Melasma is a common hyperpigmentation disorder, primarily affecting women, especially those with darker skin. Melasma typically appears on the face as dark, irregularly shaped spots and patches. Although melasma is not physically harmful, studies have shown that it can lead to psychological problems and impact quality of life, including reduced self-esteem, which in turn leads to limitations in social activities, anxiety, and depressive symptoms [11, 23, 24, 29].

Due to its complex pathogenesis and high recurrence rate, definitive treatment for melasma is challenging, and post-treatment results are not always effective or long-lasting. Lasers are currently considered a powerful method for reducing and breaking down pigment, but in clinical practice, many cases of melasma improve well after a few laser sessions only to recur several months later, sometimes even darker than before.

This article focuses on the following key questions: why does melasma recur after effective laser treatment, and what is the role of topical products for home skincare in a long-term melasma management strategy?

Abbreviations

No.	Term	Explanation
1	Melanocyte	Pigment cell
2	Melanosomes	Pigment granules
3	Melanogenesis	Melanin synthesis process
4	PIH (Post-Inflammatory Hyperpigmentation)	Post-inflammatory hyperpigmentation
5	VEGF (Vascular Endothelial Growth Factor)	Vascular endothelial growth factor
6	MASI (Melasma Area and Severity Index)	Melasma Area and Severity Index
7	NMA (Network Meta-Analysis)	Network meta-analysis, allowing simultaneous comparison of multiple treatment methods
8	Plasminogen	Proenzyme (zymogen), inactive form of plasmin
9	Plasmin	Active enzyme formed from plasminogen
10	Endothelin-1	A peptide consisting of 21 amino acids. In the skin, ET-1 can also be produced by keratinocytes
11	PGE2 (Prostaglandin E2)	Mediator involved in the inflammatory pathway
12	TNF-α (Tumor Necrosis Factor-alpha); IL-1 (Interleukin-1); IL-6 (Interleukin-6); IL-8 (Interleukin-8)	Proinflammatory cytokines
13	MDA (Malondialdehyde)	Reactive aldehyde, produced when polyunsaturated fatty acids (PUFAs) in cell membranes are oxidized
14	ROS (Reactive oxygen species)	Reactive oxygen species
15	In vitro	In vitro experiment
16	Ex vivo	Study on tissue or organs removed from the body and maintained under laboratory conditions
17	FN (Fibronectin)	A glycoprotein of the extracellular matrix (ECM)
18	MIF (Macrophage Migration Inhibitory Factor)	Macrophage Migration Inhibitory Factor, a proinflammatory cytokine
19	Collagen type IV	A crucial type of collagen in the basement membrane

I. Melasma - a multifactorial and recurrent hyperpigmentation disorder

1.1. Causes and pathogenesis of melasma

Many recent studies agree that melasma is a multifactorial hyperpigmentation disorder, resulting from the interaction of external factors (solar radiation), endocrine factors  (sex hormones and pregnancy), as well as skin inflammation (such as contact dermatitis and cosmetic procedures), or in individuals with a genetic predisposition. Advances in understanding the contributing factors and pathogenesis have driven the development of new treatment methods and preventive solutions.

Melasma is not merely a consequence of excessive melanin synthesis in melanocytes, but rather the result of interactions among multiple factors: UV and visible light radiation, inflammatory signals, changes in dermal vascular components, basement membrane damage, and endocrine factors. Due to its multi-layered pathogenic mechanism and chronic, recurrent nature, the goal of melasma treatment is not just to reduce existing pigment, but also to control the factors that sustain the condition to limit recurrence [4, 10].

In parallel with the pathway focusing on melanin pigment, histopathological studies of melasma-affected skin also show chronic subclinical inflammation, vascular changes (angiogenesis, vasodilation), and basement membrane damage—factors believed to contribute to the persistence and recurrence of melasma rather than merely being accompanying consequences [4].

