What is the healing process of mouth wounds?

What is the healing process of mouth wounds?

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When we have an external wound, blood generally tends to clot there, forming a layer of solid scab.

Yesterday, while brushing my teeth, I somehow hurt my gums and it got all bloody. However, it did not clot, neither did it hurt just after the incident.

After maybe like 12 or 15 hrs I had trouble opening my lips and when I looked at the spot in the mirror the gum tissue around and on the wound had colored white/yellowish.

Our mouths are supposed to be the among the most contaminated parts of the human body, so why do mouth wounds heal in just about a week and don't get infected?

What is the healing mechanism found in the mouth tissue, because I figure it is completely different from the processes in wounds occurring in the external skin.

To build on the answers from @Armatus and @S-Sunil

The healing mechanism involves the inflammatory process, which is the same in almost the entire body. In particular in both skin and mucosa (both referred to as "epithelial" tissues), when there is a break, platelets and clotting factors clot off any bleeding vessels, white blood cells (neutrophils and macrophages in particular) collect and destroy any bacteria, dead cells and muck, and then the process of regeneration occurs (with ongoing inflammation), where stem cells in the surrounding tissue regrow cells, new blood vessels may be formed and scar tissue is laid down to give extra strength. Eventually after these stages of healing, there is "remodelling" where the structure basically gets better.

As to why oral wounds heal quickly and don't get infected that much? There are a bunch of reasons. One is that the head and neck has an excellent blood supply- just think of scalp wounds where you bleed like crazy but then they heal very well. Another is that mucous membranes have immune functions that stop invading microbes. Generally speaking we divide this into "innate" immunity which is a general response, and "adaptive" immunity which is tailored towards specific bugs. The mucosa has both. There are neutrophils and macrophages (innate) which live in that area, there are lymphoid patches (like lymph nodes, and adaptive), there are immunoglobulins specific to mucosa (IgA) which is adaptive in nature, and the epithelial lining cells themselves will signal to the rest of the immune system if there is damage or an infection. Plus, saliva itself has chemicals and enzymes which break down oral bugs.

Most of the oral bacteria themselves are not particularly invasive. Just think, every time you brush your teeth, you cause multiple abrasions in your mouth. In fact, measurable amounts of bacteria from the mouth end up in your bloodstream every time you brush your teeth! And yet, we don't end up with bloodstream infections as a result. This is partially because the rest of our immune system (and the structure of our heart and vessels) is intact, and partially because oral bacteria are not very invasive or pathogenic. They kind of have a sweet deal living in your mouth minding their own business and not killing their host, and even causing infection in an oral wound would make their continued survival less likely.

In addition I should probably point out that skin has a great deal of bacteria on it as well, and yet we rarely get infections from them (unless colonised by an invasive species), for the same reasons.

The mucosa ("slimey" skin) of course has different properties from your epidermis (outer skin) but the wound healing process is pretty much the same; the blood clotting process might be different though. About this I'm not entirely sure, but my best guess is that the "scab" is washed away by mucus and only the clots inside vessels remain, making them invisible from outside.

The white/yellowish colour is the underlying layer of fatty tissue. Chances are your wound does get infected but your immune system is able to clear it away easily. If infection is a bit heavier, it can strain the immune cells a bit more and some of them may die - you can then see them as pus (which is mostly white blood cells).

The mechanism of oral wound healing is similar to that elsewhere in the body. Depending on the type/ extend of wound, it may be primary or secondary.The clot and the encrustations are the part of the healing process.

How to heal a cut in your mouth faster (For both Adults and Children)

Are you wondering how to heal a cut in your mouth faster? in this post, I will take you through step by step guides on you to get that wound in your mouth to heal quickly.

Wounds in your mouth can heal up faster only if you practice good oral hygiene, a study has revealed. A cut in your mouth may be outside your mouth (your lips) or inside of the same (your tongue, gum, etc).

Both children and adults do get minor injuries in their mouth, tongue, and lips most times. This may be caused by sporting activities like amateur boxing, chewing and climbing.

Your mouth i.e the gums, tongue, and lips are very rich in blood supply, and when cuts happen, these areas normally bleed profusely. This is why you really need to learn how to heal a cut in your mouth faster to stop the bleeding and infections.

