​RETHINKING PIGMENTARY AGING: FROM MELANIN LOAD TO MELANOCYTE-FIBROBLAST CROSS-TALK

Melanocyte fibroblast crosstalk is central in pigmentary aging. This holds true across phototypes I to VI. It is particularly visible in darker skin where chronological and structural aging progress more slowly, yet pigmentary disorders dominate the clinical picture.¹⁻³

Fibroblasts mainly sit in the dermis. Melanocytes mainly sit above them in the epidermis. Fibroblasts send chemical messages to melanocytes. These messages tell melanocytes how active to be. They also influence how much pigment reaches the surface and how evenly it is distributed.⁴⁻⁸

Some messages dampen pigment production, for example DKK1. Other messages like Neuregulin 1 enhance pigment production. Together these signals shape baseline skin tone. They also shape how dark spots and uneven tone appear with age.⁴⁻⁷

With time and sun exposure fibroblasts and melanocytes change. Some become senescent. Senescent melanocytes use more glucose and produce more lactate. They transport pigment granules less efficiently. This contributes to mottled dark and light areas.¹⁰ ¹¹

Lighter skin tends to show early wrinkles and fine lines. Darker skin shows later wrinkling but more pronounced lentigines, post inflammatory hyperpigmentation and tone irregularities.¹⁻³ Structural aging is slower in darker phototypes. Pigmentary aging is relatively faster.¹⁻³ ¹²

Future interventions should extend beyond lowering melanin synthesis alone. Classic tools such as tyrosinase inhibitors, antioxidants, hydroquinone, the original Kligman trio and newer triple combinations mainly reduce melanogenesis and accelerate epidermal pigment clearance. In addition, next‑generation strategies should rebalance fibroblast secretomes and dermo‑epidermal crosstalk and reduce senescence‑related stress in melanocytes. This systems‑level approach is relevant across all phototypes and is particularly critical in phototypes V and VI.⁸ ¹⁰ 

​Let´s have a closer look......

INTRODUCTION
Cutaneous pigmentation depends on melanin synthesis within melanocytes, on melanosome biogenesis and transfer, and on the spatial distribution of pigment across the epidermis.¹³ Fitzpatrick phototypes I to VI capture broad differences in melanin quantity, melanosome size, and melanosome packaging.¹³ However these physical differences do not fully explain observed patterns of skin aging across ethnicities.

Epidemiologic and clinical series show that individuals with phototypes I and II develop wrinkles and dermal laxity earlier and more severely than individuals with phototypes V and VI at comparable ages and environmental exposures.¹⁻³ In contrast darker phototypes exhibit a disproportionate prevalence of pigmentary conditions such as solar lentigines, melasma, post inflammatory hyperpigmentation and mottled dyschromia, despite comparatively preserved dermal structure and lower wrinkle scores.¹⁻³ ¹² This divergence suggests that regulation of pigment quality and distribution is at least as important as melanin load in shaping perceived skin aging.

Dermal fibroblasts have emerged as key regulators of pigmentation. They do so through secretion of paracrine factors that influence melanocyte proliferation, dendricity, melanogenesis and melanosome transfer.⁴⁻⁸ ¹² A recent synthesis of data from melasma, solar lentigines, photoaging and vitiligo concluded that fibroblasts in hyperpigmented lesions secrete increased levels of melanogenesis promoting factors and altered extracellular matrix components, whereas fibroblasts in depigmented lesions tend to express higher levels of inhibitory or non supportive mediators.⁸ These findings place the fibroblast at the center of a pigment control network and may also be relevant for idiopathic guttate hypomelanosis, characterized by tiny white spots on sun exposed sites such as shins and forearms, for which I have been searching for effective appearance improving strategies for many years.

In parallel, senescent melanocytes have been identified in chronically photoexposed skin. They display a distinct metabolic and secretory phenotype that can drive local pigmentary changes and paracrine inflammation.¹⁰ ¹¹ ¹⁴ Taken together, these observations support a dermo‑epidermal “tone orchestration” model in which the states of fibroblasts and melanocytes jointly shape pigmentary aging, with the final clinical picture amplified in a phototype specific manner.

DERMAL SIGNALING TO MELANOCYTES

DKK1 and Wnt β catenin
DKK1 is a secreted inhibitor of the Wnt β catenin pathway. It is strongly expressed by palmoplantar fibroblasts, that is, fibroblasts from the palms of the hands and the soles of the feet. These regions are relatively hypopigmented and have thin epidermis.⁴ Yamaguchi and colleagues showed that DKK1 expression is higher in palmoplantar fibroblasts compared with non‑palmoplantar fibroblasts, and that recombinant (lab‑produced) DKK1 at one hundred nanograms per milliliter suppresses melanocyte proliferation and melanogenic protein expression. ⁴

In melanocytes DKK1 reduces tyrosinase (the key melanin‑producing enzyme), dopachrome tautomerase, Pmel17, MART 1 and MITF. It decreases β catenin and increases phosphorylated GSK3β.⁴ In reconstructed skin models DKK1 decreases melanin content and epidermal thickness. It also reduces melanosome transfer by downregulating PAR 2 in keratinocytes.⁴ These data provide a mechanistic explanation for the pale and thin phenotype of palmoplantar skin and illustrate the potency of a single fibroblast derived factor in modulating pigmentation.
​
In vitiligo skin DKK1 expression is increased in lesional dermis. Exogenous DKK1 induces p16 expression in melanocytes and promotes senescence in vitro.¹⁵ This links DKK1 not only to hypopigmentation but also to melanocyte aging. Taken together these observations define DKK1 as a strong inhibitory paracrine signal that shapes local pigment patterns. This pattern suggests that long term high levels of DKK1 or similar inhibitory signals in small areas of the dermis could also help drive hypopigmented conditions such as idiopathic guttate hypomelanosis, by both slowing melanocyte activity and accelerating melanocyte aging in those spots.

