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PubMed2005

[Experimental study of tissue engineered bone with cryopreservation on healing of bone defects].

OBJECTIVE: To investigate the effect of tissue engineered bone with cryopreservation on healing of bone defects and to explore feasibility of cryopreservation for tissue engineered bone. METHODS: Tissue engineered bones were constructed with osteoblasts being seeded onto bio-derived materials made from fresh human bones,and they were preserved at 4 degrees C and - 196 degrees C for 3 months and 6 months respectively. They were applied to repair segmental bone defects of rabbit's radius while the tissue engineered bone without cryopreservation and bio-derived materials were brought into control groups. The experiment was divided into groups A3, A6, B3, B6, C and D (group A3: tissue engineered bones were preserved at 4 degrees C for 3 months; group A6: tissue engineered bones were preserved at 4 degrees C for 6 months; group B3:tissue engineered bones were preserved at --196 degrees C for 3 months; group B6:tissue engineered bones were preserved at - 196 degrees C for 6 months; group C: tissue engineered bones without cryopreservation; group D: bio-derived materials). Macroscopical and histological examination were done at the 2nd, 4th, 6th, 12th weeks, X-ray examination was done at the 6th, 12th weeks and biomechanics were determined at 12th weeks after operation respectively. RESULTS: Macroscopical observation showed no significant differences among group A3, A6, B3, B6 and C, but less new bone formation and more obvious boundary in group D were observed. Histological observation showed more collagen and new bone around the edge of implant of group A3, A6, B3, B6 and C than group D, and histological evaluation showed significant differences between group D and other groups (P <0.05). Radiographic observation showed no absorbability of the implant cortex and less new bone formation in group D, but the unity between implant and host bone, medullary cavity reopened, disappearance of fracture line and fine bone modelling were observed in other groups at 12 weeks after operation. Biomechanics between group D and other groups showed significant differences (P< 0. 05). CONCLUSION: Cryopreservation (4 degrees C and - 196 degrees C) were capable of preserving tissue engineered bone for long time, and tissue engineered bone with cryopreservation has significant effect on healing of bone defects. The methods fit clinical application.

Animals↗
PubMedDate not supplied

Intramuscular bone induction by the simultaneous administration of recombinant human bone morphogenetic protein 2 and bisphosphonate for autobone graft.

An ideal substitute for bone graft is autobone tissue, of which there is an ample supply of the required form and with vascularity. Our strategy is to generate intramuscular autogenous bone by administering recombinant human bone morphogenetic protein 2 (rhBMP-2) with beta-tricalcium phosphate (beta-TCP) as a carrier, and to transplant this bone as a muscle-pedicled autograft. However, in a previous study (Jingushi et al., J. Orthop. Sci. 7, 490, 2002), bone resorption occurred early after bone induction. This study was conducted to determine whether rhBMP-2-induced bone tissue could be maintained by simultaneous administration of bisphosphonate, and to investigate whether the induced bone could be used for bone grafting. In this study, we first applied rhBMP-2 alone to a beta-TCP disk and inoculated it into rat quadriceps muscle. Bone area and the number of tartrate-resistant acid phosphatase (TRAP)-positive cells in the induced bone disk peaked at 2 weeks, and induced bone resorption occurred later. Bisphosphonate and rhBMP-2 were then simultaneously applied to a beta-TCP disk and inoculated as in the first experiment. The addition of bisphosphonate decreased the number of TRAP-positive cells and increased the bone area and compression strength at 4 weeks. In the last experiment, a rhBMP-2 applied beta-TCP disk treated with or without bisphosphonate was free-grafted to parietal bone 4 weeks after inoculation. Both bone disks united similarly. We concluded that the concurrent use of bisphosphonate prevented bone absorption attributed to osteoclast activity after bone induction by rhBMP-2. The bisphosphonate application did not disturb the union of induced bone to host bone.

Animals↗
PubMed2001

[Clinical application of bone metabolism markers to disuse bone atrophy].

