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Treatment of peri-implantitis using guided bone regeneration and bone grafts, alone or in combination, in beagle dogs. Part 1: Clinical findings and histologic observations.

The purpose of this study was to evaluate and compare the treatment of ligature-induced peri-implantitis using guided bone regeneration and two bone grafts alone and in combination. Mandibular premolars and first molars were extracted from four beagle dogs and after 3 months of healing, three Brånemark implants were placed on each side of the mandibles. Following abutment connection 3 months later, experimental peri-implantitis was induced by tying plaque-retentive ligatures around all abutments. Ligatures and abutments were removed after 3 months, and bony defects measured and treated with either: (1) debridement only; (2) debridement plus resorbable hydroxyapatite; (3) debridement plus canine freeze-dried demineralized bone; (4) debridement plus guided bone regeneration; (5) debridement plus resorbable hydroxyapatite and guided bone regeneration; or (6) debridement plus canine freeze-dried demineralized bone and guided bone regeneration. Pretreatment and 4-month-posttreatment comparison revealed a significant but variable degree of clinically appreciable hard tissue fill with all treatment procedures. Guided bone regeneration procedures resulted in the greatest fill, followed by bone grafts alone and flap debridement. There was no significant difference between guided bone regeneration and both guided bone regeneration/graft combinations; therefore, guided bone regeneration procedures appear to be a predictable treatment for plaque-induced peri-implant defects.

Alveolar Bone Loss↗

Temporal bone dynamics, the hard way. Formation, growth, modeling, repair and quantum type bone remodeling in the otic capsule.

This review presents studies in which temporal bone dynamics were monitored in undecalcified human and animal materials by combined microradiography and osteofluorochromic time labeling. The results are interpreted in accordance with modern concepts of spatial and temporal organization of bone behavior in an attempt to contribute to a new basis for understanding the structure and function of the bony otic capsule. In postcartilaginous development, perilabyrinthine bone formed a separate functional unit in which growth and modeling were absent. Consequently, all drift movements bypassed the bone present inside a narrow perilabyrinthine zone, which in effect maintained a so-called drift barrier enclosing the entire inner ear. In baseline bone remodeling and repair-associated remodeling transients, secondary osteons were distributed centrifugally with respect to inner ear spaces, and the average osteonal size decreased towards the inner ear, suggesting a progressive inhibition of bone resorption towards inner ear spaces. No histological capsular component proved resistant to bone resorption during modeling and remodeling. Instead the dynamic behaviour of any moiety of capsular bone appeared to depend on its spatial relation to the membranous labyrinth rather than on histological characteristics. This spatial organization of perilabyrinthine bone development and turnover is responsible for the unique histology of capsular bone and may explain the accumulation of fatigue micro-cracks which can be found in human perila byrinthine bone. These findings suggests the role of inner ear tissues as a functional matrix in control of capsular bone dynamics even beyond fetal life.

Animals↗

Bone sialoprotein in serum of patients with malignant bone diseases.

Bone sialoprotein (BS), a protein synthesized by osteoblasts and osteoclasts and highly modified posttranslationally, constitutes a predominant fraction of the noncollagenous organic matrix in human bone. We report an assessment of serum concentrations of BS in patients with malignant bone diseases. In patients with bone metastases (according to scintigraphic criteria), serum BS concentrations were greater than in patients without bone metastases (P <0.05). However, ROC curve analysis revealed that serum BS was inferior to serum bone alkaline phosphatase in discriminating between patients with and without bone metastases. Patients with bone metastases showed a weak correlation between serum BS concentrations and bone formation markers. Only "traditional" markers of bone formation-but not BS-were correlated with urinary deoxypyridinoline (P <0.01). Liver and kidney dysfunction had no significant influence on BS values in these patients (as assessed by analysis of variance; P >0.05). In multiple myeloma patients treated with corticosteroids and bisphosphonates, BS concentrations were lower than in tumor patients without bone metastases (P <0.001), and the correlation between BS concentrations and the number of bisphosphonate courses applied was significant (r = -0.578; P <0.05). In postmenopausal women, serum BS concentrations averaged 142% greater than in premenopausal women. Further studies should be done, therefore, to elucidate whether serum BS is able to predict high bone turnover after menopause.

