials in osteopenic bone and the importance of careful evaluation of the healing rate and bone maturation degree around implanted biomaterials.

Alloys↗
PubMed2002

[Application of autogenous bone grafting with vascular anastomosis in treatment of nonunion of fracture and bone defect].

OBJECTIVE: To present a surgical choice for nonunion and bone defect. METHODS: From November 1994 to October 1997, 17 cases of nonunion of fracture and massive bone defect were treated by autogenous iliac bone and fibular bone with vascular anastomosis. Of 17 cases, there were 10 cases of nonunion of bone fracture, 7 cases of bone defect following tumor resection (4 cases of benign and 3 cases of malignant). Autogenous fibular bone grafting with vascular anastomosis, ranging from 12 cm to 29 cm in length, were employed in 12 cases; autogenous iliac bone grafting, ranging from 7 cm x 3 cm to 9 cm x 5 cm in size, were utilized in the other 5 cases. All of 17 cases were followed up for 10 months to 5 years, 3 years and 7 months in average, and were evaluated from clinical manifestation. RESULTS: Bone union was achieved in 10 cases of nonunion of fracture after bone grafting, bony refilling of the bone defect was observed in 4 cases due to benign tumor and 1 case due to malignant tumor. The other 2 cases of malignant tumor died from lung metastasis of the tumor 10 months and 12 months after bone grafting, respectively. CONCLUSION: Bone grafting is an effective surgical option in treatment of nonunion of fracture and bone defect.

Adolescent↗
PubMed2003

Stereo visualization of 3D trabecular bone structures produced by bone remodelling simulation.

Adult human bone is constantly being renewed by a process known as remodelling. For cancellous bone this renewal process occurs at the interface between bone and marrow where bone is depleted by osteoclasts and rebuilt by osteoblasts. This remodelling process allows bone to repair itself. Software simulators for bone remodelling provide insight into the bone remodelling process; they allow investigation into bone form and structural properties, and they also allow the emulation of bone diseases and possible treatments for these diseases over long periods of time. BONESIM is a software that simulates bone remodelling in terms of Basic Multi-cellular Units (BMUs). 3D visualization of trabecular bone and its attributes is an essential tool in understanding this remodelling process for cancellous bone. It enables the bone researcher to quickly understand the dynamic behaviour of remodelling, the resulting geometry of the bone structure and it allows alternative remodelling scenarios to be compared. This paper presents the volume visualization technique that has been developed to provide this visualization tool.

Adult↗
PubMed1991

Difference in size of bone islands formed by isolated bone cells transplanted intramuscularly under various conditions.

Bone cells isolated from the whole calvaria (2 x 10(6)) from either central or peripheral parts of parietal bones (1 x 10(6)) and from scapulas (2 x 10(6)) were allowed to adhere to devitalized calvarial bones in the number indicated in brackets and transplanted intramuscularly (supported transplants). Whole calvaria bone cells (2.4 or 8 x 10(6) cells per transplant) were also injected intramuscularly as free transplants. Calvarial cells produced solid bone islands with small intraosseous cavities, while bone formed by scapular cells contained large medullary spaces. The size of bone islands formed in transplants and the shortest distance between the neighbor islands were measured. The results of these measurements were similar in all groups of free transplants. The size of bone islands formed in supported transplants of cells from the whole calvaria or from central and peripheral parts of parietal bones was also roughly similar, but the shortest distance between islands was larger than in the free transplants. Furthermore, in these groups of transplants bone islands considerably larger than the largest islands in free transplants were present. Scapular bone cells formed islands much larger than those produced by calvarial cells. Bone islands formed by calvarial cells in free transplants were separated by bands of fibrous tissue which was absent in supported transplants. It appears that this tissue could limit growth and/or fusion of neighbor bone islands and in this manner influence their size. The population of transplanted scapular cells contained numerous stromal elements which could form an exclusion area inaccessible to local cells from the site of transplantation and thus favour formation of large bone islands within this area.

Animals↗
PubMed2005

Microcracks in cortical bone: how do they affect bone biology?

Microcrack accumulation in cortical bone has been implicated in skeletal fragility and stress fractures. These cracks have also been shown to affect the mechanical and material properties of cortical bone. Their growth has been linked to osteocyte apoptosis and the initiation of the remodeling process, which also has a role in their repair. Clinically, osteoporosis is diagnosed using dual energy x-ray absorptiometry. However, evidence now indicates that bone mass alone is insufficient to satisfactorily explain the skeletal fragility of osteoporosis and consideration needs to be given to bone quality in the diagnosis and treatment of the disease. Bone quality includes parameters such as trabecular and cortical microarchitecture, morphology, bone turnover, degree of mineralization of the bone matrix, and significantly, the amount of microdamage present in the bone. Current clinical treatments concentrate on the inhibition of osteoclast activity to maintain bone mass in osteoporotic patients. However, these cells have a major role in removing existing microcracks from the bone matrix, and hence the use of bone resorption- inhibiting drugs may lead to insufficient bone repair and therefore an increase in microdamage accumulation and loss of bone quality.

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