Another aim of this post is to teach you how to handle these cuts in your mouth at home.

Do you have children runny around? it is very important you learn this step by step guide so as to offer quick first aid treatment whenever they get their mouth injured.

Research has found out that cuts inside the mouth recover quicker because the cells and tissue in the mouth are always ready to regenerate itself and heal faster provided you are healthy orally without any infections.

Many times, the cut is left open and stitches are not needed. But if it requires stitches to help with healing or to stop bleeding, you need to meet a Doctor ASAP. In this case, where the cuts are not that minor, you will require the treatment from a qualified Doctor.


In Greek mythology, the Rod of Asclepius is a serpent-entwined rod wielded by the Greek god Asclepius. Wounded patients could be healed if they were brought to the temple and the serpent licked their wounds during the night (Gardner, 1925). The Rod of Asclepius is still used as a symbol associated with modern medicine and health care. Wound healing is a primary survival mechanism that is largely taken for granted. Although, wound healing has long been considered a primary aspect of medical practice, disturbed wound healing is infrequently discussed in the literature, and there is no acceptable classification to describe wound healing processes in the oral region.

Wound healing entails a sequence of complex biological processes (Bielefeld et al., 2013). All tissues follow an essentially identical pattern to promote healing with minimal scar formation. One fundamental difference between would healing and regeneration is that all tissues are capable of renewal, but healed tissue does not always possess the same functionality or morphology as the lost tissue (Takeo et al., 2015). Moreover, wound healing is a protective function of the body that focuses on quick recovery (Wong et al., 2013), whereas the process of regeneration in an hostile environment takes more time. In particular, the oral cavity is a remarkable environment in which wound healing occurs in warm oral fluid that contains millions of microorganisms.

The present review provides a basic overview of wound healing, focusing on specific characteristics of the process of wound healing in the oral cavity. We also discuss local and general factors that play roles in achieving efficient wound healing.

Why do mouth wounds heal so quickly?

Scientists have long known that wounds inside the mouth repair themselves very rapidly but the secret of this fast regeneration has largely remained a mystery.

To find clues, Ramiro Iglesias-Bartolome and colleagues at the National Cancer Institute in Washington, recruited a group of thirty healthy human volunteers and induced small wounds, either inside their mouths or on their skin. As the wounds healed over the next six days, the researchers collected biopsies at different time points.

Analysing which genes were active in the mouth compared to the skin revealed some notable differences. For one thing, genes associated with inflammation were less active in the oral wounds. On the other hand, the oral wounds showed greater activity of a gene that regulates stem cells, SOX2. When the researchers engineered mice that overproduced SOX2 in the outer layer of their skin, they found that skin wounds healed faster than compared to a control group.

Though these are early results, the authors say that their findings could help develop therapies to accelerate the healing process and improve wound care in patients.

The research is published in Science Translational Medicine.


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A new approach to understanding the biology of wound healing

Credit: Pixabay/CC0 Public Domain

Our bodies frequently heal wounds, like a cut or a scrape, on their own. However patients with diabetes, vascular disease, and skin disorders, sometimes have difficulty healing. This can lead to chronic wounds, which can severely impact quality of life. The management of chronic wounds is a major cost to healthcare systems, with the U.S alone spending an estimated 10-20 billion dollars per year. Still, we know very little about why some wounds become chronic, making it hard to develop effective therapeutics to promote healing. New research from Jefferson describes a novel way to sample the cells found at wounds—using discarded wound dressings. This non-invasive approach opens a window into the cellular composition of wounds, and an opportunity to identify characteristics of wounds likely to heal versus those that become chronic, as well as inform the development of targeted therapies.

The study was published in Scientific Reports on September 15th.

"Studying wound healing in humans is very challenging, and we know very little about the process in humans," says Andrew South, Ph.D., Associate Professor in the Department of Dermatology and Cutaneous Biology and one of the lead authors of the study. "What we do know is from animal studies, and animal skin and the way it heals is very different from human skin."

