Changes in the osteocyte lacunocanalicular network with aging

Tiede-Lewis, LeAnn M.; Dallas, Sarah L.

doi:10.1016/j.bone.2019.01.025

Cited by 73 publications

(68 citation statements)

References 139 publications

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“…Many factors, including aging, osteoporosis, inflammatory diseases, and systemic diseases, disrupt osteocyte functions ( 2 , 41 , 76 , 80 ). Aging causes 15–30% reduction in lacunar density or osteocyte numbers ( 81 ).…”

Section: Disturbed Osteocyte Function Can Cause Metabolic Bone Diseasmentioning

confidence: 99%

The Osteocyte as the New Discovery of Therapeutic Options in Rare Bone Diseases

2020

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Osteocytes are the most abundant (~95%) cells in bone with the longest half-life (~25 years) in humans. In the past osteocytes have been regarded as vestigial cells in bone, since they are buried inside the tough bone matrix. However, during the last 30 years it has become clear that osteocytes are as important as bone forming osteoblasts and bone resorbing osteoclasts in maintaining bone homeostasis. The osteocyte cell body and dendritic processes reside in bone in a complex lacuno-canalicular system, which allows the direct networking of osteocytes to their neighboring osteocytes, osteoblasts, osteoclasts, bone marrow, blood vessels, and nerves. Mechanosensing of osteocytes translates the applied mechanical force on bone to cellular signaling and regulation of bone adaptation. The osteocyte lacuno-canalicular system is highly efficient in transferring external mechanical force on bone to the osteocyte cell body and dendritic processes via displacement of fluid in the lacuno-canalicular space. Osteocyte mechanotransduction regulates the formation and function of the osteoblasts and osteoclasts to maintain bone homeostasis. Osteocytes produce a variety of proteins and signaling molecules such as sclerostin, cathepsin K, Wnts, DKK1, DMP1, IGF1, and RANKL/OPG to regulate osteoblast and osteoclast activity. Various genetic abnormality-associated rare bone diseases are related to disrupted osteocyte functions, including sclerosteosis, van Buchem disease, hypophosphatemic rickets, and WNT1 and plastin3 mutation-related disorders. Meticulous studies during the last 15 years on disrupted osteocyte function in rare bone diseases guided for the development of various novel therapeutic agents to treat bone diseases. Studies on genetic, molecular, and cellular mechanisms of sclerosteosis and van Buchem disease revealed a role for sclerostin in bone homeostasis, which led to the development of the sclerostin antibody to treat osteoporosis and other bone degenerative diseases. The mechanism of many other rare bone diseases and the role of the osteocyte in the development of such conditions still needs to be investigated. In this review, we mainly discuss the knowledge obtained during the last 30 years on the role of the osteocyte in rare bone diseases. We speculate about future research directions to develop novel therapeutic drugs targeting osteocyte functions to treat both common and rare bone diseases.

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Section: Disturbed Osteocyte Function Can Cause Metabolic Bone Diseasmentioning

confidence: 99%

The Osteocyte as the New Discovery of Therapeutic Options in Rare Bone Diseases

2020

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“…Changes of lacunar shapes were observed in osteopenia, osteoporosis and osteoarthritis based on imaging of one sample in human knees 8 . Age related changes have been documented in several studies showing a decrease in the density of lacunae and a loss of dendrites altering the correct communication between osteocytes 9 .…”

mentioning

confidence: 99%

Assessment of the human bone lacuno-canalicular network at the nanoscale and impact of spatial resolution

Pacureanu

Olivier

et al. 2020

Sci Rep

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cécile olivier 1,2 , peter cloetens 2 & françoise peyrin 1,2* Recently, increasing attention has been given to the study of osteocytes, the cells that are thought to play an important role in bone remodeling and in the mechanisms of bone fragility. the interconnected osteocyte system is deeply embedded inside the mineralized bone matrix and lies within a closely fitted porosity known as the lacuno-canalicular network. However, quantitative data on human samples remain scarce, mostly measured in 2D, and there are gaps to be filled in terms of spatial resolution. In this work, we present data on femoral samples from female donors imaged with isotropic 3D spatial resolution by magnified X-ray phase nano computerized-tomography. We report quantitative results on the 3D structure of canaliculi in human femoral bone imaged with a voxel size of 30 nm. We found that the lacuno-canalicular porosity occupies on average 1.45% of the total tissue volume, the ratio of the canalicular versus lacunar porosity is about 37.7%, and the primary number of canaliculi stemming from each lacuna is 79 on average. The examination of this number at different distances from the surface of the lacunae demonstrates branching in the canaliculi network. We analyzed the impact of spatial resolution on quantification by comparing parameters extracted from the same samples imaged with 120 nm and 30 nm voxel sizes. To avoid any bias related to the analysis region, the volumes at 120 nm and 30 nm were registered and cropped to the same field of view. Our results show that the measurements at 120 and 30 nm are strongly correlated in our data set but that the highest spatial resolution provides more accurate information on the canaliculi network and its branching properties.

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“…Osteocytes regulate osteoclast recruitment and activity being the major source of both MCS-F and RANK-L and control osteoblasts activity through the production of Wnt signaling modulators, such as sclerostin [86]. Age-dependent changes in the lacuno-canalicular system underlying the osteocyte network have been described [65]. Histomorphometric studies on human bone showed that lacunar density decreases in a linear manner with age, with a significant reduction ranging from 15 to 30% in aged bone [39,40].…”

Section: Osteocytesmentioning

confidence: 99%

Molecular Basis of Bone Aging

Corrado

Cici

Rotondo

et al. 2020

IJMS

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A decline in bone mass leading to an increased fracture risk is a common feature of age-related bone changes. The mechanisms underlying bone senescence are very complex and implicate systemic and local factors and are the result of the combination of several changes occurring at the cellular, tissue and structural levels; they include alterations of bone cell differentiation and activity, oxidative stress, genetic damage and the altered responses of bone cells to various biological signals and to mechanical loading. The molecular mechanisms responsible for these changes remain greatly unclear and many data derived from in vitro or animal studies appear to be conflicting and heterogeneous, probably due to the different experimental approaches; nevertheless, understanding the main physio-pathological processes that cause bone senescence is essential for the development of new potential therapeutic options for treating age-related bone loss. This article reviews the current knowledge concerning the molecular mechanisms underlying the pathogenesis of age-related bone changes.

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Changes in the osteocyte lacunocanalicular network with aging

Cited by 73 publications

References 139 publications

The Osteocyte as the New Discovery of Therapeutic Options in Rare Bone Diseases

The Osteocyte as the New Discovery of Therapeutic Options in Rare Bone Diseases

Assessment of the human bone lacuno-canalicular network at the nanoscale and impact of spatial resolution

Molecular Basis of Bone Aging

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