problem solving exercise can a skin wound turn deadly

• Publications Podiatry Today Today's Wound Clinic Wound Management & Prevention Wounds

Keeping Them Moving: How Activity Benefits the Healing Patient

by Hy-Tape International

Maintaining an active lifestyle is critical to good health; this is especially true for patients recovering from wounds or extended hospital stays. Robust activity can improve mental health, reduce the risk of infection, and accelerate wound healing. 1 Staying active can be challenging for patients with wounds, however, and it is critical that health care professionals take steps to enable their patients to stay as active as possible.

The Healing Benefits of Activity

Aside from the long-term benefits to heart health, mental health, and longevity, exercise provides many direct and indirect benefits to patients healing from wounds. Physical activity can promote rapid wound healing, reduce oxidative damage, and promote a healthy lifestyle. This can improve patient outcomes and reduce the costs of treatment. 1

Exercise Benefits Mental Health – There is ample evidence that exercise promotes good mental health, reduces the effects of depression, and causes people to report a greater level of happiness. These effects are especially important for those who have had an extended stay in a hospital or who are in a long-term care facility because these populations may be at greater risk of developing mental health problems. 2

Exercise Reduces Inflammation – Inflammation is one of the major causes of delayed healing. Research shows that wounds with low levels of inflammation heal much more quickly and completely. Exercise and other physical activity have been shown to reduce the level of inflammatory markers in the blood, thus helping to reduce the level of inflammation and promote rapid healing. Reduced inflammation may also provide palliative benefits by decreasing pain and discomfort in wounds. 1

Exercise Reduces Oxidative Damage – Exercise and other physical activity have also been shown to prevent damage from free radicals, thereby further helping to promote rapid healing. This is particularly important in populations such as the older adults and diabetic patients, who may have elevated levels of free radicals. 1

How to Keep Patients Active

Although there are many benefits to staying active, it is often difficult for patients with wounds. Pain, difficulty keeping wound dressings in place, and damage from ultraviolet (UV) light can all pose challenges. Health care professionals can help encourage their patients to stay active by following wound care practices that minimize the impact on patients’ mobility and way of life.

Encourage Activity – Health care professionals should regularly talk to their patients about their activity level and encourage them to engage in activities that are safe and comfortable for them. Whether it is swimming, running, or taking a short walk around their room, every activity helps. By having an open conversation about the importance of staying active and about the patient’s capabilities, it is possible to help patients heal faster and stay safe.

Use Longer-Lasting Dressings and Adhesives – Dressing changes can be time consuming and frustrating, particularly when dressings become loosened during physical activity. By using dressings and medical adhesives that stay secure longer, it is possible to minimize this issue.

Protect from UV Damage – UV damage can delay wound healing and cause irritation. A dressing and adhesive that protect patients from the sun will allow patients to go outside without fear of impeding their healing.

Keep Dressings Waterproof – Vigorous exercise can produce a large amount of sweat. This can cause major problems for many dressing adhesives, which may come loose if exposed to water. Adhesives that are waterproof allow patients to exercise without fear of losing their dressings.

Keeping patients with wounds active can be challenging, but it is not an insurmountable task. By talking to patients about their abilities and choosing medical dressings with adhesives suited to vigorous exercise, health care professionals can help their patients maintain an active life and promote rapid healing.

1. Keylock K, Young H. Delayed wound healing: can exercise accelerate it?. Int J Exerc Sci. 2010;3(3):70–8.

2. Craft LL, Perna FM. The benefits of exercise for the clinically depressed. Prim Care Companion J Clin Psychiatry. 2004;6(3):104–11.

About the Company

Hy-Tape International offers high-quality adhesive tape and has served the market for 70 years. Tapes are available in strips, patches, and kit rolls giving health care providers a wide range of options for securing dressings and devices. Free product samples are available at www.hytape.com or by calling 1-800-248-0201.

Industry Voices is brought to you by health care industry sponsors. All content is developed and paid for by the sponsoring company. Kestrel Health Information, Inc. is not involved in the creation of this content. 

The views and opinions expressed in this blog are solely those of the author, and do not represent the views of WoundSource, HMP Global, its affiliates, or subsidiary companies.

More from this Author

Helicoll® skin substitute: unique biocompatible scaffold that allows the growth of cells and blood vessels within 4 to 5 days resulting in accelerated skin tissue regeneration.

Diabetic Foot Ulcers: Topical Management Strategies

Secondary Wound Dressing Application: Tips to Extend Wear Time

From the blog.

Latest News

Subscribe to the WoundSource eNewsletter

The latest in wound care delivered to your inbox every Friday.

Follow WoundSource

Tweets by WoundSource

Ohio State nav bar

The Ohio State University

• BuckeyeLink
• Find People
• Search Ohio State

Study: Exercise Helps Speed Wound Healing In Older Adults

COLUMBUS , Ohio – The body's ability to heal even small skin wounds normally slows down as we age. But a new study in older adults finds that regular exercise may speed up the wound-healing process by as much as 25 percent.

“This is the first time we've been able to document this kind of enhancement associated with exercise,” said Charles Emery , a professor of psychology and the lead author of the Ohio State University study.

The faster that a wound heals, the less chance it will become infected.

The results appear in a recent issue of the Journal of Gerontology: Medical Sciences .

The study included 28 healthy older adults ranging in age from 55 to 77 (average age was 61). The participants hadn't exercised regularly for at least six months prior to the study. For the research, about half (13) of them exercised three times a week for three months. The other 15 participants served as controls and were asked not to change their physical activity habits during the study period.

Each subject received a small puncture wound on the back of the upper arm. Adults in the exercise group started working out about a month before the wound procedure; this gave their bodies enough time to adapt to a regular exercise program.

The wounds were about 1/8-inch across and deep. The researchers photographed the wounds three times a week until the wounds were no longer visible (about six to seven weeks).

The exercise sessions began with 10 minutes of warm-up floor exercises and stretching followed by 30 minutes of pedaling on a stationary bike. After that, participants either jogged or walked briskly on a treadmill for 15 minutes, followed by about 15 minutes of strength training. All sessions ended with five minutes of cool-down exercises.

At the end of the study, the researchers found that skin wounds healed an average of 10 days faster in the people who exercised (29 days in the exercise group versus 39 days in the non-exercise group.)

Each participant completed assessments of exercise endurance and stress at the beginning and end of the study. The exercise endurance test, completed on a treadmill, measured each subject's aerobic fitness level by measuring how much oxygen he or she consumed while working out.

The researchers also collected saliva samples from each participant in order to measure levels of cortisol, a primary stress hormone. High cortisol levels indicate that the body is under stress; prior studies have suggested that exercise is associated with lower levels cortisol.

Lastly, each subject completed a questionnaire called the Perceived Stress Scale. This scale let the researchers determine how stressful the respondents perceived their lives to be.

At the end of the study, the researchers found that skin wounds healed an average of 10 days faster in the people who exercised (29 days in the exercise group vs. 39 days in the non-exercise group.)

Not surprisingly, exercise endurance increased in the group that worked out, but remained the same in the non-exercise group.

The researchers were somewhat surprised to find a sharp increase in cortisol levels in the exercise group. The hormone is typically boosted by stress, and other studies have suggested that exercise may lower levels of stress.

“The stress of exercise may enhance the regulation of cortisol,” Emery said. “This increase in cortisol levels may represent a biological pathway by which exercise helps wounds heal.”

There were no changes in perceived stress in either group but none of the adults in this study reported any significant distress in their lives at the beginning of the study.

The current study supports the results of a related study on wound healing conducted at Ohio State a few years ago. That work compared wound-healing rates between older adults caring for a loved one with Alzheimer's disease to rates of older adults who weren't caregivers.

The healing rates of those who weren't caregivers was similar to the healing rates of the non-exercisers in the current studying – wounds in both groups healed in about 40 days. Wounds among older caregivers took about 20 percent longer to completely heal.

“The findings from both studies indicate that the effect of exercise we found in the current study truly represents an enhanced rate of wound healing in older adults,” Emery said.

The next step is to determine if older adults who report a fair amount of stress in their lives – such as dealing with the death of a spouse or financial troubles – get the same kind of benefit from exercise.

Emery conducted this study with Ohio State colleagues Janice Kiecolt-Glaser , professor of psychiatry and psychology; Ronald Glaser , director of both the Center for Stress and Wound Healing and the Institute for Behavioral Medicine Research ; William Malarkey , associate director of the Center for Stress and Wound Healing; and David Frid, who is currently with Pfizer, Inc.

Support for this work came from several organizations within the National Institutes of Health : the National Heart, Lung and Blood Institute ; the National Institute on Aging ; the National Institute of Dental and Craniofacial Research ; the National Cancer Institute ; and the National Center for Research Resources .

Contact: Charles Emery, (614) 688-3061;

[email protected]

Written by Holly Wagner, (614) 292-8310; [email protected]

Contact: Admissions | Webmaster | Page maintained by University Communications

Request an alternate format of this page | Web Services Status | Nondiscrimination notice

A monthly newsletter from the National Institutes of Health, part of the U.S. Department of Health and Human Services

Search form

October 2023

Print this issue

To Heal a Wound

Helping the Skin Fix Itself

You’ve likely had countless cuts and scrapes in your life. Normally, when you get a small skin wound, your body can repair it quickly. But sometimes, the repair process doesn’t work properly. If this happens, even a tiny tear in the skin can have trouble healing. That can lead to pain and distress and pose a risk for dangerous—or even deadly—infections.

Wounds that don’t heal for three months or more are called chronic wounds. Your risk for getting a chronic wound increases with age. But there are ways you can help your body to heal.

Rebuilding Skin

When you have an open wound, blood can get out of the body, and germs can get in.

“So the body’s goal is to seal that wound as quickly as possible,” says Dr. Maria Morasso, a skin biology researcher at NIH.

This normally involves an orderly series of steps. First, a clot forms over the wound to prevent blood loss. Next, cells from the immune system The system that protects your body from invading viruses, bacteria, and other microscopic threats. move into the area. These remove dead and damaged cells from the wound. This makes room for new, healthy cells. Immune cells also fight off any germs in the area, like bacteria. This process causes inflammation—heat, swelling, and redness—around the wound.

The body next starts to make new cells to replace the damaged tissue. Finally, your skin begins to heal and creates a scar. This process is called remodeling.

Too much scarring can cause problems after a wound heals. Large scars may prevent nearby muscles and joints in the body from working properly. Scientists are looking for ways to help minimize this scarring.

Not all tissues in the body scar, explains Dr. Kaitlyn Sadtler, who studies the immune system at NIH. For example, the liver and the tissues inside the mouth can heal perfectly. Her lab and others are studying these tissues to find ways to coax other organs to grow back better.

Roadblocks to Healing

There are different ways the wound-healing process can go wrong. For example, too little or too much inflammation can lead to problems, Morasso explains.

Too much inflammation can damage nearby tissue. It can also prevent immune cells in a wound from working the way they’re supposed to.

If immune cells aren’t working properly or if there’s too little inflammation, new tissue may not form over the wound. Then your body may not be able to protect itself from germs. If germs get into a wound, infection can set in. Untreated infections can lead to serious complications and become life-threatening.

Health conditions that interfere with blood flow around a wound can also affect the healing process. These conditions include diabetes or problems with blood vessels, such as varicose veins. Smoking, obesity, and aging can also make wounds heal more slowly. Slow healing can put you at higher risk of developing a chronic wound.

If you have diabetes, getting your blood glucose (or blood sugar) under control is crucial for healing, explains Dr. Geoffrey Gurtner, a surgeon who specializes in wound healing at the University of Arizona. High blood glucose levels “make a wound-healing problem much worse,” he says.

People with diabetes are at high risk of developing chronic wounds on their feet called foot ulcers. So it’s important to wear well-fitted shoes and check your feet regularly. This is true for everyone with diabetes, whether or not your blood glucose is under control, Gurtner says. But it’s especially important if you have nerve damage to your feet.

People with blood vessel problems may be advised to wear compression stockings to help stop small wounds from forming. And everyone can take steps to keep small cuts and scrapes clean and healthy. See the Wise Choices box for more about wound care.

If you have a wound that won’t heal, talk with your doctor. They may consider removing some of the old, damaged tissue to start the healing process again. Or, they may give you special bandages or antibiotics. Some people may need surgery to place new skin over the wound or a special type of cast.

But new treatments are needed to help chronic wounds heal better, Gurtner says.

Finding New Treatments

Researchers are working to develop new ways to treat chronic wounds. Morasso and her team are comparing mouth wounds—which heal very rapidly—with normal skin wounds and nonhealing wounds.

Her team’s recent study showed that diabetic foot ulcers lacked two proteins that are found in wounds that heal normally. Because the proteins were missing, immune cells weren’t able to move into the wounds.

“If we can find key proteins, we could target them with drugs to increase or decrease them as needed,” says Morasso. “This could help boost healing.”