1.2. Why does melasma tend to recur?

The chronic and recurrent nature of melasma is a point consistently emphasized in research articles, regardless of the chosen treatment protocol.

Some commonly cited reasons include:

• Melanocyte populations persist in the skin even after existing pigment has been removed, and these cells in individuals with melasma are often more sensitive to environmental stimuli.
• Initial triggers (sunlight, visible light, hormones, heat) often continue in daily life after treatment.
• Skin protection from light radiation is often not as complete in practice as theoretically recommended.
• Underlying inflammation and oxidative stress may not be thoroughly controlled.
• The skin barrier is weakened by the condition itself or by previous treatment interventions.
• Endocrine factors (pregnancy, oral contraceptives, endocrine disorders) remain among the most frequently reported risk factors.

From this, a guiding principle can be deduced: melasma treatment should not only target existing pigment but also consider the mechanisms that continue to promote and control the formation of new pigment.

II. Lasers in melasma treatment

2.1. Physical principles and commonly used laser types

Lasers for melasma treatment are one of the most popular methods today because they yield faster results than many other approaches. This method is particularly suitable for those who have tried various other treatments without noticeable improvement. In 1983, Anderson and Parrish first described the use of laser therapy for dermatological conditions. They observed that pigmented structures in tissues have specific thermal and absorption characteristics, allowing them to be targeted for selective destruction by certain radiation wavelengths, while minimizing damage to surrounding tissues [2].

Laser therapy is a treatment method for melasma and can be particularly beneficial for patients with melasma resistant to topical treatments or chemical peels, or for patients who desire faster improvement. Similar to chemical peels, these treatment modalities promote melanin removal but do not directly impact melanin production [28].

Lasers target areas of melasma, freckles, or dark spots. Based on optical principles, melanin acts as a chromophore that absorbs light energy. Depending on the technology (Q-switched, picosecond, IPL (Intense pulsed light), non-ablative fractional laser, etc.), the absorbed energy is converted into photothermal or photoacoustic effects, damaging or fragmenting the melanin-containing structures, thereby reducing pigment manifestation clinically. This process helps to lighten melasma, reduce hyperpigmentation, and promote smoother, more even-toned skin.

Laser and light-based devices used in melasma treatment include:

-       IPL (Intense Pulsed Light)

-       Fractional lasers, including non-ablative fractional and ablative fractional lasers

• Er:Glass 1540 nm/1550 nm Laser
• Er:YAG 2940 nm Laser
• CO₂ 10,600 nm Laser

-       Ablative lasers

-       Fractional lasers with transdermal drug delivery

-       Q-switched lasers (QSLs): QS 1064 nm, QS 585/595 nm Laser

-       Fractional Q-switched lasers:

• QS Nd:YAG fractional laser
• Fractional QS ruby laser 694 nm

-       Picosecond laser

-       Sublative lasers, including:

• Fractional laser 1927 nm
• Thulium fiber laser

-       Other types of lasers, such as: Copper bromide laser

-       Combination techniques, including:

• Ablative CO₂ laser + Q-switched alexandrite laser 755 nm
• IPL + QS 1064 nm toning laser
• Low-fluence QS 1064 nm + QS 585 nm gold toning
• Low-fluence QS 1064 nm + fractional laser 1550 nm
• Fractional Er:YAG laser 2940 nm + QS Nd:YAG (QSNY)
  

In the 2000s, low-fluence Q-switched Nd:YAG laser (LFQSNY), often referred to as laser toning (LT), became widely used and accepted as a new gold standard in melasma treatment in Asia, where the demand for melasma treatment is very high. This technique involves multiple treatment sessions (usually around 10 sessions) with a 1064nm Q-switched Nd:YAG laser weekly or bi-weekly, with low fluence (typically 1–3 J/cm²), a collimated beam with a large spot size, and a frequency of 5–10 Hz [18].

