Scientific Skincare - Acne Scars vs Acne Marks
Skincare,  Acne,  Lasers

Acne Scars vs Acne Marks | A Guide To The Different Causes & Treatment Options.

Have you ever had a breakout clear up, only to find that you have been left with skin texture irregularities and discolouration? You’re not alone. Acne affects up to 80% of 18-30-year-olds and 5% of those over 30 [1], 95% of which experience some degree of scarring [2]. But why do we get acne? Why does acne leave scars and marks? What’s the difference between acne scars vs acne marks? And, for the love of all that is good, how do we get rid of acne scars and acne marks?

Fear not, for here is everything you need to know about acne scars, acne marks, and the difference between them.

Acne Scars vs Acne Marks - An Exhaustive Guide

What Is Acne?

Acne (acne vulgaris) is an inflammatory skin condition that is caused by multiple overlapping factors. It is most commonly experienced on the face, back, and chest, as these areas contain the highest number of oil (sebaceous) glands.

What Causes Acne?

Acne is caused by hormones, increases in oil production, dead skin cell build-up, p-acnes bacteria, and inflammatory responses.

Hormones affect how oil glands work and can encourage the production of excess oil (sebum). In addition, hormones can alter the rate of skin cell turnover which can cause an abnormal build up of dead skin cells on the surface of the skin. The influence of hormones on acne is the reason why the majority of people experience some form of breakouts during puberty and why it is common for women to experience breakouts at certain points during their menstrual cycle.

The propionibacterium-acnes (p-acnes) bacteria live within sebaceous glands and use the sebum produced as energy to multiply. Usually, this causes no problem. However, when there is an excessive production of sebum that gets trapped within the hair follicles due to dead skin cell build-up on the surface of the skin, the p-acnes bacteria are able to multiply at an increased rate.

This rise in p-acnes bacteria leads to inflammation and causes the body to send white blood cells into the hair follicle to ‘fight’ the bacteria. It is this process that causes the papules and pustules that are characteristic of acne.

There are a number of other factors that can influence acne (e.g. diet, pollution, stress), however, all these factors contribute to acne by either altering hormones, increasing sebum production, and/or increasing inflammation.

In addition, twin studies have highlighted that acne vulgaris is highly heritable, with genetics responsible for up to 81% of individual differences in acne [3]. In other words, if your parents or siblings had (or still have) acne, you’re more likely to have it too.

So, now we have a better idea of what acne is and what causes it, why does it leave scarring and discolouration? Are there different causes for acne scars vs acne marks?

Why Does Acne Leave Scars?

Acne scars are caused by an altered wound healing response to skin inflammation. Scars, in general, represent the endpoint of the wound healing process, which consists of four stages; haemostasis, inflammation, granulation tissue formation, and matrix remodelling [4][5][6].

The Wound Healing Response

Haemostasis

Haemostasis is the process by which the body prevents bleeding. During this part of the wound healing process, platelets seal off the damaged blood vessels, causing them to constrict. These platelets attach to collagen and secrete various different substances, including growth factors, which then initiate the next phase of wound healing. Haemostasis occurs within minutes of the initial skin injury. In terms of acne lesion healing and scarring, haemostasis is only likely to take place if acne lesions have been picked at.

Inflammation

After blood flow has been stopped, blood vessels relax again which leads to reddening of the skin (erythema). In addition, melanin production may be stimulated. Wound repair requires communication between cells and this communication involves proteins called cytokines and growth factors. Cytokines stimulate cells to move, whereas growth factors stimulate cells to either divide and produce more cells or release certain substances. One such substance is collagen, which is required to form the extracellular matrix.

Granulation Tissue Formation/Proliferation

The proliferation stage of wound healing is characterised by the creation of new blood vessels, collagen deposition, granulation tissue formation, wound contraction, and epithelialisation. Growth factors stimulate the multiplication of fibroblasts as well as encouraging their movement toward the healing wound. These fibroblasts then create new collagen.

Matrix Remodelling

Cytokines encourage fibroblasts and epithelial cells to secrete enzymes known as Matrix Metalloproteases (MMPs) that degrade the extracellular matrix and allow remodelling. MMPs are balanced by Tissue Inhibitors of Metaloproteases (TIMPs) that are released to inactivate them. When MMPs are not balanced by TIMPs, they can destroy growth factors and degrade newly formed collagen and tissue.

Altered Wound Healing Response In Acne Scarring

The key point to note here is that a normal wound healing response requires a balance of MMPs and TIMPs. An imbalance in these enzymes leads to an abnormal production and degradation of collagen during the acne wound healing process and thus acne scarring. When MMPs/TIMPs are unbalanced in favour of MMPs, there is a destruction of collagen in the dermis that results in atrophic scars. In contrast, when MMPs/TIMPs are unbalanced in favour of TIMPs, there is an overproduction of collagen that results in hypertrophic scars [4][7].

Basically, atrophic scars are indented scars that result from the destruction of collagen during the wound healing process, while hypertrophic scars are raised scars that result from too much collagen being produced during the wound healing process.

In 80-90% of cases, true acne scars are atrophic [7].

Why Does Acne Leave Scars?

Types of Acne Scars

In addition to textural scarring, that can be classified as mild, moderate, or severe and is due to collagen over- or under-production, there is another type of acne scarring that is known as ‘macular acne scars’ [4] but is more commonly referred to as ‘acne marks’. 

What’s The Difference Between Acne Scars Vs Acne Marks?

The difference between acne scars vs acne marks lies in both their appearance and their underlying causes. As mentioned, true acne scarring (atrophic or hypertrophic) is caused by an underproduction or overproduction of collagen (respectively) during the wound healing process. In contrast, it is thought that acne marks are due to remaining inflammation that is partly caused by the slow break-down of the non-surviving p-acnes bacteria in the hair follicle [8].

This inflammation is visible in individuals with fair skin (Fitzpatrick Type I & II) as red acne marks (post-inflammatory erythema; PIE) and in individuals with darker skin (Fitzpatrick Type III – VI) as brown acne marks (post-inflammatory hyperpigmentation; PIH) [9][10]. However, it is not uncommon for individuals to experience both PIE and PIH at the same time.

PIH and PIE both tend to resolve themselves with time, thus differing from true acne scars [11].

The key distinction is that acne marks are flat and either red or brown in colour, whereas acne scars are textural irregularities [4].

Red acne marks = PIE

Brown acne marks = PIH

Raised acne scars = Hypertrophic

Indented acne scars = Atrophic

What's The Difference Between Acne Scars vs Acne MarksTypes of Acne Scars vs Acne Marks

PIH Acne Marks vs PIE Acne Marks

The difference between PIH vs PIE is not just down to the colour of the acne marks, but how these acne marks are caused. Both PIH and PIE are caused by inflammation or skin injury. However, in PIH, this inflammation causes an increase in the production of pigment. Specifically, melanin is overproduced by melanocytes (melanin-producing cells) and transferred to surrounding keratinocytes (skin cells) [10].

In contrast, PIE results due to the blood vessel dilation associated with wound healing. The appearance of which is worsened by the fact that the skin is thinner during the healing process [11]. Some evidence also suggests that acne is associated with skin barrier dysfunctions and that the residual erythema associated with PIE is largely due to damage and dehydration in the skins outermost layer – the stratum corneum [12].

Another difference between PIH vs PIE may be purely down to the type of melanin produced in response to inflammation. There are two basic types of melanin that are found in human skin; eumelanin and pheomelanin. Eumelanin is the type of melanin that springs to mind when discussing pigmentation as it is brown/black in colour, more prevalent in darker skin types, and has a photoprotective effect. Pheomelanin, on the other hand, is yellow/reddish in colour, is more prevalent in fairer skin types, is photo-unstable, and may even promote skin cancer [13].

