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In 2008 zijn drie landbouwbedrijven op landgoed Twickel begonnen met de omschakeling naar een natuurgericht bedrijf volgens het concept Boeren voor Natuur. Daartoe is eind 2007 een langjarig contract afgesloten tussen de betrokken ondernemers en samenwerkende overheden. Gedurende een periode van vijf jaar wordt de ontwikkeling op de voet gevolgd. Dit rapport doet verslag van de monitoringsresultaten van het tweede jaar, 2009. De volgende aspecten zijn in de monitoring meegenomen: bedrijfsvoering en veterinaire zaken, ecologie (vogels, vegetatie), waterhuishouding en maatschappelijke omgeving. De successievelijke jaren worden uiteindelijk in een eindverslag gebundeld.

Het gaat goed met de konijnen in onze heide- en stuifzandgebieden; na de dramatische achteruitgang van enkele jaren geleden zijn de aantallen het afgelopen jaar weer duidelijk toegenomen. Dat is goed voor de natuur, maar het heeft ook consequenties voor het voorkomen van sommige plantensoorten. Door konijnenvraat krijgt bijvoorbeeld de jeneverbes amper de kans zich te verjongen, zo constateren onderzoekers van Alterra

Contains fulltext : 69065.pdf (publisher's version ) (Closed access), The process of bone remodeling is carried out by 'basic multicellular units' of osteoclasts and osteoblasts. Osteoclasts excavate a resorption space that is subsequently filled with new bone by osteoblasts. In cortical bone osteoclasts dig tunnels through solid bone, in cancellous bone they dig trenches across the trabecular surface. Osteoblasts fill these tunnels and trenches, creating osteons and hemi-osteons, respectively. Both the osteons of cortical bone and the trabeculae of cancellous bone are aligned to the dominant loading direction, indicating that BMU's are mechanically regulated. How mechanical forces guide these cells is still uncertain. We hypothesize that strain-induced osteocyte signals inhibit osteoclast activity and stimulate osteoblast activity. This hypothesis was implemented in a finite element-based bone adaptation model, that was extended with a cell simulation model. This allowed us to examine tunneling and trenching by osteoclasts. We found that our simulations capture key features of BMU-based remodeling: (1) cortical BMU's create load-aligned osteons; (2) cancellous BMU's move across the surface of trabeculae instead of piercing them; (3) resorption-formation coupling occurs in response to strains around resorption sites; and (4) resorbing osteoclasts target nearby regions of osteocyte death, thus providing a mechanism for bone repair.

Bisphosphonates are antiresorptive drugs commonly used to treat osteoporosis. It is not clear, however, what the influence of the time point of treatment is. Recently developed in vivo micro-computed tomographic (CT) scanners offer the possibility to study such effects on bone microstructure in rats. The aim of this study was to determine the influence of early and late zoledronic acid treatment on bone in ovariectomized rats, using in vivo micro-CT. Twenty-nine female Wistar rats were divided into the following groups: ovariectomy (OVX, n = 5), OVX and zoledronic acid (ZOL) at week 0 (n = 8), OVX and ZOL at week 8 (n = 7), and sham (n = 9). CT scans were made of the proximal tibia at weeks 0, 2, 4, 8, 12, and 16; and bone structural parameters were determined in the metaphysis. Two fluorescent labels were administered to calculate dynamic histomorphometric parameters. At week 16, all groups were significantly different from each other in bone volume fraction (BV/TV), connectivity density, and trabecular number (Tb.N), except for the early ZOL and control groups which were not significantly different for any structural parameter. After ZOL treatment at week 8, BV/TV, structure model index, Tb.N, and trabecular thickness significantly improved in the late ZOL group. The OVX and ZOL groups showed, respectively, higher and lower bone formation rates than the control group. Early ZOL treatment inhibited all bone microstructural changes seen after OVX. Late ZOL treatment significantly improved bone microstructure, although the structure did not recover to original levels. Early ZOL treatment resulted in a significantly better microstructure than late treatment. However, late treatment was still significantly better than no treatment.

Contains fulltext : 69065.pdf (publisher's version ) (Closed access), The process of bone remodeling is carried out by 'basic multicellular units' of osteoclasts and osteoblasts. Osteoclasts excavate a resorption space that is subsequently filled with new bone by osteoblasts. In cortical bone osteoclasts dig tunnels through solid bone, in cancellous bone they dig trenches across the trabecular surface. Osteoblasts fill these tunnels and trenches, creating osteons and hemi-osteons, respectively. Both the osteons of cortical bone and the trabeculae of cancellous bone are aligned to the dominant loading direction, indicating that BMU's are mechanically regulated. How mechanical forces guide these cells is still uncertain. We hypothesize that strain-induced osteocyte signals inhibit osteoclast activity and stimulate osteoblast activity. This hypothesis was implemented in a finite element-based bone adaptation model, that was extended with a cell simulation model. This allowed us to examine tunneling and trenching by osteoclasts. We found that our simulations capture key features of BMU-based remodeling: (1) cortical BMU's create load-aligned osteons; (2) cancellous BMU's move across the surface of trabeculae instead of piercing them; (3) resorption-formation coupling occurs in response to strains around resorption sites; and (4) resorbing osteoclasts target nearby regions of osteocyte death, thus providing a mechanism for bone repair.