Mechanical stress on bone is one of the determinants of bone morphology, bone mineral density and bone strength. Therefore, disuse accelerates bone resorption, especially of cancellous bone, and consequently bone becomes atrophic and fragile. Osteocytes embedded in the bone matrix respond to mechanical load and changes of bone metabolism. The gapjunction of the long processes of osteocytes plays an important role in transmitting mechanical load through intracellular signal transmitters (cAMP, cGMP) and extracellular signal transmitters (PGE(2), IGF- I , IGF- II , TGF-beta) , to induce bone formation by osteoblasts and bone resorption by osteoclasts, or a combination of the two. Bone metabolism markers reflect activities of osteoblasts and osteoclasts, so they provide information on bone turnover and bone metabolism. Bone resorption markers characteristically increase and remain high during bed rest and disuse, whereas ambulation and exercise, as in kinesiotherapy, decrease bone resorption markers. As for treatments of disuse bone atrophy, from the bone metabolic and pharmacological viewpoint, anti-resorption agents are recommended to inhibit bone loss. Bisphosphonates which are strong anti-resorption agents, are expected to inhibit bone resorption. Calcitonin and vitamin K(2) which are also anti-resorption agents effectively, reduce bone loss due to disuse and bed rest.

English Abstract↗
PubMed1999

Markers of bone turnover predict postmenopausal forearm bone loss over 4 years: the OFELY study.

The ability of biochemical markers to predict the rate of postmenopausal bone loss is still controversial. To investigate this issue further, baseline levels of a panel of specific and sensitive biochemical bone markers were correlated to the rate of change of forearm bone mineral density (BMD) assessed by four measurements over a 4-year period using dual-energy X-ray absorptiometry in a large population-based prospective cohort of 305 women aged 50-88 years (mean 64 years), 1-38 years postmenopausal. In the whole population, higher baseline levels of bone formation (serum osteocalcin and serum type I collagen N-terminal propeptide) and bone resorption markers (urinary N-telopeptides; urinary and serum C-telopeptides) were significantly associated with faster BMD loss (r = -0.19 to -0.30, p < 0.001), independently of age. In women within 5 years of menopause that have the highest rate of bone loss, the predictive value of bone markers was increased with correlation coefficients reaching 0.53. Women with an abnormally high bone turnover, i.e., with levels of bone markers at baseline 2 SD above the mean of premenopausal women, had a rate of bone loss that was 2- to 6-fold higher than women with a low turnover (p = 0.01-0.0001) according to the marker. When the population was categorized according to quartiles of bone markers at baseline, a similar relationship between increased levels of bone markers and faster rate of bone loss was found (p = 0.008-0.0001). In the logistic regression model, the odds-ratio of fast bone loss, defined as the rate of bone loss in the upper tertile of the population, was increased by 1.8- to 3.2-fold for levels of biochemical markers in the high turnover group compared with levels within the premenopausal range, with, however, a limited value for identifying individual fast bone losers. We conclude that increased levels of some of the new biochemical markers of bone turnover are associated with greater radial bone loss. Because increased bone loss is associated with an increased risk of fracture, bone turnover markers may be useful to improve the prediction of the risk of osteoporosis in postmenopausal women.

Aged↗
PubMed2005

Effect of alendronate administration on bone mineral density and bone strength in castrated rats.

Castration of male rats leads to increased bone turnover and osteopenia. This study was conducted to examine the effects of the aminobisphosphonate alendronate on castration-induced bone changes. Bisphosphonates are drugs that inhibit bone turnover by decreasing the resorption. Since they suppress bone remodeling, they may also prevent the repair of microdamage and decrease bone strength. Although the mechanical properties of bones are directly related to the determination of fracture risk, bisphosphonate effects on the related variables have scarcely been investigated. Twenty-four male Wistar rats at two months of age were castrated or sham-operated to evaluate the effects of long-term administration (six months) of sodium alendronate at a dose of 1 mg/kg/day. The bones were tested mechanically by a three-point bending test in a Mini Bionix (MTS) testing system. High bone remodeling seen in castrated rats expressed by increased TrACP and B-ALP was suppressed by alendronate administration. Bone from castrated rats was characterized by a reduction in bone density as well as ash, calcium and phosphate content. Castration significantly altered mechanical properties of bone and femoral cortical thickness. When castrated rats were treated with high dose of alendronate, the changes in bone density resulting from castration were entirely prevented, and mechanical analysis revealed preserved mechanical strength of femur and cortical thickness. We conclude that castration induces cortical bone loss associated with high bone turnover in the male rat, and this bone loss can be prevented by alendronate through the inhibition of osteoclastic activity, while preserving the mechanical properties of bone. These results document the efficacy of alendronate, even at high doses, in preventing bone loss, loss of bone mechanical strength, and the rise in biochemical bone turnover indicators due to castration in rats, and raises the possibility that a alendronate could be equally effective in humans.

Acid Phosphatase↗
PubMedDate not supplied

[Study of renal osteodystrophy by bone biopsy. Age as an independent factor. Diagnostic value of bone remodeling markers].