Dr. South and his lab study a group of inherited skin diseases called epidermolysis bullosa (EB), where wound healing is severely impaired. Patients, often from birth, suffer from blisters and lesions that are slow to heal, and some become chronic. In a subset of patients, chronic wounds are at high risk of developing into aggressive skin cancer. At this time, it is very difficult to predict which wounds in a given patient will heal, and which won't. Being able to sample the wounds is a key to understanding the mechanisms behind healing.

"Performing a biopsy to sample the cells in the wound would help us understand the differences between these wounds," says Dr. South "But biopsy in these patients is extremely painful and could delay healing of the wound even further. On the other hand, collecting these bandages that are just going to be thrown away, it poses no harm to the patient, and can be applied to a variety of conditions where wounds don't heal properly."

The researchers, which included collaborators in Chile and Austria, collected and analyzed 133 discarded wound dressings from 51 EB patients. Both acute and chronic wounds were sampled, with acute defined as present for 21 days or less, and chronic as present for more than 3 months.

"Previous studies had used wound dressings or bandages to collect fluid and look at what proteins are in there," says Dr. South. "But no one has actually looked at what cells are present. Applying the techniques our lab frequently uses, we were able to isolate viable or living cells from the dressings."

The researchers recovered a large number of cells from the dressings, often in excess of a 100 million. The larger the wound, and the more time a dressing was on a wound, the more number of cells were recovered.

The researchers then characterized the cells to see what type of cells are present at the wound. They detected a variety of immune cells including lymphocytes, granulocytes or neutrophils, and monocytes or macrophages. When comparing dressings from acute and chronic wounds, they found a significantly higher number of neutrophils at chronic wound sites. Neutrophils are the first line of defense in our immune system, and when a wound starts to form, they're the first ones to arrive at the scene.

"Previous findings from animal studies and protein analysis of human wound dressings had supported the idea that when neutrophils hang around longer than they should, that stalls the healing process and can lead to chronicity," says Dr. South. "Our findings support that theory more definitively, by showing that chronic wounds are characterized by higher levels of neutrophils."

These findings give more insight into wound healing, and could help develop therapies that promote the process for instance, those that neutralize excess neutrophils, or recruit macrophages, the immune cells that begin the next stage in healing after neutrophils.

The researchers now plan to expand on their technique, by further analyzing the individual cells collected from the wound dressings, and the genetic material inside them. "Currently we're working with colleagues in Santiago, Chile on collecting dressings from EB patients over a period of time," says Dr. South. "This allows us to follow patients longitudinally, and observe a wound and how its cellular composition changes as it heals or doesn't heal."

The team hopes that this will reveal genetic markers that can predict healing or chronicity.

"This method of sampling could be an alternative to bothersome swabs or blood draws, which are especially hard to do in newborns," says Dr. South. "Since we know EB can present at birth, this technique could give us really early insight into the how severe the disease might be."

While the current study focuses on EB, Dr. South and his colleagues hope that this technique can be applied to a variety of other conditions, such as diabetic foot ulcers and vascular leg ulcers.

"The field of wound healing has been crying out for a better understanding of what drives a chronic wound," says Dr. South. "This technique could be transformative, and eventually help patients live more comfortable and healthy lives."

Bixin action in the healing process of rats mouth wounds

Oral lesions that manifest as ulcer lesions are quite common and can cause discomfort to the patient. Searching for drugs to accelerate the healing of these lesions is nonstop process. Bixin is a molecule found in annatto (urucum) seeds and is considered a viable therapeutic option to treat such lesions due to its anti-inflammatory, anti-oxidant, and healing properties. Therefore, the present study aimed to evaluate the effect of the bixin solution in the ulcer healing process in the oral mucosa of rats. Ulcers were induced with punches of 0.5 cm in the middle of the dorsum of the tongue of 64 Wistar rats. The animals were randomly divided into 8 groups, in which 4 groups were treated with saline solution, while the other 4 were treated with the bixin solution. The animals were sacrificed in the periods 2, 7, 14, and 21 days after the beginning of the treatment. The species were histologically processed and stained with hematoxylin/eosin and picrosirius. Fibroblasts, reepithelialization, and wound contraction could be observed, as could the quantification of neutrophils, macrophages, plasma cells, lymphocytes, and mature and immature collagen. On the seventh day, the experimental group, when compared to the control group, presented a higher proliferation of fibroblasts, more advanced reepithelialization, and a higher contraction in the wounds. A reduction in the average number of neutrophils in the experimental group, when compared to the control group, could be observed in all periods (p=0.000). Up to two days, the total collagen area was higher (p=0.044) in the experimental group (4139.60±3047.51t han in the control group (1564.81±918.47). The deposition of mature collagen, on the 14(th) day, was higher (p=0.048) in the experimental group (5802.40±3578.18) than in the control group (1737.26±1439.97). The results found in the present study indicate that the bixin solution inhibits the acute inflammatory response with a minor average number of neutrophils and accelerates reepithelialization, wound contraction and collagen maturation, thus illustrating that this solution does in fact represent an important adjuvant in the treatment of ulcers.