Contains fulltext : 69065.pdf (publisher's version ) (Closed access), The process of bone remodeling is carried out by 'basic multicellular units' of osteoclasts and osteoblasts. Osteoclasts excavate a resorption space that is subsequently filled with new bone by osteoblasts. In cortical bone osteoclasts dig tunnels through solid bone, in cancellous bone they dig trenches across the trabecular surface. Osteoblasts fill these tunnels and trenches, creating osteons and hemi-osteons, respectively. Both the osteons of cortical bone and the trabeculae of cancellous bone are aligned to the dominant loading direction, indicating that BMU's are mechanically regulated. How mechanical forces guide these cells is still uncertain. We hypothesize that strain-induced osteocyte signals inhibit osteoclast activity and stimulate osteoblast activity. This hypothesis was implemented in a finite element-based bone adaptation model, that was extended with a cell simulation model. This allowed us to examine tunneling and trenching by osteoclasts. We found that our simulations capture key features of BMU-based remodeling: (1) cortical BMU's create load-aligned osteons; (2) cancellous BMU's move across the surface of trabeculae instead of piercing them; (3) resorption-formation coupling occurs in response to strains around resorption sites; and (4) resorbing osteoclasts target nearby regions of osteocyte death, thus providing a mechanism for bone repair.

Bisphosphonates are antiresorptive drugs commonly used to treat osteoporosis. It is not clear, however, what the influence of the time point of treatment is. Recently developed in vivo micro-computed tomographic (CT) scanners offer the possibility to study such effects on bone microstructure in rats. The aim of this study was to determine the influence of early and late zoledronic acid treatment on bone in ovariectomized rats, using in vivo micro-CT. Twenty-nine female Wistar rats were divided into the following groups: ovariectomy (OVX, n = 5), OVX and zoledronic acid (ZOL) at week 0 (n = 8), OVX and ZOL at week 8 (n = 7), and sham (n = 9). CT scans were made of the proximal tibia at weeks 0, 2, 4, 8, 12, and 16; and bone structural parameters were determined in the metaphysis. Two fluorescent labels were administered to calculate dynamic histomorphometric parameters. At week 16, all groups were significantly different from each other in bone volume fraction (BV/TV), connectivity density, and trabecular number (Tb.N), except for the early ZOL and control groups which were not significantly different for any structural parameter. After ZOL treatment at week 8, BV/TV, structure model index, Tb.N, and trabecular thickness significantly improved in the late ZOL group. The OVX and ZOL groups showed, respectively, higher and lower bone formation rates than the control group. Early ZOL treatment inhibited all bone microstructural changes seen after OVX. Late ZOL treatment significantly improved bone microstructure, although the structure did not recover to original levels. Early ZOL treatment resulted in a significantly better microstructure than late treatment. However, late treatment was still significantly better than no treatment.

Item does not contain fulltext, We developed a finite element model to preclinically test cemented hip implants for damage accumulation, including cement crack formation, creep, and stem migration. Using this model, we simulated the mechanical failure processes of four cemented total hip arthroplasty implants (Lubinus SPII, Mueller Curved, Exeter and Charnley, all with known clinical results) during cyclic normal walking and stair-climbing loads. These four implants were selected to ascertain whether the simulation predicted greater damage development around clinically inferior stems, whether clinically inferior designs could be identified by an initial stress analysis without the prediction of cement damage, and whether the simulation could predict high implant subsidence rates in combination with minimal cement damage. Based on the predicted cement crack patterns and crack formation rates, the simulation correctly identified the clinically inferior implant designs. Based only on the initial stress analysis under a stair-climbing load, it was not possible to identify clinically inferior designs. High subsidence values and minimal cement damage were predicted for the Exeter implant, similar to clinical findings. Our findings suggest the simulation may be effective in differentiating between a range of implants and design features.

Solid Free-Form Fabrication (SFF) technologies allow the fabrication of anatomical 3D scaffolds from computertomography (CT) or magnetic resonance imaging (MRI) patients’ dataset. These structures can be designed and fabricatedwith a variable, interconnected and accessible porous network, resulting in modulable mechanical properties, permeability,and architecture that can be tailored to mimic a specific tissue to replace or regenerate. In this study, we evaluatedwhether anatomical meniscal 3D scaffolds with matching mechanical properties and architecture are beneficial formeniscus replacement as compared to meniscectomy. After acquiring CT and MRI of porcine menisci, 3D fiber-deposited(3DF) scaffolds were fabricated with different architectures by varying the deposition pattern of the fibers comprising thefinal structure. The mechanical behaviour of 3DF scaffolds with different architectures and of porcine menisci was measuredby static and dynamic mechanical analysis and the effect of these tissue engineering templates on articular cartilagewas assessed by finite element analysis (FEA) and compared to healthy conditions or to meniscectomy. Results show that3DF anatomical menisci scaffolds can be fabricated with pore different architectures and with mechanical propertiesmatching those of natural menisci. FEA predicted a beneficial effect of meniscus replacement with 3D scaffolds in differentmechanical loading conditions as compared to meniscectomy. No influence of the internal scaffold architecture wasfound on articular cartilage damage. Although FEA predictions should be further confirmed by in vitro and in vivo experiments,this study highlights meniscus replacement by SFF anatomical scaffolds as a potential alternative to meniscectomy.

