The COVID-19 pandemic, the respiratory infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), had infected over 225 million people and had caused more than 4.5 million deaths worldwide (data of September 2021). The clinical manifestations of COVID-19 range from asymptomatic to severe forms. A mild spectrum of manifestations with a favorable prognosis is present in most patients. Nevertheless, commonly in elderly patients with several comorbidities SARS-CoV-2 infection may be exacerbated by acute respiratory distress syndrome with a consequent high risk of death. Literature data demonstrated that SARS-CoV-2 is strongly related to SARS-CoV-1, which causes the severe acute respiratory syndrome. Epidemiological data from the SARS-CoV-1 pandemic identified musculoskeletal consequences, such as myalgias, muscle dysfunction, osteoporosis, and osteonecrosis, as frequent sequelae in patients with moderate and severe forms of this disease. Recent studies also indicated significant musculoskeletal dysfunction in patients with COVID-19, although the relationship is still unclear, and few data are available. However, the presence of ACE2 and TMPRSS2, the keyholes of SARS-CoV-2, were also identified in muscle cells (vascular cells such as endothelial cells, smooth muscle cells, pericytes, muscle stem cells, macrophages, adaptive immune cells, and myonuclei), synovium cells (including fibroblasts, monocytes, B cells, and T), cartilage cells (hypertrophic, and effector chondrocytes and homeostatic chondrocytes), bone cells (osteoblasts). These findings indicate these musculoskeletal as potential sites of direct SARS-CoV-2 infection. Furthermore, corticosteroid treatment and a greater number of immunotherapies, such as IL-1 and IL-6 inhibitors, may also impact the recovery of musculoskeletal function.
This Research Topic will focus on the following themes:
1) ACE2 and TMPRSS2 expression in musculoskeletal tissues and cells
2) systemic inflammation role in bone and joint tissue physiology in patients with COVID-19
3) potential link between COVID-19 severity and musculoskeletal tissue damage
4) epidemiological data and molecular modeling and biochemical signaling studies able to identify musculoskeletal targets of COVID-19 infection
5) roles of COVID-19 therapies on musculoskeletal systems (e.g., corticosteroid and immunotherapies)
6) and COVID-19 long-term consequences on musculoskeletal systems
In this Research Topic, we welcome Original Research, Review, and Perspective articles on short-term and long-term musculoskeletal consequences in patients with mild-to-severe COVID-19 infection. Manuscripts submitted in this Research Topic should include, but not be limited to:
• ACE2 and TMPRSS2 and other human proteases related to COVID-19, e.g., furin, cathepsin L and B, elastase, trypsin and factor X, expression in musculoskeletal tissue;
• Role of systemic inflammation in bone and joint tissue physiology in patients with COVID-19, e.g. IL-1beta, IL-6, CXCL10, IL-17, TNF-alpha;
• Link between COVID-19 severity, comorbidity, age and aging, gender and musculoskeletal damage;
• epidemiological data and molecular modeling and biochemical signaling studies that identify musculoskeletal targets of COVID-19;
• Adverse effects of specific COVID-19 therapies on musculoskeletal systems;
• Post-COVID-19 syndrome (persistent symptoms at the post-viral stage of the disease) in musculoskeletal system.
With this Research Topic, we hope to promote greater insight into the potential relationship between COVID-19 and the musculoskeletal system.
The COVID-19 pandemic, the respiratory infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), had infected over 225 million people and had caused more than 4.5 million deaths worldwide (data of September 2021). The clinical manifestations of COVID-19 range from asymptomatic to severe forms. A mild spectrum of manifestations with a favorable prognosis is present in most patients. Nevertheless, commonly in elderly patients with several comorbidities SARS-CoV-2 infection may be exacerbated by acute respiratory distress syndrome with a consequent high risk of death. Literature data demonstrated that SARS-CoV-2 is strongly related to SARS-CoV-1, which causes the severe acute respiratory syndrome. Epidemiological data from the SARS-CoV-1 pandemic identified musculoskeletal consequences, such as myalgias, muscle dysfunction, osteoporosis, and osteonecrosis, as frequent sequelae in patients with moderate and severe forms of this disease. Recent studies also indicated significant musculoskeletal dysfunction in patients with COVID-19, although the relationship is still unclear, and few data are available. However, the presence of ACE2 and TMPRSS2, the keyholes of SARS-CoV-2, were also identified in muscle cells (vascular cells such as endothelial cells, smooth muscle cells, pericytes, muscle stem cells, macrophages, adaptive immune cells, and myonuclei), synovium cells (including fibroblasts, monocytes, B cells, and T), cartilage cells (hypertrophic, and effector chondrocytes and homeostatic chondrocytes), bone cells (osteoblasts). These findings indicate these musculoskeletal as potential sites of direct SARS-CoV-2 infection. Furthermore, corticosteroid treatment and a greater number of immunotherapies, such as IL-1 and IL-6 inhibitors, may also impact the recovery of musculoskeletal function.
This Research Topic will focus on the following themes:
1) ACE2 and TMPRSS2 expression in musculoskeletal tissues and cells
2) systemic inflammation role in bone and joint tissue physiology in patients with COVID-19
3) potential link between COVID-19 severity and musculoskeletal tissue damage
4) epidemiological data and molecular modeling and biochemical signaling studies able to identify musculoskeletal targets of COVID-19 infection
5) roles of COVID-19 therapies on musculoskeletal systems (e.g., corticosteroid and immunotherapies)
6) and COVID-19 long-term consequences on musculoskeletal systems
In this Research Topic, we welcome Original Research, Review, and Perspective articles on short-term and long-term musculoskeletal consequences in patients with mild-to-severe COVID-19 infection. Manuscripts submitted in this Research Topic should include, but not be limited to:
• ACE2 and TMPRSS2 and other human proteases related to COVID-19, e.g., furin, cathepsin L and B, elastase, trypsin and factor X, expression in musculoskeletal tissue;
• Role of systemic inflammation in bone and joint tissue physiology in patients with COVID-19, e.g. IL-1beta, IL-6, CXCL10, IL-17, TNF-alpha;
• Link between COVID-19 severity, comorbidity, age and aging, gender and musculoskeletal damage;
• epidemiological data and molecular modeling and biochemical signaling studies that identify musculoskeletal targets of COVID-19;
• Adverse effects of specific COVID-19 therapies on musculoskeletal systems;
• Post-COVID-19 syndrome (persistent symptoms at the post-viral stage of the disease) in musculoskeletal system.
With this Research Topic, we hope to promote greater insight into the potential relationship between COVID-19 and the musculoskeletal system.
