Docosahexaenoic acid inhibits bone remodeling and vessel formation in the osteochondral unit in a rat model

Xie, Yinhao; Zhou, Wei; Zhong, Zhihong; H, Yu; Zhang, Ping; Shen, Huawei

doi:10.1016/j.biopha.2019.108811

Cited by 10 publications

(13 citation statements)

References 41 publications

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“…Moreover, menisci, ligaments, tendons, and adipose depots are all responsible for biomechanical stability and joint function [ 5 ]. Hands, knees, and hips are particularly affected by OA, and more specifically, the articular bodies, capsules, bursae, cartilage menisci, ligaments, and muscles [ 1 , 4 , 7 ]. The osteochondral unit consists of cartilage, subchondral bone, and calcified cartilage.…”

Section: Introductionmentioning

confidence: 99%

“…The osteochondral unit consists of cartilage, subchondral bone, and calcified cartilage. This unit, essential for load distribution and joint movement, is modified as OA progresses [ 1 , 2 , 4 ]. In the early stages of disease onset, the cortical plate and subchondral bone undergo rapid bone remodeling, with concomitant bone loss and increased porosity.…”

Section: Introductionmentioning

confidence: 99%

“…Changes in calcified cartilage and tidemark destruction are related to the improper passage of substances and vessel generation. Modification of the osteochondral unit leads to unbalanced load distribution with consequent cartilage destruction, which, over time, determines OA onset and progression [ 1 , 2 ]. Furthermore, alterations in subchondral bone are responsible for the different crosstalks between chondrocytes and bone cells, which contribute to cartilage destruction [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

“…Modification of the osteochondral unit leads to unbalanced load distribution with consequent cartilage destruction, which, over time, determines OA onset and progression [ 1 , 2 ]. Furthermore, alterations in subchondral bone are responsible for the different crosstalks between chondrocytes and bone cells, which contribute to cartilage destruction [ 1 ]. Chondrocytes, responsible for bone formation, are damaged by proinflammatory action of interleukins and metalloproteinases [ 1 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, alterations in subchondral bone are responsible for the different crosstalks between chondrocytes and bone cells, which contribute to cartilage destruction [ 1 ]. Chondrocytes, responsible for bone formation, are damaged by proinflammatory action of interleukins and metalloproteinases [ 1 , 7 ]. Furthermore, chondrocytes express molecules such as VEGF (vascular endothelial growth factor), MMP-13 (matrix metallopeptidase 13), and RUNX2 (runt-related transcription factor 2), implicated in hypertrophy and differentiation [ 1 , 2 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

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The Role of Nutraceuticals in Osteoarthritis Prevention and Treatment: Focus on n-3 PUFAs

Oppedisano

Bulotta²,

Maiuolo

et al. 2021

Oxidative Medicine and Cellular Longevity

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Osteoarthritis (OA) is a disease caused by joint degeneration with massive cartilage loss, and obesity is among the risk factors for its onset, though the pathophysiological mechanisms underlying the disease and better therapeutic approach still remain to be assessed. In recent years, several nutraceutical interventions have been investigated in order to define better solutions for preventing and treating OA. Among them, polyunsaturated fatty acids (n-3 PUFAs) appear to represent potential candidates in counteracting OA and its consequences, due to their anti-inflammatory, antioxidant, and chondroinductive effects. PUFAs have been found to counteract the onset and progression of OA by reducing bone and cartilage destruction, inhibiting proinflammatory cytokine release, reactive oxygen species (ROS) generation, and the NF-κB pathway’s activation. Moreover, a diet rich in n-3 PUFAs and their derivatives (maresins and resolvins) demonstrates beneficial effects on associated pain reduction. Finally, it has been shown that together with the anti-inflammatory and antioxidant properties of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, their antiapoptotic and antiangiogenic effects contribute in reducing OA development. The present review is aimed at assessing evidence suggesting the potential benefit of nutraceutical supplementation with PUFAs in OA management according to their efficacy in targeting relevant pathophysiological mechanisms responsible for inflammation and joint destruction processes, and this may represent a novel and potentially useful approach in OA prevention and treatment. For that purpose, a PubMed literature survey was conducted with a focus on some in vitro and in vivo studies and clinical trials from 2015 to 2020.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

The Role of Nutraceuticals in Osteoarthritis Prevention and Treatment: Focus on n-3 PUFAs

Oppedisano

Bulotta²,

Maiuolo

et al. 2021

Oxidative Medicine and Cellular Longevity

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Osteoblastic STAT3 Is Crucial for Orthodontic Force Driving Alveolar Bone Remodeling and Tooth Movement

Gong

Sun

Yang

et al. 2020

Journal of Bone and Mineral Research

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Mechanical force is essential to shape the internal architecture and external form of the skeleton by regulating the bone remodeling process. However, the underlying mechanism of how the bone responds to mechanical force remains elusive. Here, we generated both orthodontic tooth movement (OTM) model in vivo and a cyclic stretch-loading model in vitro to investigate biomechanical regulation of the alveolar bone. In this study, signal transducer and activator of transcription 3 (STAT3) was screened as one of the mechanosensitive proteins by protein array analysis of cyclic stretch-loaded bone mesenchymal stem cells (BMSCs) and was also proven to be activated in osteoblasts in response to the mechanical force during OTM. With an inducible osteoblast linage-specific Stat3 knockout model, we found that Stat3 deletion decelerated the OTM rate and reduced orthodontic force-induced bone remodeling, as indicated by both decreased bone resorption and formation. Both genetic deletion and pharmacological inhibition of STAT3 in BMSCs directly inhibited mechanical force-induced osteoblast differentiation and impaired osteoclast formation via osteoblast-osteoclast cross-talk under mechanical force loading. According to RNA-seq analysis of Stat3-deleted BMSCs under mechanical force, matrix metalloproteinase 3 (Mmp3) was screened and predicted to be a downstream target of STAT3. The luciferase and ChIP assays identified that Stat3 could bind to the Mmp3 promotor and upregulate its transcription activity. Furthermore, STAT3-inhibitor decelerated tooth movement through inhibition of the bone resorption activity, as well as MMP3 expression. In summary, our study identified the mechanosensitive characteristics of STAT3 in osteoblasts and highlighted its critical role in forceinduced bone remodeling during orthodontic tooth movement via osteoblast-osteoclast cross-talk.

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Malat1 attenuated the rescuing effects of docosahexaenoic acid on osteoarthritis treatment via repressing its chondroprotective and chondrogenesis activities

Lu¹,

Yang²,

Li³

et al. 2022

Biomedicine & Pharmacotherapy

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Docosahexaenoic acid inhibits bone remodeling and vessel formation in the osteochondral unit in a rat model

Cited by 10 publications

References 41 publications

The Role of Nutraceuticals in Osteoarthritis Prevention and Treatment: Focus on n-3 PUFAs

The Role of Nutraceuticals in Osteoarthritis Prevention and Treatment: Focus on n-3 PUFAs

Osteoblastic STAT3 Is Crucial for Orthodontic Force Driving Alveolar Bone Remodeling and Tooth Movement

Malat1 attenuated the rescuing effects of docosahexaenoic acid on osteoarthritis treatment via repressing its chondroprotective and chondrogenesis activities

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