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The occurrence mechanism and clinical diagnosis and treatment of melasma have become the focus of dermatologists. Previous studies have not fully understood melasma, believing that the disease is only related to sun exposure and increased pigmentation. Treatment only focuses on pigmentation issues, resulting in poor results and poor patient satisfaction. With the continuous development of basic research on melasma and new clinical diagnosis and treatment technologies in recent years, dermatologists have a better understanding of the disease, more accurate diagnosis and treatment, and significantly improved treatment effects. We searched for the literature using the keywords "Melasma", "chloasma", "diagnosis of facial hypermelanoses" and "chloasma" in PubMed and CNKI, and further refined the search using "guidline", "consensus", "pathogenesis", "guidelines" and "consensus". We found that there are no clinical diagnosis and treatment guidelines for melasma abroad. This article uses the "Chinese Expert Consensus on the Diagnosis and Treatment of Chloasma (2021 Edition)" [2] published in the "Chinese Journal of Dermatology" in 2021 as a reference, and combines the research progress at home and abroad to interpret the causes, mechanisms, clinical manifestations, staging and classification, and treatment of melasma, aiming to enhance dermatologists' understanding of the disease, guide clinical diagnosis and treatment, improve the treatment effect of the disease, and reduce recurrence.
I. Causes and Predisposing Factors
Genetic background, ultraviolet radiation and sex hormones are classic factors affecting melasma. Recent studies have found that blue light, air pollution, mental and psychological stress, the use of inferior cosmetics with excessive mercury/lead content, cooking/occupational heat exposure, thyroid disease, female reproductive system diseases, etc. can also induce or aggravate chloasma.
1. Genetic background
People with Fitzpatrick type III to V skin color are more susceptible to the disease, and 40% to 60% of patients have a family history, which is related to the age of onset and the severity of the disease [3].
2,Ultraviolet and blue light radiation
Previous studies on chloasma pigmentation have mainly focused on ultraviolet rays, especially long-wave ultraviolet rays (ultraviolet A, UVA) and medium-wave ultraviolet rays (ultraviolet B, UVB), which can directly stimulate melanocytes to synthesize melanin [4]. The latest research has found that ultraviolet light can stimulate keratinocytes, mast cells, and fibroblasts to regulate melanin production through paracrine secretion, and is also involved in inflammatory response, angiogenesis, photoaging and other processes; blue light activates melanocytes to produce pigmentation, and this effect is even more obvious than UVA [5].
3,sex hormones
The prevalence of melasma increases in people who are pregnant, taking oral contraceptives, and receiving other sex hormone therapies. Studies have shown that estrogen amplifies the effect of ultraviolet light on melanin production by directly acting on melanocytes or indirectly acting on keratinocytes and melanin transfer. It can also increase the number of blood vessels, change vascular hemodynamics, and aggravate melasma lesions [6].
4、Air pollution
It may be related to the fact that pollutants in the form of particulate matter and polycyclic aromatic hydrocarbons in the air enter the skin through nanoparticles, producing excessive reactive oxygen species (ROS), leading to increased melanin production［7］.
5、Psychological factors
Patients with melasma show higher anxiety scores［8］. It may be related to the fact that stress induces the hypothalamus to produce α-melanocyte stimulating hormone (ɑMSH) and adrenocorticotropic hormone (ACTH) precursor peptide to promote melanin increase.
6、Poor-quality cosmetics
Lead and mercury ions can compete with copper ions to inhibit tyrosinase and inactivate it, reducing melanin formation. However, long-term use of poor-quality cosmetics will cause excessive heavy metals to be absorbed and deposited in the dermis through skin appendages such as hair follicles and sebaceous glands, inducing pigmentation and damaging the skin barrier, inducing chloasma［9］.
7、Heat exposure
A multi-center cross-sectional survey in India showed that the severity of chloasma was positively correlated with heat exposure such as cooking and high-intensity lighting［10］.
8,Systemic diseases
Motahhareh et al. [11] found that the levels of serum thyroid stimulating hormone (TSH), anti-thyroid peroxidase antibody (TPO) and anti-thyroglobulin antibody (ATG) were significantly increased in patients with melasma, suggesting that thyroid disease may have a certain relationship with the occurrence and development of melasma; people with female reproductive system diseases are more susceptible to melasma, which may be related to the disorder of sex hormone levels.
