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PubMed2003

In vivo evaluation of bone marrow stromal-derived osteoblasts-porous calcium phosphate ceramic composites as bone graft substitute for lumbar intervertebral spinal fusion.

STUDY DESIGN: Autogenous bone marrow stromal-derived osteoblasts-porous calcium phosphate ceramic composites were constructed in vitro under cell culture for 48 hours and implanted as a bone graft substitute for lumbar intervertebral spinal fusion in rabbits. OBJECTIVES: To evaluate the efficacy of autogenous bone marrow stromal-derived osteoblasts-porous calcium phosphate ceramic composites as an alternative to autogenous graft materials in a lumbar interbody spinal fusion model. SUMMARY OF BACKGROUND DATA: Bone marrow contains a population of rare progenitor cells capable of differentiating into bone, cartilage, muscle, tendon, and other connective tissues. These cells can be induced and differentiated into osteogenic osteoblasts with addition of osteogenic supplements. Combining bone marrow stromal-derived osteoblasts with porous ceramics gave rise to bone tissue in subcutaneous sites and repaired critical size segmental femoral defects. Little work has been done in the spine to assess fusion rates and associated biomechanical characteristics. METHODS: Five experimental groups were evaluated: sham operation (Group I); porous calcium phosphate ceramics alone (Group II); autogenous tricortical iliac crest (Group III); bone marrow stromal-derived osteoblasts-calcium phosphate ceramic composites (Group IV); bone marrow stromal-derived osteoblasts-calcium phosphate ceramic composites with rhBMP-2 (Group V). All rabbits were killed 12 weeks after surgery, and the spinal fusion segments underwent the evaluation of gross inspection, manual palpation, radiography, computed tomography, nondestructive biomechanical testing, and histologic analysis. RESULTS: Successful spinal fusion was achieved by manual palpation in 100% (6/6) of animals in Group IV and Group V, 66.7% (4/6) in Group III, 50% (3/6) in Group II, and 0% (0/6) in Group I. Radiographic studies showed that minimal disc height loss was observed with ceramic blocks than with autograft. Biomechanical testingconfirmed that spines from Group IV and Group V were statistically significantly stiffer in flexion, extension, left and right bending, and left and right torsion than Group III and Group II. Histologic analysis demonstrated a qualitative increase of bone formation in fusion mass in Group IV and Group V versus all other groups. The size of fusion mass and the stiffness of fusion segments were greatest in Group V. CONCLUSION: The results indicate that bone marrow stromal-derived osteoblasts-calcium phosphate ceramic composites may provide an alternative to autogenous graft materials for lumbar interbody spinal fusion. Adding recombinant human bone morphogenetic protein-2 into the composites may reinforce the biomechanical stiffness for spinal fusion segments. Porous calcium phosphate ceramics alone were not suitable as a bone graft substitute for lumbar interbody spinal fusion.

Animals↗
PubMed1992

Effects of etidronate-mediated suppression of bone remodeling on aluminum-induced de novo bone formation.

The mechanism by which aluminum chloride stimulates de novo bone formation is unknown. To evaluate the role of bone remodeling and mature osteoblastic function in aluminum-induced neoosteogenesis, we compared the osteogenic effects of aluminum in normal beagles to those in animals with low turnover osteomalacia induced by treatment with etidronate [1-hydroxyethane-1,1-diphosphoric acid (HEBP)]. As assessed by quantitative bone histomorphology, beagles treated with HEBP developed low turnover osteomalacia characterized by a 78% reduction in osteoblast number, a 5.5-fold increase in osteoid volume, complete absence of active mineralization, and diminished resorption surfaces compared to untreated controls. The iv administration of aluminum chloride to normal dogs generated new trabecular structures in the marrow cavity consistent with induction of de novo bone formation. This response consisted of increased trabecular bone volume and number, accumulation of woven osteoid, and increased number of bone-forming cells. The concomitant administration of HEBP failed to prevent induction of de novo bone formation by aluminum. Instead, the neoosteogenic process was superimposed on low turnover osteomalacia in HEBP-treated dogs. Serum aluminum concentrations were increased 2-fold, whereas bone aluminum accumulation was reduced by 58% in HEBP- and aluminum-treated dogs compared to that in aluminum-treated controls. These findings indicate that aluminum stimulation of neoosteogenesis in beagles is independent of mature osteoblast function, normal bone remodeling, and total bone aluminum accumulation. Rather, aluminum-induced de novo bone formation appears to result from stimulation of mesenchymal precursors to form a primitive type of bone which is distinct from coupled bone formation.

