The many adaptations of bone

Currey, John D.

doi:10.1016/s0021-9290(03)00124-6

Cited by 404 publications

(346 citation statements)

References 31 publications

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“…Woven bone formation is associated with pathological overload, 17,18 fracture healing, 19 and other scenarios where a rapid rate of bone formation occurs. 20 Despite its fundamental importance to restoring or maintaining skeletal integrity under challenging conditions, the material properties of woven bone are not well known. Several factors make it difficult to characterize woven bone: it is often mixed with other types of bone [e.g., in fibrolamellar (also called plexiform) bone, which is a mix of woven and lamellar bone 20 ] or with cartilage (e.g., in a fracture callus 19 ); it is usually a temporary tissue associated with a high rate of turnover; its microstructure and organization are highly variable.…”

Section: Discussionmentioning

confidence: 99%

“…20 Despite its fundamental importance to restoring or maintaining skeletal integrity under challenging conditions, the material properties of woven bone are not well known. Several factors make it difficult to characterize woven bone: it is often mixed with other types of bone [e.g., in fibrolamellar (also called plexiform) bone, which is a mix of woven and lamellar bone 20 ] or with cartilage (e.g., in a fracture callus 19 ); it is usually a temporary tissue associated with a high rate of turnover; its microstructure and organization are highly variable. In one of the few studies from which woven bone properties can be estimated, Torzilli et al 21,22 tested cortical bone from skeletally immature dogs.…”

Section: Discussionmentioning

confidence: 99%

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Bone formation after damaging in vivo fatigue loading results in recovery of whole‐bone monotonic strength and increased fatigue life

Silva¹,

Touhey²

2006

Journal Orthopaedic Research

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Bone has a remarkable capacity for self-repair. We previously reported a woven bone response after damaging in vivo fatigue loading of the rat ulna that led to a rapid recovery of wholebone strength. In the current study we asked: does the bone response in the 12 days after damaging fatigue loading result in a bone that has normal fatigue properties? The right forelimbs of 52 adult rats were subjected to a single bout of in vivo fatigue loading. Nonloaded left forelimbs were used as controls. Ulnar geometric properties were assessed by peripheral quantitative computed tomography (pQCT) and ex vivo mechanical properties were assessed by three-point bending. On day 0, ulnae from loaded forelimbs had a 15-20% reduction in stiffness and ultimate force versus controls (p < 0.10), indicative of structural damage. On day 12, bone area at the midshaft was increased by 27% (p < 0.001) and microCT scans revealed periosteal woven bone at this site. This bone response led to a recovery of the monotonic properties of loaded ulnae at day 12 versus control (stiffness, p ¼ 0.73; ultimate force, p ¼ 0.96). Importantly, fatigue testing ex vivo at day 12 demonstrated significantly greater fatigue life in in vivo loaded ulnae versus controls (p < 0.001). Additionally, the slope of the fatigue-life curve was significantly less in loaded versus control ulnae (p < 0.002). We conclude that woven bone ''repair'' of a bone damaged by fatigue loading restores whole-bone strength and enhances resistance to further damage by repetitive loading. ß

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Bone formation after damaging in vivo fatigue loading results in recovery of whole‐bone monotonic strength and increased fatigue life

Silva¹,

Touhey²

2006

Journal Orthopaedic Research

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“…It was shown that application of 2000 microstrain macroscopically to a piece of bone resulted in greater microscopic strain surround osteocyte lacunae of over 30,000 microstrain (87). Osteons, canaliculi, and lacunae are potential stress concentrators (27). It was found that perilacunar tissue strain levels in many lacunae exceed global applied strain.…”

