Why do lips heal fast

Why do lips heal fast

We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

Whenever I have any cut in my lips ,it gets healed in 2-3 days so why do lips get healed faster as compared to other body parts?

According to this article:

Wet or moist wound treatment significantly reduces the time required for re-epithelialization

Since the lips are (normally) constantly being moistened by saliva, this could be the reason you experience accelerated cut healing.

Sunburned Lips: The Best Ways to Soothe and Heal Them, According to Dermatologists

Protect your pucker from damaging UV rays this summer.

All parts of the body are susceptible to sunburn, but some more than others—whether it’s because the sun hits the body area directly or because you didn&apost apply sunscreen. Your lips are a particularly vulnerable spot. Preventing sunburned lips should be a priority, not only so you avoid painful redness and swelling but because sunburned lips can raise your risk of skin cancer.

13 Amazing Facts About Your Lips

What is there to say about lips? They're essential equipment for eating and speaking, of course. And whistling. And kissing. And we'd look pretty silly without them, wouldn't we?

But if you think that's all there is to say--and know--about human lips, you're in for a big surprise. Just take a look at our list of 13 fascinating facts about lips:

FACT: Your lips are unique.

Many animal species have lips, of course. But only human lips have such a distinct border between the pinkish, reddish parts and the surrounding skin, according to LiveScience. Scientists call this the "vermilion border."

FACT: Your lips can help you choose a mate.

It's hard to kiss without lips, and some scientists believe that kissing plays a key role in mate selection. It seems that locking lips brings potential mates close enough that they exchange biological information--via sniffing another's pheromones. Women are believed to prefer the scent of men whose immune systems differ from their own--and pheromones may be a key to this determination.

FACT: That fleshy bump in the middle of your upper lip has a name.

In fact, that fleshy bump has a few names, including procheilion, labial tubercle, or tuberculum labii superioris.

FACT: Your lips can say something about your sexuality.

Hard to believe, but recent research links the shape of a woman's lips with her ability to achieve orgasm. Specifically, a Scottish psychologist named Stuart Brody found that women with a prominent tubercle of the upper lip are better able to achieve vaginal orgasm. Who knew?

FACT: Bigger is generally better.

When it comes to attracting the opposite sex, big lips are better, the BBC reported. That is, at least where a woman's lips are concerned. But women seem to prefer men with medium-sized lips, a University of Louisville psychologist told the BBC in 2003.

FACT: Your lips aren't the world's biggest.

Unless you're Kristina Rei, that is. The young Russian woman is said to have the world's biggest lips, and no wonder. She underwent multiple silicone injections, all part of an effort to make her lips like those of Jessica Rabbit of the hit 1988 movie Who Framed Roger Rabbit? Did she succeed? See for yourself.

FACT: Lips haven't always been used for kissing.

"Kissing was very restricted up until very recently to areas of Asia--Southeast Asia mainly--and Europe until the conquests in the 1500s," Dr. Vaughn Bryant, professor of anthropology at Texas A&M University, said in a written statement. "No one in the New World kissed, no one in Oceania kissed, the Eskimos didn't kiss, people in sub-Saharan Africa didn't kiss." According to Bryant, kissing started in India and spread slowly after soldiers under the command of Alexander the Great brought the custom home with them.

FACT: It takes many muscles to pucker up.

To pucker up for a kiss - or to play that trumpet - you have to contract your orbicularis oris. Scientists used to think the orbicularis oris was a single sphincter muscle inside the lips. But now we know it's actually a complex of four muscles.

FACT: Red lips can make you rich.

Some have said that lipstick makes women more attractive to men because it makes the lips look more like the vagina's labia. Hmm. But one thing that seems clear is that wearing red lipstick can pay off for women. In a recent study from France, sociologists showed that waitresses who wear red lipstick earn bigger tips--though only from male customers. Waitresses' red lipstick had no effect on the generosity of female customers.

FACT: Lips can become paralyzed.

People suffering from a form of facial paralysis known as Bell's palsy can have trouble smiling or frowning. The condition is caused by damage to the facial nerves. Fortunately, people with Bell's palsy generally recover with time.

FACT: Lips don't sweat.

No wonder--lips simply don't have sweat glands. Since sweat glands also help keep the skin moisturized, that means lips tend to dry out faster than other parts of the body.

FACT: Blood gives your lips their reddish hue.

The skin of the lips is thinner than skin elsewhere on the body, consisting of three to five cellular layers instead of up to 16. Thinner skin means it's easier to see the blood vessels underneath. Of course, this effect is more pronounced in people with light-colored skin.

FACT: Lips get thinner as you age.

Lips get their shape in part from collagen. But as the body ages, the body produces less of this critical protein, and the lips start to lose their plumpness, dermatologist Dr. D'Anne Kleinsmith told Real Simple. Another factor, she said, is ultraviolet light from sunlight. "One way to help preserve the fullness of your lips is to protect them from the sun by wearing a lipstick or lip balm with sunscreen," Dr. Kleinsmith told the magazine.

How to heal dry chapped lips due to harsh weather

Exposure to harsh weather and wind pull moisture out of your skin, including your lips. The solution is to moisturize your dry lips with a simple, high quality lip balm.

The two tried and true lip care products that I use in my practice are my Natural Lip Balm and Vanicream Lip Protectant SPF 30. Both are deeply hydrating and will soothe chapped lips. They both come in convenient tubes so that you can easily carry them with you and use them throughout the day. - Dermatologist Dr. Cynthia Bailey

  • The Natural Lip Balmis ideal for anytime use.
  • When you are outdoors in the sun, use the Vanicream Lip SPF Protectantbecause you need to protect your delicate lip skin from the sun’s harmful UV rays.

Unless you are constantly out in harsh weather (think fishermen and skiers), your lips should respond quickly once you are using the right lip balm. These two products are the best lip balms to care for your lips!

How Your Lip Color Will Heal

Days 1-2: You love your new lip color!

Your lip color will appear brighter than it will heal. Your lips will also feel swollen and tender. Your color will begin to darken temporarily throughout the day as the pigment oxidizes.

Days 3-14: Swelling will have finished.

Your lips will feel dry and start the flaking process. Allow shedding to happen naturally. As your lips flake, it will appear that your lip color is very light and "frosty". This is only temporary as you are still healing. Over the next several days your lip color will reappear until it fully blooms.

Days 28-42: It’s time for your follow up.

By this time your lips are fully healed and it’s recommended that you come back in to touch up any color that might have healed too light or at all imperfectly. Applying a second layer of new color will build off of your previous color, creating a more saturated and longer-lasting lip. During this appointment, you also have the opportunity to further adjust the shape if desired.

How lip wound heals

Generally, wound healing process elapses four major stages—hemostasis, inflammation, proliferation, and remodeling. These four stages may need weeks to years to complete, depending on the severity of the wound and properness of the wound care in promoting healing. If you are expecting a proper wound healing process for your wounded lip, consider some of the factors contributing to its healing, such as:

  • The depth of the wound.
  • The direction of the wound.
  • Sun exposure.
  • Dressing types.
  • The cause of the wound.

However, some people experience a very slow healing with a palatal wound—the wound located on the upper or lower lip, as even a small movement of the lips causes the wound to crack and re-bleed. Hence, some questions raised, do palatal wounds heal differently from the wounds located on the other body parts? In fact, wounded lip will elapse similar healing process with any wounds in any parts of the body. Surprisingly, the wound can possibly heal faster and prone less to infection than wounds on the other parts of the body. The main stages of lip wound healing process are:

  • Hemostasis—bleeding, which occurs as body natural way of cleansing injured part. Although oral wounds may bleed a lot, it heals in quite faster period compared to the other wounds located in other body parts.
  • Inflammation—which is caused by secreted chemicals by the body which functions to kill bacteria around the wound site. Lips which are wounded by contacts with rough surface, for instance, will bleed and swell for some days before starting the entire healing process.
  • Proliferation—which is signed by the formation of some new skin cells. During this stage, epidermal cells migrate from the wound edge, causing the wounded site to enclose. During the proliferation stage, the wound site might have lighter tone than its surrounding. Scabs may also form in this period to protect delicate skin tissues.
  • Remodeling—collagen is produced and will strengthen the skin around the wound site. Fibers are reorganized and tissue integrity increases, so that the process can be longer than three other stages.