In this sense, the difference between PIH vs PIE may simply be down to the different types of melanin expressed by different skin types.

PIE Acne Marks Vs PIH Acne Marks

 

Atrophic Acne Scars vs Hypertrophic Acne Scars

As mentioned earlier, the majority of true acne scars (80-90%) are atrophic, meaning that they leave skin indentations due to an underproduction of collagen during the wound healing process.

Atrophic scars are further categorised into three separate groups:

  • Icepick scars account for the majority of atrophic scars (60-70%) and are usually narrow, v-shaped, and extend into the deep dermis. They are deeper than they are wide.
  • Boxcar scars account for about 20-30% of atrophic scars and are wider, round-to-oval in shape, and have sharply defined vertical edges. They can be shallow or deep, but do not tend to be deeper than ice-pick scars. In general, they are wider than they are deep.
  • Rolling scars are the least common (15-25%), but the widest form of atrophic scars. They are due to a fibrous anchoring of the dermis to the subcutaneous tissue that leads to shadowing and a rippling effect on the surface of the skin. These scars can be smoothed out if stretched [1][7].

Hypertrophic acne scars are a lot less common and are typically pink, raised, and firm and are more similar to other skin scars (e.g. from surgery). They are more common on the body rather than the face and are more likely to occur in darker skin types [4].

Icepick Acne Scars vs Boxcar Acne Scars vs Rolling Acne Scars

How To Treat Acne Scars Vs Acne Marks

First things first, it is important to ensure that active acne is treated before trying to improve the appearance of acne scars, otherwise, new scars will continue to form. The early treatment of active acne remains the most effective way to prevent or reduce acne scarring [14].

The current treatment for atrophic acne scars usually requires procedures such as laser resurfacing, dermabrasion, microneedling, radiofrequency, dermal fillers, or subcision and excisional techniques (cutting under the scar or cutting out the scar) [1]. Some laser treatments can help improve the appearance of PIE and PIH acne marks as well.

Laser Treatments For Acne Marks Vs Acne Scars

Laser treatments use focused beams of light to treat several skin conditions. Within the skin, there are various light-absorbing molecules known as chromophores. These chromophores absorb energy from light photons that are absorbed through the skin. Different wavelengths of light are absorbed by different chromophores, such as melanin, haemoglobin, and water [15].

When absorbed, the light photon transfers energy to the chromophore which can then produce a thermal, mechanical, or chemical change in and around the chromophore. Selective thermolysis refers to the ability of a wavelength of light to selectively target, heat, and damage specific chromophores in the target tissue, without damaging the surrounding tissue [16].

For example, vascular lasers use selective thermolysis to selectively destroy blood vessels in the dermis [17]. Basically, vascular lasers penetrate the skin and heat the small blood vessels which destroys the vessel walls and coagulates the blood inside. The body then breaks down the old coagulated blood and absorbs it into the bloodstream where it can eventually be excreted. This process is similar to how a bruise heals.

Vascular Lasers for Acne Scars Vs Acne Marks

Vascular lasers generally have a wavelength somewhere between 400 and 600 nanometres (nm). This is due to the fact that their target chromophore is oxyhaemoglobin, which is the substance that gives blood its bright red colour. Oxyhaemoglobin absorbs light within the yellow and green range, especially at wavelengths of 418nm, 542nm, and 577nm [18].

In addition, some vascular lasers can encourage collagen production. Although the heat is targeted at blood vessels, it can also diffuse into the surrounding tissue which can boost collagen production [19]. This means that some vascular lasers may be able to help improve the appearance of indented scars, such as atrophic scars, as well as PIE acne marks.

Examples of vascular lasers:

  • Pulsed Dye Laser (PDL) – 585-595nm (e.g. V-Beam Laser) – Considered the gold-standard treatment for PIE.
  • Potassium Titanyl Phosphate (KTP) Laser – 532nm.
  • Nd:YAG/ Microsecond-pulsed NdYAG Laser – 1064nm (e.g. Laser Genesis) – More suitable for diffuse redness.

Research has demonstrated that acne scarring, as well as the redness associated with acne scarring,  can be improved by up to 68% after one or two treatments with PDL [18]. In one study, two sessions of 595nm PDL improved PIE in 90% of patients by 57.6% [20]. Another study reported a 47.8% reduction in acne scars after PDL treatment [21].

KTP lasers have less of an effect on collagen production and atrophic scars but are still effective at treating scar-associated erythema with some studies suggesting that they are equally as effective as PDL [22].

Microsecond-pulsed Nd:YAG lasers bulk heat the papillary dermis to reduce superficial erythema and boost collagen production which suggests that they can treat both PIE acne marks and atrophic acne scars. In addition, long-pulsed Nd:YAG lasers are able to heat oil glands and reduce oil production, as well as reduce acne inflammation [23].

In fact, in one case report of four patients, a single session of Nd:YAG was sufficient enough to treat mild to moderate acne and reduce acne scarring. Furthermore, at a follow-up, these improvements appeared to be long-term as no reoccurrences of acne were noted [24]. PDL and KTP are also able to treat active acne outbreaks, which means that treatment can begin before acne has fully resolved and may even help prevent further scarring.

However, vascular lasers often cause bruising, although, this is to be expected and usually resolves within 7-14 days [25]. Furthermore, vascular lasers should be used with caution in darker skin types due to the risks of pigmentation changes. Darkening of skin pigmentation (hyperpigmentation) can occur with PDL and may last up to 6 weeks after treatment. Whereas, lightening of skin pigmentation (hypopigmentation) can occur with both PDL and KTP but generally resolves within 3-6 months [25].

Note: Vascular lasers are also pretty good at hair removal so they may be unsuitable for men who have scarring in the beard area and want to keep their facial hair.

Other Non-Ablative Lasers for Acne Scars Vs Acne Marks

The vascular lasers mentioned above are examples of non-ablative lasers. This means that they are able to deliver energy into the dermis without damaging the epidermis and thus require a lot less downtime than traditional ablative lasers.

While the Nd:YAG laser does target haemoglobin, it is not strictly a vascular laser. Its preferred chromophore target is water, which means that it is able to induce collagen remodelling. In addition, it is also able to target melanin to a certain extent [26].

Nd:YAG lasers can offer around 20-30% improvement for atrophic acne scars [27]. In one study, eight sessions of 1064nm Nd:YAG laser led to an average improvement of atrophic acne scars by 29.4% [28].

Nd:YAG lasers are less likely to cause pigmentation issues in darker skin types (compared to vascular lasers), although there is still some risk.

Non-ablative fractionated lasers also stimulate collagen remodelling by targeting water chromophores with variable absorption by melanin and haemoglobin, the main difference being that they deliver energy through microchannels [29].

Examples of non-ablative fractional lasers:

  • Fractional Er:glass laser – 1540nm.
  • Fractional Erbium-Doped Laser (EDL) – 1550nm (e.g. Fraxel Re:store).

In one study, an Er:glass laser improved atrophic acne scars by over 50% after 6 months, in 92% of patients treated [30]. Another study found a similar improvement in 62.5% of patients treated [31]. The effectiveness of this laser on atrophic scars appears to vary depending on scar type. For example, boxcar scars demonstrated a 52.9% improvement, rolling scars a 43.1% improvement, and icepick scars a 25.9% improvement after six sessions of a 1540nm fractionated laser. Furthermore, the improvement in boxcar scars was statistically significant after four sessions of treatment [32].

EDL has demonstrated similar effectiveness by improving atrophic acne scarring by 51-75% in 87% of patients [33]. In addition, it has demonstrated some ability to improve disorders of hyperpigmentation, although this research has mainly focussed on melasma and other sun-induced pigmentation [34].

