Cancellous Bone Surface Research Articles

Selection of sagittal split ramus osteotomy technique based on skeletal anatomy and planned distal segment movement: Current therapy

The most common osteotomy of the mandible for the correction of dentofacial deformities is the sagittal split ramus osteotomy (SSRO). Trauner and Obwegeser 1 Trauner R. Obwegeser H. The surgical correction of mandibular prognathism and retrognathia with consideration for genioplasty. Oral Surg Oral Med Oral Pathol. 1957; 10: 677 Abstract Full Text PDF PubMed Scopus (650) Google Scholar popularized this technique in 1957 for correction of prognathism and retrognathism. They developed a technique for performing an SSRO that involved extensive soft tissue dissection and a horizontal corticotomy on the medial and lateral aspects in the vertical ramus to the posterior border. They found that this technique provided good contact of wide cancellous bone surfaces that resulted in quick bony union. However, there are complications inherent in this technique, including excessive swelling and bleeding, intraoperative trauma to the temporomandibular joint, damage to the inferior alveolar nerve (IAN), and unfavorable fractures of the proximal and/or distal segments of the mandible. Unfavorable fractures can result in infection, sequestration of fragments, delayed union, malunion, or fibrous union of the osteotomy sites.

Growth hormone can reverse glucocorticoid-induced low bone turnover on cortical but not on cancellous bone surfaces in adult Wistar rats

We evaluated the effect of glucocorticoids (GC) and growth hormone (GH) on cortical and cancellous bone turnover in adult rats using random vertical sections giving valid measurements of bone surfaces and bone formation parameters. GH administration could reverse GC-induced osteopenia and low bone turnover of cortical bone. However, GH could not reverse the GC-induced low bone turnover of cancellous bone. Methods: Seventy female Wistar rats, 7 months of age, were divided into five groups: (1) start control, (2) saline, (3) GC 9 mg/kg/day (Solu Medrol), (4) GH 5 mg/kg/day, and (5) GC 9 mg/kg/day + GH 5 mg/kg/day, and injected for 3 months. The vertebral body was examined using dynamic histomorphometry and biomechanical tests. Nonparametric methods were used. Results: Glucocorticoid administration induced a low bone turnover state of both the cortical and cancellous bone of the vertebral body, without altering the absolute amount of bone or the biomechanical competence of the vertebral body. GH administration induced a small increase in longitudinal bone growth and ventral modeling drift. This growth increased the total amount of cortical, endocortical, and cancellous bone in the vertebra. The biomechanical competence of a 3.5-mm-high cylinder of the central vertebral body was also increased due to an increase in the amount of cortical bone, whereas the total amount of cancellous bone in the cylinder was unaltered. The cancellous bone density (CBV) was, however, increased due to thicker trabeculae probably induced by an accelerated mineral appositional rate (MAR) induced by GH. GH also increased longitudinal and ventral modeling drifts in the GC-injected animals. GH increased the amount of cortical bone and also the amount of cancellous bone close to the epiphyseal growth plate, whereas the cancellous bone volume of the central vertebral cylinder was unaffected by GH administration in GC-injected animals. GH could also increase parameters of bone formation (bone mineralizing surface (MS) and MAR) on cortical bone surfaces in GC-injected animals, whereas parameters of bone formation [MS and bone formation rates (BFR)] on cancellous bone surfaces were even lower than those of animals injected with GC alone. Conclusion: GH can reverse GC-induced low bone turnover on cortical but not on cancellous bone surfaces.

Interleukin 10-deficient mice develop osteopenia, decreased bone formation, and mechanical fragility of long bones

