Osteoporosis and Covid-19: Detected similarities in bone lacunar-level alterations via combined AI and advanced synchrotron testing

Buccino, Federica; Zagra, Luigi; Longo, Elena; D’Amico, Lorenzo; Banfi, Giuseppe; Berto, Filippo; Tromba, Giuliana; Vergani, L.

doi:10.1016/j.matdes.2023.112087

Cited by 14 publications

(9 citation statements)

References 77 publications

(78 reference statements)

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“…In light of all the gathered data, it is crucial to consider the potential therapeutic impact of rosavin on the prevention and treatment of complications associated with osteoporosis, particularly fractures. As BMD decreases and osteoclastogenesis increases in the course of osteoporosis, alterations occur in the microarchitecture of the bone, including the dysmorphic morphology of trabecular lacunae [60,61]. The emergence of such changes in the bone tissue structure could serve as a predictive factor for the rapid onset of osteoporotic fractures.…”

Section: Discussionmentioning

confidence: 99%

The Role of Rosavin in the Pathophysiology of Bone Metabolism

Wojdasiewicz,

Turczyn,

Lach-Gruba

et al. 2024

IJMS

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Rosavin, a phenylpropanoid in Rhodiola rosea’s rhizome, and an adaptogen, is known for enhancing the body’s response to environmental stress. It significantly affects cellular metabolism in health and many diseases, particularly influencing bone tissue metabolism. In vitro, rosavin inhibits osteoclastogenesis, disrupts F-actin ring formation, and reduces the expression of osteoclastogenesis-related genes such as cathepsin K, calcitonin receptor (CTR), tumor necrosis factor receptor-associated factor 6 (TRAF6), tartrate-resistant acid phosphatase (TRAP), and matrix metallopeptidase 9 (MMP-9). It also impedes the nuclear factor of activated T-cell cytoplasmic 1 (NFATc1), c-Fos, the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and mitogen-activated protein kinase (MAPK) signaling pathways and blocks phosphorylation processes crucial for bone resorption. Moreover, rosavin promotes osteogenesis and osteoblast differentiation and increases mouse runt-related transcription factor 2 (Runx2) and osteocalcin (OCN) expression. In vivo studies show its effectiveness in enhancing bone mineral density (BMD) in postmenopausal osteoporosis (PMOP) mice, restraining osteoclast maturation, and increasing the active osteoblast percentage in bone tissue. It modulates mRNA expressions by increasing eukaryotic translation elongation factor 2 (EEF2) and decreasing histone deacetylase 1 (HDAC1), thereby activating osteoprotective epigenetic mechanisms, and alters many serum markers, including decreasing cross-linked C-telopeptide of type I collagen (CTX-1), tartrate-resistant acid phosphatase 5b (TRACP5b), receptor activator for nuclear factor κ B ligand (RANKL), macrophage-colony-stimulating factor (M-CSF), and TRAP, while increasing alkaline phosphatase (ALP) and OCN. Additionally, when combined with zinc and probiotics, it reduces pro-osteoporotic matrix metallopeptidase 3 (MMP-3), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α), and enhances anti-osteoporotic interleukin 10 (IL-10) and tissue inhibitor of metalloproteinase 3 (TIMP3) expressions. This paper aims to systematically review rosavin’s impact on bone tissue metabolism, exploring its potential in osteoporosis prevention and treatment, and suggesting future research directions.

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Section: Discussionmentioning

confidence: 99%

The Role of Rosavin in the Pathophysiology of Bone Metabolism

Wojdasiewicz,

Turczyn,

Lach-Gruba

et al. 2024

IJMS

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“…Research findings suggest resemblances between bones affected by osteoporosis and those affected by Covid-19, particularly evident at the lacunar level. 28 OC, originating from the monocyte/macrophage lineage (pre-OC), are exclusive bone-resorbing cells crucial for bone development and remodeling, actively contributing to musculoskeletal tissue damage.…”

Section: Discussionmentioning

confidence: 99%

The abortive SARS‐CoV‐2 infection of osteoclast precursors promotes their differentiation into osteoclasts