Seeing these stages, it becomes clear that sufficient blood supply and anti-bacterial agent are some of the most important factors determining how fast a wound is going to heal. Hence, why palatal or lip wound can heal very quickly and less prone to infection can be explained as follow:


  • Hemostasis(blood clotting): Within the first few minutes of injury, platelets in the blood begin to stick to the injured site. They change into an amorphous shape, more suitable for clotting, and they release chemical signals to promote clotting. This results in the activation of fibrin, which forms a mesh and acts as "glue" to bind platelets to each other. This makes a clot that serves to plug the break in the blood vessel, slowing/preventing further bleeding. [5][6]
  • Inflammation: During this phase, damaged and dead cells are cleared out, along with bacteria and other pathogens or debris. This happens through the process of phagocytosis, where white blood cells engulf debris and destroy it. Platelet-derived growth factors are released into the wound that cause the migration and division of cells during the proliferative phase.
  • Proliferation (growth of new tissue): In this phase, angiogenesis, collagen deposition, granulation tissue formation, epithelialization, and wound contraction occur. [7] In angiogenesis, vascular endothelial cells form new blood vessels. [8] In fibroplasia and granulation tissue formation, fibroblasts grow and form a new, provisional extracellular matrix (ECM) by excreting collagen and fibronectin. [7] Concurrently, re-epithelialization of the epidermis occurs, in which epithelial cells proliferate and 'crawl' atop the wound bed, providing cover for the new tissue. [9] In wound contraction, myofibroblasts decrease the size of the wound by gripping the wound edges and contracting using a mechanism that resembles that in smooth muscle cells. When the cells' roles are close to complete, unneeded cells undergo apoptosis. [7]
  • Maturation (remodeling): During maturation and remodeling, collagen is realigned along tension lines, and cells that are no longer needed are removed by programmed cell death, or apoptosis.

Timing is important to wound healing. Critically, the timing of wound re-epithelialization can decide the outcome of the healing. [11] If the epithelization of tissue over a denuded area is slow, a scar will form over many weeks, or months [12] [13] If the epithelization of a wounded area is fast, the healing will result in regeneration. [13]

Wound healing is classically divided into hemostasis, inflammation, proliferation, and remodeling. Although a useful construct, this model employs considerable overlapping among individual phases. A complementary model has recently been described [1] where the many elements of wound healing are more clearly delineated. The importance of this new model becomes more apparent through its utility in the fields of regenerative medicine and tissue engineering (see Research and development section below). In this construct, the process of wound healing is divided into two major phases: the early phase and the cellular phase: [1]

The early phase, which begins immediately following skin injury, involves cascading molecular and cellular events leading to hemostasis and formation of an early, makeshift extracellular matrix that provides structural staging for cellular attachment and subsequent cellular proliferation.

The cellular phase involves several types of cells working together to mount an inflammatory response, synthesize granulation tissue, and restore the epithelial layer. [1] Subdivisions of the cellular phase are:

    and inflammatory components (within 1–2 days) -mesenchymal interaction: re-epithelialization (phenotype change within hours, migration begins on day 1 or 2) and myofibroblasts: progressive alignment, collagen production, and matrix contraction (between day 4 and day 14) and angiogenesis (begins on day 4)
  1. Dermal matrix: elements of fabrication (begins on day 4, lasting 2 weeks) and alteration/remodeling (begins after week 2, lasting weeks to months—depending on wound size). [1]

Just before the inflammatory phase is initiated, the clotting cascade occurs in order to achieve hemostasis, or stop blood loss by way of a fibrin clot. Thereafter, various soluble factors (including chemokines and cytokines) are released to attract cells that phagocytise debris, bacteria, and damaged tissue, in addition to releasing signaling molecules that initiate the proliferative phase of wound healing.

Clotting cascade Edit

When tissue is first wounded, blood comes in contact with collagen, triggering blood platelets to begin secreting inflammatory factors. [15] Platelets also express sticky glycoproteins on their cell membranes that allow them to aggregate, forming a mass. [7]

Fibrin and fibronectin cross-link together and form a plug that traps proteins and particles and prevents further blood loss. [16] This fibrin-fibronectin plug is also the main structural support for the wound until collagen is deposited. [7] Migratory cells use this plug as a matrix to crawl across, and platelets adhere to it and secrete factors. [7] The clot is eventually lysed and replaced with granulation tissue and then later with collagen.

Platelets, the cells present in the highest numbers shortly after a wound occurs, release mediators into the blood, including cytokines and growth factors. [15] Growth factors stimulate cells to speed their rate of division. Platelets release other proinflammatory factors like serotonin, bradykinin, prostaglandins, prostacyclins, thromboxane, and histamine, [3] which serve several purposes, including increasing cell proliferation and migration to the area and causing blood vessels to become dilated and porous. In many ways, extravasated platelets in trauma perform a similar function to tissue macrophages and mast cells exposed to microbial molecular signatures in infection: they become activated, and secrete molecular mediators – vasoactive amines, eicosanoids, and cytokines – that initiate the inflammatory process.

Vasoconstriction and vasodilation Edit

Immediately after a blood vessel is breached, ruptured cell membranes release inflammatory factors like thromboxanes and prostaglandins that cause the vessel to spasm to prevent blood loss and to collect inflammatory cells and factors in the area. [3] This vasoconstriction lasts five to ten minutes and is followed by vasodilation, a widening of blood vessels, which peaks at about 20 minutes post-wounding. [3] Vasodilation is the end result of factors released by platelets and other cells. The main factor involved in causing vasodilation is histamine. [3] [15] Histamine also causes blood vessels to become porous, allowing the tissue to become edematous because proteins from the bloodstream leak into the extravascular space, which increases its osmolar load and draws water into the area. [3] Increased porosity of blood vessels also facilitates the entry of inflammatory cells like leukocytes into the wound site from the bloodstream. [17] [18]

Polymorphonuclear neutrophils Edit

Within an hour of wounding, polymorphonuclear neutrophils (PMNs) arrive at the wound site and become the predominant cells in the wound for the first two days after the injury occurs, with especially high numbers on the second day. [19] They are attracted to the site by fibronectin, growth factors, and substances such as kinins. Neutrophils phagocytise debris and kill bacteria by releasing free radicals in what is called a 'respiratory burst. [20] [21] They also cleanse the wound by secreting proteases that break down damaged tissue. Functional neutrophils at the wound site only have life-spans of around 2 days, so they usually undergo apoptosis once they have completed their tasks and are engulfed and degraded by macrophages. [22]

Other leukocytes to enter the area include helper T cells, which secrete cytokines to cause more T cells to divide and to increase inflammation and enhance vasodilation and vessel permeability. [17] [23] T cells also increase the activity of macrophages. [17]

Macrophages Edit

One of the macrophage's roles is to phagocytize other expended phagocytes, [24] bacteria and damaged tissue, [19] and they also debride damaged tissue by releasing proteases. [25]