Aluminum↗
PubMed2002

The effect of bone marrow transplantation on the osteoblastic differentiation of human bone marrow stromal cells.

Osteoporosis is a serious and relatively common complication of transplantation procedures. However, little is known about the exact mechanism or severity of osteoporosis complicated by bone marrow transplantation (BMT). We conducted both ex vivo and clinical studies to identify the mechanism and extent of bone loss after BMT. In a prospective clinical study, we intended to identify the changes in bone turnover markers and bone mineral density (BMD) after BMT. During a 1-yr follow-up, BMD was measured before BMT and 1 yr after BMT in 67 patients undergoing BMT. Biochemical markers of bone formation and resorption were measured in all patients at short-term intervals during the yearlong follow-up. In ex vivo study, we cultured human bone marrow cells of normal controls and BMT recipients in osteogenic medium and compared their osteogenic potential. Using a DNA fingerprinting method, we also investigated the origin of bone marrow stromal cells that were harvested 3-4 wk after BMT. In a clinical study of 67 patients undergoing BMT, the mean serum carboxy-terminal cross-linked telopeptide of type I collagen increased progressively until 4 wk after BMT. Thereafter, it began to decrease and reached basal values after 1 yr. Serum osteocalcin decreased progressively until 3 wk after BMT and reached basal values after 3 months. One year after BMT, lumbar spine BMD had decreased by 3.3% (P < 0.05), and total proximal femoral BMD had decreased by 8.9% (P < 0.001). For the ex vivo study, bone marrow was obtained from healthy donors (n = 7) and transplant recipients (n = 7). Then, mononuclear cells including marrow stromal cells were isolated and cultured to osteoblastic lineage. Alkaline phosphatase activities of each group were measured by the time course of secondary culture, and the mineralizing potentials were compared between the two groups. Cells cultured in our system showed characteristics of osteoblast-like cells differentiated from marrow stromal cells. They were initially in a fibroblastic-like spindle shape and became cuboidal with the formation of nodules that were later confluent. The cells were stained to both alkaline phosphatase histochemistry and Von Kossa histochemistry, demonstrating that these cells were of osteoblastic lineage differentiating from marrow stromal cells. The mean time required for the near-confluence in the primary culture was 15 and 22.9 d in healthy donors and transplant recipients, respectively (P = 0.003). Alkaline phosphatase activity was significantly lower in the bone marrow recipients than in the healthy donors at d 7 and 10 of the secondary cultures. The period at which peak activity of alkaline phosphatase was reached was also delayed in the osteoblasts derived from BMT recipient bone marrow compared with those of healthy donors. Using Von Kossa histochemistry, much more mineralization was observed in osteoblasts of healthy donors than those of BMT recipients. After BMT, although the peripheral mononuclear cells in the recipients were of donor origin, the bone marrow stromal cells were of recipient origin according to the PCR analysis using YNZ 22 mini-satellite probe. In conclusion, the differentiation of bone marrow stromal cells into osteoblasts was impaired after BMT, and this might contribute to post-BMT bone loss.

Adolescent↗
PubMed1998

The effects of twelve weeks of bed rest on bone histology, biochemical markers of bone turnover, and calcium homeostasis in eleven normal subjects.

