AndrewW, thanks for yours and others feedback.Yes of course, the...

AndrewW, thanks for yours and others feedback.

Yes of course, the single best reference in regards to this that I can commend to you is:


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2873929/

That was reference 8 in that post of mine above. Worth a read but its fairly involved....if others just don't have the time, here is the crux paragraph...think of it as an Executive Summary....

This ONE paragraph supports the multiple ways our incredible drug works, multi pronged effectiveness"





The functional mechanism of pentosan for OA is as follows. In the cartilage, pentosan reduces cartilage degradation by directly and indirectly affecting inflammatory mediators such as MMP-3, IL-1 and TNF-alpha. Pentosan increased the amount of proteoglycan incorporated into the extracellular matrix. In the synovium, pentosan increases both the synthesis and the molecular weight of hyaluronan. In addition, pentosan has anti-inflammatory function and strong fibrinolytic activity, which improves the blood flow not only in the synovium but also in the subchondral bone.







Perhaps to humbly add some Mozz thoughts if I can, how does Pentosan increase this HWHA? One way certainly could be by affecting directly and indirectly the inflammatory mediators. This enforces Dr Ravi's findings of NF-kB:








In truth there is more to learn about the MOA specifically in terms of HA production...we have other clues like this possible mechanism from a different reference:


"Glucosamine therapy for OA can be expected to increase synovial HA production by providing rate-limiting substrate. In addition, certain sulfated glycosaminoglycans and polysaccharides - including chondroitin sulfate (CS), dermatan sulfate, and pentosan polysulfate - stimulate synovial HA production, apparently owing to a hormone-like effect triggered by the binding of these polymers to membrane proteins of synovial cells.¹


Lots to discover on our continuing journey.




DYOR






REFERENCE
1) https://pubmed.ncbi.nlm.nih.gov/10859690/