Adult↗

[Experimental study on repair of mandibular defect by allogenic decalcified bone compounded with autogeneic bone marrow in rabbits].

Twenty adult rabbits were used in our experiment. The bone defects were made at the lower border of the bilateral mandible. A compound bone graft (allogenic decalcified bone with autogeneic bone marrow, ADB) was implanted in the right bone defect as the experimental group. The left mandible was taken as the control group and autogeneic cancellous bone was grafted. The process of new bone formation was evaluated by X-ray plain film, 99Tc-PYP Scintigraphy, histological, and histochemical, and transmmission electronic microscope examinations. The results demonstrated histogically that ADB induced new bone formation. The quantity of new bone produced by compound bone graft in the experimental group was much more than that in control group (P < 0.05). The compound bone graft can promote and accelerate bone defect healing.

Animals↗

Iliac trabecular bone formation predicts radial trabecular bone density changes in type 1 osteoporosis.

In 28 patients with idiopathic or postmenopausal type 1 (spinal crush fracture) osteoporosis, resorption indices and dynamic measurements of trabecular bone formation based on in vivo tetracycline labeling in 7.5 mm transiliac biopsies have been compared with trends in radial cortical and trabecular bone density measured with computed tomography. Positive correlations were observed between trabecular bone density trends in the radius and indices of bone formation in the ilium. These were improved when one of the two resorption indices was included with a formation index in bivariate regressions. Marked interindividual variations in radial bone density trends were also seen in cortical bone. These correlated poorly with trends in trabecular bone. Weak negative relationships between cortical bone trends and indices relating to bone formation and resorption were observed, but a positive association was seen with single-labeled surfaces on iliac trabeculae. If, as has been suggested, there are periodic variations in bone formation, the results suggest that axial and peripheral trabecular bone density trends are synchronized in osteoporosis, perhaps in response to systemic factors, such as circulating hormones.

Aged↗

In vivo fatigue microcracks in human bone: material properties of the surrounding bone matrix.

Human bones sustain fatigue damage in the form of in vivo microcracks as a result of the normal everyday loading activities. These microcracks appear to preferentially accumulate in certain regions of bone and most notably in interstitial bone matrix areas. These are remnants of old bone tissue left unremodelled, which show a higher than average mineral content and consequently the occurrence of microcracks has been attributed to the possible brittleness brought about by such hypermineralisation. There is a need, therefore, for information on the in situ bone matrix properties in the vicinity of such in vivo microcracks to elucidate the possible causes of their appearance. The present study examined the elastic, strain rate (viscous) and plastic properties of bone matrix in selectively targeted areas by nanoindentation and in both quasistatic and dynamic mode. The results showed that in vivo crack areas are not as stiff as some well-known extremely mineralised and brittle bone examples (bulla, rostrum); the strain rate effects of crack regions were identical to those of other regions of human bone and agreed well with values collected for human bone in the past at the macroscale; while the plasticity index of the crack regions was also not statistically different from most bone examples (including human at random, bovine, bulla and rostrum) except antler, which showed lower plasticity and thus a greater fraction of elastic recovery in indentation energy. It is difficult, therefore, to explain the susceptibility of these interstitial regions to crack in terms of the mineral content and its after-effects on elasticity, viscosity and plasticity alone, but one need to attribute the cracks to the cumulative loading history of these areas, or raise the suggestion that these areas of bone matrix are in some measure 'aged' or material/quality defective.

Aged↗

Systemic zoledronate precoating of a bone graft reduces bone resorption during remodeling.

