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Inflammatory signs of arthritis are not affected by the removal of osteoclasts, suggesting that osteoclasts are strictly linked to bone damage but not to the inflammatory features of arthritis.
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The upper extremities also experience bone damage but to a much lesser extent.
These findings support the theory that bone damage is not exclusively a consequence of synovitis [ 7].
However, direct bone damage does not seem to be essential, given that inhibition of the activity of the osteoclasts did not prevent bone formation in animal experiments [ 6].
These results suggest that MRI bone oedema may be a pre-erosive feature and that bone damage may not be coupled with joint inflammation in PsA.
There was damage, but not outright destruction.
In rheumatoid arthritis (RA), bone damage on radiographs presents not only as erosions but also as periarticular osteoporosis.
Interestingly, a combination of Scl-Ab with TNFi was necessary to achieve repair, whereas inhibition of either Scl-Ab or TNFi alone only blocked progression of bone and cartilage damage but could not reverse it.
Interestingly, a study examining a murine model of premature aging that exhibits increased nuclear DNA damage due to deficiency of a repair enzyme found a significant increase in age-related bone loss but not in cartilage damage [ 87].
Some were damaged but not devastated.
The experiments presented here employed intra-cardiac injection, which does not cause bone damage directly and the resulting metastatic foci in these experiments are likely to involve relatively few cells.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com