This study was undertaken to examine the effects of 12 weeks of skeletal unloading on parameters of calcium homeostasis, calcitropic hormones, bone histology, and biochemical markers of bone turnover in 11 normal subjects (9 men, 2 women; 34 +/- 11 years of age). Following an ambulatory control evaluation, all subjects underwent 12 weeks of bed rest. An additional metabolic evaluation was performed after 12 days of reambulation. Bone mineral density declined at the spine (-2.9%, p = 0.092) and at the hip (-3.8%, p = 0.002 for the trochanter). Bed rest prompted a rapid, sustained, significant increase in urinary calcium and phosphorus as well as a significant increase in serum calcium. Urinary calcium increased from a pre-bed rest value of 5.3 mmol/day to values as high as 73 mmol/day during bed rest. Immunoreactive parathyroid hormone and serum 1,25-dihydroxyvitamin D declined significantly during bed rest, although the mean values remained within normal limits. Significant changes in bone histology included a suppression of osteoblastic surface for cancellous bone (3.1 +/- 1.3% to 1.9 +/- 1.5%, p = 0.0142) and increased bone resorption for both cancellous and cortical bone. Cortical eroded surface increased from 3.5 +/- 1.1% to 7.3 +/- 4.0% (p = 0.018) as did active osteoclastic surface (0.2 +/- 0.3% to 0.7 +/- 0.7%, p = 0.021). Cancellous eroded surface increased from 2.1 +/- 1.1% to 4.7 +/- 2.2% (p = 0.002), while mean active osteoclastic surface doubled (0.2 +/- 0.2% to 0.4 +/- 0.3%, p = 0.020). Serum biochemical markers of bone formation (osteocalcin, bone-specific alkaline phosphatase, and type I procollagen extension peptide) did not change significantly during bed rest. Urinary biochemical markers of bone resorption (hydroxyproline, deoxypyridinoline, and N-telopeptide of type I collagen) as well as a serum marker of bone resorption (type I collagen carboxytelopeptide) all demonstrated significant increases during bed rest which declined toward normal during reambulation. Thus, under the conditions of this study, the human skeleton appears to respond to unloading by a rapid and sustained increase in bone resorption and a more subtle decrease in bone formation.

Adult↗
PubMed2006

[Vascularization in transplantation of gene modified tissue engineered bone for repairing bone defect].

OBJECTIVE: To study the vascularization of the composite of bone morphogenetic protein 2 (BMP-2) gene transfected marrow mesenchymal stem cells (MSCs) and biodegradable scaffolds in repairing bone defect. METHODS: Adenovirus vector carrying BMP-2 (Ad-BMP-2) gene transfected MSCs and gene modified tissue engineered bone was constructed. The 1.5 cm radial defect models were made on 60 rabbits, which were evenly divided into 4 groups randomly (n= 15, 30 sides). Different materials were used in 4 groups: Ad-BMP-2 transfected MSCs plus PLA/PCL (group A), Ad-Lacz transfected MSCs plus PLA/PCL (group B), MSCs plus PLA/PCL (group C) and only PLA/PCL scaffolds (group D). The X-ray, capillary vessel ink infusion, histology, TEM, VEGF expression and microvascular density counting (MVD) were made 4, 8, and 12 weeks after operation. RESULTS: In group A after 4 weeks, foliated formed bones image was observed in the transplanted bones, new vessels grew into the bones, the pores of scaffolds were filled with cartilage callus, osteoblasts with active function grew around the microvessels, and VEGF expression and the number of microvessels were significantly superior to those of other groups, showing statistically significant difference (P<0.01); after 8 weeks, increasingly more new bones grew in the transplanted bones, microvessels distended and connected with each other, cartilage callus changed into trabecular bones; after 12 weeks, lamellar bone became successive, marrow cavity recanalized, microvessels showed orderly longitudinal arrangement. In groups B and C, the capability of bone formation was weak, the regeneration of blood vessels was slow, after 12 weeks, defects were mostly repaired, microvessels grew among the new trabecular bones. In group D, few new vessels were observed at each time, after 12 weeks, broken ends became hardened, the defected area was filled with fibrous tissue. CONCLUSION: BMP-2 gene therapy, by up-regulating VEGF expression, indirectly induces vascularization of grafts, promotes the living of seed cells, and thus accelerates new bone formation.

Animals↗
PubMed1987

Effects of a 120 day period of bed-rest on bone mass and bone cell activities in man: attempts at countermeasure.