Despite unraveling key mechanisms and players in physiological and pathological tissue repair, these findings have not yet led to a substantial improvement in patient care. Translating novel technologies and concepts in the field of tissue repair into standardized therapies has several challenges. When considering therapeutic strategies to restore diseased or damaged tissues, it is crucial to realize that most wound-healing pathologies are due to a combination of underlying systemic disease with regional/anatomical factors that cause tissue stress, an ulcerative lesion, and/or scar formation ( Figs. 1 to ​ to3). 3 ). The best treatment approach for wound healing is to normalize the underlying (systemic) cause and simultaneously administer local treatment. Similarly, at the wound site, a combination of therapies may be required because it is unlikely that replacing a single tissue component, growth factor, ECM scaffold, or cell type will be optimal on its own. Rather, a comprehensive understanding of how these different components act together in time and space to successfully restore tissue function will be required.

Interactions between ECM and growth factors

Traditionally, the ECM was considered to be an inert, space-filling material providing mechanical support and tissue integrity. However, in recent years, it has become clear that the matrix also provides a bioactive structure that fundamentally controls cell behavior through chemical and mechanical signals (136). The diverse role of the ECM in organ function is probably best revealed by observing mutant gene defects in human disease, alongside the systematic analysis of ECM functions in genetically modified model organisms (137). These studies have revealed that ECM controls organ development and subsequent function through cell anchorage, integrin-mediated activation and signaling, transduction of mechanical forces, and the sequestering, release, and activation of soluble growth factors. For example, Marfan syndrome, a connective tissue disorder, is caused by mutations in the gene that encodes fibrillin-1, leading to reduced levels of extracellular fibrillin-rich microfibrils, which normally act as a TGFβ reservoir. Thus, although caused by a mutation in an ECM molecule, selected disease manifestations of Marfan syndrome reflect disturbances in TGFβ signaling (138).

Several ECM-based therapeutic systems for tissue repair and regeneration have reached the clinic or are in clinical trials [reviewed in (72)]. Collagen- or fibrin-based products are the most established ECMs being used clinically to guide regeneration of different tissues, including skin, heart valves, trachea, muscle, and tendon (71, 139). These products are used as carriers for transplanted cells, as acellular scaffolds, or as an immediate coverage for large trauma- or disease-associated skin defects. Many of these products have shown efficacy for the treatment of difficult-to-heal skin wounds (140). However, most of the clinical studies on collagen- and fibrin-based materials have not been controlled (for example, ECM alone without cellular component) or have been compared only to standard wound dressings, and their mechanisms of healing action remain speculative.

To advance the field of wound healing, it will be important to understand the relative efficacy of currently available products and how they work. By extrapolating from principles of developmental morphogenesis, an engrafted fibrin matrix is an appropriate natural material that can be modified to respond to the dynamic requirements of the repair microenvironment in both time and space (141-143). In experimental models of bone or skin repair, it has been shown that covalent attachment of growth factors and recombinant fibronectin fragments into a fibrin scaffold can provide spatiotemporally controlled release of the growth factor and enhance growth factor–matrix interactions that ultimately significantly reduce the morphogen concentrations required for effective tissue generation (142). These studies have also confirmed the essential role of the ECM for efficient delivery of growth factors for induction of blood vessel growth (141, 143). Timely restoration of blood vessel supply in therapeutic tissue repair approaches remains an unresolved need in all aspects of regenerative medicine.