The authors studied ultrastructural changes within melanosomes using transmission electron microscopy. They observed a reduction in the number of epidermal melanocyte dendrites after laser treatment. Laser treatment caused selective photothermolysis of stage IV melanosomes, while melanocytes remained intact and only melanosomes were destroyed. The authors concluded that laser toning is an effective method for treating melasma through subcellular selective photothermolysis [26].

Today, picosecond lasers (Picos) are a new type of laser with ultra-short pulse durations ranging from 300-900 picoseconds. These lasers produce more of a photomechanical effect than a photothermal effect, which helps to fragment pigment more effectively while minimizing thermal damage to surrounding tissue. Picosecond lasers used in melasma treatment primarily include picosecond Nd:YAG laser 1.064 nm (PSNYL) and picosecond alexandrite laser 755nm (PSAL). Studies show that non-fractional PSAL achieves better and faster melasma clearance rates compared to Q-switched Nd:YAG laser (QSNYL) [19].

2.2. Efficacy and Limitations of Laser Treatment

2.2.1 Melasma Recurrence After Laser Treatment

The key point to distinguish clearly: lasers can reduce existing pigmentation, but this does not mean they reduce the sensitivity of melanocytes or eliminate environmental triggers. A ScienceDirect overview of lasers and light in melasma treatment notes that although these methods are clearly effective in the short term, the recurrence rate over time remains high, and some techniques also carry the risk of post-inflammatory hyperpigmentation or hypopigmentation. Therefore, the commonly observed outcome in practice is: lasers help clear pigmentation, leading to significant clinical improvement, but if light exposure, inflammation, and oxidative stress persist, melanogenesis can restart and melasma can return [28].

Why melasma can still recur after successful laser treatment:

• Melanocytes remain capable of responding to stimuli: Lasers reduce existing melanin but do not eliminate melanocytes. When continuously exposed to environmental or hormonal stimuli, melanocytes can still be reactivated, leading to increased tyrosinase activity and pigment resynthesis [10].
• Visible light and UV radiation continue to stimulate melanogenesis: In addition to UV radiation, visible light has been shown to stimulate hyperpigmentation, especially in darker skin types – this is why protecting the skin from visible light, not just UV, becomes an important part of the post-laser maintenance strategy [10].
• Inflammation and damage to the skin barrier: Both environmental factors and the laser procedure itself can cause local inflammatory reactions. The nature of energy-based treatment is to create controlled tissue damage, and this damage always entails a local inflammatory response. If this inflammatory response is not well-controlled, it can become the very factor that promotes melanogenesis and leads to post-inflammatory hyperpigmentation (PIH) – a commonly reported complication after laser procedures for melasma, especially in darker skin types or when energy parameters are inappropriate [7].
• Vascular component of melasma: Melasma skin exhibits increased vascular proliferation and higher VEGF expression compared to adjacent healthy skin, creating a microenvironment that nourishes melanocyte activity. Laser modalities primarily targeting melanin do not necessarily fully control the vascular component of melasma, while vascular abnormalities are considered one of the factors that can contribute to the persistence of the condition [15].
  

Therefore, post-treatment skincare is not just about soothing, but should also be seen as part of a strategy to limit factors that can promote pigment recurrence.

2.2.2 Clinical Treatment Data and Melasma Recurrence

The effectiveness of various laser therapies in improving the Melasma Area and Severity Index (MASI) and the occurrence of side effects, analyzed by network meta-analysis (NMA). A review analyzed a network meta-analysis of 39 randomized controlled clinical trials involving 1,394 patients, showing that Q-switched Nd:YAG laser (QSND) was the most effective monotherapy among the compared laser groups, but QSND combined with topical medication was still superior to QSND alone (mean difference -4.21; 95% confidence interval: -6.80 to -1.63) [21].

Another systematic review of 42 studies (2009-2022) noted that low-fluence Q-switched Nd:YAG laser (LFQSNY) is generally safe and effective, but can cause patchy hypopigmentation with high cumulative energy [18].