Macrophages function in regeneration [26] [27] and are essential for wound healing. [19] They are stimulated by the low oxygen content of their surroundings to produce factors that induce and speed angiogenesis [20] and they also stimulate cells that reepithelialize the wound, create granulation tissue, and lay down a new extracellular matrix. [28] By secreting these factors, macrophages contribute to pushing the wound healing process into the next phase. They replace PMNs as the predominant cells in the wound by two days after injury. [24]

The spleen contains half the body's monocytes in reserve ready to be deployed to injured tissue. [29] [30] Attracted to the wound site by growth factors released by platelets and other cells, monocytes from the bloodstream enter the area through blood vessel walls. [31] Numbers of monocytes in the wound peak one to one and a half days after the injury occurs. [23] Once they are in the wound site, monocytes mature into macrophages. Macrophages also secrete a number of factors such as growth factors and other cytokines, especially during the third and fourth post-wounding days. These factors attract cells involved in the proliferation stage of healing to the area. [15]

In wound healing that result in incomplete repair, scar contraction occurs, bringing varying gradations of structural imperfections, deformities and problems with flexibility. [32] Macrophages may restrain the contraction phase. [27] Scientists have reported that removing the macrophages from a salamander resulted in failure of a typical regeneration response (limb regeneration), instead bringing on a repair (scarring) response. [33] [34]

Decline of inflammatory phase Edit

As inflammation dies down, fewer inflammatory factors are secreted, existing ones are broken down, and numbers of neutrophils and macrophages are reduced at the wound site. [19] These changes indicate that the inflammatory phase is ending and the proliferative phase is underway. [19] In vitro evidence, obtained using the dermal equivalent model, suggests that the presence of macrophages actually delays wound contraction and thus the disappearance of macrophages from the wound may be essential for subsequent phases to occur. [27]

Because inflammation plays roles in fighting infection, clearing debris and inducing the proliferation phase, it is a necessary part of healing. However, inflammation can lead to tissue damage if it lasts too long. [7] Thus the reduction of inflammation is frequently a goal in therapeutic settings. Inflammation lasts as long as there is debris in the wound. Thus, if the individual's immune system is compromised and is unable to clear the debris from the wound and/or if excessive detritus, devitalized tissue, or microbial biofilm is present in the wound, these factors may cause a prolonged inflammatory phase and prevent the wound from properly commencing the proliferation phase of healing. This can lead to a chronic wound.

About two or three days after the wound occurs, fibroblasts begin to enter the wound site, marking the onset of the proliferative phase even before the inflammatory phase has ended. [35] As in the other phases of wound healing, steps in the proliferative phase do not occur in a series but rather partially overlap in time.

Angiogenesis Edit

Also called neovascularization, the process of angiogenesis occurs concurrently with fibroblast proliferation when endothelial cells migrate to the area of the wound. [36] Because the activity of fibroblasts and epithelial cells requires oxygen and nutrients, angiogenesis is imperative for other stages in wound healing, like epidermal and fibroblast migration. The tissue in which angiogenesis has occurred typically looks red (is erythematous) due to the presence of capillaries. [36]

Angiogenesis occurs in overlapping phases in response to inflammation:

  1. Latent period: During the haemostatic and inflammatory phase of the wound healing process, vasodilation and permeabilisation allow leukocyte extravasation and phagocytic debridement and decontamination of the wound area. Tissue swelling aids later angiogenesis by expanding and loosening the existing collagenous extracellular matrix.
  2. Endothelial activation: As the wound macrophages switches from inflammatory to healing mode, it begins to secrete endothelial chemotactic and growth factors to attract adjacent endothelial cells. Activated endothelial cells respond by retracting and reducing cell junctions, loosening themselves from their embedded endothelium. Characteristically the activated endothelial cells show enlarged nucleoli.
  3. Degradation of endothelial basement membrane: The wound macrophages, mast cells and the endothelial cells themselves secrete proteases to break down existing vascular basal lamina.
  4. Vascular sprouting: With the breakdown of endothelial basement membrane, detached endothelial cells from pre-existing capillaries and post-capillary venules can divide and migrate chemotactically towards the wound, laying down new vessels in the process. Vascular sprouting can be aided by ambient hypoxia and acidosis in the wound environment, as hypoxia stimulates the endothelial transcription factor, hypoxia inducible factor (HIF) to transactivate angiogenic genes such as VEGF and GLUT1. Sprouted vessels can self-organise into luminal morphologies, and fusion of blind channels give rise to new capillary networks.
  5. Vascular maturation: the endothelium of vessels mature by laying down new endothelial extracellular matrix, followed by basal lamina formation. Lastly the vessel establishes a pericyte layer.

Stem cells of endothelial cells, originating from parts of uninjured blood vessels, develop pseudopodia and push through the ECM into the wound site to establish new blood vessels. [20]

Endothelial cells are attracted to the wound area by fibronectin found on the fibrin scab and chemotactically by angiogenic factors released by other cells, [37] e.g. from macrophages and platelets when in a low-oxygen environment. Endothelial growth and proliferation is also directly stimulated by hypoxia, and presence of lactic acid in the wound. [35] For example, hypoxia stimulates the endothelial transcription factor, hypoxia-inducible factor (HIF) to transactivate a set of proliferative genes including vascular endothelial growth factor (VEGF) and glucose transporter 1 (GLUT1).

To migrate, endothelial cells need collagenases and plasminogen activator to degrade the clot and part of the ECM. [3] [19] Zinc-dependent metalloproteinases digest basement membrane and ECM to allow cell migration, proliferation and angiogenesis. [38]

When macrophages and other growth factor-producing cells are no longer in a hypoxic, lactic acid-filled environment, they stop producing angiogenic factors. [20] Thus, when tissue is adequately perfused, migration and proliferation of endothelial cells is reduced. Eventually blood vessels that are no longer needed die by apoptosis. [37]

Fibroplasia and granulation tissue formation Edit

Simultaneously with angiogenesis, fibroblasts begin accumulating in the wound site. Fibroblasts begin entering the wound site two to five days after wounding as the inflammatory phase is ending, and their numbers peak at one to two weeks post-wounding. [19] By the end of the first week, fibroblasts are the main cells in the wound. [3] Fibroplasia ends two to four weeks after wounding.

As a model the mechanism of fibroplasia may be conceptualised as an analogous process to angiogenesis (see above) - only the cell type involved is fibroblasts rather than endothelial cells. Initially there is a latent phase where the wound undergoes plasma exudation, inflammatory decontamination and debridement. Oedema increases the wound histologic accessibility for later fibroplastic migration. Second, as inflammation nears completion, macrophage and mast cells release fibroblast growth and chemotactic factors to activate fibroblasts from adjacent tissue. Fibroblasts at this stage loosen themselves from surrounding cells and ECM. Phagocytes further release proteases that break down the ECM of neighbouring tissue, freeing the activated fibroblasts to proliferate and migrate towards the wound. The difference between vascular sprouting and fibroblast proliferation is that the former is enhanced by hypoxia, whilst the latter is inhibited by hypoxia. The deposited fibroblastic connective tissue matures by secreting ECM into the extracellular space, forming granulation tissue (see below). Lastly collagen is deposited into the ECM.

In the first two or three days after injury, fibroblasts mainly migrate and proliferate, while later, they are the main cells that lay down the collagen matrix in the wound site. [3] Origins of these fibroblasts are thought to be from the adjacent uninjured cutaneous tissue (although new evidence suggests that some are derived from blood-borne, circulating adult stem cells/precursors). [39] Initially fibroblasts utilize the fibrin cross-linking fibers (well-formed by the end of the inflammatory phase) to migrate across the wound, subsequently adhering to fibronectin. [37] Fibroblasts then deposit ground substance into the wound bed, and later collagen, which they can adhere to for migration. [15]

Granulation tissue functions as rudimentary tissue, and begins to appear in the wound already during the inflammatory phase, two to five days post wounding, and continues growing until the wound bed is covered. Granulation tissue consists of new blood vessels, fibroblasts, inflammatory cells, endothelial cells, myofibroblasts, and the components of a new, provisional extracellular matrix (ECM). The provisional ECM is different in composition from the ECM in normal tissue and its components originate from fibroblasts. [28] Such components include fibronectin, collagen, glycosaminoglycans, elastin, glycoproteins and proteoglycans. [37] Its main components are fibronectin and hyaluronan, which create a very hydrated matrix and facilitate cell migration. [31] Later this provisional matrix is replaced with an ECM that more closely resembles that found in non-injured tissue.

