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Nutrients
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Nutritional Supplements for Bone Health
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Nutritional Supplements for Bone Health

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Public Health".

Deadline for manuscript submissions: closed (5 October 2024) | Viewed by 19699

Special Issue Editor

Dr. Yan Wen

E-Mail Website
Guest Editor
Key Laboratory of Trace Elements and Endemic Diseases of National Health Commission, Collaborative Innovation Center of Endemic Disease and Health Promotion for Silk Road Region, School of Public Health, Health Science Center, Xi’an Jiaotong University, Xi’an 710061, China
Interests: bone and cartilage integrity; osteoarthropathy; Kashin–Beck disease; mycotoxin

Special Issue Information

Dear Colleagues,

Bone health is of great importance to our daily activities and is maintained using multiple nutrients under a complicated regulatory system. Nutritional supplements are developed and utilized to keep and improve our bone health under pathological status or during specific life stages. In this context, there are many issues to address. Numerous studies have focused on this topic to help improve the supplement usage strategy. We organized this Special Issue aiming to collect and spread the most current and valuable data on this topic, which we believe will eventually boost the general bone health of the public.

We are enthusiastic about your original research, no matter whether it is population-based or animal-based, in vivo or in vitro, and clinical or basic. Meanwhile, we also welcome meta-analyses and reviews in which up-to-date summaries and informative results are provided. Any other opinions from experts on this topic are more than welcome.

Dr. Yan Wen
Guest Editor

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • bone health
  • nutrients
  • nutritional supplements
  • bone development
  • osteochondropathy

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Published Papers (7 papers)