Sadtler and her lab are studying how biomaterials can help wound healing. Biomaterials can be made from substances found in the human body or synthetically designed. Her team is testing whether biomaterials can be engineered to release different drugs at different times. These drugs would draw different immune cells into a wound in the order they’re needed for healing.

“Immune cells are the body’s defenders. But they’re also the construction workers that help build new tissues,” Sadtler explains. “We’re looking at how we can use them to heal wounds and prevent scar tissue.”

Researchers are working on “smart bandages” that could help wounds heal, too. These use features like electrical stimulation to boost wound healing. Smart bandages can also monitor wounds for signs of infection in real time.

Gurtner and others recently tested smart bandages in mice. They found that wounds underneath the bandage healed faster than those covered with a normal dressing.

“I think we’re going to see this type of bandage in the clinic in the near future,” Gurtner says.

For now, he encourages anyone with a wound that’s not healing to ask their doctor for a referral to a wound-care center if possible.

“These exist in most communities now,” he says. “Having the kind of coordinated care they provide really makes a big difference for helping wounds heal.”

Related Stories

All About Acne

3D Repairs for Damaged Skin

Focus on Your Feet!

Learn About Burn Care

NIH Office of Communications and Public Liaison Building 31, Room 5B52 Bethesda, MD 20892-2094 [email protected] Tel: 301-451-8224

Editor: Harrison Wein, Ph.D. Managing Editor: Tianna Hicklin, Ph.D. Illustrator: Alan Defibaugh

Attention Editors: Reprint our articles and illustrations in your own publication. Our material is not copyrighted. Please acknowledge NIH News in Health as the source and send us a copy.

For more consumer health news and information, visit health.nih.gov .

For wellness toolkits, visit www.nih.gov/wellnesstoolkits .

How Exercise Affects Your Skin, The Good And Bad

On Assignment For HuffPost

Does it really need to be said that exercise is good for you? The list of ways in which it’s beneficial is long and varied, from building muscle to improving your mood ― to maybe even giving you more radiant skin .

But while exercise helps keep skin healthy, it can also irritate your outer layer, causing breakouts. And hives. And rashes. And infections. Workouts can lead to acne and redness and a whole host of other issues. Fortunately, there are ways to mitigate these effects (and they’re pretty easy, too).

First, let’s start with the how and why exercise benefits your skin.

How working out may positively impact your skin

“Exercise has innumerable benefits for the body overall and especially for our skin,” said Corey L. Hartman , a board-certified dermatologist and founder of Skin Wellness Dermatology in Birmingham, Alabama.

Most of that good has to do with the way your workout gets your heart pumping. “During exercise, the heart rate increases and improves blood circulation, which helps to deliver oxygen and nutrients to the skin,” Hartman told HuffPost. “This rush of oxygen and nutrients promotes the development of collagen to prevent skin sagging and regenerates new skin cells to keep the skin glowing and exfoliating properly.”

While the verdict is still out on just how much exercise can improve the visual appearance of your skin, early evidence shows promise for overall skin health, wound healing and anti-aging, according to Jordan V. Wang, a dermatologist at Laser & Skin Surgery Center of New York . Like Hartman, Wang said that increased blood flow to the skin is one big benefit, explaining that nutrient-rich blood can “flush out unwanted byproducts of skin cells and contribute to having a healthy glow.”

The anti-inflammatory effects of exercise may play a positive role as well. “Too much inflammation can contribute to damaging key proteins in our body, which can affect normal and healthy functioning,” Wang said. This may extend to the skin too, although Wang was clear that more research is needed to determine exactly how far these benefits go.

Brian B. Adams , a board-certified dermatologist, chair of dermatology at the University of Cincinnati College of Medicine, and the university’s director of sports dermatology, was less enthusiastic when asked about the particular benefits that exercise might have for skin. “People always ask me this question,” he said. “There are no direct beneficial effects on the skin from exercise. People who have recently worked out might have an erythematous glow and some people think that that looks good.”

How exercise can negatively affect your skin

Without appropriate precautions, your workouts can cause new skin problems and exacerbate existing conditions.

“Exercise can increase sweat, and that can cause certain skin conditions to flare,” Hartman said. These may include acne, eczema and folliculitis, an inflammation of hair follicles. “Moist conditions on our skin can encourage the normal bacteria that live on our skin and function positively to suddenly overgrow, clogging pores and leading to pus bumps and painful acne nodules,” he said.

The combination of sweat, tight-fighting clothing and high friction can also bring problems. “For example, rashes in folded areas, such as the inner thighs, knees and elbows, can worsen with chronic rubbing from running or weight lifting routines,” Wang said.

How to mitigate these issues while still getting in your workouts

Fortunately, there are ways to minimize the bad so you can reap more of the good.

Before you work out, apply emollients or thick creams that provide a barrier to protect areas experiencing high friction, like those aforementioned inner thighs, knees and elbows. If you’ll be outside, make sure to wear SPF to prevent sun damage. Wang even suggests wearing a product with antioxidants — especially if you’re in a city — to protect against pollution.

After exercise, washing your face can remove the buildup of sweat, oil and environmental pollutants that may lead to acne, but getting out of your clothes and into a shower is even better. “The best way to control the negative effects of exercise on skin is to remove all sweaty workout clothes as quickly as possible after a workout, especially those that are tight-fitting. ... Taking a shower promptly after a workout also helps to keep bacteria numbers manageable,” Hartman said.

Shedding those compression pants, in particular, can be helpful in preventing folliculitis, which often shows up as red, pimple-like bumps on your butt. “Use of a benzoyl peroxide wash in the shower a few times per week can also prevent these bumps from occurring,” Wang said.

And if you’re noticing drier skin, that may be due to sodium-rich sweat. While a shower will help rinse the sweat off (and moisturizer will help rehydrate skin), Adams goes one step further and suggests skipping soap when it comes to your arms, legs, back and chest. “Only water needs to hit these areas to keep you clean,” he shared, adding that you should still make sure you’re soaping up your face, underarms and groin.

For more insidious problems, like infections, foot fungus and warts, Adams advises that you always wear foot protection in locker room showers and surrounding areas, where viruses and fungi can hide. For more extreme cases, take some time off from working out and call your doctor.

These days, your skin may develop an additional irritation: mascne (that’s acne caused by wearing a mask). Safely exercising outside your home now often means that a mask is needed, which doesn’t make skin happy. “[Masks] function much like tight-fitting workout clothes and keep all the oil, bacteria and sweat in place where they can band together to clog pores and cause acne,” Hartman said.

Mascne can be mitigated by always wearing a clean mask and by cleaning your skin soon after a workout.

Adams has seen many cases of rosacea over the last year, too. “Heat is one of the major triggers of rosacea and one’s breath is nearly 100 degrees,” he said. “So when someone constantly exposes their face to 100-degree heat because the mask contains that temperature, they risk flaring the number of bumps and degree of redness on their cheeks, chin and nose.”

Even without a mask, exercise can worsen rosacea due to the heat and increased circulation. Those prone to rosacea should try to reduce overheating when they can.

While exercise’s list of potential negatives for your skin may be long, don’t let that keep you from working out. The benefits of exercise on the body are clear, and the outlook is good that some of those positives may extend to the skin. With some extra care (and a good shower), you’ll reap the benefits of the post-workout glow a little longer.

From Our Partner

Huffpost shopping’s best finds, more in life.

COVID-19: What you need to know about the current coronavirus outbreak

• General Dermatology
• Cosmetic Dermatology
• Skin Cancer

Clinical Research Institute

• Insurance Information
• Patient Forms
• Care Instructions
• Awards & Honors
• Outreach Program

Top 5 Benefits of Exercise for Skin Health

September 22, 2020

The coronavirus (COVID-19) pandemic has resulted in some challenging life changes for many of us. From transitioning to working at home to teaching kids at the dinner table, life has been a little different for many of us since March. However, the life changes we’re experiencing during the pandemic haven’t all been negative. Many of us are getting to spend a little more quality time with our families. Additionally, people are using their saved commute times to make some positive health changes, including eating better and improving exercise routines. For patients at U.S. Dermatology Partners who struggle with chronic skin conditions, there may be questions about how exercise will impact skin health. According to Dr. Amy McClung of U.S. Dermatology Partners Brodie Lane in Austin, Texas , “Many people think that exercising has a negative effect on their skin. Teens with acne, especially, worry about this. However, with proper care, exercising isn’t bad for your skin at all, in fact, it can be good for your skin health. During annual skin exams with a dermatologist, patients should ask for personalized skincare recommendations to ensure health while exercising.” In this blog, you can learn more about some of the many benefits of exercising for your skin and whole-body health and the steps you can take to keep your skin looking and feeling great.

According to Dr. McClung, “I  know that people with sensitive or acne-prone skin and those with chronic conditions like rosacea or psoriasis may be concerned that exercise will only lead to skin issues, but exercise is an important part of a healthy lifestyle for everyone. That includes people with skin health concerns. Even though you may need to adjust your skincare routine slightly, exercising regularly has fewer negative effects than positive for your skin’s health.” Below, Dr. McClung walks through just five of the benefits of exercise for skin health.

1 – Improved Blood Flow to Nourish Cells

When we exercise, the blood is pumped through our body, working our heart muscles and circulating blood and oxygen. This increased blood flow during exercise can also result in improved circulation even when you’re not exercising. That means all of our body’s cells, including skin cells, are nourished by this blood flow, leading to improved vitality and more effective cellular repair and replacement.

2 – Improved Blood Flow Removes Toxins from Skin

In addition to more effectively delivering vital nutrients to the body’s cells, improved blood flow also means toxins are removed from the body more efficiently. According to Dr. McClung, “If you think about your bloodstream as a highway for your cell’s essential nutrients and waste removal, exercise increases the highway speed, which means that all the nutrients are getting where they need to be more quickly and waste or toxins are leaving the cells more quickly. So, your cells are getting more of what they need and being less affected by potentially damaging waste by-products and toxins. It’s a win-win for all of our cells, including those that make up our skin.”

3 – Decreased Stress Improves Outcomes for Chronic Skin Conditions

The U.S. Dermatology Partners blog has recently featured posts about the negative impact of stress on skin and hair, especially for those who suffer from chronic skin conditions like acne, eczema, rosacea, and psoriasis. Stress triggers numerous physiological responses within the body that can cause breakouts, inflammation, and allergic skin reactions. Exercise actually decreases the body’s elevated hormonal and immune responses to stress. This can minimize the risk of chronic skin condition breakouts and flare-ups. It also keeps the immune system healthy and better able to respond if needed to combat skin and whole-body health concerns.

4 – Prevent & Reverse the Signs of Aging

A research study that examined the skin of individuals who were 65 and older revealed some impressive findings. The study took a base sample of the community members’ skin. Then, these individuals were asked to maintain a moderate aerobic exercise routine for three months. When testing the skin after the three month exercise period, the findings were remarkable. The skin of the individuals who were exercising more frequently closely resembled healthy skin for individuals of much younger ages, between 20 and 40. In the past, dermatologists believed that exercising could help to keep skin looking healthier, but this recent research tells us exercising may actually make it possible for you to turn back the clock for your skin. With just thirty minutes of aerobic exercise each day, you may just start looking younger.

Dr. McClung says, “I love telling patients that exercising may help them to look younger! There is more and more scientific evidence supporting the fact that appropriate exercise keeps people looking younger for longer. That being said, if you’re exercising outdoors, it’s important to take steps to protect your skin from sun damage. Additionally, extremely exhausting and overtaxing exercise routines may also have negative effects on the skin’s appearance as well as damaging overall health. You should talk to your physician or a trainer about exercise routines that are appropriate for you.”

5 – Improved Overall Health Places Less Stress on Skin

Finally, we know that our skin is a barrier organ that protects the rest of the body from potential damage. Unfortunately, when the immune system is engaged in keeping the body healthy due to poor health, our skin health will suffer.  Regular exercise is an essential part of maintaining good whole-body health, which means your body has the necessary nutrients available to keep skin looking and feeling its best.

Tips for Maintaining Skin Health as You Exercise

According to Dr. McClung, “People with chronic skin conditions like acne or eczema may see a temporary flare-up when they start exercising, but in the long term, these conditions typically improve. I know it can be frustrating to deal with a breakout, but it’s worth it to achieve the long term benefits.” Some of the steps you can take to protect your skin health while maintaining an exercise routine are included below:

• Clean skin – After you exercise, you should take a shower whenever possible. Use gentle skin cleansers on the whole body, and don’t forget to wash your face.
• Dress appropriately – Wear loose-fitting, moisture-wicking clothing to avoid issues like chafing, irritation, and rashes.
• Wear sunscreen – If you’re exercising outdoors, it’s essential to apply sunscreen of SPF 30 or higher (and reapply at least every two hours). Whenever possible, avoid exercising outdoors during the peak sun exposure hours between 10 am and 4 pm.
• Treat skin – If you notice your skin is chafing, rashes appear, or blisters form, make sure you treat these skin conditions right away. Additionally, you should take steps to treat flare-ups or breakouts in chronic skin conditions like eczema, rosacea, psoriasis, and acne based on your dermatologist’s recommendations.