A randomized controlled trial, published in Frontiers in Medicine (2023), directly compared PSNYL: picosecond Nd:YAG 1064nm laser, PSAL: picosecond alexandrite 755nm laser, and 2% hydroquinone cream (HO) in 59 patients with Fitzpatrick III-IV melasma, followed for 24 weeks. All three groups showed statistically significant improvement in MASI scores compared to baseline, with the picosecond Nd:YAG laser group demonstrating superior MASI reduction compared to both other groups.

Figure: Results of MASI score changes from baseline in three groups.
PSNYL: picosecond Nd:YAG laser (1.064 nm); PSAL: picosecond alexandrite laser (755 nm); HQ: hydroquinone (2%) [19].

The most notable point is that despite all patients being instructed on strict sun protection throughout the study, a recurrence rate was recorded in 6.8% (4/59) of patients, and post-inflammatory hyperpigmentation appeared at a similar rate in all three treatment groups – although these manifestations were all transient and resolved spontaneously within 1-6 months. From these observations, the authors concluded that no single therapy is comprehensively effective for melasma, and combining two or three treatment methods based on different pathogenetic mechanisms often yields better results than monotherapy – a conclusion from actual clinical data, directly reinforcing the multi-modal pigment control argument presented in Section III of this article [19].

In Vietnam, a study conducted at Can Tho Dermatology Hospital (2024-2025) on 55 melasma patients treated with picosecond Nd:YAG 1064nm laser recorded a continuous and statistically significant decrease in the average Melasma Area and Severity Index (MASI) score, from 10.49 at baseline to 3.26 after 20 weeks of follow-up, accompanied by a gradual decrease in the incidence of new lesions over time. The most common side effects recorded at week 20 were transient stinging, dry skin, itching, and redness, all of which resolved spontaneously. This data reflects well on the short-term efficacy and safety of picosecond lasers in Vietnamese patients; however, as this is a cross-sectional study with a limited follow-up period of 20 weeks, this data is insufficient to conclude on the long-term recurrence rate after treatment cessation – which is the core issue analyzed in this article, and the period when the role of home maintenance skincare becomes most evident [17].

III. Application of Topical Therapy in the Strategy for Managing and Controlling Melasma After Laser Treatment

Laser treatment and topical therapy do not compete but rather complement each other, acting synergistically at different mechanistic links and stages. Instead of expecting lasers to end melasma, a more appropriate view, given the pathophysiology of melasma, is that lasers help rapidly reduce pigment load, while controlling and managing factors that promote pigment recurrence should be entrusted to topical therapy combined with strict sun protection and long-term skin barrier care. A comprehensive topical product for the post-laser treatment phase needs to consider multiple targets simultaneously, rather than just a single mechanism:

• Melanogenesis: the process of melanin biosynthesis in melanocytes.
• Melanosome transfer: the process of pigment granule transport to keratinocytes.
• Oxidative stress: free radicals generated by UV and visible light.
• Inflammatory signaling: inflammatory signals that contribute to maintaining melanocyte activation.
• Photoaging/skin barrier dysfunction: the structural foundation of the skin indirectly affecting pigment expression.

In 2026, a comprehensive review combining meta-analysis summarized 11 randomized controlled trials on 461 melasma patients, directly comparing the effectiveness of combining laser/light with topical products versus using either method alone, evaluated by MASI scores at various time points. The most notable finding was not whether the combination was more effective, but how the difference in efficacy emerged over time: at week 4, the combination group did not show a significant difference compared to monotherapy, but by week 8, the advantage became clear and statistically significant, and continued to widen through weeks 12 and 16. In other words, the benefits of combining laser/light with topical treatment became more pronounced over time, reinforcing the role of sustained pigment control rather than just focusing on immediate post-procedure efficacy. [13].