​Neuregulin 1 SCF and endothelin 1

Neuregulin 1 is a fibroblast derived ligand ((a signaling molecule that binds a specific receptor) for ERBB receptors on melanocytes. It promotes melanocyte growth and differentiation. In skin equivalent models fibroblasts from darker skin express higher levels of neuregulin 1 and induce greater pigmentation than fibroblasts from lighter skin.⁶ ⁷ Supplementation of neuregulin 1 decreases L* values (makes the skin model appear darker on the color scale) by approximately one to three units in reconstructed epidermis, with the largest changes observed in dark skin models.⁶

Neuregulin 1 increases melanocyte size and dendricity and raises melanin content.⁶ ⁷ These effects demonstrate that baseline differences in fibroblast neuregulin 1 expression can account in part for interindividual and interethnic differences in constitutive pigmentation. The pathway seems to work in all phototypes. What changes is how strongly it is expressed.

​Fibroblasts also secrete stem cell factor, endothelin 1, hepatocyte growth factor and keratinocyte growth factor. These factors increase melanocyte proliferation, dendrite formation and melanogenesis in co culture and reconstructed skin models.⁵ ⁸ ¹² Conditioned media from fibroblasts taken from melasma or solar lentigo lesions raise tyrosinase activity and melanin content in melanocytes compared with media from nearby normal skin.⁵ ⁸ Together, these observations support a distinct lesional fibroblast (fibroblasts taken directly from the pigmented lesion) signature in acquired hyperpigmentation.

The emerging view is that a fibroblast melanogenic secretome, comprising neuregulin 1, stem cell factor, endothelin 1 and related cytokines, acts as a positive regulatory module. DKK1 and other Wnt antagonists act as negative regulators.⁴⁻⁸ ¹² Clinical pigmentation represents the net result of these opposing influences on a melanocyte network whose baseline activity is set by phototype.

SENESCENT MELANOCYTES AND GLYCOLIC REPROGRAMMING
Senescent melanocytes in photoexposed skin show durable cell cycle arrest and a senescence associated secretory phenotype.¹⁰ ¹¹ ¹⁴ A recent study developed a UV induced senescent melanocyte model. Transcriptomic and metabolic profiling revealed profound changes in energy metabolism.¹⁰ ¹¹

Senescent melanocytes consume approximately twice as much glucose as non senescent controls. They produce about three point three times more lactate.¹⁰ ¹¹ These shifts indicate strong glycolytic reprogramming. They resemble the Warburg effect described in other senescent and neoplastic cells.

Functional analysis showed that senescent melanocytes exhibit melanosome transport dysfunction. Pigment granules accumulate in perinuclear regions and fewer reach distal dendrites and the surrounding keratinocytes.¹⁰ ¹¹ ¹⁴ This defect aligns with clinical observations of mottled hyperpigmented and hypopigmented macules in photoaged skin and may also contribute to the small, sharply demarcated hypopigmented macules seen in idiopathic guttate hypomelanosis, as a working hypothesis. In this sense, clusters of senescent melanocytes and fibroblasts create a hostile microenvironment for normal pigment homeostasis.

​Pharmacologic inhibition of glycolysis in this model reduced p16 and p21 expression. It attenuated senescence associated secretory phenotype markers. It partially restored melanosome transport.¹⁰ ¹¹ These findings demonstrate that metabolic state is causally linked to pigmentary dysfunction in senescent melanocytes.

Melanocyte density and melanosome content increase from phototypes I and II to phototypes V and VI.¹³ In darker phototypes a given fraction of melanocytes entering senescence affects a larger absolute pigment load. This may help explain the heavy burden of focal dyschromia seen in phototypes V and VI despite relative preservation of dermal architecture.¹⁻³ ¹²

PHOTOAGED FIBROBLASTS AND PIGMENTARY FEEDBACK 
Fibroblasts from photoaged skin differ from those from young photo protected skin. They show:
▌ reduced collagen synthesis
▌ altered extracellular matrix remodelling 
▌ increased expression of inflammatory mediators¹⁶ 
▌ changes in pigment related signals

In reconstructed skin models fibroblasts from photoaged facial skin induce darker epidermis than fibroblasts from young skin. Epidermal L* values  are lower. Melanin content is higher. Expression of melanogenic genes is increased. These differences are statistically significant.⁵ ⁹ The findings indicate that age modified fibroblasts can drive and maintain hyperpigmentation.

Single cell RNA sequencing of human dermis has defined multiple fibroblast subpopulations: papillary fibroblasts, reticular fibroblasts, secretory fibroblasts, pro inflammatory fibroblasts. Aging shifts the population toward secretory and inflammatory phenotypes.¹⁶ This is associated with decreased collagen gene expression and altered paracrine (changed cell‑to‑cell signaling via secreted factors) output.

These changes are observed in skin from different ancestries. The qualitative direction appears conserved. The clinical manifestations vary with phototype. In phototypes I and II structural aging features, such as wrinkles and laxity, dominate. In phototypes V and VI pigmentary changes are more visually prominent relative to structural decline.¹⁻³ ⁸ ¹² This is consistent with shared molecular pathways acting within distinct baseline contexts.