Visit U.S. Dermatology Partners for Annual Skin Exams

When you’re ready for an annual skin exam, the U.S. Dermatology Partners team would love to see you. You can schedule an in-office skin exam using our simple online scheduling request form .

If you’re not ready to visit us in the office, especially if you’re in a high-risk patient category, we are continuing to offer online teledermatology services. You can quickly and easily get started with your online visit by filling out our virtual appointment request form or calling the U.S. Dermatology Partners location near you.

Find a location near me

Featured provider.

Amy McClung, MD, FAAD

Search Blog Posts

Most Popular

• What Is the Safest Tattoo Removal?
• What Is Microneedling?
• Top Ways to Prevent and Treat Acne Scars
• The Best Facial Anti-Aging Products and Procedures

Our Locations

Find a location near me, featured blog posts, u.s. dermatology partners announces the opening of second granbury, texas office.

Granbury, Texas – U.S. Dermatology Partners is pleased to announce the opening of a second office location in Granbury, Texas. ...

U.S. Dermatology Partners Awarded Best Company Outlook Award By Comparably

Dallas, Texas - U.S. Dermatology Partners Awarded Best Company Outlook Award By Comparably...

U.S. Dermatology Partners Welcomes Juan Estrada, MD to Kyle, Texas

Kyle, Texas – U.S. Dermatology Partners is pleased to welcome Board-Certified Dermatologist Dr. Juan Estrada to their Kyle, Texas office....

Red Light Therapy: A Revolutionary Approach to Skin and Health

Red light therapy is considered one of the newest and most innovative skin rejuvenati...

Ready to Get Started?

Find a Location

Request an Appointment

Find a Service

Find a Provider

COVID-19 Information

Sign Up for Our Newsletter!

Get the latest updates on news, specials and skin care information.

• Email This field is for validation purposes and should be left unchanged.

Popular Conditions & Treatments

Skin Cancer Treatment

Botox and Injectables

Annual Skin Examinations

Eczema and Dermatitis

Moles and Warts

Acne Treatments

• Privacy Policy |
• Non-Discrimination Policy |

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

• Publications
• Account settings

Preview improvements coming to the PMC website in October 2024. Learn More or Try it out now .

• Advanced Search
• Journal List
• Cold Spring Harb Perspect Med
• v.5(1); 2015 Jan

Wound Healing and Skin Regeneration

Makoto takeo.

1 The Ronald O. Perelman Department of Dermatology, New York University, School of Medicine, New York, New York 10016

2 Department of Cell Biology, New York University, School of Medicine, New York, New York 10016

The skin is a complex organ consisting of the epidermis, dermis, and skin appendages, including the hair follicle and sebaceous gland. Wound healing in adult mammals results in scar formation without any skin appendages. Studies have reported remarkable examples of scarless healing in fetal skin and appendage regeneration in adult skin following the infliction of large wounds. The models used in these studies have offered a new platform for investigations of the cellular and molecular mechanisms underlying wound healing and skin regeneration in mammals. In this article, we will focus on the contribution of skin appendages to wound healing and, conversely, skin appendage regeneration following injuries.

In adult skin, wound healing causes scar tissue that lacks appendages; however, some skin appendages (e.g., hair follicles) may serve important roles during the healing process.

The skin is an intricate structure composed of the epidermis and dermis, including the subcutaneous fat, or dermal adipocyte layer. Environmental challenges to the barrier include penetration of harmful UV rays from the sun, invasion of harmful pathogens, and evaporation of water. Importantly, the skin also protects the underlying organs, a function necessary for the survival of the organism. As a protective shield for the body from the external environment, the skin is constantly exposed to potential injury, and thus wound healing is a vital process for the survival of all higher organisms. Epidermal appendages such as hair follicles, nails, and sweat glands help maintain and protect the skin and their important roles in wound healing continue to be elucidated. Better understanding of the cellular and molecular mechanisms underlying wound healing will ultimately allow us to influence and accelerate the wound repair/regeneration process. This will benefit severe burn patients and amputees, especially in cases of extensive tissue loss and scarring.

Wound healing is a conserved evolutionary process among species and encompasses spatially and temporally overlapping processes including inflammation, blood clotting, and cellular proliferation and extracellular matrix (ECM) remodeling ( Seifert et al. 2012b ; Richardson et al. 2013 ). However, the outcome of wound healing in the skin differs between species. Some lower vertebrates including fish (zebrafish) and amphibians (axolotl and Xenopus ) possess the ability to perfectly regenerate skin. It is known that after full-thickness excisional wounds in Xenopus froglets and axolotols, the entire skin, including secretory appendages, regenerates ( Yokoyama et al. 2011 ; Seifert et al. 2012b ). During this process, even the pigmentation pattern of the skin can be fully re-established ( Seifert et al. 2012b ). Zebrafish skin can also recover its striped pigmentation pattern following wounding, as well as regenerate subcutaneous adipocytes and scales during the healing process, making the regenerated skin almost indistinguishable from the original one ( Richardson et al. 2013 ).

In contrast, it is challenging for adult mammals, including humans, to achieve such regeneration. Typically, wound healing in adult mammals results in scar tissue that lack skin appendages. Although scar formation can meet the requirements of the skin’s fundamental function in preventing infection and dehydration, this process can also be unfavorable. Because of its obviously distinct appearance from the original intact skin, the scar formed as a result of injuries or burns can result in devastating cosmetic and psychological consequences, reducing the quality of life of the individual. Furthermore, skin appendages are an integral part of the skin’s biological and physiological function. For example, skin epithelial appendages contribute epidermal cells for wound healing. Additionally, the hair follicle and sebaceous gland confer additional roles for the skin as sensory and thermoregulatory organs ( Chen et al. 1997 ; Li et al. 2011 ). Consequently, scar formation prevents the complete recovery of skin function. Thus, the ability to restore the skin to its original state is highly valued. Interestingly, studies have reported remarkable examples of scarless healing in fetal skin and appendage regeneration in adult skin following the infliction of large wounds. The models used in these studies have offered a new platform for investigations of the cellular and molecular mechanisms underlying wound healing and skin regeneration in mammals. These may provide important insights into the regeneration of missing structures and redevelopment of fully functional skin. In this chapter, we will focus on the contribution of skin appendages to wound healing and, conversely, skin appendage regeneration following injuries.

RE-EPITHELIALIZATION AND EPITHELIAL STEM CELLS

The mammalian epidermis is a stratified squamous epithelium whose maintenance relies on proliferation and differentiation of the basal layer of the epidermis. As basal epidermal cells differentiate and move toward the surface, they give rise to suprabasal cells and the granular layer and eventually terminally differentiate into enucleated corneocytes composing the stratum corneum. As the outermost layer of the organism, the epidermis is constantly exposed to multiple forms of injury. Failure to re-epithelialize injured skin causes the loss of the barrier function of the organ, dehydration, infection or even death. Hence, rapid closure of the wound site by migration and proliferation of epithelial cells is critical to restore the barrier function that is vital for organism survival. A vast amount of evidence now shows that the presence and function of resident epithelial stem cells in adult skin fuel the re-epithelialization process.

Mascré et al. (2012) used two distinct promoters: Keratin14 that targets basal cells in the epidermis including a progenitor population that proliferates and differentiates, and Involculin that solely targets a committed progenitor cell population. Following wounding, both populations are recruited to the wound area but it is predominantly progeny of Keratin 14 expressing cells that survive long term, in contrast to progeny of Involculin expressing cells that were lost earlier. This study illustrates the importance of relatively undifferentiated cells in the basal layer of the skin epithelium, and their contribution to epidermal repair following injury.

Lineage tracing with mice that ubiquitously labels all keratinocytes of follicular origin ( Shh-Cre;R26R-lacZ ) showed that follicular cells can be converted to epidermal cells ( Levy et al. 2007 ). Several distinct progenitor populations located in the hair follicle, including the bulge, upper bulge, hair follicle junctional zone next to the sebaceous gland and infundibulum have all been shown to contribute to the regenerating skin. Using label retaining techniques to trace the fate of slow cycling stem cells in the skin, hair follicle stem cells located in the bulge area of the hair follicle were shown to mobilize to the upper follicle ( Taylor et al. 2000 ) and then to the skin epidermis after wounding ( Tumbar et al. 2004 ). Consistent with these findings, transplantation studies have also shown that the bulge region from R26-LacZ adult vibrissal follicles can contribute progenitors to reform the hair follicle, sebaceous gland, as well as the epidermis ( Oshima et al. 2001 ). Subsequently, genetic tracing of Keratin 15 expressing epithelial stem cells located in the bulge/secondary hair germ region of the hair follicle showed that these cells migrate to the epidermis toward the center of the wound following full-thickness exisional wounds ( Ito et al. 2005 ; Levy et al. 2005 ). Genetic ablation of K15 + cells does not result in defects in normal epidermal homeostasis suggesting that they only shift to epidermal cells in response to wounding. This illustrates that wounding perturbs epidermal homeostasis by cell depletion, resulting in recruitment of epithelial cells in the hair follicle that give rise to epidermal cells to promote re-epithelialization. Following migration to the epidermis, K15 + epithelial stem cell progeny acquire an epidermal phenotype based on biochemical marker analysis. However, the observation that most of these cells disappear in the wound epidermis suggests that hair follicle bulge stem cells are primarily involved in the acute cell injury phase of wound repair ( Fig. 1 ).

Contributions of hair follicle stem cells to re-epithelialization. ( A ) Schematic illustration of bulge stem cell markers that contribute to re-epithelialization. ( B ) Lineage tracing of K15 + hair follicle stem cells after excisional wound using K15-LacZ mice. LacZ-positive cells were not found in IFE at 2 d after wounding ( right panel). At 5 d, LacZ + cells start to migrate from hair follicle to wound center ( middle panel). At 8 d after wounding, re-epithelialization is completed and about 26% of re-epithelialized cells are lacZ + ( left panel). (From Ito et al. 2005 ; reprinted, with permission.)

Lrig1 was the first marker identified for the junctional zone (isthmus) between the hair follicle bulge, sebaceous gland and infundibulum ( Jensen et al. 2009 ). Lrig1 expressing cells can give rise to all adult epidermal lineages in skin reconstitution assays ( Jensen et al. 2009 ). In contrast, more recent genetic labeling analysis revealed that Lrig1 + cells within the pilosebaceous unit contribute to neither the hair follicle nor the interfollicular epidermis, but solely the sebaceous gland or infundibulum during homeostasis ( Page et al. 2013 ). After wounding, Lrig1 cells originating from the pilosebaceous compartment migrate to the wound area and persist up to 1 year in the regenerating IFE, and contribute permanently to the regenerating tissue following wounding ( Page et al. 2013 ). Similarly, Lgr6-positive cells identified in the isthmus area are shown to contribute to re-epithelialization ( Snippert et al. 2010 ). Isolation of Lgr6-positive cells enabled them to reconstitute all of the epithelial lineages of the skin and form hair follicle bearing skin when combined with inductive dermal cells in transplantation assays. Genetic tracing showed that Lgr6 + cells give rise to epidermis and participate in the hair follicle formation seen in the center of the wound. Lgr6 + cells persisted long term in the wound area suggesting that these cells have the ability to maintain or reacquire the self-renewing capacity following exit from their original niche within the isthmus. These studies establish that progenitors residing in compartments other than the bulge including the isthmus and junctional zone convert into self-sustaining epidermal stem cells in response to trauma. Furthermore, the study by Brownell et al. (2011) showed that Gli1 + upper bulge cells contribute to the epidermal healing to establish long-term progenitors following wounding. Interestingly, following skin denervation, Gli1 + cells can still contribute to the initial re-epithelialization but they are not maintained in the regenerated epidermis. These results suggest that Gli1 + K15 − upper bulge cells depend on a perineural stem cell niche for their ability to adopt epidermal stem cell fate after wounding. These studies suggest that extrinsic niche derived signals may determine the ability of follicular keratinocytes to become long-term epidermal progenitors after migrating from the hair follicle. Currently, it is not known how much the re-epithelialized area is occupied by epithelial stem cells nor how they are patterned in the re-epithelialized layer. Understanding these may provide a platform to investigate mechanisms of how cells from distinct lineages show different persistence in the new epidermis. Moreover, understanding the extent of how the adult skin epidermis is capable of regenerating stem cells will define whether re-epithelialization in wounded mammals represents the true regeneration process.