Item does not contain fulltext, We developed a finite element model to preclinically test cemented hip implants for damage accumulation, including cement crack formation, creep, and stem migration. Using this model, we simulated the mechanical failure processes of four cemented total hip arthroplasty implants (Lubinus SPII, Mueller Curved, Exeter and Charnley, all with known clinical results) during cyclic normal walking and stair-climbing loads. These four implants were selected to ascertain whether the simulation predicted greater damage development around clinically inferior stems, whether clinically inferior designs could be identified by an initial stress analysis without the prediction of cement damage, and whether the simulation could predict high implant subsidence rates in combination with minimal cement damage. Based on the predicted cement crack patterns and crack formation rates, the simulation correctly identified the clinically inferior implant designs. Based only on the initial stress analysis under a stair-climbing load, it was not possible to identify clinically inferior designs. High subsidence values and minimal cement damage were predicted for the Exeter implant, similar to clinical findings. Our findings suggest the simulation may be effective in differentiating between a range of implants and design features.

Item does not contain fulltext, We developed a finite element model to preclinically test cemented hip implants for damage accumulation, including cement crack formation, creep, and stem migration. Using this model, we simulated the mechanical failure processes of four cemented total hip arthroplasty implants (Lubinus SPII, Mueller Curved, Exeter and Charnley, all with known clinical results) during cyclic normal walking and stair-climbing loads. These four implants were selected to ascertain whether the simulation predicted greater damage development around clinically inferior stems, whether clinically inferior designs could be identified by an initial stress analysis without the prediction of cement damage, and whether the simulation could predict high implant subsidence rates in combination with minimal cement damage. Based on the predicted cement crack patterns and crack formation rates, the simulation correctly identified the clinically inferior implant designs. Based only on the initial stress analysis under a stair-climbing load, it was not possible to identify clinically inferior designs. High subsidence values and minimal cement damage were predicted for the Exeter implant, similar to clinical findings. Our findings suggest the simulation may be effective in differentiating between a range of implants and design features.

Solid Free-Form Fabrication (SFF) technologies allow the fabrication of anatomical 3D scaffolds from computertomography (CT) or magnetic resonance imaging (MRI) patients’ dataset. These structures can be designed and fabricatedwith a variable, interconnected and accessible porous network, resulting in modulable mechanical properties, permeability,and architecture that can be tailored to mimic a specific tissue to replace or regenerate. In this study, we evaluatedwhether anatomical meniscal 3D scaffolds with matching mechanical properties and architecture are beneficial formeniscus replacement as compared to meniscectomy. After acquiring CT and MRI of porcine menisci, 3D fiber-deposited(3DF) scaffolds were fabricated with different architectures by varying the deposition pattern of the fibers comprising thefinal structure. The mechanical behaviour of 3DF scaffolds with different architectures and of porcine menisci was measuredby static and dynamic mechanical analysis and the effect of these tissue engineering templates on articular cartilagewas assessed by finite element analysis (FEA) and compared to healthy conditions or to meniscectomy. Results show that3DF anatomical menisci scaffolds can be fabricated with pore different architectures and with mechanical propertiesmatching those of natural menisci. FEA predicted a beneficial effect of meniscus replacement with 3D scaffolds in differentmechanical loading conditions as compared to meniscectomy. No influence of the internal scaffold architecture wasfound on articular cartilage damage. Although FEA predictions should be further confirmed by in vitro and in vivo experiments,this study highlights meniscus replacement by SFF anatomical scaffolds as a potential alternative to meniscectomy.

Contains fulltext : 49817.pdf (publisher's version ) (Closed access), The paradigm that bone metabolic processes are controlled by osteocyte signals have been the subject of investigation in many recent studies. One hypothesis is that osteoblast formation is enhanced by these signals, and that osteoclast resorption is enhanced by the lack of them. Reduced, or absent, osteocyte signaling can be an effect of reduced mechanical loading (disuse) or of defects in the canalicular network, due to microcracks. This would mean that bone is resorbed precisely there where it is mostly needed. In our study, we addressed this apparent contradiction. The purpose was to investigate how alternative strain-based local stimuli for osteoclasts to resorb bone would affect remodeling and adaptation of the trabecular architecture. For this purpose, a computer-simulation model was used, which couples morphological and mechanical effects of local bone metabolism to changes in trabecular architecture and density at large. Six resorption characteristics were studied in the model: (I) resorption occurs spatially random, (II) resorption is enhanced or (III) strongly enhanced where there is disuse, (IV) resorption is enhanced or (V) strongly enhanced where there are high strains, i.e. overload, and (VI) resorption is enhanced where there is disuse and where there are high strains. Results showed that the rates of structural adaptation to alternative loading were higher for disuse-controlled resorption than for overload-controlled resorption. Architecture and mass remained stable for all cases except (V) in which the structure deteriorated as in osteoporotic bone. We conclude that, given the potential of osteoblasts to form bone in highly strained areas, based on signals from osteocytes, osteoclast resorption can normally be compensated for.