Section: Tissue Strain Substrate Deformation Cell Deformationmentioning

confidence: 99%

Osteocytes, mechanosensing and Wnt signaling

Bonewald¹,

Johnson²

2008

Bone

926

760

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The majority of bone cell biology focuses on activity on the surface of the bone with little attention paid to the activity that occurs below the surface. However, with recent new discoveries, osteocytes, cells embedded within the mineralized matrix of bone, are becoming the target of intensive investigation. In this article, the distinctions between osteoblasts and their descendants, osteocytes, are reviewed. Osteoblasts are defined as cells that make bone matrix and osteocytes are thought to translate mechanical loading into biochemical signals that affect bone (re)modeling. Osteoblasts and osteocytes should have similarities as would be expected of cells of the same lineage, yet these cells also have distinct differences, particularly in their responses to mechanical loading and utilization of the various biochemical pathways to accomplish their respective functions. For example, the Wnt/ β-catenin signaling pathway is now recognized as an important regulator of bone mass and bone cell functions. This pathway is important in osteoblasts for differentiation, proliferation and the synthesis bone matrix, whereas osteocytes appear to use the Wnt/β-catenin pathway to transmit signals of mechanical loading to cells on the bone surface. New emerging evidence suggests that the Wnt/β-catenin pathway in osteocytes may be triggered by crosstalk with the prostaglandin pathway in response to loading which then leads to a decrease in expression of negative regulators of the pathway such as Sost and Dkk1. The study of osteocyte biology is becoming an intense area of research interest and this review will examine some of the recent findings that are reshaping our understanding of bone/bone cell biology. KeywordsOsteocytes; bone; Wnt/β-catenin signaling; Mechanosensation; Mechanical loading Osteocytes compose over 90-95% of all bone cells in the adult skeleton and are thought to respond to mechanical strain to send signals of resorption or formation (70). Osteocytes are usually regularly dispersed throughout the mineralized matrix especially in cortical bone. These cells are connected to each other and cells on the bone surface through dendritic processes that occupy tiny canals called canaliculi (For review see (17)). Not only do these cells communicate with each other and with cells on the bone surface but their dendritic processes are in contact with the bone marrow (59) giving them the potential to recruit osteoclast precursors to stimulate bone resorption (133)(12) and to regulate mesenchymal stem cell differentiation (48).

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“…The invasion of endothelial cells precedes the ingress of both osteoclasts, which remove the transverse septae, and osteoblasts, which deposit bone onto the remaining longitudinal calcified cartilage cores to form the bony trabeculae of the primary spongiosa. (29) Remodeling of the primary spongiosa takes place over a defined space in close proximity to the growth plate; (30,31) the precise mechanisms controlling remodeling here are unclear. In remodeling sites in the rest of the skeleton, a variety of interlinked mechanisms have been identified that regulate the site and degree of mineralization activity, including the presence of mineralization inhibitors such as pyrophosphate (32) and osteopontin, (33) and the potential mineral nucleation initiator bone sialoprotein, which may act in concert with alkaline phosphatase.…”

Section: Mineralization Of Bone Matrixmentioning

confidence: 99%

“…(65) Toughness is a measure of energy dissipation and cannot be easily estimated in an anisotropic material. Both strength and toughness are influenced by inhomogeneity (30) and interface properties, (64) which can be highly localized. Fracture resistance extends beyond the intrinsic material properties of bone to encompass all levels of scale up to the whole bone.…”

Section: Energy Dissipation In Bone and Fracture Toughening Mechanismsmentioning

confidence: 99%

Bone Material Properties in Osteogenesis Imperfecta

Bishop

2016

Journal of Bone and Mineral Research

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Osteogenesis imperfecta entrains changes at every level in bone tissue, from the disorganization of the collagen molecules and mineral platelets within and between collagen fibrils to the macroarchitecture of the whole skeleton. Investigations using an array of sophisticated instruments at multiple scale levels have now determined many aspects of the effect of the disease on the material properties of bone tissue. The brittle nature of bone in osteogenesis imperfecta reflects both increased bone mineralization density-the quantity of mineral in relation to the quantity of matrix within a specific bone volume-and altered matrix-matrix and matrix mineral interactions. Contributions to fracture resistance at multiple scale lengths are discussed, comparing normal and brittle bone. Integrating the available information provides both a better understanding of the effect of current approaches to treatment-largely improved architecture and possibly some macroscale toughening-and indicates potential opportunities for alternative strategies that can influence fracture resistance at longer-length scales.

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The many adaptations of bone

Cited by 404 publications

References 31 publications

Bone formation after damaging in vivo fatigue loading results in recovery of whole‐bone monotonic strength and increased fatigue life

Bone formation after damaging in vivo fatigue loading results in recovery of whole‐bone monotonic strength and increased fatigue life

Osteocytes, mechanosensing and Wnt signaling

Bone Material Properties in Osteogenesis Imperfecta

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