Growth factors (PDGF, TGF-β) and fibronectin encourage proliferation, migration to the wound bed, and production of ECM molecules by fibroblasts. Fibroblasts also secrete growth factors that attract epithelial cells to the wound site. Hypoxia also contributes to fibroblast proliferation and excretion of growth factors, though too little oxygen will inhibit their growth and deposition of ECM components, and can lead to excessive, fibrotic scarring.

Collagen deposition Edit

One of fibroblasts' most important duties is the production of collagen. [36]

Collagen deposition is important because it increases the strength of the wound before it is laid down, the only thing holding the wound closed is the fibrin-fibronectin clot, which does not provide much resistance to traumatic injury. [20] Also, cells involved in inflammation, angiogenesis, and connective tissue construction attach to, grow and differentiate on the collagen matrix laid down by fibroblasts. [40]

Type III collagen and fibronectin generally begin to be produced in appreciable amounts at somewhere between approximately 10 hours [41] and 3 days, [37] depending mainly on wound size. Their deposition peaks at one to three weeks. [28] They are the predominating tensile substances until the later phase of maturation, in which they are replaced by the stronger type I collagen.

Even as fibroblasts are producing new collagen, collagenases and other factors degrade it. Shortly after wounding, synthesis exceeds degradation so collagen levels in the wound rise, but later production and degradation become equal so there is no net collagen gain. [20] This homeostasis signals the onset of the later maturation phase. Granulation gradually ceases and fibroblasts decrease in number in the wound once their work is done. [42] At the end of the granulation phase, fibroblasts begin to commit apoptosis, converting granulation tissue from an environment rich in cells to one that consists mainly of collagen. [3]

Epithelialization Edit

The formation of granulation tissue into an open wound allows the reepithelialization phase to take place, as epithelial cells migrate across the new tissue to form a barrier between the wound and the environment. [37] Basal keratinocytes from the wound edges and dermal appendages such as hair follicles, sweat glands and sebacious (oil) glands are the main cells responsible for the epithelialization phase of wound healing. [42] They advance in a sheet across the wound site and proliferate at its edges, ceasing movement when they meet in the middle. In healing that results in a scar, sweat glands, hair follicles [43] [44] and nerves do not form. With the lack of hair follicles, nerves and sweat glands, the wound, and the resulting healing scar, provide a challenge to the body with regards to temperature control. [44]

Keratinocytes migrate without first proliferating. [45] Migration can begin as early as a few hours after wounding. However, epithelial cells require viable tissue to migrate across, so if the wound is deep it must first be filled with granulation tissue. [46] Thus the time of onset of migration is variable and may occur about one day after wounding. [47] Cells on the wound margins proliferate on the second and third day post-wounding in order to provide more cells for migration. [28]

If the basement membrane is not breached, epithelial cells are replaced within three days by division and upward migration of cells in the stratum basale in the same fashion that occurs in uninjured skin. [37] However, if the basement membrane is ruined at the wound site, reepithelization must occur from the wound margins and from skin appendages such as hair follicles and sweat and oil glands that enter the dermis that are lined with viable keratinocytes. [28] If the wound is very deep, skin appendages may also be ruined and migration can only occur from wound edges. [46]

Migration of keratinocytes over the wound site is stimulated by lack of contact inhibition and by chemicals such as nitric oxide. [48] Before they begin to migrate, cells must dissolve their desmosomes and hemidesmosomes, which normally anchor the cells by intermediate filaments in their cytoskeleton to other cells and to the ECM. [23] Transmembrane receptor proteins called integrins, which are made of glycoproteins and normally anchor the cell to the basement membrane by its cytoskeleton, are released from the cell's intermediate filaments and relocate to actin filaments to serve as attachments to the ECM for pseudopodia during migration. [23] Thus keratinocytes detach from the basement membrane and are able to enter the wound bed. [35]

Before they begin migrating, keratinocytes change shape, becoming longer and flatter and extending cellular processes like lamellipodia and wide processes that look like ruffles. [31] Actin filaments and pseudopodia form. [35] During migration, integrins on the pseudopod attach to the ECM, and the actin filaments in the projection pull the cell along. [23] The interaction with molecules in the ECM through integrins further promotes the formation of actin filaments, lamellipodia, and filopodia. [23]

Epithelial cells climb over one another in order to migrate. [42] This growing sheet of epithelial cells is often called the epithelial tongue. [45] The first cells to attach to the basement membrane form the stratum basale. These basal cells continue to migrate across the wound bed, and epithelial cells above them slide along as well. [45] The more quickly this migration occurs, the less of a scar there will be. [49]

Fibrin, collagen, and fibronectin in the ECM may further signal cells to divide and migrate. Like fibroblasts, migrating keratinocytes use the fibronectin cross-linked with fibrin that was deposited in inflammation as an attachment site to crawl across. [25] [31] [42]

As keratinocytes migrate, they move over granulation tissue but stay underneath the scab, thereby separating the scab from the underlying tissue. [42] [47] Epithelial cells have the ability to phagocytize debris such as dead tissue and bacterial matter that would otherwise obstruct their path. Because they must dissolve any scab that forms, keratinocyte migration is best enhanced by a moist environment, since a dry one leads to formation of a bigger, tougher scab. [25] [37] [42] [50] To make their way along the tissue, keratinocytes must dissolve the clot, debris, and parts of the ECM in order to get through. [47] [51] They secrete plasminogen activator, which activates plasminogen, turning it into plasmin to dissolve the scab. Cells can only migrate over living tissue, [42] so they must excrete collagenases and proteases like matrix metalloproteinases (MMPs) to dissolve damaged parts of the ECM in their way, particularly at the front of the migrating sheet. [47] Keratinocytes also dissolve the basement membrane, using instead the new ECM laid down by fibroblasts to crawl across. [23]

As keratinocytes continue migrating, new epithelial cells must be formed at the wound edges to replace them and to provide more cells for the advancing sheet. [25] Proliferation behind migrating keratinocytes normally begins a few days after wounding [46] and occurs at a rate that is 17 times higher in this stage of epithelialization than in normal tissues. [25] Until the entire wound area is resurfaced, the only epithelial cells to proliferate are at the wound edges. [45]

Growth factors, stimulated by integrins and MMPs, cause cells to proliferate at the wound edges. Keratinocytes themselves also produce and secrete factors, including growth factors and basement membrane proteins, which aid both in epithelialization and in other phases of healing. [52] Growth factors are also important for the innate immune defense of skin wounds by stimulation of the production of antimicrobial peptides and neutrophil chemotactic cytokines in keratinocytes.