Myriad synthetic materials are being explored preclinically for diverse reparative approaches, typically as three-dimensional microenvironments to mimic the features of natural ECM (144). The major challenge in developing synthetic biomaterials for clinical applications is reproducing the complexity of form and dynamics of function of the wound microenvironment (144). Early developments focused on materials where only a few biological moieties were integrated now, so-called hybrid materials provide multiplexed signaling in a temporal sequence, recapitulating the complexity of the regenerative tissue environment. Poly(ethylene glycol) (PEG) is a commonly used synthetic component of these hybrid systems because of its favorable biocompatibility and chemical properties. Bioactive components have been integrated into PEG-based hydrogel matrices, including heparin, cyclic RGD (Arg-Gly-Asp) adhesion peptides, and growth factors (145). PEG-based matrices that are responsive to physical (light) or chemical (enzymes) stimuli have been created to reproduce the dynamics of the reparative process, by modulating the local milieu in time and space (146).

Future studies will need to prove the functionality of these complex synthetic materials for encouraging new tissue growth in vivo, under physiological and pathological wound conditions. Nevertheless, engineering synthetic biomaterials opens up avenues for investigating the systematic and independent variation of biomolecular and mechanical features of wound healing. In this regard, biomaterials research could provide a better understanding of how the ECM and its mechanical forces affect cell invasion, growth, and differentiation (147-149). Thus, although synthetic biomaterials are currently simplified mimics of natural ECM, the capacity to manipulate and direct fundamental cell functions and to apply this knowledge to tissue growth and repair will be a cornerstone for the future of regenerative medicine.

Cell-based therapies

The currently applied and FDA-approved cellular products for regenerative therapies in the clinic use primary human cells. Primary cells have obvious limitations yields and proliferation rates are low, and for some tissues𠅏or example, neurons, heart, and muscle�lls do not divide at all. With advances in stem cell biology as well as techniques to isolate, expand, and engraft stem cells, a new and exciting era has opened for cellular therapy in regenerative medicine.

Over the past decade, stem cells from bone marrow, adipose tissue, adult blood, cord blood, epidermis, and hair follicle have been investigated in numerous preclinical studies and a few clinical pilot studies. Along these lines, clinical studies have shown that bone marrow– and adipose tissue�rived MSCs can augment the repair process when applied locally to chronic skin wounds in patients (96, 150). A recent clinical trial reported improved wound healing and increased mechanical skin stability in children with recessive dystrophic epidermolysis bullosa (RDEB) after allogeneic bone marrow or umbilical cord blood transplantation (151).

Currently, there is no FDA-approved stem cell product on the market for the treatment of skin wounds. We can perhaps learn lessons from other organ systems, such as the heart. Acute myocardial infarction and chronic ischemic heart disease have been targets for numerous phase 1/2 clinical trials using stem cells for tissue regeneration and repair. Those studies have proven that cardiac stem cell therapy is relatively well tolerated and feasible (152). For conclusions regarding the efficacy of cardiac stem cells, we will need to wait for completion of ongoing, large-scale, phase 3 trials. Similarly, the tissue repair field will learn from the final outcomes of ongoing clinical trials applying bone marrow MSCs in the treatment of articular cartilage defects, bone defects, or idiopathic pulmonary fibrosis.

Recent developments in reprogramming skin and other differentiated cells into induced pluripotent stem cells (iPSC) provide a new cell source that can potentially be used for therapy. It has been shown that human skin equivalents can be created entirely from fibroblasts and keratinocytes generated from patients’ iPSCs, and that healthy cells can be generated from reprogrammed cells from patients with RDEB (153, 154). More recently, revertant keratinocytes of a junctional epidermolysis bullosa patient with compound heterozygous COL17A1 mutations used an iPSC approach to generate genetically corrected keratinocytes (155). In addition, iPSCs have been shown to ameliorate diabetic polyneuropathy (a neuropathic disorder associated with diabetes mellitus) in mice (156), and to activate an angiogenic response in mice with hindlimb ischemia (157).

