Comparative Analysis of Bone Structural Parameters Reveals Subchondral Cortical Plate Resorption and Increased Trabecular Bone Remodeling in Human Facet Joint Osteoarthritis

Netzer, Cordula; Distel, Pascal; Wolfram, Uwe; Deyhle, Hans; Jost, Gregory F.; Schären, Stefan; Geurts, Jeroen

doi:10.3390/ijms19030845

Cited by 12 publications

(18 citation statements)

References 34 publications

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“…These results are also fully in line with the demonstration that the crucial effect of PTH (1-34) is to improve only the “dynamic” bone formation instead of the “static” one during bone repair in transcortical holes experimentally drilled in rat femur [47]. On the contrary, in some pathologies, like facet joint osteoarthritis (FJOA), remodeling of the subchondral trabecular bone compartment is characterized by increased trabecular number, rather than trabecular thickening [48]; this observation can be explained with the impairment of viability of osteocytes (i.e., the bone mechanosensor) inside the trabecular bone due to osteoarthritis, so that static osteogenesis (instead of dynamic one) is activated, through the recruitment of osteoprogenitor cells by endothelial-derived growth factors, giving rise to the formation of new trabeculae. Moreover, Kumabe and coworkers [43] showed that the administration of PTH (1–34) increases union rate and accelerates bone healing in rat refractory fracture models, suggesting that such a drug could become a useful therapy for accelerating fracture healing in patients at high risk of delayed union or nonunion.…”

Section: Discussionsupporting

confidence: 73%

Interaction among Calcium Diet Content, PTH (1-34) Treatment and Balance of Bone Homeostasis in Rat Model: The Trabecular Bone as Keystone

Ferretti

Cavani²,

Rovedatti³

et al. 2019

IJMS

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The present study is the second step (concerning normal diet restoration) of the our previous study (concerning the calcium-free diet) to determine whether normal diet restoration, with/without concomitant PTH (1-34) administration, can influence amounts and deposition sites of the total bone mass. Histomorphometric evaluations and immunohistochemical analysis for Sclerostin expression were conducted on the vertebral bodies and femurs in the rat model. The final goals are (i) to define timing and manners of bone mass changes when calcium is restored to the diet, (ii) to analyze the different involvement of the two bony architectures having different metabolism (i.e., trabecular versus cortical bone), and (iii) to verify the eventual role of PTH (1-34) administration. Results evidenced the greater involvement of the trabecular bone with respect to the cortical bone, in response to different levels of calcium content in the diet, and the effect of PTH, mostly in the recovery of trabecular bony architecture. The main findings emerged from the present study are (i) the importance of the interplay between mineral homeostasis and skeletal homeostasis in modulating and guiding bone’s response to dietary/metabolic alterations and (ii) the evidence that the more involved bony architecture is the trabecular bone, the most susceptible to the dynamical balance of the two homeostases.

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Section: Discussionsupporting

confidence: 73%

Interaction among Calcium Diet Content, PTH (1-34) Treatment and Balance of Bone Homeostasis in Rat Model: The Trabecular Bone as Keystone

Ferretti

Cavani²,

Rovedatti³

et al. 2019

IJMS

View full text Add to dashboard Cite

show abstract

“…These results are also fully in line with the demonstration that the crucial effect of PTH(1-34) is to improve only the "dynamic" bone formation instead of the "static" one during bone repair in transcortical holes experimentally drilled in rat femur [47]. On the contrary, in some pathologies, like facet joint osteoarthritis (FJOA), remodeling of the subchondral trabecular bone compartment is characterized by increased trabecular number, rather than trabecular thickening [48]; this observation can be explained with the impairment of viability of osteocytes (i.e. the bone mechanosensor) inside the trabecular bone due to osteoarthritis, so that static osteogenesis (instead of dynamic one) is activated, through the recruitment of osteoprogenitor cells by endothelialderived growth factors, giving rise to the formation of new trabeculae.…”

Section: Discussionsupporting

confidence: 82%

Interplay among calcium diet content, PTH(1-34) treatment and balance of bone homeostases in rat model: the trabecular bone as keystone

