Acne.org Products
Hey everybody. I have some acell sheets but I've tried to use them on hidden imperfections and they haven't worked. For example:I cut out some raised freckles on my chest and followed proper procedure with the acell sheets(well, at least I tried to follow proper procedure). I've come to the conclusion that the acell sheets are impossible to use on small wounds because they simply don't fill the wound. They just lay on top and contribute nothing. The sheets weren't even degrading or changing that brownish color they're supposed to because they weren't even in contact with the wound. The sheets are probably only supposed to be used for very large wounds. So I'm going to ask again if anyone can help me find a way to grind the sheets into powder. I emailed acell and they won't reveal the information. I thought I heard somewhere(maybe even on this thread) that someone has a tutorial of how to do it...?? I tried freezing the sheets but nothing happens. Like they literally don't even get 1 degree colder which is weird. Help me find this and you'll soon find out what acell can do for you. I can be your hero. I can be the pioneer. I won't leave this thread no matter what my results are. It doesn't seem that difficult. Small injuries(the opening of scars) are the smallest injuries you can have that scar and don't regenerate. So if you aid the process with a $200 product that's job is to heal things scarlessly then you won't scar. I know other acell trials don't seem amazingly promising but they are also dealing with insane injuries. We're basically going to be healing cuts on our faces. If you find out how to make acell sheets into powdered form I can help put this ridiculous scar battle to bed. Help me help you. Thanks everyone.
and another failure of acell. and they goa
@ eternal:
no failure. only wrong treatment. sheets will not work on a small scar.
I hope the powder form will help.
NEO
Hey Neomike, I really really like to be optimistic as well. But somehow I find myself veering toward's eternal's side. I really can't be blame as if Acell is really the solution for it all, how can you explain it hasn't been used for scar revision after being released for 2 years already?
Just a thought. I'm not trying to steer anyone's mind to another particular direction. Maybe, i'm wrong, or maybe u're wrong. But im just saying, if it can work (Which I really really hope so), why hasn't it been use for scars? It's as simple as that.
I have heard many explanations for it not being used from it being a conspiracy by the medical industry to continue forcing consumers to use lasers (Which I think it's a little far fetch and is comparable to the "we have never landed on the moon" theory). Again, let me re-emphasize that I do not know the truth but it's based purely on my own personal opinion.
Another theory would be that they're still testing the potential of the product, do not want to offer 100% guarantee in case of a backfire (Does not regenerate skin perfectly). This sounds more convincing, as from the earlier photos of Acell, we see regeneration on the animals wound that is certainly very impressive without a doubt, the one on Dr Jones website was a failure. Again, maybe he didn't follow the exact procedures and did not kept the wound moist.
I think that the second explanation is likely as medical products are complex and requires extensive testing. Moreover, we do not know the exact mechanism of scarless healing and thus Acell might not want to risk a lawsuit on giving a 100% guarantee. Also, because a strict procedure has to be followed through application and the healing process, it might not produce optimal results if you do not follow instructions.
But then again still, I would think they would have a least a trial to test their product on scars (Which they never have mentioned?).
I just wish someone can shed some light on this..
Hey everybody. I have some acell sheets but I've tried to use them on hidden imperfections and they haven't worked. For example:I cut out some raised freckles on my chest and followed proper procedure with the acell sheets(well, at least I tried to follow proper procedure). I've come to the conclusion that the acell sheets are impossible to use on small wounds because they simply don't fill the wound. They just lay on top and contribute nothing. The sheets weren't even degrading or changing that brownish color they're supposed to because they weren't even in contact with the wound. The sheets are probably only supposed to be used for very large wounds. So I'm going to ask again if anyone can help me find a way to grind the sheets into powder. I emailed acell and they won't reveal the information. I thought I heard somewhere(maybe even on this thread) that someone has a tutorial of how to do it...?? I tried freezing the sheets but nothing happens. Like they literally don't even get 1 degree colder which is weird. Help me find this and you'll soon find out what acell can do for you. I can be your hero. I can be the pioneer. I won't leave this thread no matter what my results are. It doesn't seem that difficult. Small injuries(the opening of scars) are the smallest injuries you can have that scar and don't regenerate. So if you aid the process with a $200 product that's job is to heal things scarlessly then you won't scar. I know other acell trials don't seem amazingly promising but they are also dealing with insane injuries. We're basically going to be healing cuts on our faces. If you find out how to make acell sheets into powdered form I can help put this ridiculous scar battle to bed. Help me help you. Thanks everyone.
