Tag: scarring

Categories : Dermatology Injury & TraumaTags :

The Face Scars Less than the Body – New Study Explains Why

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Photo by Tom Jur on Unsplash

The face is privileged when it comes to scarring after injury. A Stanford Medicine study in mice not only discovers why but also finds a drug that helps skin from other sites regenerate.

Tweaking a pattern of wound healing established millions of years ago may enable scar-free injury repair after surgery or trauma, Stanford Medicine researchers have found. If results from their study, which was conducted in mice, translate to humans, it may be possible to avoid or even treat the formation of scars anywhere on or within the body.

Scarring is more than a cosmetic problem. Scars can interfere with normal tissue function and cause chronic pain, disease and even death. It’s estimated that about 45% of deaths in the United States are due to some type of fibrosis – usually of vital organs like the lungs, liver or heart.

Scars on the skin’s surface, while rarely fatal, are stiffer and weaker than normal skin and they lack sweat glands or hair follicles, making it difficult to compensate for temperature changes.

Surgeons have known for decades that facial wounds heal with less scarring than injuries on other parts of the body. This phenomenon makes evolutionary sense: Rapid healing of body wounds prevents death from blood loss, infection or impaired mobility, but healing of the face requires that the skin maintain its ability to function well.

“The face is the prime real estate of the body,” said professor of surgery Michael Longaker, MD. “We need to see and hear and breathe and eat. In contrast, injuries on the body must heal quickly. The resulting scar may not look or function like normal tissue, but you will likely still survive to procreate.”

Exactly how this discrepancy happens has remained a mystery, although there were some clues.

“The face and scalp are developmentally unique,” said professor of surgery Derrick Wan, MD. “Tissue from the neck up is derived from a type of cell in the early embryo called a neural crest cell. In this study we identified specific healing pathways in scar-forming cells called fibroblasts that originate from the neural crest and found that they drive a more regenerative type of healing.”

Activating this pathway in even a subset of fibroblasts around small wounds on the abdomen or backs of mice caused them to heal with much less scarring – similar to untreated facial or scalp wounds.

Longaker, the Deane P. and Louise Mitchell Professor in the School of Medicine, and Wan, the Johnson & Johnson Distinguished Professor in Surgery II, are the senior authors of the study, which was published January 22 in Cell. Plastic surgery resident Michelle Griffin, MD, PhD, and clinical and postdoctoral scholar Dayan Li, MD, PhD, are the lead authors of the research.

“Many of the authors on this paper are fellow physician scientists,” said Li, who is board certified in dermatology. “This project was inspired by what we’ve observed in our patients – facial wounds in general heal with less scarring. We wanted to understand, mechanistically, why this is.”

Proteins determine scarring

Li and his colleagues used laboratory mice to investigate differences in wound healing at various sites on the animals’ bodies. They anesthetised the mice before creating small skin wounds on the face, scalp, back and abdomen. The wounds were stabilised by suturing small plastic rings around them to prevent differences in mechanical forces as the animals moved. Mice were given pain relief during the healing process.

After 14 days, the wounds on the face and scalp expressed lower levels of proteins known to be involved in scar formation as compared with those on the abdomen or back of the animals. The sizes of the scars were also smaller.

The researchers then transplanted skin from the face, scalp, back and abdomen of mice onto the backs of control mice. After the transplants had engrafted, they repeated the experiment on the transplanted skin. As before, wounds in the skin transplanted from the faces of the donor mice expressed lower levels of scarring-associated proteins.

Additionally, Li and his colleagues isolated fibroblasts from skin samples from the four body sites in the donor mice and injected them into the backs of control mice. They observed reduced levels of scarring-associated proteins on the recipient animals’ backs injected with fibroblasts from the donor animals’ faces as compared with fibroblasts from the scalp, back or abdomen.

Now that we understand this pathway and the implications of the differences among fibroblasts that arise from different types of stem cells, we may be able to improve wound healing after surgeries or trauma.”