Although these studies established that hair follicle epithelial stem cells contribute to re-epithelialization, a recurring question has been whether the hair follicle is necessary for wound healing of hair bearing skin. A study that experimentally addressed this entailed wounding Edaradd cr/cr mice that lack hair follicles in the tail skin ( Langton et al. 2008 ). They showed that the tail skin of these mutant mice do not close their wounds as efficiently as control tail skin containing hair follicles. However, after an initial lag period, the wound re-epithelializes at the same rate. From these results, it was concluded that hair follicle cells accelerate the onset of wound healing but are not necessary for wound healing. The relevance of hair follicles to wound healing was also shown by a study that investigated the influence of hair cycle stages on the rate of wound healing. Ansell et al. (2011) showed that wound-healing rates were different depending on the hair cycle stage, in which wound healing was faster, during the anagen phase of hair follicle cycling in vivo. This was likely caused by the extensive blood vessel network, relative immunosuppression, reduction in cell adhesion genes, and increase in developmental pathway genes by follicular epithelial cells during the anagen stage compared with the telogen stage. This is consistent with another study that showed that anagen hair follicles produce angiogenic factors ( Mecklenburg et al. 2000 ). More recently, it was shown that mice deficient for the proapoptotic Sept4 /ARTS gene have elevated numbers of hair follicle stem cells as a result of reduced apoptosis ( Fuchs et al. 2013 ), which normally occurs in the catagen phase ( Ito et al. 2004 ). Sept4 /ARTS− / − mice display significant improvement in wound healing. Furthermore, this phenotype depended on K15-expressing hair follicle stem cells as indicated by lineage tracing.

Taken together, these studies illustrate the vital function of hair follicles as a cellular reservoir for healing skin and as a signaling center that affects the behavior of nonhair follicle cells.

SCARLESS WOUND-HEALING PROCESS IN MAMMALS

In association with re-epithelialization, the restoration of dermis takes place by migration and proliferation of fibroblasts. The response of fibroblasts during wound healing determines the outcome of tissue repair. In response to wounding, macrophages and fibroblasts release growth factors that lead to further fibroblast migration and proliferation. They also release inflammatory cytokines to induce the immune response to protect against external pathogens in the wound. These fibroblasts also produce collagens and other extracellular matrix proteins to aid in wound repair. While collagen and ECM deposition are required to close the wound efficiently, they are also deleteriously responsible for fibrosis and scarring of the skin. Recent studies have shown an essential role for intradermal adipocytes in fibroblast activation and migration ( Schmidt and Horsley 2013 ), suggesting that multiple cell types in the dermis function to activate the fibroblast proliferation and migration necessary to repair the dermis. Recently, transplantation and lineage tracing have identified two distinct dermal lineages that give rise to the upper and lower dermis, respectively. Following wounding, both cell types are recruited to the wounded area. One population forms the lower dermis in the initial injury response. In contrast, the progeny that gives rise to the upper dermis is recruited during re-epithelialization and provides an environment for new hair follicle formation in the wounded area. This study illustrates the importance of the dermal contribution to not only wound healing, but also to appendage regeneration ( Driskell et al. 2013 ).

In 1970, a seminal article reported that rabbit fetuses can heal wounds without the appearance of scar formation ( Somasundaram and Prathap 1970 ). Since then, similar observations have been reported in other mammals, including sheep, mice, rats, and humans ( Somasundaram and Prathap 1970 ; Burrington 1971 ; Sopher 1972 ; Rowlatt 1979 ; Hallock 1985 ). In Somasundaram and Prathap’s study ( Hallock 1985 ), a 0.5-cm disc of skin of either newborn or fetal (14–25 d after gestation) rabbits was excised. In newborn rabbits, wound contraction and scab formation are observed by 6 days after wounding, resulting in granulation tissue development and scar formation. In contrast, a compact layer of spindle-shaped cells, two to three cells thick, initially covered the fetal wound surface. There was no apparent sign of wound contraction, subsequent granulation tissue development, or scar formation. These pioneering studies did not describe or discuss whether and how skin appendage regeneration accompanied the scarless wound healing, presumably because of limitations in distinguishing between embryonic development processes of skin appendages and wound-induced de novo regeneration of skin appendages at that time.

Since then, scar-free wound healing of human fetuses was reported in 1979 ( Rowlatt 1979 ), and subsequent efforts have been directed at investigating the mechanisms underlying scar-free wound healing by comparing the wound-healing processes between scarless and scarring wounds in multiple animal models. A key difference identified in fetal wound healing is a low inflammatory reaction owing to the absence of a fully developed immune system. In scarless wounds, neutrophils, macrophages, and mast cells have differences in size and maturity when compared with scarring wounds ( Satish and Kathju 2010 ; Wulff et al. 2012 ). Intriguingly, Urodeles such as newts, capable of perfectly regenerating multiple organs including the skin and limb, are immunodeficient compared with other amphibians such as Xenopus that show a more limited ability to regenerate (reviewed by Cohen 1971 ). The correlation between the immune system and competence for regeneration led to a traditional hypothesis in wound-healing studies: inflammation may restrict regeneration by promoting fibrosis and scar formation.

The inflammatory response marks one of the earliest responses in the adult skin to wounding stimuli, and a number of studies have shown that immune cell infiltration and signaling play a key role in scar formation and fibrosis. Immune cells and macrophages accumulate at a wound site not only to fight against invading microorganisms but also to produce various growth factors such as FGFs and TGF-β to guide re-epithelialization, fibroblast repopulation and ECM remodeling. Therefore it is plausible that scarring or fibrosis during skin repair is promoted by cytokines or growth factors produced by the inflammatory response. However, a similar cocktail of growth factors sufficient to promote scar formation may also be provided by skin resident cells even in the absence of a well-developed immune system. In contrast to the seminal work by Barbul et al., which showed that immunodeficient Foxn1 null adult mice that lack T lymphocytes close wounds without scar formation ( Barbul et al. 1989 ), subsequent studies in other immunodeficient mouse models, such as Rag1-deficient mice and SCID (severe combined immune deficiency) mice, which lack both B and T lymphocytes, showed that wounds on these mice heal with scar formation ( Gawronska-Kozak et al. 2006 ). Similarly, it is reported that thymus-depleted mice and mice treated with immunosuppressants also heal with scar formation ( Gawronska-Kozak et al. 2006 ). These results suggest that scar formation is not merely dependent on the degree of the lymphocyte-mediated inflammatory response to wounding.

In efforts to identify the distinct molecular characteristics in scarless wound healing, Dang et al. (2003) analyzed the expression of matrix metalloproteinases (MMP) and their inhibitor TIMPs in scarless wounds and scarring wounds in rats. They made full-thickness excisional wounds on the dorsum of E16 and E19 fetal rats in which wounds heal without or with scars, respectively. They compared gene expression of MMPs and TIMPs at 24, 48, and 72 h after wounding and found that scarless wounds have greater MMP expression relative to TIMPs in wounds that heal with a scar. More recently, Colwell et al. made excisional wounds on the dorsal back skin of E17 fetal mice and 3-wk-old postnatal mice, respectively. They compared gene expression profiles between scarless fetal wounds and scarring postnatal wounds by microarray at 1, 12, and 24 h, and found that upregulation of genes involved in DNA transcription and repair, cell-cycle regulation, protein homeostasis, and intracellular signaling is detected more rapidly in response to wounding in fetal wounds ( Colwell et al. 2008 ). Additionally, comparisons of scarless fetal wounds and adult wounds report that one of the most prominent and consistent differences between the two is the high expression of TGF-β3 in mouse and rat fetus ( Cowin et al. 2001 ; Soo et al. 2003 ). Shah et al. showed that administration of exogenous TGF-β3 into the dermis at the margins of a full-thickness wound for 3 days reduced monocyte and macrophage accumulation in the wound area, resulting in reduced scar formation with decreased fibronectin and collagen I and III deposition in the early stages of wound healing ( Shah et al. 1995 ). These studies suggest that production of TGF-β3 may be a key factor to achieving scar-free wound healing. These basic animal studies pave the way to clinical trials to control scar formation in humans, which show that injection of recombinant human TGF-β3 after injury or surgical removal of scar tissue significantly reduces scar formation ( Occleston et al. 2008 ; So et al. 2011 ). Despite these advancements, there is still no treatment that completely prevents scar formation and induces regeneration of skin appendages including hair follicles.

REGENERATION OF SKIN APPENDAGES—HAIR FOLLICLE NEOGENESIS

Several of the molecular and cellular events that orchestrate mammalian wound healing have been elucidated over the past several years. However, there is still a lack of therapeutic interventions that lead to perfect scarless skin regeneration that includes appendages in the adult skin. Research aimed to influence the wound repair process to promote regenerative healing requires experimental models in which molecular and cellular interactions can be efficiently dissected. Previous studies established that de novo hair follicles form in the wound area by recapitulating embryonic hair follicle development, illustrating the remarkable regenerative capacity of the adult skin ( Ito et al. 2007 ). Moreover, this phenomenon occurred in normal wild-type mice and therefore serves as a powerful model to study how growth and patterning mechanisms can be properly activated and used to regenerate missing appendages.

Hair follicle formation typically only occurs during embryonic development under homeostatic conditions. During embryonic development, cellular interactions between epithelial and mesenchymal cells lead to the formation of a hair placode and dermal papilla, and their reciprocal interactions lead to morphogenesis and growth of the hair follicle. Coordinated activation of several key signaling pathways including Wnt/β-catenin and BMP regulators is essential for this process ( Fig. 2 ) ( Millar 2002 ; Schmidt-Ullrich and Paus 2005 ; Myung and Ito 2012 ; Sennett and Rendl 2012 ). Once the hair follicle forms, hair is produced cyclically by interactions between epithelial stem cells in the hair follicle bulge/secondary hair germ area and dermal papilla cells throughout life ( Cotsarelis et al. 1990 ; Kishimoto et al. 2000 ; Botchkarev et al. 2001 ; Ito et al. 2002 , 2004 ; Rendl et al. 2008 ; Greco et al. 2009 ; Zhang et al. 2009 ; Enshell-Seijffers et al. 2010 ; Garza et al. 2011 ; Clavel et al. 2012 ; Oshimori and Fuchs 2012 ; Myung et al. 2013 ).

Schematic illustration of molecular mechanisms during hair follicle morphogenesis ( top ) and neogenesis ( bottom ).

Mouse models with small punch wounds (∼6 mm) heal largely by contraction (note that contraction accounts for ∼90% of repair of mouse skin), while hair follicles fail to regenerate in the wound site ( Ito et al. 2007 ). In contrast, after a large wound is made on the back skin (1 cm 2 in 3 wk old, or 2.25 cm 2 in <7 wk old), contraction stops before wound closure leaving a measurable wound scar area. Re-epithelialization of large wounds occurs approximately 2 wk after wounding in adult mice. Remarkably, although there is a lack of hair follicles in the wound area at the completion of re-epithelialization, de novo hair follicles are found in this area 2–3 d after re-epithelialization. It is unknown how hair follicle neogenesis occurs only in the center of the wounds and is absent in the peripheral area of wounds. During hair follicle neogenesis, expression of several genes that are required for embryonic hair follicle development, such as Wnt10b, Lef1, and Shh, were observed. Moreover, in transgenic mice in which epithelial cells secrete the Wnt inhibitor, Dkk1, wound closure occurs normally, while hair neogenesis is inhibited. Similar defects were also observed in another transgenic mouse that lacks epithelial Wntless (Wls) expression, which is required for Wnt ligand secretion ( Myung et al. 2013 ). In contrast, the number of regenerated hair germs significantly increased in K14-Wnt7a transgenic mice that overexpress Wnt7a in the epidermis. These results suggest that the secretion of Wnt ligands from the epidermis promotes hair follicle neogenesis in adult mice ( Fig. 2 ).

A more recent study from Gay et al. (2013) showed the role of FGF9 secretion from γδ-T cells and activation of Wnt signaling in dermal fibroblasts on hair follicle neogenesis ( Fig. 2 ). They found that following large full-thickness excisional wounds, γδ-T immune cells accumulate within the wound site and secrete FGF9 before re-epithelialization. Subsequently, FGF-9 induces Wnt2 expression in dermal fibroblasts, which in turn leads to activation of Wnt signaling in dermal fibroblast in an autocrine manner and induces FGF-9 expression in Wnt-activated dermal fibroblasts. In mice that lack γδ-T cells ( Tcrb −/− mice ) or FGF-9 expression specifically in T cells ( Lck-Cre:Fgf9 fl/fl mice), wound closure occurs normally, while Wnt signaling is abrogated in dermal fibroblasts, resulting in decreased hair neogenesis. These findings showed that the interplay between immune cells and skin fibroblasts recruited to the wound site is essential to the activation of molecular pathways that promote hair follicle regeneration. On the other hand, another study showed that application of prostaglandin (PGD 2 ), an inflammatory mediator, inhibits hair neogenesis while new hair formation is enhanced in mice that lack a receptor for PGD 2 , GPR44 ( Nelson et al. 2013 ). These results suggest that inflammatory mediators involved in wound healing have the ability to modulate hair follicle regeneration in the wound area.