From my opinion, this could from variables like: the trauma you created was not enough to attract intercellular cells to the ecm, the ECM did not fit in the wound, the ECM was mobile in the wound by a lot of movement, maybe the sheet was denatured etc.
I only wait for something that has ' decorin' that by the way there is no product in phase of test with decorin to treat scars, this is hopeless to me. there is a product that just proposed the patent with decorin, but I believe that serious but easy to give with a biologist that needs money and to ask to him that it provides decorin to me
and also JUVISTA, that ''--- improves the scar in 30 %--- ; and my theory is that, after waiting for 1 year the scar, already improved in 30 percent, returning to apply juvista
-----(and thus to repeat the cycle 4 times in 4 years) -------
until the 100 scar is reduced almost to percent, is a theory. another thing lamentably we do not have.
and another serious interesting thing a ECM no desnaturaliced (that contains already decorina)
as it says seabs, but is none in phase of development that I know.
the ECM one that there is today for sale as acell is NOT no desnaturaliced.i don't know why,or maybe yes path , no work.
year 2010?
and we followed in the prehistory concerning regeneration of scars, and my fear is that probably this follows thus for a long time. forgive my ' realist'
hopefully the boys of the forum bring positive new features to us on we needed them to promises.
Just throwing this out there. http://reverseskinaging.com/copper-peptide...anticancer.html
Also, if this part of the article is true, then maybe we should rethink the use of Tretinoin.
Tretinoin-treated keloid-producing fibroblasts secreted more TGF-beta1 than did controls at 120 hours (P<.05). Keloid-producing fibroblasts treated with copper tripeptide secreted less TGF-beta1 than did controls at 24 hours (P<.05); a similar trend was observed in normal fibroblasts. CONCLUSIONS: Normal fibroblasts treated with tretinoin produced more bFGF than did controls, and this might partially explain the clinically observed tightening effects of tretinoin. Normal and keloid-producing dermal fibroblasts treated with copper tripeptide secreted less TGF-beta1 than did controls, suggesting a possible clinical use for decreasing excessive scar formation.
Just throwing this out there. http://reverseskinaging.com/copper-peptide...anticancer.html
Also, if this part of the article is true, then maybe we should rethink the use of Tretinoin.
Tretinoin-treated keloid-producing fibroblasts secreted more TGF-beta1 than did controls at 120 hours (P<.05). Keloid-producing fibroblasts treated with copper tripeptide secreted less TGF-beta1 than did controls at 24 hours (P<.05); a similar trend was observed in normal fibroblasts. CONCLUSIONS: Normal fibroblasts treated with tretinoin produced more bFGF than did controls, and this might partially explain the clinically observed tightening effects of tretinoin. Normal and keloid-producing dermal fibroblasts treated with copper tripeptide secreted less TGF-beta1 than did controls, suggesting a possible clinical use for decreasing excessive scar formation.
copper tripeptide = decorin?
more info about copper tripeptide: http://www.skinbiology.com/copperpeptidere...20Hair%20Growth
Just throwing this out there. http://reverseskinaging.com/copper-peptide...anticancer.html
Also, if this part of the article is true, then maybe we should rethink the use of Tretinoin.
Tretinoin-treated keloid-producing fibroblasts secreted more TGF-beta1 than did controls at 120 hours (P<.05). Keloid-producing fibroblasts treated with copper tripeptide secreted less TGF-beta1 than did controls at 24 hours (P<.05); a similar trend was observed in normal fibroblasts. CONCLUSIONS: Normal fibroblasts treated with tretinoin produced more bFGF than did controls, and this might partially explain the clinically observed tightening effects of tretinoin. Normal and keloid-producing dermal fibroblasts treated with copper tripeptide secreted less TGF-beta1 than did controls, suggesting a possible clinical use for decreasing excessive scar formation.