The effects of immobilization on bone mass and bone remodeling in patients with spinal cord injuries are known to simulate weightlessness-induced bone changes in astronauts. Nevertheless, immobilization has never been investigated using histomorphometric studies in healthy volunteers. Twenty healthy male volunteers participated in a '120 day bed-rest' experiment in the USSR. Bone biopsy cores of iliac crest were taken before and at the end of the period of bed-rest. The subjects were divided into five groups. Five subjects underwent a normal ambulatory life (control subjects); three subjects were placed on continuous bed-rest for 120 days (complete immobilization); four subjects were immobilized and underwent a controlled training program; four subjects were immobilized and received treatment with potassium diphosphonate (ethane-1,hydroxy-1,diphosphonate 900 mg/day, per os); and four subjects were immobilized and received diphosphonate plus physical exercise. Parameters of bone mass and bone cellular activities (osteoblastic formation and osteoclastic resorption) were measured using automatic and semi-automatic image analysis systems. Bone mass remained constant in each group. Cellular activity measurements showed that in completely immobilized men, the mineralization rate was lower than in controls without change in osteoid parameters; in contrast, osteoclastic parameters were increased. In immobilized men given the training program, bone formation was normal and bone resorption was increased. In immobilized men treated with diphosphonate, osteoid parameters and resorption activity were decreased. In immobilized men with diphosphonate plus training, the osteoid parameters and the resorption activity were reduced but to a lesser degree than in immobilized men with diphosphonate alone. Failure of bone loss in normal immobilized subjects differed from results found in paraplegic patients. However, a decrease in mineralization rate and an increase in bone resorption activity were found in both studies. Exercise stimulated bone resorption and diphosphonate inhibited the osteoclastic activity. These data emphasize the difficulties in finding good models to stimulate spaceflight conditions on earth. Comparative studies must be done using bone biopsies to determine more precisely the effects of weightlessness on the human skeleton.

Adult↗
PubMed1992

Abnormal bone remodelling in patients with myelomatosis and normal biochemical indices of bone resorption.

We studied bone biopsies from 26 patients with myelomatosis with apparently normal skeletal metabolism. Quantitative histomorphometric measurements suggested that skeletal disease was progressive despite normocalcaemia and normal urinary excretion rates of calcium and hydroxyproline. When biopsies were divided according to the involvement of marrow by plasma cells, bone resorption--as judged by the eroded surface--increased significantly the greater plasma cell burden. Osteoclasts were frequent with moderate tumour burdens, but there was no further increase in the number of osteoclasts when plasma cell infiltration increased by more than 50% of bone marrow. Contrary to expectation, the numbers of osteoblasts and bone formation rates were increased with bone biopsies with moderate tumour burden, but were markedly lower when plasma cell infiltration occupied more than 50% of bone marrow, due to a decreased functional capacity of osteoblasts. We conclude that skeletal bone disease in myeloma is commonly progressive despite apparently stable bone disease as judged by biochemical measurements. The major mechanism of bone loss in myelomatosis is increased osteoclastic resorption but decreased bone formation contributes to bone loss with heavy plasma cell burdens. Urinary excretion of calcium and hydroxyproline provide insensitive indices of bone resorption in myelomatosis.

Alkaline Phosphatase↗
PubMed2007

Bone morphogenetic proteins-signaling plays a role in tendon-to-bone healing: a study of rhBMP-2 and noggin.

BACKGROUND: Successful anterior cruciate ligament reconstruction requires secure healing between tendon and bone. HYPOTHESIS: Bone morphogenetic protein-signaling plays an important role in tendon-to-bone healing. rhBMP-2, a powerful osteoinductive agent, can improve tendon-bone interdigitation. STUDY DESIGN: Controlled laboratory study. METHODS: The study was designed in 2 phases: Phase I consisted of a dose-response study where 21 New Zealand White rabbits underwent bilateral anterior cruciate ligament reconstructions. Rabbits received either rhBMP-2 (11.5, 50, or 115 microg) or noggin (10, 15, 30, or 100 ng) (a potent bone morphogenetic proteins inhibitor) delivered in an injectable calcium phosphate matrix. Animals were sacrificed at 2 weeks and histomorphometric analyses were performed. In phase II, 60 rabbits underwent bilateral anterior cruciate ligament reconstructions and were assigned to 3 groups: rhBMP-2 (115 microg), noggin (30 ng) in a calcium phosphate carrier, and calcium phosphate carrier alone. Animals were sacrificed at 2, 4, and 8 weeks and histomorphometric and biomechanical analyses were performed. RESULTS: rhBMP-2 treatment led to a significant increase in the width of new bone formation at the tendon-bone interface in a dose-dependent fashion (0.24-0.35 mm vs 0.13-0.16 mm in controls). All dosages of noggin inhibited new bone formation (0.06-0.1 mm vs 0.15-0.16 mm in controls); however, there was no dose-dependent effect in the concentrations studied. In the phase II study, rhBMP-2 resulted in a significant increase in new bone formation (81%, 89%, and 113%) at increasing time periods compared with controls. Tunnel diameters in the rhBMP-2 group were significantly smaller (15%-45%) than in the carrier group. The negative effect of noggin was not sustained, as new bone formation increased with time. The rhBMP-2 group demonstrated significantly increased stiffness at 8 weeks, while there was no significant difference in ultimate tensile load when compared with the other 2 groups. CONCLUSION: rhBMP-2 demonstrated a strong, positive dose-dependent effect on osteointegration at the tendon-bone junction. In contrast, noggin decreased osteointegration. No tunnel widening was detected with rhBMP-2 using the calcium phosphate carrier. CLINICAL RELEVANCE: Further studies are needed to investigate the potential clinical application of enhancing healing and decreasing recovery time using bone morphogenetic proteins in soft tissue ligament reconstruction.