Although de novo hair follicles formed in the wound were repopulated with functional epithelial stem cells that possess the ability to drive cyclical growth of the new hair follicles, most of the neogenic hairs were unpigmented ( Ito et al. 2007 ; Chou et al. 2013 ). It is believed that formation of unpigmented hair follicle was caused by the lack of melanocytes in the wound area. In the normal skin, melanocyte stem cells (McSCs), responsible for hair pigmentation, are located in the hair follicle bulge and secondary hair germ niche together with epithelial stem cells ( Nishimura et al. 2002 ). The coordinated activation of these two stem cell populations through co-activation of Wnt signaling results in pigmented hair production ( Rabbani et al. 2011 ). McSCs in the hair follicles that surround the wound migrate upward and populate the wound epidermis ( Fig. 3 ) ( Chou et al. 2013 ). It was also found that the distribution of epidermal melanocytes is restricted to the wound periphery, and epidermal melanocytes are occasionally found in the wound center where hair neogenesis occurs. In instances where melanocytes are able to migrate to the center, epidermal melanocytes participate in hair neogenesis. As de novo hair follicles develop, McSCs are re-established in the newly formed bulge, and these hair follicles produce pigmented hair. These results indicate that when melanocytes are present in the region of the skin where de novo hair follicle formation occurs, these cells can properly interact with epidermal and dermal cells to participate in hair follicle neogenesis after wounding.

Contribution of hair follicle–derived melanocytes to hair follicle neogenesis. ( A–C ) Hair regeneration from newly formed hair follicle in wound area. Note that almost all hair lack pigment. ( D ) Distribution of hair follicle derived melanocytes in the wound in Dct-LacZ reporter mice in which melanocyte including McSCs are labeled with LacZ. Most of the epidermal melanocytes are restricted to the wound periphery, and only a few melanocytes are found in the center of wound where hair follicle neogenesis occurs (red dashed line). ( E ) Occasional pigmented hair regeneration. ( F ) Whole mount view of newly formed hair follicle that produce pigmented hair. Note the presence of McSCs in the bulge. ( G ) Schematic illustration of the contribution of hair follicle–derived melanocytes to hair follicle neogenesis. Scale bars, 1 mm. ( A–C from Ito et al. 2007 ; reproduced, with permission; D–G from Chou et al. 2013 ; reproduced, with permission.)

Recently, similar hair follicle neogenesis was reported in another mouse strain, the African spiny mouse (Acomys) ( Seifert et al. 2012a ). Sixty percent of the total dorsal surface area of these mice are torn up as a result of autotomy and regenerate pigmented hair follicles within 30 d after autotomy. Acomys can also regenerate hair follicles after 4 mm 2 small wounds unlike other mice. Moreover, the wound-healing process of Acomys shared similar characteristics observed in mammalian fetuses, such as slow deposition of the extracellular matrix and high-level expression of collagen III. These observations suggest that hair follicle neogenesis may occur more effectively when the wound-healing process is similar to what occurs in fetuses.

CONCLUDING REMARKS AND REMAINING QUESTIONS

Previous studies have established the contribution of skin appendages to wound healing. How wounding stimuli recruit stem cells for re-epithelialization is not fully understood. Further understanding of the molecular mechanisms underlying the plasticity of epithelial stem cells in the hair follicle will be necessary to design strategies to efficiently exploit stem cells to enhance tissue regeneration during wound healing. At the same time, it is now clear that wound stimuli can trigger the skin to engage embryonic programs to regenerate hair follicles in adult mice. The relationship between scarless healing and the ability to regenerate epidermal appendages in the wound site is currently unclear. Wound-induced scar formation and epidermal appendage regeneration likely share some common signals or mechanisms. However, it is unknown how the mechanisms that lead to these two distinct consequences of wound healing are synchronized. For example, it is still unclear whether precluding scar formation is a prerequisite to permit the skin to regenerate its appendage or whether the addition of morphogenetic signals in the presence of scar formation can promote epidermal appendage formation. To integrate our understanding of wound healing and appendage regeneration, it will be important to dissect how molecular signals that are activated at each stage of the wound-healing process influence the behavior of each skin cell type and how these signals ultimately promote scarring and/or appendage regeneration.

Interestingly, epidermal appendage regeneration also impacts surrounding cells. This concept is illustrated by a study that showed that epithelial stabilization of β-catenin in adult skin, known to trigger de novo hair follicle formation, confers embryonic characteristics to surrounding dermal cells ( Collins et al. 2011 ). These observations suggest that epidermal appendage formation is not merely a result of regenerative healing, but may be allowing regenerative healing of surrounding dermal cells. Importantly, on amputation of the mouse digit tip, regeneration of underlying mesenchymal bone occurs only in association with nail regeneration ( Fig. 4 ) ( Borgens 1982 ; Zhao and Neufeld 1995 ; Mohammad et al. 1999 ; Takeo et al. 2013 ). Wound healing following digit amputations proximal to the visible nail plate lacks nail regeneration and ends with scarring. These studies highlight the possibility that epidermal appendage formation emits multiple morphogens that signal to other cell types in a paracrine manner. Little is known about the interplay between heterotypic cells that coordinately orchestrate wound healing and regeneration. Dissecting the molecular crosstalk between epidermal appendage regeneration and dermal repair may provide important clues to instruct dermal cells to engage embryonic/regenerative programs and reduce scarring. These future studies hold the promise to develop novel and innovative approaches to exploit our cumulative understanding of signals that govern epidermal appendage regeneration and wound healing.

Relationship between nail regeneration and digit regeneration. Alcian blue/alizarin red staining of mouse digit at 5 weeks after distal ( A ), or proximal ( B ) amputation. When a digit is amputated at the distal level, both nail and underlying mesenchymal digit bone regenerates A , while neither nail nor digit bone regenerates from proximal amputation B . (Panel B is from Takeo et al. 2013 ; reproduced, with permission.)

ACKNOWLEDGMENTS

W.L. is supported by the NYU Kimmel Stem Cell Center and NYSTEM training Grant C026880. M.I. is supported by the U.S. National Institutes of Health, National Institute of Arthritis and Musculoskeletal and Skin Diseases Grant 1R01AR59768-01A1, and the Ellison Medical Foundation.

Editors: Anthony E. Oro and Fiona M. Watt

Additional Perspectives on The Skin and Its Diseases available at www.perspectivesinmedicine.org

