Bone loss in hepatitis B virus-infected patients can be associated with greater osteoclastic activity independently of the retroviral use

Dessordi, Renata; Watanabe, Lígia Moriguchi; Guimarães, Mariana P.; Romão, Elen Almeida; Martinelli, Ana de Lôurdes Candolo; Cruz, Raquel Santana da; Navarro, Anderson Marliere

doi:10.1038/s41598-021-89486-9

Cited by 6 publications

(3 citation statements)

References 32 publications

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“…Exploring the involvement of nuclear factor erythroid 2-related factor 2, a major regulator of antioxidant defence mechanisms [ 55 ], and assessing mitochondrial redox status in bone cells exposed to TDF could provide valuable insights. Additionally, HIV or hepatitis B infection could cause bone loss independently of treatment [ 56 , 57 ]. Therefore, the bone loss caused by TDF could be compounded by the infections and should be examined with proper study design to delineate the effects between the drug and the infection.…”

Section: Discussionmentioning

confidence: 99%

Effects of Tenofovir Disoproxil Fumarate on Bone Quality beyond Bone Density—A Scoping Review of the Literature

Hashwin Singh,

Jashwin Singh,

Chin

2024

Pharmaceuticals

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Tenofovir disoproxil fumarate (TDF) is a widely used pharmacological agent for the treatment of human immunodeficiency virus infection. While prolonged exposure to TDF has been associated with a decrease in bone mineral density (BMD) and increased fracture risk, limited discussion exists on its effects on various aspects of bone quality. This scoping review aims to provide a comprehensive overview of the impact of TDF on bone quality beyond BMD. A literature search was conducted using the PubMed and Scopus databases to identify studies investigating the effects of TDF on bone quality. Original research articles written in English, irrespective of study type or publication year, were included in the review. Seven articles met the inclusion criteria. Findings indicate that prolonged exposure to TDF adversely affects bone microarchitecture and strength, impeding fracture healing and skeletal microdamage repair. The observed effects suggest a complex interplay involving bone cell signalling, cytokines and bone remodelling processes as potential mechanisms underlying TDF’s impact on bone quality. As a conclusion, TDF impairs bone remodelling and microarchitecture by influencing dynamic bone cell behaviour and signalling pathways. Future studies should delve deeper into understanding the intricate negative effects of TDF on bone and explore strategies for reversing these effects.

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Section: Discussionmentioning

confidence: 99%

Effects of Tenofovir Disoproxil Fumarate on Bone Quality beyond Bone Density—A Scoping Review of the Literature

Hashwin Singh,

Jashwin Singh,

Chin

2024

Pharmaceuticals

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“… 18 Dessordi et al reported that patients with a Hepatitis B infection had lower BMD and higher serum levels of osteoclast markers than controls, suggesting that chronic viral infection may enhance bone resorption independently of antiretroviral therapy. 16 Oh et al reported that patients with chronic Hepatitis B infection in South Korea had increased risks of osteoporosis compared to the general population, as evidenced by a 9% higher fracture rate and an upward trend of osteoporotic fractures from 2007 to 2016. 17 Baeg et al reported that male patients with Hepatitis B virus infection had lower BMD in the femur and lumbar spine than those without the infection.…”

Section: Discussionmentioning

confidence: 99%

Association between hepatitis A seropositivity and bone mineral density in adolescents and adults: a cross-sectional study using NHANES data

Yu,

Hu,

Wang

et al. 2024

Sao Paulo Med. J.

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BACKGROUND: Osteoporosis, characterized by decreased bone density and increased fracture risk, imposes significant physical, psychosocial, and financial burdens. Early detection and prevention are crucial for managing osteoporosis and reducing the risk of fractures. OBJECTIVES: To investigate the relationship between Hepatitis A seropositivity and bone mineral density (BMD) in adolescents and adults and to explore the potential link between Hepatitis A infection and osteoporosis risk. DESIGN AND SETTING: This cross-sectional study used data from the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2018 to evaluate the association between hepatitis A seropositivity and BMD in 15,693 participants. METHODS: Multivariable regression analysis was used to calculate the mean BMD and standard error for adolescents and adults, followed by an independent z-test to determine whether there was a significant difference between the seropositive and seronegative groups. RESULTS: Hepatitis A seropositive adolescents and adults had lower BMD than their seronegative counterparts, with significant differences in lumber spine (mean difference = -0.03 g/cm2, P < 0.01 for both age groups) and pelvis BMDs (mean difference = -0.02 g/cm2, P < 0.01 for the adult age groups), after adjusting for various covariates. CONCLUSIONS: This study confirmed that both adolescent and adult individuals seropositive for Hepatitis A antibodies had reduced BMD among both adolescents and adults, especially in the adult group. This finding suggests a possible link between Hepatitis A infection and risk of osteoporosis.