PHOTOTYPE SUBGROUPS I II II IV V VI 

A functional grouping into three phototype clusters is useful. It reflects common mechanisms with different amplification.

Subgroup I and II includes very fair and fair skin. These types have low eumelanin content. They have fewer melanocytes. They have smaller and less dense melanosomes.¹³ They burn easily and wrinkle early. Aging is driven mainly by dermal matrix degradation and actinic damage. Pigmentary issues such as lentigines occur but are not usually the dominant aesthetic concern.¹ ³ ¹² ¹⁶

Subgroup III and IV includes intermediate skin tones. These types show both wrinkles and pigmentary issues. Melasma and solar lentigines are common.² ³ Fibroblast secretome changes contribute to these lesions. However the overall aging phenotype is mixed, with structural and pigmentary components of similar weight.² ⁸ ¹²

Subgroup V and VI includes dark brown and black skin. These types have high melanocyte activity. They have large and densely packed melanosomes. They exhibit strong natural photoprotection and delayed wrinkling.¹⁻³ ¹³ They also show high prevalence of solar lentigines, post inflammatory hyperpigmentation and mottled tone with age.¹⁻³ ⁸ ¹²
​
In this subgroup fibroblast secretome shifts and senescent melanocytes act upon a high capacity pigmentary system. Modest changes in DKK1, neuregulin 1, stem cell factor or endothelin 1 can produce clinically conspicuous tone alterations.⁴⁻⁸ ¹⁰ ¹¹ ¹⁴ Thus over time, these changes establish a hostile dermo‑epidermal environment for balanced pigmentation, favouring pigmentary aging over structural aging.

FROM BRIGHTENING TO DERMO EPIDERMAL ORCHESTRATION

Conventional “brightening” or “hyperpigmentation” strategies act mainly on melanocytes. They focus on inhibiting tyrosinase and downstream melanogenesis, while largely overlooking the roles of fibroblasts, cellular senescence and metabolism.

The crosstalk model suggests a broader approach built on three complementary levers.

First dermal secretome modulation. Peptides and botanical fractions can be selected or designed to influence fibroblast output. They may normalize neuregulin 1, stem cell factor and endothelin 1. They may tune Wnt related signalling and DKK1. The goal is restoration of balanced crosstalk rather than blunt suppression of pigmentation.⁵ ⁸ ¹²

Second melanocyte focused modulation. Tyrosinase inhibitors, PAR 2 modulators and antioxidants remain central. They should be optimized for barrier compatibility and irritation control. This is particularly important in phototypes V and VI where post inflammatory hyperpigmentation risk is high and baseline melanogenesis is strong.⁴ ¹² ¹⁴
​
Third senescence informed strategies. Actives with senomorphic potential may reduce the senescence associated secretory phenotype without inducing excessive cell death. Examples include certain flavonoids, resveratrol like molecules and carotenoids.¹⁰ ¹¹ ¹⁴ They can be combined with metabolic support and antioxidant systems. They may help shift melanocytes away from a glycolysis high senescent state.

​For darker phototypes an optimal regimen would integrate these three layers. It would:

▌support dermal matrix integrity
▌normalize fibroblast messaging
▌stabilize melanocyte metabolism 
▌reduce oxidative stress
▌modulate melanin synthesis and transfer in a controlled way
▌respect barrier integrity and minimize irritation

This perspective is unique because it reframes “brightening” as dermo epidermal tone orchestration, links pigmentary aging to fibroblast secretomes and senescent melanocyte metabolism, and translates these mechanisms into concrete, phototype inclusive intervention levers.

Take care!
​Anne-Marie

References

1. Yamaguchi Y Brenner M Hearing VJ. The role of melanin in skin of color. J Invest Dermatol. 2014 134 4 875 880.
2. Alexis AF et al. Ethnic considerations in aging skin. J Clin Aesthet Dermatol. 2012 5 4 25 37.
3. Taylor SC et al. Diverse presentations of aging in skin of color. J Am Acad Dermatol. 2009 60 5 S41 S50.
4. Yamaguchi Y et al. Regulation of skin pigmentation and thickness by Dickkopf 1. J Cell Biol. 2007 176 3 367 379.
5. Araki K et al. Photoaged fibroblasts promote epidermal pigmentation in reconstructed skin. J Dermatol Sci. 2010 59 1 21 29.
6. Tanimura S et al. Neuregulin 1 regulates constitutive color and melanocyte function. J Invest Dermatol. 2010 130 3 846 854.
7. Doi H et al. Fibroblast derived neuregulin 1 and skin pigmentation. Pigment Cell Melanoma Res. 2010 23 6 822 830.
8. Li S et al. Emerging roles of dermal fibroblasts in hyperpigmentation and hypopigmentation. J Cosmet Dermatol. 2025 24 1 e16790.
9. Precise role of dermal fibroblasts on melanocyte pigmentation. Greentech technical paper. 2017.
10. Wang X et al. Senescent melanocytes driven by glycolytic changes are characterized by melanosome transport dysfunction. Theranostics. 2023 13 12 3914 3933.
11. Wang X et al. Supplementary data to senescent melanocytes driven by glycolytic changes. Theranostics. 2023 13 12 e3914.
12. Alexis AF Sergay AB. Management of dyschromia in skin of color. Cutis. 2019 104 5 320 324.
13. Costin GE Hearing VJ. Human skin pigmentation. J Investig Dermatol Symp Proc. 2007 12 1 20 23.
14. Campisi J. Aging cellular senescence and cancer. Nat Rev Mol Cell Biol. 2013 14 4 257 263.
15. Kang HY et al. Dickkopf 1 in vitiligo skin. Br J Dermatol. 2010 163 2 287 294.
16. Sole Boldo L et al. Single cell transcriptomes reveal age related loss of fibroblast priming. Commun Biol. 2020 3 1 188.

