Climate change, environmental pollution, and virus epidemics have sharply increased the number of patients suffering from respiratory diseases in recent years. Prolonged periods of illness and drug use increase the occurrence of complications in these patients. Osteoporosis is the common bone metabolism disease with respiratory disturbance, which affects prognosis and increases mortality of patients. The problem of osteoporosis in patients with respiratory diseases needs more attention. In this review, we concluded the characteristics of osteoporosis in some respiratory diseases including COPD, asthma, COVID-19, tuberculosis, and lung cancer. We revealed that hypoxia was the common pathogenesis of osteoporosis secondary to respiratory diseases, with malnutrition and corticosteroid abuse driving the progression of osteoporosis. Hypoxia-induced ROS accumulation and activated HIF-1α lead to attenuated osteogenesis and enhanced osteoclastogenesis in patients with respiratory diseases. Tuberculosis and cancer also invaded bone tissue and reduced bone strength by direct infiltration. For the treatment of osteoporosis in respiratory patients, oral-optimized bisphosphonates were the best treatment modality. Vitamin D was a necessary supplement, both for calcium absorption in osteogenesis and for improvement of respiratory lesions. Reasonable adjustment of the dose and course of corticosteroids according to the etiology and condition of patients is beneficial to prevent the occurrence and development of osteoporosis. Additionally, HIF-1α was a potential target for the treatment of osteoporosis in respiratory patients, which could be activated under hypoxia condition and involved in the process of bone remodeling.

Extrapulmonary complications of different organ systems have been increasingly recognized in patients with severe or chronic Coronavirus Disease 2019 (COVID-19). However, limited information on the skeletal complications of COVID-19 is known, even though inflammatory diseases of the respiratory tract have been known to perturb bone metabolism and cause pathological bone loss. In this study, we characterize the effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on bone metabolism in an established golden Syrian hamster model for COVID-19. SARS-CoV-2 causes significant multifocal loss of bone trabeculae in the long bones and lumbar vertebrae of all infected hamsters. Moreover, we show that the bone loss is associated with SARS-CoV-2-induced cytokine dysregulation, as the circulating pro-inflammatory cytokines not only upregulate osteoclastic differentiation in bone tissues, but also trigger an amplified pro-inflammatory cascade in the skeletal tissues to augment their pro-osteoclastogenesis effect. Our findings suggest that pathological bone loss may be a neglected complication which warrants more extensive investigations during the long-term follow-up of COVID-19 patients. The benefits of potential prophylactic and therapeutic interventions against pathological bone loss should be further evaluated.

The use of standard procedures for the diagnosis of osteoporosis and assessment of fracture risk significantly decreased during the COVID-19 pandemic, while the incidence of fragility fractures was mostly unaltered. Both COVID-19 per se and its treatments are associated with a negative impact on bone health. Preclinical models show that mice infected with SARS-CoV2 even without symptoms display loss of trabecular bone mass two weeks post infection, due to increased numbers of osteoclasts. Osteoporosis medications do not aggravate the clinical course of COVID-19, while preclinical data suggests possible beneficial effects of some therapies. While vitamin D deficiency is clearly associated with a worse clinical course of COVID-19, evidence of improved patient outcome with vitamin D supplementation is lacking. Osteoporosis treatment should not be generally discontinued, and recommendations for substituting therapies are available. Osteoporosis therapies do not interfere with the efficacy or side-effect profiles of COVID-19 vaccines and should not be stopped or indefinitely delayed because of vaccination.

Aim The COVID-19 pandemic has influenced the management of many chronic conditions including osteoporosis as resources are re-allocated to urgent care. Methods This mini-review summarizes the effects of COVID-19 on diagnosis and management of osteoporosis. Evidence regarding possible effects of osteoporosis medications on COVID-19 outcomes and the relationship of COVID-19 vaccination to osteoporosis care is reviewed. Finally, initiation and maintenance of osteoporosis treatment during the pandemic are highlighted. Results The use of standard procedures for the diagnosis of osteoporosis and assessment of fracture risk significantly decreased during the COVID-19 pandemic, while the incidence of fragility fractures was mostly unaltered. Both COVID-19 per se and its treatments are associated with a negative impact on bone health. Osteoporosis medications do not aggravate the clinical course of COVID-19, while preclinical data suggests possible beneficial effects of some therapies. While vitamin D deficiency is clearly associated with a worse clinical course of COVID-19, evidence of outcome improvement through vitamin D supplementation is lacking. Osteoporosis treatment should not be generally discontinued, and recommendations for substituting therapies are available. Osteoporosis therapies do not interfere with the efficacy or side-effect profiles of COVID-19 vaccines and should not be stopped or indefinitely delayed because of vaccination. Conclusion The diagnosis and management of osteoporosis are challenging during the COVID-19 pandemic. Osteoporosis medications are safe and effective and should be continued. Further studies will elucidate the impact of the COVID-19 pandemic on long-term bone health.

Extrapulmonary complications of different organ systems have been increasingly recognized in patients with severe or chronic Coronavirus Disease 2019 (COVID-19). However, limited information on the skeletal complications of COVID-19 is known, even though inflammatory diseases of the respiratory tract have been known to perturb bone metabolism and cause pathological bone loss. In this study, we characterized the effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on bone metabolism in an established golden Syrian hamster model for COVID-19. SARS-CoV-2 causes significant multifocal loss of bone trabeculae in the long bones and lumbar vertebrae of all infected hamsters. The bone loss progressively worsens from the acute phase to the post-recovery phase. Mechanistically, the bone loss was associated with SARS-CoV-2-induced cytokine dysregulation which upregulates osteoclastic differentiation of monocyte-macrophage lineage. The pro-inflammatory cytokines further trigger a second wave of cytokine storm in the skeletal tissues to augment their pro-osteoclastogenesis effect. Our findings in this established hamster model suggest that pathological bone loss may be a neglected complication which warrants more extensive investigations during the long-term follow-up of COVID-19 patients. The benefits of potential prophylactic and therapeutic interventions against pathological bone loss should be further evaluated. Abstract Figure Graphical abstract SARS-CoV-2 infection causes pathological bone loss in golden Syrian hamsters through induction of cytokine storm and inflammation-induced osteoclastogenesis.

Purpose The coronavirus disease 2019 (COVID-19) has both directly and indirectly affected osteoporosis diagnosis and treatment throughout the world. Methods This mini-review summarizes the available evidence regarding the effects of COVID-19, its treatment, and the consequences of the pandemic itself on bone health. Additionally, we review evidence and expert recommendations regarding putative effects of osteoporosis medications on COVID-19 outcomes and vaccine efficacy and summarize recommendations for continuation of osteoporosis treatment during the pandemic. Results The use of standard screening procedures to assess for osteoporosis and fracture risk declined dramatically early in the pandemic, while rates of fragility fractures were largely unchanged. COVID-19, its treatments, and public health measures to prevent viral spread are each likely to negatively affect bone health. Osteoporosis treatments are not known to increase risk of adverse events from COVID-19, and preclinical data suggest possible beneficial effects of some therapies. Vitamin D deficiency is clearly associated with adverse outcomes from COVID-19, but it remains unclear whether vitamin D supplementation may improve outcomes. Osteoporosis treatment should be continued whenever possible, and recommendations for substituting therapies, if required, are available. Conclusion The COVID-19 pandemic has decreased screening and disrupted treatment for osteoporosis. Osteoporosis medications are safe and effective during the pandemic and should be continued whenever possible. Further studies are needed to fully understand the impact of the COVID-19 pandemic on long-term bone health.