The spectrum of bone disease in uremic patients on hemodialysis has changed in the last years. Undecalcified bone biopsy with histomorphometric measurements and tetracycline labelling remains the gold standard for diagnosis of the different forms of renal osteodystrophy. But because of its invasive nature and complicated laboratory processing a number of non-invasive biochemical parameters have been proposed. The aim of our study was to determine the prevalence of the different forms of renal osteodystrophy in our patients in hemodialysis. Moreover we analyse the correlation between several biochemical parameters and the histological findings and evaluate their diagnostic and predictive value. Transiliac bone biopsies were performed in seventy three uremic patients (31 males) on chronic hemodialysis and static and dynamic parameters were measured. Serum levels of intact parathyroid hormone (iPTH), osteocalcin (OC), total alkaline phosphatase (FAT) and bone alkaline phosphatase (FAO) were determined. High-bone remodelling (50 pts, 68.5%) predominates over low-bone remodelling (23 pts, 31.5%). The distribution of the different types of bone disease was: Mild hyperparathyroidism 8 pts, Osteitis fibrosa 37 pts, Mixed lesions 5 pts, Adynamic bone disease 21 pts and Osteomalacia 2 pts. Six of our 73 patients were diabetics and they had adynamic bone disease (4 pts), osteomalacia (1 pt) and osteitis fibrosa (1 pt). Patients older than 50 years presented lower cellular activity (osteoblast surface, ObS/BS) and lower bone formation rate (BFR/BS). iPTH showed different correlation with these parameters of bone formation in patients above and below 50 years old suggesting that older patients need higher levels of PTH to obtain a determined level of bone formation. iPTH, OC, FAT and FAO correlated with the majority of histomorphometric indices of bone formation and resorption, though the best correlations were those with iPTH. The diagnostic and predictive value of these bone markers is better with high-bone remodelling. Serum levels of FAT > 300 U/l, OC > 150 ng/ml, FAO > 40 ng/ml and iPTH > 200 pg/ml showed a positive predictive value of 1 (with a specificity of 1, but sensibility below 0.78 except for iPTH that is 0.95) in the diagnosis of high-bone remodelling. After an analysis with ROC curves the cut-off value to differentiate high from low-bone remodelling was obtained. iPTH level > 200 pg/ml combined with one of the other markers (FAT > 150 U/l, FAO > 30 ng/ml or OC > 100 ng/ml) are predictive of high-bone remodelling, while values below those figures are predictive of low-bone remodelling.

Age Factors↗
PubMed1994

Effect of bone mineral particles on the porosity of bone cement.

Bone particle-impregnated bone cement is investigated in vitro, which could be used to improve fixation between bone and cement interface by ingrowth of tissues that may replace bone particles. Inorganic bone particles (150-300 microns diameter) were mixed with regular bone cement powder by 0, 10, 20, and 30% by weight and implanted into the pre-drilled intramedullary canal (11cm long, 10mm diameter) of canine femur. A 4mm diameter, 10mm long stainless steel rod was implanted to simulate the prosthesis. The specimens were cut into 2mm thick discs transversely along the long axis of the bone and ground to examine with a confocal laser microscope. Diametral tensile strength tests were performed for the 0, 10, 20, and 30% bone particle impregnated bone cement discs without the intramedullary implant. Present results show that mixing bone particles with bone cement decreased the number of pores and porosity but increased the size of pores. The analysis of porosity distribution showed no significant difference between bone cement and bone particle-impregnated bone cement. Also, the strength of the bone particle-impregnated bone cement decreased linearly with increased amount of bone particles in spite of the decreased percent porosity. Using a bone particle-impregnated bone cement along with a pre-coated implant could be one of the solutions to the problems in the fixation of total joint arthroplasty.

Animals↗
PubMedDate not supplied

Radiographic analysis of regenerated bone around endosseous implants in the canine using recombinant human bone morphogenetic protein-2.