• Ansel DM, Kloepper JE, Thomason HA, Paus R, Hardman MJ 2011. Exploring the “hair growth–wound healing connection”: Anagen phase promotes wound re-epithelialization . J Invest Dermatol 131 : 518–528. [ PubMed ] [ Google Scholar ]
• Barbul A, Shawe T, Rotter SM, Efron JE, Wasserkrug HL, Badawy SB 1989. Wound healing in nude mice: A study on the regulatory role of lymphocytes in fibroplasia . Surgery 105 : 764–769. [ PubMed ] [ Google Scholar ]
• Borgens RB 1982. Mice regrow the tips of their foretoes . Science 217 : 747–750. [ PubMed ] [ Google Scholar ]
• Botchkarev VA, Botchkareva NV, Nakamura M, Huber O, Funa K, Lauster R, Paus R, Gilchrest BA 2001. Noggin is required for induction of the hair follicle growth phase in postnatal skin . FASEB J 15 : 2205–2214. [ PubMed ] [ Google Scholar ]
• Brownell I, Guevara E, Bai CB, Loomis CA, Joyner AL 2011. Nerve-derived sonic hedgehog defines a niche for hair follicle stem cells capable of becoming epidermal stem cells . Cell Stem Cell 8 : 552–565. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Burrington JD 1971. Wound healing in the fetal lamb . J Pediatr Surg 6 : 523–528. [ PubMed ] [ Google Scholar ]
• Chen W, Kelly MA, Opitz-Araya X, Thomas RE, Low MJ, Cone RD 1997. Exocrine gland dysfunction in MC5-R-deficient mice: Evidence for coordinated regulation of exocrine gland function by melanocortin peptides . Cell 91 : 789–798. [ PubMed ] [ Google Scholar ]
• Chou WC, Takeo M, Rabbani P, Hu H, Lee W, Chung YR, Carucci J, Overbeek P, Ito M 2013. Direct migration of follicular melanocyte stem cells to the epidermis after wounding or UVB irradiation is dependent on Mc1r signaling . Nat Med 19 : 924–929. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Clavel C, Grisanti L, Zemla R, Rezza A, Barros R, Sennett R, Mazloom AR, Chung CY, Cai X, Cai CL, et al. 2012. Sox2 in the dermal papilla niche controls hair growth by fine-tuning BMP signaling in differentiating hair shaft progenitors . Dev Cell 23 : 981–994. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Cohen N 1971. Amphibian transplantation reactions—Review . Am Zool 11 : 193. [ Google Scholar ]
• Collins CA, Kretzschmar K, Watt FM 2011. Reprogramming adult dermis to a neonatal state through epidermal activation of β-catenin . Development 138 : 5189–5199. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Colwell AS, Longaker MT, Peter Lorenz H 2008. Identification of differentially regulated genes in fetal wounds during regenerative repair . Wound Repair Regen 16 : 450–459. [ PubMed ] [ Google Scholar ]
• Cotsarelis G, Sun TT, Lavker RM 1990. Label-retaining cells reside in the bulge area of pilosebaceous unit: Implications for follicular stem cells, hair cycle, and skin carcinogenesis . Cell 61 : 1329–1337. [ PubMed ] [ Google Scholar ]
• Cowin AJ, Holmes TM, Brosnan P, Ferguson MW 2001. Expression of TGF-β and its receptors in murine fetal and adult dermal wounds . Eur J Dermatol 11 : 424–431. [ PubMed ] [ Google Scholar ]
• Dang CM, Beanes SR, Lee H, Zhang X, Soo C, Ting K 2003. Scarless fetal wounds are associated with an increased matrix metalloproteinase-to-tissue-derived inhibitor of metalloproteinase ratio . Plast Reconstr Surg 111 : 2273–2285. [ PubMed ] [ Google Scholar ]
• Driskell RR, Lichtenberger BM, Hoste E, Kretzschmar K, Simons BD, Charalambous M, Ferron SR, Herault Y, Pavlovic G, Ferguson-Smith AC, et al. 2013. Distinct fibroblast lineages determine dermal architecture in skin development and repair . Nature 504 : 277–281. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Enshell-Seijffers D, Lindon C, Kashiwagi M, Morgan BA 2010. β-Catenin activity in the dermal papilla regulates morphogenesis and regeneration of hair . Dev Cell 18 : 633–642. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Fuchs Y, Brown S, Gorenc T, Rodriguez J, Fuchs E, Steller H 2013. Sept4 /ARTS regulates stem cell apoptosis and skin regeneration . Science 341 : 286–289. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Garza LA, Yang CC, Zhao T, Blatt HB, Lee M, He H, Stanton DC, Carrasco L, Spiegel JH, Tobias JW, et al. 2011. Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells . J Clin Invest 121 : 613–622. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Gawronska-Kozak B, Bogacki M, Rim JS, Monroe WT, Manuel JA 2006. Scarless skin repair in immunodeficient mice . Wound Repair Regen 14 : 265–276. [ PubMed ] [ Google Scholar ]
• Gay D, Kwon O, Zhang Z, Spata M, Plikus MV, Holler PD, Ito M, Yang Z, Treffeisen E, Kim CD, et al. 2013. Fgf9 from dermal γδ-T cells induces hair follicle neogenesis after wounding . Nat Med 19 : 916–923. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Greco V, Chen T, Rendl M, Schober M, Pasolli HA, Stokes N, Dela Cruz-Racelis J, Fuchs E 2009. A two-step mechanism for stem cell activation during hair regeneration . Cell Stem Cell 4 : 155–169. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Hallock GG 1985. In utero cleft lip repair in A/J mice . Plast Reconstr Surg 75 : 785–790. [ PubMed ] [ Google Scholar ]
• Ito M, Kizawa K, Toyoda M, Morohashi M 2002. Label-retaining cells in the bulge region are directed to cell death after plucking, followed by healing from the surviving hair germ . J Invest Dermatol 119 : 1310–1316. [ PubMed ] [ Google Scholar ]
• Ito M, Kizawa K, Hamada K, Cotsarelis G 2004. Hair follicle stem cells in the lower bulge form the secondary germ, a biochemically distinct but functionally equivalent progenitor cell population, at the termination of catagen . Differentiation 72 : 548–557. [ PubMed ] [ Google Scholar ]
• Ito M, Liu Y, Yang Z, Nguyen J, Liang F, Morris RJ, Cotsarelis G 2005. Stem cells in the hair follicle bulge contribute to wound repair but not to homeostasis of the epidermis . Nat Med 11 : 1351–1354. [ PubMed ] [ Google Scholar ]
• Ito M, Yang Z, Andl T, Cui C, Kim N, Millar SE, Cotsarelis G 2007. Wnt-dependent de novo hair follicle regeneration in adult mouse skin after wounding . Nature 447 : 316–320. [ PubMed ] [ Google Scholar ]
• Jensen KB, Collins CA, Nascimento E, Tan DW, Frye M, Itami S, Watt FM 2009. Lrig1 expression defines a distinct multipotent stem cell population in mammalian epidermis . Cell Stem Cell 4 : 427–439. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Kishimoto J, Burgeson RE, Morgan BA 2000. Wnt signaling maintains the hair-inducing activity of the dermal papilla . Genes Dev 14 : 1181–1185. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Langton AK, Herrick SE, Headon DJ 2008. An extended epidermal response heals cutaneous wounds in the absence of a hair follicle stem cell contribution . J Invest Dermatol 128 : 1311–1318. [ PubMed ] [ Google Scholar ]
• Levy V, Lindon C, Harfe BD, Morgan BA 2005. Distinct stem cell populations regenerate the follicle and interfollicular epidermis . Dev Cell 9 : 855–861. [ PubMed ] [ Google Scholar ]
• Levy V, Lindon C, Zheng Y, Harfe BD, Morgan BA 2007. Epidermal stem cells arise from the hair follicle after wounding . FASEB J 21 : 1358–1366. [ PubMed ] [ Google Scholar ]
• Li L, Rutlin M, Abraira VE, Cassidy C, Kus L, Gong S, Jankowski MP, Luo W, Heintz N, Koerber HR, et al. 2011. The functional organization of cutaneous low-threshold mechanosensory neurons . Cell 147 : 1615–1627. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Mascré G, Dekoninck S, Drogat B, Youssef KK, Brohee S, Sotiropoulou PA, Simons BD, Blanpain C 2012. Distinct contribution of stem and progenitor cells to epidermal maintenance . Nature 489 : 257–262. [ PubMed ] [ Google Scholar ]
• Mecklenburg L, Tobin DJ, Muller-Rover S, Handjiski B, Wendt G, Peters EM, Pohl S, Moll I, Paus R 2000. Active hair growth (anagen) is associated with angiogenesis . J Invest Dermatol 114 : 909–916. [ PubMed ] [ Google Scholar ]
• Millar SE 2002. Molecular mechanisms regulating hair follicle development . J Invest Dermatol 118 : 216–225. [ PubMed ] [ Google Scholar ]
• Mohammad KS, Day FA, Neufeld DA 1999. Bone growth is induced by nail transplantation in amputated proximal phalanges . Calcif Tissue Int 65 : 408–410. [ PubMed ] [ Google Scholar ]
• Myung P, Ito M 2012. Dissecting the bulge in hair regeneration . J Clin Invest 122 : 448–454. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Myung PS, Takeo M, Ito M, Atit RP 2013. Epithelial Wnt ligand secretion is required for adult hair follicle growth and regeneration . J Invest Dermatol 133 : 31–41. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Nelson AM, Loy DE, Lawson JA, Katseff AS, Fitzgerald GA, Garza LA 2013. Prostaglandin D 2 inhibits wound-induced hair follicle neogenesis through the receptor, Gpr44 . J Invest Dermatol 133 : 881–889. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Nishimura EK, Jordan SA, Oshima H, Yoshida H, Osawa M, Moriyama M, Jackson IJ, Barrandon Y, Miyachi Y, Nishikawa S 2002. Dominant role of the niche in melanocyte stem-cell fate determination . Nature 416 : 854–860. [ PubMed ] [ Google Scholar ]
• Occleston NL, Laverty HG, O’Kane S, Ferguson MW 2008. Prevention and reduction of scarring in the skin by transforming growth factor β3 (TGF-β3): From laboratory discovery to clinical pharmaceutical . J Biomater Sci Polym Ed 19 : 1047–1063. [ PubMed ] [ Google Scholar ]
• Oshima H, Rochat A, Kedzia C, Kobayashi K, Barrandon Y 2001. Morphogenesis and renewal of hair follicles from adult multipotent stem cells . Cell 104 : 233–245. [ PubMed ] [ Google Scholar ]
• Oshimori N, Fuchs E 2012. Paracrine TGF-β signaling counterbalances BMP-mediated repression in hair follicle stem cell activation . Cell Stem Cell 10 : 63–75. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Page ME, Lombard P, Ng F, Gottgens B, Jensen KB 2013. The epidermis comprises autonomous compartments maintained by distinct stem cell populations . Cell Stem Cell 13 : 471–482. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Rabbani P, Takeo M, Chou W, Myung P, Bosenberg M, Chin L, Taketo MM, Ito M 2011. Coordinated activation of Wnt in epithelial and melanocyte stem cells initiates pigmented hair regeneration . Cell 145 : 941–955. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Rendl M, Polak L, Fuchs E 2008. BMP signaling in dermal papilla cells is required for their hair follicle-inductive properties . Genes Dev 22 : 543–557. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Richardson R, Slanchev K, Kraus C, Knyphausen P, Eming S, Hammerschmidt M 2013. Adult zebrafish as a model system for cutaneous wound-healing research . J Invest Dermatol 133 : 1655–1665. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Rowlatt U 1979. Intrauterine wound healing in a 20 week human fetus . Virchows Arch A Pathol Anat Histol 381 : 353–361. [ PubMed ] [ Google Scholar ]
• Satish L, Kathju S 2010. Cellular and molecular characteristics of scarless versus fibrotic wound healing . Dermatol Res Pract 2010 : 790234. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Schmidt BA, Horsley V 2013. Intradermal adipocytes mediate fibroblast recruitment during skin wound healing . Development 140 : 1517–1527. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Schmidt-Ullrich R, Paus R 2005. Molecular principles of hair follicle induction and morphogenesis . Bioessays 27 : 247–261. [ PubMed ] [ Google Scholar ]
• Seifert AW, Kiama SG, Seifert MG, Goheen JR, Palmer TM, Maden M 2012a. Skin shedding and tissue regeneration in African spiny mice ( Acomys ) . Nature 489 : 561–565. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Seifert AW, Monaghan JR, Voss SR, Maden M 2012b. Skin regeneration in adult axolotls: A blueprint for scar-free healing in vertebrates . PLoS ONE 7 : e32875. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Sennett R, Rendl M 2012. Mesenchymal-epithelial interactions during hair follicle morphogenesis and cycling . Semin Cell Dev Biol 23 : 917–927. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Shah M, Foreman DM, Ferguson MW 1995. Neutralisation of TGF-β1 and TGF-β2 or exogenous addition of TGF-β3 to cutaneous rat wounds reduces scarring . J Cell Sci 108 : 985–1002. [ PubMed ] [ Google Scholar ]
• Snippert HJ, Haegebarth A, Kasper M, Jaks V, van Es JH, Barker N, van de Wetering M, van den Born M, Begthel H, Vries RG, et al. 2010. Lgr6 marks stem cells in the hair follicle that generate all cell lineages of the skin . Science 327 : 1385–1389. [ PubMed ] [ Google Scholar ]
• So K, McGrouther DA, Bush JA, Durani P, Taylor L, Skotny G, Mason T, Metcalfe A, O’Kane S, Ferguson MW 2011. Avotermin for scar improvement following scar revision surgery: A randomized, double-blind, within-patient, placebo-controlled, phase II clinical trial . Plast Reconstr Surg 128 : 163–172. [ PubMed ] [ Google Scholar ]
• Somasundaram K, Prathap K 1970. Intra-uterine healing of skin wounds in rabbit foetuses . J Pathol 100 : 81–86. [ PubMed ] [ Google Scholar ]
• Soo C, Beanes SR, Hu FY, Zhang X, Dang C, Chang G, Wang Y, Nishimura I, Freymiller E, Longaker MT, et al. 2003. Ontogenetic transition in fetal wound transforming growth factor-β regulation correlates with collagen organization . Am J Pathol 163 : 2459–2476. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Sopher D 1972. The response of rat fetal membranes to injury . Ann R Coll Surg Engl 51 : 240–249. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Takeo M, Chou WC, Sun Q, Lee W, Rabbani P, Loomis C, Taketo MM, Ito M 2013. Wnt activation in nail epithelium couples nail growth to digit regeneration . Nature 499 : 228–232. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Taylor G, Lehrer MS, Jensen PJ, Sun TT, Lavker RM 2000. Involvement of follicular stem cells in forming not only the follicle but also the epidermis . Cell 102 : 451–461. [ PubMed ] [ Google Scholar ]
• Tumbar T, Guasch G, Greco V, Blanpain C, Lowry WE, Rendl M, Fuchs E 2004. Defining the epithelial stem cell niche in skin . Science 303 : 359–363. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Wulff BC, Parent AE, Meleski MA, DiPietro LA, Schrementi ME, Wilgus TA 2012. Mast cells contribute to scar formation during fetal wound healing . J Invest Dermatol 132 : 458–465. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Yokoyama H, Maruoka T, Aruga A, Amano T, Ohgo S, Shiroishi T, Tamura K 2011. Prx-1 expression in Xenopus laevis scarless skin–wound healing and its resemblance to epimorphic regeneration . J Invest Dermatol 131 : 2477–2485. [ PubMed ] [ Google Scholar ]
• Zhang YV, Cheong J, Ciapurin N, McDermitt DJ, Tumbar T 2009. Distinct self-renewal and differentiation phases in the niche of infrequently dividing hair follicle stem cells . Cell Stem Cell 5 : 267–278. [ PMC free article ] [ PubMed ] [ Google Scholar ]
• Zhao W, Neufeld DA 1995. Bone regrowth in young mice stimulated by nail organ . J Exp Zool 271 : 155–159. [ PubMed ] [ Google Scholar ]

Welcome to Sanova Dermatology, your premier source for cosmetic, medical, and surgical dermatology. We blend experience, education, technology, compassion, and exceptional skills to provide you with an unparalleled quality of care. Our state-of-the-art facilities are equipped with the most advanced technology, and our team of caring professionals are trained in the latest techniques.

Home / Blog / How Does Exercise Effect The Skin?

How Does Exercise Effect The Skin?

Posted on April 17, 2017 in Skin Care , How To Stay Healthy , Beauty Tips , Outdoor Fun , Anti-Aging , Wrinkles , Fitness

It’s no secret that exercise is good for you. It helps you maintain a healthy weight , improves cardiovascular health and even aids in sleep and mood regulation. But, you may not know it’s also good for the skin!

Exercise Keeps Your Skin Younger Longer

Indirectly, exercise is part of an overall healthier lifestyle. Regular exercise keeps harmful stress levels at bay. This is good news for people who struggle with skin conditions that are exacerbated by stress. Do look here for the best clothing for larger people that will be suitable for doing any exercises effortlessly.

Directly, exercise improves the circulation to the skin. “Increased blood and oxygen flow to the cells flushes out free radicals that contribute to the signs of aging ,” explains Johnston. Increased skin cell turnover that can come with exercise can also mean healthier, glowing skin .

Skin Science

Research backs it up. A study done on people who led sedentary lifestyles versus those who exercised regularly showed marked differences in both the outer layer (stratum corneum) which gets thicker with age, and the inner layer (dermis) which gets thinner with age. The active group showed skin with younger characteristics than the inactive group.

Not only that, but when they retested the sedentary group of people after just three months of regular exercise , they found that the skin layers showed improvement. “This means that even if you haven’t been active in the past, starting an exercise routine now can have a positive impact on your skin ,” Johnston says.

Exercising Caution

It’s important that you care for your skin properly when you exercise. For example, if you are jogging , cycling or doing other outdoor activities be sure you are protecting your skin. Cover yourself with light, loose-fitting clothing, wear a hat and sunglasses and apply sunscreen. Also, wash your skin with gentle soap to reduce the chance of clogged pores from sweating.

Now you have another good reason to begin a fitness routine! For more information about healthy skin, contact Sanova Dermatology today.

Sorry, no locations are in this area. Check out the areas below:

Latest Specials & Promotions

• SBA Dermatology 1900 Saint James Place Suite: 600 Houston, TX 77056 (713) 850-0240
• Metairie 111 Veterans Boulevard Suite: 406 Metairie, LA 70005 (504) 838-8225
• Uptown 3434 Prytania St. Suite: 310 New Orleans, Louisiana 70115 (504) 897-5899
• Old Metairie 701 Metairie Road Suite: 2A205 Metairie, LA 70005 (504) 836-2050
• Bee Cave & Lakeway 3944 RR 620 S. Bldg. 6 Suite: 201 Bee Cave, TX 78738 (512) 366-8568
• Lafayette 1245 Camellia Boulevard Suite: 300 Lafayette, LA 70508 (337) 839-2773
• Baton Rouge 6411 Perkins Road Suite: 100 Baton Rouge, LA 70808 (225) 303-9500
• Steiner Ranch 5145 North FM 620 Rd Suite: B-110 Austin, Texas 78732 (512) 266-0007
• Pflugerville 1601 E. Pflugerville Parkway Suite: 1102 Pflugerville, Texas 78660 (512) 252-3700
• Dripping Springs 13830 Sawyer Ranch Road Suite: 304 Dripping Springs, TX 78620 (512) 829-0009
• Central Austin 3705 Medical Parkway Suite: 340 Austin, Texas 78705 (512) 454-3781
• North Austin 12319 North Mopac Expressway Suite: 100 Austin, Texas 78758 (512) 837-3376

Book appointment by

Choose your area, baton rouge, bee cave & lakeway, old metairie, sba dermatology, north austin, central austin, dripping springs, pflugerville, steiner ranch, helyn alvarez, md, daniel barron, pa-c, suzanne bruce, md, daniel a. carrasco, md, kristy charles, md, ryan couvillion, md, megan couvillion, md, gretchen donnes, pa-c, leigh ellen eubanks, md, elizabeth foley, do, natalie gibson, pa-c, miriam l. hanson, md, alicia haslauer, pa-c, agezi igboko, fnp-c, haneen issa, pa-c, jennifer jordan, pa-c, ted lain, md, mba, adam j. mamelak, md, sharon meyer, md, lesley ott, fnp-c, melanie pickett, md, jeffrey c. poole, md, chad prather, md, maria “gabi” prudhomme, fnp-c, marcela ramirez, fnp-c, diana reyes, pa-c, israel rodriguez, pa-c, katharine saussy, md, megan shelton, md, candace thrash, md, mamina turegano, md, jennifer vickers, md, micah williams, pa-c, laura williams, md.

