Quantifying the osteocyte network in the human skeleton

Buenzli, Pascal R.; Sims, Natalie A.

doi:10.1016/j.bone.2015.02.016

Cited by 235 publications

(194 citation statements)

References 77 publications

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“…Although extensive cell-cell contact exists within the osteocyte network (Buenzli and Sims, 2015) and between boneforming osteoblasts, and contact-dependent mechanisms are recognised to control bone formation (Tonna and Sims, 2014), it is not clear how membrane-bound ephrin B2 could influence cell function in chondrocytes since these cells are isolated from each other by the cartilaginous matrix. There are two possibilities: ephrin B2 might be capable of autocrine signalling through EPHB4, which is also expressed by hypertrophic chondrocytes (Wang et al, 2014); alternatively, there might be cell-cell contact between hypertrophic chondrocytes.…”

Section: Discussionmentioning

confidence: 99%

Chondrocytic EphrinB2 promotes cartilage destruction by osteoclasts in endochondral ossification

et al. 2016

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There was an error published in Development 143, 648-657.In the Materials and Methods section the murine Efnb2 gene mutation was incorrectly listed as Efnb2 tm1And . The correct annotation for the floxed allele that we used in our experiments is Efnb2 tm2And . This was a nomenclature error and does not affect the results or conclusions of the paper.We thank Monika Tomczuk, scientific curator of Mouse Genome Informatics at The Jackson Laboratory, for alerting us to this mistake.We apologise for any confusion that this error may have caused. Osteoclasts at the growth plate had an abnormal morphology and expressed low levels of tartrate-resistant acid phosphatase; this was not observed in more mature bone. Electron microscopy revealed a lack of sealing zones and poor attachment of Osx1Cre.Efnb2 Δ/Δ osteoclasts to growth plate cartilage. Osteoblasts at the growth plate were also poorly attached and impaired in their ability to deposit osteoid. By 6 months of age, trabecular bone mass, osteoclast morphology and osteoid deposition by Osx1Cre.Efnb2 Δ/Δ osteoblasts were normal. Cultured chondrocytes from Osx1Cre. Efnb2 Δ/Δ neonates showed impaired support of osteoclastogenesis but no significant change in Rankl (Tnfsf11) levels, whereas Adamts4 levels were significantly reduced. A population of ADAMTS4 + early hypertrophic chondrocytes seen in controls was absent from Osx1Cre.Efnb2 Δ/Δ neonates. This suggests that Osx1Cre-expressing cells, including hypertrophic chondrocytes, are dependent on ephrin B2 for their production of cartilagedegrading enzymes, including ADAMTS4, and this might be required for attachment of osteoclasts and osteoblasts to the cartilage surface during endochondral ossification.

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Section: Discussionmentioning

confidence: 99%

Chondrocytic EphrinB2 promotes cartilage destruction by osteoclasts in endochondral ossification

et al. 2016

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“…Interestingly, in T2DM patients circulating levels of sclerostin, an osteocyte-derived factor, is elevated [21][22][23], suggesting that osteocyte physiology may be altered. As osteocytes are organized as a communication network inside the bone matrix [40], we postulated that T2DM might also disturb the osteocyte network organization and communication processes. In the present study, we focused our attention on studying the osteocyte network and its perilacunar mineralization in a high fat fed murine model of type 2 diabetes.…”

Section: Discussionmentioning

confidence: 99%

High fat-fed diabetic mice present with profound alterations of the osteocyte network

Mabilleau

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Flatt

et al. 2016

Bone

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Diabetes mellitus is considered to be an independent risk factor for bone fragility fractures. Reductions in bone mass, observed only with type 1 diabetes mellitus, as well as modifications of bone microarchitectures and tissue material properties are landmarks of diabetes-related bone alterations. An interesting feature observed in type 2 diabetes mellitus (T2DM) is the augmented concentration in circulating sclerostin. This observation prompts us to hypothesize that modifications of osteocyte network and perilacunar mineralization occur in T2DM. As such, the aims of the present study were to ascertain by quantitative backscattered electron imaging, confocal microscopy and image analysis, modifications of perilacunar tissue mineral density, osteocyte morphology and osteocyte network topology in a mouse model of high fat-induced type 2 diabetes. As compared with lean control animals, diabetic mice exhibited a significant 48% decrease in perilacunar mineralization heterogeneity although mean perilacunar mineralization was unchanged. Furthermore, in diabetic animals, osteocyte volume was significantly augmented by 34% with no change in the overall number of dendrite processes. Finally, the network topology was profoundly modified in diabetic mice with increases in the mean node degree, mean node volume and hub numbers whilst the mean link length was reduced. Overall, it appeared that in diabetic animals, the dendritic network exhibited features of a scale-free network as opposed to the single-scale characteristic observed in lean controls. However, it is important to ascertain whether diabetic patients exhibit such modifications of the osteocyte network and whether anti-diabetic drugs could restore normal osteocyte and network parameters, thereby improving bone quality and protecting against fragility fractures.

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“…Effects of CLCF1/CRLF1 composite cytokines on the musculoskeletal system CLCF1 and CRLF1 are expressed within the developing murine skeleton, both in limb buds [9,46] and in embryonic muscle and cartilage [11]. In a mouse model of ectopic bone formation, CRLF1 was detected by in situ hybridization in the cells that produce bone matrix (osteoblasts), and by the cells that constitute bone's internal neuron-like cellular network (osteocytes [47]) [48]. Although in situ detection has not been carried out in adult tissue, CLCF1, CRLF1 and CNTFR (but not NP) mRNAs are detected in cultured murine primary osteoblasts [12,49].…”

Section: Effects Of Clcf1 and Crlf1 Composite Cytokines On The Neuralmentioning

confidence: 99%

Cardiotrophin-like cytokine factor 1 (CLCF1) and neuropoietin (NP) signalling and their roles in development, adulthood, cancer and degenerative disorders

Quantifying the osteocyte network in the human skeleton

Cited by 235 publications

References 77 publications

Chondrocytic EphrinB2 promotes cartilage destruction by osteoclasts in endochondral ossification

Chondrocytic EphrinB2 promotes cartilage destruction by osteoclasts in endochondral ossification

High fat-fed diabetic mice present with profound alterations of the osteocyte network

Cardiotrophin-like cytokine factor 1 (CLCF1) and neuropoietin (NP) signalling and their roles in development, adulthood, cancer and degenerative disorders

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