BACKGROUND: Cartilage degeneration often occurs after osteosynthesis of a devascularized intermediary fragment in a joint fracture, in mosaicplasty or in whole-joint toe-to-finger transplantation. Hypothetically, the degeneration is secondary to a collapse of the transferred subchondral bone as it remodels during high mechanical load. Bisphosphonates are used to reduce resorption of necrotic bone. We tested a systemic pretreatment before harvesting the graft in order to protect the bone and cartilage against collapse and secondary arthrosis. METHODS: Rats were given one zoledronate injection and bone grafts were harvested. The grafts were frozen, thawed and placed into bone chambers, and implanted into another batch of rats. Graft resorption and new bone formation was measured by histomorphometric analysis and compared with untreated grafts. RESULTS: In the remodeled area of the controls, the graft was almost totally resorbed and replaced by bone marrow. In the zoledronate-treated specimens, the graft remained and the graft trabeculas were lined with new bone. By histomorphometry, the total amount of bone (graft plus new bone) within the remodeled area was 16% in the zoledronate-treated grafts and 5% in the controls (p = 0.003). INTERPRETATION: A bone graft can be pretreated with bisphosphonate and remain protected against resorption once implanted again.

Animals↗

The role of cortical bone and its microstructure in bone strength.

Bone's mechanical competence and its fragility in particular depend to a certain extent on the structure and microstructure of the cortical bone compartment. Beyond bone mineral density (BMD) and bone mineral content, a variety of other features of cortical bone contribute to whole bone's resistance to fracture. Structural properties of cortical bone most commonly employed as surrogate for its mechanical competence include thickness of the cortex, cortical cross-sectional area and area moment of inertia. But microstructural properties such as cortical porosity, crystallinity or the presence of microcracks also contribute to bone's mechanical competence. Microcracks in particular not only weaken the cortical bone tissue but also provide an effective mechanism for energy dissipation. Bone is a damageable, viscoelastic composite and most of all a living material capable of self-repair and thus exhibits a complex repertoire of mechanical properties. This review provides an overview of a variety of features of cortical bone known to provide mechanical competence and how these features may be applied for fracture risk prediction.

Aging↗

Perinatal testosterone surge is required for normal adult bone size but not for normal bone remodeling.

Although testosterone (T) has striking effects on mature skeletal size and structure, it is not clear whether this depends exclusively on adult circulating levels of T or whether additional early-life factors also play a role. We have compared the androgen-deficient hypogonadal (hpg) mutant mouse with intact, orchidectomized, and T-treated non-hpg mice to determine relative contributions of adult and perinatal T to bone growth and development. At 3 wk of age, although trabecular and cortical bone structure was normal, bone turnover was significantly altered in hpg male mice; osteoid volume (OV/BV) and osteoblast surface (ObS/BS) were significantly lower and osteoclast surface (OcS/BS) significantly higher in hpg mice compared with age-matched non-hpg mice, pointing to a role for the perinatal T surge in determining bone turnover levels before sexual maturity. At 9 wk of age, the hpg bone phenotype mimicked closely that of age-matched non-hpg mice that had been orchidectomized at 3 wk of age, including low trabecular bone mass and high bone turnover. These bone phenotypes of hpg and orchidectomized non-hpg mice were all prevented by replacement doses of T or dihydrotestosterone (DHT), suggesting that these are determined by adult sex steroid hormones. In contrast, a short bone phenotype that could not be prevented by T or DHT treatment was observed in 9-wk-old hpg mice yet not in intact or castrated non-hpg mice. These data suggest a role for the perinatal T surge in determining adult bone length and confirms that adult circulating T determines adult bone density.

Androgens↗

Leptin treatment induces loss of bone marrow adipocytes and increases bone formation in leptin-deficient ob/ob mice.