 
This article is intended purely for education and reflection. It does not replace a consultation with your own dermatologist, physician or other qualified health professional, nor does it serve as diagnosis, treatment plan or product recommendation. Always discuss your individual skin concerns, conditions with a trusted medical expert who knows your history and can examine you in person.

In simple terms, milky toners are micro‑emulsified barrier and hydration vehicles presented in a texture that people actually want to use.

WHAT MAKES THE TONER “MILKY”?

Despite the diversity in branding, most milky toners are built on the same four pillars.

1. Humectant‑rich water phase
   Glycerin and hyaluronic acid are used again and again. Both increase stratum corneum hydration and reduce TEWL for up to 24 hours after a single application.⁶,⁷ Poly‑γ‑glutamic acid appears in some barrier‑centric milky toners. In keratinocyte and reconstructed skin models, it upregulates filaggrin and involucrin, boosts hyaluronic‑acid synthases and increases aquaporin‑3, pointing to barrier and hydration benefits beyond simple water binding.¹¹
2. Modest lipid phase for barrier support
   Light plant oils, esters, fatty alcohols and ceramides deliver emolliency without the heaviness of a cream. Ceramide‑containing lotions and physiologic lipid mixtures outperform non‑physiologic moisturizers on hydration and TEWL and restore barrier function in dry and eczematous skin.⁸,⁹ That same logic underpins cream‑in‑toner architectures and many ceramide‑rich milky toners.
3. Film‑forming polysaccharides
   β‑Glucan and fungal polysaccharides such as Tremella fuciformis (“snow mushroom”) add water‑binding, barrier‑supportive and anti‑inflammatory properties.¹⁰–¹² β‑Glucan‑containing creams have been shown to reduce symptoms and improve clinical scores in atopic dermatitis.¹⁰,¹²
4. Soothing and micro‑inflammation modulators
   Niacinamide, centella asiatica, panthenol and colloidal oatmeal are key recurring actors. Niacinamide increases ceramide synthesis, improves barrier function, reduces TEWL and improves signs such as fine lines and dyspigmentation.¹³,¹⁸ Centella asiatica improves elasticity and scar appearance and reduces inflammatory mediators.¹⁹ Panthenol accelerates barrier recovery in tape‑stripping models.¹⁴Colloidal oatmeal reduces itch, improves EASI/SCORAD and enhances quality of life in atopic dermatitis.¹⁶,¹⁷

​Optically, these micro‑emulsions scatter light and appear milky. Functionally, the interplay of humectants, lipids and polymers explains the immediate cushioning, “plumped” feel.⁵–⁹ For combination or oily‑dehydrated skin, this can make a well‑formulated milky toner a single, efficient post‑cleanser step.

WHAT MILKY TONERS DO FOR SKIN

Hydration
Humectant‑rich toners and light emulsions raise skin capacitance and hydration for at least 24 hours and continue to improve with regular use.⁶,⁷ In one open‑label trial, a hyaluronic‑acid cream improved hydration and lowered TEWL for a full day.⁶ Combining glycerin, hyaluronic acid and poly‑γ‑glutamic acid, as found in many modern milky formats, is therefore well supported by in vivo and ex vivo work.⁶,⁷,¹¹

Barrier repair
Ceramides and physiologic lipids are central to barrier‑focused milky toners. In adults with moderate eczema, a ceramide‑dominant cream and cleanser regimen significantly improved hydration and reduced TEWL vs placebo over 28 days.⁹ A separate trial with a ceramide lotion in dry skin showed similar improvements.⁸ Niacinamide (2–5%) upregulates sphingolipid synthesis, increases ceramide content and reduces TEWL in vivo.¹³,¹⁸ β‑Glucan and colloidal oatmeal add additional anti‑inflammatory and barrier‑supportive activity, especially relevant for atopic and dry skin.¹⁰,¹²,¹⁶,¹⁷

Soothing micro‑inflammation
Centella asiatica extracts improve elasticity and scar appearance and reduce inflammatory mediators, supporting their use as soothing, anti‑inflammatory cosmetic actives.¹⁹ Panthenol’s effect on barrier recovery explains its frequent use after procedures.¹⁴ Niacinamide combines barrier and anti‑inflammatory actions, resulting in less redness and better tolerance of active routines.¹³,¹⁸

​Penetration and “prep”
Hydrated stratum corneum is more permeable: corneocytes swell, and diffusional pathways change.⁶,²⁰While dedicated “toner as penetration enhancer” randomized trials are rare, in vitro and biophysical data support the idea that a hydrated, lipid‑replenished barrier allows more even and predictable penetration of subsequent actives than a dry, compromised one.²⁰
For routines that include retinoids, acids or procedures, a humectant‑ and lipid‑rich milky step straight after cleansing is therefore a rational, comfort‑enhancing choice, not just a cosmetic extra.