EDL is often considered the frontline treatment for atrophic scars but it can also help improve erythema as it has a long wavelength that can destroy blood vessels in the dermis. In one study, 1550nm EDL improved the appearance of PIE after just one treatment [35]. Another study found that this laser improved PIE equally as well as 595nm PDL. Furthermore, the patients that received the EDL laser were more satisfied with their treatment than those who received PDL (91.7% compared to 75% satisfaction levels, respectively) [36].

Fractional lasers can activate the herpes simplex virus (HSV) and trigger cold sores in 0.3-2% of cases and, for this reason, antiviral prophylaxis should be given to anyone with a history of facial HSV undergoing fractional laser treatment [37]. In addition, fractional lasers can cause acne flare-ups in 2-10% of patients and should be avoided in those with active acne outbreaks [25].

Ablative Lasers for Acne Scars Vs Acne Marks

Ablative lasers are fairly extreme treatments as they cause extensive injury to the skin and often require antibiotic prophylaxis. They are painful and come with increased risk of pigmentation issues, scarring, and infections. However, significant clinical improvements can be seen after only one treatment which means they are often considered the gold standard in acne scarring treatment.

Ablative laser treatments should only be performed by qualified medical professionals with the right training and experience.

The target chromophore of these lasers is the water in the skin and, although they have longer wavelengths, this means they are less able to penetrate the dermis [38].

Examples of ablative lasers include:

  • CO2 Laser – 10,600nm
  • Er:YAG Laser – 2940nm
  • Fractional CO2 Laser – 10,600nm
  • Fractional Er:YAG – 2940nm
  • Fractional Er:YSGG – 2790nm

The CO2 10,600nm laser emits light in the far infra-red spectrum. The laser has demonstrated significant immediate and long-term improvements in atrophic acne scarring after one single treatment. In one study, 60 patients experienced 69% improvement of atrophic scars one month after treatment, which increased to 79% eighteen-months after treatment. However, it caused erythema that lasted fourteen weeks and one-third of the patients experienced temporary hyperpigmentation [39].

Similar results can be found with other ablative lasers and with fractional ablative lasers to a lesser extent.

IPL Treatment for Acne Scars Vs Acne Marks

Intense Pulsed Light (IPL) is not a true laser as it does not have a specific wavelength. Instead, it is made up of a combination of different wavelengths (500-1200nm) and filters can be applied to enhance different effects [40]. For this reason, IPL is a bit of a “Jack of all trades, master of none” as it can treat several conditions at once (including erythema and hyperpigmentation) but is less effective at treating anyone condition [26][40].

Due to the fact that it can also boost collagen, improve erythema, and improve hyperpigmentation, IPL may provide a treatment option for atrophic scars as well as PIE and PIH. However, multiple treatments are needed and caution is required in order to prevent PIH in darker skin types [26].

Radiofrequency Treatments for Acne Scars Vs Acne Marks

Radiofrequency treatments deliver a current of energy into the skin which produces heat (around 65°C to 75°C) in the dermis without heating and damaging the epidermis. This temperature alters the natural qualities of collagen in the dermis, allowing collagen production and remodelling and providing a tightening effect [41]. This is a similar thermolysis effect to that used by laser treatments but via a high frequency alternating current rather than light energy.

Fractional radiofrequency treatments take this one step further and use microneedles to pierce the skin in order to deliver radiofrequency energy deep into the dermis.

In one study, four patients received radiofrequency treatments for acne scarring, three of which experienced an improvement of 25% or more. Improvements were initially noticed after the second treatment [42]. In another study, over 73% of patients saw improvements in atrophic acne scarring, with icepick scars having the best response to treatment, followed by rolling, then boxcar scars [43].

In general, an improvement of 25-75% can be expected after 3 to 4 treatment sessions, with optimal results three months after the final treatment due to the time required for fibroblast production and upregulation of collagen production [44].

While radiofrequency treatments appear to help improve acne scars, they do not have much of an effect on acne marks. In addition, there have been some reports of radiofrequency treatments causing facial fat loss.

Microneedling for Acne Scars Vs Acne Marks

Microneedling uses tiny needles to puncture the skin and create micro-channels into the dermis. The idea behind microneedling is to create a controlled trauma to the skin in order to initiate a wound healing response and growth factor release, thus stimulating collagen production and deposition [4]. In addition, the micro-channels created can enhance skin penetration of topical products.

In one study, five microneedling sessions improved acne scarring by 50-75% [45]. Other research suggests that microneedling treatments are as effective as non-ablative fractional laser treatments at improving the appearance of acne scars [46]. In addition, microneedling is particularly effective for acne scarring when combined with topical platelet-rich plasma (PRP) as it can increase improvement from 45.8% to 62.2% [47]. However, microneedling does not appear to improve acne marks.

Chemical Peels/Hydroxy Acids for Acne Scars Vs Acne Marks

Hydroxy acids, such as glycolic acid, lactic acid, and salicylic acid act as chemical exfoliants by helping to remove dead skin cells and loosen the top layer of skin. They generally fall into three main categories; alpha-hydroxy acids (AHAs; e.g. glycolic acid, lactic acid), beta-hydroxy acids (BHAs; e.g. salicylic acid), and poly-hydroxy acids (PHAs; e.g. lactobionic acid) [48].

Hydroxy acids can speed-up the resolution of acne marks by increasing skin cell turnover, which means that skin pigment is brought to the surface of the skin and shed via normal epidermal desquamation faster. In addition, some alpha-hydroxy acids may prevent the production of melanin by inhibiting tyrosinase (an enzyme needed for melanin production) [49].

Chemical peels use hydroxy acids at higher concentrations than are available over the counter which causes injury to the skin and stimulates collagen production and remodelling [50]. This means that chemical peels can be an effective treatment for acne scarring as well as PIH acne marks. However, only certain types of acne scars appear to respond to chemical peels. For example, one study investigated the effect of glycolic acid peels vs salicylic-mandelic acid peels on active acne lesions, acne scarring, and PIH. Both of the chemical peels were able to improve small, depressed scars but not icepick or deep boxcar scars. However, the salicylic-mandelic chemical peel was more effective at improving active acne lesions and PIH. In addition, less side effects, including hyperpigmentation, were observed with the salicylic-mandelic acid peels [51].

This research would suggest that chemical peels and hydroxy acids aren’t able to offer a huge improvement in acne scars but may be able to improve acne marks, especially PIH.

In addition, lower concentrations of lactic acid, such as those able to be bought OTC, can increase stratum corneum ceramide levels and reduce TEWL, resulting in a superior lipid barrier [52]. This means that they may be able to help improve PIE acne marks too.

CROSS Technique For Acne Scars vs Acne Marks

Unlike the above-mentioned chemical peels, the Chemical Reconstruction Of Skin Scars (CROSS) technique may be able to improve atrophic acne scars, particularly boxcar and icepick acne scars. The CROSS technique uses high-strength (65-100%) trichloroacetic acid (TCA), which is applied to the base of the scar to destroy the epithelial wall and encourage dermal remodelling [7].

In one study, 12 patients received four treatments with the CROSS technique (using 100% TCA) spaced four weeks apart. All patients experienced at least 50% improvement in icepick acne scars, with the vast majority experiencing more than 70% improvement [53].

A larger study of 53 patients found that the CROSS technique with 70% TCA was able to improve the appearance of boxcar acne scars by more than 50% in the majority of patients. In addition, over 80% of the patients were satisfied with their results [54].

Other research has found that the CROSS technique is equally as effective as fractional EDL for the treatment of icepick scars, however, EDL provided better improvements for rolling acne scars [55].