–Derrick Wan

“We found you don’t need to change or manipulate all fibroblasts within the tissue to have a positive outcome,” Li said. “When we injected fibroblasts that we had genetically altered to more closely resemble facial fibroblasts, we saw that the back incisions healed very much like facial incisions, with reduced scarring, even when the transplanted fibroblasts made up only 10% to 15% of the total number of surrounding fibroblasts. Changing just a few cells can trigger a cascade of events that can cause big changes in healing.”

A less-fibrotic wound healing

Digging deeper, the researchers identified changes in gene expression between facial fibroblasts and those from other parts of the body and followed these clues to identify a signaling pathway involving a protein called ROBO2 that maintains facial fibroblasts in a less-fibrotic state. They also saw something interesting in the genomes of fibroblasts making ROBO2.

“In general, the DNA of the ROBO2-positive cells is less transcriptionally active, or less available for binding by proteins required for gene expression,” Li said. “These fibroblasts more closely resemble their progenitors, the neural crest cells, and they might be more able to become the many cell types required for skin regeneration.”

In contrast, the DNA in fibroblasts from other sites of the body allows free access to genes like collagen that are involved in the creation of scar tissue.

“It seems that, in order to scar, the cells must be able to express these pro-fibrotic genes,” Longaker said. “And this is the default pathway for much of the body.”

ROBO2 doesn’t act alone. It triggers a signalling pathway that results in the inhibition of another protein called EP300 that facilitates gene expression. EP300 plays an important role in some cancers, and clinical trials of a small drug molecule that can inhibit its activity are underway. Li and his colleagues found that using this pre-existing small molecule to block EP300 activity in fibroblasts prone to scarring caused back wounds to heal like facial wounds.

“Now that we understand this pathway and the implications of the differences among fibroblasts that arise from different types of stem cells, we may be able to improve wound healing after surgeries or trauma,” Wan said.

The findings are likely to extend to internal scarring as well, Longaker said. “There’s not a million ways to form a scar,” he said. “This and previous other findings in my lab suggest there are common mechanisms and culprits regardless of the tissue type, and they strongly suggest there is a unifying way to treat or prevent scarring.”

By Krista Conger

Source: Stanford University Medical Center

Categories : Injury & Trauma Regenerative MedicineTags :

Hope for Severe Burns Patients with New Skin Substitutes

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A dermal matrix – one of the latest advancements to regenerate skin after severe burns.

Severe burns remain one of the most challenging injuries to treat, causing high disease and death rates worldwide, but Australian researchers have flagged some promising new approaches that could save lives and dramatically improve patient recovery.

In a comprehensive review published in Advanced Therapeutics, researchers from the University of South Australia (UniSA), University of Adelaide and Royal Adelaide Hospital (RAH) explore the latest advancements in dermal substitutes – biochemicals used to replace damaged skin – with a particular focus on combating infection and enhancing tissue regeneration following catastrophic burns.

The researchers say that despite decades of progress, traditional treatments such as skin grafting often fail to provide adequate healing and infection control, leading to prolonged hospital stays and soaring healthcare costs.

According to the lead authors Dr Zlatko Kopecki and Dr Bronwyn Dearman, the urgency to develop safer, more effective solutions has never been greater.

“Infections are a major cause of complications and mortality in burn patients,” says Dr Kopecki, a Research Fellow at UniSA’s Future Industries Institute.

“We must innovate beyond conventional methods and develop therapies that regenerate tissue while actively preventing infections.”

Each year, approximately 2423 Australians are admitted to hospital with burn-related injuries, 74% of whom require surgery, including a skin graft. Globally, 180 000 people die from burns each year, and approximately 10 million are hospitalised, costing healthcare systems $112 billion worldwide.

The review highlights that while many commercial skin substitutes exist, very few offer integrated antimicrobial protection – a critical factor given the vulnerability of burn wounds to bacterial invasion and sepsis.

