Reframing melasma through the language of management, from pigment formation to home-care planning. This section examines how skin pigmentation develops.
“Director, I had laser treatment last year. Why has it come back?”
This question returns without fail at the end of summer. The patches had clearly faded through spring. By August, however, brown discoloration had spread again across the cheekbones. Answering this question requires understanding how pigment forms and where that pathway breaks down to create melasma. This explains why aggressive procedures may backfire, why melasma requires management, and why home care matters as much as professional treatment.
This column has three parts. They cover pigment formation, the pigmentation encountered in aesthetic practice, and practical management strategies.
PART 1
How Pigment Forms and Where the Process Breaks Down
1. Start with the Normal Pigment Pathway
Melanocytes reside in the basal layer, the deepest layer of the epidermis. These pigment-producing cells appear repeatedly throughout this column. Pigment follows four stages from formation to elimination.
- A signal, such as ultraviolet exposure, reaches the skin.
Melanocytes receive instructions to produce pigment. - Melanin is synthesized inside the cell. It forms within intracellular structures called melanosomes.
- The pigment is transferred to nearby cells. Melanocytes extend dendrites and deliver pigment to surrounding keratinocytes.
- The pigment is shed with dead skin cells. Pigment-containing keratinocytes move upward and eventually detach.
The third and fourth stages are especially important. Visible brown coloration comes from pigment-containing keratinocytes, not the melanocytes themselves. The epidermis renews approximately every four weeks through skin turnover. If this pathway functions normally, pigment is naturally removed. Think of melanocytes as factories, melanosomes as production lines, and melanin as the product. The product is delivered to nearby shops, or keratinocytes. When those shops close, their remaining inventory leaves with them. Persistent pigment therefore indicates excessive production, impaired elimination, or both. Unfortunately, melasma involves both processes.
2. Melasma Disrupts Three Points in This Pathway
① Production — Activity Increases, Not the Number of Factories
Melasma is sometimes described as an increase in melanocyte numbers, but this is not precise. Multiple studies found no clear difference between melasma lesions and adjacent normal skin. Instead, melanocytes were larger, had longer dendrites, and showed greater activity of enzymes involved in melanin production. The issue is cellular activity, not cell count. This distinction fundamentally changes the management strategy. If cell numbers increased, reducing them might be logical. When activity rises, however, reducing activating factors is more appropriate. The existing factory is operating around the clock rather than new factories being built. Reducing incoming orders is more fundamental than trying to destroy the factory.
Studies comparing melasma lesions with surrounding normal skin have not consistently found significantly more melanocytes. Instead, they reported cellular enlargement and increased pigment-synthesis activity.
② Elimination — Pigment Leaks Downward
A thin boundary called the basement membrane separates the epidermis from the dermis. When intact, pigment remains within the epidermis and exits upward with dead skin cells. Prolonged ultraviolet exposure can damage this membrane. Some pigment then moves in the opposite direction and enters the dermis. Macrophages capture this pigment, allowing it to remain for extended periods. It is no longer governed by the skin turnover cycle. This helps explain why exfoliation and topical brightening ingredients alone may not sufficiently reduce melasma.
Consider water spilled onto a carpet. A fresh spill is easily wiped away. Once water penetrates the layer underneath, surface wiping cannot remove it. Melasma is similarly difficult to eliminate quickly when the basement membrane is damaged. Histological studies found basement membrane damage in 83% to 95.5% of lesions, depending on the assessment method.
Melanocytes may also extend downward through gaps in the damaged boundary and into the dermis. This resembles roots growing through a drainage hole in a flowerpot. The pigment factory itself then spans the lower level, or dermis. As a result, epidermis-focused management alone may not easily clear established melasma.
③ Signaling — Orders Continue Rising from the Dermis
Melasma is not limited to the epidermis. Changes also occur within the dermis. Chronically sun-exposed fibroblasts age and continuously release signals that promote melanin production. Increased blood vessels and inflammatory cell infiltration may occur alongside these changes.
One point requires clarification.
Fibroblasts do not intentionally request more pigment. These signals belong to a repair program originally designed for wound recovery. Damaged skin requires regeneration. Covering the affected area with pigment may also help protect it from ultraviolet exposure. This is a reasonable response to acute damage.
Problems arise when repeated ultraviolet damage ages fibroblasts and prevents these signals from switching off. Senescent fibroblasts remain in place, but their secretions change. Younger cells mainly produce structural proteins, such as collagen. Senescent cells increasingly release degradative enzymes and various signaling molecules. Melanocytes interpret some of these substances as activation commands.
The damage signal therefore remains active even without a wound or anything left to repair. Melanocytes receive that signal and continue working.