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Research

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22 pages, 4075 KiB  
Article
Supplementation with a Whey Protein Concentrate Enriched in Bovine Milk Exosomes Improves Longitudinal Growth and Supports Bone Health During Catch-Up Growth in Rats
by Jorge García-Martínez, Rafael Salto, María D. Girón, Íñigo M. Pérez-Castillo, Pilar Bueno Vargas, Jose D. Vílchez, Azahara Linares-Pérez, Manuel Manzano, María T. García-Córcoles, Ricardo Rueda and José M. López-Pedrosa
Nutrients 2024, 16(22), 3814; https://doi.org/10.3390/nu16223814 - 7 Nov 2024
Cited by 1 | Viewed by 1505
Abstract
Background: Undernutrition impairs linear growth while restoration of nutritional provisions leads to accelerated growth patterns. However, the composition of the nutrition provided is key to facilitating effective catch-up growth without compromising bone quantity, quality, and long-term health. Methods: We evaluated the role of [...] Read more.
Background: Undernutrition impairs linear growth while restoration of nutritional provisions leads to accelerated growth patterns. However, the composition of the nutrition provided is key to facilitating effective catch-up growth without compromising bone quantity, quality, and long-term health. Methods: We evaluated the role of a whey protein concentrate enriched in bovine milk exosomes (BMEs) in modulating the proliferative properties of human chondrocytes in vitro and studied how these effects might impact bone quantity and quality measured as longitudinal tibia growth, bone mineral content (BMC) and density (BMD), and trabecular micro-CT parameters in stunted rats during catch-up growth. Results: BMEs promoted proliferation in C28/I2 human chondrocytes mediated by mTOR-Akt signaling. In a stunting rat model, two-week supplementation with BMEs during refeeding was associated with improved tibia BMD, trabecular microstructure (trabecular number (Tb. N.) and space (Tb. Sp.)), and a more active growth plate (higher volume, surface, and thickness) compared to non-supplemented stunted rats. Positive effects on physis translated to significantly longer tibias without compromising bone quality when extending the refeeding period for another two weeks. Conclusions: Overall, BME supplementation positively contributed to longitudinal bone growth and improved bone quantity and quality during catch-up growth. These findings might be relevant for improving diets aimed at addressing the nutritional needs of children undergoing undernutrition during early life. Full article
(This article belongs to the Special Issue Nutritional Supplements for Bone Health)
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18 pages, 14985 KiB  
Article
Hesperetin Attenuates T-2 Toxin-Induced Chondrocyte Injury by Inhibiting the p38 MAPK Signaling Pathway
by Chunqing Lu, Wenjing Yang, Fang Chu, Sheng Wang, Yi Ji, Zhipeng Liu, Hao Yu, Shaoxiao Qin, Dianjun Sun, Zhe Jiao and Hongna Sun
Nutrients 2024, 16(18), 3107; https://doi.org/10.3390/nu16183107 - 14 Sep 2024
Cited by 2 | Viewed by 1384
Abstract
Background: Hesperetin, a flavonoid derived from citrus fruits, exhibits potent antioxidant and anti-inflammatory activities and has been implicated in cartilage protection. However, its effectiveness against T-2 toxin-induced knee cartilage damage remains unclear. Methods: In this study, high-throughput sequencing analysis was employed to identify [...] Read more.
Background: Hesperetin, a flavonoid derived from citrus fruits, exhibits potent antioxidant and anti-inflammatory activities and has been implicated in cartilage protection. However, its effectiveness against T-2 toxin-induced knee cartilage damage remains unclear. Methods: In this study, high-throughput sequencing analysis was employed to identify the key signaling pathways involved in T-2 toxin-induced articular cartilage damage in rats. Animal models were divided into the following groups: control, low-dose T-2 toxin, high-dose T-2 toxin, T-2 toxin + hesperetin, hesperetin, and vehicle. Pathological staining and immunohistochemistry were used to assess pathological changes, as well as the expression levels of the cartilage matrix-related proteins MMP13 and collagen II, along with the activation of the p38 MAPK signaling pathway. Additionally, primary rat chondrocytes were cultured to establish an in vitro model for investigating the underlying mechanism. Results: High-throughput sequencing analysis revealed the involvement of the MAPK signaling pathway in T-2 toxin-induced articular cartilage damage in rats. Hesperetin intervention in T-2 toxin-exposed rats attenuated pathological cartilage damage. Immunohistochemistry results demonstrated a significant reduction in collagen II protein expression in the high-dose T-2 toxin group (p < 0.01), accompanied by a significant increase in MMP13 protein expression (p < 0.01). In both the articular cartilage and the epiphyseal plate, the T-2 toxin + hesperetin group exhibited significantly higher collagen II protein expression than the high-dose T-2 toxin group (p < 0.05), along with significantly lower MMP13 protein expression (p < 0.05). Hesperetin inhibited the over-activation of the p38/MEF2C signaling axis induced by T-2 toxin in primary rat chondrocytes. Compared to the T-2 toxin group, the T-2 toxin + hesperetin group showed significantly reduced phosphorylation levels of p38 and protein expression levels of MEF2C (p < 0.001 or p < 0.05). Moreover, the T-2 toxin + hesperetin group exhibited a significant decrease in MMP13 protein expression (p < 0.05) and a significant increase in collagen II protein expression (p < 0.01) compared to the T-2 toxin group. Conclusions: T-2 toxin activates the p38 MAPK signaling pathway, causing knee cartilage damage in rats. Treatment with hesperetin inhibits the p38/MEF2C signaling axis, regulates collagen II and MMP13 protein expression, and reduces cartilage injury significantly. Full article