Nice cite I'll book mark that one too.
Regarding fibroblasts, by suppressing fibroblasts decorin has completely stopped scarring (not limited, but stopped) at 200nv, with no apoptosis to normal tissues.
It is the protein that stops your normal unwounded tissues from scarring by keeping your fibrils slender. Also after you exercise it protects your muscles from fibrosis E.g. if you exercise your body floods your muscles wioth decorin to stop fibrosis.
so 99 pages is too much to read here, what is the deal with Acell, is it FDA approved, are doctors using it, does it work?
We've seen the acell heal without scarring and a bit scarring (on a large area). However we know if an ECM is not denatured, then the fibers in the collagen will stay slender, they will aattract decorin(the stuff that keeps your non wounded tissues from scarring, the stuff that has completely stopped scarring) etc. these intercellular cells will then knit the the 100% site specific tissue, the wound will remodel like your non wounded tissues do. On the other hand if it is denatured you will get scarring the fibers will over express collagen(scar) and the body will treat the wound similar to the way it usually treats a wound.
so 99 pages is too much to read here, what is the deal with Acell, is it FDA approved, are doctors using it, does it work?
We've seen the acell heal without scarring and a bit scarring (on a large area). However we know if an ECM is not denatured, then the fibers in the collagen will stay slender, they will aattract decorin(the stuff that keeps your non wounded tissues from scarring, the stuff that has completely stopped scarring) etc. these intercellular cells will then knit the the 100% site specific tissue, the wound will remodel like your non wounded tissues do. On the other hand if it is denatured you will get scarring the fibers will over express collagen(scar) and the body will treat the wound similar to the way it usually treats a wound.
Seabs, you've said that numerous times already. Im sure everyone is familiar with the denatured ECM and its abilities already. But the main point is, who has this denatured ECM in their hands, how to get it,and who is going to use it for scar removal?
I think that is a more important question.
so 99 pages is too much to read here, what is the deal with Acell, is it FDA approved, are doctors using it, does it work?
We've seen the acell heal without scarring and a bit scarring (on a large area). However we know if an ECM is not denatured, then the fibers in the collagen will stay slender, they will aattract decorin(the stuff that keeps your non wounded tissues from scarring, the stuff that has completely stopped scarring) etc. these intercellular cells will then knit the the 100% site specific tissue, the wound will remodel like your non wounded tissues do. On the other hand if it is denatured you will get scarring the fibers will over express collagen(scar) and the body will treat the wound similar to the way it usually treats a wound.
Seabs, you've said that numerous times already. Im sure everyone is familiar with the denatured ECM and its abilities already. But the main point is, who has this denatured ECM in their hands, how to get it,and who is going to use it for scar removal?
I think that is a more important question.
Agree.
so 99 pages is too much to read here, what is the deal with Acell, is it FDA approved, are doctors using it, does it work?
We've seen the acell heal without scarring and a bit scarring (on a large area). However we know if an ECM is not denatured, then the fibers in the collagen will stay slender, they will aattract decorin(the stuff that keeps your non wounded tissues from scarring, the stuff that has completely stopped scarring) etc. these intercellular cells will then knit the the 100% site specific tissue, the wound will remodel like your non wounded tissues do. On the other hand if it is denatured you will get scarring the fibers will over express collagen(scar) and the body will treat the wound similar to the way it usually treats a wound.
Seabs, you've said that numerous times already. Im sure everyone is familiar with the denatured ECM and its abilities already. But the main point is, who has this denatured ECM in their hands, how to get it,and who is going to use it for scar removal?
I think that is a more important question.
Agree.
hey seabs....
I ask, if a oriented membrane of colagen (with a guidance of fibrillas of colagen similar to the normal skin) is applied on the skin, reduces the healing and allows regeneration? or it needs to include decorin obligatorily?