Ideal endosseous implant placement involves a congruent bony housing in close apposition to the implant surface. Clinical situations are encountered, however, in which the entire implant surface cannot be in close apposition to bone. In these instances, bone grafting materials are generally used to regenerate bone around the implant. In this study, a biologically active bone differentiation factor, recombinant human bone morphogenetic protein-2 (rhBMP-2), was used with two different carriers to regenerate bone around implants in standardized critical-sized defects in the canine mandible. Half of the sites had a nonresorbable membrane placed over the defect. Longitudinal standardized radiographs were obtained to assess the amount of bone regeneration on the mesial and distal of the implants after 4 and 12 weeks of healing. Ninety-six implants were placed in 12 fox-hounds. Bone fill was determined by linear measurement of bone on the radiographs, and changes in bone density were evaluated by computer-assisted densitometric image analysis of discrete areas adjacent to the implant. After 4 weeks of healing, nonmembrane sites had significantly greater bone height than membrane-protected sites. Following 12 weeks of healing, sites treated with rhBMP-2 had significantly greater bone formation than untreated sites. Sites treated with rhBMP-2 and a membrane had the greatest bone fill, followed by sites treated with rhBMP-2 but no membrane. Sites without rhBMP-2, whether with or without a membrane, had less bone fill than sites with rhBMP-2. At 12 weeks, sites with a membrane resulted in significantly more gain in bone density than sites without a membrane. Furthermore, sites treated with a collagen carrier resulted in greater gains in bone density than sites treated with a polylactide/glycolide carrier. The results from this study demonstrate by radiographic evidence that new bone formation in critical-sized defects around implants is dependent on time after defect treatment, the type of carrier used, the use of a barrier membrane, and the presence of rhBMP-2. In addition, these findings suggest that rhBMP-2, a bone differentiation factor, can significantly stimulate bone formation around endosseous dental implants.

Analysis of Variance↗
PubMedDate not supplied

Biochemical parameters of bone metabolism in bone metastases of solid tumors (review).

The role of biochemical markers of bone metabolism in the diagnosis and monitoring of bone metastases in solid tumors is reviewed. Emphasis is on the recently developed markers, which may provide a more accurate quantitation of bone metabolism. In metastatic bone disease, bone formation and resorption become uncoupled processes, leading to predominantly osteoblastic or osteolytic metastases. In osteolytic metastases, bone resorption is enhanced without appropriate acceleration of bone formation. In osteolytic metastases the resorption markers are indicated for the detection of bone metastases. Urinary pyridinium cross-links and serum collagen telopeptides are sensitive and specific markers of bone resorption. These markers, can often identify bone metastases before visualization by imaging techniques. When osteolytic lesions are responding to treatment the physiologic coupling between bone resorption and formation is partly restored. An increase in formation markers, bone specific isoenzyme of alkaline phosphatase (BSAP), osteocalcin (OC) and carboxyterminal propeptide of collagen type I (PICP), will then closely reflect restoration of coupling. In osteoblastic metastases, bone formation markers can accurately indicate early and advanced bone involvement. Bone resorption markers are less sensitive in these osteoblastic lesions. The collagen telopeptides however, are resorption markers with the ability to detect early bone metastases. Osteoblastic lesions responding to therapy are indicated by declining values of formation as well as resorption markers. The precise role of the recently developed markers of bone metabolism in early diagnosis and monitoring of bone metastases needs further evaluation in longitudinal studies. Since the delicate derangements in bone metabolism may be obscured in mixed patient groups, these studies should address uniform patient groups with respect to the primary tumor type.

Biomarkers↗
PubMed2004

Dissociation between global markers of bone formation and direct measurement of spinal bone formation in osteoporosis.

UNLABELLED: Regional bone metabolism measured using 18F-fluoride PET was assessed in 72 postmenopausal women classified as normal, osteopenic, or osteoporotic. Lower values of regional bone formation activity at the lumbar spine were seen in osteoporotic women, whereas global markers of bone formation were significantly increased. INTRODUCTION: Evaluations of global bone remodeling have revealed that increased bone turnover is a feature of patients with osteoporosis. The noninvasive functional imaging technique of 18F-fluoride positron emission tomography (PET) allows the direct quantitative assessment of bone metabolism at specific sites in the skeleton, including the clinically important site of the lumbar spine. MATERIALS AND METHODS: The aim of this study was to compare regional skeletal kinetics in 72 postmenopausal women (mean age, 61 years) classified as normal, osteopenic, or osteoporotic according to their BMD T score at the lumbar spine. Each woman had a dynamic PET scan of the lumbar spine after injection of 90 MBq 18F-fluoride ion and measurements of biochemical markers of bone formation and resorption. The arterial plasma input function was derived using aorta arterial activity from the PET image. Time-activity curves were obtained by placing regions of interest over the lumbar vertebrae. A three-compartmental model was used to calculate bone blood flow (K1) and the net plasma clearance of tracer to bone mineral (Ki), reflecting regional osteoblastic activity (ml/minutes/ml). Rate constants k2, k3, and k4, which describe transport between plasma, the extracellular fluid (ECF) compartment, and the bone mineral compartment, were also measured. RESULTS: The net uptake of fluoride to the bone mineral compartment (Ki) was significantly lower in the osteoporotic group compared with both the osteopenic and normal groups, with a mean difference of 0.005 ml/minutes/ml (16.7%). The fraction of the tracer in the extravascular tissue space that underwent specific binding to bone mineral (k3/k2 + k3) was also significantly reduced in the women classified as osteoporotic. In contrast, levels of bone-specific alkaline phosphatase (BSALP) were significantly higher in the osteoporotic group compared with the normal and osteopenic groups by 35% and 27%, respectively. A significant negative correlation (r = -0.41) was observed between levels of BSALP and the fraction of the tracer that underwent specific binding to bone mineral. CONCLUSION: Lower values of Ki, a measurement of regional bone formation activity, were seen in women classified as osteoporotic, whereas levels of BSALP, a measure of global bone formation, were significantly increased. These findings are suggestive of increased global skeletal bone turnover in women with postmenopausal osteoporosis but with relatively reduced regional bone formation at the predominantly trabecular site of the lumbar spine.

