Topographically induced bone formation in vitro: Implications for bone implants and bone grafts

Gray, Colin; Boyde, A.; Jones, Siana

doi:10.1016/8756-3282(95)00456-4

Cited by 102 publications

(53 citation statements)

References 16 publications

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“…The exact factors involved in this ''coupling'' are not known but proposed mechanisms include release of growth factors from bone matrix, mediators (''coupling factors'') released from osteoclasts, changes in the local strain environment, TRAP signaling, and surface contour effects. [46][47][48][49] Osteoblast activity and bone formation may therefore have been affected by inhibition in osteoclast activity with reduced remodeling along the SFx line.…”

Section: Discussionmentioning

confidence: 99%

Selective and non‐selective cyclooxygenase inhibitors delay stress fracture healing in the rat ulna

Kidd

Cowling

et al. 2012

Journal Orthopaedic Research

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Anti-inflammatory drugs are widely used to manage pain associated with stress fractures (SFxs), but little is known about their effects on healing of those injuries. We hypothesized that selective and non-selective anti-inflammatory treatments would retard the healing of SFx in the rat ulna. SFxs were created by cyclic loading of the ulna in Wistar rats. Ulnae were harvested 2, 4 or 6 weeks following loading. Rats were treated with non-selective NSAID, ibuprofen (30 mg/kg/day); selective COX-2 inhibition, [5,5-dimethyl-3-3 (3 fluorophenyl)-4-(4 methylsulfonal) phenyl-2 (5H)-furanone] (DFU) (2.0 mg/kg/day); or the novel c5a anatagonist PMX53 (10 mg/kg/ day, 4 and 6 weeks only); with appropriate vehicle as control. Quantitative histomorphometric measurements of SFx healing were undertaken. Treatment with the selective COX-2 inhibitor, DFU, reduced the area of resorption along the fracture line at 2 weeks, without affecting bone formation at later stages. Treatment with the non-selective, NSAID, ibuprofen decreased both bone resorption and bone formation so that there was significantly reduced length and area of remodeling and lamellar bone formation within the remodeling unit at 6 weeks after fracture. The C5a receptor antagonist PMX53 had no effect on SFx healing at 4 or 6 weeks after loading, suggesting that PMX53 would not delay SFx healing. Both selective COX-2 inhibitors and non-selective NSAIDs have the potential to compromise SFx healing, and should be used with caution when SFx is diagnosed or suspected. ß

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Section: Discussionmentioning

confidence: 99%

Selective and non‐selective cyclooxygenase inhibitors delay stress fracture healing in the rat ulna

Kidd

Cowling

et al. 2012

Journal Orthopaedic Research

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“…[7][8][9][10][11][12][13] More recently, cell responses to nano-topography have begun to be elucidated, and it appears that these reactions can be very strong. Epitenon cells have been shown to be unable to adhere to pillars of 200-nm height produced by electron beam lithography.…”

Section: Introductionmentioning

confidence: 99%

Nonadhesive nanotopography: Fibroblast response to poly(n‐butyl methacrylate)‐poly(styrene) demixed surface features

Dalby¹,

Riehle²,

Johnstone³

et al. 2003

J Biomedical Materials Res

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It is becoming clear that cells do not only respond to micrometric scale topography, but may also respond to topography at the nanometric scale. Nano-fabrication methods such as electron beam lithography are, however, expensive and time consuming. Polymer demixing of poly(styrene) and poly(4-bromostyrene) has been found to produce nano-scale islands of reproducible height, and the islands have been previously shown to effect cell events such as adhesion, spreading, proliferation, and differentiation. This study uses demixed poly(styrene) and poly(n-butyl methacrylate) to produce nano-islands with closer packing and narrower widths compared with those previously studied. Observations have been made of morphological and cytoskeletal changes in human fibroblasts interacting with 10- and 50-nm-high islands. The methods used included scanning electron microscopy, fluorescent microscopy, and optical microscopy. The results indicated that the cells do not respond differently to the 10-nm islands compared with planar samples but, in contrast, the 50-nm islands are nonadhesive.

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“…Alternatively, decades of research have shown that surface topography can directly stimulate bone cell differentiation and function on various material substrates, including polymers (Fu et al, 2010;Watari et al, 2012;Wilkinson et al, 2011;You et al, 2010), titanium (Brunette, 1988;Gittens et al, 2011;, ceramics (Webster, 2000;Zhang et al, 2014), and tissue (Gray et al, 1996). Topographical control of cell fate is a complex phenomenon that can occur through focal adhesion clustering and downstream focal adhesion kinase (FAK) signalling (McNamara et al, 2010).…”

Section: Nl Davison Et Almentioning

confidence: 99%

Influence of surface microstructure and chemistry on osteoinduction and osteoclastogenesis by biphasic calcium phosphate discs

Davison

Su²,

Yuan³

et al. 2015

eCM

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It has been reported that surface microstructural dimensions can influence the osteoinductivity of calcium phosphates (CaPs), and osteoclasts may play a role in this process. We hypothesised that surface structural dimensions of ≤ 1 μm trigger osteoinduction and osteoclast formation irrespective of macrostructure (e.g., concavities, interconnected macropores, interparticle space) or surface chemistry. To test this, planar discs made of biphasic calcium phosphate (BCP: 80 % hydroxyapatite, 20 % tricalcium phosphate) were prepared with different surface structural dimensions -either ~ 1 μm (BCP1150) or ~ 2-4 μm (BCP1300) -and no macropores or concavities. A third material was made by sputter coating BCP1150 with titanium (BCP1150Ti), thereby changing its surface chemistry but preserving its surface structure and chemical reactivity. After intramuscular implantation in 5 dogs for 12 weeks, BCP1150 formed ectopic bone in 4 out of 5 samples, BCP1150Ti formed ectopic bone in 3 out of 5 samples, and BCP1300 formed no ectopic bone in any of the 5 samples. In vivo, large multinucleated osteoclast-like cells densely colonised BCP1150, smaller osteoclast-like cells formed on BCP1150Ti, and osteoclast-like cells scarcely formed on BCP1300. In vitro, RAW264.7 cells cultured on the surface of BCP1150 and BCP1150Ti in the presence of osteoclast differentiation factor RANKL (receptor activator for NF-κB ligand) proliferated then differentiated into multinucleated osteoclast-like cells with positive tartrate resistant acid phosphatase (TRAP) activity. However, cell proliferation, fusion, and TRAP activity were all significantly inhibited on BCP1300. These results indicate that of the material parameters tested -namely, surface microstructure, macrostructure, and surface chemistry -microstructural dimensions are critical in promoting osteoclastogenesis and triggering ectopic bone formation.

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Topographically induced bone formation in vitro: Implications for bone implants and bone grafts

Cited by 102 publications

References 16 publications

Selective and non‐selective cyclooxygenase inhibitors delay stress fracture healing in the rat ulna

Selective and non‐selective cyclooxygenase inhibitors delay stress fracture healing in the rat ulna

Nonadhesive nanotopography: Fibroblast response to poly(n‐butyl methacrylate)‐poly(styrene) demixed surface features

Influence of surface microstructure and chemistry on osteoinduction and osteoclastogenesis by biphasic calcium phosphate discs

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