However, there isn’t any evidence to suggest that the CROSS technique may improve the appearance of acne marks. In some circumstances, it may also lead to temporary PIH.

Treatment Options For Acne Marks vs Acne Scars

 

Preventative Treatment Of Acne Scars Vs Acne Marks

Recent research demonstrates that early and effective acne treatment can reduce the formation of new scars. It appears to be the early inflammatory pathways that cause both the development of acne lesions and the subsequent atrophic scars and inhibiting these pathways may prevent acne scarring.

Topical retinoids are able to inhibit one of the most important inflammatory pathways associated with acne and acne scarring. In fact, not only can retinoids help prevent scarring by treating acne, but they can also treat existing acne scarring. A topical combination of 0.3% adapalene and 2.5% benzoyl peroxide was significantly better than a control cream at reducing acne scarring over a 24-week treatment period. In addition, it prevented new scars from forming, unlike the control cream [56].

A 0.3% adapalene gel, alone, demonstrated similar results. In this study, the retinoid was applied once daily for the first 4-weeks, then twice daily for the following 20 weeks. After the 24-week study period, both the patients and the investigators reported significant improvements by up to 89% [57].

Furthermore, topical retinoid treatment (0.1% Tazarotene gel) proved to be as effective as microneedling at improving atrophic acne scarring [58].

Retinoids can also be combined with other topical treatments for enhanced effects. For example, one study investigated a combination of 0.025% retinoic acid and 12% glycolic acid for acne scars. After 12-weeks of use, a significant improvement in acne scars was observed in 91.4% of the patients [59]. Another study combined 0.1% retinaldehyde and 6% glycolic acid and found that it significantly improved active acne lesions, acne scaring, and both PIE and PIH acne marks [60].

Combined, this research suggests that retinoids are effective at treating both acne scars and acne marks, especially when combined with glycolic acid.

Silicone Gels and Sheets For Acne Scars vs Acne Marks

Silicone gels have demonstrated effectiveness at treating scars, with some research suggesting that they can reduce scar texture by 86%, scar colour by 84%, and scar height by 68% [61].

These results are thought to be due to one or more of the several actions of silicone gels:

  • Increasing stratum corneum hydration and reducing collagen production
  • Protecting scarred tissue from bacteria and thus preventing bacteria-induced collagen production.
  • Regulating growth factors which normalises collagen production in abnormal scar tissue [62].

As you can see, silicone gels and sheeting may be beneficial for PIE acne marks and hypertrophic acne scars, but are unlikely to have much of an effect on atrophic acne scars or PIH acne marks. In fact, the majority of research regarding silicone gels and sheets for scars has been focussed on hypertrophic scars and keloid scars [61], both of which are fairly rare in acne.

Other Topical Treatments For Acne Marks vs Acne Scars

While there aren’t many other topical treatments for atrophic acne scars, there are plenty of options for acne marks. Both PIE and PIH will eventually resolve on their own, however, there are certain skincare ingredients that can help fade these acne marks faster.

With both PIE and PIH acne marks, the most important treatment is addressing the underlying inflammatory condition (e.g. acne) and preventing further marks from occurring. For example, by avoiding picking, scratching, and rubbing at the skin and protecting the skin from UV radiation [63]. The same can be said for atrophic and hypertrophic acne scarring too.

The majority of topical treatments for PIH involve inhibiting tyrosinase, a key enzyme that is essential for the production of melanin [64], or increasing the rate of skin cell turnover in order to increase the speed that skin pigment is shed from the skin.

In terms of PIE, effective topical treatments are those that repair stratum corneum barrier function and increase skin hydration, as well as those that reduce inflammation and blood vessel dilation. Similarly to PIH, PIE may resolve faster with the use of ingredients that increase skin cell turnover.

In addition, there are a number of ingredients that can help improve both PIE and PIH acne marks. These ingredients have been extensively covered in other articles, so only a summary of the ingredients and their effects will be covered here. For a full discussion of the research, please see the below links.

Read More:

Topical Treatments for PIE

Topical Treatments for PIH

Topical Treatments For PIE vs PIH Acne Marks

To provide a summary of the topical treatments for PIE vs PIH acne marks, here is a table demonstrating the ingredients that work for either PIE, PIH, or both, as well as how they work.

IngredientMechanism of Action
PIHPIE
HydroquinoneInhibits tyrosinase

Interferes with DNA & RNA synthesis

Destroys melanocytes

Degrades melanosomes [64]

None
RetinoidsIncreases epidermal turnover [64]

Inhibits inflammatory pathways [56]

Increases epidermal turnover [64]

Inhibits inflammatory pathways [56]

Azelaic AcidInhibits tyrosinase

Inhibits DNA synthesis of abnormal melanocytes [65]

Reduces Inflammation [66]

Reduces Inflammation [66]
NiacinamideDecreases the transfer of melanosomes from melanocytes to keratinocytes (a.k.a. stops pigment leaking into skin cells) 

Interferes with cell signalling pathways between keratinocytes and melanocytes [67]

Stabilises the skins barrier function and improves skin hydration by increasing levels of ceramides, free fatty acids, and cholesterol in the stratum corneum [68]

Reduces Inflammation

Promotes wound healing [69]

Vitamin CInhibits tyrosinase [70]Plays crucial role in the formation and regulation of stratum corneum lipids and ceramides [71]

Promotes wound healing

Reduces inflammation

Improves the appearance of capillary skin

Improves skin barrier function [72]

N-Acetyl Glucosamine (NAG)Inhibits tyrosinase glycosylation [73]None
MequinolInhibits tyrosinase [64]None
Kojic AcidInhibits tyrosinase [74]Reduces inflammation [75]
ArbutinInhibits tyrosinase

Prevents maturation of melanosomes [64]

None
Licorice ExtractInhibits tyrosinase

Disperses melanin [64]

Reduces inflammation [76]
Soy ExtractInhibits transfer of melanosomes from melanocytes to keratinocytes [64]None
ResveratrolInhibits the transcription of tyrosinase and regulates it thereafter  [77]Reduces inflammation [78] 
ZincPossibly plays a role in tyrosinase metabolism [79]Reduces inflammation [79]
Hydroxy AcidsIncrease skin cell turnover [48]

Glycolic acid and lactic acid may inhibit tyrosinase [80]

Increase skin cell turnover [48]

Lactic acid can increase stratum corneum ceramide levels and reduce TEWL [52]

CeramidesNoneImprove stratum corneum barrier function and skin hydration 

Reduce inflammation [81]

Silicone GelNoneImproves stratum corneum barrier function and skin hydration [62]
Grean Tea (EGCG)May suppress melanin production [82]Regulates pathways involved in inflammatory responses [83]
CytokininsUnknown but does reduce hyperpigmentation associated with photoaging [84]Reduces inflammation

Improves stratum corneum barrier function and skin hydration [85]

Treatment Options for PIE vs PIH Acne Marks

 

Summary

Acne Scars vs Acne Marks

Acne scars and acne marks have different causes, however, these causes share an underlying similarity – inflammation.

Acne scars are textural irregularities, whereas acne marks are discolouration. Red acne marks are called post-inflammatory erythema and brown acne marks are called post-inflammatory hyperpigmentation. 

Atrophic Acne Scars vs Hypertrophic Acne Scars

Acne scars are formed due to an altered wound healing response that causes an imbalance of MMPs (Matrix Metallaproteases) and TIMPs (Tissue Inhibitors of Metallaproteases) and leads to either too much collagen production (more TIMPs than MMPs) or too little collagen production (more MMPs than TIMPs).

When too much collagen is produced during the wound healing response, it can cause hypertrophic or keloid scars. Both of these types of acne scars are rare and mainly occur on the body.