3.1 Impact on Melanin Biosynthesis in Melanocytes

The group of active ingredients that impact the melanin biosynthesis step is quite diverse and familiar to both dermatologists and users: Hydroquinone, Thiamidol, Arbutin, Azelaic Acid, Vitamin C derivatives, Tranexamic Acid... Each group has its own molecular mechanism, but the commonality is that they all target the early stages and the process of new pigment synthesis, rather than just removing already formed pigment.

Among these, Arbutin works by temporarily blocking enzymes. Studies on human melanocytes show that Arbutin inhibits tyrosinase activity in a competitive and reversible manner, meaning it directly competes with L-tyrosine at the enzyme's active site without altering the expression of the gene encoding tyrosinase. In other words, Arbutin does not destroy or permanently inhibit melanocytes, but temporarily blocks the enzyme responsible for melanin synthesis while it is present on the skin [22].

Tranexamic Acid: A Different Approach

Tranexamic acid (TA) approaches the problem of pigmentation in a completely different way from other active ingredients. TA is a synthetic derivative of lysine that inhibits the plasminogen/plasmin system. Many recent studies describe its mechanism as follows: under the influence of UV radiation, keratinocytes increase the expression of plasminogen activator, converting plasminogen into plasmin; plasmin then promotes the release of inflammatory mediators and melanocyte-stimulating factors, thereby initiating melanogenesis [1, 16].

By inhibiting the conversion of plasminogen to plasmin, TA reduces this signaling cascade, thereby indirectly reducing light-induced melanocyte activation. Another aspect frequently reported is the link between the plasmin pathway and angiogenic factors such as VEGF. Inhibiting the plasmin formation pathway is believed to reduce the expression of VEGF and endothelin-1, two factors associated with the vascular proliferation often observed in melasma skin histopathology. This is why TA is often mentioned not only as an anti-hyperpigmenting agent but also considered in the vascular hypothesis of melasma [1, 16]. This is a fundamental difference compared to the mechanism of Niacinamide, and also why these active ingredients are often combined in the same formula rather than replacing each other.

A retrospective study published in 2025 on 121 melasma patients compared the efficacy of Q-switched alexandrite 755 nm laser combined with topical tranexamic acid (TA) versus topical TA alone. Of these, 61 patients received combination treatment with laser and TA, while 60 patients used only TA. Results showed that the combination group achieved a treatment response rate of 93.44%, which was statistically significantly higher than 81.67% in the TA-only group. After treatment, the combination group also had significantly lower MASI scores, lesion color intensity and area, melanin index, as well as certain pigmentary and vascular characteristics on dermoscopy compared to the control group. [20].

3.2 Impact on Melanosome Transfer Process

In addition to inhibiting synthesis, another approach targets the transport of pigment particles (melanosomes) from melanocytes to keratinocytes, which is a decisive step in whether the pigment actually appears on the skin surface. Niacinamide is an active ingredient that has been researched and proven effective in influencing this pathway. In a study by Hakozaki et al. published in the British Journal of Dermatology, Niacinamide does not directly inhibit tyrosinase but acts at the transport stage: reducing melanosome transfer by 35-68% in co-culture models of melanocytes and keratinocytes. Clinically, using Niacinamide for four weeks showed a significant reduction in hyperpigmentation compared to the control group [14].

In addition to its role in transport, Niacinamide has also been noted for its anti-inflammatory activity in in vitro and animal models, by reducing the expression of several pro-inflammatory cytokines such as TNF-α, IL-1, IL-6, IL-8, as well as reducing UVB-induced PGE2 production [12].

Regarding sebum control, this efficacy has clearer clinical evidence: a randomized controlled study by Draelos et al. on both Japanese and Caucasian subjects showed that 2% Niacinamide significantly reduced sebum excretion rate after 4-6 weeks of use [9]. This sebum control mechanism is indirectly related to limiting post-inflammatory hyperpigmentation (PIH related to acne), rather than a direct mechanism for melasma treatment. Niacinamide can be described as an active ingredient with a dual role in formulations: it partly helps control triggering factors (inflammation, sebum) and directly acts on pigment transport. This provides a reasonable basis for explaining the presence of Niacinamide in a multi-target melasma control formulation, while still noting that most data on its anti-inflammatory effect at the cytokine level comes from in vitro/animal models, and direct clinical evidence on melasma skin still primarily focuses on the melanosome transfer inhibition mechanism [14]. 