SOME MILKY AND NEAR‑MILKY FORMULAS 

​Rice‑ and oat‑based milky toners

Beauty of Joseon – Glow Replenishing Rice Milk Toner
This bi‑phase toner has a hydrating rice and amino‑acid phase plus a kaolin‑based powder phase that gently absorbs sebum.⁵⁶–⁶⁰ Rice extracts and amino acids provide antioxidants, vitamins and moisturising starches, while kaolin tempers shine without stripping.⁵⁶–⁶⁰ Centella asiatica, panthenol, sodium hyaluronate and ceramides match the evidence for centella, panthenol and ceramides in soothing and barrier repair.¹³,¹⁴,¹⁸,¹⁹ The result is a milky yet softly matte finish that works well for oily‑dehydrated skin.

Purito – Oat‑in Silky Toner
This formula is built around a high proportion of oat‑derived fractions (around 60–70%).²³ It uses colloidal oatmeal, oat kernel extract and β‑glucan as its backbone. Colloidal oatmeal and β‑glucan both have clinical evidence for reducing symptoms and improving barrier status in atopic dermatitis.¹⁰,¹²,¹⁶,¹⁷ Panthenol and niacinamide add further support for barrier repair and sensitivity reduction.¹³,¹⁴,¹⁸ In practice, it behaves as a calming milky toner for fragile or post‑stressed skin.

TIRTIR – Milk Skin Toner (The original)
TIRTIR’s rice toner combines rice bran extract, niacinamide, ceramides, panthenol, centella asiatica, two peptides (copper tripeptide‑1 (GHK‑Cu) and acetyl hexapeptide‑8) and one of my favourite ingredients of all time glycyrrhiza glabra (Licorice) root extract in a milky emulsion.²⁵ Rice bran offers antioxidants and moisturising lipids; ceramides and panthenol support barrier recovery; niacinamide benefits barrier, pigment and sebum balance; centella and licorice root extract provide anti‑inflammatory support.¹³,¹⁴,¹⁸,¹⁹ It is a strong example of a “one and done” milky toner that can carry much of the hydration, barrier and glow workload in a minimal routine. TIRTIR also offers a lighter, more sebum‑controlling version with 4% niacinamide, rice bran and ceramide, targeted more to oily/acne‑prone skin.

Ferment‑ and peptide‑driven milky toners

The Ordinary – Saccharomyces Ferment 30% Milky Toner
This product sits between milky toner and treatment essence. It contains 30% saccharomyces ferment with 3% fermented N‑acetylglucosamine (NAG) as a non‑acid exfoliant.²⁹ NAG loosens corneocyte cohesion and, in other contexts, supports brightening in combination with niacinamide.² The ferment fraction adds amino acids, peptides and osmolytes, which likely support hydration and barrier integrity, although specific clinical data on this exact ferment are limited.²⁹

Squalane is used as a lightweight emollient, and non‑ionic surfactants and emulsifiers build the milky, low‑viscosity texture.²⁹ In brand testing (38 subjects), a single use provided all‑day hydration and improved barrier strength, findings that fit independent data on humectant‑ and emollient‑rich emulsions.⁵–⁷ Clinically, it can be positioned as a non‑acid exfoliating milky toner for skins that struggle with traditional acids but still benefit from controlled desquamation.

Peptide‑forward milky toners

Peptide‑heavy milky toners (including copper‑peptide formats like GHK‑Cu) use the milky vehicle as a comfortable platform for signal peptides. Preclinical and early clinical work suggests GHK‑Cu can stimulate collagen synthesis, support wound healing and facilitate tissue remodelling.²² These formulas sit at the treatment‑heavy end of the milky spectrum and can be thought of as light peptide serums wrapped in a reassuring milky base. Examples include TIRTIR Milk Skin Toner, which adds copper tripeptide‑1 and acetyl hexapeptide‑8 to a rice‑ and ceramide‑based milky chassis,²⁵ and numbuzin No. 9 NAD⁺ PDRN Glow Boosting Toner, which pushes the concept further with NAD⁺, PDRN and a blend of around 50 peptides in an essence‑rich, near‑milky texture.¹,²²

Watery hydrating toners as contrast

Haruharu Wonder – Black Rice Hyaluronic Toner
This is a clear, essence‑like toner combining fermented black rice, betaine and hyaluronic acid.²⁶ Brand data report more than 40% improvement in moisture and texture after 14 days, in line with independent work on humectant‑rich toners and TEWL reduction.⁶,⁷ It is an excellent hydrating solution, but it remains strictly watery rather than milky.

Anua – Heartleaf 77% Soothing Toner
A very lightweight toner with 77% heartleaf (Houttuynia cordata) extract plus humectants, marketed for soothing and oil balance.²⁷ Internal testing shows strong subjective calming and measurable changes in hydration and sebum over two weeks, consistent with a humectant‑rich, anti‑inflammatory solution.⁶,⁷,²⁷

SKIN1004 – Madagascar Centella Probio‑Cica Essence Toner
This essence‑toner combines multiple hyaluronic‑acid fractions, ceramide NP, betaine and a refined centella complex.²⁸ Mechanistically, it mirrors the evidence for centella, HA and ceramides in anti‑inflammatory, hydrating and barrier‑repair effects.⁶–⁹,¹⁴,¹⁹ The major difference is galenics: it remains a clear, watery vehicle, essentially the watery cousin of barrier‑centric milky toners.
Products such as Acwell licorice toner, Biodance Sea Kelp pads or Eqqualberry “Swimming Pool” toner follow similar hydrating and soothing concepts in watery formats and illustrate how adding an emulsion phase changes both function and sensorial payoff.