Animals↗
PubMed1985

Multicellular tumor spheroid interactions with bone cells and bone.

In vitro coculture techniques were used to study HSDM1C1 murine fibrosarcoma multicellular tumor spheroid (HSDM1C1-MTS) interactions with mouse calvarial bone cells having osteoblastic characteristics and mouse bone explants. HSDM1C1-MTS attached to confluent bone cell monolayers and their attachment rate was quantified. HSDM1C1-MTS interaction with bone cells was further demonstrated by the release of 3H-deoxyuridine from prelabeled bone cells during coculture with multicellular tumor spheroids. HSDM1C1-MTS-induced cytotoxicity was mimicked by the addition of 10(-5) M prostaglandin E2 (PGE2) to 3H-deoxyuridine-labeled bone cells. The effects of low (10(-9) M) and high (10(-5) M) concentrations of PGE2 on bone cell proliferation were also studied. Higher concentrations of PGE2 inhibited bone cell proliferation. HSDM1C1-MTS resorbed living explants in the presence of indomethacin, suggesting that other tumor cell products may also participate in bone resorption. HSDM1C1-MTS caused direct bone resorption as measured by the significantly elevated release of 45Ca from prelabeled, devitalized calvaria. However, the growth of a confluent bone cell layer on devitalized, 45Ca-prelabeled calvaria resulted in a significant reduction in the amount of 45Ca released subsequent to the seeding of HSDM1C1-MTS onto the explants. Bone cells at the bone surface may act as a barrier against invasion and tumor cell-mediated bone resorption. Violation of this cellular barrier is achieved, in part, by tumor cell products.

Animals↗
PubMed2003

Anterior lumbar intervertebral fusion with artificial bone in place of autologous bone.

The feasibility of anterior lumbar intervertebral fusion with artificial bone in place of autogenous bone was investigated. Porous hydroxyapatite (HA)/ZrO2 ceramics loading bone morphogenetic protein (BMP) were implanted after removal of lumbar vertebral disc in rabbits. The adjacent intervertebral discs were also removed by the same way and autogenous illic bone was implanted. SEM observation and biomechanical test were carried out. Compound bone had a bit lower osteoinductive activity than autogenous bone by SEM (Osteoinductive activity of artificial bone in 12 weeks was the same as that of autogenous bone in 9 weeks). Biomechanical test revealed that compound bone had lower anti-pull strength than autogenous bone (P < 0.001), but there was no significant difference in anti-pull strength between compound bone at 12th week and autogenous bone at 9th week (P > 0.05). It was concluded that compound bone could be applied for anterior spinal fusion, especially for those patients who can't use autogenous bone.

Animals↗
PubMed1999

Changes in bone mass and bone turnover following distal forearm fracture.

Bone loss occurs close to a fracture and is associated with increased bone turnover. Fracture healing itself results in increased markers of bone turnover. But the exact patterns of these changes after different fractures are unclear. We aimed to investigate the changes in bone density and biochemical markers following distal forearm fracture. Twenty women (mean age 63 years) were recruited following fracture of the distal radius and ulna. Bone mineral density (BMD) of the hand and forearm were measured by dual-energy X-ray absorptiometry (DXA) and quantitative ultrasound (QUS) of the fingers was measured at 0, 6, 12, 26 and 52 weeks after fracture. Serum and urine samples were collected at 0, 3 and 7 days and at 2, 4, 6, 12, 26 and 52 weeks after fracture to measure markers of bone turnover. For bone formation we measured: bone alkaline phosphatase (iBAP), osteocalcin (Oc), procollagen type I N-terminal propeptide (PINP); and for bone resorption: tartrate-resistant acid phosphatase (TRAcP), free deoxypyridinoline (iFDpd), N-telopeptides of type I collagen (NTx). We used the nonfractured limb to calculate values for baseline BMD and amplitude-dependent speed of sound (AD-SoS). There was a decrease in BMD at the hand and in AD-SoS of the fingers after forearm fracture (p<0.001). This bone loss was maximal for BMD by 6 weeks at 9% (p<0. 001) and remained decreased at 52 weeks. AD-SoS decreased at 12 weeks by 3% (p<0.01) and recovered completely by 52 weeks. Bone formation markers increased between 2 and 4 weeks by 13-52% (p<0. 001), and were still elevated at 52 weeks. Bone resorption markers increased between 2 and 6 weeks by 18-35% and returned to baseline at 52 weeks (TRAcP remained elevated). We conclude that BMD decreased distal and immediately proximal to the fracture line when measured with DXA and QUS. Bone loss after distal forearm fracture did not recover by 52 weeks and most bone turnover markers did not return to baseline.