UNLABELLED: Normal mice and leptin-deficient ob/ob mice were treated with leptin to study effects on osteogenesis and adipogenesis in bone marrow. Leptin treatment significantly decreased bone marrow adipocyte size and number in ob/ob mice while increasing bone formation, BMC, and BMD. The results suggest that, in leptin-sensitive animals, the reduction in marrow adipocytes has positive effects on bone formation. INTRODUCTION: Adipocytes, osteoblasts, and osteoclasts have leptin receptors, and leptin can also affect bone metabolism indirectly through its receptors in the hypothalamus. We examined the effects of leptin treatment on bone formation, BMD, and marrow adipocyte population in normal mice and leptin-deficient ob/ob mice. MATERIALS AND METHODS: At the age of 15 weeks, mice were implanted with Alzet osmotic pumps for subcutaneous delivery of treatment solutions (saline, 2.5 microg leptin/day, or 10 microg leptin/day) for 14 days at a delivery rate of 0.25 microl/h. Bone formation was assessed using fluorochrome labels, cell populations were quantified using histomorphometry, and bone densitometry was measured using DXA. We also used a Luminex Beadlyte assay system to quantify cell survival markers in bone marrow samples. RESULTS AND CONCLUSIONS: Results indicate that both doses of leptin decreased the number of marrow adipocytes in ob/ob mice by >20% (p < 0.05) compared with PBS-treated ob/ob mice. The decrease in adipocyte number with leptin treatment is accompanied by an increase in concentration of the apoptosis marker caspase-3 in bone marrow adipocytes and hematopoietic cells. Both leptin doses also significantly (p < 0.05) increased the percentage of fluorochrome-labeled tibial endosteal surface by >30% compared with PBS-treated ob/ob mice. Leptin treatment increased whole body BMC by >30% in the ob/ob mice receiving the highest leptin dose. Leptin treatment provided no increase in bone formation, BMC, or BMD in normal, leptin-replete mice.

Adipocytes↗

Skeletal retention of bisphosphonate (pamidronate) and its relation to the rate of bone resorption in patients with breast cancer and bone metastases.

UNLABELLED: Bisphosphonate pharmacokinetics may affect individual responses. Skeletal retention of pamidronate infused monthly to patients with bone metastases was highly variable (12-98%) and did not diminish with time, showing the capacity of the skeleton to retain large amounts of bisphosphonate. Relationships between skeletal retention of pamidronate and rate of bone resorption are complex and depend on previous treatment and the total amount of retained bisphosphonate. INTRODUCTION: Bisphosphonates (BPs) given intravenously every 3-4 weeks are effective in the management of metastatic bone disease from breast cancer, but responses among patients vary, and it is not known whether current dose and dose intervals are appropriate for an individual patient. An influence of pharmacokinetics of BPs on antiresorptive action may contribute to this variation in response. To test this hypothesis, we determined the skeletal retention of intravenous pamidronate and its association to the rate of bone resorption in patients with bone metastases from breast cancer. MATERIALS AND METHODS: In a cross-sectional study, 24-h urinary excretion of pamidronate and the biochemical marker of bone resorption N-terminal telopeptide of type 1 collagen and serum alkaline phosphatase were measured in 40 patients with bone metastases from breast cancer at the beginning, after 3-6 months, and after 1 year of treatment with intravenous pamidronate 90 mg every 3-4 weeks. RESULTS AND CONCLUSIONS: Skeletal retention (dose--amount excreted into urine) 2 days after infusion varied between 12% and 98% (mean, 62%) of the administered dose, but there were no differences in retention between patients receiving pamidronate for the first time or after 3-6 months or after 1 year of treatment. Retention of pamidronate was related to the prevalent rate of bone turnover in previously untreated patients, whereas no such relationship was found in previously treated patients. Rate of bone resorption after treatment seemed to be related to the amount of pamidronate retained. During 1 year of treatment, retention of pamidronate remained constant, indicating no saturation of skeletal binding sites with treatment. The variability in retention among individual patients can be attributed to the number of available binding sites. This is related, however, to bone turnover only before the start of treatment. The apparent relationships between skeletal retention and antiresorptive effect could have implications for the design of optimal therapeutic regimens with BPs in patients with bone metastases from breast cancer.

Aged↗

Disruption of the p53 gene results in preserved trabecular bone mass and bone formation after mechanical unloading.