Pathogenesis
It was previously believed that melanocytes were the only cells involved in the progression of melasma. It has been confirmed that fibroblasts, sebaceous gland cells, keratinocytes, vascular endothelial cells, mast cells, etc. also play a certain role, involving biological processes such as increased pigment synthesis and transport disorders, basement membrane destruction, vascular proliferation and blood stasis, inflammatory response, skin barrier damage, and photoaging [12]. Increased melanin synthesis and transport disorders are the most widely recognized biological characteristics of melasma. The genes involved in melanogenesis, such as tyrosinase (TYＲ), tyrosine-related protein 1 (TYＲP1) and microphthalmia-associated transcription factor (MITF), are upregulated in the lesion area, and the increase in melanocyte dendrites and mitochondria are strong supporting evidence [13]. However, recent studies have found that the above factors, especially the large amount of ROS produced after ultraviolet radiation, can directly stimulate the oxidation process of melanocytes, leading to increased melanin synthesis; damage the basement membrane zone, hinder melanin transport, and enter the dermis to cause persistent pigmentation [14]; at the same time, it induces fibroblasts, sebaceous gland cells, etc. to secrete melanin-stimulating factors such as α-MSH, basic fibroblast growth factor (basic fibroblast growth factor, BFGF), hepatocyte growth factor (hepatocyte growth factor, HGF), stem cell factor (stem cell factor, SCF), etc., activate TYＲ and TYＲP1 [1, 15-16], and promote increased pigment synthesis; blue light induces increased pigment production, which may be related to the induction of multimeric TYＲ/TYＲP-related protein complexes to regulate melanin production after the activation of opsin 3 [17].
2, vascular proliferation and blood stasis
The latest studies have found that the expression of vascular endothelial growth factor (VEGF) and endothelin 1 (ET-1) in the lesions of patients with melasma is significantly increased, and the number and diameter of small blood vessels in the dermis are significantly increased compared with normal skin［6,18］; the hematocrit, reduced hemoglobin, and erythrocyte sedimentation rate are increased, the capillaries in the lesions are dilated, and blood stasis is present［19］.
3、Inflammatory response
In melasma lesions, the expression of Toll-like receptor (TLＲ) -2 and TLR-4 is upregulated, promoting the release of prostaglandin E2 (PGE2) and SCF, increasing the expression of IL-1β, IL-17, stem cell factor receptor (c-kit receptor, c-kit), and cyclooxygenase-2 (COX-2), activating MITF and TYＲ/TYＲP1, and promoting melanogenesis［20-21］. Recent studies have also shown that UVB radiation promotes the release of PGE2 and SCF by stimulating keratinocytes to secrete IL-1β, upregulating the expression of TYＲ/TＲP-1, and inducing increased melanogenesis［22］.
4、Skin barrier damage
The water content of the stratum corneum in the lesion area of chloasma patients decreases, the transepidermal water loss (TEWL) value increases, the stratum corneum becomes thinner, and the barrier repair rate is delayed［23］; the expression of epidermal keratin, cornified mantle protein and acid ceramidase is abnormal, the skin barrier is damaged, and the P53/POMC (pro-opiomelanocortin)/TＲP1 signaling pathway is further promoted to increase the pigmentation induced by ultraviolet rays［24-25］. 5. Photoaging: Ultraviolet radiation causes skin elastic fibers to degenerate [14]. Visible light can induce keratinocytes to produce ROS and proinflammatory cytokines, and may induce matrix metalloproteinase (MMP) expression through the EGFＲ-ERK pathway, promoting skin photoaging [26]. Therefore, in recent years, some scholars have proposed that melasma is a manifestation of photoaging [1]. 6. Mast cells: The number of mast cells in the lesion area of melasma patients increases and their function is active [27]. UV radiation stimulates mast cell degranulation to release histamine, which binds to H2 receptors on the surface of melanocytes and induces increased melanin production [28]; releases trypsin, activates MMP to degrade the extracellular matrix and destroy the basement membrane zone [29], and participates in skin photoaging and pigment transport disorders; produces VEGF, transfers
III. Diagnosis and differential diagnosis
1,Diagnosis
Melasma can be diagnosed comprehensively based on the patient's medical history, typical clinical manifestations, and non-invasive detection techniques such as reflectance confocal microscopy (RCM), slide compression, and Wood lamp. The 2021 consensus for the first time divides melasma into stages and types, including active and stable phases of melasma; melanized type (M type) and melanized with vascularized type (M + V type) [2, 31].
