Volume 32, Issue 1 (3-2025)
RJMS 2025, 32(1): 1-28 |
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Ghaznavi H, Shirvaliloo M, Shirvalilou S, Sheervalilou R, Rigi S. Long-term Effects of Coronavirus on Bone Health and Muscle Efficiency in Recovered Patients from COVID-19: Risk Factors, Possible Mechanisms and Therapeutic Approaches. RJMS 2025; 32 (1) :1-28
URL: http://rjms.iums.ac.ir/article-1-8629-en.html
URL: http://rjms.iums.ac.ir/article-1-8629-en.html
Assistant Professor of Molecular Medicine, Pharmacology Research Center, Zahedan University of Medical Sciences, Zahedan, Iran , sheervalilour@tbzmed.ac.ir
Abstract: (1114 Views)
Background & Aims: As of February 21, 2023, which marks the third anniversary of of the coronavirus disease or COVID-19 outbreak, more than 757 million cases have been confirmed and roughly 6.8 million deaths have been reported worldwide. COVID-19 is the third widespread disease caused by a coronavirus in the last 20 years. Although severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) had high mortality rates, they did not culminate into global pandemics.
COVID-19 is highly variable in terms of the severity of the symptoms. A cross-sectional study of 31,472 cases in China in February 2020 reported that most infected individuals (81%) developed mild to moderate disease, with 14% suffering from severe respiratory disease and 5% suffering from the critical disease. Mild symptoms include fever, respiratory symptoms (cough and sore throat), loss of taste and/or smell, headache, muscle pain (myalgia), and gastrointestinal symptoms (nausea, vomiting, and/or diarrhea). Patients with moderate disease have involvement of the lower respiratory tract with symptoms such as shortness of breath and pseudo-pneumonia with moderate intensity, which can manifest as a respiratory rate of 20-29 per minute with 94% oxygen saturation in room air at sea level. Severe type of COVID-19 can be characterized by symptoms such as shortness of breath at rest, respiratory distress, respiratory rate more than 30 times per minute, oxygen saturation ≤ 93% in room air at sea level, or arterial oxygen pressure drop to less than 300 mm Hg. It appears. Critical disease is defined by symptoms including respiratory failure, shock or multi-organ failure. People with severe and critical illness are at increased risk of death or developing complications such as arrhythmia, acute kidney injury, thromboembolic events and septic shock. Even in those who recover from a COVID-19 infection, regardless of the severity of the disease, some people have persistent symptoms, known as prolonged COVID-19.
Preliminary clinical evidence indicates an increase in vertebral fractures, blood calcium deficiency (hypocalcemia), vitamin D deficiency, and a decrease in bone mineral density in COVID-19 patients. Additionally, lower bone mineral density is associated with more severe viral infection. Preclinical models have shown bone density loss and increased osteoclastogenesis. Bone density loss associated with COVID-19 infection can be the result of many factors that directly affect bone, such as elevated inflammation, NLRP3 inflammasome activation, induction of Th17 cells, hypoxic environment, and changes in RANKL/OPG signaling.
In addition, COVID-19 can have indirect effects on the skeleton and muscles. Mechanical breakdown may occur with severe illness (such as bed rest) or with loss of body mass index and muscle wasting, which has been shown to coincide with COVID-19. Muscle wasting can also cause systemic problems that may affect bone structure. Medications used in the treat COVID-19 might also have a negative effect on bone. Ultimately, COVID-19 may also worsen conditions such as diabetes and negatively affect kidney function, all of which can contribute to bone loss and increase fracture risk. Patients with coronavirus had reduced bone mineral density, which was initially thought to be related to corticosteroid treatment. However, decreased bone mineral density was also observed in acute stage patients, suggesting that bone loss can occur independently of treatment.