Acid Phosphatase↗
PubMed1998

Osteocyte-bone lining cell system at the origin of steady ionic current in damaged amphibian bone.

A wound-generated steady electric current was measured by a two-dimensional vibrating probe system in the metatarsal bones of 22 adult frogs (Xenopus laevis) placed in amphibian Ringer. Inward currents were recorded entering a micrometric hole drilled through the cortex at middiaphyseal level. These steady state currents (mean +/- SD 8.50 +/- 2.77 microA/cm2) last approximately 2 hours, were dependent on the presence of sodium in the incubation medium, were no more detectable after fixation, and were reduced to background level when the cell membranes were solubilized. These results agree with previous recordings of metatarsal bones of weanling mice, under identical conditions. Both results suggest that the measured ionic currents have a cellular origin. Metatarsal bones of adult amphibian were purposely selected for this study because, unlike mammalian bones, their shafts are avascular and only contain an osteocyte-bone lining cell system, as documented by scanning and transmission electron observations. Thus, unlike the data from previous investigations on mammals, the results succeeded in giving the first convincing evidence that the osteocyte-bone lining cell system is the origin of damage-generated ionic currents. As damage exposes bone ionic compartment to plasma, damage-generated ionic currents are representative of ion fluxes at bone plasma interface, and cells at the origin of the current generate the driving force of such fluxes. By demonstrating that osteocytes and bone lining cells are at the origin of the current, this study suggests that the osteocyte-bone lining cell system, though operating as a cellular membrane partition, regulates ionic flow between bone and plasma. Since strain-related adaptive remodeling could also depend on ionic characteristics and flow of the bone fluid through the osteocyte lacuno-canalicular network, the results reported here support the view that osteocyte and bone lining cells may constitute a functional syncytium involved in mineral homeostasis as well as in bone adaptation to mechanical loading.

Animals↗
PubMed2006

Alveolar bone graft for patients with cleft lip/palate using bone particles and titanium mesh: A quantitative study.

PURPOSE: This study evaluated the bone volume, height, and width that can be obtained in alveolar ridge augmentation using titanium mesh and autogenous bone particles in patients with cleft lip/palate. PATIENTS AND METHODS: Subjects were 15 patients with cleft lip/palate requiring tertiary bone graft for implant therapy. Computed tomography (CT) scans were taken before removing the mesh, from 1 to 21 months after bone grafting. Forty-three reconstructed images corresponding to the positions for implant placement were selected for this study. The percent defect filled with bone (%BONE), defined as the percentage of newly formed bone in the space created by the mesh, was measured for image analyses. In linear analyses, 4 parameters were used: increased bone height (IBH), percent increased bone height (%IBH), increased bone width (IBW), and percent increased bone width (%IBW). Factors influencing the quantitative data and the clinical courses of placed implants were also explored. RESULTS: The average %BONE was 91.1%. IBH averaged 4.4 mm, whereas %IBH averaged 88.5%. IBW averaged 4.6 mm, whereas %IBW averaged 86.4%. Little correlation was present between the quantitative data and patient age, or time interval. A significant correlation was identified between the data for span of the grafted area and %BONE (correlation coefficient value = -0.36). However, the diminishing rate was very low. No implants were lost postoperatively. CONCLUSIONS: Alveolar ridge augmentation with titanium mesh and autogenous bone particles from the anterior iliac crest has very high predictability as a preimplant procedure in patients with cleft lip/palate.

Adolescent↗
PubMed2005

Evaluation of the relationship between periapical lesions/sclerotic bone and general bone density as a possible gauge of general health among 80-year-olds.