We tested the hypothesis that mechanical unloading facilitates signaling of p53, an important modulator of cell cycling and apoptosis, in bone marrow cells and thereby reduces trabecular bone volume (BV). We performed histomorphometric analyses and bone marrow cell cultures in tail-suspended (TS) p53 null (p53-/-) and wild-type (p53+/+) mice. Eight-week-old male mice were assigned to four groups after 1-week acclimatization: p53+/+ + ground control (GC), p53+/+ + TS, p53-/- + GC, and p53-/- + TS. Bilateral tibial samples were used for analysis. The histomorphometric parameters of trabecular structure, formation and resorption did not differ between the p53-/- + GC and p53+/+ + GC groups. Trabecular BV in p53+/+ + TS mice was significantly reduced to 45% of that in the p53+/+ + GC group after one week of TS. In contrast, BV in p53-/- + TS mice was preserved at the same level as that in the p53-/- + GC group. The bone formation rate (BFR) was significantly reduced in p53+/+ + TS but not in p53-/- + TS mice. Unloading significantly increased trabecular osteoclast number (Oc.N) and surface in p53+/+ + TS mice compared with the p53+/+ + GC group, but the difference was not significant between p53-/- + TS and p53-/- + GC mice. In bone marrow cell culture, the numbers of alkaline phosphatase-positive (ALP+) colony-forming units fibroblastic (CFU-f) and mineralized nodules were significantly reduced in p53+/+ + TS, but not p53-/- + TS mice. [3H]thymidine incorporation into bone marrow cells was higher in p53-/- mice than in p53+/+ mice, independent of mechanical loading or unloading. Flow cytometric cell cycle analysis revealed that unloading significantly increased the percentage of hypoploid bone marrow cells in p53+/+ mice relative to that in p53+/+ + GC mice, but there was no significant difference in ploidy between p53-/- + TS and p53-/- + GC mice. Expression levels of p53 and p21 mRNAs were enhanced after TS in bone marrow cells from p53+/+ mice. Our data show that trabecular bone mass and bone formation were preserved after tail-suspension in p53-/- mice, closely associated with ALP+ CFU-f and mineralized nodule formation in marrow cultures obtained from tibias of p53-/- mice. We speculate that bone loss due to mechanical unloading may be related to facilitation of intracellular p53-p21 signaling.

Animals↗

A histological study on experimental tooth movement into bone induced by recombinant human bone morphogenetic protein-2 in beagle dogs.

OBJECTIVE: The purpose of this preliminary study was to examine experimental tooth movement into newly generated bone induced by recombinant human bone morphogenetic protein-2 (rhBMP-2). METHOD: After extraction of the maxillary first premolars, bone defects were surgically created in eight adult beagle dogs using a 5-mm-diameter trepan bar. According to which material was grafted into the bone defects, animals were divided into the following four groups: (1) the rhBMP-2 group in which rhBMP-2 with a poly[ D,L-(lactide-co-glycolide)]/gelatin sponge complex was implanted; (2) the spongiosa group in which spongiosa from the tibia was grafted; (3) the nongrafted group in which no material was embedded; and (4) the control group in which only tooth extraction was performed. The osteoinductive activity of rhBMP-2 and tooth movement into the newly generated bone were examined by histological and morphometric comparisons of each group. RESULTS: Considerable new bone formation was observed at the grafted site both in the rhBMP-2 and in the spongiosa groups. The area of generated bone in the rhBMP-2 group was significantly greater than that in the spongiosa group. Newly generated bone, in both the rhBMP-2 and spongisosa groups, showed a similar histological response to orthodontic force as in normal alveolar bone in the control group. However, root resorption occurred on the pressure side in the rhBMP-2 group. CONCLUSION: These results indicated that rhBMP-2 might constitute an alternative material to autogeneous bone grafting for alveolar cleft defects. Further studies regarding tooth movement into generated bone induced by rhBMP-2 are suggested.

Absorbable Implants↗

Contribution of bone mineral density and bone turnover markers to the estimation of risk of osteoporotic fracture in postmenopausal women.