Absorptiometry, Photon↗
PubMed2007

Platelet-rich plasma inhibits demineralized bone matrix-induced bone formation in nude mice.

BACKGROUND: It is unclear whether platelet-rich plasma is a clinically effective adjunct to osteoinductive agents such as demineralized bone matrix. It contains platelet-derived growth factor (PDGF), which decreases osteoinduction by human demineralized bone matrix in nude-mouse muscle, suggesting that platelet-rich plasma may also have a negative impact. This study tested the hypothesis that platelet-rich plasma reduces demineralized bone matrix-induced bone formation and that this effect varies with donor-dependent differences in platelet-rich plasma and demineralized bone matrix. METHODS: Human platelet-rich plasma was prepared from blood from six men (average age [and standard error of the mean], 29.2 +/- 2.4 years). Platelet numbers were determined, and growth factors were quantified before and after platelet activation. Human demineralized bone matrix from two donors (demineralized bone matrix-1 and demineralized bone matrix-2) was mixed with activated platelet-rich plasma and was implanted bilaterally in the gastrocnemius muscle in eighty male nude mice (eight implants per variable). Fifty-six days after implantation, the hindlimb calf muscles were harvested for histological analysis. Osteoinduction was evaluated with use of a qualitative score and morphometric measurements of ossicle size, new bone formation, and residual demineralized bone matrix. RESULTS: Compared with platelet-poor plasma, platelet-rich plasma preparations exhibited a fourfold increase in the platelet count, a fifteenfold increase in the amount of transforming growth factor-beta, a sixfold increase in the amount of PDGF-BB, a fivefold increase in the amount of PDGF-AA, and a twofold increase in the amount of PDGF-AB. Demineralized bone matrix-1 was more osteoinductive than demineralized bone matrix-2, as determined on the basis of a greater ossicle area. The effect of platelet-rich plasma was either neutral or inhibitory depending on the demineralized bone matrix batch. When used with demineralized bone matrix-1, platelet-rich plasma did not alter the qualitative score or overall ossicle size, but it decreased the new bone area. When used with demineralized bone matrix-2, platelet-rich plasma reduced the qualitative score, ossicle area, and new bone area and increased the amount of residual demineralized bone matrix. The effects on osteoinduction also varied with the donor of the platelet-rich plasma. CONCLUSIONS: Platelet-rich plasma decreased the osteoinductivity of demineralized bone matrix implanted in immunocom-promised mice, and the activities of both demineralized bone matrix and platelet-rich plasma were donor-dependent.

Adult↗
PubMed1995

Bone metabolic markers in bone metastases.

The efficacy and cost/performance benefit of radionuclide bone scintigraphy in monitoring metastatic bone activity remain controversial. Recently developed bone metabolic markers are expected to play an additional role in the diagnosis of bone metastasis. We measured osteoclastic and osteoblastic markers in 267 patients with breast cancer (100 with bone metastasis), 38 patients with prostatic cancer (25 with bone metastasis), 50 patients with lung cancer (12 with bone metastasis) and 33 patients with miscellaneous cancers (13 with bone metastasis) and compared the values in the presence and absence of bone metastasis. Bone metabolic markers, both osteoclastic and osteoblastic, increased significantly in patients with bone metastasis. In breast cancer (bone metastasis is mostly of the mixed type), osteoclastic markers were good in detecting bone metastasis. In prostatic cancer (bone metastasis is mostly osteoblastic), osteoclastic and osteoblastic markers were equally effective in detecting bone metastasis. In lung cancer (bone metastasis is mostly osteolytic), osteoclastic markers were elevated preferentially in bone metastasis. Over all, osteoclastic markers were more sensitive in the diagnosis of bone metastasis, and among osteoclastic markers, serum pyridionoline-cross-linked carboxyterminal telopeptide was the most efficient in both specificity (91.0%) and sensitivity (48.6%) for detecting bone metastasis.