The paper discusses emerging technologies such as Kerecis, a novel fish skin graft with inherent antimicrobial properties, and NovoSorb BTM, a synthetic biodegradable matrix that resists bacterial colonisation without relying on antibiotics.

Both products represent a new generation of dermal substitutes with enhanced potential to protect and heal complex burns.

Kerecis comes from wild Atlantic cod, caught from a sustainable fish stock in pristine Icelandic waters and processed using renewable energy. It stands out for retaining natural omega-3 fatty acids, which have strong antimicrobial effects and promote wound healing.

Meanwhile, NovoSorb BTM’s unique polyurethane matrix offers structural resilience even in infected wounds, providing a vital scaffold for tissue regeneration.

“These materials demonstrate a shift towards multifunctional therapies that combine structural support with infection resistance,” says Dr Dearman, Principal Medical Scientist for the Skin Engineering Laboratory at the RAH and an Adjunct Lecturer at the University of Adelaide.

“Such innovations are crucial, particularly as antibiotic-resistant infections continue to rise globally,” she says.

The review calls for the next wave of research to integrate active antimicrobial agents directly into 3D dermal scaffolds that support cell growth, reducing the reliance on antibiotics and temporary dressings.

Beyond infection control, the research points to scarless healing as the future frontier of burn care.

By combining smart biomaterials with cell-based therapies, scientists aim to regenerate skin that restores its full function – an outcome that could revolutionise the recovery for millions of burn survivors worldwide.

Source: University of South Australia

Categories : Injury & Trauma Regenerative MedicineTags :

Controlling Fibrosis with the Right Mechanical Forces

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Photo by Kampus Production: https://www.pexels.com/photo/man-in-blue-and-black-crew-neck-shirt-8638036/

The cells in human bodies are subject to both chemical and mechanical forces. But until recently, scientists have not understood much about how to manipulate the mechanical side of that equation. That’s about to change.

“This is a major breakthrough in our ability to be able to control the cells that drive fibrosis,” said Guy Genin, professor of mechanical engineering in the McKelvey School of Engineering at Washington University in St. Louis, whose research was just published in Nature Materials.

Fibrosis is an affliction wherein cells produce excess fibrous tissue. Fibroblast cells do this to close wounds, but the process can cascade in unwanted places. Examples include cardiac fibrosis; kidney or liver fibrosis, which precedes cancer; and pulmonary fibrosis, which can cause major scarring and breathing difficulties. Every soft tissue in the human body, even the brain, has the potential for cells to start going through a wound-healing cascade when they’re not supposed to, according to Genin.

The problem has both chemical and mechanical roots, but mechanical forces seem to play an outsized role. WashU researchers sought to harness the power of these mechanical forces, using a strategic pull and tug in the right mix of directions to tell the cell to shut off its loom of excess fibre.

In the newly published research, Genin and colleagues outline some of those details, including how to intervene in tension fields at the right time to control how cells behave.

“The direction of the tension these cells apply matters a lot in terms of their activation state,” said Nathaniel Huebsch, an associate professor of biomedical engineering at McKelvey Engineering and co-senior author of the research, along with Genin and Vivek Shenoy at the University of Pennsylvania.

The forces

The human body is constantly in motion, so it should come as no surprise that force can encode function in cells. But what forces, how much force and in which direction are some of the questions that the Center for Engineering MechanoBiology examines.

“The magnitude of tension will affect what the cell does,” Huebsch said. But tension can go in many different directions. “The discovery that we present in this paper is that the way stress pulls in different directions makes a difference with the cell,” he added.

Pulling in multiple directions in a nonuniform manner, called tension anisotropy (imagine a taffy pull) is a key force in kicking off fibrosis, the researchers found.

“We’re showing, for the first time, using a structure with a tissue, we’re able to stop cell cytoskeletons from going down a pathway that will cause contraction and eventual fibrosis,” Genin said.