In osteoporosis, the main cause for concern is the increase in the risk of fractures. The level of bone mineral density (BMD) measured by various techniques has been shown to be a strong predictor of fracture risk in postmenopausal women. However, half of patients with incident fractures have BMD value above the diagnostic threshold of osteoporosis defined as a T-score of -2.5 SD or more below the average value of young healthy women. Clearly there is a need for improvement in the identification of patients at risk for fracture. Several prospective studies have shown that an increased bone resorption evaluated by specific biochemical markers was associated with increased risk of the hip, spine and non-vertebral fractures independently of BMD. The use of bone markers in individual patients may be appropriate in some situations, especially in women who are not detected at risk by BMD measurements. For example, in the OFELY study including 668 postmenopausal women followed prospectively over 9 years, we found that among the 115 incident fractures, 54 (47%) actually occurred in non-osteoporotic women. Among these women, the combination of bone markers and history of previous fracture was highly predictive of fracture risk. Thus, bone markers may be used in the assessment of fracture risk in selected cases in which BMD and clinical risk factors are not enough to take a treatment decision. Advances in our knowledge of bone matrix biochemistry, most notably of post-translational modifications in type I collagen, may allow identification of biochemical markers that reflect changes in the material property of bone, which is an important determinant of bone strength. Preliminary in vitro studies indicate that the extent of post-translational modifications of collagen--which can be reflected in vivo by the measurement of the urinary ratio between native and isomerised type I collagen--play a role in determining the mechanical competence of cortical bone, independently of BMD. Further studies in osteoporosis should explore the changes in these biochemical parameters of bone matrix as they may represent a key component of bone quality.

Biomarkers↗

[Biochemical markers of bone metabolism and bone tissue losses after allotransplantation of the cadaveric kidney: a cross-sectional].

The biochemical markers of bone metabolism (osteocalcin (OC), C- and N-terminal procollagen I propeptides (PICP) and PINP), bone alkaline phosphatase (BALP), deoxypyridinoline (DPD), beta-crosslaps (beta-CL), bone acid phosphatase (BAP), osteoprotegerin (OPG), insulin-like growth factor I (IGF-I), and parathyroid hormone (PTH)), daily urinary calcium excretion (DUCE) (intestinal calcium absorption), and lumbar and hip bone mineral density (BMD) were determined in 195 patients (78 females and 74 males with normal function of the grafted kidney and 11 females and 31 males with chronic renal failure (CRF) 40 +/- 33 months after renal transplantation (RT). All RT recipients received triple immunosuppressive therapy (cyclosporin, prednisolone, and azathioprine). All groups showed a significant increase in resorption markers and a moderate increase in bone formation markers (except BALP), which suggested bone remodeling dissociation, as well as elevated levels of PTH and OPG and decreased DUCE and BMD in the vertebral column and hip. Increased bone metabolism and decreased intestinal calcium absorption were largely pronounced in CRF. In the majority of recipients, the BMD reduction in the vertebral column and hip was moderate (osteopenia) and only in male recipients with CRF, axial osteopenia was concurrent with peripheral osteoporosis. The main predictor of accelerated bone metabolism and BMD losses following RT was hyperparathyroidism mainly caused by decreased renal graft function. Decreased IGF-I may be a cause of bone remodeling dissociation after RT/ and the increase in OPG seems to be compensatory, which suppresses bone resorption and reduces bone losses.

Biomarkers↗

Removal of bone in CT angiography of the cervical arteries by piecewise matched mask bone elimination.