3.3 Control of oxidative stress

A 2024 study that evaluated the systemic oxidative status in melasma patients reported an imbalance between oxidants and antioxidants, where malondialdehyde (MDA - a marker of lipid peroxidation) concentration increased correlating with both the severity and area of melasma lesions. This indicates that oxidative stress not only accompanies but likely participates in the disease progression, rather than being merely a secondary consequence of UV radiation [25].

Mechanistically, UV and visible light increase the production of reactive oxygen species (ROS) in melanocytes and keratinocytes. Since melanin synthesis itself produces a certain amount of ROS, melanocytes are inherently more sensitive to oxidative stress than many other skin cell types. When the endogenous antioxidant system is overloaded or its activity is reduced, accumulated ROS will activate intracellular signals that promote melanogenesis, while also contributing to inflammation and overall skin aging [6].

A meta-analysis published in 2023 on the role of antioxidants in treating melasma and vitiligo revealed a rather cautious picture: most clinical studies on antioxidants for melasma have small sample sizes, are often combined with other treatments, making it difficult to isolate the individual efficacy of each active ingredient, and the overall evidence is still limited. In other words, the biological basis for the role of oxidative stress in melasma is quite strong, but clinical evidence for specific antioxidants is still accumulating and not yet sufficient to confidently affirm their efficacy as monotherapy [27].

Among common antioxidants on the market are Coenzyme Q10, Idebenone, Glutathione, Tocopherol derivatives, and various plant extracts. Most data on these active ingredients come from in vitro or ex vivo studies on their free radical neutralizing capabilities, with not many independent, controlled clinical trials on melasma patients. It is reasonable to expect these active ingredients to work synergistically as an antioxidant system in managing melasma.

3.4 Supporting skin quality and structural factors related to melasma

Most active ingredients target the stages of pigment synthesis and transport. However, after melanin has been delivered to keratinocytes, there is still one final stage that determines whether the pigment persists long in the skin: the rate of pigment elimination through epidermal turnover, and the level of local basal inflammation, which is one of the reasons why melasma tends to recur. This is why active ingredients that support skin regeneration are directly linked to the strategy of controlling and managing melasma.

Bakuchiol is a plant-derived monoterpene phenol, primarily extracted from the seeds and leaves of Psoralea corylifolia. Chemically, Bakuchiol is not analogous to Retinol or any retinoid; studies show it induces some gene expression changes similar to Retinol, but through different molecular mechanisms [5].

A direct comparative study of Bakuchiol with Retinol on human dermal fibroblast models and reconstructed epidermal models showed that Bakuchiol increased the expression of type I and VII collagen and fibronectin (structural components of the extracellular matrix ECM and basement membrane), while also promoting re-epithelialization in an in vitro wound healing model, being equivalent to or superior to Retinol in some indices. The same study noted that Bakuchiol reduced PGE2 and MIF (two inflammatory mediators) to an extent comparable to Retinol [3].

In terms of the pathogenesis of melasma, this is a noteworthy point: basement membrane damage and chronic inflammation are two factors contributing to the persistence of melasma, with basement membrane damage believed to be related to the phenomenon of pigment leakage into the dermis (a component of deep melasma, which responds poorly to superficial treatment). Supporting components related to the structure of the extracellular matrix and the dermo-epidermal junction, including type VII collagen and fibronectin, can therefore be seen as a mechanism to support skin structural quality. However, there is currently no clinical evidence directly proving that Bakuchiol reduces the risk of melasma recurrence.