Cosmetic appointments require a $100 deposit, which will be applied towards your procedure at the time of your appointment.

To schedule your appointment, please select an available appointment time below. If you desire an earlier appointment , please call our office at (337) 839-2773 and we will do our best to accommodate you sooner.

*Cosmetic appointments require a $100 deposit to schedule, this amount will be applied towards your procedure at the time of your visit.

• Cosmetic Botox - Botox or Dysport Treatment only
• Cosmetic Filler - Dermal filler Appointment only
• Cosmetic Botox + Filler - A Botox/Dysport AND Dermal filler appointment
• Botox + Filler Consultation - If you are NEW to Sanova Dermatology, please select this appointment type so that we can do an initial consultation.

To schedule your appointment, please select an available appointment time below. If you desire an earlier appointment , please call our office at (512) 366-8568 and we will do our best to accommodate you sooner. *Cosmetic appointments require a $100 deposit to schedule, which will be applied towards your procedure at the time of your visit.

To schedule your appointment, please select an available appointment time below. If you desire an earlier appointment , please call our office at (504) 836-2050 and we will do our best to accommodate you sooner.

To schedule your appointment, please select an available appointment time below. If you desire an earlier appointment , please call our office at (504) 897-5899 and we will do our best to accommodate you sooner.

*Cosmetic appointments require a $100 deposit to schedule, which will be applied towards your procedure at the time of your visit.

To schedule your appointment, please select an available appointment time below. If you desire an earlier appointment , please call our office at 512-837-3376 and we will do our best to accommodate you sooner. *Cosmetic appointments require a $100 deposit to schedule, which will be applied towards your procedure at the time of your visit.

• Aesthetic Consultant - Preliminary Consult - A preliminary discussion with our Aesthetic Consultant about your aesthetic goals and discuss cosmetic treatment options

To schedule your appointment, please select an available appointment time below. If you desire an earlier appointment , please call our office at (512) 454-3781 and we will do our best to accommodate you sooner. *Cosmetic appointments require a $100 deposit to schedule, which will be applied towards your procedure at the time of your visit.

To schedule your appointment, please select an available appointment time below. If you desire an earlier appointment , please call our office at (512) 829-0009 and we will do our best to accommodate you sooner. *Cosmetic appointments require a $100 deposit to schedule, which will be applied towards your procedure at the time of your visit.

To schedule your appointment, please select an available appointment time below. If you desire an earlier appointment , please call our office at (512) 252-3700 and we will do our best to accommodate you sooner. *Cosmetic appointments require a $100 deposit to schedule, which will be applied towards your procedure at the time of your visit.

To schedule your appointment, please select an available appointment time below. If you desire an earlier appointment , please call our office at (512) 266-0007 and we will do our best to accommodate you sooner. *Cosmetic appointments require a $100 deposit to schedule, which will be applied towards your procedure at the time of your visit.

If you need an appointment earlier than 48 hours, please call the location to check availability.

Diseases & conditions

Everyday care, darker skin tones, cosmetic treatments, public health programs, find a dermatologist.

• For AAD Members
• Coronavirus Resource Center
• Skin cancer
• A to Z diseases
• A to Z videos
• Skin care basics
• Skin care secrets
• Injured skin
• Sun protection
• Hair & scalp care
• Nail care secrets
• Diseases & Conditions
• Your safety
• Age spots & dark marks
• Cellulite & fat removal
• Hair removal
• Scars & stretch marks
• Younger-looking skin
• Skin cancer awareness
• Free skin cancer screenings
• Kids' camp
• Good Skin Knowledge
• Shade Structure grants
• Skin Cancer, Take a Hike!™
• Awareness campaigns
• Flyers & posters
• Get involved
• What is a dermatologist?
• FAAD: What it means
• How to select a dermatologist
• Your digital health
• Prior authorization
• Dermatologists team up to improve patient care
• DIY acne treatment
• How dermatologists treat
• Skin care: Acne-prone skin
• Is it really acne?
• Types & treatments
• Childhood eczema
• Adult eczema
• Insider secrets
• Types of hair loss
• Treatment for hair loss
• Causes of hair loss
• Hair care matters
• What is psoriasis
• Diagnosis & treatment
• Skin, hair & nail care
• What is rosacea
• Skin care & triggers
• Types and treatment
• Find skin cancer
• Prevent skin cancer
• Raise awareness
• Español
• Basic skin care
• Dry, oily skin
• Tattoos and piercings
• Anti-aging skin care
• For your face
• For your skin routine
• Preventing skin problems
• Bites & stings
• Burns, cuts, & other wounds
• Itch relief
• Poison ivy, oak & sumac
• Shade, clothing, and sunscreen
• Sun damage and your skin
• Aprenda a proteger su piel del sol
• Nail care basics
• Manicures & pedicures
• Light spots
• Razor bumps
• Caring for Black hair
• Scalp psoriasis
• Weaves & extensions
• Central centrifugal cicatricial alopecia
• Frontal fibrosing alopecia
• Hairstyles that pull can cause hair loss
• Acanthosis nigricans
• Acne keloidalis nuchae
• Hidradenitis suppurativa
• Keloid scars
• Lupus and your skin
• Sarcoidosis and your skin
• More diseases & conditions
• Lesson plans and activities
• Planes de lecciones y actividades
• Community grants
• Finding accurate health information
• Health apps
• Wearable medical devices
• Telemedicine
• Taking pictures of your skin
• Protect your information

Both the CDC and the FDA warn against treating this common childhood condition on your own with non-prescription treatments. See what they recommend.

Find answers to questions patients ask about this newer treatment option, including, “What’s involved in switching from a biologic to a biosimilar?”

Everyone's at risk for skin cancer. These dermatologists' tips tell you how to protect your skin.

Find out what may be causing the itch and what can bring relief.

Find out why dark spots appear and what can fade them.

If you have what feels like razor bumps or acne on the back of your neck or scalp, you may have acne keloidalis nuchae. Find out what can help.

You can expect permanent results in all but one area. Do you know which one?

If you want to diminish a noticeable scar, know these 10 things before having laser treatment.

It can smooth out deep wrinkles and lines, but the results aren’t permanent. Here’s how long botox tends to last.

Use these professionally produced online infographics, posters, and videos to help others find and prevent skin cancer.

Free to everyone, these materials teach young people about common skin conditions, which can prevent misunderstanding and bullying.

You can search by location, condition, and procedure to find the dermatologist that’s right for you.

A dermatologist is a medical doctor who specializes in treating the skin, hair, and nails. Dermatologists care for people of all ages.

How your workout can affect your skin

Working out affects skin in good and not-so-good ways. here is how to protect it while getting fit..

Working out regularly can help maintain your weight, boost your overall mood and self-esteem, motivate you to eat healthier, and do wonders for your skin. However, not taking the right precautions while working out can cause acne to flare, skin infections, and other skin issues. As much as we benefit from those feel-good endorphins, all of that sweat can clog our pores, cause breakouts, chafing, and more. Your best form of defense is understanding the good, along with the bad, so you can prepare and protect your skin.

Here, we spoke with leading board-certified dermatologists on what to do before and after your workout to prevent unwanted issues.

Get that glow

Once you have cooled down and chugged some water after exercise, you likely noticed your radiant, flushed skin. There’s a reason why so many fitness enthusiasts rave about this feeling, and why many cosmetic companies try to replicate it: it’s naturally attractive.

Board-certified dermatologist with a private practice in Chicago, Edidiong Kaminska, MD, FAAD, says this allure is created by an increase of blood flow to all organs, including our largest one, the skin. "This provides oxygen and nutrients to the skin cells and clears impurities from the skin, creating a post-workout glow," she says.

Another way fitness improves our skin’s appearance is through stress management and sleep regulation. Because burning calories also burns off anxiety, it can decrease the likelihood or severity of skin conditions like acne, eczema, or psoriasis, since stress can play a role in those conditions. And when you stick to a manageable workout schedule, you tend to sleep better. Plus, with more hours of shut eye, those pesky dark eye circles are less common too, Dr. Kaminska adds.

The downside of sweat

If you’re in a challenging boot camp or a hot vinyasa yoga class, it feels like sweat is coming from everywhere. And that’s because it is! While sweating is a healthy way to release build-up and impurities, it can also clog up your pores, causing breakouts and other skin issues on your face and throughout your body, especially if you are wearing heavy makeup or other acne-causing products.

Dr. Kaminska also says excessive sweating can lead to seborrheic dermatitis, or dandruff, especially if you’re already prone to this condition. This is because dandruff is caused by a yeast that lives on our skin (and thrives in warm, moist environments), and when it overgrows, it begins to flake or itch.

And if you’re someone who likes to hit the ground running—literally—you could experience chafing. Though relatively harmless and short-lasting, Dr. Kaminska says it can become painful, especially as your thighs rub together, creating friction.

Protect your skin during a workout

You shouldn’t skip your favorite fitness class or routine because you’re worried about skin-related issues. Instead, Dr. Kaminska says, there are some proactive, preventive measures you can take before you lace up your sneakers. These include:

Skip makeup. Sometimes, it’s easy to forget the swipe of foundation you applied in the morning when you’re scrambling to squeeze in an hour of workout time before relaxing at the end of the day. It may not seem like a big deal, but Dr. Kaminska says sweat mixed in with makeup is much more damaging to skin, because your pores are "clogged" before the workout even begins. It’s better to wash your face with a gentle cleanser before picking up a dumbbell.

Never skip sun protection . Any time you work up a sweat outdoors, it’s essential to protect your skin from the sun by staying in the shade whenever possible and wearing sun-protective clothing. Many fitness apparel brands make hats, sunglasses, and clothing that are not only comfortable to wear while active, but also provide UV protection. Apply a broad-spectrum, water-resistant sunscreen with an SPF of at least 30 to all skin not covered by clothing. Choose a sunscreen that says "non-comedogenic" or "won’t clog pores" on the label. Not only does it prevent skin cancer, but it will help your appearance remain more youthful for longer. And don’t forget, if you’re enjoying a long fitness session—like marathon training—you’ll need to reapply your sunscreen every two hours or after swimming or sweating. To further protect your skin from the elements, if working out in the cold makes your skin chapped and windburned, consider applying some moisturizer or petroleum jelly before heading outside. Don’t skip sun protection if taking this step, however.

Choose the right fabrics . The next time you’re updating your workout wardrobe, look for synthetic fabrics like nylon or polyester or garments that say "moisture-wicking" on the label. These materials "wick" sweat away from your skin and dry quickly, which help prevent clogged pores and even cool down your overall body temperature. Make sure your workout clothes fit loosely, because tight clothing or accessories can rub against and irritate your skin.

Get fitted for the right shoes . While everyone has a shoe size, athletic sneakers are not one-size-fits-all, because feet are unique to each person. This is why Dr. Kaminska suggests being fitted at a running or athletic store. Having shoes that fit well reduces blisters and injuries alike. Other ways to prevent blisters while working out include wearing nylon or moisture-wicking socks and if needed, applying soft bandages as extra protection to areas on your feet, like your heels, that are prone to blistering.

Stay clean . Avoid contact with equipment or towels that aren’t clean. Use a clean towel to gently pat sweat from your skin while working out, and make sure to disinfect shared equipment before and after use to avoid spreading germs. When possible, use your own equipment, like a yoga mat, to avoid sharing germs.

How to protect your skin after a workout

You mustered up the energy, you put in the work, and now it’s time for the reward. Before you treat yourself to a high-protein snack or begin your binge-watching of the evening, Dr. Kaminska says to give your skin a little post-workout TLC by hopping in the shower. "This clears the skin of sweat, oils, and bacteria, and helps to keep pores clean," she continues.

"If you cannot shower, at least wash your face with a gentle, non-comedogenic cleanser or wipe skin that tends to break out with pads containing salicylic acid." Change into clean clothing, too.

And one more thing: Do not go barefoot in the shower or the locker room at a gym. Public locker rooms are high-traffic areas, and may not be cleaned as well or as often as they should be, so you run the risk of skin infections like fungus or warts. A travel pair of flip-flops is enough to keep you safe.

