Quantification of remodeling parameter sensitivity—assessed by a computer simulation model

Thomsen, Jesper Skovhus; Mosekilde, Li.; Mosekilde, E.

doi:10.1016/s8756-3282(96)00231-1

Cited by 13 publications

(10 citation statements)

References 48 publications

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“…Accepting the principle that bone has to be deposited on a pre-existing bone surface, many authors have considered the perforation or fenestration of the trabeculae as irreversible. (2,20,22,23) Indeed, this was consistent with the progressive age-related loss of entire structural elements. (24) Overall, it is generally believed that large perforations (100 -400 m) are irreversible alterations of bone architecture.…”

Section: Perforations: the Dogmasupporting

confidence: 75%

“…Now, what about bone apposition on the perforated trabecular plate? Accepting the principle that bone has to be deposited on a pre‐existing bone surface, many authors have considered the perforation or fenestration of the trabeculae as irreversible (2,20,22,) , 23 . Indeed, this was consistent with the progressive age‐related loss of entire structural elements (24) .…”

Section: Discussionmentioning

confidence: 99%

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Irreversible Perforations in Vertebral Trabeculae?

Banse

Devogelaer

Delloye

et al. 2003

Journal of Bone and Mineral Research

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In human cancellous bone, osteoclastic perforations resulting from normal remodeling were generally considered irreversible. In human vertebral samples, examined by backscatter electron microscopy, there was clear evidence of bridging of perforation defects by new bone formation. Hence trabecular perforations may not be irreversible.Introduction: Preservation of the trabecular bone microarchitecture is essential to maintain its load-bearing capacity and prevent fractures. However, during bone remodeling, the osteoclasts may perforate the platelike trabeculae and disconnect the structure. Large perforations (Ͼ100 m) are generally considered irreversible because there is no surface on which new bone can be laid down. In this work, we investigated the outcome of these perforations on human vertebral cancellous bone. Materials and Methods: Using backscatter electron microscopy, we analyzed 264 vertebral bone samples from the thoracic and lumbar spine of nine subjects (44 -88 years old). Nine fields (2 ϫ 1.5 mm) were observed on each block. Several bone structural units (BSUs) were visible on a single trabecula, illustrating a dynamic, historical aspect of bone remodeling. A bridge was defined as a single and recent BSU connecting two segments of trabeculae previously separated by osteoclastic resorption. They were counted and measured (length and breadth, m). Results and Conclusion: We observed 396 bridges over 2376 images. By comparison, we found only 15 microcalluses on the same material. The median length of the bridge was 165 m (range, 29 -869 m); 86% being longer than 100 m and 35% longer than 200 m. Their breadth was 56 m (range, 6 -255 m), but the thinnest were still in construction. Bridges were found in all nine subjects included in the study, suggesting that it is a common feature of normal vertebral bone remodeling. These observations support the hypothesis that perforation could be repaired by new bone formation. and hence, might not be systematically irreversible.

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Section: Perforations: the Dogmasupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Irreversible Perforations in Vertebral Trabeculae?

Banse

Devogelaer

Delloye

et al. 2003

Journal of Bone and Mineral Research

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“…As body weight and tibial length were not altered by the transgene, it appears that periosteal osteoblasts in the transgenic mice have a greater osteogenic response for a given range of body weights. This is of particular interest in light of the suggestion that age-related deficiencies in the anabolic potential of osteoblasts may be a major contributor to age-related bone loss in humans (29). The change in osteoblast activity was associated with wider tibiae and femora in OSVDR mice.…”

Section: Discussionmentioning

confidence: 99%

Increased formation and decreased resorption of bone in mice with elevated vitamin D receptor in mature cells of the osteoblastic lineage

et al. 2000

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The microarchitecture of bone is regulated by complex interactions between the bone-forming and resorbing cells, and several compounds regulate both actions. For example, vitamin D, which is required for bone mineralization, also stimulates bone resorption. Transgenic mice overexpressing the vitamin D receptor solely in mature cells of the osteoblastic bone-forming lineage were generated to test the potential therapeutic value of shifting the balance of vitamin D activity in favor of bone formation. Cortical bone was 5% wider and 15% stronger in these mice due to a doubling of periosteal mineral apposition rate without altered body weight or calcium homeostatic hormone levels. A 20% increase in trabecular bone volume in transgenic vertebrae was also observed, unexpectedly associated with a 30% reduction in resorption surface rather than greater bone formation. These findings indicate anabolic vitamin D activity in bone and identify a previously unknown pathway from mature osteoblastic cells to inhibit osteoclastic bone resorption, counterbalancing the known stimulatory action through immature osteoblastic cells. A therapeutic approach that both stimulates cortical anabolic and inhibits trabecular resorptive pathways would be ideal for treatment of osteoporosis and other osteopenic disorders.

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“…Cortical and trabecular components were accounted for by assigning two different ranges of apparent density (Fyhrie & Carter 1986), thus avoiding the need to describe their heterogeneous microstructures. Density-based simulations of trabecular bone adaptation have been addressed in many continuum approaches (Frost 1964;Cowin 1984;Fyhrie & Carter 1986;Reeve 1986;Huiskes et al 1987;Brown et al 1990;Martin 1991;Thomsen et al 1996;Adachi et al 1998;Langton et al 1998;Hernandez et al 2000) and have been reviewed before (Cowin 1993;Jacobs 2000;Hart 2001). To name only some of the approaches, several groups (Carter & Hayes 1976;Cowin 1984;Fyhrie & Carter 1986;Huiskes et al 1987;Beaupre et al 1990;Weinans et al 1992;Van Rietbergen et al 1993) proposed strain as the driving force for remodelling.…”

Section: Biologymentioning

confidence: 99%

In silico biology of bone modelling and remodelling: adaptation

Gerhard

Webster

Lenthe

et al. 2009

Phil. Trans. R. Soc. A.

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Modelling and remodelling are the processes by which bone adapts its shape and internal structure to external influences. However, the cellular mechanisms triggering osteoclastic resorption and osteoblastic formation are still unknown. In order to investigate current biological theories, in silico models can be applied. In the past, most of these models were based on the continuum assumption, but some questions related to bone adaptation can be addressed better by models incorporating the trabecular microstructure. In this paper, existing simulation models are reviewed and one of the microstructural models is extended to test the hypothesis that bone adaptation can be simulated without particular knowledge of the local strain distribution in the bone. Validation using an experimental murine loading model showed that this is possible. Furthermore, the experimental model revealed that bone formation cannot be attributed only to an increase in trabecular thickness but also to structural reorganization including the growth of new trabeculae. How these new trabeculae arise is still an unresolved issue and might be better addressed by incorporating other levels of hierarchy, especially the cellular level. The cellular level sheds light on the activity and interplay between the different cell types, leading to the effective change in the whole bone. For this reason, hierarchical multi-scale simulations might help in the future to better understand the biomathematical laws behind bone adaptation.

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Quantification of remodeling parameter sensitivity—assessed by a computer simulation model

Cited by 13 publications

References 48 publications

Irreversible Perforations in Vertebral Trabeculae?

Irreversible Perforations in Vertebral Trabeculae?

Increased formation and decreased resorption of bone in mice with elevated vitamin D receptor in mature cells of the osteoblastic lineage

In silico biology of bone modelling and remodelling: adaptation

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