Keratinocytes continue migrating across the wound bed until cells from either side meet in the middle, at which point contact inhibition causes them to stop migrating. [31] When they have finished migrating, the keratinocytes secrete the proteins that form the new basement membrane. [31] Cells reverse the morphological changes they underwent in order to begin migrating they reestablish desmosomes and hemidesmosomes and become anchored once again to the basement membrane. [23] Basal cells begin to divide and differentiate in the same manner as they do in normal skin to reestablish the strata found in reepithelialized skin. [31]

Contraction Edit

Contraction is a key phase of wound healing with repair. If contraction continues for too long, it can lead to disfigurement and loss of function. [32] Thus there is a great interest in understanding the biology of wound contraction, which can be modelled in vitro using the collagen gel contraction assay or the dermal equivalent model. [27] [53]

Contraction commences approximately a week after wounding, when fibroblasts have differentiated into myofibroblasts. [54] In full thickness wounds, contraction peaks at 5 to 15 days post wounding. [37] Contraction can last for several weeks [46] and continues even after the wound is completely reepithelialized. [3] A large wound can become 40 to 80% smaller after contraction. [31] [42] Wounds can contract at a speed of up to 0.75 mm per day, depending on how loose the tissue in the wounded area is. [37] Contraction usually does not occur symmetrically rather most wounds have an 'axis of contraction' which allows for greater organization and alignment of cells with collagen. [54]

At first, contraction occurs without myofibroblast involvement. [55] Later, fibroblasts, stimulated by growth factors, differentiate into myofibroblasts. Myofibroblasts, which are similar to smooth muscle cells, are responsible for contraction. [55] Myofibroblasts contain the same kind of actin as that found in smooth muscle cells. [32]

Myofibroblasts are attracted by fibronectin and growth factors and they move along fibronectin linked to fibrin in the provisional ECM in order to reach the wound edges. [25] They form connections to the ECM at the wound edges, and they attach to each other and to the wound edges by desmosomes. Also, at an adhesion called the fibronexus, actin in the myofibroblast is linked across the cell membrane to molecules in the extracellular matrix like fibronectin and collagen. [55] Myofibroblasts have many such adhesions, which allow them to pull the ECM when they contract, reducing the wound size. [32] In this part of contraction, closure occurs more quickly than in the first, myofibroblast-independent part. [55]

As the actin in myofibroblasts contracts, the wound edges are pulled together. Fibroblasts lay down collagen to reinforce the wound as myofibroblasts contract. [3] The contraction stage in proliferation ends as myofibroblasts stop contracting and commit apoptosis. [32] The breakdown of the provisional matrix leads to a decrease in hyaluronic acid and an increase in chondroitin sulfate, which gradually triggers fibroblasts to stop migrating and proliferating. [19] These events signal the onset of the maturation stage of wound healing.

When the levels of collagen production and degradation equalize, the maturation phase of tissue repair is said to have begun. [20] During maturation, type III collagen, which is prevalent during proliferation, is replaced by type I collagen. [17] Originally disorganized collagen fibers are rearranged, cross-linked, and aligned along tension lines. [31] The onset of the maturation phase may vary extensively, depending on the size of the wound and whether it was initially closed or left open, [28] ranging from approximately 3 days [41] to 3 weeks. [56] The maturation phase can last for a year or longer, similarly depending on wound type. [28]

As the phase progresses, the tensile strength of the wound increases. [28] Collagen will reach approximately 20% of its tensile strength after 3 weeks, increasing to 80% by 12th week. The maximum scar strength is 80% of that of unwounded skin. [57] Since activity at the wound site is reduced, the scar loses its red appearance as blood vessels that are no longer needed are removed by apoptosis. [20]

The phases of wound healing normally progress in a predictable, timely manner if they do not, healing may progress inappropriately to either a chronic wound [7] such as a venous ulcer or pathological scarring such as a keloid scar. [58] [59]

Many factors controlling the efficacy, speed, and manner of wound healing fall under two types: local and systemic factors. [2]

Local factors Edit

  • Moisture keeping a wound moist rather than dry makes wound healing more rapid and with less pain and less scarring [60]
  • Mechanical factors
  • Faulty technique of wound closure and necrosis
  • Foreign bodies. Sharp, small foreign bodies can penetrate the skin leaving little surface wound but causing internal injury and internal bleeding. For a glass foreign body, "frequently, an innocent skin wound disguises the extensive nature of the injuries beneath". [61] First-degree nerve injury requires a few hours to a few weeks to recover. [62] If a foreign body passes by a nerve and causes first-degree nerve injury during entry, then the sensation of the foreign body or pain due to internal wounding may be delayed by a few hours to a few weeks after entry. A sudden increase in pain during the first few weeks of wound healing could be a sign of a recovered nerve reporting internal injuries rather than a newly developed infection.
  • Low oxygen tension
  • Perfusion

Systemic factors Edit

In the 2000s, there were proposed the first Mathematical models of the healing process, based on simplified assumptions and on a system of differential equations solved through MATLAB. The data shed an experimental evidence for which the "rate of the healing process" appears to be "highly influenced by the activity and size of the injury itself as well as the activity of the healing agent." [70]

Up until about 2000, the classic paradigm of wound healing, involving stem cells restricted to organ-specific lineages, had never been seriously challenged. Since then, the notion of adult stem cells having cellular plasticity or the ability to differentiate into non-lineage cells has emerged as an alternative explanation. [1] To be more specific, hematopoietic progenitor cells (that give rise to mature cells in the blood) may have the ability de-differentiate back into hematopoietic stem cells and/or transdifferentiate into non-lineage cells, such as fibroblasts. [39]

Stem cells and cellular plasticity Edit

Multipotent adult stem cells have the capacity to be self-renewing and give rise to different cell types. Stem cells give rise to progenitor cells, which are cells that are not self-renewing, but can generate several types of cells. The extent of stem cell involvement in cutaneous (skin) wound healing is complex and not fully understood.

It is thought that the epidermis and dermis are reconstituted by mitotically active stem cells that reside at the apex of rete ridges (basal stem cells or BSC), the bulge of hair follicles (hair follicular stem cell or HFSC), and the papillary dermis (dermal stem cells). [1] Moreover, bone marrow may also contain stem cells that play a major role in cutaneous wound healing. [39]

In rare circumstances, such as extensive cutaneous injury, self-renewal subpopulations in the bone marrow are induced to participate in the healing process, whereby they give rise to collagen-secreting cells that seem to play a role during wound repair. [1] These two self-renewal subpopulations are (1) bone marrow-derived mesenchymal stem cells (MSC) and (2) hematopoietic stem cells (HSC). Bone marrow also harbors a progenitor subpopulation (endothelial progenitor cells or EPC) that, in the same type of setting, are mobilized to aid in the reconstruction of blood vessels. [39] Moreover, it is thought that extensive injury to skin also promotes the early trafficking of a unique subclass of leukocytes (circulating fibrocytes) to the injured region, where they perform various functions related to wound healing. [1]

Wound repair versus regeneration Edit

An injury is an interruption of morphology and/or functionality of a given tissue. After injury, structural tissue heals with incomplete or complete regeneration. [71] [72] Tissue without an interruption to the morphology almost always completely regenerates. An example of complete regeneration without an interruption of the morphology is non-injured tissue, such as skin. [73] Non-injured skin has a continued replacement and regeneration of cells which always results in complete regeneration. [73]

There is a subtle distinction between 'repair' and 'regeneration'. [1] [71] [72] Repair means incomplete regeneration. [71] Repair or incomplete regeneration, refers to the physiologic adaptation of an organ after injury in an effort to re-establish continuity without regards to exact replacement of lost/damaged tissue. [71] True tissue regeneration or complete regeneration, [72] refers to the replacement of lost/damaged tissue with an ‘exact’ copy, such that both morphology and functionality are completely restored. [72] Though after injury mammals can completely regenerate spontaneously, they usually do not completely regenerate. An example of a tissue regenerating completely after an interruption of morphology is the endometrium the endometrium after the process of breakdown via the menstruation cycle heals with complete regeneration. [73]