Cell therapies will continue to contribute to regenerative medicine in the 21st century. However, fundamental questions regarding the optimal cell populations for treatment of a chronic condition (for example, multipotent versus pluripotent), favorable route and time point of cell delivery (after injury, for example), the cells’ mode of action, survival and integration of transplanted cells, and whether cells can establish and maintain identity in new microenvironment still need to be addressed (158). Beside these biological questions, safety issues and complex regulatory requirements provide additional major challenges in the advancement of developing cell-based therapies for wound healing (159).

Meaningful clinical endpoints and study design

From our early understanding of the pathomechanisms involved in inhibition of healing, it became clear that targeting a single molecule or a cellular process will not work alone rather, combinatorial treatment approaches are needed. Ultimately, the most important step in bringing therapy to patients rests on successful clinical trials. The development and approval process of treatment modalities for wound healing has seen a large number of drug/biologic failures, with only one drug (Regranex) and two biologic devices (Apligraf and Dermagraft) having obtained approval for efficacy from the FDA in the past 15 years.

Clinical trial design in the area of chronic wounds faces multiple challenges (160). Heterogeneity of patients and their wounds (even within the same category of chronic wound) indicates a need for better diagnostic stratification of patients who are being included in clinical trials. Defining inclusion and exclusion criteria is another challenge, because patients with chronic wounds have underlying chronic illnesses and are often undergoing additional systemic therapies, raising the question of drug-drug interaction and drugs’ multiple pharmacodynamic actions. For example, “hard-to-heal” wound inclusion criteria range from wounds that are large and long-standing (ϡ year) and have been treated with all available therapies without success, to wounds that show 㱀% closure in 4 weeks of standard of care. Such inclusion/exclusion criteria will also greatly influence patient recruitment and consequently duration and expense of the trial. Variability of wound healing “standard of care” between clinics, academic centers, private sector, regions of the city, country, or parts of the world all contribute to difficulty in obtaining cumulative, large data sets from multicenter trials.

There is an ongoing debate in the field regarding defining endpoints. Complete (100%) closure, rate of closure, reduction in size, recurrence, and “surrogate endpoints” (early changes in wound size that are intended to predict the true, meaningful clinical endpoint) are all potential primary and/or secondary outcomes (161). One has to compare with the field of cancer and ask: How many cancer treatments would be available today if complete cure was the only accepted outcome of clinical trials? A more unified approach in standardizing protocols and defining endpoints�side 100% closure—in clinical trial design is desperately needed. A better understanding of local patient population, demographics, and socioeconomics will be important in clinical trial design.

The wound-healing community, including The Wound Healing Society (, the American Association for Advancement of Wound Care (, the Canadian Association of Wound Care (, and the Mexican Association for Comprehensive Wound Care (, is currently in the process of formulating consolidated guidelines for each of the common types of ulcers. It is anticipated that these guidelines will lead to standardized, evidence-based clinical protocols. In a further collaborative effort, the Wound Healing Society and the American Association for the Advancement of Wound Care have initiated discussions with the FDA to develop expanded, clinically relevant, evidence-based primary endpoints for clinical trials.

Molecular Factors Underlie Mouth’s Head Start on Healing

IRP researchers discovered the reason that skin tissue (pictured above) heals more slowly than tissue in the mouth.

As an impatient eater, I find myself burning or biting the inside of my mouth more often than I’d like. Fortunately, these injuries tend to heal within a day or two, whereas wounds like nicking my finger with a knife or scraping my knee seem to take a week or longer to disappear. My personal impressions have now been confirmed by a new NIH study that uncovered major differences in the way the mouth and skin repair themselves, pointing to potential therapeutic targets that could speed healing. 1

While common injuries can take longer to mend than we’d like, certain conditions like the foot sores caused by diabetes heal agonizingly slowly or not at all. Such ‘chronic’ wounds can lead to infection or amputations and substantially reduce patients’ quality of life while driving up medical costs.

While clinicians have long believed that wounds to the inside of the mouth heal faster than skin injuries, these suspicions had never been scientifically validated. IRP investigators Maria Morasso, Ph.D., and J. Silvio Gutkind, Ph.D., set out to investigate those suspected disparities.

“Rather than rely on anecdotal evidence, we needed to learn whether it was a real difference,” says Dr. Gutkind, who has since moved to the University of California, San Diego. “Once we established it was real, we wanted to catalogue all the changes at the cellular and molecular levels that occurred in each place to explain why oral wounds heal faster than skin wounds.”