Contains fulltext : 49319.pdf (publisher's version ) (Closed access), Osteoarthritis (OA) is a multifactorial disease, associated with articular cartilage degeneration and eventually joint destruction. The phases of the disease have been described in detail, and mechanical factors play an important role in the initiation of OA, but many questions remain about its etiology. Swelling of cartilage, one of the earliest signs of damage, is proportional to the amount of collagen damage. This strongly suggests that damage to the collagen network is an early event in cartilage degeneration. The goal of this study was to determine the mechanical cause of early collagen damage in articular cartilage after mechanical overloading. Both the shear strain along the fibrils and the maximum fibril strains were evaluated as possible candidates for causing collagen damage. This evaluation was done by comparing the locations of maximum shear and tensile strains with the locations of initial collagen damage after mechanical overloading in bovine explants as found using antibodies directed against denatured type II collagen (Col2-3/4M). Collagen damage could be initiated by excessive shear strains along the collagen fibrils, and by excessive fibrils strains. The locations of collagen damage after mechanical overloading were highly dependent on the cartilage thickness, with thinner cartilage being more susceptible to damage than thicker samples.

Contains fulltext : 51270.pdf (publisher's version ) (Closed access)

Contains fulltext : 51134.pdf (publisher's version ) (Closed access), Longitudinal growth of long bones takes place at the growth plates. The growth plate produces new bone trabeculae, which are later resorbed or merged into the cortical shell. This process implies transition of trabecular metaphyseal sections into diaphyseal sections. We hypothesize that the development of cortical bone is governed by mechanical stimuli. We also hypothesize that trabecular and cortical bone share the same regulatory mechanisms for adaptation to mechanical loads. To test these hypotheses, we monitored the development of the tibial cortex in growing pigs, using micro-computer tomography and histology. We then tested the concept that regulatory mechanisms for trabecular bone adaptation can also explain cortical bone development using our mechanical stimulation theory, which could explain trabecular bone (re)modelling. The main results showed that, from the growth plate towards the diaphysis, the pores of the trabecular structure were gradually filled in with bone, which resulted in increased density and cortical bone. The computer model largely predicted this morphological development. We conclude that merging of metaphyseal trabeculae into cortex is likely to be governed by mechanical stimuli. Furthermore, cortex development of growing long bones can be explained as a form of trabecular bone adaptation, without the need for different regulatory mechanisms for cortical and trabecular bone.

Contains fulltext : 49817.pdf (publisher's version ) (Closed access), The paradigm that bone metabolic processes are controlled by osteocyte signals have been the subject of investigation in many recent studies. One hypothesis is that osteoblast formation is enhanced by these signals, and that osteoclast resorption is enhanced by the lack of them. Reduced, or absent, osteocyte signaling can be an effect of reduced mechanical loading (disuse) or of defects in the canalicular network, due to microcracks. This would mean that bone is resorbed precisely there where it is mostly needed. In our study, we addressed this apparent contradiction. The purpose was to investigate how alternative strain-based local stimuli for osteoclasts to resorb bone would affect remodeling and adaptation of the trabecular architecture. For this purpose, a computer-simulation model was used, which couples morphological and mechanical effects of local bone metabolism to changes in trabecular architecture and density at large. Six resorption characteristics were studied in the model: (I) resorption occurs spatially random, (II) resorption is enhanced or (III) strongly enhanced where there is disuse, (IV) resorption is enhanced or (V) strongly enhanced where there are high strains, i.e. overload, and (VI) resorption is enhanced where there is disuse and where there are high strains. Results showed that the rates of structural adaptation to alternative loading were higher for disuse-controlled resorption than for overload-controlled resorption. Architecture and mass remained stable for all cases except (V) in which the structure deteriorated as in osteoporotic bone. We conclude that, given the potential of osteoblasts to form bone in highly strained areas, based on signals from osteocytes, osteoclast resorption can normally be compensated for.

Contains fulltext : 49319.pdf (publisher's version ) (Closed access), Osteoarthritis (OA) is a multifactorial disease, associated with articular cartilage degeneration and eventually joint destruction. The phases of the disease have been described in detail, and mechanical factors play an important role in the initiation of OA, but many questions remain about its etiology. Swelling of cartilage, one of the earliest signs of damage, is proportional to the amount of collagen damage. This strongly suggests that damage to the collagen network is an early event in cartilage degeneration. The goal of this study was to determine the mechanical cause of early collagen damage in articular cartilage after mechanical overloading. Both the shear strain along the fibrils and the maximum fibril strains were evaluated as possible candidates for causing collagen damage. This evaluation was done by comparing the locations of maximum shear and tensile strains with the locations of initial collagen damage after mechanical overloading in bovine explants as found using antibodies directed against denatured type II collagen (Col2-3/4M). Collagen damage could be initiated by excessive shear strains along the collagen fibrils, and by excessive fibrils strains. The locations of collagen damage after mechanical overloading were highly dependent on the cartilage thickness, with thinner cartilage being more susceptible to damage than thicker samples.

Contains fulltext : 51270.pdf (publisher's version ) (Closed access)

Contains fulltext : 51134.pdf (publisher's version ) (Closed access), Longitudinal growth of long bones takes place at the growth plates. The growth plate produces new bone trabeculae, which are later resorbed or merged into the cortical shell. This process implies transition of trabecular metaphyseal sections into diaphyseal sections. We hypothesize that the development of cortical bone is governed by mechanical stimuli. We also hypothesize that trabecular and cortical bone share the same regulatory mechanisms for adaptation to mechanical loads. To test these hypotheses, we monitored the development of the tibial cortex in growing pigs, using micro-computer tomography and histology. We then tested the concept that regulatory mechanisms for trabecular bone adaptation can also explain cortical bone development using our mechanical stimulation theory, which could explain trabecular bone (re)modelling. The main results showed that, from the growth plate towards the diaphysis, the pores of the trabecular structure were gradually filled in with bone, which resulted in increased density and cortical bone. The computer model largely predicted this morphological development. We conclude that merging of metaphyseal trabeculae into cortex is likely to be governed by mechanical stimuli. Furthermore, cortex development of growing long bones can be explained as a form of trabecular bone adaptation, without the need for different regulatory mechanisms for cortical and trabecular bone.