(This article belongs to the Special Issue Nutritional Supplements for Bone Health)
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15 pages, 5592 KiB  
Article
Apoptosis and Inflammation Involved with Fluoride-Induced Bone Injuries
by Miao Wang, Kangting Luo, Tongtong Sha, Qian Li, Zaichao Dong, Yanjie Dou, Huanxia Zhang, Guoyu Zhou, Yue Ba and Fangfang Yu
Nutrients 2024, 16(15), 2500; https://doi.org/10.3390/nu16152500 - 31 Jul 2024
Cited by 2 | Viewed by 2163
Abstract
Background: Excessive fluoride exposure induces skeletal fluorosis, but the specific mechanism responsible is still unclear. Therefore, this study aimed to identify the pathogenesis of fluoride-induced bone injuries. Methods: We systematically searched fluoride-induced bone injury-related genes from five databases. Then, these genes were subjected [...] Read more.
Background: Excessive fluoride exposure induces skeletal fluorosis, but the specific mechanism responsible is still unclear. Therefore, this study aimed to identify the pathogenesis of fluoride-induced bone injuries. Methods: We systematically searched fluoride-induced bone injury-related genes from five databases. Then, these genes were subjected to enrichment analyses. A TF (transcription factor)–mRNA–miRNA network and protein–protein interaction (PPI) network were constructed using Cytoscape, and the Human Protein Atlas (HPA) database was used to screen the expression of key proteins. The candidate pharmacological targets were predicted using the Drug Signature Database. Results: A total of 85 studies were included in this study, and 112 osteoblast-, 35 osteoclast-, and 41 chondrocyte-related differential expression genes (DEGs) were identified. Functional enrichment analyses showed that the Atf4, Bcl2, Col1a1, Fgf21, Fgfr1 and Il6 genes were significantly enriched in the PI3K-Akt signaling pathway of osteoblasts, Mmp9 and Mmp13 genes were enriched in the IL-17 signaling pathway of osteoclasts, and Bmp2 and Bmp7 genes were enriched in the TGF-beta signaling pathway of chondrocytes. With the use of the TF–mRNA–miRNA network, the Col1a1, Bcl2, Fgfr1, Mmp9, Mmp13, Bmp2, and Bmp7 genes were identified as the key regulatory factors. Selenium methyl cysteine, CGS-27023A, and calcium phosphate were predicted to be the potential drugs for skeletal fluorosis. Conclusions: These results suggested that the PI3K-Akt signaling pathway being involved in the apoptosis of osteoblasts, with the IL-17 and the TGF-beta signaling pathways being involved in the inflammation of osteoclasts and chondrocytes in fluoride-induced bone injuries. Full article
(This article belongs to the Special Issue Nutritional Supplements for Bone Health)
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20 pages, 2536 KiB  
Article
Lycopene Promotes Osteogenesis and Reduces Adipogenesis through Regulating FoxO1/PPARγ Signaling in Ovariectomized Rats and Bone Marrow Mesenchymal Stem Cells
by Bingke Xia, Xuan Dai, Hanfen Shi, Jiyuan Yin, Tianshu Xu, Tianyuan Liu, Gaiyue Yue, Haochen Guo, Ruiqiong Liang, Yage Liu, Junfeng Gao, Xinxiang Wang, Xiaofei Chen, Jinfa Tang, Lili Wang, Ruyuan Zhu and Dongwei Zhang
Nutrients 2024, 16(10), 1443; https://doi.org/10.3390/nu16101443 - 10 May 2024
Cited by 1 | Viewed by 1646
Abstract
Recent interest in preventing the development of osteoporosis has focused on the regulation of redox homeostasis. However, the action of lycopene (LYC), a strong natural antioxidant compound, on osteoporotic bone loss remains largely unknown. Here, we show that oral administration of LYC to [...] Read more.
Recent interest in preventing the development of osteoporosis has focused on the regulation of redox homeostasis. However, the action of lycopene (LYC), a strong natural antioxidant compound, on osteoporotic bone loss remains largely unknown. Here, we show that oral administration of LYC to OVX rats for 12 weeks reduced body weight gain, improved lipid metabolism, and preserved bone quality. In addition, LYC treatment inhibited ROS overgeneration in serum and bone marrow in OVX rats, and in BMSCs upon H2O2 stimulation, leading to inhibiting adipogenesis and promoting osteogenesis during bone remodeling. At the molecular level, LYC improved bone quality via an increase in the expressions of FoxO1 and Runx2 and a decrease in the expressions of PPARγ and C/EBPα in OVX rats and BMSCs. Collectively, these findings suggest that LYC attenuates osteoporotic bone loss through promoting osteogenesis and inhibiting adipogenesis via regulation of the FoxO1/PPARγ pathway driven by oxidative stress, presenting a novel strategy for osteoporosis management. Full article
(This article belongs to the Special Issue Nutritional Supplements for Bone Health)
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14 pages, 2460 KiB  
Article