When too little collagen is produced during the wound healing process, the skin can be left with indented scars that are referred to as atrophic scars. There are three main types of atrophic acne scars; icepick, boxcar, and rolling.

Icepick acne scars are deeper than they are wide, boxcar scars are wider than they are deep, and rolling scars have a ripple effect that can be smoothed out when stretched.

PIH Acne Marks vs PIE Acne Marks

During the wound healing process, inflammation can stimulate melanin production. There are two main types of melanin in the skin; eumelanin (black/brown in colour) and pheomelanin (red/yellow in colour).

Both PIE and PIH may also be partly due to the slow break-down of non-surviving (not destroyed by the body’s immune response) p-acnes bacteria in the hair follicle. In addition, PIE results from the blood vessel dilation associated with wound healing.

The key difference between PIE vs PIH is that PIE presents as red marks and generally affects those with fair skin, while PIH presents as brown marks and generally affects those with darker skin. However, it is not unusual for some people to experience both PIE and PIH, and in some circumstances, PIE may lead to PIH.

How To Treat Acne Scars Vs Acne Marks

The first step in treating both acne scars and acne marks is through the prevention of further scarring by addressing underlying inflammation and active acne. Retinoids are particularly good for this as they inhibit some inflammatory pathways associated with acne and acne scarring. In addition, they are able to treat existing acne scars and marks, particularly when combined with low concentrations of glycolic acid.

Laser treatment may also help improve the appearance of both acne scars and acne marks, for example:

  • Vascular Lasers
    • Good for – active acne, PIE.
    • May also be good for – atrophic and hypertrophic scars.
    • Not so good for – PIH, darker skin types.
  • Non-Ablative Fractional Lasers
    • Good for – atrophic and hypertrophic scars, PIH.
    • May also be good for – PIE.
    • Not so good for – active acne.
  • Ablative Fractional Lasers
    • Good for – atrophic and hypertrophic scars.
    • Not so good for – PIH, pain adverse people, people prone to keloid scarring.
  • IPL
    • Good for – PIE, PIH.
    • May be good for – atrophic scars.
    • Not so good for – hypertrophic scars, quick results.

In addition, radiofrequency treatments and microneedling can be helpful for acne scars but not acne marks. Whereas chemical peels can be useful for acne marks but not acne scars, with the exception of the TCA CROSS technique which is particularly effective for boxcar and icepick acne scars.

These treatments need to be used with caution in individuals prone to PIH as they may cause further PIH (although this is usually temporary).

Topical Treatments For PIE vs PIH

Effective topical treatments for PIH are those that prevent melanin production by inhibiting tyrosinase, or those that increase skin cell turnover in order to resolve PIH faster. Whereas, effective treatments for PIE are those that improve stratum corneum barrier function, reduce inflammation, or reduce blood vessel dilation.