DR BOUHON “GLASS SKIN SERUM”: GLASS‑SKIN LOGIC, MILKY‑TONER PHILOSOPHY

Dr Bouhon’s The Glass Skin Serum shows how the glass‑skin, barrier‑support story has moved into a German pharmacy‑adjacent brand and format. It is not milky in texture, but its design and role in the routine are very close to a modern milky toner step.³⁰

The formula combines 5% niacinamide, centella asiatica extract, panthenol, glycerin, sodium hyaluronate, glycyrrhiza glabra (licorice) root extract, yeast extract, inulin (as a prebiotic sugar), postbiotics from porcelain flower (Hoya lacunosa) and allantoin in an ultra-light, non‑occlusive base.³⁰ Inulin and postbiotic ferments help support a balanced skin microbiome; allantoin contributes additional soothing and skin‑conditioning effects on top of the barrier‑ and calming benefits from niacinamide, centella and panthenol.¹³,¹⁴,¹⁸,¹⁹

Glycyrrhiza glabra (licorice) root extract is as mentioned before, one of my favourite multitasking actives with soothing and very strong antioxidant properties: it can help calm visible redness and inflammation, support a more even tone and, and is evidence based among the more potent botanical antioxidants to counter free radical activity in general, lipid peroxidation and uniquely, also that induced by blue light, which we know can cause DNA-damage, pigmentation (especially in darker phototypes) and thus negatively affect both skin quality and long‑term skin health.

Clinical data report up to 34% reduction in visible pores, 20% improvement in evenness, and 100% of subjects perceiving healthier‑looking skin and wrinkle reduction after 28 days; 95% reported smoother skin.³⁰ These endpoints (pore visibility, evenness, glow) are exactly what many consumers describe as “glass skin.” They are achieved using the same families of barrier‑, microbiome‑ and tone‑modulating actives that sit at the heart of modern milky toners,³⁰ delivered in a very pleasant ultra-lightweight serum‑like texture¹³,¹⁴,¹⁸,¹⁹ that pairs especially well with Dr Bouhon’s The Centella Barrier Cream containing zinc PCA, making this duo genuinely beneficial for a wide range of skin types: from dry to even more oily skin types. The serum comes in a luxe black glass dropper bottle, the cream in a beautiful high quality glass pump; both are fragrance free and odourless, and make a truly elegant pairing. Both my 21‑year‑old daughter and I are genuinely obsessed.
​
TEXTURE AS A DRIVER OF COMPLIANCE

Texture is not a detail; it is a compliance tool. Large consumer datasets show that sensoriality and texture are among the main reasons people repurchase skincare and haircare.¹–³
EEG‑based work now confirms this at brain level. Moist, smooth, easy‑to‑spread emulsions trigger more favourable neural responses in sensorimotor regions linked to touch and emotional regulation than draggy or sticky vehicles, and those patterns line up with stated preference.²¹
If a vehicle is unpleasant, even the best evidence‑based active will not be used consistently, especially relevant in daily‑use categories such as sunscreens, retinoids and barrier care. Milky toners deliberately sit at the point where sound mechanism and pleasant texture meet: hydration, barrier repair, soothing and sometimes controlled exfoliation or peptide signalling, all in a format the skin and brain “like.”

The current wave of milky toners, Dr Bouhon’s The Glass Skin Serum and The Centella Barrier Cream is not just a passing social‑media craze. It reflects a deeper shift towards barrier‑first formulation, ferment‑driven hydration and a growing recognition that texture itself is an active part of effective skincare design.