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“…In particular, the viral protein “nef” induces bone loss by promoting the assembly of OCs on the bone-resorbing sealing zone by activating Src (a key regulator of podosome formation in OCs) [ 14 ]. Furthermore, a cross-sectional study reported that the use of nucleoside/nucleotide analogs such as tenofovir reduced the BMD in hepatitis B virus (HBV) infected patients thereby simultaneously enhancing the risk of developing osteoporosis-related fractures in the long run [ 15 , 16 ]. Importantly, bone resorptive biochemical marker such as deoxypyridinoline in the urine of HBV-infected patients further supports its bone resorptive potential.…”

Section: Introductionmentioning

confidence: 99%

Long-term implications of COVID-19 on bone health: pathophysiology and therapeutics

et al. 2022

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Background SARS-CoV-2 is a highly infectious respiratory virus associated with coronavirus disease (COVID-19). Discoveries in the field revealed that inflammatory conditions exert a negative impact on bone metabolism; however, only limited studies reported the consequences of SARS-CoV-2 infection on skeletal homeostasis. Inflammatory immune cells (T helper—Th17 cells and macrophages) and their signature cytokines such as interleukin (IL)-6, IL-17, and tumor necrosis factor-alpha (TNF-α) are the major contributors to the cytokine storm observed in COVID-19 disease. Our group along with others has proven that an enhanced population of both inflammatory innate (Dendritic cells—DCs, macrophages, etc.) and adaptive (Th1, Th17, etc.) immune cells, along with their signature cytokines (IL-17, TNF-α, IFN-γ, IL-6, etc.), are associated with various inflammatory bone loss conditions. Moreover, several pieces of evidence suggest that SARS-CoV-2 infects various organs of the body via angiotensin-converting enzyme 2 (ACE2) receptors including bone cells (osteoblasts—OBs and osteoclasts—OCs). This evidence thus clearly highlights both the direct and indirect impact of SARS-CoV-2 on the physiological bone remodeling process. Moreover, data from the previous SARS-CoV outbreak in 2002–2004 revealed the long-term negative impact (decreased bone mineral density—BMDs) of these infections on bone health. Methodology We used the keywords “immunopathogenesis of SARS-CoV-2,” “SARS-CoV-2 and bone cells,” “factors influencing bone health and COVID-19,” “GUT microbiota,” and “COVID-19 and Bone health” to integrate the topics for making this review article by searching the following electronic databases: PubMed, Google Scholar, and Scopus. Conclusion Current evidence and reports indicate the direct relation between SARS-CoV-2 infection and bone health and thus warrant future research in this field. It would be imperative to assess the post-COVID-19 fracture risk of SARS-CoV-2-infected individuals by simultaneously monitoring them for bone metabolism/biochemical markers. Importantly, several emerging research suggest that dysbiosis of the gut microbiota—GM (established role in inflammatory bone loss conditions) is further involved in the severity of COVID-19 disease. In the present review, we thus also highlight the importance of dietary interventions including probiotics (modulating dysbiotic GM) as an adjunct therapeutic alternative in the treatment and management of long-term consequences of COVID-19 on bone health.

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Bone loss in hepatitis B virus-infected patients can be associated with greater osteoclastic activity independently of the retroviral use

Cited by 6 publications

References 32 publications

Effects of Tenofovir Disoproxil Fumarate on Bone Quality beyond Bone Density—A Scoping Review of the Literature

Effects of Tenofovir Disoproxil Fumarate on Bone Quality beyond Bone Density—A Scoping Review of the Literature

Association between hepatitis A seropositivity and bone mineral density in adolescents and adults: a cross-sectional study using NHANES data

Long-term implications of COVID-19 on bone health: pathophysiology and therapeutics

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