A Metabolomics Study of Feces Revealed That a Disturbance of Selenium-Centered Metabolic Bioprocess Was Involved in Kashin–Beck Disease, an Osteoarthropathy Endemic to China
by Yan Wen, Bingyi Wang, Panxing Shi, Xiaoge Chu, Sirong Shi, Yao Yao, Lu Zhang and Feng Zhang
Nutrients 2023, 15(21), 4651; https://doi.org/10.3390/nu15214651 - 2 Nov 2023
Cited by 1 | Viewed by 1519
Abstract
Background: Kashin–Beck disease (KBD) is a distinct osteoarthropathy in China with an unclear pathogenesis. This study aims to explore whether perturbations in the intestine metabolome could be linked to KBD individuals. Methods: An investigation was conducted in KBD endemic villages and [...] Read more.
Background: Kashin–Beck disease (KBD) is a distinct osteoarthropathy in China with an unclear pathogenesis. This study aims to explore whether perturbations in the intestine metabolome could be linked to KBD individuals. Methods: An investigation was conducted in KBD endemic villages and fecal samples were collected. After applying inclusion and exclusion criteria, a total of 75 subjects were enrolled for this study, including 46 KBD (including 19 Grade I KBD and 27 Grade II KBD) and 29 controls. Untargeted metabolomics analysis was performed on the platform of UHPLC-MS. PLS-DA and OPLS-DA were conducted to compare the groups and identify the differential metabolites (DMs). Pathway analysis was conducted on MPaLA platform to explore the functional implication of the DMs. Results: Metabolomics analysis showed that compared with the control group, KBD individuals have a total of 584 differential metabolites with dysregulated levels such as adrenic acid (log2FC = −1.87, VIP = 4.84, p = 7.63 × 10−7), hydrogen phosphate (log2FC = −2.57, VIP = 1.27, p = 1.02 × 10−3), taurochenodeoxycholic acid (VIP = 1.16, log2FC = −3.24, p = 0.03), prostaglandin E3 (VIP = 1.17, log2FC = 2.67, p = 5.61 × 10−4), etc. Pathway analysis revealed several significantly perturbed pathways associated with KBD such as selenium micronutrient network (Q value = 3.11 × 10−3, Wikipathways), metabolism of lipids (Q value = 8.43 × 10−4, Reactome), free fatty acid receptors (Q value = 3.99 × 10−3, Reactome), and recycling of bile acids and salts (Q value = 2.98 × 10−3, Reactome). Subgroup comparisons found a total of 267 differential metabolites were shared by KBD vs. control, KBD II vs. control, and KBD I vs. control, while little difference was found between KBD II and KBD I (only one differential metabolite detected). Conclusions: KBD individuals showed distinct metabolic features characterized by perturbations in lipid metabolism and selenium-related bioprocesses. Our findings suggest that the loss of nutrients metabolism balance in intestine was involved in KBD pathogenesis. Linking the nutrients metabolism (especially selenium and lipid) to KBD cartilage damage should be a future direction of KBD study. Full article
(This article belongs to the Special Issue Nutritional Supplements for Bone Health)
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13 pages, 2875 KiB  
Article
Anti-Osteoporotic Potential of Water Extract of Anethum graveolens L. Seeds
by Seon-A Jang, Sung-Ju Lee, Youn-Hwan Hwang and Hyunil Ha
Nutrients 2023, 15(19), 4302; https://doi.org/10.3390/nu15194302 - 9 Oct 2023
Cited by 2 | Viewed by 1655
Abstract
Anethum graveolens L., known as European dill, is a versatile herb widely used in both traditional medicine and culinary practices. Despite its long-standing history, the potential impact of the water extract of A. graveolens seeds (WEAG) on bone health remains unexplored. In this [...] Read more.
Anethum graveolens L., known as European dill, is a versatile herb widely used in both traditional medicine and culinary practices. Despite its long-standing history, the potential impact of the water extract of A. graveolens seeds (WEAG) on bone health remains unexplored. In this study, we investigated the influence of WEAG on osteoclast differentiation and assessed its potential as an anti-osteoporotic agent. WEAG hindered osteoclast differentiation through the suppression of receptor activator of nuclear factor-κB ligand (RANKL) expression in osteoclast-supporting cells and by directly targeting osteoclast precursor cells. WEAG significantly reduced the expression of key osteoclastogenic transcription factors, namely c-Fos and NFATc1, typically induced by RANKL in osteoclast precursors. This reduction was attributed to the suppression of both MAPKs and NF-κB pathways in response to RANKL. In vivo experiments further revealed that WEAG administration effectively reduces trabecular bone loss and weight gain triggered by ovariectomy, mimicking postmenopausal osteoporosis. Furthermore, our comprehensive phytochemical analysis of WEAG identified a range of phytochemical constituents, associated with bone health and weight regulation. Notably, we discovered a specific compound, isorhamnetin-3-O-glucuronide, within WEAG that exhibits anti-osteoclastogenic potential. Overall, this research elucidated the beneficial effects and mechanistic basis of WEAG on osteoclast differentiation and bone loss, indicating its potential as a viable alternative to address bone loss in conditions like postmenopause. Full article
(This article belongs to the Special Issue Nutritional Supplements for Bone Health)
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Review