1. Staging
Chloasma clinical staging is divided into active stage and stable stage. Active stage: Recently, the lesions have expanded in area, deepened in color, and reddened. The lesions are red after scratching. Most of them fade when the slide is pressed. Under RCM, there are more high-refractive dendritic and starburst-shaped melanocytes in the basal layer of the epidermis, and there are varying numbers of mononuclear cells with medium refraction infiltration in the superficial dermis, and some high-refractive chromophages can be seen. Stable stage: Recently, the lesions have not expanded in area, deepened in color, and reddened. The lesions are not red after scratching. Most of them do not fade when the slide is pressed. Under RCM, there are fewer dendritic melanocytes in the basal layer of the epidermis, and the dendrites are shorter than those of the active stage melanocytes. Starburst-shaped melanocytes are rare, and the number of mononuclear cells infiltrating the superficial dermis is reduced.
1. Classification
Based on the involvement of blood vessels, it is divided into 2 types: ①M type: the lesions do not fade when the slide is pressed, and the color contrast between the lesion area and the non-lesion area increases under the Wood lamp; ②M + V type: the lesions partially fade when the slide is pressed, and the color contrast between the lesion area and the non-lesion area under the Wood lamp is not significantly increased. According to the location of the pigment, it is divided into 2 types: ①epidermal type (increased epidermal pigment); ②mixed type (increased epidermal pigment + melanophages in the superficial dermis). This classification is of guiding significance for the judgment of treatment effect.
2,Differential diagnosis
This disease needs to be differentiated from freckles, brown-blue nevus, nevus of Ota, melanosis and post-inflammatory pigmentation.
IV. Treatment
The 2021 consensus no longer focuses solely on pigmentation issues, but emphasizes the importance of avoiding triggers, inhibiting angiogenesis, anti-inflammation, repairing the skin barrier, and resisting photoaging in the treatment of melasma. It is combined with the use of freckle-removing and whitening functional skin care products, combined with clinical staging and classification, and combined with systemic and topical medications, chemical peels, lasers and traditional Chinese medicine treatments [2, 32-34].
1、Basic treatment
1. Avoid triggers
Avoid excessive sun exposure; Avoid taking drugs that cause changes in sex hormone levels; Maintain a good mood and mentality; Avoid using inferior cosmetics with excessive mercury and lead content; Reduce cooking/occupational heat exposure, etc.
2. Sun protection
Should be carried out throughout the entire treatment process of melasma. It is recommended to use a broad-spectrum (UVA +, UVB +, blue light) sunscreen with a sun protection factor (SPF) ≥ 30 and a UVA protection grade (PA) + + + for a long time. On the basis of topical sunscreen, it is recommended to strengthen sun protection, such as sun umbrellas, sun hats, sun masks, etc., which is beneficial to the prevention and treatment of chloasma, improve the efficacy and reduce recurrence.
3. Freckle removal and whitening functional skin care products
According to the latest pathogenesis of chloasma, freckle removal and whitening skin care products that inhibit pigmentation, anti-inflammatory, anti-oxidation, inhibit angiogenesis and restore skin barrier have significant effects on the treatment of chloasma, which is better than simple topical pigment removal preparations. They can be used alone or combined with drugs, chemical peeling or photoelectric treatment according to the staging/typing of chloasma. This type of functional skin care products also plays an irreplaceable role in the maintenance treatment of chloasma. Dermatologists should understand its active ingredients, clinical applications and precautions.
4. Treatment of related diseases Actively treat related chronic diseases that may induce or aggravate chloasma, such as thyroid disease, female reproductive system diseases, etc.
