Composition of the cement line and its possible mechanical role as a local interface in human compact bone

Burr, David B.; Schaffler, Mitchell B.; Frederickson, Richard G.

doi:10.1016/0021-9290(88)90132-7

Cited by 260 publications

(175 citation statements)

References 28 publications

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“…Frasca [8] showed that the cement line interface between osteons and interstitial bone is relatively weak which means that it may reduce the shear strength of osteonal bone but slipping at this interface may relax shear stresses, reduce strain energy and therefore may slow crack propagation. Burr et al [5] showed that the cement line is a region of reduced mineralization and provides a relatively ductile interface with the surrounding bone matrix which has the qualities required to promote crack initiation but slow crack growth in compact bone. Infibre-reinforced composite materials, the crack can enter the fibre interface and then become trapped by deflection and blunting.…”

Section: Discussionmentioning

confidence: 99%

The effect of bone microstructure on the initiation and growth of microcracks

O’Brien

Taylor

Lee

2005

Journal Orthopaedic Research

185

138

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Osteonal bone is often compared to a composite material and to metals as discontinuities within the material may provide sites of stress concentration for crack initiation and serve as barriers to crack growth. However, little experimental data exist to back up these hypotheses. Fluorescent chelating agents were applied at specific intervals to bone specimens fatigue tested in cyclic compression at a stress range of 80 MPa. The failed specimens were sectioned and labelled microcracks identified using UV epifluorescence microscopy. Microcrack lengths were measured and their relationship to cement lines surrounding secondary osteons recorded. Microcrack length at the time of encountering a cement line was also measured. Microcracks of less than 100 pm stopped growing when they encountered a cement line. Microcracks of greater than 1OOpm in length continued to grow after encountering a cement line surrounding an osteon. Only microcracks greater than 300 pm in length were capable of penetrating osteons and these microcracks were the only ones which were observed to cause failure in the specimen. These experimental data support the hypothesis that secondary osteons act as barriers to crack propagation in compact bone. However, it shows that this microstructural barrier effect is dependent on the crack length at the time of encountering an osteon. For the vast majority of cracks, osteons act as barriers to growth but for the minority of cracks that are long enough and do break through the cement line, an osteon may actually act as a weakness in the bone and facilitate crack propagation.

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Section: Discussionmentioning

confidence: 99%

The effect of bone microstructure on the initiation and growth of microcracks

O’Brien

Taylor

Lee

2005

Journal Orthopaedic Research

185

138

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“…Crack splitting, deflection, and twist are extrinsic toughening mechanisms that consume energy that would otherwise be used to propagate the crack forward, thereby decreasing the local stress intensity actually experienced at the crack tip, essentially doubling the fracture toughness of cortical bone (26,30). The loss of this toughening mechanism in bisphosphonate-treated bone suggests that unlike in untreated bone, where highly mineralized cement line boundaries surrounding osteons represent the most favorable crack path, in bisphosphonate-treated tissue the greater homogenization of mineralization may lead to cement lines not acting as a boundary to direct transverse crack propagation, resulting in a corresponding loss in fracture resistance (30)(31)(32).…”

Section: Loss Of Extrinsic Toughening With Long-term Bisphosphonatementioning

confidence: 99%

Atypical fracture with long-term bisphosphonate therapy is associated with altered cortical composition and reduced fracture resistance

Lloyd

Gludovatz

Riedel

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

131

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Bisphosphonates are the most widely prescribed pharmacologic treatment for osteoporosis and reduce fracture risk in postmenopausal women by up to 50%. However, in the past decade these drugs have been associated with atypical femoral fractures (AFFs), rare fractures with a transverse, brittle morphology. The unusual fracture morphology suggests that bisphosphonate treatment may impair toughening mechanisms in cortical bone. The objective of this study was to compare the compositional and mechanical properties of bone biopsies from bisphosphonate-treated patients with AFFs to those from patients with typical osteoporotic fractures with and without bisphosphonate treatment. Biopsies of proximal femoral cortical bone adjacent to the fracture site were obtained from postmenopausal women during fracture repair surgery (fracture groups, n = 33) or total hip arthroplasty (nonfracture groups, n = 17). Patients were allocated to five groups based on fracture morphology and history of bisphosphonate treatment [+BIS Atypical: n = 12, BIS duration: 8.2 (3.0) y; +BIS Typical: n = 10, 7.7 (5.0) y; +BIS Nonfx: n = 5, 6.4 (3.5) y; −BIS Typical: n = 11; −BIS Nonfx: n = 12]. Vibrational spectroscopy and nanoindentation showed that tissue from bisphosphonate-treated women with atypical fractures was harder and more mineralized than that from bisphosphonatetreated women with typical osteoporotic fractures. In addition, fracture mechanics measurements showed that tissue from patients treated with bisphosphonates had deficits in fracture toughness, with lower crack-initiation toughness and less crack deflection at osteonal boundaries than that of bisphosphonate-naïve patients. Together, these results suggest a deficit in intrinsic and extrinsic toughening mechanisms, which contribute to AFFs in patients treated with long-term bisphosphonates.atypical fracture | bisphosphonates | subtrochanteric fracture | fracture toughness | FTIR imaging

