Investigating Osteocytic Perilacunar/Canalicular Remodeling

Yee, Cristal S.; Schurman, Charles A.; White, Carter R.; Alliston, Tamara

doi:10.1007/s11914-019-00514-0

Cited by 41 publications

(35 citation statements)

References 115 publications

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“…In reality, the adaptation process is more dynamic, so that the first bone (re)modeling would already have an influence on the fluid flow pattern. Additionally, osteocytes may be even able to actively manipulate the permeability of certain canaliculi, for example by perilacunar/canalicular remodeling ( 62 ) and/or obstructing the fluid flow with their cell processes. Such an active control of the fluid flow would allow indirect communication between osteocytes ( 63 ).…”

Section: Discussionmentioning

confidence: 99%

The mechanoresponse of bone is closely related to the osteocyte lacunocanalicular network architecture

Tol

Schemenz

Wagermaier

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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Organisms rely on mechanosensing mechanisms to adapt to changes in their mechanical environment. Fluid-filled network structures not only ensure efficient transport but can also be employed for mechanosensation. The lacunocanalicular network (LCN) is a fluid-filled network structure, which pervades our bones and accommodates a cell network of osteocytes. For the mechanism of mechanosensation, it was hypothesized that load-induced fluid flow results in forces that can be sensed by the cells. We use a controlled in vivo loading experiment on murine tibiae to test this hypothesis, whereby the mechanoresponse was quantified experimentally by in vivo micro-computed tomography (µCT) in terms of formed and resorbed bone volume. By imaging the LCN using confocal microscopy in bone volumes covering the entire cross-section of mouse tibiae and by calculating the fluid flow in the three-dimensional (3D) network, we could perform a direct comparison between predictions based on fluid flow velocity and the experimentally measured mechanoresponse. While local strain distributions estimated by finite-element analysis incorrectly predicts preferred bone formation on the periosteal surface, we demonstrate that additional consideration of the LCN architecture not only corrects this erroneous bias in the prediction but also explains observed differences in the mechanosensitivity between the three investigated mice. We also identified the presence of vascular channels as an important mechanism to locally reduce fluid flow. Flow velocities increased for a convergent network structure where all of the flow is channeled into fewer canaliculi. We conclude that, besides mechanical loading, LCN architecture should be considered as a key determinant of bone adaptation.

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Section: Discussionmentioning

confidence: 99%

The mechanoresponse of bone is closely related to the osteocyte lacunocanalicular network architecture

Tol

Schemenz

Wagermaier

et al. 2020

Proc. Natl. Acad. Sci. U.S.A.

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“…Osteocytes not only facilitate mechanosensation as described in Table 1, but also control bone structure (amount and quality) through mineralization inhibitors such as dentin matrix protein-1, fetuin-A, and Wnt inhibitor (Poole et al, 2005;Feng et al, 2006;Coen et al, 2009;Liu et al, 2009;Rauner et al, 2012). Although it was thought that osteocytes remain inactive until the next bone remodeling cycle (Mikuni-Takagaki, 1999;Kamioka et al, 2001;Zhao et al, 2002;Knothe-Tate et al, 2004;Datta et al, 2008), it is now accepted that osteocytes constantly remodel the surrounding extracellular matrix (Yee et al, 2019). Another fate of osteoblasts is to become bone lining cells, which cover the freshly formed endosteal bone surface thus forming a physical barrier to avoid the process of osteoclast adhesion and bone resorption.…”

Section: Stimulators Of Osteoblast Functionsmentioning

confidence: 99%

Destroy to Rebuild: The Connection Between Bone Tissue Remodeling and Matrix Metalloproteinases

Hardy

Fernández-Patrón

2020

Front. Physiol.

