Scarless Healing

6,892 posts in this topic

Think about say... when Obama's presidency began. Feels like pretty recently, right? That was more than five years ago. Time flies.

And I refer you to my above speculation that we could aquire it as soon as it is available for veterinary use which will be in a year or so.

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Pretty sure they mentioned "we expected it to be out in a year or two" because its a class 2 device or something

Edited by bloodwar44

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Now I should say I bought resveratrol but it came as powder in capsules and it doesn't seem to absorb into the skin (even when mixing with a gel) so I have started taking it orally in a total of ten capsules so far. I have observed slight improvements as verified by before and after photographs and on about a handful of spots on the scar tissue I see an improvement in the texture meaning a thinner and more "granulated" texture.

And I don't know if the improvement I have seen is because of the resveratrol and if so if it's because of that which I tried to apply directly on the skin or that which I took orally or a combination. I can say that all my scars are past the "remodeling phase" so any improvement shouldn't happen by itself other than reduction of redness which is not what I'm talking about. Keep in mind as I've said before that mine are hypertrophic so I don't know how this translates to acne.

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Upon further research, I've come to some conclusions about the differences between hypertrophic and atrophic scarring, resveratrol and decorin, and the potential use of resveratrol and decorin in scar treatment.

I had previously believed that atrophic scarring was simply an over expression of collagen, similar to hypertrophic scarring, and that the depressed appearance was a result of the scar tissue preventing the skin from stretching properly. Dissatisfied with this theory, I began to research the pathology of atrophic scarring. I was woefully disappointed in the lack of verifiable scientific explanation. Many sources claimed that, as opposed to hypertrophy, which is an excess of tissue in response to a wound, atrophy occurs when there is a loss of tissue, be it collagen, muscle, or fat. This explanation seemed logical, but I still failed to understand why, if there isn't any legitimate scar tissue in an atrophic scar, the collagen, muscle, and fat don't simply regenerate. After all, we know that collagen is capable of regenerating, as evidenced by the prevalence of hypertrophic scar tissue after a wound. If the human body was not capable of producing collagen, hypertrophic scars would not exist. And we know that muscles are capable of regenerating as well. And so, this brought me to fat tissue. Evidently, fat cells are not capable of regenerating on their own, or at least, they regenerate at a very slow rate. This would explain why atrophic scars persist in spite of a lack of dense collagen which inhibits proper regeneration. However, this does not explain why acne is more prone to scarring when picked at. Certainly, minor damage to the surface of the skin is not capable of producing loss of fat tissue.

Eager to learn more about the pathology of atrophy, I stumbled upon a research paper that further enlightened me. The research paper stated, "Fibroblasts and keratinocytes produce enzymes including those that determine the architecture of the extracellular matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs. MMPs are extracellular matrix (ECM) degrading enzymes that interact and form a lytic cascade for ECM remodeling. As a consequence, an imbalance in the ratio of MMPs to tissue inhibitors of MMPs results in the development of atrophic or hypertrophic scars. Inadequate response results in diminished deposition of collagen factors and formation of an atrophic scar while, if the healing response is too exuberant, a raised nodule of fibrotic tissue forms hypertrophic scars." [1] In other words, atrophic scarring is not a scar at all, at least not by common definition. Rather, atrophic scarring is a lack of a scar. This was an intriguing find, but disappointingly, this paper still does not answer the question of why the collagen does not regenerate, and fails to mention loss of fat tissue in the pathology of atrophy.

If this theory of atrophy proves true, it means that resveratrol and decorin may not have an effect on atrophic scarring as previously hoped for. Resveratrol and decorin improve scars primarily via destruction of collagen, which is beneficial in scars which display an over expression of collagen, but may not be beneficial in atrophic scarring. Theoretically, resveratrol/decorin-induced destruction could promote new collagen production in atrophic scarring in a similar manner to that of lasers or chemical peels. However, there is also the possibility that resveratrol and decorin could cause a worsening of the scar and its appearance by further damaging tissue.

In conclusion, it appears that the pathology of hypertrophic scarring is better understood than the pathology of atrophic scarring. I would be thankful for anyone who could point to scientific evidence and research which further clarifies the cause and pathology of atrophic scarring.

Sources:

[1] http://www.hindawi.com/journals/drp/2010/893080/#B19

Edited by Bozo
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Now I'll just add a speculation here and that is that once it's approved for veterinary use in a year from now I assume it's the same product as will later be approved for human use so I think there can be a possibility to just buy it under the pretense of treating a wounded pet but instead use it on yourself.

Not unless you have an M.D. accomplice. Excision is a requirement if you are concerned with pre-existing scars.