PIH Treatments By Mechanism Of ActionPIE Treatments By Mechanism Of Action

References

  1. Jacob, C., Dover, J. & Kaminer, M. (2001). ‘Acne scarring: a classification system and review of treatment options.’, J Am Acad Dermatol., 45(1), 109-117. Available at: https://www.ncbi.nlm.nih.gov/pubmed/11423843/
  2. Werschler, W., Herdener, R., Ross, V. & Zimmerman, E. (2015). ‘Treating Acne Scars: What’s New?’, J Clin Aesthet Dermatol., 8(Supp 8), 2-8. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4570086/
  3. Bataille, V., Snieder, H., MacGregor, A., Sasieni, P., & Spector, T. (2002). ‘The influence of genetics and environmental factors in the pathogenesis of acne: a twin study of acne in women’. Journal of Investigative Dermatology, 119, 317-322. Available at: https://www.jidonline.org/article/S0022-202X(15)30101-9/fulltext
  4. Fabbrocini, G., Annunziata, M., D’Arco, V. et al. (2010). ‘Acne Scars: pathogenesis, classification and treatment’, Derm Res Pract., Article ID 893080. Available at: https://www.hindawi.com/journals/drp/2010/893080/
  5. Orsted, H., Keast, D., Lalande, L. & Megie, M. (2004). ‘Basic principles of wound healing’, Wound Care Canada, 9(2), 4-12. Available at: http://www.wrha.mb.ca/professionals/woundcare/documents/PrinciplesWoundHealing_WCCSpring2011.pdf
  6. Martin, P. & Leibovich, S. (2005). ‘Inflammatory cells during wound repair: the good, the bad, and the ugly.’ Trends Cells Biol., 15(11), 599-607. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16202600?dopt=AbstractPlus
  7. Connolly, D., Vu, H., Mariwalla, K. & Saedi, N. (2017). ‘Acne Scarring – pathogenesis, evaluation, and treatment options’, J Clin Aesthet Dermatol., 10(9), 12-23. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5749614/
  8. Vowels, B., Yang, S. & Leyden, J. (1995). ‘Induction of proinflammatory cytokines by a soluble factor of Propionibacterium acnes: implications for chronic inflammatory acne’. Infect Immun., 63(8), 3158-3165. Available at: https://www.ncbi.nlm.nih.gov/pubmed/7542639/
  9. Kircik, L. (2014). ‘Re-evaluating Treatment Targets in Acne Vulgaris: Adapting to a New Understanding of Pathophysiology’. J Drug Dermatol., 13(6), Sup s57, Available at: http://jddonline.com/articles/dermatology/S1545961614S0057X
  10. Davis, E. & Callender, V. (2010). ‘Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of colour’. J Clin Aesthet Dermatol., 3(7), 20-31. Available at: https://www.ncbi.nlm.nih.gov/pubmed/20725554/
  11. Bae-Harboe, Y. & Graber, E. (2013). ‘Easy as PIE (Postinflammatory Erythema)’. J Clin Aesthet Dermatol., 6(9), 46-47. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3780804/
  12. Yamamoto, A., Takenouchi, K. & Ito, M. (1995). ‘Impaired water barrier function in acne vulgaris’, Arch Dermatol Res., 287(2), 214-218. Available at: https://www.ncbi.nlm.nih.gov/pubmed/7763094
  13. Nasti, T. & Timares, L. (2015). ‘Invited review MC1R, Eumelanin and pheomelanin: their role in determining the susceptibility to skin cancer’, Photochem Photobiol., 91(1), 188-200. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299862/
  14. Williams, H., Dellavale, R. & Garner, S. (2012). ‘Acne Vulgaris’, The Lancet, 379(9813), 361-372. Available at: https://www.ncbi.nlm.nih.gov/pubmed/21880356/
  15. Farkas, J., Hoopman, J. & Kenkel, J. (2013). ‘Five parameters you must understand to master control of your laser/light-based devices’, Aesth Surg J., 33(7), 1059-1064. Available at: https://watermark.silverchair.com/33-7-1059.pdf?token=AQECAHi208BE49Ooan9kkhW_Ercy7Dm3ZL_9Cf3qfKAc485ysgAAAlMwggJPBgkqhkiG9w0BBwagggJAMIICPAIBADCCAjUGCSqGSIb3DQEHATAeBglghkgBZQMEAS4wEQQMW7yMDrwBOPGttWMEAgEQgIICBgOWFrIX9Z82lfRxOdat4Yb-9w03nvuj_i0AR_BvhrAd9ueBHiMROqavukqpU9E3PGeCcWkpMwPUcX5wn1B3OiTc_3u7Ulsk1nioIp9e5bjgse_c5M4kQ1h59U0JNGp1B1kslOBVpEhuC-jk2xj2L9U42Frem7XYbyBWayl1gwy9Ir08bF7F_x6gO9xPWkM5q6ra9Vfgd6bfqt_K4d0D64poE4lHLvazUmHl-EZs1JnoswFM2noE5JRHyS7NkxXjFY7GTifpBk5DdTeEEHBbOW_zFk54YmUuO3thPqqIj24IJtpZS7R1r7deoqalzc1w_MvjGJeVUzB46g5SM008J8BwtAORhmyYRHIzDxOnwfBHCfZ0hDuIAtPS3h54Noxv7z8BdyQB6r3LOJcqLO6KZTqEIZW_T_so40sF5v5pcQt66VnDN8iQw0A3vrK90DDHlReKBjsZlHb19WJLT2SpH2EY_5TeO08-osZiut32MtT93S1sv0ZHTcRROMVrMxxkHRt_58rJ1TLt-ykjClzfZuF9MyU2OoK8rBIYHEWkdJE495SYJC_UP5umBloSpZhc79yB58bYYIQVnaY9tQqOtIO5CXBgaoMUzmlO01TC8UCrTPYGeTQG8uwrJLyBKlxBS_CU-y1LEyGXCPHjO8zF3LgyuMvP__Dnek6nBjzIJp4X6l6awJwb
  16. Patil, U. & Dhami, L. (2008). ‘Overview of lasers’, Indian J Plast Surg., 41(Supp), pp. S101-S113. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2825126/
  17. Anderson, R. & Parrish, J. (1983). ‘Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation’. Science, 220(4596), 524-527. Available at: https://www.ncbi.nlm.nih.gov/pubmed/6836297/
  18. Alster, T. & McMeekin, T. (1996). ‘Improvement of facial acne scars by the 585nm flashlamp-pumped pulsed dye laser’. J Am Acad Dermatol, 35(1), 79-81. Available at: https://www.ncbi.nlm.nih.gov/pubmed/8682969/
  19. Seaton, E., Mouser, P., Charakida, A., Alam, S., Seldon, P. & Chu, A. (2006). ‘Investigation of the mechanism of action of nonablative pulsed-dye laser therapy in photorejuvination and inflammatory acne vulgaris’. Br J Dermatol, 155(4), 748-755. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16965424/
  20. Yoon, H., Lee, D., Kim, S., Park, K. & Youn, S. (2008). ‘Acne erythema improvement by long-pulsed 595-nm pulsed-dye laser treatment: a pilot study’. J Dermatolog Treat, 19(1), 38-44. Available at: https://www.ncbi.nlm.nih.gov/pubmed/18273723
  21. Patel, N. & Clement, M. (2002). ‘Selective nonablative treatment of acne scarring with 585 nm flashlamp pulsed dye laser’. Dermatol Surg, 28(10), 942-945. Available at: https://www.ncbi.nlm.nih.gov/pubmed/12410680/
  22. Kaney, T., Tanzi, E. & Alster, T. (2016). ‘Comparison of 532 nm Potassium Titanyl Phosphate Laser and 595 nm Pulsed Dye Laser in the treatment of Erythematous Surgical Scars: A randomized, controlled, open-label study’. Dermatol Surg., 42(1), 70-76. Available at: https://www.ncbi.nlm.nih.gov/pubmed/26673432/
  23. Bencini, P., Luci, A., Galimbetti, M. & Ferranti, G. (1999). ‘Long-term epilation with long-pulsed neodymium:YAG laser’. Dermatol Surg, 25(3), 175-178. Available at: https://www.ncbi.nlm.nih.gov/pubmed/10193962
  24. Sult, R. (2014). ‘CASE REPORT: Treatment of Acne Vulgaris with Long-Pulsed 1064 nm Nd:Yag Laser’. J Laser Health Acad., Vol. 2014 (1), Available at: https://www.laserandhealthacademy.com/media/objave/academy/priponke/57_60_sult_laha_2014_1.pdf
  25. Nanni, C. (2000). ‘Handling Complications of laser treatment’. Dermatologic Therapy, 13(1), 127-139. Available at: https://onlinelibrary.wiley.com/doi/pdf/10.1046/j.1529-8019.2000.00013.x
  26. Rao, J. (2011). ‘Treatment of acne scarring’, Facial Plast Surg Clin North Am., 19(2), 275-291. Available at: https://www.ncbi.nlm.nih.gov/pubmed/21763989/
  27. Tanzi, E. & Alster, T. (2002). ‘Treatment of atrophic facial acne scars with a dual-mode Er:YAG laser’, Dermatol Surg., 28(7), 551-555. Available at: https://www.ncbi.nlm.nih.gov/pubmed/12135504/
  28. Lipper, G. & Perez, M. (2006). ‘Nonablative acne scar reduction after a series of treatments with a short-pulsed 1,064-nm neodymium:YAG laser.’, Dermatol Surg., 32(8), 998-1006. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16918561/
  29. Cohen, B., Brauer, J. & Geronemus, R. (2016). ‘Acne scarring: A review of available therapeutic lasers’, Lasers Surg Med., 48(2), 95-115. Available at: https://www.ncbi.nlm.nih.gov/pubmed/26414762/