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Bone is a dynamic organ that undergoes constant remodeling, an energetically costly process by which old bone is replaced and localized bone defects are repaired to renew the skeleton over time, thereby maintaining skeletal health. This review provides a general overview of bone's main players (bone lining cells, osteocytes, osteoclasts, reversal cells, and osteoblasts) that participate in bone remodeling. Placing emphasis on the family of extracellular matrix metalloproteinases (MMPs), we describe how: (i) Convergence of multiple protease families (including MMPs and cysteine proteinases) ensures complexity and robustness of the bone remodeling process, (ii) Enzymatic activity of MMPs affects bone physiology at the molecular and cellular levels and (iii) Either overexpression or deficiency/insufficiency of individual MMPs impairs healthy bone remodeling and systemic metabolism. Today, it is generally accepted that proteolytic activity is required for the degradation of bone tissue in osteoarthritis and osteoporosis. However, it is increasingly evident that inactivating mutations in MMP genes can also lead to bone pathology including osteolysis and metabolic abnormalities such as delayed growth. We argue that there remains a need to rethink the role played by proteases in bone physiology and pathology.

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“…The potential interactions between the systematic changes of pregnancy and lactation and skeletal mechano-sensitivity are likely mediated by osteocytes, the primary mechanosensory cells in bone. In addition to osteoblasts and osteoclasts, osteocytes are also able to directly modulate their surrounding tissue during reproduction, by removing mineral from the surrounding matrix and/or forming new bone tissue on the surfaces of their lacunae [71,72]. More recent studies have confirmed that this process of osteocyte PLR occurs in various conditions, most notably during lactation, and is thought to play a role in maintaining mineral homeostasis [19][20][21]73].…”

Section: Lactation-induced Osteocytic Perilacunar/canalicular Remodelmentioning

confidence: 99%

“…Furthermore, despite recent advances in our understanding of PLR and its role during reproduction and lactation [71,72], little is known on the exact signals that trigger osteocytic PLR and how PLR triggered by lactation may affect bone over the long-term. Recent data reported that compared to virgin rats, estrogen deficiency by ovariectomy triggers osteocytic PLR and improves mechano-responsiveness in rats with reproduction and lactation history [89].…”

Section: Future Directions: Challenges and Unresolved Questionsmentioning

confidence: 99%

Mechanical Regulation of the Maternal Skeleton during Reproduction and Lactation

Liu

Wang

Bakker

et al. 2019

Curr Osteoporos Rep

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Purpose of review: This review summarizes recently published data on the effects of pregnancy and lactation on bone structure, mechanical properties, and mechano-responsiveness in an effort to elucidate how the balance between the structural and metabolic functions of the skeleton is achieved during these physiological processes. Recent findings: While pregnancy and lactation induce significant changes in bone density and structure to provide calcium for fetal/infant growth, the maternal physiology also comprises several innate compensatory mechanisms that allow for the maintenance of skeletal mechanical integrity. Both clinical and animal studies suggest that pregnancy and lactation lead to adaptations in cortical bone structure to allow for rapid calcium release from the trabecular compartment while maintaining whole-bone stiffness and strength. Moreover, extents of lactation-induced bone loss and weaning-induced recovery are highly dependent on a given bone's load-bearing function, resulting in better protection of the mechanical integrity at critical load-bearing sites. The recent discovery of lactation-induced osteocytic peri-lacunar/canalicular remodeling (PLR) indicates a new means for osteocytes to modulate mineral homeostasis and tissue-level mechanical properties of the maternal skeleton. Furthermore, lactation-induced PLR may also play an important role in maintaining the maternal skeleton's load-bearing capacity by altering osteocyte's microenvironment and modulating the transmission of anabolic mechanical signals to osteocytes.

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Investigating Osteocytic Perilacunar/Canalicular Remodeling

Cited by 41 publications

References 115 publications

The mechanoresponse of bone is closely related to the osteocyte lacunocanalicular network architecture

The mechanoresponse of bone is closely related to the osteocyte lacunocanalicular network architecture

Destroy to Rebuild: The Connection Between Bone Tissue Remodeling and Matrix Metalloproteinases

Mechanical Regulation of the Maternal Skeleton during Reproduction and Lactation

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