OBJECTIVES: To evaluate the incidence among 80-year-olds of periapical lesions as detected on panoramic radiographs and to determine the relationship between sclerotic bone around the periapical lesions to heel bone density, body height, and hand-grip strength. STUDY DESIGN: Six hundred fifty-nine panoramic radiographs (262 males, 397 females), obtained from 80-year-old residents of Fukuoka Prefecture, Japan, were used for evaluation of periapical lesions. These findings were correlated with physical examination results to determine the relationship to general health. RESULTS: Of 659 panoramic radiographs, 31 (5%) were noted to have periapical lesions. Average size of the 31 periapical lesions was 6.1 +/- 2.2 mm. Of the 31 periapical lesions, 21 (68%) were accompanied by linear or diffuse types of sclerotic bone. Of the 21 sclerotic bones, 10 (48%) were of a linear type of sclerotic bone and 11 (52%) of a diffuse type of sclerotic bone. Of the 11 diffuse types of sclerotic bone, 10 (91%) were in the mandible and 1 (9%) in the maxilla. Periapical lesions in the mandible were more frequently accompanied by a diffuse type of sclerotic bone than those in the maxilla (P < .01). The hand-grip strength of those having periapical lesions, accompanied by a diffuse type of sclerotic bone, was stronger than those having no periapical lesions (P < .01) and those accompanied by a linear type of sclerotic bone (P < .03). However, there was no relationship between presence of sclerotic bone and heel bone density or body height. CONCLUSIONS: Periapical lesions accompanied by a diffuse type of sclerotic bone were more frequently seen in the mandible of 80-year-olds. To evaluate the clinical significance of sclerotic bone around periapical lesions in 80-year-olds, further study to evaluate the significance of endodontic treatment needs to be done.

Aged↗
PubMed2001

Predictive value of Singh index and bone mineral density measured by quantitative computed tomography in determining the local cancellous bone quality of the proximal femur.

OBJECTIVE: The purpose of this study was to assess the predictive value of the Singh index as well as quantitative computed tomography for the in vitro local mechanical competence of the cancellous bone of the proximal femur. DESIGN: An experimental study examining the relation between mechanical properties and bone mineral density of the femoral neck determined in vitro and the clinical estimated Singh index on X-rays. BACKGROUND: Evaluation of the predictive value of the Singh index, an inexpensive and simple technique for the mechanical properties of the cancellous bone of the proximal femur. METHODS: The bone quality of the proximal femur of 34 patients undergoing total hip replacement was estimated by roentgenography using the Singh index. Bone mineral density was quantified by quantitative computed tomography using cylindrical cancellous bone biopsies harvested during the total hip replacement procedure by a new biopsy method. The mechanical properties of the bone specimens (Young's modulus, strength and maximum energy absorption E(max)) were measured by mechanical testing of the bone biopsies. RESULTS: A strong correlation of the Singh index versus material properties of cancellous bone was noted (r=0.66 for Young's modulus, r=0.73 for strength and r=0.69 for E(max), P<0.0001). The correlations of bone mineral density measured by quantitative computed tomography versus Young's modulus, strength and energy absorption E(max) were significant. Strength was predicted best (r=0.82; P<0.0001), followed by E(max) (r=0.79; P<0.0001) and Young's Modulus (r=0.73; P<0.0001). CONCLUSIONS: We conclude, that assessment of bone mineral density by quantitative computed tomography is a reliable and precise method for the estimation of cancellous bone material properties. The Singh index provides a rough estimate for the mechanical competence of the proximal femur. It is inexpensive, simply to assess and can in some cases replace the measurement of bone mineral density, notably in cases of marked decrease in bone density.

Aged↗
PubMed2000

Bone conduction experiments in humans - a fluid pathway from bone to ear.