In some instances, after a tissue breakdown, such as in skin, a regeneration closer to complete regeneration may be induced by the use of biodegradable (collagen-glycoaminoglycan) scaffolds. These scaffolds are structurally analogous to extracellular matrix (ECM) found in normal/un-injured dermis. [74] Fundamental conditions required for tissue regeneration often oppose conditions that favor efficient wound repair, including inhibition of (1) platelet activation, (2) inflammatory response, and (3) wound contraction. [1] In addition to providing support for fibroblast and endothelial cell attachment, biodegradable scaffolds inhibit wound contraction, thereby allowing the healing process to proceed towards a more-regenerative/less-scarring pathway. Pharmaceutical agents have been investigated which may be able to turn off myofibroblast differentiation. [75]

A new way of thinking derived from the notion that heparan sulfates are key player in tissue homeostasis: the process that makes the tissue replace dead cells by identical cells. In wound areas, tissue homeostasis is lost as the heparan sulfates are degraded preventing the replacement of dead cells by identical cells. Heparan sulfate analogues cannot be degraded by all known heparanases and glycanases and bind to the free heparin sulfate binding spots on the ECM, therefore preserving the normal tissue homeostasis and preventing scarring. [76] [77] [78]

Repair or regeneration with regards to hypoxia-inducible factor 1-alpha (HIF-1a). In normal circumstances after injury HIF-1a is degraded by prolyl hydroxylases (PHDs). Scientists found that the simple up-regulation of HIF-1a via PHD inhibitors regenerates lost or damaged tissue in mammals that have a repair response and the continued down-regulation of Hif-1a results in healing with a scarring response in mammals with a previous regenerative response to the loss of tissue. The act of regulating HIF-1a can either turn off, or turn on the key process of mammalian regeneration. [79] [80]

Scarless wound healing Edit

Scarless wound healing is a concept based on the healing or repair of the skin (or other tissue/organs) after injury with the aim of healing with subjectively and relatively less scar tissue than normally expected. Scarless healing is sometimes mixed up with the concept of scar free healing, which is wound healing which results in absolutely no scar (free of scarring). However they are different concepts.

A reverse to scarless wound healing is scarification (wound healing to scar more). Historically, certain cultures consider scarification attractive [81] however, this is generally not the case in the modern western society, in which many patients are turning to plastic surgery clinics with unrealistic expectations. Depending on scar type, treatment may be invasive (intralesional steroid injections, surgery) and/or conservative (compression therapy, topical silicone gel, brachytherapy, photodynamic therapy). [82] Clinical judgment is necessary to successfully balance the potential benefits of the various treatments available against the likelihood of a poor response and possible complications resulting from these treatments. Many of these treatments may only have a placebo effect, and the evidence base for the use of many current treatments is poor. [83]

Since the 1960s, comprehension of the basic biologic processes involved in wound repair and tissue regeneration have expanded due to advances in cellular and molecular biology. [84] Currently, the principal goals in wound management are to achieve rapid wound closure with a functional tissue that has minimal aesthetic scarring. [85] However, the ultimate goal of wound healing biology is to induce a more perfect reconstruction of the wound area. Scarless wound healing only occurs in mammalian foetal tissues [86] and complete regeneration is limited to lower vertebrates, such as salamanders, and invertebrates. [87] In adult humans, injured tissue are repaired by collagen deposition, collagen remodelling and eventual scar formation, where fetal wound healing is believed to be more of a regenerative process with minimal or no scar formation. [86] Therefore, foetal wound healing can be used to provide an accessible mammalian model of an optimal healing response in adult human tissues. Clues as to how this might be achieved come from studies of wound healing in embryos, where repair is fast and efficient and results in essentially perfect regeneration of any lost tissue.

The etymology of the term scarless wound healing has a long history. [88] [89] [90] In print the antiquated concept of scarless healing was brought up the early 20th century and appeared in a paper published in the London Lancet. This process involved cutting in a surgical slant, instead of a right angle… it was described in various Newspapers. [88] [89] [90]

Cancer Edit

After inflammation, restoration of normal tissue integrity and function is preserved by feedback interactions between diverse cell types mediated by adhesion molecules and secreted cytokines. Disruption of normal feedback mechanisms in cancer threatens tissue integrity and enables a malignant tumor to escape the immune system. [91] [92] An example of the importance of the wound healing response within tumors is illustrated in work by Howard Chang and colleagues at Stanford University studying Breast cancers. [8]

Oral collagen supplements Edit

Preliminary results are promising for the short and long-term use of oral collagen supplements for wound healing and skin aging.Oral collagen supplements also increase skin elasticity, hydration, and dermal collagen density. Collagen supplementation is generally safe with no reported adverse events. Further studies are needed to elucidate medical use in skin barrier diseases such as atopic dermatitis and to determine optimal dosing regimens. [93]

Wound Dressings Edit

Modern wound dressing to aid in wound repair have undergone considerable research and development in recent years. Scientists aim to develop wound dressings which have the following characteristics: [94]

  • Provide wound protection
  • Remove excess exudate properties
  • Maintain a humid environment
  • Have high permeability to oxygen
  • Easily removed from a wound site
  • Non-anaphylactic characteristics

Cotton gauze dressings have been the standard of care, despite their dry properties that can adhere to wound surfaces and cause discomfort upon removal. Recent research has set out to improve cotton gauze dressings to bring them closer in line to achieve modern wound dressing properties, by coating cotton gauze wound dressing with a chitosan/Ag/ZnO nanocomposite. These updated dressing provide increase water absorbency and improved antibacterial efficacy. [94]

Wound cleansing Edit

Dirt or dust on the surface of the wound, bacteria, tissue that has died, and fluid from the wound may be cleaned. The evidence supporting the most effective technique is not clear and there is insufficient evidence to determine conclude whether cleaning wounds is beneficial for promoting healing or whether wound cleaning solutions (polyhexamethylene biguanide, aqueous oxygen peroxide, etc.) are better than sterile water or saline solutions to help venous leg ulcers heal. [95] It is uncertain whether the choice of cleaning solution or method of application makes any difference to venous leg ulcer healing. [95]

Considerable effort has been devoted to understanding the physical relationships governing wound healing and subsequent scarring, with mathematical models and simulations developed to elucidate these relationships. [96] The growth of tissue around the wound site is a result of the migration of cells and collagen deposition by these cells. The alignment of collagen describes the degree of scarring basket-weave orientation of collagen is characteristic of normal skin, whereas aligned collagen fibers lead to significant scarring. [97] It has been shown that the growth of tissue and extent of scar formation can be controlled by modulating the stress at a wound site. [98]

The growth of tissue can be simulated using the aforementioned relationships from a biochemical and biomechanical point of view. The biologically active chemicals that play an important role in wound healing are modeled with Fickian diffusion to generate concentration profiles. The balance equation for open systems when modeling wound healing incorporates mass growth due to cell migration and proliferation. Here the following equation is used:

where ρ represents mass density, R represents a mass flux (from cell migration), and R0 represents a mass source (from cell proliferation, division, or enlargement). [99] Relationships like these can be incorporated into an agent-based models, where the sensitivity to single parameters such as initial collagen alignment, cytokine properties, and cell proliferation rates can be tested. [100]

Successful wound healing is dependent on various cell types, molecular mediators and structural elements. [101]

Primary intention Edit

Primary intention is the healing of a clean wound without tissue loss. [101] In this process, wound edges are brought together, so that they are adjacent to each other (re-approximated). Wound closure is performed with sutures (stitches), staples, or adhesive tape or glue.