Regarding clinical data, a randomized, double-blind study by Dhaliwal et al. published in the British Journal of Dermatology (2019) directly comparing 0.5% Bakuchiol with 0.5% Retinol in 44 participants over 12 weeks showed that both groups significantly improved wrinkles and hyperpigmentation, with no statistical difference between the two groups, while the Retinol group reported significantly more peeling and stinging [8].

Some topical formulations today also combine peptides, often with the aim of supporting aspects related to signs of aging and overall skin quality, complementing a comprehensive pigment control and management strategy.

3.5 Skincare stages after laser treatment

The role of topical homecare products should be categorized by stage:

Immediate post-treatment phase: The top priority is to restore the skin barrier, control inflammation, and strictly apply sun protection. At this stage, the skin is sensitive and easily damaged, so strong active ingredients should not be automatically introduced immediately, but rather follow the treating physician's instructions.

Stabilized skin phase: After the skin barrier has recovered and acute inflammation has subsided, pigment-controlling products can gradually be introduced into the skincare routine, with dosage and frequency according to the physician's instructions, depending on the type of laser and the individual's skin response.

Maintenance phase: This is the longest and most decisive phase in whether melasma recurs. The trio of topical pigment control, sun protection, and skin barrier care needs to be maintained regularly and long-term to control factors that continue to promote repigmentation after the laser has completed its role in reducing the initial pigment load.

IV. Application in multi-action formulations

A general overview to visualize how a comprehensive multi-action topical formulation works at different stages to control and manage melasma is as follows:

• Melanogenesis: Tranexamic Acid, Dark Fade Complex, Arbutin, Vitamin C Derivatives
• Melanosome Transfer: Niacinamide
• Oxidative Stress: CoQ10, Idebenone, Glutathione
• Photoaging/skin quality: Bakuchiol, supportive Peptides

oh!oh! Dark Spot Fading Serum is a specific example of how to build a multi-target topical formulation, with 10% Niacinamide, 3% Tranexamic Acid, 2.5% Dark Fade Complex, 1% Bakuchiol, the antioxidant system CoQ10 - Idebenone - Glutathione, and 1% peptide complex MSR™ Blend. What is noteworthy is not the number of active ingredients in the formula, but the systematic arrangement: each group of active ingredients is placed correctly at each stage and link of the melasma pathogenesis mechanism, developed with a multi-target orientation to support the pigment care process in the stabilized skin phase after procedures, with the timing of use needing to be appropriate for the skin condition and the instructions of the treating specialist.

V. Conclusion

Melasma treatment should not be viewed merely as the process of removing existing melanin pigment. Lasers and other energy-based methods can rapidly and significantly reduce the existing pigment load, but melanocytes themselves, environmental triggers, inflammation, and oxidative stress continue after the procedure. Therefore, controlling signals that continue to promote melanogenesis, melanosome transfer, oxidative stress, and photoaging—through at-home topical products combined with strict sun protection—still plays a crucial role in the long-term strategy for maintaining melasma treatment results.

VI. References

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2. Anderson, R.R. and J.A. Parrish, Selective photothermolysis: precise microsurgery by selective absorption of pulsed radiation. Science, 1983. 220(4596): p. 524-527.

3. Bluemke, A., et al., Multidirectional activity of bakuchiol against cellular mechanisms of facial ageing - Experimental evidence for a holistic treatment approach. Int J Cosmet Sci, 2022. 44(3): p. 377-393.

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6. Denat, L., et al., Melanocytes as instigators and victims of oxidative stress. J Invest Dermatol, 2014. 134(6): p. 1512-1518.

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8. Dhaliwal, S., et al., Prospective, randomized, double‐blind assessment of topical bakuchiol and retinol for facial photoageing.British Journal of Dermatology, 2019. 180(2): p. 289-296.

9. Draelos, Z.D., A. Matsubara, and K. Smiles, The effect of 2% niacinamide on facial sebum production. J Cosmet Laser Ther, 2006. 8(2): p. 96-101.