Bone loss is a common complication of human inflammatory bowel disease (IBD), but its mechanisms are not understood completely. We investigated bone metabolism in interleukin-10-deficient ( IL-10-/- ) mice, an animal model with IBD features. IL-10-/- male mice (8- and 12-weeks-old) and their age-matched wild-type counterparts (C57BL/6J) were studied. Bone mass of the femur was determined by ashing. Tibial cancellous and cortical bone mass and formation was measured by static and dynamic histomorphometry. Biomechanical strength of the femur was tested. Primary bone marrow stromal cell cultures were used to assess osteoblast generation. Serum levels of 25-OH vitamin D 3, insulin-like growth factor-1 (IGF-1), parathyroid hormone, osteocalcin, and deoxy-pyridinoline cross-links were measured. The presence of colitis was determined histologically, and by IL-12 and interferon-gamma (IFN-gamma) secretion from cultured colonic explants. Eight- and 12-week-old IL-10-/- mice developed osteopenia of both cancellous and cortical bone, evidenced by lower femoral ash weight, cancellous bone area and surface, trabecular number, and decreased cortical bone area and width. Osteopenia was associated with mechanical fragility, manifested by decreased stiffness and mechanical load at fracture, and was caused by suppressed bone formation, indicated by decreased cancellous double-labeled surface, mineralizing surface, serum osteocalcin level, and mineralized nodule number in bone marrow stromal cell cultures. IL-10-/- mice with colitis had significantly less bone mass compared with IL-10-/- mice without colitis. IL-10-/- mice develop the hallmarks of osteoporosis, that is, reduced bone mass, increased mechanical fragility, and suppressed bone formation. The presence of colitis is an important contributor to osteoporosis in IL-10-/- mice.

The Classic: Revision of Aseptic Loose Total Hip Arthroplasties

The Classic: Revision of Aseptic Loose Total Hip Arthroplasties

Mechanotransduction of bone cells in vitro: mechanobiology of bone tissue.

Mechanical force plays an important role in the regulation of bone remodelling in intact bone and bone repair. In vitro, bone cells demonstrate a high responsiveness to mechanical stimuli. Much debate exists regarding the critical components in the load profile and whether different components, such as fluid shear, tension or compression, can influence cells in differing ways. During dynamic loading of intact bone, fluid is pressed through the osteocyte canaliculi, and it has been demonstrated that fluid shear stress stimulates osteocytes to produce signalling molecules. It is less clear how mechanical loads act on mature osteoblasts present on the surface of cancellous or trabecular bone. Although tissue strain and fluid shear stress both cause cell deformation, these stimuli could excite different signalling pathways. This is confirmed by our experimental findings, in human bone cells, that strain applied through the substrate and fluid flow stimulate the release of signalling molecules to varying extents. Nitric oxide and prostaglandin E2 values increased by between two- and nine-fold after treatment with pulsating fluid flow (0.6 +/- 0.3 Pa). Cyclic strain (1000 microstrain) stimulated the release of nitric oxide two-fold, but had no effect on prostaglandin E2. Furthermore, substrate strains enhanced the bone matrix protein collagen I two-fold, whereas fluid shear caused a 50% reduction in collagen I. The relevance of these variations is discussed in relation to bone growth and remodelling. In applications such as tissue engineering, both stimuli offer possibilities for enhancing bone cell growth in vitro.

Interrelationships between structural parameters of cancellous bone reveal accelerated structural change at low bone volume.

This study shows that change to cancellous bone structure is bone volume-dependent in a nonlinear manner. At low bone volume (< 15%), trabecular thickness and trabecular separation change at a much greater rate than at higher bone volume. This suggests that the structural integrity of the cancellous bone may become rapidly compromised when bone volume falls below a critical value. While bone mass is the major determinant of bone strength, this mass-based paradigm does not fully account for the contribution of the bone microstructure to mechanical efficiency. Geometric models of cancellous bone structure have been formulated based on stylized representations of the trabecular elements, where the relationships between bone volume and bone surface of cancellous bone are complex and reflect the modulating effect on the cancellous bone structure of bone remodeling at the trabecular surfaces. Using the plate model of cancellous bone structure, the interrelationships between parameters of cancellous bone structure have been studied. Two hundred eighty histological sections of human cancellous bone from eight skeletal sites were analyzed. The structural parameters of cancellous bone (BV/TV, BS/TV, BS/BV, Tb.Th, Tb.Sp, Tb.N, and TBPf) were obtained. This study shows that change to cancellous bone structure is bone volume-dependent in a nonlinear manner. At low bone volume (< 15%), structural parameters of cancellous bone, such as trabecular thickness and trabecular separation, change at a much greater rate than at higher bone volume. This suggests that the structural integrity of the cancellous bone may become rapidly compromised when bone volume falls below a critical value. These data describe the complex relationships between bone mass and structure in cancellous bone that are often overlooked in the mass-based paradigm of bone strength. Histomorphometric descriptors of cancellous bone structure highlight the potential for accelerated deterioration of the structure with low bone volume, which leads to increased risk of fracture. From a clinical viewpoint, estimation of an individual's fracture risk is constrained to noninvasive techniques, which only provide bone mineral density or bone mineral content. Therefore, there is a need to better correlate measurement of bone mass with measurements of structural parameters.