I ask this so that there is a scientist that this to test in humans with a membrane of colagen, that has the particularitity of being oriented, with a guidance similar to fibrillas of colagen of our skin.
so 99 pages is too much to read here, what is the deal with Acell, is it FDA approved, are doctors using it, does it work?
We've seen the acell heal without scarring and a bit scarring (on a large area). However we know if an ECM is not denatured, then the fibers in the collagen will stay slender, they will aattract decorin(the stuff that keeps your non wounded tissues from scarring, the stuff that has completely stopped scarring) etc. these intercellular cells will then knit the the 100% site specific tissue, the wound will remodel like your non wounded tissues do. On the other hand if it is denatured you will get scarring the fibers will over express collagen(scar) and the body will treat the wound similar to the way it usually treats a wound.
Seabs, you've said that numerous times already. Im sure everyone is familiar with the denatured ECM and its abilities already. But the main point is, who has this denatured ECM in their hands, how to get it,and who is going to use it for scar removal?
I think that is a more important question.
Agree.
hey seabs....
I ask, if a oriented membrane of colagen (with a guidance of fibrillas of colagen similar to the normal skin) is applied on the skin, reduces the healing and allows regeneration? or it needs to include decorin obligatorily?
I ask this so that there is a scientist that this to test in humans with a membrane of colagen, that has the particularitity of being oriented, with a guidance similar to fibrillas of colagen of our skin.
Hey eterna,
I'm lost in translation a little bit here, but I assume you mentioned collagen, and the fibers(fibrils) in the collagen? From the knowledge I have, our bodies regenerate when the fibrils in our collagen stays slender. Decorin keeps the fibers slender. But decorin is almost absent in new wounds and in new wounds fibroblasts over express collagen, making the fibers too thick.
renovo web page:
----
2 x within patient efficacy trials with a 12 month assessment endpoint to establish efficacy. The first of these Phase 3 trials is underway and is expected to report data in H1 2011. The second Phase 3 efficacy trial is expected to commence in H2 2011 and report data in 2013.-------
they stretch the tests until the 2013? when ready on sale juvista then? in the 2050? :-s
surely after 2013 they initiate phase 4, and later the 5 and thus... (sarcasm)
this is so dissapointing
renovo web page:
----
2 x within patient efficacy trials with a 12 month assessment endpoint to establish efficacy. The first of these Phase 3 trials is underway and is expected to report data in H1 2011. The second Phase 3 efficacy trial is expected to commence in H2 2011 and report data in 2013.-------
they stretch the tests until the 2013? when ready on sale juvista then? in the 2050? :-s
surely after 2013 they initiate phase 4, and later the 5 and thus... (sarcasm)
this is so dissapointing
any clue whats in it so we can recreate it?
opinions about this news of March of 2008? :
From The Times March 4, 2008
Renovo shares plunge as new scar prevention drug fails second trialLilly Peel Recommend? (1) Renovo lost half its value on the stock market yesterday after announcing the failure of the latest trial of Juvista, its scar prevention drug, which had been touted as a breakthrough product with a potential $12 billion (A6 billion) market.
http://business.timesonline.co.uk/tol/busi...icle3479317.ece
Hey guys,
something brand new:
http://www.ncbi.nlm.nih.gov/pubmed/2009811...mp;ordinalpos=2
So, it seams as if not only growth factors are important for scarless regeneration. Genes for neurodevelopment are important too.
Maybe this will be a better point to start with. It's really interesting. There are so many different approaches. But nothing really makes scars better. We will see.
stay tuned.