The lowdown on post-workout products

You’ve done your cool-down and some stretching and now it’s time to clean up. With so many products available, how do you know you are choosing the right one for use post-workout? We asked board-certified dermatologist Farah Moustafa, MD, FAAD, director of lasers and cosmetics and assistant professor at Tufts University School of Medicine, to share specific ingredients in cleansers and more:

Cleanser . Go for a wash with salicylic acid or benzoyl peroxide, which help clean your pores and fight bacteria. Because salicylic acid is oil-soluble, it can penetrate effectively into our pores and provide deep exfoliation as well as prevention of excess oil production. This helps treat whiteheads, blackheads, and other inflammatory acne, she explains. Benzoyl peroxide wash kills the bacteria that causes acne and can also help reduce body odor after a workout (also caused by bacteria). Benzoyl peroxide can sometimes be irritating for people with sensitive skin, so approach it with caution, and avoid using it at the same time as products with other drying ingredients, like salicylic acid. If you don’t have any cleanser nearby, lukewarm water alone will go a long way to help prevent breakouts, Dr. Moustafa says.

Deodorant/antiperspirant . While antiperspirants reduce sweating and odor, deodorants mask the scent. When shopping for these, check if it has “aluminum chloride,” which Dr. Moustafa says blocks our sweat ducts, cutting back on the amount of sweat. Higher concentrations are more effective and are often labeled as “clinical strength.” She recommends applying deodorant after your shower on dry skin and then again before the workout for the best effectiveness.

Related AAD resources

How to prevent skin conditions in athletes

How to prevent common skin infections at the gym

Last updated: 5/27/21

Microsoft no longer supports your browser, please upgrade to Internet Explorer 10+

• About Our Supporters

Exercise and stretching with burn injuries

Why do I need to stretch and exercise after a burn injury?

Acute or early on after the injury.

When somebody has a burn injury the body reacts in ways that lead to loss of movement, loss of muscle strength and endurance. This is due to a combination pain, prolonged bed rest and not moving as one would normally do. Also with large burns the body reacts by using more energy than usual and it is often challenging to eat enough food to match the energy being consumed.

It is common to have swelling where the burn is and surrounding areas. Exercise is a very good way of reducing any swelling that occurs.

After the burn has healed

When burn injuries heal, the body commonly reacts by making scars that want to tighten and cause the skin to lose its ability to stretch and move as it would normally do. This along with any weakness that comes after the time in hospital recovering means that regular exercise becomes very important to recovery and getting back to life after a burn. It may take some time before you are back to normal activity after the burn has healed so exercise is very important in achieving this.

What exercises do I need to do?

When your burn injuries are healing the therapist will be guiding you on specific exercises for you and your injury and wounds. They will start immediately and will be aimed at maintaining all the movement you had before the injury. Getting up and walking around and doing as much of the normal activities such as feeding yourself, washing and dressing as you can is very important. As well you will have specific exercises for the areas of the body that are burned which are important. The more moving and exercising that you do the more likely that recovery from the injury will be good.

There is often pain and discomfort with burn injuries while they are healing. It is important that pain does not stop stretching and exercises being done. The timing of any pain relief medication needs to be managed so that the exercises can be done to there best effect. Also incorporating exercises into an activity that is useful or fun can be a distraction from any pain or discomfort. Generally the more frequent the exercises are done the easier and more comfortable they become.

There may be times while the burn wound is healing that you will not be able to move that part of the body such as after a skin grafting operation. This is important for healing and the health team caring for you will give specific instructions on what can be done or not done with stretching and exercises.

Exercise and stretches continue to be very important after the burn wound has healed, particularly if the body is making scar tissue. Scar tissue causes the skin to be tight and less stretchable. This ‘active’ tightening of the scars and skin commonly goes on for 12 to 18 months. The burn therapist will give specific stretching exercises for each person depending on where the burn injury is, how long it took to heal and if operations were required to heal the burn.

The newly healed skin can often feel tight and can feel like a ‘burning’ sensation during exercises that stretch the skin. This is because the scars are actively trying to tighten and shorten.

The newly healed skin can often be dry so it is important that stretching exercises are done when the skin has had moisturiser rubbed in as this will help with the exercises and protect the skin from damaging.

With large area burn injuries the new scarred skin may not be able to sweat and therefore help your body to cool itself when exercising. It may be important that you do exercises in cooler environments such as air-conditioning, making sure you drink plenty of water and minimising the amount of clothing you have on while exercising.

Exercise and stretching will be aimed at maintaining and improving movement, and maintaining strength and endurance. Don’t forget, incorporating exercises into an activity that is useful or fun can be a distraction from any pain or discomfort and the more frequent the exercises are done the easier and more comfortable they become.

When to seek further assistance:

• If you are finding it difficult to do the stretches and exercises that your therapist has given to you to do
• If your movement and ability to do things for yourself is getting worse
• If you have new wounds or skin breakdown

When any of the above occurs or for further assistance contact your treating therapist or the medical team that looked after your burn.

Subscribe to updates

Subscribe to our newsletter and receive updates in your inbox.

• Terms of Use
• Rights & Responsibilities

SKIN HEALTH

After a Spinal Cord Injury, there are specific risks for your skin that can dramatically affect health and mobility, but are preventable with the right knowledge and equipment. In this section, you will learn how a spinal cord injury (SCI) changes your skin, how to protect and care for your skin post-injury, and ways to prevent the most common risks and concerns. You’ll learn how to prevent pressure injuries, how to troubleshoot if problems do arise, and where to get help when you need it.

• What does skin do?
• How does skin change after SCI?
• Pressure injuries: definition and stages
• Pressure Injuries: causes and risk factors
• Preventing pressure injuries
• What to do if you have a pressure injury
• Who Can I Talk to About This?
• Conclusion & Resources

INTRODUCTION

After an injury to the spinal cord, the nerves that communicate the sensations of pressure and discomfort and make us aware of the need to change position may no longer work or be as reliable as they were before injury. These nerves are unable to accurately alert you to imminent injury like a scald from hot water or skin pinched by a seatbelt. After SCI, the loss of this important information from the skin’s surface means that your body is no longer able to unconsciously protect itself from injury, so using conscious awareness becomes a new everyday task in order to protect your skin.

After SCI, your skin changes in several other important ways that may not be obvious at first.

• Skin itself changes, changing colour and temperature. The loss of nerve connection from the skin to the nervous system below the injury disrupts thousands of tiny fibres in the skin that control how the skin responds to stimuli. Both skin and nails become thinner, more brittle and can be more vulnerable to dryness and injury.
• Circulation of blood and lymph changes affect your skin after SCI:  Without the squeeze of muscles in the calf and thigh against the veins in your legs, blood and lymph pool and only sluggishly return back to the chest area, leading to fluid collection in the legs and feet. Compression stockings are often used in hospital to reduce swelling and risk of deep vein thrombosis (DVT) , but can also be worn regularly at home to help leg circulation and reduce swelling.
• Slowed circulation also contributes to slower wound healing  below the injury level, and can also lead to fluid collection in the legs and feet, by slowing the flow of wound healing cells and building blocks to wound sites and delaying the removal of fluid and byproducts of healing from the wound.

These changes after injury mean that living with SCI puts your skin at high risk for developing a pressure injury , which are injuries to the skin and the tissue that lies beneath the skin. Pressure injuries commonly develop on areas of skin that cover a bony area – such as the tailbone, sit bones , hips, or heels. Pressure injuries can also occur in places where the skin folds over on itself, such as the folds of the groin.  They can start very small, but can quickly turn into a serious problem which may require a person to be on bed rest for weeks or even months while it heals.

DID YOU KNOW?

Preventing skin problems is much easier than treating skin problems after SCI.

Pressure Injury Prevention wallet card

Spin Doctor Article: SCI, Edema and your skin

WHAT DO I NEED TO KNOW?

Stages of pressure injuries.

There are four stages of pressure injuries that range from reddening of the skin (Stage 1) to deep wounds that go through all layers of the tissue down to the bone (Stage IV). They can be very hard to treat and very slow to heal. Sometimes, the injury starts under your skin and you can’t see it right away. These are called deep tissue injuries, and once they present themselves, they often show up as a dark red/purple colour. It’s important to take any discolouration of the skin seriously, and try to prevent it from getting worse.

Main Causes of Pressure Injuries

• Pressure : Lying or sitting still for too long reduces the blood supply to the skin and tissues under the skin, as they become “pinched” between the bone and the sitting/lying surface.
• . Pressure can also be a result of inadequate sitting or sleeping surfaces, tight clothing, seams, or buttons.
• Friction : Skin can get damaged by dragging across different surfaces, such as during a sliding board/pivot transfer, or from the sling used during a ceiling lift transfer.
• Shearing : Skin can get damaged from the shearing of tissues against each other, such as from sliding down in bed or sliding forward in the wheelchair.

 Other Risk Factors

These factors are well known to increase the risk of developing a pressure injury, or to delay wound healing. This is not an exhaustive list, but are some of the most common contributors:

• Moisture/Dampness : The skin becomes fragile and more prone to skin breakdown when moist – such as from sweat, urine, or stool. It is important to keep the skin free from moisture as much as possible.
• Sensory Loss : Sensory changes or sensory loss below the level of injury are very common after SCI. This results in our body not receiving the signal that it is time to change position or that we are in a position that is causing discomfort to our skin and tissues.
• Poor nutrition/hydration : A poor diet that is low in vitamins and protein can make skin more likely to be damaged and delay healing. Your skin, like other organs in your body, also needs proper hydration to stay healthy, so drinking enough water is crucial.
• Smoking:  Smoking decreases the blood flow to the skin, which makes it more fragile and can also delay healing. 

People with SCI have a 50-80% chance of having a pressure injury in their lifetime.

Pressure Ulcers: Consumer Guide

WHAT CAN I DO?  

Studies have shown that people with spinal cord injuries have a 50-80% chance of having a pressure injury in their lifetime. It is much easier to prevent a pressure injury than to heal a pressure injury, so every person with SCI should know and practice these prevention strategies every day.

Check your skin twice every day

• A red spot that does not go away after removing the cause of pressure (~15-20 minutes) is a pressure injury! Catching it at this stage is crucial so that you can find the cause and make changes to prevent it from getting worse.
• Always check bony areas (back, elbows, tailbone, sit-bones, knees, heels). You can use a mirror to check yourself, if you are able to. If you can’t check yourself, learn to direct others (i.e. a caregiver) to check for you.

Shift your weight

• Weight shift every 15 minutes for 30 seconds to 1 minute.
• If you are in a manual chair, lean forward onto your elbows, or lean to the side to shift your weight.
• If you are in a power chair, tilt your chair 45- 60 degrees (almost lying down).
• In bed, find out how many turns you need each night to keep your skin healthy.

Ensure proper surfaces

Work with your health care professionals, such as your OT and PT, to ensure your surfaces (cushion, mattress, backrest) are right for you, and that they are adequate to relieve and distribute pressure and prevent pressure injuries.

Transfer safely

Ensure you have enough clearance during transfer – don’t drag yourself across surfaces (such as the wheel of manual chair). If you use an overhead lift, ensure your sling is placed properly in order to prevent friction or shearing.

Keep your skin clean and dry

Read about Foot Care from Bonnie Venables Nybo, GF Strong Rehabilitation Centre’s SCI Outpatient Nurse

• Bowel and bladder accidents can cause skin problems. Try to stick to your bladder and bowel routine to prevent having accidents.
• If you are having bowel and bladder problems that you are not able to manage, be sure to seek help from health care providers.
• If exercising, make sure to change out of sweaty clothes and clean your skin.
• Remember your feet! Care for your skin includes your feet and toenails!

Take care of your equipment

• Check your cushion every day – if it’s an air cushion – is the inflation correct? Is it on your chair the right way?
• Make sure all your equipment is working and in good shape.
• Every 3-5 years have an occupational therapist or physiotherapist check the fit of your equipment. If you don’t have an OT or PT, ask your family physician for a referral to GF Strong’s outpatient spinal cord program or the local health unit to access these services.

Eat a proper diet and drink plenty of water

• Eat a healthy diet following Canada’s Food Guide  and ensure you maintain a healthy weight.
• Drink water to keep well hydrated. Dark urine or a low amount of urine are signs of dehydration.
• For more information on eating well, contact a dietician in BC through HealthLinkBC’s 811 hotline. 

Pressure Injury Trouble Spots: The photos below show common areas that are at risk for pressure injury, both sitting in a wheelchair and in bed. Make sure to check these areas during your skin checks every day, and take action when you see any red spots particularly in these areas.

A red spot that does not go away after removing the cause of pressure is a pressure injury!

Campbell Biology 11th Edition by Lisa Urry,Michael Cain,Steven Wasserman,Peter Minorsky,Jane Reece

721252-11-1PE AID: 4685 | 17/03/2017 The ... View Answer

Why don’t you like this exercise?

• Perks Center
• Homeschooling
• Campus Reps
• Influencers
• Privacy Policy
• Terms Of Service
• Community Guidelines

• Referral Program
• Chrome Extension
• Get it on the App Store
• Get it on Google Play