Contains fulltext : 49319.pdf (publisher's version ) (Closed access), Osteoarthritis (OA) is a multifactorial disease, associated with articular cartilage degeneration and eventually joint destruction. The phases of the disease have been described in detail, and mechanical factors play an important role in the initiation of OA, but many questions remain about its etiology. Swelling of cartilage, one of the earliest signs of damage, is proportional to the amount of collagen damage. This strongly suggests that damage to the collagen network is an early event in cartilage degeneration. The goal of this study was to determine the mechanical cause of early collagen damage in articular cartilage after mechanical overloading. Both the shear strain along the fibrils and the maximum fibril strains were evaluated as possible candidates for causing collagen damage. This evaluation was done by comparing the locations of maximum shear and tensile strains with the locations of initial collagen damage after mechanical overloading in bovine explants as found using antibodies directed against denatured type II collagen (Col2-3/4M). Collagen damage could be initiated by excessive shear strains along the collagen fibrils, and by excessive fibrils strains. The locations of collagen damage after mechanical overloading were highly dependent on the cartilage thickness, with thinner cartilage being more susceptible to damage than thicker samples.

Contains fulltext : 51270.pdf (publisher's version ) (Closed access)

Van oudsher zijn hellinggraslanden soortenrijk, maar in de loop van de twintigste eeuw is de omvang sterk teruggelopen. Herstelbeheer heeft voor de kalkgraslandflora weliswaar tot verbetring geleid, maar herstel van de hele gradiënt (van plateau tot dal) is niet bereikt. In 2004 is daarom een OBN onderzoek gestart naar de oorzaken van de achteruitgang en de mogelijkheden voor herstel van bodem, vegetatie en fauna

It is widely believed that mechanical forces affect trabecular bone structure and orientation. The cellular mechanisms involved in this relationship, however, are poorly understood. In earlier work we developed a theoretical, computational framework, coupling bone-cell metabolic expressions to the local mechanical effects of external bone loading. This theory is based on the assumption that osteocytes within the bone tissue control the recruitment of bone-resorbing osteoclasts and bone-forming osteoblasts, by sending strain-energy-density (SED) related signals to trabecular surfaces through the osteocytic, canalicular network. The theory explains the known morphological effects of external bone-loading variations in magnitude and frequency. It also explains the development of osteoporosis, as an effect of increased osteoclast resorption due to estrogen deficiency in postmenopausal women, and to reduced physical activity levels in general. However, the theory uses lumped variables to represent the mechanisms of osteocyte mechano-sensing and signaling. The question is whether these mechanisms could not be specified in a more realistic way. On the one hand, anabolic osteocyte signals might be triggered by the local mechanical loading variables they experience directly, as we assumed in our original theory. On the other hand, osteocyte signals might be triggered by fluid flow in the osteocytic network at large, as was suggested by others. For that purpose we compared the effects of SED, maximal principal strain and volumetric strain as representing local loading variables, to their spatial gradients on the morphological predictions of our computational model. We found that, in concept, they all produced reasonable trabecular structures. However, the predicted trabecular morphologies based on SED as the triggering variable were more realistic in dimensions and relevant metabolic parameters.

It is widely believed that mechanical forces affect trabecular bone structure and orientation. The cellular mechanisms involved in this relationship, however, are poorly understood. In earlier work we developed a theoretical, computational framework, coupling bone-cell metabolic expressions to the local mechanical effects of external bone loading. This theory is based on the assumption that osteocytes within the bone tissue control the recruitment of bone-resorbing osteoclasts and bone-forming osteoblasts, by sending strain-energy-density (SED) related signals to trabecular surfaces through the osteocytic, canalicular network. The theory explains the known morphological effects of external bone-loading variations in magnitude and frequency. It also explains the development of osteoporosis, as an effect of increased osteoclast resorption due to estrogen deficiency in postmenopausal women, and to reduced physical activity levels in general. However, the theory uses lumped variables to represent the mechanisms of osteocyte mechano-sensing and signaling. The question is whether these mechanisms could not be specified in a more realistic way. On the one hand, anabolic osteocyte signals might be triggered by the local mechanical loading variables they experience directly, as we assumed in our original theory. On the other hand, osteocyte signals might be triggered by fluid flow in the osteocytic network at large, as was suggested by others. For that purpose we compared the effects of SED, maximal principal strain and volumetric strain as representing local loading variables, to their spatial gradients on the morphological predictions of our computational model. We found that, in concept, they all produced reasonable trabecular structures. However, the predicted trabecular morphologies based on SED as the triggering variable were more realistic in dimensions and relevant metabolic parameters.

