We were never able to get around to studying how tendons are damaged in vivo .. or how they heal up. But this and other pathologies could be quite interesting.
John Kastelic
Houston
Hi John,
Thanks for the great question - the project is still in progress... From our mouse study of hypercholesteremia and tendons, we saw that exposure of tenocytes to oxidized LDL caused them to reduce their expression of collagen, and upregulate expression of specific MMPs, which would indicate that the disease is expressed at the cellular and peri-cellular levels. This led to an overall reduction in the modulus and failure strength of the tendons. Hopefully we'll have more information about this as our studies (slowly!) progress... I share your hunch that mechanical loading could predispose to the progression of xanthoma (by creating a slightly more pro-inflammatory condition), but I think it's not necessary for the condition to develop.
Alex
In my eyes the epidermal layer of the skin as well as striated and non-striated Muscle tissue to include ligaments depending on consumption, health and familial susceptibility for a diverse ailment diagnostic and prognostic discovery and inaccurate treatment options, referrals, and choices. DSM criteria on mild/moderate/severe in psychiatry/psychology can get a proposal?
Michael S.
Back in the 70's we were given the impression that collagen and tropo-collagen were all replicated perfectly as identical molecules. The thinking was that the crosslinking and binding might be increasing with age. But with disease, that may not be the case. There could be some imperfectly replicated material which might not link an bind into fibrils quite the same. This might account for the lower modulus and strenght that apparently can accompany some disease conditions. Alternatively, one could speculate that the average size of collagen fibrils and their muco polysaccharide environment might also be alterred in some disease conditions.
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