Animal experiments in this laboratory have led to the suggestion that a major pathway in bone conduction stimulation to the inner ear is via the skull contents (brain and CSF). This hypothesis was now tested in humans. Auditory nerve brainstem evoked responses could be recorded in neonates to bone conduction stimulation over the fontanelle and audiometric responses were obtained in neurosurgical patients with the bone vibrator on the skin over a craniotomy. There were no differences in threshold between these responses and those obtained to bone conduction stimulation over skull bone in the same subjects. Audiometric thresholds in response to bone vibrator stimulation of the eye (a 'natural craniotomy') were no different from those to bone stimulation delivered to several sites on the head. Thus there is no need to vibrate bone in order to obtain 'bone conduction' responses. Bone vibrator thresholds to stimulation at the head region with thinnest bone (temporal) were better than those to stimulation at the forehead region which has much thicker bone, implying that the vibrations penetrate the skull at the site of the vibrator. In addition, the magnitude of vibration (acceleration) measured at various sites around the head in response to bone vibrator stimulation at a fixed point on the forehead generally decreased with distance from the point of vibration. Therefore it seems that the vibrations produced by a bone vibrator at a point on the head are also able to penetrate the skull, setting up audio-frequency pressures in the CSF which spread by fluid communications to the inner ear fluids, exciting the ear.

Adolescent↗
PubMed2002

Relationships between trabecular bone remodeling and bone vascularization: a quantitative study.

Beside its well-known role in bone development, vascularization plays a major role in bone cell migration for bone remodeling and metastatic tumor invasion. However, the various techniques used to identify vessels in bone have never been tested for trabecular bone vessel quantification, whereas bone remodeling quantitative parameters are commonly assessed. In this context, we developed and compared various histological techniques used to visualize blood vessels in rat bone in order to quantify them. First, several products were tested by intracardiac infusion to opacify the bone vascular network. The best results were obtained using either an India ink-1% agarose solution or an India ink-saturated barium sulfate solution followed by X-ray microradiography. Second, to identify the types of vessels, we also performed histoenzymology and immunohistochemistry stainings. Neither alkaline phosphatase (for endothelial cells) nor adenosine triphosphatase (ATPase) stainings (for smooth muscle cells) provided a low enough background to allow for vessel identification and quantification. For immunohistochemistry, various specific vessel constituents were analyzed: laminin, smooth muscle cell alpha-actin, factor VIII, and lectin Griffonia simplifolia. Anti-laminin and anti-smooth muscle cell alpha-actin antibodies gave the best results for quantification. Third, after optimization of these techniques, we performed quantitative bone and vessel histomorphometry on two groups of 12 rats each, for which bone remodeling and vessel number and area parameters were measured. No statistical differences were observed between the two groups, confirming the reproducibility of our measurements. A significant relationship was found between vessel number and histodynamic parameters; that is, bone formation rate correlated positively with India ink-positive vessel area (p < 0.009, r2 = 0.54) and alpha-actin-positive vessel number (p < 0.05, r2 = 0.66). Furthermore, we report reproducible techniques for visualization and quantification of vessels in bone that also allowed for simultaneous conventional bone histomorphometry. This methodology should help researchers to better understand the functional and anatomical relationship between trabecular bone and its vascularization during normal or pathological processes.

Adenosine Triphosphatases↗
PubMed1997

Temporal expression of PTHrP during endochondral bone formation in mouse and intramembranous bone formation in an in vivo rabbit model.

Expression of parathyroid hormone-related protein (PTHrP) messenger RNA (mRNA) and protein was investigated throughout the developmental progression of endochondral bone formation in mouse and intramembranous bone formation in an in vivo model in rabbit, using in situ hybridization and immunohistochemistry. Endochondral bone formation was investigated in a developing embryo, newborn, and adult mouse. In fetal long bones through to newborn (day 7), PTHrP mRNA and protein were consistently expressed in chondrocytes within the proliferative, transitional, and hypertrophic zones. In addition, high levels of PTHrP were also detected in osteoblasts on the surface of trabecular bone surfaces. Similarly, at the adult stage (week 7), PTHrP mRNA and protein were consistently expressed in chondrocytes at epiphyseal ends of the subarticular cartilage, within cortical periosteum, as well as in osteoblasts located at the metaphyseal trabecular bone surfaces. Using an in vivo intramembranous bone formation model in rabbits, expression of PTHrP mRNA and protein was demonstrated in preosteoblasts prior to trabecular bone formation (1-week bone harvest). As bone formed (2-, 3-, and 4-week bone tissue harvests), PTHrP mRNA and protein were highly expressed in actively synthesizing osteoblasts and in those osteocytes embedded within the superficial layers of the bone matrix. Lining osteoblasts and osteocytes buried deeply in the bone matrix displayed weak or no signal for PTHrP. The pattern of spatial and temporal expression of PTHrP demonstrated in cartilage cells and osteoblasts in the two systems suggests an important role of PTHrP in both endochondral and intramembranous bone formation.

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