Sviercz,

Jarmoluk,

Godoy Coto

et al. 2024

Journal of Medical Virology

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The Coronavirus Disease 2019 (COVID‐19) pandemic has resulted in the loss of millions of lives, although a majority of those infected have managed to survive. Consequently, a set of outcomes, identified as long COVID, is now emerging. While the primary target of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is the respiratory system, the impact of COVID‐19 extends to various body parts, including the bone. This study aims to investigate the effects of acute SARS‐CoV‐2 infection on osteoclastogenesis, utilizing both ancestral and Omicron viral strains. Monocyte‐derived macrophages, which serve as precursors to osteoclasts, were exposed to both viral variants. However, the infection proved abortive, even though ACE2 receptor expression increased postinfection, with no significant impact on cellular viability and redox balance. Both SARS‐CoV‐2 strains heightened osteoclast formation in a dose‐dependent manner, as well as CD51/61 expression and bone resorptive ability. Notably, SARS‐CoV‐2 induced early pro‐inflammatory M1 macrophage polarization, shifting toward an M2‐like profile. Osteoclastogenesis‐related genes (RANK, NFATc1, DC‐STAMP, MMP9) were upregulated, and surprisingly, SARS‐CoV‐2 variants promoted RANKL‐independent osteoclast formation. This thorough investigation illuminates the intricate interplay between SARS‐CoV‐2 and osteoclast precursors, suggesting potential implications for bone homeostasis and opening new avenues for therapeutic exploration in COVID‐19.

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“…Of note, when comparing SARS-CoV-2-infected patients with never-infected controls, no differences were observed in serum angiotensin converting enzyme-2 (ACE-2) levels and no correlations were observed between ACE-2 levels and either OPG levels or DXA T-score measurements [ 33 ]. Another study examined the bone from total hip arthroplasties from controls, osteoporotic, and patients infected with SARS-CoV-2 at most 12 months prior to the total hip arthroplasties to determine if differences in bone quality, as measured by mechanics and lacunar geometry, existed [ 34 •]. Femoral heads were tested with synchrotron image-guided failure assessment to determine structure and mechanics.…”

Section: Clinical Evidence Of Sars-cov-2 Infection-related Bone Lossmentioning

confidence: 99%

“…Control sample size was five females, osteoporotic sample size was five females, and SARS-CoV-2-infected sample size was five males and five females. Multiple test samples were taken from these patients, but biological sample size remained low [ 34 •]. Further work will need to be done to determine the long-term effects of SARS-CoV-2 infection on BMD and fracture risk, especially in patients who were not hospitalized with SARS-CoV-2 infection.…”

Section: Clinical Evidence Of Sars-cov-2 Infection-related Bone Lossmentioning

confidence: 99%

COVID-19 and Bone Loss: A Review of Risk Factors, Mechanisms, and Future Directions

Creecy,

Awosanya,

Harris

et al. 2024

Curr Osteoporos Rep

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Purpose of Review SARS-CoV-2 drove the catastrophic global phenomenon of the COVID-19 pandemic resulting in a multitude of systemic health issues, including bone loss. The purpose of this review is to summarize recent findings related to bone loss and potential mechanisms. Recent Findings The early clinical evidence indicates an increase in vertebral fractures, hypocalcemia, vitamin D deficiencies, and a loss in BMD among COVID-19 patients. Additionally, lower BMD is associated with more severe SARS-CoV-2 infection. Preclinical models have shown bone loss and increased osteoclastogenesis. The bone loss associated with SARS-CoV-2 infection could be the result of many factors that directly affect the bone such as higher inflammation, activation of the NLRP3 inflammasome, recruitment of Th17 cells, the hypoxic environment, and changes in RANKL/OPG signaling. Additionally, SARS-CoV-2 infection can exert indirect effects on the skeleton, as mechanical unloading may occur with severe disease (e.g., bed rest) or with BMI loss and muscle wasting that has also been shown to occur with SARS-CoV-2 infection. Muscle wasting can also cause systemic issues that may influence the bone. Medications used to treat SARS-CoV-2 infection also have a negative effect on the bone. Lastly, SARS-CoV-2 infection may also worsen conditions such as diabetes and negatively affect kidney function, all of which could contribute to bone loss and increased fracture risk. Summary SARS-CoV-2 can negatively affect the bone through multiple direct and indirect mechanisms. Future work will be needed to determine what patient populations are at risk of COVID-19-related increases in fracture risk, the mechanisms behind bone loss, and therapeutic options. This review article is part of a series of multiple manuscripts designed to determine the utility of using artificial intelligence for writing scientific reviews.

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Osteoporosis and Covid-19: Detected similarities in bone lacunar-level alterations via combined AI and advanced synchrotron testing

Cited by 14 publications

References 77 publications

The Role of Rosavin in the Pathophysiology of Bone Metabolism

The Role of Rosavin in the Pathophysiology of Bone Metabolism

The abortive SARS‐CoV‐2 infection of osteoclast precursors promotes their differentiation into osteoclasts

COVID-19 and Bone Loss: A Review of Risk Factors, Mechanisms, and Future Directions

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