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11. Espósito, M.C.C., et al., Depression, anxiety, and self‐esteem in women with facial melasma: an Internet‐based survey in Brazil. International Journal of Dermatology, 2021. 60(9): p. e346.

12. Farris, P. and T. Lain, Niacinamide: a multi-functional cosmeceutical ingredient. Practical Dermatology, 2022. 15: p. 62-63.

13. Fithria, R.F., et al., Laser and light-based therapies combined with topical agents for melasma: A systematic review and meta-analysis. Medicine (Baltimore), 2026. 105(2): p. e46579.

14. Hakozaki, T., et al., The effect of niacinamide on reducing cutaneous pigmentation and suppression of melanosome transfer.Br J Dermatol, 2002. 147(1): p. 20-31.

15. Kim, E.H., et al., The vascular characteristics of melasma. Journal of dermatological science, 2007. 46(2): p. 111-116.

16. Konisky, H., et al., Tranexamic acid in melasma: A focused review on drug administration routes. J Cosmet Dermatol, 2023. 22(4): p. 1197-1206.

17. Lam, T., et al., Treatment outcomes of melasma using picosecond Nd: YAG 1064nm laser at Can Tho Dermatology Hospital.Tạp chí Y học Việt Nam, 2025. 556(2).

18. Lee, Y.S., et al., The low-fluence Q-switched Nd: YAG laser treatment for melasma: a systematic review. Medicina, 2022. 58(7): p. 936.

19. Liang, S., et al., Comparison of the efficacy and safety of picosecond Nd: YAG laser (1,064 nm), picosecond alexandrite laser (755 nm) and 2% hydroquinone cream in the treatment of melasma: a randomized, controlled, assessor-blinded trial.Frontiers in medicine, 2023. 10: p. 1132823.

20. Liu, X. and C. Liao, Value of Q-switched 755-nm alexandrite laser combined with topical tranexamic acid in the treatment of melasma. Am J Transl Res, 2025. 17(3): p. 1651-1661.

21. Ma, W., et al., Efficacy and safety of laser‐related therapy for melasma: a systematic review and network meta‐analysis.Journal of Cosmetic Dermatology, 2023. 22(11): p. 2910-2924.

22. Maeda, K. and M. Fukuda, Arbutin: mechanism of its depigmenting action in human melanocyte culture. J Pharmacol Exp Ther, 1996. 276(2): p. 765-9.

23. Maranzatto, C.F.P., et al., Psychometrican analysis and dimensional structure of the Brazilian version of melasma quality of life scale (MELASQoL-BP). Anais brasileiros de dermatologia, 2016. 91(4): p. 422-428.

24. Pollo, C., et al., Factors associated with quality of life in facial melasma: a cross‐sectional study. International journal of cosmetic science, 2018. 40(3): p. 313-316.

25. Rahimi, H., et al., Evaluation of systemic oxidative stress in patients with melasma. Journal of Cosmetic Dermatology, 2024. 23(1): p. 284-288.

26. Sarkar, R., et al., Lasers in melasma: a review with consensus recommendations by Indian Pigmentary Expert Group. Indian Journal of Dermatology, 2017. 62(6): p. 585.

27. Speeckaert, R., et al., The impact of antioxidants on vitiligo and melasma: a scoping review and meta-analysis. Antioxidants, 2023. 12(12): p. 2082.

28. Trivedi, M., F. Yang, and B. Cho, A review of laser and light therapy in melasma. International journal of women's dermatology, 2017. 3(1): p. 11-20.

29. Yalamanchili, R., V. Shastry, and J. Betkerur, Clinico-epidemiological Study and Quality of Life Assessment in Melasma.Indian J Dermatol, 2015. 60(5): p. 519.

 

Note: This article is a scientific summary and does not replace the diagnosis or advice of a dermatologist. The effectiveness of all topical products depends on individual skin type and must be used under professional guidance, especially during the post-laser procedure period.