The researchers began by taking two tiny pieces of tissue from healthy volunteers — one from the skin under the armpit and one from the inside of the cheek — using a minimally painful biopsy technique routinely used by doctors. The scientists then examined the biopsy sites every three days for 15 days total. Some of the volunteers also had a second biopsy taken from the same locations either two or five days after the first.

The experiment confirmed that the oral biopsies healed much more quickly than the skin biopsies. In addition, by examining the activity of a wide array of genes in the two biopsy sites across the course of the study, the researchers discovered that numerous genes related to healing and infection prevention were already active in the mouth but not in the skin when the first biopsy was taken. Moreover, the activity of these genes rose in the skin in the days after the first biopsy but changed much less over time and quickly returned to the baseline level in the mouth tissue. The researchers concluded that the mouth is uniquely set up for healing, with important molecular processes already revved up and ready to go even before an injury occurs.

“The mouth is constantly having small abrasions due to chewing and it’s really rich in microorganisms, so you really want to make sure that the wound heals as quickly as possible,” Dr. Morasso says. “Those factors might have yielded pressures to develop mechanisms for quicker wound resolution compared to the skin.”

By comparing their own findings to those of related studies, the researchers were able to hone in on four specific genes that code for transcription factors, proteins that regulate the activity of other genes. Two of these transcription factor genes, PITX1 and SOX2, were much more active in cells from the uninjured mouth than cells from uninjured skin. Reducing the activity of PITX1 and SOX2 in mouth cells grown in petri dishes tamped down healing-related processes, whereas increasing their activity in skin cells ramped up those molecular pathways. Finally, mice genetically designed to have greater SOX2 activity in their skin healed much more quickly than mice with no SOX2 activity in their skin.

Dr. Morasso now plans to investigate the specific genes and molecular processes controlled by the transcription factors the study identified. Eventually, this research could help produce therapeutics that hasten healing and reduce scarring in both typical and chronic wounds. Dr. Gutkind, for his part, believes their work could provide insights into the development of oral cancers, which rely on the same cell division and movement processes that contribute to healing.

“Only in the NIH Intramural Research Program can these sorts of collaborations happen so quickly,” Dr. Gutkind says. “It’s a great example of team science where distinct but complementary expertise can be melded into something that is unique and would never have been able to be done individually.”

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What is the healing process of mouth wounds? - Biology

Wounds in the mouth heal more slowly in women and older adults, a new study at the University of Illinois at Chicago reveals.//

"While wounds to the skin heal more quickly in women than in men, our study suggested the opposite is true for healing of wounds inside the mouth," said Dr. Phillip Marucha, head of periodontics at the UIC College of Dentistry.

"We discovered that, regardless of age, men's mouth wounds heal faster than women's."

Older women were at the highest risk for delayed healing, their wounds closing half as slowly as younger men, Marucha said. The findings of the study, he said, could have important implications for surgical practices.

"There are an increasing number of surgical procedures being performed in older populations," Marucha said. "A greater emphasis needs to be placed on accelerating the healing process. Discovering the reasons behind these age and sex differences will help us improve treatment, and postsurgical recovery times may be reduced."

The study consisted of creating a small, standardized circular wound, half the diameter of a pencil, between the first and second molar of 212 male and female volunteers aged 18 to 35 years and 50 to 88 years. The wounds were videographed at the same time for seven consecutive days to assess closure.

Testosterone may help mouth wounds heal faster in men, said Christopher Engeland, research assistant professor at UIC and lead author of the study.

"It's a potent anti-inflammatory hormone that is abundant in saliva," he said.

Women are generally more prone to inflammatory diseases, such as rheumatoid arthritis, Engeland said. In skin, women's wounds heal faster than men's in part because inflammation causes them to close faster.

"The more inflammation a person has inside the mouth, the slower wounds appear to heal," Engeland said. "We were surprised to learn that oral wounds heal more slowly in women than in men. It's one of the few times in the field of healing where men have an advantage over women.

"This indicates that the healing process in skin and mouth tissues is different in some fundamental way not previously expected."