Huebsch, who pioneered microscopic models and scaffolds for testing these tension fields that act on cells, explained that tentacle-like microtubules establish tension by emerging and casting out in a direction. Collagen around the cell pulls back on that tubule and becomes aligned with it.

“We discovered that if you could disrupt the microtubules, you would disrupt that whole organization and you would potentially disrupt fibrosis,” Huebsch said.

And, though this research was about understanding what goes wrong to cause fibrosis, there is still much to learn about what goes right with fibroblasts, connective tissue cells, especially in the heart, he added.

 “In tissues where fibroblasts are typically well aligned, what is stopping them from activating to that wound-healing state?” Huebsch asked.

Personalised treatment plans

Along with finding ways to prevent or treat fibrosis, Genin and Huebsch said doctors can look for ways to apply this new knowledge about the importance of mechanical stress to treatment of injuries or burns. The findings could help address the high fail rate for treatments of elderly patients with injuries that require reattaching tendon to bone or skin to skin.

For instance, in rotator cuff injuries, there is compelling evidence that patients must start moving their arm to recover function, but equally compelling evidence that patients should immobilise the arm for better recovery. The answer might depend on the amount of collagen a patient produces and the stress fields at play at the recovery site.

By understanding the multidirectional stress fields’ impact on the cell structure, doctors may be able to look at specific patients’ repair and determine a personalised treatment plan.

For instance, a patient who has biaxial stress coming from two directions at the site of injury will potentially need to exercise more to trigger cell repair, Genin said. However, another patient showing signs of uniaxial stress, meaning stress is pulling only one direction, any movement could over-activate cells, so in that case, the patient should keep the injury immobilised. All that and more is still to be worked out and confirmed, but Genin is excited to begin.

“The next generation of disease we’re going to be conquering are diseases of mechanics,” Genin said.

Source: Washington University in St. Louis

Categories : Cardiovascular Disease New Compounds and TreatmentsTags :

An Experimental Drug to Prevent Post-heart Attack Heart Failure

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Scientists at UCLA have developed a first-of-its-kind experimental therapy that has the potential to enhance heart repair following a heart attack, preventing the onset of heart failure. After a heart attack, the heart’s innate ability to regenerate is limited, causing the muscle to develop scars to maintain its structural integrity. This inflexible scar tissue, however, interferes with the heart’s ability to pump blood, leading to heart failure in many patients – 50% of whom do not survive beyond five years.

The new therapeutic approach aims to improve heart function after a heart attack by blocking a protein called ENPP1, which is responsible for increasing the inflammation and scar tissue formation that exacerbate heart damage. The findings, published in Cell Reports Medicine, could represent a major advance in post-heart attack treatment.

The research was led by senior author Dr Arjun Deb, a professor of medicine and molecular, cell and developmental biology at UCLA.

“Despite the prevalence of heart attacks, therapeutic options have stagnated over the last few decades,” said Deb, who is also a member of the UCLA Broad Stem Cell Research Center. “There are currently no medications specifically designed to make the heart heal or repair better after a heart attack.”

The experimental therapy uses a therapeutic monoclonal antibody engineered by Deb and his team. This targeted drug therapy is designed to mimic human antibodies and inhibit the activity of ENPP1, which Deb had previously established increases in the aftermath of a heart attack.

The researchers found that a single dose of the antibody significantly enhanced heart repair in mice, preventing extensive tissue damage, reducing scar tissue formation and improving cardiac function. Four weeks after a simulated heart attack, only 5% of animals that received the antibody developed severe heart failure, compared with 52% of animals in the control group.

This therapeutic approach could become the first to directly enhance tissue repair in the heart following a heart attack; an advantage over current therapies that focus on preventing further damage but not actively promoting healing. This can be attributed to the way the antibody is designed to target cellular cross-talk, benefitting multiple cell types in the heart, including heart muscle cells, the endothelial cells that form blood vessels, and fibroblasts, which contribute to scar formation. 