2, , Staging and classification treatment
1. Active stage Avoid phototherapy and acid peeling, and choose basic treatment combined with systemic and topical medication.
a. Systemic medication
① Tranexamic acid: It has the effects of reducing melanin synthesis, inhibiting the transport of melanin particles to the superficial layer of the epidermis and vascular proliferation. ② Glycyrrhizic acid: It inhibits mast cell degranulation, reduces the production of inflammatory factors, and has anti-inflammatory effects. ③ Vitamin C and vitamin E: Vitamin C can prevent DOPA oxidation and inhibit melanin synthesis, and vitamin E has a strong antioxidant effect. The combined use of the two can enhance the therapeutic effect. ④ Glutathione: The sulfhydryl group in the molecule can inhibit its activity by binding to the copper ion in tyrosinase and reduce melanin production. It is often used in combination with vitamin C.
b. Topical drugs
① Hydroquinone and its derivatives: competitively inhibit tyrosinase, inhibit DOPA production and reduce melanin production, and are the first-line topical treatment drugs for chloasma. ② Retinoic acid: promote epidermal exfoliation and accelerate black shedding. ③ Azelaic acid: inhibit tyrosinase activity, reduce melanin production and prevent melanin from being transported to the epidermis. ④ Tranexamic acid: In addition to the above three types of effects, studies have shown that topical tranexamic acid can also repair the skin barrier.
2. Stable period
Combined with systemic and topical drug treatments, such as fruit acid peeling and photoelectric treatment.
a. Fruit acid peeling
Promote the replacement of keratinocytes and accelerate the discharge of melanin particles, thereby reducing pigmentation and brightening the skin.
b. Photoelectric treatment
①M type: Q-switched laser, picosecond laser, etc. can selectively photothermally blast melanin and accelerate melanin metabolism. Among them, picosecond laser can also stimulate collagen synthesis and improve photoaging. ②M + V type: frequency-doubled Nd: YAG/high-energy potassium titanyl phosphate (KTP) laser, pulsed dye laser, intense pulsed light, etc. target pigments while selectively acting on oxygenated hemoglobin to raise its temperature and coagulate it, causing blood vessels to coagulate and destroy blood vessels, thereby improving vascular proliferation.
3、Treatment with Traditional Chinese Medicine
Traditional Chinese medicine believes that patients with melasma suffer from liver depression and qi stagnation, qi stagnation and blood stasis, spleen and stomach weakness, and liver and kidney deficiency. The treatment should be based on soothing the liver, strengthening the spleen and tonifying the kidney, regulating qi, activating blood circulation and removing blood stasis. Clinically, it is necessary to treat based on syndrome differentiation.
4、Combined treatment
Chloasma has many causes and a complex pathogenesis. Single treatment is ineffective. It is necessary to avoid chloasma-inducing factors, and use sun protection and freckle-removing and whitening functional skin care products throughout the entire treatment process. According to the patient's clinical stage and classification, and taking into account factors such as pigment, blood vessels, inflammation, skin barrier, photoaging, etc., a variety of treatment methods should be used in combination for the best effect.
V. Summary and Outlook
With the improvement of the understanding of the pathogenesis of melasma, melasma is no longer a simple pigmentation problem. Various cell types, blood vessels, inflammation, skin barrier and photoaging processes all play an important role. Treatment methods targeting new targets are gradually becoming popular, and the treatment effect of melasma has been significantly improved. We should further increase the interpretation and promotion of guidelines, formulate a comprehensive treatment plan according to the stage and type of the disease, combined with the causes and pathogenesis of melasma, and incorporate sun protection and the use of freckle-removing and whitening functional skin care products throughout the treatment of melasma. This is an effective strategy for the long-term management of melasma. Although the diagnosis and treatment of melasma have achieved encouraging results in the past few decades, there is a lack of research on drugs for the treatment of melasma. Studies have shown that anti-hormone therapy, vascular endothelial growth factor inhibitors and intradermal injection of platelet-rich plasma (PRP) [34] are effective in the treatment of melasma. Topical products that block blue light can prevent immediate and persistent pigmentation caused by blue light [35]. It is imperative to clarify the efficacy and safety of these emerging therapies in large-scale trials. It is believed that with the development of evidence-based medicine, there will be new breakthroughs in the treatment of melasma.
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