Primary intention can only be implemented when the wound is precise and there is minimal disruption to the local tissue and the epithelial basement membrane, e.g. surgical incisions. [102]

This process is faster than healing by secondary intention. [101] There is also less scarring associated with primary intention, as there are no large tissue losses to be filled with granulation tissue, though some granulation tissue will form. [101]

  • Examples of primary intention include: well-repaired lacerations, well reduced bone fractures, healing after flap surgery.
  • Early removal of dressings from clean or clean-contaminated wounds does affect primary healing of wounds. [103] [better source needed]

Secondary intention Edit

  • Secondary intention is implemented when primary intention is not possible because of significant tissue damage or loss, usually due to the wound having been created by major trauma. [102]
  • The wound is allowed to granulate.
  • Surgeon may pack the wound with a gauze or use a drainage system.
  • Granulation results in a broader scar.
  • Healing process can be slow due to presence of drainage from infection.
  • Wound care must be performed daily to encourage wound debris removal to allow for granulation tissue formation.
  • Using antibiotics or antiseptics for the surgical wound healing by secondary intention is controversial. [104]
  • Examples: gingivectomy, gingivoplasty, tooth extraction sockets, poorly reduced fractures, burns, severe lacerations, pressure ulcers.
  • There is insufficient evidence that the choice of dressings or topical agents affects the secondary healing of wounds. [105]
  • There is lack of evidence for the effectiveness of negative pressure wound therapy in wound healing by secondary intention. [106]

Tertiary intention Edit

(Delayed primary closure or secondary suture):

  • The wound is initially cleaned, debrided and observed, typically 4 or 5 days before closure.
  • The wound is purposely left open.
  • Examples: healing of wounds by use of tissue grafts.

If the wound edges are not reapproximated immediately, delayed primary wound healing transpires. This type of healing may be desired in the case of contaminated wounds. By the fourth day, phagocytosis of contaminated tissues is well underway, and the processes of epithelization, collagen deposition, and maturation are occurring. Foreign materials are walled off by macrophages that may metamorphose into epithelioid cells, which are encircled by mononuclear leukocytes, forming granulomas. Usually the wound is closed surgically at this juncture, and if the "cleansing" of the wound is incomplete, chronic inflammation can ensue, resulting in prominent scarring.

Following are the main growth factors involved in wound healing:

  • Activated macrophages
  • Keratinocyte and fibroblast mitogen
  • Keratinocyte migration formation
  • Activated macrophages
  • T-lymphocytes
  • Keratinocytes
    and epithelial cell proliferation
  • Expression of antimicrobial peptides
  • Expression of chemotactic cytokines
  • Epithelial and endothelial cell proliferation
  • Hepatocyte motility
  • Mesenchymal cells
  • Vascular permeability
  • Endothelial cell proliferation
  • Platelets
  • Macrophages
  • Endothelial cells
  • Smooth muscle cells
  • Keratinocytes
    , macrophage, fibroblast and smooth muscle cell chemotaxis
  • Granulocyte, macrophage and fibroblast activation
  • Fibroblast, endothelial cell and smooth muscle cell proliferation , fibronectin and hyaluronan production
  • Angiogenesis
  • Wound remodeling
  • Integrin expression regulation
  • Macrophages
  • T-lymphocytes
  • Endothelial cells
  • Fibroblasts
  • Fibroblast chemotaxis
  • Fibroblast and keratinocyte proliferation
  • Keratinocyte migration
  • Angiogenesis
  • Wound contraction
  • Matrix (collagen fibers) deposition
  • Platelets
  • T-lymphocytes
  • Macrophages
  • Endothelial cells
  • Keratinocytes
  • Smooth muscle cells
  • Fibroblasts
  • Granulocyte, macrophage, lymphocyte, fibroblast and smooth muscle cell chemotaxis synthesis
  • Angiogenesis
  • Fibroplasia
  • Matrix metalloproteinase production inhibition
  • Keratinocyte proliferation
  • Keratinocytes
  • Keratinocyte migration, proliferation and differentiation

The major complications are many:

  1. Deficient scar formation: Results in wound dehiscence or rupture of the wound due to inadequate formation of granulation tissue.
  2. Excessive scar formation: Hypertrophic scar, keloid, desmoid.
  3. Exuberant granulation (proud flesh).
  4. Deficient contraction (in skin grafts) or excessive contraction (in burns).
  5. Others: Dystrophic calcification, pigmentary changes, painful scars, incisional hernia

Other complications can include infection and Marjolin's ulcer.

Advancements in the clinical understanding of wounds and their pathophysiology have commanded significant biomedical innovations in the treatment of acute, chronic, and other types of wounds. Many biologics, skin substitutes, biomembranes and scaffolds have been developed to facilitate wound healing through various mechanisms. [108] This includes a number of products under the trade names such as Epicel, Laserskin, Transcyte, Dermagraft, AlloDerm/Strattice, Biobrane, Integra, Apligraf, OrCel, GraftJacket and PermaDerm. [109]

Causes of Peeling Lips

People usually have a tendency to bite their lips at times of stress and tensions. The biting of lips leads to the formation of wounds. The skin of the lips then begins to peel out when these wounds begin to heal. Therefore one must always leave the lips alone during stressful hours.

Licking of lips is another one very common habit observed in most people. The licking of lips causes the lips to dry even faster and thereby leaving the skin dry, which gradually begin to peel out if proper moisturization is not given.

Cold and dry weather is also one of the major reasons which result in the peeling of lips.

Natural agents such as wind, sunlight, and dust may also sometimes lead to peeling lips. When exposed to these agents, the skin of the lips begins to dry out and develop cracks which cause bleeding and peeling of lips.

Excessive use of cosmetic products such as lipsticks, lip glosses, and lip liners also leads to the dryness and chapping of lips, which further causes peeling lips which are extremely painful.

The Only Way to Use Vaseline on Chapped Lips

Both statements run rampant online. And it can be incredibly difficult to pare down these ChapStick-size nuggets of truth into reliable shopping decisions.

Here’s the catch: When people say “Vaseline,” they mean petroleum jelly (also called petrolatum), a mixture of mineral oils and waxes that’s been on the market for more than 150 years. It’s almost like “Kleenex” vs. “tissue,” except that Vaseline is 100 percent petroleum jelly.

While people have long used Vaseline to help heal minor cuts, scrapes, and burns as well as to moisturize dry skin, your lip skin is a different story from the rest of your body. Your lips are thinner than many other parts of your face, which makes them more vulnerable to the environment. And that slight blush? It’s likely because they’re the inside-out in-between of hair-producing skin tissue (outside) and mucous membrane (inside).

We’re all familiar with this thick jelly (probably because it’s pretty affordable and widely available) — but how does it stack up to all the noisy claims on the internet? Let’s take a look.

Short answer: No. If you’re actually talking about petroleum and not the brand, then it depends on ingredient sourcing and, to be honest, your goals. If you’re talking about Vaseline specifically, it’s how you use it that matters.

Vaseline is a type of moisturizer called an occlusive. Occlusives hold in moisture. They’re different from humectants, which draw in moisture from the air.

When you apply Vaseline to your lips, the petroleum jelly acts as a protective barrier and prevents moisture from escaping. It’s not going to add moisture.

If you lick your lips before applying Vaseline and nothing else, you might make chapped lips worse because lips don’t retain water very well. Theoretically, you could work around that by applying a moisturizer before Vaseline to really pack a hydrating punch.

Allergy research also suggests petroleum jelly may improve the skin barrier in people with eczema. A strong skin barrier means less dry, irritated skin.

In short, you can safely use Vaseline as part of your skin care routine, as many people have for a long time.

Remember: Refined white petroleum jelly — aka Vaseline — is what you’re looking for. It’s generally safe for gentle external use. Just don’t inhale it, eat it, or apply it to sensitive areas (it’s no lube).

What you don’t want is unrefined petroleum jelly. Vaseline is refined, meaning that after the petroleum jelly has been collected, it goes through a process to filter out the harmful, cancerous elements people are worried about.