Methods of preventing or reducing scarring with decorin or biglycan
Decorin-treated wounds have been found to exhibit essentially no detectable scarring
The decorin-treated wounds were histologically normal and resembled fetal wounds in the first two trimesters.
something new from the troops:
http://www.afirm.mil/index.cfm?pageid=rese...ealing.overview
they are using autologous fat transfer. interesting.
what do you think? who will be the first with a good treatment? the military?
and here the research report from 2009:
substitute of juvidex: 'KITOSCELL' this gel like juvidex, inhibits tgf1
this document this in spanish, I could not translate it. to pay attention to the images of the scars as 30 are reduced percent in 8 months, they are results similar to those of JUVISTA tgf3.
and the best thing is than it is applied every day on the scar, is not necessary the revision. to pay attention to the photos of keloids. if it reduces keloids it reduces everything.
and the best thing of everything is than this on sale, is not a promise is a reality
http://kitoscell.com/images/Kitoscell%20Monografia.pdf
a weekly application of tca applying this gel every day I believe that it increases its effect
Methods of preventing or reducing scarring with decorin or biglycan
Decorin-treated wounds have been found to exhibit essentially no detectable scarring
The decorin-treated wounds were histologically normal and resembled fetal wounds in the first two trimesters.
lamentably it is only the patent.
there is no commercial name even..
A Novel Regenerative Tissue Matrix (RTM) Technology for Connective Tissue Reconstruction
VOLUME: 19 PUBLICATION DATE: Jun 01 2007
Sidebars_in_article:
Issue:
6
author:
John R. Harper, PhD and David J. McQuillan, PhD
The goal of regenerative medicine is to recapitulate in adult wounded tissue the intrinsic regenerative processes that are involved in normal adult tissue maintenance. Recent advances allow adult wounds to heal in a similar fashion to the regenerative healing that is also present during fetal development. Research suggests that tissue loss or injury that occurs during early fetal development can be corrected by a regenerative mechanism since fetal wound healing appears to occur without scar formation.1 However, later in the gestational development there is a transition from the regenerative to the reparative healing process, which utilizes fibrosis and scar formation to replace damaged or otherwise wounded connective tissue. Scar does not have the native structure, function, and physiology of the original normal tissue.
When a wound exceeds a critical deficit it requires a scaffold to organize tissue replacement, and 3 pathways or mechanisms of action may exist for the body to respond to the implanted material (Figure 1). A synthetic material or an extracellular matrix (ECM) that has been intentionally crosslinked to avoid enzymatic degradation will elicit a foreign body response towards the implant resulting in encapsulation. Foreign bodies have an increased potential for long-term infection and extrusion of the implant. When a temporary, resorbable synthetic or a poorly processed ECM is employed for wound closure, an inflammatory response will result in resorption of the implant with the deposition of a reparative scar to close the wound. In contrast, a regenerative tissue matrix (RTM), comprising a structurally and biochemically intact ECM implanted at the wound site, supports the appropriate cascade of cellular events characteristic of tissue regeneration ultimately leading to remodeling and transition of the RTM to tissue resembling that which was lost. Therefore, it is critical to understand these differing mechanisms of action in order to understand how the process for preparing the ECM determines which mechanism of action will be utilized by the body.
While regenerative healing is characterized by the restoration of the structure, function, and physiology of damaged or absent tissue, reparative healing is characterized by wound closure through scar formation. Reparative healing begins with the deposition of a provisional protein scaffold of fibrin as a result of hemostasis. Although transitory in nature, this fibrin scaffold serves to organize the healing process through several functional activities.2 Initial platelet activation triggers a release of growth factors and other morphogens that become deposited within the fibrin scaffold. In addition to the immobilized growth factors, this scaffold contains cell adhesion proteins that exhibit specific binding to a variety of integrin receptors found on the surface of inflammatory fibroblasts and lymphocytes. These interactions coupled with accommodative protease activity stimulate cell migration into the scaffold. The eventual fibrinolysis and matrix elaboration by the cells within the provisional scaffold along with vascularization of this new connective tissue ultimately results in scar tissue formation. This tissue has a characteristic structure, cellularity, and vascular pattern that are clearly distinguishable from the original, native connective tissue prior to injury. While scar tissue often serves a critical role in the survival of an organism, clinically it is considered a pathological state exhibiting suboptimal functional, biomechanical, and physiological characteristics compared to normal, native connective tissue.