Initial findings from preclinical studies also show that the antibody therapy safely decreased scar tissue formation without increasing the risk of heart rupture – a common concern after a heart attack. However, Deb acknowledges that more work is needed to understand potential long-term effects of inhibiting ENPP1, including potential adverse effects on bone mass or bone calcification. 

Deb’s team is now preparing to move this therapy into clinical trials. The team plans to submit an Investigational New Drug, or IND, application to the U.S. Food and Drug Administration this winter with the goal of beginning first-in-human studies in early 2025. These studies will be designed to administer a single dose of the drug in eligible individuals soon after a heart attack, helping the heart repair itself in the critical initial days after the cardiac event.

While the current focus is on heart repair after heart attacks, Deb’s team is also exploring the potential for this therapy to aid in the repair of other vital organs.

“The mechanisms of tissue repair are broadly conserved across organs, so we are examining how this therapeutic might help in other instances of tissue injury,” said Deb, who is also the director of the UCLA Cardiovascular Research Theme at the David Geffen School of Medicine. “Based on its effect on heart repair, this could represent a new class of tissue repair-enhancing drugs.”

Categories : Injury & Trauma NeurologyTags :

Scarring after Spinal Cord Injury is More Complex than Previously Thought

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Fibrotic scar 14d after spinal cord injury, red – Col1a1+ perivascular fibroblast derived cells Photo: Daniel Holl

New research has found that scar formation after spinal cord injuries is more complex than previously thought. Scientists at Karolinska Institutet have identified two types of perivascular cells as key contributors to scar tissue, which hinders nerve regeneration and functional recovery. These findings, published in Natural Neuroscience, are also relevant for other brain and spinal cord injuries and could lead to targeted therapies for reducing scarring and improving outcomes.

The central nervous system (CNS) has very limited healing abilities. Injuries or autoimmune diseases like multiple sclerosis often lead to permanent functional deficits. 

Regardless of the injury’s cause, the body responds by forming a boundary around the damaged tissue, which eventually becomes permanent scar tissue. 

Two contributing cell types

While scar tissue seals the damaged area, it also prevents functional repair. After spinal cord injuries, scar tissue blocks the regeneration of nerve fibers that connect the brain with the body, resulting in paralysis after severe injuries.

The research team led by Christian Göritz at Karolinska Institutet has made significant progress in understanding how scar tissue forms in the CNS. The group now identified two distinct types of perivascular cells, which line different parts of blood vessels, as the major contributors to fibrotic scar tissue after spinal cord injury. Depending on the lesion’s location, the two identified cell types contribute differently.

“We found that damage to the spinal cord activates perivascular cells close to the damaged area and induces the generation of myofibroblasts, which consequently form persistent scar tissue,” explains first author Daniel Holl, researcher at the Department of Cell and Molecular Biology.

By examining the process of scar formation in detail, the researchers hope to identify specific therapeutic targets to control fibrotic scarring.

Categories : Injury & Trauma Regenerative MedicineTags :

Transplanted Hair Follicles Successfully Reduced Scars

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Photo by Diana Polekhina on Unsplash

By treating skin scars in three volunteers with hair follicle transplants, researchers found that the scarred skin began to behave more like uninjured skin. According to the results published in Nature Regenerative Medicine, the scarred skin harboured new cells and blood vessels, remodelled collagen to restore healthy patterns, and even expressed genes found in healthy unscarred skin.

The findings could lead to better treatments for scarring both on the skin and inside the body, leading to hope for patients with extensive scarring, which can impair organ function and cause disability.

Lead author Dr Claire Higgins, of Imperial’s Department of Bioengineering, said: “After scarring, the skin never truly regains its pre-wound functions, and until now all efforts to remodel scars have yielded poor results. Our findings lay the foundation for exciting new therapies that can rejuvenate even mature scars and restore the function of healthy skin.”