Estrogen receptor-alpha dependency of estrogen's stimulatory action on cancellous bone formation in male mice.

We examined whether estrogen receptor (ER)alpha is required for estrogen to stimulate cancellous bone formation in long bones of male mice. 17 beta-Estradiol (E(2)) was administered to ER alpha(-/-) male mice or wild-type (WT) littermate controls at 40, 400, or 4000 microg/kg by daily sc injection for 28 d and histomorphometric analysis performed at the distal femoral metaphysis. In WT mice, treatment with E(2) (40 microg/kg per d) increased the proportion of cancellous bone surfaces undergoing mineralization and stimulated mineral apposition rate. In addition, higher doses of E(2) induced the formation of new cancellous bone formation surfaces in WT mice. In contrast, E(2) had little effect on any of these parameters in ER alpha(-/-) mice. Immunohistochemistry was subsequently performed using an ER alpha-specific C-terminal polyclonal antibody. In WT mice, ER alpha was expressed both by cancellous osteoblasts and a significant proportion of mononuclear bone marrow cells. Immunoreactivity was also observed in cancellous osteoblasts of ER alpha(-/-) mice, resulting from expression of the activation function-1-deficient 46-kDa ER alpha isoform previously reported to be expressed in normal osteoblasts and bones of ER alpha(-/-) mice. Taken together, our results suggest that estrogen stimulates bone formation in mouse long bones via a mechanism that requires the presence of full-length ER alpha possessing activation function-1.

Inhibition of cyclo-oxigenase-2 activity does not abolish the anabolic effect of prostaglandin E2 in vivo or in vitro.

It was previously reported that the expression of cyclo-oxigenase-2 (COX-2) is induced by prostaglandin E(2) (PGE(2)) in vitro in an osteogenic cell line and organ culture, suggesting an autoamplification mechanism. In this study, we first tested whether this phenomenon also occurs in bone tissue in vivo and found that a single anabolic dose of PGE(2) (5 mg/kg) induced (between 30 and 120 min) in rat tibiae, an increase in the mRNA level of COX-2 (2.5- to 9-fold) but not that of COX-1. Secondly, to test whether COX-2 activity in generating endogenous prostaglandins (PGs) is required for the in vivo anabolic properties of PGE(2), young male rats were injected daily with either vehicle (8% ethanol) or 5 mg/kg PGE(2) for 21 days. PGE(2)-injected rats received, 45 min prior to PGE(2), either dimethyl sulphoxide (as vehicle) or one of two doses of NS-398, a selective COX-2 inhibitor: a low dose (3 mg/kg) or a high dose (10 mg/kg). PGE(2) increased bone formation (measured as cancellous mineralizing surface, mineral apposition rate and bone formation rate) and bone mass (measured as cancellous bone area and surface and cortical width). None of these increases was suppressed by pre-administration of NS-398. In contrast, the high dose of NS-398 effectively suppressed an increase in rat hind-paw volume induced by a local carrageenan injection. Furthermore, since COX-2 inactivation may affect PG receptor expression, we found that pre-administration of NS-398 did not abolish the induction in EP(4) receptor mRNA levels, caused by PGE(2) in rat bone tissue. For in vitro testing, rat femoral bone marrow stromal cell cultures were initiated and were incubated in the absence or presence of PGE(2) at 100 nM (as an inducer) and with increasing concentrations of NS-398 (10(-8) M to 10(-5) M) for 21 days, after which time mineralized (Von-Kossa positive) nodules were counted. PGE(2) increased nodule formation as previously reported; however, NS-398 reduced nodule formation in both control and PGE(2)-treated cultures to the same extent. We conclude that while the level of COX-2 mRNA is increased in vivo by administration of PGE(2), inhibition of its activity (i.e. generation of endogenous PGs) does not abolish the anabolic effect of PGE(2).

The static and cyclic strength of a bone-cement bond.