Contains fulltext : 59366.pdf (publisher's version ) (Closed access), The purpose of this study was to examine the effect of mineralization on the mechanical properties of embryonic bone rudiments. For this purpose, four-point bending experiments were performed on unmineralized and mineralized embryonic mouse ribs at 16 and 17 days of gestational age. Young's modulus was calculated using force-displacement data from the experiment in combination with finite element analysis (FEA). For the unmineralized specimens, a calculated average for the Young's modulus of 1.11 (+/- 0.62) MPa was established after corrections for sticking to the four-point bending device and aspect ratio, which is the ratio between the length of the bone and its diameter. For the mineralized specimens, the value was 117 (+/- 62) MPa after corrections. Hence, Young's moduli of embryonic bone rudiments increase by two orders of magnitude within 1 day, during endochondral ossification. As an effect, the hypertrophic chondrocytes in the calcifying cartilage experience a significant change in their mechanical environment. The chondrocytes are effectively stress shielded, which means that they do not carry stresses since stresses are supported by the stiffest parts of the tissue, which are in this case the diaphyseal cortex and the calcified matrix. The deformability of the hypertrophic chondrocytes is, therefore, severely reduced. Since the transition is so sudden and enormous, it can be seen as a process of 'catastrophic' proportion for the hypertrophic chondrocytes. The subsequent resorption of calcified cartilage and the expansion of the marrow cavity could be consequential to stress shielding.

Contains fulltext : 58450.pdf (publisher's version ) (Closed access), We studied reconstruction of the anterior cruciate ligament (ACL) in skeletally mature goats. In one group, the autogenous tissue was augmented with polydioxanone (PDS), the other group had no augmentation. Histological complete incorporation and remodeling of the transplant was found in both groups. The newly formed connective tissues gradually assumed the microscopic properties of the normal ligament. The augmented group showed a delay in remodeling and maturation of the fiber bundles. Mechanically, the PDS-augmented transplants were stronger than the nonaugmented transplants immediately after surgery. During the first 6 weeks, a rapid decrease in strength of the augmented transplants was found, whereas the strength of the nonaugmented group gradually increased. The results of our experiment do not favor augmentation of autografts in reconstruction of the ACL.

Item does not contain fulltext

Contains fulltext : 59366.pdf (publisher's version ) (Closed access), The purpose of this study was to examine the effect of mineralization on the mechanical properties of embryonic bone rudiments. For this purpose, four-point bending experiments were performed on unmineralized and mineralized embryonic mouse ribs at 16 and 17 days of gestational age. Young's modulus was calculated using force-displacement data from the experiment in combination with finite element analysis (FEA). For the unmineralized specimens, a calculated average for the Young's modulus of 1.11 (+/- 0.62) MPa was established after corrections for sticking to the four-point bending device and aspect ratio, which is the ratio between the length of the bone and its diameter. For the mineralized specimens, the value was 117 (+/- 62) MPa after corrections. Hence, Young's moduli of embryonic bone rudiments increase by two orders of magnitude within 1 day, during endochondral ossification. As an effect, the hypertrophic chondrocytes in the calcifying cartilage experience a significant change in their mechanical environment. The chondrocytes are effectively stress shielded, which means that they do not carry stresses since stresses are supported by the stiffest parts of the tissue, which are in this case the diaphyseal cortex and the calcified matrix. The deformability of the hypertrophic chondrocytes is, therefore, severely reduced. Since the transition is so sudden and enormous, it can be seen as a process of 'catastrophic' proportion for the hypertrophic chondrocytes. The subsequent resorption of calcified cartilage and the expansion of the marrow cavity could be consequential to stress shielding.

Contains fulltext : 58450.pdf (publisher's version ) (Closed access), We studied reconstruction of the anterior cruciate ligament (ACL) in skeletally mature goats. In one group, the autogenous tissue was augmented with polydioxanone (PDS), the other group had no augmentation. Histological complete incorporation and remodeling of the transplant was found in both groups. The newly formed connective tissues gradually assumed the microscopic properties of the normal ligament. The augmented group showed a delay in remodeling and maturation of the fiber bundles. Mechanically, the PDS-augmented transplants were stronger than the nonaugmented transplants immediately after surgery. During the first 6 weeks, a rapid decrease in strength of the augmented transplants was found, whereas the strength of the nonaugmented group gradually increased. The results of our experiment do not favor augmentation of autografts in reconstruction of the ACL.

Item does not contain fulltext

Item does not contain fulltext

Contains fulltext : 58450.pdf (publisher's version ) (Closed access), We studied reconstruction of the anterior cruciate ligament (ACL) in skeletally mature goats. In one group, the autogenous tissue was augmented with polydioxanone (PDS), the other group had no augmentation. Histological complete incorporation and remodeling of the transplant was found in both groups. The newly formed connective tissues gradually assumed the microscopic properties of the normal ligament. The augmented group showed a delay in remodeling and maturation of the fiber bundles. Mechanically, the PDS-augmented transplants were stronger than the nonaugmented transplants immediately after surgery. During the first 6 weeks, a rapid decrease in strength of the augmented transplants was found, whereas the strength of the nonaugmented group gradually increased. The results of our experiment do not favor augmentation of autografts in reconstruction of the ACL.