Edited by JT1986

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Pretty sure they mentioned "we expected it to be out in a year or two" because its a class 2 device or something

They -suddenly- interrupted the process with the acute wound trial. Had they kept on track, they could have met the timeframe quoted last summer. It's a bummer, but we can't blame them for trying to trying to break free from those "niche markets" that were quoted earlier this year.

To be honest, even I am surprised despite keeping up with them. I expected them to maintain the trials limited to controllable protocols (i.e. Let the wound close, drastically reduce the probability of infection, then remove the tissue and use the scaffold). Depending on the protocol of the new trial, they may be trying to directly apply the HG into the original wound (after removing debris, etc.) a la bacta gel. Completely unexpected.

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If animal trials starts from 2011 and end in 2015, human trials start from 2016 late or maybe even 2017 and end up in 2021 plus a year if there is any procastrination and market availability

We will get it at 2022 if everything goes smoothly i think

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Out of curiosity, what ever happened to Acell's Matristem? I've looked into it, but cannot find anything verifiable about it related to the prevention of scarring. It seems to kind of fallen out of focus, and I'm curious as to why this is. I would be interested to see if, considering that atrophic scars simply result from a loss of collagen, theoretically, injections of Matristem into the depression would repair collagen damage. If all goes well, you wouldn't even have to excise the scar. This is the promising part about atrophic scars not actually being scar tissue. You could theoretically promote growth, regrowth, and regeneration from within without damaging the skin, because there is no over expression of scar tissue preventing proper regeneration, which is the case in hypertrophic and other forms of scarring.

I'm not completely positive at this point, but I believe that atrophic scars resist healing and persist due to damage of the extracellular matrix within the skin. If you injected a foreign ECM into the depression, such as Matristem or DHG, then it should solve the issue.

Someone correct me if I'm wrong.

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@bozo, as far as i know:

1. If acne scars destroy fat and cant regenerate it is right.. yet dextran hydrogel regenerate 3rd degreee burn which is far deeper in skin than acne scars

2. Even if it ddestroy ECM, dextran hydrogel serve its function as ECM, i've read this before...

Hope my answer helps

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If animal trials starts from 2011 and end in 2015, human trials start from 2016 late or maybe even 2017 and end up in 2021 plus a year if there is any procastrination and market availability

We will get it at 2022 if everything goes smoothly i think

You are aware that the first porcine test was basically a repetition of the murine trial on a different model and that they basically spent all of 2012 and most of 2013 inactive... Right? Edited by JT1986

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If animal trials starts from 2011 and end in 2015, human trials start from 2016 late or maybe even 2017 and end up in 2021 plus a year if there is any procastrination and market availability

We will get it at 2022 if everything goes smoothly i think

You are aware that the first porcine test was basically a repetition of the murine trial on a different model and that they basically spent all of 2012 and half of 2013 inactive... Right?
Well, no im not...

I just thought it was this order :

1. Mice

2. Porcine

3. Human

Simply without repetition of the first subjects

Edited by thecureforscars

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Interesting news and thanks for posting the website, thecureforscars.

I think it's important for us to remember that while we all want the dextran hydrogel to work and be on the market ASAP, Gerecht's lab is also doing other research that likely divides her time and their resources. This year alone they have 14 published articles, some connected to the work going on with the hydrogel and some not (they're involved heavily in cancer research as well).

Also, on the subject of a timeline, going off their original quoted timeframe for approval after starting human trials (if the FDA considers the hydrogel a device) of 18-24 months that would put us somewhere in the neighborhood of 2018-2019 for when the hydrogel hits the market (if human trials start in mid-late 2016 as written on the website). It's not ideal, but quicker than many people were speculating about on the board.

Obviously, this is all just an estimate based on present information, which could change drastically. I hope they have a paper upcoming for what results they've gathered so far, but in my previous conversations with Dr. Sun he said that was unlikely (although, he works at Columbia now and at the time of the email so he could be wrong).

JT1986, have you been in direct contact with them recently?

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Golfpanther and everyone, i may have an opinion to reply Bozo as stated in my second last post, but bozo there stated that atrophic scars are different than hyperthropic and keloid scars...

We all should reconsider about this.. even if hydrogel works, our acne atrophic scar may not get the same result im afraid

What do you guys think?

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Pretty sure they mentioned "we expected it to be out in a year or two" because its a class 2 device or something

They -suddenly- interrupted the process with the acute wound trial. Had they kept on track, they could have met the timeframe quoted last summer. It's a bummer, but we can't blame them for trying to trying to break free from those "niche markets" that were quoted earlier this year.

To be honest, even I am surprised despite keeping up with them. I expected them to maintain the trials limited to controllable protocols (i.e. Let the wound close, drastically reduce the probability of infection, then remove the tissue and use the scaffold). Depending on the protocol of the new trial, they may be trying to directly apply the HG into the original wound (after removing debris, etc.) a la bacta gel. Completely unexpected.

this is very sad news, guess i was wrong to bet on hydrogels...