Ferretti¹,

Cavani²,

Rovedatti³

et al. 2019

Preprint

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The present study is the second step (concerning the normal-diet restoration) of the our previous one (concerning the calcium-free diet) to determine whether the normal-diet restoration, with/without concomitant PTH(1-34) administration, can influence amounts and deposition sites of the total bone mass. Histomorphometric evaluations and immunohistochemical analysis for Sclerostin expression were conducted on the vertebral bodies and femurs  in rat model. The final goals are: i) to define timing and manners of bone mass changes when calcium is restored in the diet; ii) to analyze the different involvement of the two bony architectures having different metabolism (i.e. trabecular versus cortical bone); iii) to verify the eventual role of PTH(1-34) administration. Results evidenced the greater involvement of the trabecular bone with respect to the cortical one, in answering to different calcium diet content, and the effect of PTH mostly in the recovery of trabecular bony architecture. The main findings emerged from the present study are: i) the importance of the interplay between mineral homeostasis and skeletal homeostasis in modulating and guiding bone answers to dietary/metabolic alterations and ii) the evidence that the more involved bony architecture is the trabecular one, the most susceptible to the dynamical balance of the two homeostases.

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“…Evaluation of histological changes in articular cartilage is an important way to comprehend the progression of OA . In the present study, we assessed the 3D characteristics and morphology changes of cartilage and subchondral bone to illuminate the influence of BMSCs‐exosomes on LFJ‐OA.…”

Section: Discussionmentioning

confidence: 99%

“…30 Evaluation of histological changes in articular cartilage is an important way to comprehend the progression of OA. 38,39 In the present study, we assessed the 3D characteristics and morphology changes of cartilage and subchondral bone to illuminate the influence of BMSCs-exosomes on LFJ-OA. On the basis of a PPCT imaging, a loss of integrity of the osteochondral junction was detected after LFJ-OA induction, chartered as reduced cartilage thickness and volume, decreased surface area, and architectural destruction in the subchondral bone.…”

Section: Discussionmentioning

confidence: 99%

BMSCs‐Derived Exosomes Ameliorate Pain Via Abrogation of Aberrant Nerve Invasion in Subchondral Bone in Lumbar Facet Joint Osteoarthritis

Ding

et al. 2019

Journal Orthopaedic Research

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Lumbar facet joint osteoarthritis (LFJ OA) is regarded as one of the common causes of low back pain (LBP). The pathogenesis and underlying mechanism of this disease are largely unknown, there is still no effective disease‐modifying therapy. This study aims to investigate the efficacy of exosomes derived from bone marrow mesenchymal stem cells (BMSCs) on the pathogenesis and behavioral signs of LBP in the LFJ OA mouse model. The pathogenetic change in cartilage and aberrant nerve invasion in the subchondral bone of LFJ in a mouse model after treatment with BMSC‐exosomes was evaluated. BMSC‐exosomes could relieve pain via abrogation of aberrant CGRP‐positive nerve and abnormal H‐type vessel formation in the subchondral bone of LFJ. Moreover, BMSC‐exosomes attenuated cartilage degeneration and inhibited tartrate‐resistant acid phosphatase expression and RANKL‐RANK‐TRAF6 signaling activation to facilitate subchondral bone remodeling. These results indicated that BMSC‐exosomes could relive behavioral signs of LBP and pathological processes in LFJ OA. BMSC‐exosomes have a prominent protective effect and might be a potential therapeutic option for the treatment of LFJ OA causing LBP. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 38:670–679, 2020

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Comparative Analysis of Bone Structural Parameters Reveals Subchondral Cortical Plate Resorption and Increased Trabecular Bone Remodeling in Human Facet Joint Osteoarthritis

Cited by 12 publications

References 34 publications

Interaction among Calcium Diet Content, PTH (1-34) Treatment and Balance of Bone Homeostasis in Rat Model: The Trabecular Bone as Keystone

Interaction among Calcium Diet Content, PTH (1-34) Treatment and Balance of Bone Homeostasis in Rat Model: The Trabecular Bone as Keystone

Interplay among calcium diet content, PTH(1-34) treatment and balance of bone homeostases in rat model: the trabecular bone as keystone

BMSCs‐Derived Exosomes Ameliorate Pain Via Abrogation of Aberrant Nerve Invasion in Subchondral Bone in Lumbar Facet Joint Osteoarthritis

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