Bone Homeostasis and Repair: Forced Into Shape

Castillo, Alesha B.; Leucht, Philipp

doi:10.1007/s11926-015-0537-9

Cited by 21 publications

(17 citation statements)

References 93 publications

(99 reference statements)

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“…An unstable implant can induce gradual bone resorption similar to when mechanical movement at the site of a fracture contributes to the development of non-union associated with bone resorption [122][123][124]. Some studies have demonstrated that mechanical forces generated either by joint fluid or the implant surface can also lead to bone resorption [115,[125][126][127][128][129].…”

Section: Mechanical Osteolysis and Synergies With Inflammatory Agentsmentioning

confidence: 99%

Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment

Goodman

Gallo

2019

JCM

152

149

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Clinical studies, as well as in vitro and in vivo experiments have demonstrated that byproducts from joint replacements induce an inflammatory reaction that can result in periprosthetic osteolysis (PPOL) and aseptic loosening (AL). Particle-stimulated macrophages and other cells release cytokines, chemokines, and other pro-inflammatory substances that perpetuate chronic inflammation, induce osteoclastic bone resorption and suppress bone formation. Differentiation, maturation, activation, and survival of osteoclasts at the bone–implant interface are under the control of the receptor activator of nuclear factor kappa-Β ligand (RANKL)-dependent pathways, and the transcription factors like nuclear factor κB (NF-κB) and activator protein-1 (AP-1). Mechanical factors such as prosthetic micromotion and oscillations in fluid pressures also contribute to PPOL. The treatment for progressive PPOL is only surgical. In order to mitigate ongoing loss of host bone, a number of non-operative approaches have been proposed. However, except for the use of bisphosphonates in selected cases, none are evidence based. To date, the most successful and effective approach to preventing PPOL is usage of wear-resistant bearing couples in combination with advanced implant designs, reducing the load of metallic and polymer particles. These innovations have significantly decreased the revision rate due to AL and PPOL in the last decade.

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Section: Mechanical Osteolysis and Synergies With Inflammatory Agentsmentioning

confidence: 99%

Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment

Goodman

Gallo

2019

JCM

152

149

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“…44,46 The actual level of strain at which these changes occur is controversial and currently debated, 117 but the amount of new bone formed appears to correlate with the magnitude and rate of strain. 26 Many of the concepts expressed in the mechanostat model have been demonstrated experimentally. A mouse model of in vivo tibial loading showed that, in response to cyclic compressive load, there was decreased endosteal bone resorption and increased bone deposition beneath the periosteum and endosteum of the cortex.…”

Section: Mechanical Forces and Bone Adaptation Wolff's Law And The Mementioning

confidence: 99%

“…72,123 Thus, cyclical loading with recovery periods is thought to create a more effective bone response, and is therefore considered to be a constructive treatment for improving bone formation. 26,72 Age has a marked effect on the response of bone to mechanical loading. Many studies in children have shown that, during growth, bone is highly responsive to loading.…”

Section: Mechanical Forces and Bone Adaptation Wolff's Law And The Mementioning

confidence: 99%

Mechanisms of bone response to injury

Dittmer

Firth

2017

J VET Diagn Invest

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Bone, despite its relatively inert appearance, is a tissue that is capable of adapting to its environment. Wolff's law, first described in the 19th century, describes the ability of bone to change structure depending on the mechanical forces applied to it. The mechanostat model extended this principle and suggested that the amount of strain a bone detects depends on bone strength and the amount of muscle force applied to the bone. Experimental studies have found that low-magnitude, high-frequency mechanical loading is considered to be the most effective at increasing bone formation. The osteocyte is considered to be the master regulator of the bone response to mechanical loading. Deformation of bone matrix by mechanical loading is thought to result in interstitial fluid flow within the lacunar-canalicular system, which may activate osteocyte mechanosensors, leading to changes in osteocyte gene expression and ultimately increased bone formation and decreased bone resorption. However, repetitive strain applied to bone can result in microcracks, which may propagate and coalesce, and if not repaired predispose to catastrophic fracture. Osteocytes are a key component in this process, whereby apoptotic osteocytes in an area of microdamage promote targeted remodeling of the damaged bone. If fractures do occur, fracture repair can be divided into 2 types: primary and secondary healing. Secondary fracture repair is the most common and is a multistage process consisting of hematoma formation and acute inflammation, callus formation, and finally remodeling, whereby bone may return to its original form.

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“…29 IGFBP-2 supported HUVEC proliferation, invasion, and tubule formation in vitro; and knockdown of IGFBP-2 reduced CD31-positive cells in vivo. In fact, cells of the osteogenic lineage are mechanically sensitive 31,[36][37][38][39][40][41][42][43][44][45][46][47][48] and their response includes release of angiogenic factors. High deformational strains and fluid flow shear stress, likely to exist in the fracture regenerate 32 when compliant fixation is used, would act upon resident cells at the fracture site including endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

Osteoblast-derived paracrine factors regulate angiogenesis in response to mechanical stimulation

et al. 2016

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Angiogenesis is a process by which new blood vessels emerge from existing vessels through endothelial cell sprouting, migration, proliferation, and tubule formation. Angiogenesis during skeletal growth, homeostasis and repair is a complex and incompletely understood process. As the skeleton adapts to mechanical loading, we hypothesized that mechanical stimulation regulates "osteo-angio" crosstalk in the context of angiogenesis. We showed that conditioned media (CM) from osteoblasts exposed to fluid shear stress enhanced endothelial cell proliferation and migration, but not tubule formation, relative to CM from static cultures. Endothelial cell sprouting was studied using a dual-channel collagen gel-based microfluidic device that mimics vessel geometry. Static CM enhanced endothelial cell sprouting frequency, whereas loaded CM significantly enhanced both frequency and length. Both sprouting frequency and length were significantly enhanced in response to factors released from osteoblasts exposed to fluid shear stress in an adjacent channel. Osteoblasts released angiogenic factors, of which osteopontin, PDGF-AA, IGBP-2, MCP-1, and Pentraxin-3 were upregulated in response to mechanical loading. These data suggest that in vivo mechanical forces regulate angiogenesis in bone by modulating "osteo-angio" crosstalk through release of paracrine factors, which we term "osteokines".

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Bone Homeostasis and Repair: Forced Into Shape

Cited by 21 publications

References 93 publications

Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment

Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment

Mechanisms of bone response to injury

Osteoblast-derived paracrine factors regulate angiogenesis in response to mechanical stimulation

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