Contains fulltext : 59366.pdf (publisher's version ) (Closed access), The purpose of this study was to examine the effect of mineralization on the mechanical properties of embryonic bone rudiments. For this purpose, four-point bending experiments were performed on unmineralized and mineralized embryonic mouse ribs at 16 and 17 days of gestational age. Young's modulus was calculated using force-displacement data from the experiment in combination with finite element analysis (FEA). For the unmineralized specimens, a calculated average for the Young's modulus of 1.11 (+/- 0.62) MPa was established after corrections for sticking to the four-point bending device and aspect ratio, which is the ratio between the length of the bone and its diameter. For the mineralized specimens, the value was 117 (+/- 62) MPa after corrections. Hence, Young's moduli of embryonic bone rudiments increase by two orders of magnitude within 1 day, during endochondral ossification. As an effect, the hypertrophic chondrocytes in the calcifying cartilage experience a significant change in their mechanical environment. The chondrocytes are effectively stress shielded, which means that they do not carry stresses since stresses are supported by the stiffest parts of the tissue, which are in this case the diaphyseal cortex and the calcified matrix. The deformability of the hypertrophic chondrocytes is, therefore, severely reduced. Since the transition is so sudden and enormous, it can be seen as a process of 'catastrophic' proportion for the hypertrophic chondrocytes. The subsequent resorption of calcified cartilage and the expansion of the marrow cavity could be consequential to stress shielding.

Item does not contain fulltext, Peak stress levels predicted in finite element analysis (FEA) usually depend on mesh density, due to singular points in the model. In an earlier study, an FEA algorithm was developed to simulate the damage accumulation process in the cement mantle around total hip replacement (THR) implants. It allows cement crack formation to be predicted, as a function of the local cement stress levels. As the simulation is driven by mesh-dependent peak stresses, predicted crack formation rates are also likely to be mesh dependent. The aim of this study was to evaluate the mesh dependence of the predicted crack formation process, and to present a method to reduce the mesh dependence. Crack-propagation experiments were simulated. Experimental specimens, representing transverse slices of cemented THR reconstructions, were subjected to cyclic torsional loading. Crack development around the corners of the stem was monitored. The experiments were simulated using three meshes with increasing levels of mesh refinement. Crack locations and orientations were accurately predicted, and were virtually independent of the level of mesh refinement. However, the experimental crack propagation rates were overestimated considerably, increasing with mesh refinement. To eliminate the effect of stress singularities around the corners of the stem, a stress averaging algorithm was applied in the simulation. This algorithm redistributed the stresses by weighted spatial averaging. When damage accumulation was computed based on averaged stresses, the crack propagation rates predicted were independent of the level of mesh refinement. The critical distance, a parameter governing the effect of the averaging algorithm, was optimized such that the predicted crack propagation rates accurately corresponded to the experimental ones. These results are important for the validity and standardization of pre-clinical testing methods for orthopaedic implants.

Item does not contain fulltext, Rigorous preclinical testing of cemented hip prostheses against the damage accumulation failure scenario will reduce the incidence of aseptic loosening. For that purpose, a finite element simulation is proposed that predicts damage accumulation in the cement mantle and prosthetic migration. If the simulation is to become a convincing preclinical test, it should be able to distinguish between implants in a clinically relevant way, based on accurate predictions of long-term failure mechanisms of cemented hip prostheses. The algorithm was used to simulate long-term fatigue experiments on femoral reconstructions with Mueller Curved and Lubinus SPII stems. Clinically, the Mueller Curved system performs inferior to the Lubinus SPII system. The finite element simulation predicted much more cement damage around the Mueller Curved stem and showed that the entire cement mantle was involved in the failure process, which was not the case around the Lubinus SPII stem. In addition, the Mueller Curved stem was predicted to migrate more than the Lubinus SPII. The predictions showed excellent agreement with the experimental findings: similar damage locations in the cement, more damage for the Mueller Curved, similar prosthetic migration directions, and more migration for the Mueller Curved stem. This is the first time that a finite element simulation is able to differentiate between a clinically superior and an inferior implant, based on accurate simulation of the long-term failure mechanisms in a cemented reconstruction. Its use for preclinical testing purposes is corroborated.

Item does not contain fulltext, Osteoporosis is a progressive systemic skeletal condition characterized by low bone mass and microarchitectural deterioration, with a consequent increase in susceptibility to fracture. Hence, osteoporosis would be best diagnosed by in vivo measurements of bone strength. As this is not clinically feasible, our goal is to estimate bone strength through the assessment of elastic properties, which are highly correlated to strength. Previously established relations between morphological parameters (volume fraction and fabric) and elastic constants could be applied to estimate cancellous bone stiffness in vivo. However, these relations were determined for normal cancellous bone. Cancellous bone from osteoporotic patients may require different relations. In this study we set out to answer two questions. First, can the elastic properties of osteoporotic cancellous bone be estimated from morphological parameters? Second, do the relations between morphological parameters and elastic constants, determined for normal bone, apply to osteoporotic bone as well? To answer these questions we used cancellous bone cubes from femoral heads of patients with (n=26) and without (n=32) hip fractures. The elastic properties of the cubes were determined using micro-finite element analysis, assuming equal tissue moduli for all specimens. The morphological parameters were determined using microcomputed tomography. Our results showed that, for equal tissue properties, the elastic properties of cancellous bone from fracture patients could indeed be estimated from morphological parameters. The morphology-based relations used to estimate the elastic properties of cancellous bone are not different for women with or without fractures.