Four-point bending static and fatigue tests were carried out on bone-cement bonds. The effects of the pressurization and the washing of the bone joint face on the bond strength were investigated. The results are summarized as follows. When the bond surface of cancellous bone is washed prior to the application of the bone cement, both the static and fatigue strengths of the bond are increased relative to the corresponding properties of unwashed bone-cement bonds. From observations of bone-cement interfaces as well as the fracture surfaces of bone-cement specimens, it has been determined that bone cement was able to infiltrate into fine holes present in washed cancellous bone. However, such infiltration occurred to a much lesser degree in the case of unwashed cancellous bone. Increasing the molding pressure during the time of cement application to the bone from 39200 to 117600 Pa had a beneficial effect on the bending strength and fatigue properties, particularly in the case of washed bone cement specimens. An increase in molding pressure also resulted in a reduction in the amount of scatter in test results.

Estrogen-induced osteogenesis in mice is associated with the appearance of Cbfa1-expressing bone marrow cells.

Cbfa1 is a transcription factor recognised as being involved in early osteoblast differentiation during embryonic skeletogenesis. To determine whether Cbfa1 plays a similar role in bone formation in the adult, we analysed whether its expression is altered during estrogen-induced osteogenesis, following our recent studies which suggest that this response involves the generation of early osteoblast precursors within bone marrow. To facilitate identification of Cbfa1-expressing cells, these studies were performed in mice heterozygous for a cbfa1 gene deletion (cbfa1(+/-)) using beta-galactosidase (lacZ) as a genetic marker. Cbfa1-expressing cells were identified by lacZ staining of longitudinal sections of the proximal tibial metaphysis. Treatment of cbfa1(+/-) mice with 17beta-estradiol 0.5 mg/week for 24 days led to the appearance of new cancellous bone surfaces. This response was associated with a marked increase in number of Cbfa1-expressing cells within the metaphysis, consisting not only of osteoblasts on bone surfaces but also of cells within the adjacent bone marrow. We subsequently enumerated Cbfa1-expressing cells at earlier time-points following estrogen, in sections co-stained for ALP activity. After 4 days of estrogen treatment, a population of cells appeared within the marrow cavity which expressed Cbfa1, but were negative for ALP. At later time-points, large numbers of Cbfa1 + bone marrow cells were still present, but the majority of these were close to new trabecular bone surfaces at sites which showed high levels of ALP activity. An equivalent distribution of Cbfa1-expressing cells was observed in further studies where Cbfa1 expression was analysed in wild-type mice by immunohistochemistry. We conclude that estrogen-induced osteogenesis is associated with the appearance of a population of Cbfa1-expressing cells within bone marrow, which we hypothesize to represent the osteoblast precursor population responsible for subsequent new bone formation.

Cancellous bone remodeling occurs in specialized compartments lined by cells expressing osteoblastic markers.

We describe a sinus, referred to as a bone remodeling compartment (BRC), which is intimately associated with cancellous bone remodeling. The compartment is lined on its marrow side by flattened cells and on its osseous side by the remodeling bone surface, resembling a roof of flattened cells covering the bone surface. The flat marrow lining cells are in continuity with the bone lining cells at the margins of the BRC. We examined a large number of diagnostic bone biopsy specimens received during recent years in the department. Furthermore, 10 patients (8 women and 2 men, median age 56 [40-69] years) with the high turnover disease of primary hyperparathyroidism who were treated with parathyroidectomy and followed for 3 years were included in the histomorphometric study. Bone samples for the immuno-enzyme staining were obtained from an amputated extremity of child. The total cancellous bone surface covered by BRC decreases by 50% (p < 0.05) following normalization of turnover and is paralleled by a similar 50% decrease in remodeling surface (p < 0.05). The entire eroded surface and two-thirds of the osteoid surface are covered by a BRC. BRC-covered uncompleted walls are 30% (p < 0.05) thinner than those without a BRC. This indicates that the BRC is invariably associated with the early phases of bone remodeling, that is, bone resorption, whereas it closes during the late part of bone formation. Immuno-enzyme staining shows that the flat marrow lining cells are positive for alkaline phosphatase, osteocalcin, and osteonectin, suggesting that they are bone cells. The first step in cancellous bone remodeling is thought to be the lining cells digesting the unmineralized matrix membrane followed by their disappearance and the arrival of the bone multicellular unit (BMU). We suggest that the lining cell barrier persists during bone remodeling; that the old lining cells become the marrow lining cells, allowing bone resorption and bone formation to proceed under a common roof of lining cells; that, at the end of bone formation, new bone lining cells derived from the flattened osteoblasts replace the marrow lining cells thereby closing the BRC; and that the two layers of lining cells eventually becomes a single layer. The integrity of the osteocyte-lining cell system is reestablished by the new generation of lining cells. The BRC most likely serves multiple purposes, including efficient exchange of matrix constituents and minerals, routing, monitoring, or modulating bone cell recruitment, and possibly the anatomical basis for the coupling of bone remodeling.