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“…1). At the highest level of material structure in adult human bone lie the osteons (0.1-0.2 mm in diameter) that contribute to toughness by trapping microcracks (5,6) and participate in the formation of "uncracked ligaments" (7). Osteons are made of multiple 3-to 7-μm-thick sheets (lamellae) of mineralized matrix.…”

mentioning

confidence: 99%

Dilatational band formation in bone

Poundarik

Diab

Sroga

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

237

274

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Toughening in hierarchically structured materials like bone arises from the arrangement of constituent material elements and their interactions. Unlike microcracking, which entails micrometer-level separation, there is no known evidence of fracture at the level of bone's nanostructure. Here, we show that the initiation of fracture occurs in bone at the nanometer scale by dilatational bands. Through fatigue and indentation tests and laser confocal, scanning electron, and atomic force microscopies on human and bovine bone specimens, we established that dilatational bands of the order of 100 nm form as ellipsoidal voids in between fused mineral aggregates and two adjacent proteins, osteocalcin (OC) and osteopontin (OPN). Laser microdissection and ELISA of bone microdamage support our claim that OC and OPN colocalize with dilatational bands. Fracture tests on bones from OC and/or OPN knockout mice (OC −/− , OPN −/− , OC-OPN −/−;−/− ) confirm that these two proteins regulate dilatational band formation and bone matrix toughness. On the basis of these observations, we propose molecular deformation and fracture mechanics models, illustrating the role of OC and OPN in dilatational band formation, and predict that the nanometer scale of tissue organization, associated with dilatational bands, affects fracture at higher scales and determines fracture toughness of bone.noncollagenous proteins | diffuse damage | energy dissipation I n hierarchically structured materials, the composition and spatial arrangement of nanoscale elements are the key determinants of toughness (1, 2). In comparison with many man-made materials, cortical bone is well known for its superior toughness (3, 4). Bone's ability to resist crack propagation originates from its highly complex hierarchical material structure ( Fig. 1). At the highest level of material structure in adult human bone lie the osteons (0.1-0.2 mm in diameter) that contribute to toughness by trapping microcracks (5, 6) and participate in the formation of "uncracked ligaments" (7). Osteons are made of multiple 3-to 7-μm-thick sheets (lamellae) of mineralized matrix. Individual lamellae have the ability to slide past each other (8, 9), forming 60-to 130-μm-long linear microcracks (9) that provide resistance to fracture through microcrack toughening (10). Individual mineralized collagen fibrils <1μm thick, which make up the lamellae, bridge the crack surfaces and toughen the bone (7). Bone's ability to crack, and not fracture by propagating that crack, is therefore a key fundamental aspect of the toughening mechanisms at the microstructural level (10).Recent evidence suggests that bone's nanostructure contributes to bone toughness (11). The nonfibrillar and ductile extrafibrillar matrix components in bone can serve as a "glue" between stiffened mineralized collagen fibrils (11) and between fibrils and mineral platelets (12). Fibril matrix shearing (13) has been proposed to enhance bone toughness through mineral interparticle friction (14) and "sacrificial bonds," a nanoscale mechanism...

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Composition of the cement line and its possible mechanical role as a local interface in human compact bone

Cited by 260 publications

References 28 publications

The effect of bone microstructure on the initiation and growth of microcracks

The effect of bone microstructure on the initiation and growth of microcracks

Atypical fracture with long-term bisphosphonate therapy is associated with altered cortical composition and reduced fracture resistance

Dilatational band formation in bone

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