Item does not contain fulltext, Peak stress levels predicted in finite element analysis (FEA) usually depend on mesh density, due to singular points in the model. In an earlier study, an FEA algorithm was developed to simulate the damage accumulation process in the cement mantle around total hip replacement (THR) implants. It allows cement crack formation to be predicted, as a function of the local cement stress levels. As the simulation is driven by mesh-dependent peak stresses, predicted crack formation rates are also likely to be mesh dependent. The aim of this study was to evaluate the mesh dependence of the predicted crack formation process, and to present a method to reduce the mesh dependence. Crack-propagation experiments were simulated. Experimental specimens, representing transverse slices of cemented THR reconstructions, were subjected to cyclic torsional loading. Crack development around the corners of the stem was monitored. The experiments were simulated using three meshes with increasing levels of mesh refinement. Crack locations and orientations were accurately predicted, and were virtually independent of the level of mesh refinement. However, the experimental crack propagation rates were overestimated considerably, increasing with mesh refinement. To eliminate the effect of stress singularities around the corners of the stem, a stress averaging algorithm was applied in the simulation. This algorithm redistributed the stresses by weighted spatial averaging. When damage accumulation was computed based on averaged stresses, the crack propagation rates predicted were independent of the level of mesh refinement. The critical distance, a parameter governing the effect of the averaging algorithm, was optimized such that the predicted crack propagation rates accurately corresponded to the experimental ones. These results are important for the validity and standardization of pre-clinical testing methods for orthopaedic implants.

Item does not contain fulltext, Rigorous preclinical testing of cemented hip prostheses against the damage accumulation failure scenario will reduce the incidence of aseptic loosening. For that purpose, a finite element simulation is proposed that predicts damage accumulation in the cement mantle and prosthetic migration. If the simulation is to become a convincing preclinical test, it should be able to distinguish between implants in a clinically relevant way, based on accurate predictions of long-term failure mechanisms of cemented hip prostheses. The algorithm was used to simulate long-term fatigue experiments on femoral reconstructions with Mueller Curved and Lubinus SPII stems. Clinically, the Mueller Curved system performs inferior to the Lubinus SPII system. The finite element simulation predicted much more cement damage around the Mueller Curved stem and showed that the entire cement mantle was involved in the failure process, which was not the case around the Lubinus SPII stem. In addition, the Mueller Curved stem was predicted to migrate more than the Lubinus SPII. The predictions showed excellent agreement with the experimental findings: similar damage locations in the cement, more damage for the Mueller Curved, similar prosthetic migration directions, and more migration for the Mueller Curved stem. This is the first time that a finite element simulation is able to differentiate between a clinically superior and an inferior implant, based on accurate simulation of the long-term failure mechanisms in a cemented reconstruction. Its use for preclinical testing purposes is corroborated.

Item does not contain fulltext, Osteoporosis is a progressive systemic skeletal condition characterized by low bone mass and microarchitectural deterioration, with a consequent increase in susceptibility to fracture. Hence, osteoporosis would be best diagnosed by in vivo measurements of bone strength. As this is not clinically feasible, our goal is to estimate bone strength through the assessment of elastic properties, which are highly correlated to strength. Previously established relations between morphological parameters (volume fraction and fabric) and elastic constants could be applied to estimate cancellous bone stiffness in vivo. However, these relations were determined for normal cancellous bone. Cancellous bone from osteoporotic patients may require different relations. In this study we set out to answer two questions. First, can the elastic properties of osteoporotic cancellous bone be estimated from morphological parameters? Second, do the relations between morphological parameters and elastic constants, determined for normal bone, apply to osteoporotic bone as well? To answer these questions we used cancellous bone cubes from femoral heads of patients with (n=26) and without (n=32) hip fractures. The elastic properties of the cubes were determined using micro-finite element analysis, assuming equal tissue moduli for all specimens. The morphological parameters were determined using microcomputed tomography. Our results showed that, for equal tissue properties, the elastic properties of cancellous bone from fracture patients could indeed be estimated from morphological parameters. The morphology-based relations used to estimate the elastic properties of cancellous bone are not different for women with or without fractures.

KUN, 14 januari 2003, Promotor : Huiskes, R. Co-promotor : Verdonschot, N.J.J., Item does not contain fulltext

KUN, 14 januari 2003, Promotor : Huiskes, R. Co-promotor : Verdonschot, N.J.J., Item does not contain fulltext

Item does not contain fulltext, Rigorous preclinical testing of cemented hip prostheses against the damage accumulation failure scenario will reduce the incidence of aseptic loosening. For that purpose, a finite element simulation is proposed that predicts damage accumulation in the cement mantle and prosthetic migration. If the simulation is to become a convincing preclinical test, it should be able to distinguish between implants in a clinically relevant way, based on accurate predictions of long-term failure mechanisms of cemented hip prostheses. The algorithm was used to simulate long-term fatigue experiments on femoral reconstructions with Mueller Curved and Lubinus SPII stems. Clinically, the Mueller Curved system performs inferior to the Lubinus SPII system. The finite element simulation predicted much more cement damage around the Mueller Curved stem and showed that the entire cement mantle was involved in the failure process, which was not the case around the Lubinus SPII stem. In addition, the Mueller Curved stem was predicted to migrate more than the Lubinus SPII. The predictions showed excellent agreement with the experimental findings: similar damage locations in the cement, more damage for the Mueller Curved, similar prosthetic migration directions, and more migration for the Mueller Curved stem. This is the first time that a finite element simulation is able to differentiate between a clinically superior and an inferior implant, based on accurate simulation of the long-term failure mechanisms in a cemented reconstruction. Its use for preclinical testing purposes is corroborated.