This begs another question, though: Is Vaseline eco-friendly?

Not really. It’s derived from petroleum, a fossil fuel, which is obtained through oil drilling — hardly a sustainable practice in the long term. Yes, petroleum jelly is a byproduct of this drilling and is not the reason oil companies spend billions. But still, it’s not like petroleum jelly is growing on trees.

The good news is that Vaseline isn’t the only thing in the world keeping your lips soft. There are greener swaps many people swear by:

First things first: Don’t lick or pick. Soothe your lips with balms to avoid irritating them further. If your chapped lips are due to weather (like extreme cold, high winds, or super dry air), aim for tricks like heading inside, turning on a humidifier, or drinking lots of water.

For immediate relief, try exfoliating your lips. Exfoliating may seem counterproductive, but as long as your lips aren’t in too much pain and don’t have open cuts, removing dry, flaky skin will restore their softness and smoothness.

All you need to do is combine an abrasive substance, like sugar, with an emollient, like shea butter, and massage the mixture over your lips. You can also use Vaseline. Instead of mixing in an abrasive substance, rub the Vaseline over your lips with a towel or toothbrush.

After you exfoliate, apply your fave moisturizing lip balm. Balms containing the uber-moisturizing ingredients ceramide and hyaluronic fatty acids are your best bet. Top it off with Vaseline (or your fave alternative) to lock in that moisture.

Just don’t overexfoliate. Stick to a couple of times a week to avoid further damaging your lips.

Not all lip care products are good for chapped lips, no matter the sleek marketing. According to the American Academy of Dermatology, you’ll want to steer clear of:

  • chemical exfoliants like salicylic acid
  • minty ingredients like menthol and peppermint
  • cinnamon
  • citrus
  • camphor
  • eucalyptus
  • any fragrances
  • octinoxate
  • oxybenzone
  • phenol
  • propyl gallate

You know your body best. If you find that something on this list doesn’t irritate you or something that “shouldn’t” does, adjust your use accordingly. A good rule of thumb: If the product is stinging or burning, it’s not working — it’s actually hurting!

What to know about lip cancer

Lip cancer is a form of head and neck cancer that starts in the squamous cells of the lips and mouth. Early signs can include a sore or lump that does not heal on the lips or in the mouth.

According to the Skin Cancer Foundation (SCF), lip cancer accounts for about 0.6 percent of all cancers in the United States. The SCF also state that this type of cancer is most common in males with light skin over the age of 50 years. Common risk factors for lip cancer include prolonged sun exposure, heavy alcohol intake, and tobacco use.

Treatment options depend on the stage, size, and location of the tumor. However, lip cancer is often curable with early diagnosis and treatment.

In this article, we discuss the symptoms of lip cancer, the risk factors, and when to see a doctor. We also cover diagnosis, treatment, prevention, and outlook.

The most common symptom of lip cancer is a sore on the lips or inside the mouth that does not heal.

Other signs and symptoms of lip cancer can include:

  • a lump on the lips or a noticeable thickening
  • painful or numb lips
  • bleeding from the lips
  • a red or white patch on the lips
  • tightness in the jaw that results from swelling

As with other types of cancer, lip cancer may not always have obvious symptoms in the early stages. People sometimes discover that they have lip cancer during a routine visit to their dentist.

The symptoms of lip cancer can be similar to those of other conditions, so it is important to see a doctor or dentist about any unexplained lesions or bleeding from the lips.

Anyone can get lip cancer. However, certain lifestyle and environmental factors can increase a person’s risk of developing this disease.

  • heavy alcohol use
  • smoking or using tobacco products
  • prolonged exposure to natural or artificial sunlight, such as from tanning beds

Other risk factors for lip cancer include:

  • being male
  • having light-colored skin
  • being over the age of 40 years
  • being infected with certain strains of the human papillomavirus (HPV), including strains 16 and 18

A person should consult a doctor or dentist about any unusual changes to their lips or mouth, particularly lumps or other lesions that do not get better on their own.

Regular visits to the dentist increase the likelihood of detecting lip and other types of oral cancer early. It is especially important for people with a higher risk of developing lip cancer to have regular dental checkups.

If a dentist suspects or discovers lip cancer, it is essential for the individual to book an appointment with their primary care provider. A doctor can fully diagnose lip cancer and work with the person to develop an appropriate treatment plan.

A doctor will typically begin a diagnosis by reviewing a person’s symptoms, medical history, and risk factors. They may ask about:

  • the family history of cancer and other diseases
  • tobacco or alcohol consumption
  • previous or current medical conditions
  • history of dental procedures

The doctor will then carry out a physical examination of the person’s mouth. Typically, they will closely inspect the lips and the inside of the mouth for lumps and abnormalities. The doctor may also check the lymph nodes in the neck for swelling.

If the doctor suspects that a person has lip cancer, they will usually carry out a biopsy. This test involves taking a small sample of skin from the affected area and examining it under a microscope for signs of cancer.

If the biopsy confirms a diagnosis of lip cancer, the doctor will then order additional tests to help determine the stage of the cancer and whether it has spread to other areas of the body. These tests may include imaging tests and an endoscopy, or the doctor may take more tissue samples.

The type of treatment for lip cancer typically depends on:

  • the stage of the cancer
  • the size and location of the tumor
  • the person’s general health

A doctor will discuss the available treatment options with the person and work closely with them to develop a suitable treatment plan.

Standard therapy for lip cancer usually involves a combination of surgery and radiation therapy. The aim of surgery is to remove the tumor and also to restore the function and appearance of the lips. Radiation therapy involves the use of high-energy beams to kill tumor cells and prevent cancer from returning.

Other treatment options for lip cancer can include:

It is not always possible to prevent lip cancer. However, a person can reduce their risk of developing lip cancer by:

  • using appropriate sun protection when outside, including sunscreen, lip balm with SPF protection, and a hat with a brim
  • limiting or avoiding the use of tanning beds
  • reducing alcohol intake
  • quitting tobacco products and avoiding tobacco smoke
  • having regular dental checkups

According to the SCF, the most common risk factor for lip cancer is cumulative ultraviolet (UV) light exposure, which is likely to affect people who spend a lot of time in the sun or use tanning beds.

The outlook for people with lip cancer is generally good if a doctor detects and treats the disease early.

According to the American Cancer Society (ACS), the overall 5-year relative survival rate for lip cancer is 88 percent. This figure means that people with lip cancer are 88 percent as likely as those without the condition to live for at least 5 years following diagnosis.

The ACS also state that the 5-year relative survival rate for lip cancer that has not spread beyond the lip is 92 percent, while it is 61 percent when the cancer has spread to nearby tissues or lymph nodes and 24 percent when it has spread to distant parts of the body.

Early signs of lip cancer often include a lump or sore on the lips or inside the mouth that fails to heal. Lip cancer is most common in older males with light-colored skin.

The treatment options for people with lip cancer depend on the stage and size of the tumor, but standard therapy usually involves a combination of surgery and radiation therapy. Early detection and treatment of lip cancer significantly improve a person’s outlook.

People can reduce their risk of lip cancer by using sun protection, limiting alcohol intake, and avoiding the use of tobacco products. Having regular dental checkups makes the early detection of lip cancer more likely.


  1. Graent

    I suggest you visit a site that has a lot of information on this subject.

  2. Vudogor

    In my opinion, you are wrong. I'm sure. I propose to discuss it. Email me at PM, we'll talk.

  3. Doukasa

    I agree with all of the above. We can communicate on this theme. Here or at PM.

  4. Brando

    I can't take part in the discussion right now - I'm very busy. But I will return - I will definitely write what I think.

  5. Banos

    Unequivocally, excellent answer

Write a message