Although several vaccines, including mRNA vaccines, inactivated virus vaccines, adenovirus-based vaccines, and viral protein-based vaccines are now available, patients continue to be infected with COVID-19. Significantly, those who survive COVID-19 may experience long-term side effects of the disease, known as "long haulers". Some persistent symptoms include extreme fatigue, cough, chest pain, palpitations, headache, joint pain, myalgia and weakness, insomnia, diarrhea, skin rashes, hair loss, impaired balance and gait, and neurological issues such as problems memory and concentration, and generally reduced quality of life. Recently, the long-term and systemic effects of COVID-19 infection are being investigated, as researchers and health care professionals suggest co-morbidities and treatment options for those who recover. Among the systemic effects of COVID-19 mentioned, there is evidence that bones are affected and patients may be at increased risk of fractures.
Therefore, the purpose of this review is to investigate the effects of COVID-19 on the skeletal-muscular system in people who have recovered from the disease. We describe potential risk factors, and suggest possible mechanisms by which bone loss may occur. In the following, treatment approaches are examined.
Methods: In this study, original research articles and reputable review papers were searched in the Google Scholar and PubMed databases from 2019 to 2024. The keywords used included coronavirus, bone health, muscle performance, COVID-19 recovered patients, risk factors, potential mechanisms, and therapeutic approaches.
Results: Studies have shown that the inflammatory conditions resulting from coronavirus infection have direct and indirect negative impacts on bone health and muscle performance. Numerous studies in COVID-19 survivors reported significant bone tissue loss. These articles discussed potential mechanisms, including direct involvement of bone tissue cells, pre-inflammatory responses due to the cytokine storm caused by COVID-19 and/or as a result of hypoxia and oxidative stress, effects of antiviral treatments, blood biomarkers, vitamin D deficiency, the role of steroid hormones, and disruption of normal gut flora as factors influencing bone-muscle tissue loss. Additionally, probiotics and regulatory metabolites derived from normal gut flora were introduced as available therapeutic approaches.
Conclusion: There is preliminary evidence that bone mass changes after infection with the coronavirus through multiple physiological mechanisms. Many of the identified pathways are interconnected, and inflammation acts as a common link in multiple signaling cascades, such as the RANKL/OPG pathway, NLRP3, and immune cells. In addition, the inflammatory response associated with pro-inflammatory cytokines, including interleukins and tumor necrosis factor alpha, may worsen other diseases such as renal dysfunction in addition to affecting the bone remodeling process.
The current study examines the relationship and consequences of COVID-19 on bone health and muscle strength. Several possibilities show that coronavirus affects bone health directly or indirectly. The effect on bone cells, cytokine storm and gut microbiome dysbiosis, antiviral and steroid treatments, vitamin D and probiotics are the factors affecting the severity of long-term complications of COVID-19 in those who have recovered.
COVID-19 is highly variable in terms of the severity of the symptoms. A cross-sectional study of 31,472 cases in China in February 2020 reported that most infected individuals (81%) developed mild to moderate disease, with 14% suffering from severe respiratory disease and 5% suffering from the critical disease. Mild symptoms include fever, respiratory symptoms (cough and sore throat), loss of taste and/or smell, headache, muscle pain (myalgia), and gastrointestinal symptoms (nausea, vomiting, and/or diarrhea). Patients with moderate disease have involvement of the lower respiratory tract with symptoms such as shortness of breath and pseudo-pneumonia with moderate intensity, which can manifest as a respiratory rate of 20-29 per minute with 94% oxygen saturation in room air at sea level. Severe type of COVID-19 can be characterized by symptoms such as shortness of breath at rest, respiratory distress, respiratory rate more than 30 times per minute, oxygen saturation ≤ 93% in room air at sea level, or arterial oxygen pressure drop to less than 300 mm Hg. It appears. Critical disease is defined by symptoms including respiratory failure, shock or multi-organ failure. People with severe and critical illness are at increased risk of death or developing complications such as arrhythmia, acute kidney injury, thromboembolic events and septic shock. Even in those who recover from a COVID-19 infection, regardless of the severity of the disease, some people have persistent symptoms, known as prolonged COVID-19.