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22 pages, 541 KiB  
Review
Omega-3 Supplementation and Its Effects on Osteoarthritis
by Megan Shawl, Thangiah Geetha, Donna Burnett and Jeganathan Ramesh Babu
Nutrients 2024, 16(11), 1650; https://doi.org/10.3390/nu16111650 - 28 May 2024
Cited by 4 | Viewed by 8648
Abstract
Osteoarthritis (OA) is a degenerative joint disease characterized by the destruction of the articular cartilage, resulting in a pro-inflammatory response. The progression of OA is multifactorial and is influenced by the underlying cause of inflammation, which includes but is not limited to trauma, [...] Read more.
Osteoarthritis (OA) is a degenerative joint disease characterized by the destruction of the articular cartilage, resulting in a pro-inflammatory response. The progression of OA is multifactorial and is influenced by the underlying cause of inflammation, which includes but is not limited to trauma, metabolism, biology, comorbidities, and biomechanics. Although articular cartilage is the main tissue affected in osteoarthritis, the chronic inflammatory environment negatively influences the surrounding synovium, ligaments, and subchondral bone, further limiting their functional abilities and enhancing symptoms of OA. Treatment for osteoarthritis remains inconsistent due to the inability to determine the underlying mechanism of disease onset, severity of symptoms, and complicating comorbidities. In recent years, diet and nutritional supplements have gained interest regarding slowing the disease process, prevention, and treatment of OA. This is due to their anti-inflammatory properties, which result in a positive influence on pain, joint mobility, and cartilage formation. More specifically, omega-3 polyunsaturated fatty acids (PUFA) have demonstrated an influential role in the progression of OA, resulting in the reduction of cartilage destruction, inhibition of pro-inflammatory cytokine cascades, and production of oxylipins that promote anti-inflammatory pathways. The present review is focused on the assessment of evidence explaining the inflammatory processes of osteoarthritis and the influence of omega-3 supplementation to modulate the progression of osteoarthritis. Full article
(This article belongs to the Special Issue Nutritional Supplements for Bone Health)
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