IU researchers study long-term effects of COVID-19 on bone growth
New paper is now published in BONE
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I review the paper and associated pathways and the possible implications of this in:
Spike protein (inc vax) induced immunodeficiency & carcinogenesis megathread #6: consistent pathophysiological alterations after vaccination with COVID-19 vaccines. + New paper warns of osteoporosis.
IU researchers study long-term effects of COVID-19 on bone growth
Caitlin VanOverberghe Oct 04, 2021
SARS-CoV-2 can cause quick and significant bone lossâeven when infections of the virus that causes COVID-19 appear to be mild.
Researchers in the Department of Orthopaedic Surgery at Indiana University School of Medicine discovered that mouse models infected with the novel coronavirus lost approximately 25% of their bone mass within two weeks of contagion. They also found mouse models with a 63% increase in osteoclasts, the cells that cause bone to break down.
These changes were observed even in mice with mild and asymptomatic infections.
The study is part of ongoing coronavirus-related research being conducted by the Kacena Lab in Indianapolis, led by Melissa Kacena, PhD, the Vice Chair of Research for the Department of Orthopaedic Surgery. Findings will be published in the medical journal BONE.
The study raises questions about the lasting implications of the pandemic and the virusâs effects on the musculoskeletal system. The discovery will likely inspire further research into the potential bone loss experienced by people of all ages who contract COVID-19.
Decreased bone mass, or osteoporosis, can lead to brittle bones that are prone to breaks.
Elderly people have always been the most at-risk group for complications due to osteoporosis, because they are least likely to naturally regenerate lost bone matter. Because the elderly are also at a higher risk of contracting COVID-19, Kacena is studying if those who overcome the virus will now be even more likely to suffer broken bones.
And with more children contracting the Delta variant, further questions are raised about whether young people can develop adequate bones after contracting the virus. Humans donât reach peak bone mass until about age 25, Kacena said, and COVID-19 could be impacting normal bone development.
Kacena diverted her work to SARS-CoV-2 after several studies from across the country revealed that those dying from the coronavirus had high numbers of megakaryocytes built up in various organs, which causes significant issues.
Megakaryocytes are among Kacenaâs areas of expertise; she studies their relation to bone regeneration and fracture healing.
The Kacena Lab began using transgenic mouse models to further study the coronavirus and its relation to megakaryocytes and bone health. It was the first lab in Indiana and only one of a handful of labs in the United States to start conducting coronavirus-related experiments at this level.
Megakaryocytes are large bone marrow cells that produce platelets needed for blood clotting. The autopsies of those who died from COVID-19 have revealed significant megakaryocyte build-ups in the heart, lungs and brain. The labâs goal was to discover whether regulating megakaryocytes could change the severity of COVID-19 and decrease its morbidity and mortality.
From there, Kacenaâs researchers began questioning the other effects COVID-19 might be having on the body, particularly the musculoskeletal system. These inquiries ultimately led to the discovery of decreased bone matter in the coronavirus-infected mice.
Researchers found a 24.4% decrease in trabecular bone volume fraction; a 19.0% decrease in trabecular number; a 6.2% decrease in trabecular thickness; and a 9.8% increase in trabecular separation.
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So - did they determine the causative factor? Is this spike?
If spike, then can we expect to see this problem in the injected?
Inquiring bears would like to know. (it may be rhetorical)
Thanks Carp. I have a question, because I have a problem with this "asymptomatic infection" term. When the study states "These changes were observed even in mice with mild and asymptomatic infections.", does this mean that the mouse caught Covid through mucosal infection and went on to develop this bone issue while not showing any covid symptoms. OR, was the mouse injected with Covid? If the mouse was injected with Covid, then it stands to reason that the mouse would not be showing symptoms, but woudl still be suffering from the effects of the covid virus throught the parts of the body that received the injected virus. Also, when they inject the mouse is the dsed according to size in comparison to the dose that a human would generally pick up through normal infection?
Not being picky, just generally inquizative to the specifics.
Cheers