Contrary to the formation of reparative scar, connective tissue structure and physiology are maintained through a process of intrinsic tissue regeneration.3 Connective tissue is responsible for a variety of functions in the adult human and mesenchymal stem cells that are present in the bone marrow, as well as locally within tissues, are believed to enter the circulation in small quantities ultimately localizing within tissues to provide a rapid source of cells for tissue replenishment and regeneration.4,5 Through the integrin class of cell surface receptors these cells recognize and adhere to the extracellular matrix within a tissue or organ. Once bound to specific adhesion sites within the matrix, they commit to a specialized path of differentiation by responding to local growth factors, morphogens, cytokines, as well as local biomechanical forces. Once cellular differentiation has occurred the cells begin remodeling and restoring the matrix within the tissue.
The ECM in Support of Regenerative Healing
The 3 critical constituents for tissue regeneration are an intact scaffold with the appropriate initial biomechanical properties and the capacity to support the regenerative healing process, the proper binding molecules for growth factors within the scaffold that can support cell differentiation, proliferation, and migration, and lastly, cells capable of responding to growth factors and biomechanical stimuli. As the newly regenerated tissue achieves a mature cellular and vascular status, the resident cells should respond to biological and physical stimuli by remodeling the initial scaffold into a functional, metabolic tissue that performs the function of the original tissue prior to injury.
Processing is critical for the ultimate performance of the scaffold because certain physical and chemical procedures can alter structure and destroy biochemistry, which will lead to a dramatically different mechanism of action upon placement of material in the wound. Presumably, if the scaffold contains the proper structural and biochemical components and is capable of performing as the scaffold in native tissue, the regenerative process should lead to a remodeling and transition to the appropriate tissue with minimal, if any, scarring. The properly prepared ECM must be acellular and therefore not stimulate a foreign body response, which would interfere with the dynamic equilibrium that balances synthesis, degradation, and deposition of new tissue characteristic of regenerative healing.
Regenerative tissue matrices produced using the proprietary LifeCell Technology (LifeCell Corp, Branchburg, NJ), such as GraftJacketA (Wright Medical Technologies, Memphis, Tenn) and AlloDermA (LifeCell Corp, Branchburg, NJ), are created through a process that eliminates cellular materials from human skin, which act as targets of acute immunological rejection. The remaining dermal matrix retains a structurally intact basement membrane, intact collagen fibers, and elastin-rich microfibrils for biomechanical integrity, as well as the biochemical components, such as small, leucine-rich proteoglycans (decorin and biglycan) necessary to foster angiogenesis, cellular migration and the overall intrinsic regeneration process.6a11
This monograph will review existing literature on the use of GraftJacket RTM in chronic wounds, as well as document several examples of anecdotal human clinical biopsies that indicate that it is possible to replace tissue within a defect through regeneration and transition rather than through reparative scarring.
Evidence for RTM Incorporation
In successful regenerative connective tissue replacement, the RTM becomes repopulated with the patientas cells, a mature vascular network develops and the tissue becomes so well-integrated into the patient that identification of the new tissue within a clinical biopsy becomes difficult even with employment of specialized histological stains. Since neither scar tissue nor fascia contain significant amounts of elastin microfibrils in a network organization, the Verhoeff von Giesen stain is a valuable tool to identify the location of the RTM in the context of regenerative healing as compared with reparative scarring. This approach has been used previously as a means of studying the integration of RTM into the surrounding tissue.8,12,13
The difference between an acellular matrix retaining the proper structure and one with documented structural or biochemical damage is readily visualized (Figure 2). Verhoeffas staining shows RTM with normal, organized architecture, while a human dermal ECM produced by an improper freeze drying process shows destruction of the scaffold integrity.