 
Take care!
Anne-Marie

REFERENCES 

1. Cosmetics Business. Milky toners: why skin care shoppers are lapping them up. 2025.
2. Accio. Trend of toner in 2025: hydrating & milky formulas rise. 2025.
3. Accio. 2025 milky essence trends: skincare & food market insights. 2025.
4. Cleveland Clinic. Do you need a face toner? Cleveland Clinic Health Essentials. 2025.
5. Hachicha S. Trend of the week: milky toners. 2025.
6. Milani M, Sparavigna A. 24‑hour hydration and barrier effects of a hyaluronic acid cream. J Clin Aesthet Dermatol. 2017;10(5):18‑23.
7. Yuanxi Z, Wei L. Comparison of skin hydration in combination and single use of common moisturizers (cream, toner, and spray water). J Cosmet Sci. 2016;67(3):175‑183.
8. Aich P, Kumbhar S, Koppikar S, et al. Clinical evaluation of a topical ceramide lotion on skin hydration and skin barrier in healthy volunteers with dry skin. Cosmoderma. 2024;4(1):148.cosmoderma+1
9. Eichenfield LF, Tom WL, Zang J, et al. Efficacy and safety of a ceramide‑dominant cream and cleanser in moderate eczema. Dermatol Ther (Heidelb). 2020;10(4):e14970.
10. Jesenak M, Majtan J, Rennerova Z, et al. β‑Glucan cream in atopic dermatitis. Clin Cosmet Investig Dermatol. 2016;9:371‑379.
11. Kim JH, Lee J, Park H, et al. Poly‑γ‑glutamic acid from a novel Bacillus subtilis strain and its effects on skin barrier‑related gene expression. Int J Biol Macromol. 2025;xx:xx‑xx (epub ahead of print).pmc.ncbi.nlm.nih+1
12. Wang Y, Li X, Zhang Y, et al. β‑Glucan in cosmetics: applications in skin care and dermatology. Int J Cosmet Sci. 2025;47(2):145‑159.
13. Metware Bio. Ceramides vs niacinamide in barrier strengthening: comparative efficacy insights. 2025.
14. Proksch E, de Bony R, Trévisan J, et al. Topical panthenol in skin disorders. J Dermatolog Treat. 2017;28(8):728‑733.
15. Draelos ZD. Cleansing and the skin barrier. J Cosmet Dermatol. 2018;17(6):1030‑1038.
16. Fowler JF. Colloidal oatmeal in atopic dermatitis: a clinical overview. Dermatol Ther. 2017;30(3):e12576.
17. HMP Global. Clinical benefits of colloidal oatmeal in atopic dermatitis. 2016.
18. Bissett DL, Miyamoto K, Sun P, et al. Topical niacinamide: effects on sebum, pigmentation and fine lines. Dermatol Surg. 2005;31(7 Pt 2):860‑865.
19. Topical Centella asiatica and scar appearance (NCT02601105). ClinicalTrials.gov. 2015.
20. Lodén M. Emollients and barrier disorders. Am J Clin Dermatol. 2003;4(11):771‑788.
21. Kim H, Park S, Lee S, et al. EEG indicators of texture preference in cosmetic formulations. J Cosmet Sci. 2025;76(5):321‑334.
22. Pickart L, Margolina A. GHK and tissue remodelling. J Biomater Sci Polym Ed. 2015;26(1):1‑18.
23. Purito Oat‑in Silky Toner: INCI analyses, 2022–2025 (e.g. Incidecoder and brand technical sheets).
24. Beauty of Joseon Glow Replenishing Rice Milk Toner: INCI analyses, 2022–2025 (e.g. Incidecoder and retailer ingredient listings).
25. TIRTIR Milk Skin Rice Toner: INCI summaries, 2022–2025 (brand and retailer ingredient listings).
26. Haruharu Wonder Black Rice Hyaluronic Toner: ingredient and clinical claim summaries, 2024–2025.
27. ANUA Heartleaf 77% Soothing Toner: product testing summary, 2024–2025.
28. SKIN1004 Madagascar Centella Probio‑Cica Essence Toner: INCI summary, 2024.
29. The Ordinary Saccharomyces Ferment 30% Milky Toner: product information and INCI, 2025.
30. Dr Bouhon. The Glass Skin Serum: INCI and clinical results, 2024–2026. Available at: https://drbouhon.com/THE-GLASS-SKIN-SERUM/SW10187.

This article is intended for educational and informational purposes only and is not meant to diagnose, treat, cure or prevent any disease. It does not replace a consultation with a qualified healthcare professional or dermatologist, and it should not be used to make individual treatment decisions. All opinions are my own, and this article does not contain affiliate links or sponsored content.

In a 2022 cosmetic science paper, purified freshwater sponge spicules loaded with a model flavonoid showed very high dermal absorption in ex vivo porcine (pig) skin of 73.4% of the dose in the dermis, while systemic/transdermal passage remained low, indicating that they can act as an effective local dermal delivery system, similar in concept to very superficial microneedling. However, the solid human clinical data are limited to small studies, mostly formula‑specific or manufacturer‑linked. 

One small Korean trial reportedly found better wrinkle/dermal density outcomes when growth factors were combined with spicules versus growth factors alone, but methodology and controls are not robust enough to be definitive. 

The “gimmick” part of spicules comes from mainly from marketing claims which come on top; of dramatic collagen induction, scar removal, or facelift‑like tightening, which are not backed by large, independent, long‑term human trials. Available data suggest modest improvements in texture and radiance at best, mainly by boosting penetration of real actives or mechnical exfoliation by the spicules themselves. When the formula itself is weak (without robust actives) spicules will not compensate. They should be seen as a delivery aid rather than a miracle ingredient.
​
Spicules are cosmetic-grade in EU/Korea (INCI: "Spongilla lacustris Spicule") but lack FDA monograph approval as drugs, limiting claims.​

USER EXPERIENCE

Spicule‑based peels and serums have been used in aesthetic practice for at least one to two decades, with traditional sponge‑powder applications going back much further, and modern K‑beauty “bio‑microneedling” formats expanding rapidly over the past 10–15 years to an estimated nine‑figure USD market, suggesting many millions of units sold worldwide.

Most reported reactions are transient stinging, erythema, tightness, and short‑lived dryness, however the intensity of discomfort depends strongly on spicule length and density: longer and more densely packed spicules create more microchannels and a sharper, more aggressive feel, whereas shorter or lower‑density systems are better tolerated. Subjectively, many users describe the sensation as similar to handling fiberglass or prickly pear spines; sharp, prickly, and aggravating rather than a mild “tingle” with this perception increasing as spicule size and concentration rise. Patting rather than rubbing tends to reduce discomfort while still providing a penetration benefit, so application technique is important for tolerability. Given the current lack of robust long‑term human safety data, spicule products are generally not ideal for very sensitive, rosacea‑prone, or barrier‑impaired skin, and high‑frequency use in these groups should be approached with caution.

SPICULE LENGHT
Most commonly spicules measure 100–300 μm in length, determining their skin penetration depth:

▌~100 μm: Superficial penetration, targeting the stratum corneum for very gentle exfoliation and enhanced absorption, suitable for regular at-home use
▌~300 μm: Deeper but still epidermal penetration, however still less deep compared to microneedling

Therefore, when you see 100 or 300 related to spicules, it’s a reference to their physical size and penetration depth, which determines their strength and function in skincare routines. This shallow range (100–300 μm) creates microchannels to enhance active absorption without reaching the dermis or causing significant trauma/downtime. Some brands like Mediheal and ClearDea use a very short spicules, which are more gentle, however also less effective as active penetration enhancers.