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This whole HG should be approved for market in 2016 to 2017, 2 to 3 years after the animal testing began in 2014. The 2 to 3 years just like has been stated a few times. As this is a class II device, all this needs is clearance from the FDA, I've read somewhere the FDA has roughly 90 days to give clearance in 510's after filing; but this should be less with this one as I'm sure this will be 510 exempt saying the ingredients in the HG are known to be safe. You only need 'one' human test protocol (say 3month) and to show the historic data, which shows safety and effectiveness. Upon clearance they will be allowed to sell the product immediately. As the HG will already be available in the vet market; I'm guessing the manufacturing jets will also be fired up upon clearance, imo, this should allow for immediate production.

Edited by seabs135

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Golfpanther and everyone, i may have an opinion to reply Bozo as stated in my second last post, but bozo there stated that atrophic scars are different than hyperthropic and keloid scars...

We all should reconsider about this.. even if hydrogel works, our acne atrophic scar may not get the same result im afraid

What do you guys think?

Don't misunderstand me, I certainly believe that DHG will be effective in the treatment of atrophic scarring. However, the most effective method of treatment can only be speculated at this point. Theoretically, DHG should be able to be injected into the depression of an atrophic scar, thus treating the scar from within. This is because, as someone mentioned before, DHG is thought to primarily treat wounds and scars via acting as a synthetic ECM. Atrophic scarring, particularly acne scarring, results from damage to the native ECM, causing collagen damage from the inside. Contrary to what many people believe, an acne scar is not damage to the external layers of the skin, but rather to the internal layers of the skin. If the damage is on the inside, then the treatment should be effective on the inside. I theorize that this is why external treatments display modest, if any effectiveness. External treatments do not penetrate into the deep layers of the skin.

And let me clarify, the fundamental difference between a hypertrophic scar and an atrophic scar is that hypertrophic scars are the result of an over expression of collagen in response to injury, while atrophic scars are the result of an under expression of collagen due to internal damage of the ECM, and incomplete healing. This is the pathology of scars as I understand it through research. It is for this reason that treatments based on resveratrol and decorin may not be beneficial in the treatment of atrophic scarring, as they work primarily by breaking down excess collagen. However, synthetic and foreign ECM's such as DHG and Matristem would theoretically be effective in the treatment of atrophic scars by providing a scaffold for cells, promoting the regeneration of collagen. DHG and Matristem would not, however, be effective in the treatment of chronic hypertrophic scarring, as the excess collagen associated with hypertrophic scarring prevents cells from penetrating into the wound site and repairing the tissue properly. If you were to treat a hypertrophic scar with a foreign ECM, you would have to excise or otherwise dissolve the scar tissue, and then apply the scaffold to promote scar free healing of the induced wound.

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What you need to understand about the hydrogel is this:

Five weeks. 35 days.

That is all it took from application to fully restored skin in the original mice study.

Meaning when human trials start in second half of 2016 (somewhere between 1 year and 7½ months and 2 years and 1½ months from now) it will only be 5 weeks after that, that they see the results and can hopefully confirm that it works 100%. After that moment my guess is that it will be a very quick rush to approval and market. Hydrogels are safe, dextran is safe. There can be very little safety worries.

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Golfpanther and everyone, i may have an opinion to reply Bozo as stated in my second last post, but bozo there stated that atrophic scars are different than hyperthropic and keloid scars...

We all should reconsider about this.. even if hydrogel works, our acne atrophic scar may not get the same result im afraid

What do you guys think?

It's something to think about but immaterial to how the dextran hydrogel would function and be used (at least based on the trials with mice, which we're all familiar with).

The only way the dextran hydrogel works is to create a wound bed through excision or dissolving the scar tissue. At that point, the type of scar that it was (since it has now been removed from the body) is irrelevant. The dextran hydrogel would then be placed on the new wound bed that had been created and allowed to do its work.

Hopefully, it would then interfere with the normal scarring pathway for human healing and lead to a path of regeneration. It's not used as an injectable into already existing scars; it needs a wound bed to function properly. Just look at the original research paper; the investigators didn't scar the mouse, wait for scar tissue to form and then inject the hydrogel into the scar. They burned the mouse, removed the damaged tissue and then place the dextran hydrogel over the wound bed. We can assume the same methodology would be applied to humans if its found to be effective in our species.

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someone should just get more efficient employees lol. how many tests do you need to do on animals that takes 2 freaking years?

its very stupid of them to delay the market time , a cure for scars would be big and all the money from lasers would go to them the faster they release.

Edited by bloodwar44

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Not just lasers but creams and gels like mederma and kelocote as well. We are talking about a billion dollar market opportunity.

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