  30. Bencini, P., Tourlaki, A., Galimberti, M., Longo, C., Pellacani, G., DeGiorgi, V. & Guerriero, G. (2012). ‘Nonablative fractional photothermolysis for acne scars: clinical and in vivo microscopic documentation of treatment efficacy’, Dermatol Ther., 25(5), 463-467. Available at: https://www.ncbi.nlm.nih.gov/pubmed/23046026/
  31. Yoo, K., Ahn, J., Kim, J., Li, K., Seo, S. & Hong, C. (2009). ‘The use of 1540nm fractional photothermolysis for the treatment of acne scars in Asian skin: a pilot study.’, Photodermatol Phtoimmunol Photomed., 25(3), 138-142. Available at: https://www.ncbi.nlm.nih.gov/pubmed/19438992/
  32. Sardana, K., Manjihi, M., Garg, V. & Sagar, V. (2014). ‘Which type of atrophic acne scar (ice-pick, boxcar, or rolling) responds to nonablative fractional laser therapy’, Dermatol Surg., 40(3), 288-300. Available at: https://www.ncbi.nlm.nih.gov/pubmed/24447255/
  33. Alster, T., Tanzi, E. & Lazarus, M. (2007). ‘The use of fractional laser photothermolysis for the treatment of atrophic scars’, Dermatol Surg., 33(3), 295-299. Available at: https://www.ncbi.nlm.nih.gov/pubmed/17338686/
  34. Gold, M. (2010). ‘Update on Fractional Laser Technology’, J Clin Aesthet Dermatol., 3(1), 42-50. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2921736/
  35. Glaich, A., Goldberg, L., Friedman, R. & Friedman, P. (2007). ‘Fractional photothermolysis for the treatment of postinflammatory erythema resulting from acne vulgaris’. Dermatol Surg., 33(7), 842-846. Available at: https://www.ncbi.nlm.nih.gov/pubmed/17598852/
  36. Park, K., Ko, E., Seo, S. & Hong, C. (2014). ‘Comparison of fractional, nonablative, 1550-nm laser and 595-nm pulsed dye laser for the treatment of facial erythema resulting from acne: A split-face, evaluator-blinded, randomized pilot study’. J Cosm Laser Therapy., 16(3), 120-123. Available at: https://www.tandfonline.com/doi/abs/10.3109/14764172.2013.854626?journalCode=ijcl20
  37. Setyadi, H., Jacobs, A. & Markus, R. (2008). ‘Infectious complications after nonablative fractional resurfacing treatment. Dermatol Surg., 34, 301-305. Available at: https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1524-4725.2008.34331.x
  38. Brightman, L., Brauer, J. Anolik, R. et al. (2009). ‘Ablative and fractional ablative lasers’, Dermatol Clin., 27(4), 479-489. Available at: https://www.ncbi.nlm.nih.gov/pubmed/19850197/
  39. Alster, T. & Hirsch, R. (2003). ‘Single-pass CO2 laser skin resurfacing of light and dark skin: extended experience with 52 patients’, J Cosmet Laser Ther., 5(1), 39-42. Available at: https://www.ncbi.nlm.nih.gov/pubmed/12745598/
  40. Sadick, N. & Weiss, R. (2002). ‘Intense pulsed-light photorejuvenation’, Semin Cutan Med Surg., 21(4), 280-287. Available at: https://www.ncbi.nlm.nih.gov/pubmed/12512651/
  41. Fisher, G., Jacobson, L., Bernstein, L., Kim, K. & Geronemus, R. (2005). ‘Nonablative radiofrequency treatment of facial laxity’. Dermatologic Surgery, 31, 1237-1241. Available at: https://www.ncbi.nlm.nih.gov/pubmed/16176777
  42. Montesi, G., Calvieri, S., Balzani, A. & Gold, M. (2007). ‘Bipolar radiofrequency in the treatment of dermatologic imprefections: clinicopathological and immunohistochemical aspects’, J Drugs Dermatol., 6(9), 890-896. Available at: https://www.ncbi.nlm.nih.gov/pubmed/17941360
  43. Ramesh, M., Gopal, M., Kumar, S. & Talwar, A. (2010). ‘Novel technology in the treatment of acne scars: the matrix-tunable radiofrequency technology’, J Cutan Aesthet Surg., 3(2), 97-101. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2956966/
  44. Simmons, B., Griffith, R., Falto-Aizpura, L. & Nouri, K. (2014). ‘Use of radiofrequency in cosmetic dermatology: focus on nonablative treatment of acne scars’, Clin Cosmet Investig Dermatol., 7, 335-339. Available at: https://www.ncbi.nlm.nih.gov/pubmed/25540589/
  45. Dogra, S., Yadav, S. & Sarangal, R. (2014). ‘Microneedling for acne scars in Asian skin type: an effective low cost treatment modality’, J Cosmet Dermatol., 13(3), 180-187. Available at: https://www.ncbi.nlm.nih.gov/pubmed/25196684/
  46. Cachafeiro, T., Escobar, G., Maldonado, G., Cestari, T. & Corleta, O. (2016). ‘Comparison of nonablative fractional erbium laser 1340nm and microneedling for the treatment of atrophic acne scars: a randomized clinical trial’, Dermatol Surg., 42(2), 232-241. Available at: https://www.ncbi.nlm.nih.gov/pubmed/26845539/
  47. Asif, M., Kanodia, S. & Singh, K. (2016). ‘Combined autologous platelet-rich plasma with microneedling verses microneedling with distilled water in the treatment of atrophic acne scars: a concurrent split-face study’, J Cosmet Dermatol., 15(4), 434-443. Available at: https://www.ncbi.nlm.nih.gov/pubmed/26748836/
  48. Kornhauser, A., Coelho, S. & Hearing, V. (2010). ‘Applications of hydroxyl acids: classification, mechanisms, and photoactivity’, Clin Cosmet Investig Dermatol, 3, 135-142. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047947/
  49. Usuki, A., Ohashi, A., Sato, H., Ochiai, Y., Ichihashi, M. & Funasaka, Y. (2003). ‘The inhibitory effect of glycolic acid and lactic acid on melanin synthesis in melanoma cells’, Exp Dermatol., 12(Suppl. 2), 43-50. Available at: https://www.ncbi.nlm.nih.gov/pubmed/14756523/
  50. Garg, V., Sinha, S. & Sarkar, R. (2009). ‘Glycolic acid peels versus salicylic-mandelic acid peels in active acne vulgaris and post-acne scarring and hyperpigmentation: a comparative study’, Dermatol Surg., 35(1), 59-65. Available at: https://www.ncbi.nlm.nih.gov/pubmed/19076192/
  51. Garg, V., Sinha, S. & Sarkar, R. (2009). ‘Glycolic acid peels versus salicylic-mandelic acid peels in active acne vulgaris and post-acne scarring and hyperpigmentation: a comparative study’, Dermatol Surg., 35(1), 59-65. Available at: https://www.ncbi.nlm.nih.gov/pubmed/19076192/
  52. Rawlings, A., Davies, A., Carlomusto, M., Pillai, S., Zhang, K., Kosturko, R., Verdejo, P., Feinberg, C., Nguyen, L. & Chandar, P. (1996). ‘Effect of lactic acid isomers on keratinocyte ceramide synthesis, stratum corneum lipid levels and stratum corneum barrier function’, Arch Derm Res., 288(7), 383-390. Available at: https://link.springer.com/article/10.1007/BF02507107
  53. Bhardwaj, D. & Khunger, N. (2010). ‘An assessment of the efficacy and safety of CROSS technique with 100% TCA in the management of icepick acne scars’, J Cutan Aesthet Surg., 3(2), 93-96. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2956965/
  54. Agarwal, N., Gupta, L., Khare, A., Kuldeep, C. & Mittal, A. (2015). ‘Therapeutic response of 70% trichloroacetic acid CROSS in atrophic acne scars’, Dermatol Surg., 41(5), 597-604. Available at: https://www.ncbi.nlm.nih.gov/pubmed/25899884/
  55. Kim, H., Kim, T., Kwon, Y., Park, J. & Lee, J. (2009). ‘Comparison of a 1550nm Erbium:glass fractional laser anc chemical reconstruction of skin scars (CROSS) method in the treatment of acne scars: a simultaneous split-face trial’, Lasers Surg Med, 41(8), 545-549. Available at: https://www.ncbi.nlm.nih.gov/pubmed/19639620/
  56. Tan, J., Tanghetti, E., Baldwin, H., Stein Gold, L. & Lain, E. (2019). ‘The role of topical retinoids in prevention and treatment of atrophic acne scarring: Understanding the importance of early effective treatment’, J Drugs Dermatol., 18(3), 255-260. Available at: https://www.ncbi.nlm.nih.gov/pubmed/30909329
  57. Loss, M., Leung, S., Chien, A. et al. (2018). ‘Adapalene 0.3% gel shows efficacy for the treatment of atrophic scars’, Dermatol Ther., 8(2), 245-257. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6002315/