A faulty fire alarm provides a useful analogy. The fire is out, but the alarm continues sounding. Firefighters keep responding to the signal. In this comparison, fibroblasts are the alarm and melanocytes are the firefighters.
This is why melasma is not solely an epidermal issue. Addressing epidermal pigment only clears inventory from the upper floor. Meanwhile, new orders continue arriving from below. Heat and irritation may further stimulate senescent fibroblasts. Aggressive procedures may therefore backfire through dermal as well as epidermal pathways.
3. Invisible Inflammation — The Embers of Melasma
This is the most important point discussed so far. Melasma lesions involve chronic skin inflammation that is not visible. This single fact explains all subsequent management principles.
What Is Present?
Histological examination of melasma lesions reveals findings that are not expected in normal skin.
· Immune cell infiltration: T cells and macrophages are present within the affected area.
· Increased mast cells: Despite their name, these cells are unrelated to obesity. They help initiate inflammatory responses.
· Elevated inflammatory markers: Substances associated with inflammation are measured at higher levels than in unaffected areas.
· Increased blood vessels: Greater vascular density and size may create a subtle reddish tone beneath the brown pigmentation.
Why Is It Invisible?
The four classic signs of inflammation do not appear: redness, swelling, pain, and heat. This is not an obvious acute response like acne or a burn. Instead, it persists for a long period at very low intensity. It resembles embers that remain after a fire, without even visible smoke.
Why Does It Matter?
Inflammatory signaling and pigment-production signaling share many of the same pathways. Melanocytes interpret substances released by inflammatory cells as commands to produce pigment. In melasma-prone skin, irritation can therefore become a pigmentation signal.
Three practical principles follow directly from this fact.
· Why can strong stimulation backfire? It adds fuel to inflammation that is already active.
· Why should low-pH formulations be used carefully? Stinging and flushing can themselves act as pigmentation signals.
· Why is melasma managed rather than cured? Remaining embers may flare again at any time.
What Fuels the Embers?
Ultraviolet exposure is a major factor. Heat, friction, irritating cosmetics, and excessive procedures may add to it. Importantly, all these variables can be controlled. From this perspective, melasma management takes on a different meaning. It is not about removing pigment. It is about shielding the embers from further fuel. This idea runs throughout the entire column.
PRACTICAL TIP
— One Sentence Is Enough for Clients
“Melasma is not a stain on wallpaper. It is a leak coming from inside the wall. Removing the stain may make the surface look clean for several days. However, it returns because the water continues leaking. The goal is to remove the stain while slowing the leak.”
Terms such as basement membrane and melanocyte are unnecessary here. This single analogy helps clients understand why ongoing management is needed.
Melasma is not triggered by ultraviolet exposure alone. Genetics and hormones may pull the trigger, while ultraviolet exposure repeats the process each year.
References
① What Should Be Considered in Treatment of Melasma. Annals of Dermatology. PMC2991712 / Heterogeneous Pathology of Melasma and Its Clinical Implications. International Journal of Molecular Sciences. 2016. PMC4926358
② Torres-Álvarez B, Mesa-Garza IG, Castanedo-Cázares JP, et al. Histochemical and immunohistochemical study in melasma: evidence of damage in the basal membrane. American Journal of Dermatopathology. 2011;33(3):291-295.
③ Histopathological comparison of lesional and perilesional skin in melasma: A cross-sectional analysis. Indian Journal of Dermatology, Venereology and Leprology. 2019.
④ Unraveling Melasma: From Epidermal Pigmentation to Microenvironmental Dysregulation. Biology. 2025;14(10):1402. doi:10.3390/biology14101402
⑤ New Mechanistic Insights of Melasma. Clinical, Cosmetic and Investigational Dermatology. 2023. PMC9936885 / Unraveling Melasma. Biology. 2025;14(10):1402.
⑥ A Review of Postinflammatory Hyperpigmentation. Cutis. 2017. / Postinflammatory Hyperpigmentation. StatPearls. 2024. NBK559150
⑦ Honigman A, et al. Differential diagnosis of melasma and hyperpigmentation. Dermatological Reviews. 2023. doi:10.1002/der2.144
⑧ Hori Y, Kawashima M, Oohara K, Kukita A. Acquired, bilateral nevus of Ota-like macules. Journal of the American Academy of Dermatology. 1984;10(6):961-964.
⑨ Comparison of acquired bilateral nevus of Ota-like macules in men and women. Indian Journal of Dermatology, Venereology and Leprology. 2014.
⑩ The Low-Fluence Q-Switched Nd:YAG Laser Treatment for Melasma: A Systematic Review. PMC9323185
Editor SEUL, LEE
Image Shutterstock
The Signature Magazine – September 2026 Issue