Aged↗
PubMed2004

Repair of local bone erosions and reversal of systemic bone loss upon therapy with anti-tumor necrosis factor in combination with osteoprotegerin or parathyroid hormone in tumor necrosis factor-mediated arthritis.

Local bone erosion and systemic bone loss are hallmarks of rheumatoid arthritis and cause progressive disability. Tumor necrosis factor (TNF) is a key mediator of arthritis and acts catabolically on bone by stimulating bone resorption and inhibiting bone formation. We hypothesized that the concerted action of anti-TNF, which reduces inflammation and parathyroid hormone (PTH), which stimulates bone formation, or osteoprotegerin (OPG), which blocks bone resorption and could lead to repair of local bone erosions and reversal of systemic bone loss. To test this, human TNF-transgenic mice with established erosive arthritis and systemic bone loss were treated with PTH, OPG, and anti-TNF, alone or in combination. Local bone erosions almost fully regressed, on combined treatment with anti-TNF and PTH and/or OPG, suggesting repair of inflammatory skeletal lesions. In contrast, OPG and anti-TNF alone led to arrest of bone erosions but did not achieve repair. Treatment with PTH alone had no influence on the progression of bone erosions. Local bone erosions all showed signs of new bone formation such as the presence of osteoblasts, osteoid formation, and mineralization. Furthermore, systemic bone loss was completely reversed on combined treatment and this effect was mediated by osteoblast stimulation and osteoclast blockade. In summary, we conclude that local joint destruction and systemic inflammatory bone loss because of TNF can regress and that repair requires a combined approach by reducing inflammation, blocking bone resorption, or stimulating bone formation.

Animals↗
PubMed1999

Formation of bone around titanium implants placed into zero wall defects: pilot project using reinforced e-PTFE membrane and autogenous bone grafts.

BACKGROUND: Guided bone regeneration (GBR) frequently is used to augment implants with various types of bone defects. The defects often are grafted with different materials, yet there is insufficient evidence that these materials enhance bone-to-implant contacts. PURPOSE: The purpose of this pilot project was to test the principle of GBR to promote bone formation adjacent to commercially pure titanium implants placed within zero-wall defects. Histologic and histomorphometric measurements were used to evaluate new bone formation. MATERIALS AND METHODS: Under appropriate anesthesia, deep, wide defects were created within the mandibles of two large dogs. Buccolingual bone was removed to the depth of the defects leaving only the mesial and distal walls. Of the eight implants placed, three were augmented with titanium-reinforced expanded polytetrafluoroethylene (e-PTFE) barriers and autogenous bone chips. Three sites were augmented with barrier membranes only, and two sites were not augmented or grafted and served as controls. Seven months after surgery the dogs were sacrificed and block sections were taken for histologic evaluation. RESULTS: Histologic and histomorphometric measurements were used to evaluate new bone formation. Results from this evaluation revealed bone formation at the membrane-only sites and the membrane-plus-bone grafted sites. The bone grafts were completely incorporated by the newly formed marginal compact bone. For all treated sites, there was poor bone-to-implant contact. Histomorphometric measurements showed a trend toward greater bone formation at membrane-treated sites compared with control sites. However, autogenous bone grafting did not seem to affect the amount of newly regenerated bone. CONCLUSIONS: Within the limits of this pilot project, findings show trends toward bone healing, indicating constant and enhanced bone regeneration over the exposed implant. Bone contact to the implant surface generally was poor.

Animals↗
PubMed1994

Interleukin-1 receptor antagonist decreases bone loss and bone resorption in ovariectomized rats.

