Degradation of bone structural properties by accumulation and coalescence of microcracks

Danova, Nichole A.; Colopy, Sara A.; Radtke, Catherine L.; Kalscheur, Vicki L.; Markel, Mark D.; Vanderby, Ray; McCabe, Ronald P.; Escarcega, Anthony J.; Muir, Peter

doi:10.1016/s8756-3282(03)00155-8

Cited by 87 publications

(83 citation statements)

References 27 publications

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“…The cross-sectional and longitudinal strain distributions correspond well to the pattern of bone formation observed following loading; peak measures of osteogenesis occur on the medial periosteal surface, 1-3 mm distal to the midpoint [25,[27][28][29]. The strain distribution also correlates with the pattern of crack formation observed after damaging fatigue loading, where cracks are consistently observed on the medial half of the cross-section and are centered ~1 mm distal to the midpoint [20,30,31]. Because of the documented spatial patterns of ulnar bone formation and damage following rat forelimb loading, we asked if a similar pattern of angiogenesis occurs after loading.…”

Section: Introductionsupporting

confidence: 60%

“…Repeated measures analysis of variance (ANOVA) was used to assess the effects of longitudinal location (repeated factor; P4, P2, M, D2, D4), fatigue displacement level (30,45, 65, 85%) and time (3, 7, 14 days) on vascular and bone outcomes. Two-way ANOVA with Fisher's protected least significant differences post hoc tests were used to assess the effects of displacement level and time for individual locations.…”

Section: Discussionmentioning

confidence: 99%

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Damaging Fatigue Loading Stimulates Increases in Periosteal Vascularity at Sites of Bone Formation in the Rat Ulna

et al. 2007

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Bone formation in a variety of contexts depends on angiogenesis, however there are few reports of the vascular response to osteogenic skeletal loading. We used the rat forelimb compression model to characterize vascular changes after fatigue loading. The right forelimbs of 72 adult rats were loaded cyclically in vivo to one of four displacement levels, to produce four discrete levels of ulnar damage. Rats were euthanized 3-14 days after loading and their vasculature perfused with silicone rubber. Transverse histological sections were cut along the ulnar diaphysis. We quantified vessel number, average vessel area, total vessel area and bone area. On day 3 we observed a dramatic periosteal expansion near the ulnar midshaft, with significant increases in periosteal vascularity; total vessel area was increased 250-450% (p<0.001). Vascularity remained elevated on days 7 and 14. Vessel number and average vessel area were not correlated (p=0.09) and contributed independently to total vascular increases. Bone area was not increased on day 3, but on days 7 and 14 was increased significantly in all displacement groups (p<0.01) due to periosteal woven bone formation. Vascular and bone changes depended on longitudinal location (p<0.001), with peak increases 2 mm distal to the midshaft. Vascular and bone changes also depended on displacement level (p<0.005), with greater increases at higher levels of fatigue displacement. We conclude that skeletal fatigue loading induces a rapid increase in periosteal vascularity, followed by an increase in bone area. The angiogenic-osteogenic response is spatially coordinated and scaled to the level of the mechanical stimulus.

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Section: Introductionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Damaging Fatigue Loading Stimulates Increases in Periosteal Vascularity at Sites of Bone Formation in the Rat Ulna

et al. 2007

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“…Moreover, it is well established that static loading by itself leads to progressive creep of bone [4,5]. While there are several reports on the degradation of bone mechanical properties during fatigue (dynamic) loading both in vivo and ex vivo, with reported decreases in modulus [21], strength [7] and stiffness [7,11,29], similar data for in vivo creep (static) loading are lacking. Fondrk et al [12] demonstrated bone stiffness degradation during tensile creep, but they used multiple cycle tests.…”

Section: Discussionmentioning

confidence: 99%

“…In this model, dynamic compressive (fatigue) loading is applied to the forelimb, causing bending of the ulna leading to gradients in mechanical strain [17]. Peak strains are located on the medial (compressive) surface, 1-3 mm distal to the midpoint of the ulna, corresponding with sites of fatigue crack formations [11,25,29] and maximal woven bone formation [17]. Woven bone formation is stimulated in areas of high strain [2,17,25].…”

Section: Introductionmentioning

confidence: 99%

In vivo static creep loading of the rat forelimb reduces ulnar structural properties at time-zero and induces damage-dependent woven bone formation

Lynch

Silva

2008

Bone

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Periosteal woven bone forms in response to stress fractures and pathological overload. The mechanical factors that regulate woven bone formation are poorly understood. Fatigue loading of the rat ulna triggers a woven bone response in proportion to the level of applied fatigue displacement. However, because fatigue produces damage by application of cyclic loading it is unclear if the osteogenic response is due to bone damage (injury response) or dynamic strain (adaptive response). Creep loading, in contrast to fatigue, involves application of a static force. Our objectives were to use static creep loading of the rat forelimb to produce discrete levels of ulnar damage, and subsequently to determine the bone response over time. We hypothesized that 1) increases in applied displacement during loading correspond to ulnae with increased crack number, length and extent, as well as decreased mechanical properties; and 2) in vivo creep loading stimulates a damage-dependent dose-response in periosteal woven bone formation. Creep loading of the rat forelimb to progressive levels of sub-fracture displacement led to progressive bone damage (cracks) and loss of whole-bone mechanical properties (especially stiffness) at time-zero. For example, loading to 60% of fracture displacement caused a 60% loss of ulnar stiffness and a 25% loss of strength. Survival experiments showed that woven bone formed in a dose-dependent manner, with greater amounts of woven bone in ulnae that were loaded to higher displacements. Furthermore, after 14 days the mechanical properties of the loaded limb were equal or superior to control, indicating functional repair of the initial damage. We conclude that bone damage created without dynamic strain triggers a woven bone response, and thus infer that the woven bone response reported after fatigue loading and in stress fractures is in large part a response to bone damage.

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“…Previous fatigue loading studies using the rat forelimb model have documented time-zero bone damage in the form of ulnar cracks that intersect the periosteal surface. 9,14,15 The resulting osseous response consists of both periosteal modeling and intracortical remodeling. The modeling response occurs quickly, with new woven bone seen histologically on day 3 and a significant amount of woven bone formed by day 6.…”

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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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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Degradation of bone structural properties by accumulation and coalescence of microcracks

Cited by 87 publications

References 27 publications

Damaging Fatigue Loading Stimulates Increases in Periosteal Vascularity at Sites of Bone Formation in the Rat Ulna

Damaging Fatigue Loading Stimulates Increases in Periosteal Vascularity at Sites of Bone Formation in the Rat Ulna

In vivo static creep loading of the rat forelimb reduces ulnar structural properties at time-zero and induces damage-dependent woven bone formation

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

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