In maximum intensity projection (MIP) images of CT angiography (CTA) scans, the arteries are often obscured by bone. A bone removal method is presented that uses an additional, nonenhanced scan to create a mask of the bone by thresholding and dilation. After registration of the CTA scan and the additional scan, the bone in the CTA scan is masked. As the cervical area contains bones that can move with respect to each other, these bones are separated first using a watershed algorithm, and then registered individually. A phantom study was performed to evaluate and quantify the tradeoff between the removal of the bone and the preservation of the arteries contiguous to the bone. The influence of algorithm parameters and scan parameters was studied. The method was clinically evaluated with data sets of 35 patients. Best results were obtained with a threshold of 150 HU and a dilation of 8 in-plane voxels and two out-of-plane voxels. The mean width of the soft tissue layer, which is also masked, was approximately 1 mm. The mAs value of the nonenhanced scan could be reduced from 250 mAs to 65 mAs without a loss of quality. In 32 cases the bones were registered correctly and removed completely. In three cases the bone separation was not completely successful, and consequently the bone was not completely removed. The piecewise matched mask bone elimination method proved to be able to obtain MIP images of the cervical arteries free from overprojecting bone in a fully automatic way and with only a slight increase of radiation dose.

Algorithms↗

Changes in trabecular bone turnover and bone marrow cell development in tail-suspended mice.

Skeletal unloading induces trabecular bone loss in loaded bones. The tail-suspended mouse model simulates conditions associated with lack of mechanical stress such as space flight for the loaded bones. In such a model, the tail supports the body weight. The forelimbs are normally loaded and the movement of its hindlimbs is free without weight bearing. Histomorphometric analyses of the murine tibiae of the elevated hindlimbs show that trabecular bone volume rapidly diminishes within one week and stabilizes at that level in the subsequent week of tail suspension. Two-week reloading after one-week unloading completely restores trabecular bone volume, but this does not happen after two-week unloading. Unloading for one or two weeks significantly reduces bone formation rate and increases both the osteoclast surface and number compared with age-matched ground control mice. Subsequent reloading restores reduced bone formation and suppresses increased bone resorption. In bone marrow cell cultures, the numbers of alkaline phosphatase (ALP)-positive colony-forming units-fibroblastic (CFU-f) and mineralized nodules are significantly reduced, but the numbers of adherent marrow cells and total CFU-f are unaltered after tail suspension. On the other hand, subsequent reloading increases the number of adherent marrow cells. Unloading for one week significantly increases the number of tartrate-resistant acid phosphatase (TRAP)- positive multinucleated cells compared with the control level. Our data demonstrate that tail suspension in mice reduces trabecular bone formation, enhances bone resorption, and is closely associated with the formation of mineralized nodules and TRAP-positive multinucleated cells in bone marrow cultures obtained from tibiae. Two-week reloading restores bone volume reduced after one-week unloading, but does not after two-week unloading. The tail-suspended model provides a unique opportunity to evaluate the physiological and cellular mechanisms of the skeletal response to unloading and reloading.

Journal Article↗

[An experimental study on biomechanical effects due to unilateral cortical bone defect in long tubular bone].

OBJECTIVE: To investigate the biomechanics effect due to unilateral cortical bone defect of different size in long tubular bone. METHODS: Seventy-six pieces of Sanhuang cock tibial were randomly divided into 7 groups. The unilateral diaphyses cortical were drilled holes of different size, include 1.5, 2.0, 2.5, 3.0, 3.5, and 4.5 mm, performed three-points bend single experiment. The intact bone cortical group was control group. RESULTS: When there were bone structure destructions, the maximum of the bend load between 3 groups which bone defect diameter were 1.5 mm, 2.0 mm, and control was not significant difference (P = 0.824, 0.865), but the maximum of the bend load between 3 groups which bone defect diameter were 2.5, 3.0, and 3.5 mm decreasing about 14 percent of the control group (P = 0.015, 0.010, 0.021). and the maximum of the bend load which bone defect diameter were 4.5 mm decrease about 23 percent of the control group (P = 0.001). CONCLUSIONS: If the diameter of bone cortical defect is within 22.63 +/- 1.39 percent of bone cortical outer diameter, there was no reduction of the bend load. If the diameter of bone cortical defect is beyond 29.36 +/- 2.07 percent of bone cortical outer diameter, it decreases the maximum bend load of the long tubular bone, but the reduced range is not complete with direct ratio to the bone defect size.

Animals↗