Interleukin-1 (IL-1), a cytokine produced by bone marrow cells and bone cells, has been implicated in the pathogenesis of postmenopausal osteoporosis because of its potent stimulatory effects on bone resorption in vitro and in vivo. To investigate whether IL-1 plays a direct causal role in post ovariectomy bone loss, 6-mo-old ovariectomized rats were treated with subcutaneous infusions of IL-1 receptor antagonist (IL-1ra), a specific competitor of IL-1, for 4 wk, beginning either at the time of surgery or 4 wk after ovariectomy. The bone density of the distal femur was measured non invasively by dual-energy X-ray absorptiometry. Bone turnover was assessed by bone histomorphometry and by measuring serum osteocalcin, a marker of bone formation, and the urinary excretion of pyridinoline cross-links, a marker of bone resorption. Ovariectomy caused a rapid increase in bone turnover and a marked decrease in bone density which were blocked by treatment with 17 beta estradiol. Ovariectomy also increased the production of IL-1 from cultured bone marrow cells. Ovariectomy induced-bone loss was significantly decreased by IL-1ra treatment started at the time of ovariectomy and completely blocked by IL-1ra treatment begun 4 wk after ovariectomy. In both studies IL-1ra also decreased bone resorption in a manner similar to estrogen, while it had no effect on bone formation. In contrast, treatment with IL-1ra had no effect on the bone density and the bone turnover of sham-operated rats, indicating that IL-1ra specifically blocked estrogen-dependent bone loss. In conclusion, these data indicate that IL-1, or mediators induced by IL-1, play an important causal role in the mechanism by which ovariectomy induces bone loss in rats, especially following the immediate post ovariectomy period.

Animals↗
PubMed2005

Evaluating bone mass and bone quality in patients with breast cancer.

Bone remodeling is a process by which bone renews itself focally in distinct areas on cancellous (ie, trabecular) bone and/or in the Haversian systems of cortical (or compact) bone. Normal bone turnover involves the ordered metabolism of bone-resorbing cells (osteoclasts) and bone-forming cells (osteoblasts). Estrogen exerts a multitude of actions on bone tissues and is integral to bone health, and estrogen deprivation leads to accelerated bone loss. Bone strength reflects the integration of bone density and bone quality. Methods to assess bone strength fall into 3 categories: radiologic (ie, bone mineral density [BMD]), biochemical (ie, markers of bone turnover), and histologic (ie, bone biopsies for histomorphometry). The beneficial effect of aromatase inhibitors (AIs) and inactivators on breast cancer depends on reducing levels of circulating estrogens in the peripheral blood. There appears to be variability in the effects of AIs on bone in experimental animals, and this variability may not be the same in humans. In general, bone loss is an expected side effect of the AIs. For postmenopausal women receiving adjuvant anastrozole or other AIs, a BMD measurement using dual-energy x-ray absorptiometry is recommended, to be repeated every 1-2 years. Regular physical exercise is advised together with added calcium 1500 mg and vitamin D 800 U daily. If the T-score reaches a level of >2.5, or if it is between -1.5 and -2.5 in the presence of a fragility fracture or vertebral compression fracture, or if height loss > 2 cm occurs or BMD decreases > 3% in 1 year at the lumbar spine or > 5% at the femoral neck, bisphosphonate therapy should be considered.

Absorptiometry, Photon↗
PubMed2000

[Evaluation of bone mineral density and selected metabolic markers of bone in boys with constitutional delay of growth and puberty].