Hope in hair

Scar tissue in the skin lacks hair, sweat glands, blood vessels and nerves, impairing temperature regulation and sensation. Scarring can also hinder movement as well as potentially causing discomfort and emotional distress.

Compared to scar tissue, healthy skin undergoes constant remodelling by the hair follicle. Hairy skin heals faster and scars less than non-hairy skin- and hair transplants had previously been shown to aid wound healing. Inspired by this, the researchers hypothesised that transplanting growing hair follicles into scar tissue might induce scars to remodel themselves.

To test their hypothesis, Imperial researchers worked with Dr Francisco Jiménez, lead hair transplant surgeon at the Mediteknia Clinic and Associate Research Professor at University Fernando Pessoa Canarias, in Gran Canaria, Spain. They transplanted hair follicles into the mature scars on the scalp of three participants in 2017. The researchers selected the most common type of scar, called normotrophic scars, which usually form after surgery.

They took and microscope imaged 3mm-thick biopsies of the scars just before transplantation, and then again at two, four, and six months afterwards.

The researchers found that the follicles inspired profound architectural and genetic shifts in the scars towards a profile of healthy, uninjured skin.

Dr Jiménez said: “Around 100 million people per year acquire scars in high-income countries alone, primarily as a result of surgeries. The global incidence of scars is much higher and includes extensive scarring formed after burn and traumatic injuries. Our work opens new avenues for treating scars and could even change our approach to preventing them.”

Architects of skin

After transplantation, the follicles continued to produce hair and induced restoration across skin layers.

Scarring causes the epidermis to thin out, leaving it vulnerable to tears. At six months post-transplant, the epidermis had doubled in thickness alongside increased cell growth, bringing it to around the same thickness as uninjured skin.

The next skin layer down, the dermis, is populated with connective tissue, blood vessels, sweat glands, nerves, and hair follicles. Scar maturation leaves the dermis with fewer cells and blood vessels, but after transplantation the number of cells had doubled at six months, and the number of vessels had reached nearly healthy-skin levels by four months. This demonstrated that the follicles inspired the growth of new cells and blood vessels in the scars, which are unable to do this unaided.

Scarring also increases the density of collagen fibres, causing them to align and make the scar stiffer. The hair transplants reduced the fibre density, allowing them to form a healthier, ‘basket weave’ pattern, which reduced stiffness – a key factor in tears and discomfort.

The authors also found that after transplantation, the scars expressed 719 genes differently to before. Genes that promote cell and blood vessel growth were expressed more, while genes that promote scar-forming processes were expressed less.

Underling mechanism still unknown

It is not known how exactly the transplants brought about the change. Having of a hair follicle in the scar was cosmetically acceptable for the participants as the scars were on the scalp. The researchers are now working to uncover the underlying mechanisms so they can develop therapies that remodel scar tissue towards healthy skin, without the hair follicle transplant. They can then test their findings on non-hairy skin, or on organs like the heart, which can suffer scarring after heart attacks, and the liver, which can suffer scarring through fatty liver disease and cirrhosis.

Dr Higgins said: “This work has obvious applications in restoring people’s confidence, but our approach goes beyond the cosmetic as scar tissue can cause problems in all our organs.

“While current treatments for scars like growth factors focus on single contributors to scarring, our new approach tackles multiple aspects, as the hair follicle likely delivers multiple growth factors all at once that remodel scar tissue. This lends further support to the use of treatments like hair transplantation that alter the very architecture and genetic expression of scars to restore function.”

Source: Imperial College London

Categories : Diseases, Syndromes and ConditionsTags :

For Acne Scars in Dark Skin, Microneedling Beats Chemical Peels

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Chemical peels are a common treatment for acne scars, but a study published in the Journal of Clinical and Aesthetic Dermatology finds that, for patients with dark skin, microneedling is a significantly more effective treatment.