Effect of deconditioning on cortical and cancellous bone growth in the exercise trained young rats.

Exercise enhances bone growth and increases peak bone mass. The aim of this study was to determine whether or not 4 weeks of deconditioning after 8 weeks of exercise in growing rats would result in a decrease in bone gain or reverse the benefits of exercise. Fifty 4-week-old female Sprague-Dawley rats were randomized by a stratified weight method into 5 groups with 10 rats in each group: 8 weeks exercise (8EX), 8 weeks sedentary control (8S), 12 weeks exercise (12EX), 8 weeks exercise followed by 4 weeks sedentary (8EX4S), and 12 weeks sedentary control (12S). The exercise consisted of running on a treadmill with a 5 degrees slope at 24 m/minute for 1 h/day and 5 days/week. After each period of exercise, cancellous and cortical bone histomorphometry were performed on double fluorescent labeled 5-microm-thick sections of the proximal tibia and 40-microm-thick sections of the tibial shaft, respectively. Eight and 12 weeks of exercise resulted in a significant increase in the body weight and gastrocnemius muscle weight by two-way analysis of variance (ANOVA). The femoral wet weight (mg; mean +/- SD; 8EX, 781 +/- 45.1 vs. 8S, 713 +/- 40.5; p < 0.05; 12EX, 892 +/- 41.6 vs. 12S, 807 +/- 19.8; p < 0.05) was significantly higher in the exercise group than that in the respective control groups. The femoral wet weight and bone volume (BV) of the 8EX4S group (818 +/- 46.2 mg and 531 +/- 31.2 microl, respectively) were significantly lower than those of the 12EX group (p < 0.05) and did not differ significantly from those of the 12S groups. The cancellous BV was significantly higher in the 8EX and 12EX groups than that in the respective sedentary groups (p < 0.05). The cortical bone area of the tibial shaft was also significantly higher in the 12EX than that in the 12S group (p < 0.05). The increase in the cancellous BV or cortical bone area was caused by an increase in the mineral apposition rate (MAR), without a significant effect in the labeled perimeter. The bone formation rate (BFR; microm3/microm2 per day) in the cancellous bone (12EX, 27.9 +/- 7.74 vs. 12S, 15.4 +/- 4.56; p < 0.05) or periosteal surface (12EX, 127.6 +/- 27.7 vs. 12S, 79.5 +/- 18.6; p < 0.05) was significantly higher in the exercised groups than that in the respective control group (p < 0.05). Again, deconditioning resulted in a decrease in the cancellous BFR, BV, periosteal BFR, and cortical bone area to levels not significantly different from the 12S group. In conclusion, our findings showed that exercised growing rats, when deconditioned, lost the benefits gained through exercise and their bone parameters were reduced to levels not different from the sedentary control. Thus, continued exercise is required to maintain high bone mass.

Irrigation and suction technique to ensure reliable cement penetration for total knee arthroplasty

We describe a new technique to enhance the preparation of the cancellous bone surfaces in total knee arthroplasty using bone suction and pressure lavage irrigation. This technique provides dry bone surfaces on which to cement (which is particularly valuable if a tourniquet is not used) and improves significantly the penetration of cement into the tibial plateau as assessed on plain postoperative radiographs. We review the results of this new technique by analyzing depths of cement penetration on postoperative radiographs to assess whether this technique offers improvements in cement penetration and bone surface preparation. This technique offers a simple, quick, and reliable method of ensuring reliable cement penetration into the bony trabeculae during cemented total knee arthroplasty.