Clinical biopsies have been obtained from a variety of surgical applications of RTM for tissue regeneration and the samples have been studied using differential staining with hematoxylin and eosin (H&E) and Verhoeffas staining. Specimens taken by 2 surgeons from different patients at 8- and 12 months have been studied. In the first example, RTM was used to reinforce primary closure of anterior rectus fascia following ventral hernia repair. At 8 months, the patient developed another hernia adjacent to the initial RTM repair that was unrelated to the RTM repair itself. Grossly, the RTM was indistinguishable from the surrounding fascia, but a punch biopsy was taken at the midline of the initial repair through the suspected RTM tissue into the underlying rectus fascia. The tissue was cellular to an apparent cell density for fascia, vascular and well integrated with the surrounding tissue (Figure 3). A distinct tissue plane between RTM and fascia was not discernible. Upon staining for elastin, it was apparent that remnants of the RTM were present and the elastin appeared to be in the process of removal from the starting scaffold. This would be consistent with a dermal scaffold being transitioned into a fascia-like tissue. The collagen in this tissue appeared to remain intact and robust in the face of the process of elastin remodeling.
In the second example, RTM was used in a transverse rectus abdominus musculocutaneous (TRAM) flap reconstruction of a breast following mastectomy. Regenerative tissue matrix was used in the TRAM donor site to reinforce the posterior rectus fascial sheath to minimize the risk of abdominal bulging or hernia formation.14 At 12 months post reconstruction the patient required an open hysterectomy operation by another surgeon. Upon entry to the abdomen through the previous TRAM donor site, a biopsy of RTM tissue was taken that had the gross appearance of fascia. Examination of the biopsy under low magnification following H&E staining revealed a distinct plane of tissue with a robust collagen matrix, as well as a cellular and vascular density that was consistent with normal fascia and distinct from that of scar tissue. Staining for elastin demonstrated that a significant area of the fascia-like RTM tissue appeared to have been remodeled (Figure 4). Higher magnification allowed the visualization of the robust collagen network and vasculature.
Applications of RTM
Regenerative tissue matrix has been used for a variety of applications including treatment of full-thickness burns,15 soft-tissue augmentation,16 and the reconstruction of pelvic, abdominal, and chest walls.7,17 In particular, the ability to become vascularized equips the RTM with the ability to resist infection, even in the presence of contamination.18,19
Closure of tissue defects or replacement of lost tissue represents the broadest use of an RTM where the regenerative nature of the scaffold is of paramount importance to its success. Patients exhibiting multiple comorbidities, such as wound site infection, diabetes, obesity, chemotherapy, corticosteroid or radiation therapy, all of whom have a decreased ability to heal properly without complication, represent an added challenge to successful wound treatment.20
Applications of GraftJacket for the successful closure of the diabetic foot have recently been reported.21a23 Studies highlight the use of GraftJacket in challenging and compromised patients suffering from diabetes. In many of these patients microvascular occlusive disease can cause ischemia and impaired repair.24,25 Acute complications of diabetes, such as diabetic ketoacidosis,
nonketotic hyperosmolar hyperglycemia, and hypoglycemia are also detrimental to wound healing.26
In a 4-week pilot study of 40 patients, a group treated by sharp debridement followed by a single application of RTM (GraftJacket) was compared with those treated by debridement alone.21 At the end of the trial, RTM-treated wounds closed statistically faster than those treated by conventional means. Subsequently, a 16-week prospective, controlled randomized clinical study followed and compared patients in the same way.22 The authors observed 12 out of the 14 patients were healed by week 16 compared to 4 out of the 14 in the control group. Another example of the utility of RTM with this challenging patient group involved a retrospective study of deep wound healing in 17 patients with diabetes. It was reported that 14 of the 17 chronic wounds healed in the 20-week evaluation period with a single application of RTM. The mean wound duration was 8.9 A 2.7 weeks.23
Conclusion
The ability to restore structure, function, and physiology is the goal among surgeons of all specialties and may be possible through harnessing the intrinsic regenerative process in adult wound healing and tissue replacement. All biologic scaffolds are not the same because of differences in the methods used to process themamaterials that encapsulate and scar do not offer the benefits of regenerative healing but lead to suboptimal results. An RTM that is prepared properly to preserve required elements of structure and biochemistry provides a valuable resource to the clinician and enables the patient to heal by a regenerative process rather than reparative one.