Preliminary clinical evidence indicates an increase in vertebral fractures, blood calcium deficiency (hypocalcemia), vitamin D deficiency, and a decrease in bone mineral density in COVID-19 patients. Additionally, lower bone mineral density is associated with more severe viral infection. Preclinical models have shown bone density loss and increased osteoclastogenesis. Bone density loss associated with COVID-19 infection can be the result of many factors that directly affect bone, such as elevated inflammation, NLRP3 inflammasome activation, induction of Th17 cells, hypoxic environment, and changes in RANKL/OPG signaling.
In addition, COVID-19 can have indirect effects on the skeleton and muscles. Mechanical breakdown may occur with severe illness (such as bed rest) or with loss of body mass index and muscle wasting, which has been shown to coincide with COVID-19. Muscle wasting can also cause systemic problems that may affect bone structure. Medications used in the treat COVID-19 might also have a negative effect on bone. Ultimately, COVID-19 may also worsen conditions such as diabetes and negatively affect kidney function, all of which can contribute to bone loss and increase fracture risk. Patients with coronavirus had reduced bone mineral density, which was initially thought to be related to corticosteroid treatment. However, decreased bone mineral density was also observed in acute stage patients, suggesting that bone loss can occur independently of treatment.
Although several vaccines, including mRNA vaccines, inactivated virus vaccines, adenovirus-based vaccines, and viral protein-based vaccines are now available, patients continue to be infected with COVID-19. Significantly, those who survive COVID-19 may experience long-term side effects of the disease, known as "long haulers". Some persistent symptoms include extreme fatigue, cough, chest pain, palpitations, headache, joint pain, myalgia and weakness, insomnia, diarrhea, skin rashes, hair loss, impaired balance and gait, and neurological issues such as problems memory and concentration, and generally reduced quality of life. Recently, the long-term and systemic effects of COVID-19 infection are being investigated, as researchers and health care professionals suggest co-morbidities and treatment options for those who recover. Among the systemic effects of COVID-19 mentioned, there is evidence that bones are affected and patients may be at increased risk of fractures.
Therefore, the purpose of this review is to investigate the effects of COVID-19 on the skeletal-muscular system in people who have recovered from the disease. We describe potential risk factors, and suggest possible mechanisms by which bone loss may occur. In the following, treatment approaches are examined.
Methods: In this study, original research articles and reputable review papers were searched in the Google Scholar and PubMed databases from 2019 to 2024. The keywords used included coronavirus, bone health, muscle performance, COVID-19 recovered patients, risk factors, potential mechanisms, and therapeutic approaches.
Results: Studies have shown that the inflammatory conditions resulting from coronavirus infection have direct and indirect negative impacts on bone health and muscle performance. Numerous studies in COVID-19 survivors reported significant bone tissue loss. These articles discussed potential mechanisms, including direct involvement of bone tissue cells, pre-inflammatory responses due to the cytokine storm caused by COVID-19 and/or as a result of hypoxia and oxidative stress, effects of antiviral treatments, blood biomarkers, vitamin D deficiency, the role of steroid hormones, and disruption of normal gut flora as factors influencing bone-muscle tissue loss. Additionally, probiotics and regulatory metabolites derived from normal gut flora were introduced as available therapeutic approaches.
Conclusion: There is preliminary evidence that bone mass changes after infection with the coronavirus through multiple physiological mechanisms. Many of the identified pathways are interconnected, and inflammation acts as a common link in multiple signaling cascades, such as the RANKL/OPG pathway, NLRP3, and immune cells. In addition, the inflammatory response associated with pro-inflammatory cytokines, including interleukins and tumor necrosis factor alpha, may worsen other diseases such as renal dysfunction in addition to affecting the bone remodeling process.
The current study examines the relationship and consequences of COVID-19 on bone health and muscle strength. Several possibilities show that coronavirus affects bone health directly or indirectly. The effect on bone cells, cytokine storm and gut microbiome dysbiosis, antiviral and steroid treatments, vitamin D and probiotics are the factors affecting the severity of long-term complications of COVID-19 in those who have recovered.
Keywords: Corona virus (COVID-19), Bone health, Muscle efficiency, Recovered patients of COVID-19, Risk factors, Possible mechanisms, Therapeutic approaches
Type of Study: review article |
Subject:
Medical
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