Tibial antivarus closing wedge osteotomy

Antivarus lateral closing wedge osteotomy of the proximal tibia is a time-tested surgical technique. Redistribution ofweight-bearing forces within the knee joint decreases the medial compartment load and the varus knee moment. Young or middle-aged patients as well as athletes with medial unicompartmental arthritis, posterolateral instability and varus thrust, or chronic anterior cruciate ligament deficiency and varus malalignment may be candidates. The indications have expanded recently to include patients with a varus mechanical axis who are undergoing periosteal resurfacing, autogenous chondrocyte implantation, meniscal transplantation, osteochondral grafting, or multiple subchondral bone microfractures. The osteotomy is performed between the knee joint and the tibial tubercle by removing a laterally based bone wedge. The construct is stable because of osteoclasis of the medial tibial cortex, an intact periosteal hinge, and excellent apposition of broad cancellous bone surfaces. Early knee motion is possible and bone healing is expeditious. Complications can be averted by careful patient selection, precise preoperative planning, and meticulous surgical technique. The weight-bearing line method uses a full-length standing radiograph to determine the desired correction angle. The osteotomy is performed with fluoroscopic guidance through a limited exposure. Low-profile step staples provide satisfactory fixation, and no bone grafting is required. Tibial Antvarus lateral closing wedge osteotomy is a useful and reliable surgical technique.

How do changes to plate thickness, length, and face-connectivity affect femoral cancellous bone's density and surface area? An investigation using regular cellular models

Models of regular cellular-solids representing femoral head `medial group’ bone were used to (1) compare thickness data for plate-like and beam-like structures at realistic surface areas and densities; (2) test the validity of a standard formula for trabecular thickness (Tb.Th); and (3) study how systematic changes in cancellous bone thicknesses, spacing, and face-connectivity affect relative density and surface area. Models of different face-connectivities, produced by plate removal from the unit cell, were fitted to bone density and surface area data. The medial group bone was anisotropic: the supero-inferior (SI) direction was the principal direction for bone plate alignment and the plane normal to this had the largest number of bone/void intersections per unit line length ( P L). A comparison of boundary perimeter per unit area data, in planes normal to SI, with surface area data placed the medial group bone between prismatic structures in which walls are parallel to one principal direction and isotropic structures. Selective removal of plates from a closed-cell model produced a similar result. For the same relative density and surface-area, plate-like models had significantly thinner cross-sections than beam-like models. The formula for Tb.Th produced overestimates of model plate thickness by up to 20% at realistic femoral cancellous densities. Trends in data on surface area to volume ratio and density observed on sampled medial group bone could be simulated by plate thickness changes on models of intermediate face-connectivity (∼1.5) or by plate removal from models with relatively thick and short (low aspect-ratio) plates. The latter mechanism is unrealistic for it resulted in beam-like structures at low `medial group’ densities, an architecture unlike the predominantly plate-like bone in the sample.

Growth hormone increases cortical and cancellous bone mass in young growing rats with glucocorticoid-induced osteopenia.

The effects of growth hormone (GH) on linear growth, bone formation, and bone mass have been examined in glucocorticoid (GC)-injected young growing rats. Two-month-old female Wistar rats were injected for 90 days with 1, 3, 6, or 9 mg of methylprednisolone alone or in combination with 5 mg of GH. Bone mass and bone formation parameters were examined in the femoral cortical bone and in cortical bone and cancellous bone of the lumbar vertebra. GC administration dose dependently decreased growth, longitudinal growth of the vertebra, as well as the modeling drift of the cortical bone of the vertebral body and femoral diaphysis. In the vertebral cancellous bone, GC also decreased the mineralizing surface and inhibited the growth-related increase in cancellous bone volume. GH increased growth, longitudinal growth of the vertebra, as well as the modeling drift of the vertebral body and the femoral diaphysis, resulting in an increased cortical bone mass. GH also increased cancellous bone volume and the mineralizing surface of the vertebral body. In GC-injected animals, GH normalized and further increased growth, longitudinal growth, and the modeling drift of both the femoral diaphysis and the vertebral body, resulting in an increased cortical bone mass at both locations. GH also increased cancellous bone volume of the vertebral body in GC-injected animals, but GH did not, however, reverse the decreased mineralizing surface of cancellous bone induced by GC injections. In conclusion, GC administration to growing rats retards normal growth, longitudinal growth, and cortical bone modeling drift. It also decreases the cancellous bone mineralizing surface and inhibits the normal age-related increase in cancellous bone volume of the vertebral body. In the growing rat skeleton, GH can counteract these GC-induced side effects, except for the GC-induced decrease in the mineralizing surface of cancellous bone of the vertebral body, which remained unaffected by GH administration.

A Structural Approach to Renal Bone Disease

A Structural Approach to Renal Bone Disease

Flow characteristics of curing polymethyl methacrylate bone cement.