  58. Afra, T., Ramzi, M., Narang, T. et al. (2018). ‘Topical Tazarotene gel 0.1%, as a novel treatment approach for atrophic postacne scars: A randomized active-controlled clinical trial’, JAMA Facial Plast Surg., 21(2), 125-132. Available at: https://jamanetwork.com/journals/jamafacialplasticsurgery/article-abstract/2714234
  59. Chandrashekar, B., Ashwini, K., Vasanth, V. & Navale, S. (2015). ‘Retinoic acid and glycolic acid combination in the treatment of acne scars’, Indian Dermatol Online J., 6(2), 84-88. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4375771/
  60. Dreno, B., Katsambas, A., Pelfini, C. et al. (2007). ‘Combined 0.1% retinaldehyde/ 6% glycolic acid cream in prophylaxis and treatment of acne scarring’, Dermatology, 214(3), 260-267. Available at: https://www.ncbi.nlm.nih.gov/pubmed/17377389/
  61. Poston, J. (2000). ‘The use of silicone gel in the management of hypertrophic and keloid scars’, J Wound Care, 9(1), 10-6. Available at: https://www.ncbi.nlm.nih.gov/pubmed/10827662/
  62. Puri, N. & Talwar, A. (2009). ‘The efficacy of silicone gel for the treatment of hypertrophic scars and keloids’, J Cutan Aesthet Surg., 2(2), 104-106. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2918339/
  63. Lacz, N., Vafaie, J., Kihiczak, N. et al. (2004). ‘Postinflammatory hyperpigmentation: a common but troubling condition’, Int J Dermatol., 43, 362-365. Available at: https://www.ncbi.nlm.nih.gov/pubmed/15117368?dopt=Abstract
  64. Callender, V., St Surin-Lord, S., Davis, E. et al. (2011). ‘Post inflammatory hyperpigmentation: etiologic and therapeutic considerations’, Am J Clin Dermatol., 12, 87-99. Available at: https://www.ncbi.nlm.nih.gov/pubmed/21348540?dopt=Abstract
  65. Halder, R. & Richards, G. (2004). ‘Topical agents used in the management of hyperpigmentation’, Skin Therapy Letter, 9(6), Available at: https://www.skintherapyletter.com/hyperpigmentation/topical-agents/
  66. Schulte, B., Wu, W. & Rosen, T. (2015). ‘Azelaic acid: Evidence-based update on mechanism of action and clinical application’, J Drug Dermatol., 14(9), pp. 964. Available at: http://jddonline.com/articles/dermatology/S1545961615P0964X
  67. Hakozaki, T., Minwalla, L., Zhuang, J. et al. (2002). ‘The effect of niacinamide on reducing cutaneous pigmentation and suppression of melanosome transfer’, Br J Dermatol., 147(1), 20-31. Available at: https://www.ncbi.nlm.nih.gov/pubmed/12100180
  68. Tanno, O., Ota, Y., Kitamura, N., Katsube, T. & Inoue, S. (2000). ‘Nicotinamide increases biosynthesis of ceramides as well as other stratum corneum lipids to improve the epidermal permeability barrier’, Br J Derm., 143, 524-531. Available at: https://www.ncbi.nlm.nih.gov/pubmed/10971324
  69. Gehring, W. (2004). ‘Nicotinic acid/niacinamide’. Journal of Cosmetic Dermatology, 3(2), pp. 88-93. Available at: https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1473-2130.2004.00115.x
  70. Kameyama, K., Sakai, C., Kondoh, S. et al. (1996). ‘Inhibitory effect of magnesium L-ascorbyl-2-phosphate (VC-PMG) on melanogenesis in vitro and in vivo’, J Am Acad Dermatol., 34(1), pp. 29-33. Available at: https://www.ncbi.nlm.nih.gov/pubmed/8543691/
  71. Ponec, M., Weerheim, A., Kempenaar, J., Mulder, A., Gooris, G., Bouwstra, J. & Mommass, A. (1997). ‘The formation of competent barrier lipids in reconstructed human epidermis requires the presence of vitamin C’, J Invest Dermatol, 109, 348-355. Available at: https://www.jidonline.org/article/S0022-202X(15)42998-7/pdf
  72. Jaros, A., Zasada, M., Budzisz, E., Debowska, R., Gebczynska-Rzepka, M. & Rotsztejn, H. (2018). ‘Evaluation of selected skin parameters following the application of 5% vitamin C concentrate’, J Cos Derm., 18(1), pp. 236-241. Available at: https://onlinelibrary.wiley.com/doi/10.1111/jocd.12562
  73. Bissett, D., Robinson, L., Raleigh, P. et al. (2007). ‘Reduction in the appearance of facial hyperpigmentation by topical N-acetyl glucosamine’, J Cosmet Dermatol., 6(1), pp. 20-6. Available at: https://www.ncbi.nlm.nih.gov/pubmed/17348991
  74. Lim, J. (1999). ‘Treatment of melasma using kojic acid in a gel containing hydroquinone and glycolic acid’, Dermatol Surg, 25(4), 282-284. Available at: https://www.ncbi.nlm.nih.gov/pubmed/10417583
  75. Saeedi, M., Eslamifar, M. & Khezri, K. (2019). ‘Kojic acid applications in cosmetic and pharmaceutical preparations’, Biomed Pharmacother., 110, pp. 582-593. Available at: https://www.ncbi.nlm.nih.gov/pubmed/30537675
  76. Emer, J., Waldorf, H. & Berson, D. (2011). ‘Botanicals and anti-inflammatories: Natural ingredients for rosacea’, Semin Cutan Med Surg., 30, pp. 148-155. Available at: https://mdedge-files-live.s3.us-east-2.amazonaws.com/files/s3fs-public/issues/articles/Vol30_i3_Emer.pdf
  77. Na, J., Shin, J., Choi, H., Kwon, S. & Park, K. (2019). ‘Resveratrol as a multifunctional topical hypopigmenting agent’, Int J Mol Sci., 20(4), 956. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6412432/
  78. Nichols, J. & Katiyar, S. (2010). ‘Skin photoprotection by natural polyphenols: Anti-inflammatory, anti-oxidant and DNA repair mechanisms’, Arch Dermatol Res., 302(2), pp. 71. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2813915/
  79. Abendrot, M. & Kalinowska-Lis, U. (2018). ‘Zinc-containing compounds for personal care applications’, Int J Cosmet Sci., 40(4), 319-327. Available at: https://www.ncbi.nlm.nih.gov/pubmed/29734525
  80. Usuki, A., Ohashi, A., Sato, H., Ochiai, Y., Ichihashi, M. & Funasaka, Y. (2003). ‘The inhibitory effect of glycolic acid and lactic acid on melanin synthesis in melanoma cells’, Exp Dermatol., 12(Suppl. 2), pp. 43-50. Available at: https://www.ncbi.nlm.nih.gov/pubmed/14756523/
  81. Carneiro, R., Salgado, A., Raposo, S., Marto, J., Simoes, S., Urbano, M. & Ribeiro, H. (2011). ‘Topical emulsions containing ceramides: Effects on the skin barrier function and anti-inflammatory properties’, Eur J Lipid Sci., 113(8), 961-966. Available at: https://onlinelibrary.wiley.com/doi/full/10.1002/ejlt.201000495
  82. Kanlayavattanakul, M. & Lourith, N. (2017). ‘Skin hyperpigmentation treatment using herbs: A review of clinical evidences’, J Cosmet Laser Ther., 20(2), pp. 123-131. Available at: https://www.tandfonline.com/doi/abs/10.1080/14764172.2017.1368666
  83. Thiboutot, D., Thieroff-Ekerdt, R. & Graupe, K. (2003). ‘Efficacy and safety of azelaic acid (15%0 gel as a new treatment for papulopustular rosacea: results from two vehicle-controlled, randomized phase III studies’, J Am Acad Dermatol., 48(6), pp. 836-845. Available at: https://www.ncbi.nlm.nih.gov/pubmed/12789172
  84. Garcia, R., McCullough, J., Reece, B. & Massino, F. (2018). ‘Novel topical cytokinin improves coarse wrinkles and skin roughness without skin irritation’, J Drugs Dermatol., 17(7), pp. 772-779. Available at: https://europepmc.org/abstract/med/30005100
  85. McCullough, J., Garcia, M. & Reece, B. (2008). ‘A clinical study of topical pyratine 6 for improving the appearance of photodamaged skin’, Journal of Drugs in Dermatology, 7(2), pp.131-135. Available at: https://www.pyratine.com/wp-content/uploads/2015/08/Journal-of-Drugs-in-Dermatology.pdf

 

 

Spread the Science:
  •  
  •  
  •  
  •  
  •  
  •  
  •  
  •  
  •  
  •  
  •  

Laura is a skincare addict and sunscreen enthusiast with more than 10 years of experience working in healthcare and over 5 years of experience working as a nurse. She has experience in plastic and reconstructive surgery, dermatology, and aesthetics and has received training in laser treatments. Laura is currently working in healthcare education and writes for ScienceBecomesHer in her spare time. Read More.

One Comment

Leave a Reply

Your email address will not be published.