Researchers randomly assigned 60 patients with acne scars and dark skin (Fitzpatrick Skin Phototype IV to VI) to treatment with either 35% glycolic acid chemical peels or microneedling, both administered every two weeks for 12 weeks.

Microneedling therapy is a controlled skin injury that utilises instruments containing rows of thin needles that penetrate the dermis to a uniform depth. This induces rapidly-healing micropunctures with subsequent stimulation of collagen and elastin fibre production, resulting in skin remodelling.

Microneedling was initially developed as a tool for skin rejuvenation. However, it is now being used for a number of indications, which include: various forms of scars, alopecias, drug delivery, hyperhidrosis, stretch marks, and more. It is occasionally combined with delivery of radiofrequency energy, which is thought to enhance dermal remodelling and clinical effects. Despite its widespread use, data on the efficacy of microneedling are lacking.

Chemical peels involve applying a solution to the skin that removes the top layers.

Treatment produced an improvement of two points or more on the Goodman and Baron Scarring Grading System in 33% of patients who received chemical peels and 73% of patients who underwent microneedling.

“Based on the results of this study, patients whose darker skin precludes the use of stronger chemical peels, which can permanently discolour darker skin, should treat acne scars with microneedling,” said the study’s senior author Babar Rao, a professor of dermatology and pathology at Robert Wood Johnson Medical School. “For patients with lighter skin who can use stronger peels without risk of discoloration, chemical peels might still be the best option for some.”

Source: EurekAlert!

Categories : Injury & Trauma Regenerative MedicineTags :

New Wound Dressing Minimises Scarring

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Photo by Diana Polekhina on Unsplash
Photo by Diana Polekhina on Unsplash

A new wound dressing technology that can stop bleeding while preventing infection and scarring using a single material, has been developed. This technology also has potential applications in drug delivery, among other areas.

“Scarring is one of the worst consequences of severe wounds,” said Xiaoyang Wu, an associate professor in the Ben May Department of Cancer Research at the University of Chicago, noting that scar tissue formation is particularly common in human skin.

The researchers used a material science approach to develop a new method to overcome scarring, by impeding collagen synthesis by blocking transforming growth factor beta (TGF-β) – a cytokine that plays an important role in cell signaling, both in skin wound repair and tissue fibrosis.

“Increasing evidence suggests TGF-β is important in early phase wound repair for wound closure. But, later on, the signal may promote and enhance scarring,” Prof Wu said. This makes timing crucial. “We cannot simply block the signal, because that would slow down wound healing and would be dangerous for the patient,” he explained.

To get around this, the researchers came up with a delayed-release system combining a sutureless wound closure hydrogel material with a biodegradable microcapsule system, enabling them to control the release of the TGF-β inhibitor. “In this way, we can enhance skin wound repair and after 7-14 days can release the inhibitor that blocks the skin scarring process at the same time by using one material,” Prof Wu added.

The study results were recently published in Nature Communications.

At present, treatment of scarring is not ideal with little besides cosmetic surgery, and little can be done to prevent scar formation if a patient experiences a deep or messy wound. “The system we developed is very convenient for application,” said Wu, adding that the system has many possible future applications, such as drug delivery.

“We believe the novel system will have potential clinical importance in the future,” he said. To this end, the next steps include filing an investigational new drug (IND) application with the US Food and Drug Administration (FDA). Consistent manufacturing of the material is necessary and the researchers are exploring collaborations with pharmaceutical companies to move the research forward.

Since the system is a biocompatible material with adhesive properties, Wu said it has internal applications as well, adhering to and closing bleeding arteries and cardiac walls after irradiation with UV light. This was demonstrated in animal models, suggesting significant advantages as a traumatic wound sealant.

“Normal wound binding material does work well,” said Wu, noting that fibres are the most reliable material currently available, which, like surgical glue, is less biocompatible. “Biocompatibility is a significant advantage of our system,” he explained, “It is superior compared to current existing materials.”

Source: University of Chicago