During polymerization, polymethyl methacrylate bone cements have complex viscoelastic characteristics. Within a short working time they transform from dough-like consistencies to solid cements. Therefore, the time at which a cement is introduced to cancellous bone surfaces and subjected to pressure is important, to achieve optimum flow and mechanical interdigitation. Achieving adequate mechanical interlock increases the area for load transfer and reduces localized bone-cement interface stresses. The aim of this study was to measure the flow characteristics for commercial bone cements as a function of time and calculate the apparent viscosities for the curing bone cements. The capillary extrusion method was used to measure the rate of flow of the curing cement, by means of a melt flow index apparatus, which was manufactured in-house. The tests were conducted using nozzles of different lengths and under two loads. This enabled the power index value, n, and the pressure at the die entry, P0, to be calculated for each material with respect to time. Once the flow characteristics were determined, a series of formulae were used to calculate the shear rates, gamma, the shear stresses, tau, and the apparent viscosities, eta a, of the curing bone cements. The results indicated that acrylic bone cements are non-Newtonian, pseudoplastic materials, since the power index values are less than 1.0 during the curing stage. The consistency indices, K, were calculated from the shear stress versus shear rate data. The apparent viscosities of the cements were found to increase with respect to increases in time. Clinically, it was considered desirable to inject and pressurize the cement into the medullary canal while its viscosity is relatively low in order to obtain maximum interdigitation into cancellous bone, provided adequate containment and a means of pressurization can be achieved. The pseudoplastic character of bone cements is responsible for their reduction in viscosity with increased shear rate, a property that may be exploited to enhance penetration with appropriate delivery.

Intermittent parathyroid hormone administration stimulates bone formation in the mandibles of aged ovariectomized rats.

Intermittent administration of parathyroid hormone (PTH) is known to stimulate bone formation in many skeletal sites and is being investigated as a possible therapeutic agent for the treatment of osteopenic conditions, including post-menopausal osteoporosis. The purpose of this study was to determine the ability of PTH to stimulate bone formation in the mandibles of aged ovariectomized (Ovx) rats, and the results are compared with a site in the appendicular skeleton (humerus). The Ovx rat is a useful model of estrogen deficiency, replicating many aspects of post-menopausal osteoporosis. Female rats were ovariectomized or sham-operated, and one year later a group of the ovariectomized rats was treated with the 1-34 fragment of human PTH daily, five days a week for 10 weeks. During the experiment, the animals were given fluorochrome bone markers for histomorphometry. More than one year after ovariectomy or sham surgery, there were few differences in the histomorphometric indices of bone formation in the humerus or mandible. PTH treatment had no effect on dentin formation, measured in the mandibular incisor; however, most indices of bone formation-including the double-labeled surface, mineralizing surface, mineral appositional rate, new bone area, and surface-referent bone formation rates-were substantially greater in the PTH-treated group compared with both the Ovx and the Sham controls measured at the periosteal and endocortical surfaces of the humerus and the periosteal and cancellous bone surfaces of the mandible. In addition, bone formation at the alveolar crest, particularly on the buccal side, was greater in the PTH-treated group. The results from this study demonstrate that systemic intermittent PTH treatment stimulates bone formation in the mandibles in aged, estrogen-deficient animals.

The Effect of Long-Term Ovarian Hormone Deficiency on Transforming Growth Factor β and Bone Matrix Protein mRNA Expression in Rat Femora

Estrogen deficiency results in increased bone turnover and osteopenia. Decreased transforming growth factor beta (TGF-β) has been implicated as having a role in ovariectomy (OVX)-induced bone loss; however the decrease in TGF-β mRNA may simply be due to the reduction in cancellous bone volume that occurs following OVX. This investigation characterized the effect of long-term OVX (11.5 months) on mRNA levels for TGF-β, osteocalcin (OC), and type I collagen (TYPE I) and expressed these data relative to the amount of cancellous bone surface. Additionally, the short-term effect of estrogen administration on TGF-β, OC, and TYPE I mRNA was evaluated. OVX resulted in a 56% loss of bone surface. At the tissue level, TGF-β was reduced, OC was increased, and TYPE I was unchanged. Expressed relative to bone surface, TGF-β was unchanged and OC and TYPE I were significantly elevated. Four hours after estrogen administration, TGF-β mRNA was unchanged compared to vehicle-treated controls. The data suggest that bone turnover is elevated after long-term OVX, but do not suggest a direct role of TGF-β in OVX-induced bone loss.