The aim of this study was to evaluate bone mineral density and some markers of bone metabolism (alkaline phosphatase activity, osteocalcin concentration, deoxypirydinoline excretion), as well as the influence of physical activity and dietary calcium supplementation on bone density and bone metabolism in boys with a constitutional delay of growth and puberty (CDGP), in relation to calendar age, bone age and pubertal stage. The study was done in 41 boys aged 8-18 years with CDGP diagnosed on the basis of family history and typical pattern of growth, with prior exclusion of hormonal and non-hormonal causes of height deficiency. According to Tanner's criteria, boys were assigned to 4 groups corresponding to 4 stages of puberty (Tab. 1). Total body (total BMD) and lumbar spine (L2L4 BMD) bone mineral density were obtained using DEXA densitometry. The activity of alkaline phosphatase (AP) and serum osteocalcin (OC) concentration served as markers of bone formation. 24-h urinary deoxypirydinoline (DPD) excretion was a marker of bone resorption. Using a questionnaire, daily dietary calcium intake and physical activity were established. A positive correlation between calendar age, total BMD and L2L4 BMD was found (R = 0.70 and R2 = 0.49; R = 0.72 and R2 = 0.51; p < 0.001, respectively). Bone age was positively correlated with total BMD and L2L4 BMD (for both correlations R = 0.68, R2 = 0.47; p < 0.001). Total BMD adjusted for calendar age revealed osteoporosis in 4 cases (9.7%), osteopenia in 19 cases (46.3%) and normal bone density in 18 cases (43.9%). After adjustment of BMD to bone age, 2 boys (4.9%) were diagnosed with osteoporosis, 9 (21.9%) with osteopenia, and 30 (73.2%) with normal bone density. L2L4 BMD adjusted for calendar age showed osteoporosis in 6 cases (14.6%), osteopenia in 21 cases (51.2%) and normal density in 14 cases (34.2%). After adjustment of BMD to bone age, 3 boys (7.3%) were diagnosed with osteoporosis, 10 (24.4%) with osteopenia, and 28 (68.3%) with normal bone density. A significant correlation between stage of puberty, total BMD (p < 0.045) and L2L4 BMD (p < 0.001) was found. Values for total BMD and L2L4 BMD in boys with CDGP in relation to pubertal stage are presented in Table 2. Mean AP activity, serum OC concentration, DPD excretion, dietary calcium intake and physical activity in boys at consecutive stages of puberty are presented in Table 3. No significant correlation between pubertal stage, markers of bone metabolism, daily dietary calcium intake or physical activity was found. The boys were next grouped according to level of physical activity: low (< 10 h/week) or high (> 10 h/week). Table 4 summarizes the results for both groups. No significant differences between the groups were found concerning the parameters studied. Two groups with a low (< 1.2 g) and high (> 1.2 g) dietary calcium intake were also formed. The results for both groups are presented in Table 5. A significant correlation between dietary calcium intake and total BMD (R = 0.34 and R2 = 0.11; p < 0.03) was revealed. On the basis of these results it can be concluded that BMD values in boys with CDGP should be adjusted for bone age, thus significantly limiting the diagnosis of osteoporosis and osteopenia. BMD values for these boys increase with consecutive pubertal stage, while markers of bone metabolism do not reveal significant abnormalities (markers of bone formation increase until stage IV, markers of bone resorption show fluctuating values).

Absorptiometry, Photon↗
PubMed2003

[Clinical application of tissue engineered bone repair of human craniomaxillofacial bone defects].

OBJECTIVE: To explore the feasibility of tissue engineered bone formation in human being using human bone marrow stromal cells (hBMSCs) and the possibility of clinical repair of craniomaxillofacial bone defects with tissue engineered bone. METHODS: Total 11 patients of cranial defects and aperture piriformis bone depression were included in this study. The hBMSCs were isolated by Percoll gradient centrifugation from patient's bone marrow aspirated from iliac crest. The hBMSCs were cultured in vitro and induced to become osteogenic cells in the DMEM medium containing 10% self-serum, beta-glycerophosphate (10 nmol/L) dexamethasone (10(-8) mol/L), L-2-ascorbic acid (50 micro mol/L), and 1, 25 (OH)(2)VD(3)(10 nmol/L). Induced hBMSCs of passage 3 were harvested and seeded onto partly demineralized allogenic bone matrix (pDBM) to form a cell-scaffold construct and in vitro co-culture for 1 week. The defects were repaired with the cell-scaffold construct. In 3 cases of aperture piriformis bone depression, one side was repaired with hBMSC/pDBM, while the other side was repaired by pDBM alone. All cases were followed up for 1, 3, 6 months post-operation as short-term evaluation and 1 to 2.5 years post-operation as long-term evaluation by three-dimensional computerized tomography (3D-CT) and clinical examination. In 2 cases who received secondary surgery, extra engineered bone tissue and control pDBM were harvested at the implantation sites for histological examination and immunohistochemistry. RESULTS: 3D-CT demonstrated that engineered bone was formed in 3 to 6 months post-operation. Additionally, formed bone maintained stable up to 1 - 2 years without absorption. Histologically, engineered bones revealed their structures similar to that of normal bone in HE staining. Interestingly, endochondral ossification was also observed in engineered bone. Immunohistochemistry shows positive staining of osteonectin and osteocalcin in engineered and normal bones. In contrast, implanted pDBM was completely degraded in 3 - 6 months as revealed by 3D-CT. Histologically, degraded pDBM and fibrous tissue were observed in the sites where pDBM alone was implanted. CONCLUSIONS: Tissue engineered bone can be formed in human being. Engineered bone can be used to repair clinical bone defect with satisfactory result. Furthermore, the result of this study proves that tissue engineered bone is possible for clinical application.

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