Age-related changes in porosity and mineralization and in-service damage accumulation

Norman, Timothy L.; Little, Tara M.; Yeni, Yener N.

doi:10.1016/j.jbiomech.2008.06.032

Cited by 31 publications

(18 citation statements)

References 47 publications

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“…101 In contrast, cases and controls had similar indentation modulus and hardness. This suggests compensation for reduced mineralisation by a stiffer organic phase in hip fracture cases, making the bone tissue potentially less tough, 99,100 consistent with the finding of Norman et al 102 that reduced mineralisation is positively associated with diffuse damage and microcrack density.…”

Section: Mineralised Bone Tissue Heterogeneitysupporting

confidence: 56%

Role of cortical bone in hip fracture

Reeve

2017

BoneKEy Rep

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In this review, I consider the varied mechanisms in cortical bone that help preserve its integrity and how they deteriorate with aging. Aging affects cortical bone in two ways: extrinsically through its effects on the individual that modify its mechanical loading experience and 'milieu interieur'; and intrinsically through the prolonged cycle of remodelling and renewal extending to an estimated 20 years in the proximal femur. Healthy femoral cortex incorporates multiple mechanisms that help prevent fracture. These have been described at multiple length scales from the individual bone mineral crystal to the scale of the femur itself and appear to operate hierarchically. Each cortical bone fracture begins as a sub-microscopic crack that enlarges under mechanical load, for example, that imposed by a fall. In these conditions, a crack will enlarge explosively unless the cortical bone is intrinsically tough (the opposite of brittle). Toughness leads to microscopic crack deflection and bridging and may be increased by adequate regulation of both mineral crystal size and the heterogeneity of mineral and matrix phases. The role of osteocytes in optimising toughness is beginning to be worked out; but many osteocytes die in situ without triggering bone renewal over a 20-year cycle, with potential for increasing brittleness. Furthermore, the superolateral cortex of the proximal femur thins progressively during life, so increasing the risk of buckling during a fall. Besides preserving or increasing hip BMD, pharmaceutical treatments have class-specific effects on the toughness of cortical bone, although dietary and exercise-based interventions show early promise.

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Section: Mineralised Bone Tissue Heterogeneitysupporting

confidence: 56%

Role of cortical bone in hip fracture

Reeve

2017

BoneKEy Rep

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“…Relevant to the present discussion, microcrack accumulation is reportedly associated with the age-related decrease in the density of osteocyte lacunae [70]. Microdamage accumulation beyond a certain threshold appears to adversely affect the bone mechanical properties [71].…”

Section: Microcracksmentioning

confidence: 55%

Microarchitectural Changes in the Aging Skeleton

Gabet

Bab

2011

Curr Osteoporos Rep

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The age-related reduction in bone mass is disproportionally related to skeletal weakening, suggesting that microarchitectural changes are also important determinants of bone quality. The study of cortical and trabecular microstructure, which for many years was mainly based on two-dimensional histologic and scanning electron microscopy imaging, gained a tremendous momentum in the last decade and a half, due to the introduction of microcomputed tomography (μCT). This technology provides highly accurate qualitative and quantitative analyses based on three-dimensional images at micrometer resolution, which combined with finite elemental analysis predicts the biomechanical implications of microstructural changes. Global μCT analyses of trabecular bone have repeatedly suggested that the main age-related change in this compartment is a decrease in trabecular number with unaltered, or even increased, trabecular thickness. However, we show here that this may result from a bias whereby thick trabeculae near the cortex and the early clearance of thin struts mask authentic trabecular thinning. The main cortical age-related change is increased porosity due to negatively balanced osteonal remodeling and expansion of Haversian canals, which occasionally merge with endosteal and periosteal resorption bays, thus leading to rapid cortical thinning and cortical weakening. The recent emergence of CT systems with submicrometer resolution provides novel information on the age-related decrease in osteocyte lacunar density and related micropetrosis, the result of lacunar hypermineralization. Last but not least, the use of the submicrometer CT systems confirmed the occurrence of microcracks in the skeletal mineralized matrix and vastly advanced their morphologic characterization and mode of initiation and propagation.

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“…However, the fact that some bone creep is either permanent, or recovered very slowly [14], suggests additional mechanisms unrelated to fluid flow. Possibilities include the propagation of microcracks [33][34][35], slipping between osteons [36], viscoelastic deformation of collagen [27], and slipping between [28,37] or within [28] hydroxyapatite crystals. Plastic deformation must be involved, because total strains (creep plus elastic) measured in the present experiment greatly exceed those at the elastic limit of trabecular bone [30,38].…”

Section: Explanation Of Resultsmentioning

confidence: 99%

Vertebral deformity arising from an accelerated “creep” mechanism

et al. 2012

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Introduction Vertebral deformities often occur in patients who recall no trauma, and display no evident fracture on radiographs. We hypothesise that vertebral deformity can occur by a gradual creep mechanism which is accelerated following minor damage. ''Creep'' is continuous deformation under constant load. Materials and methods Forty-five thoracolumbar spine motion segments were tested from cadavers aged 42-92 years. Vertebral body areal BMD was measured using DXA. Specimens were compressed at 1 kN for 30 min, while creep in each vertebral body was measured using an optical MacReflex system. After 30 min recovery, each specimen was subjected to a controlled overload event which caused minor damage to one of its vertebrae. The creep test was then repeated. Results Vertebral body creep was measurable in specimens with BMD \0.5 g/cm 2 . Creep was greater anteriorly than posteriorly (p \ 0.001), so that vertebrae gradually developed a wedge deformity. Compressive overload reduced specimen height by 2.24 mm (STD 0.77 mm), and increased vertebral body creep by 800 % (anteriorly), 1,000 % (centrally) and 600 % (posteriorly). In 34 vertebrae with complete before-and-after data, anterior wedging occurring during the 1st creep test averaged 0.07°(STD 0.17°), and in the 2nd test (after minor damage) it averaged 0.79°(STD 1.03°). The increase was highly significant (P \ 0.001). Vertebral body wedging during the 2nd creep test was proportional to the severity of damage, as quantified by specimen height loss during the overload event (r 2 = 0.51, p \ 0.001, n = 34). Conclusions Minor damage to an old vertebral body, even if it is barely discernible on radiographs, can accelerate creep to such an extent that it makes a substantial contribution to vertebral deformity.

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Age-related changes in porosity and mineralization and in-service damage accumulation

Cited by 31 publications

References 47 publications

Role of cortical bone in hip fracture

Role of cortical bone in hip fracture

Microarchitectural Changes in the Aging Skeleton

Vertebral deformity arising from an accelerated “creep” mechanism

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