Classic microneedling needles penetrate from about 0.25 mm (250 μm) to 2.5 mm (2500 μm), much deeper than spicules. 

TYPES OF MICRONEEDLE TECHNOLOGIES – COMPARISON FROM MANUFACTURER

SPICULE CONCENTRATION CONFUSION

VT Reedle Shot, comes in various spicule concentrations (e.g., 50, 100, 300, 700), where higher numbers mean stronger micro-needling/exfoliation effects due to higher spicule density, not necessarily larger spicule size. Users report that higher concentrations like 300 or 700 have stronger exfoliating and penetrating sensations, while lower concentrations like 50 or 100 are milder. These concentration differences affect the intensity of the delivery effect and potential skin irritation. Higher concentrations create more microchannels but may increase tingling or prickling sensations and require less frequent use. Lower concentrations are gentler and can be used more regularly and are more suitable for sensitive or irritable skin.

VT describes its Cica Reedle™ spicules as “around fourteen times thinner than pores” and “smaller than pores,” without disclosing an exact micrometer size; typical facial pores are on the order of 200–300 µm in diameter, so this implies a very fine needle‑like structure. For Reedle Shot 300, VT and retailers report approximately 237,500 Cica Reedles per application, which, together with Cica Reedle’s small diameter, helps explain the pronounced “liquid microneedling” sensation and improved absorption, texture, pore visibility, and acne‑related roughness noted in marketing and user feedback. Classic Reedle Shot formulas pair Cica Reedle™ with Centella asiatica, multi‑weight hyaluronic acid, niacinamide, adenosine, propolis, and amino acids (CICA‑HYALON™ complex) for soothing, barrier support, and slow‑aging benefits. The Reti‑A Reedle Shot variants add a vitamin A complex (retinol and retinoid ester) plus bakuchiol on top of the Cica Reedle™ system, using the spicules to enhance retinoid delivery while the CICA‑HYALON™ base supports tolerability.

SPICULES + EXOSOMES
​
Medicube 1-Day Exosome Shot which is marketed as “microneedling in a bottle,” is available in 7,500 and 2,000 “microneedle” versions. 
▌7,500 spicules = Total hydrolysed sponge spicules delivered in one full application of the 7,500 version (typically 30ml bottle or single-use ampoule equivalent).
▌2,000 spicules = Total in the milder 2,000 version per application.
These are density/concentration markers for marketing and product differentiation. Key difference between both brands mentioned is that VT uses relative concentration (spicules/ml), while Medicube uses absolute count per treatment. Both scale intensity with higher numbers, but Medicube's 7,500 delivers far more spicules total despite similar density effects.

PAINLESS SPICULES
ClearDea is a brand that uses Collanetinal™ spicules of approximately 0.01 mm (11 μm) in length, i.e., very short. Because spicule length largely determines penetration depth, these collagen‑ and retinol‑coated spicules are expected to act predominantly in the very superficial layer(s) of the skin and to be gentler than longer, more prickling spicules. They are likely to be less efficient as active delivery enhancers. ​

SPICULES + CAPSULSES
​
In the SUNGBOON EDITOR gel‑cream, (tiny whitish) spicules are combined with separate capsules containing very low molecular weight (200 Da) collagen‑related ingredients, retinol, niacinamide, hyaluronic acid and panthenol in a gel-base. Spicules are designed to boost the bioavailability of the encapsulated actives by nudging them closer to the viable epidermis and superficial dermis, which may enhance visible results compared with a conventional cream of similar composition. The magnitude of this benefit, however, is tightly linked to spicule size (not disclosed for this product) and density. The formula contains 300.000 shots, which is a marketing way of saying that one jar contains approximately 300,000 individual spicules. The prickly, tingling feel from the spicules is frequently mentioned in reviews; some users enjoy it as a sign that the product is “doing something,” while others find it uncomfortable or briefly stinging. SUNGBOON recommends specifically for dry skin 2 part capsuls and 1 part gel, for oily skin 2 parts gel and 1 part capsule and for combination skin 1 part capsule and 1 part gel ratio.

​The concentration of active ingredients:
▌200 Da collagen: 1,100,000 ppb, which literally means 1,100,000 parts of a substance in 1,000,000,000 parts of the total mixture. In percentage terms, that is 0.11%. 
▌Niacinamide: 20,000,000 ÷ 1,000,000,000 = 0.02, which corresponds to 2%.
▌Retinol: 3000 ppb is 0.0003%. 
Retinol at just 0.0003% (3 ppm) barely penetrates skin: less than 1% gets through without help. Spicules' microchannels boost this 10x or more, making tiny doses far more effective. 

If SUNGBOON´S before‑and‑after photos truly reflect typical results, this product would be worth serious consideration. However, when used consistently and with appropriate skin tolerance, SUNGBOON EDITOR Deep Collagen Retinol can realistically be expected to modestly improve skin smoothness, hydration and fine lines rather than produce dramatic “filler‑like” changes. Some users experience more bouncy or firmer skin and even skin tone.

Similar, however not the same is the VT Reedle Shot 2‑step masks, which are bio‑microneedling sheet masks that combine a spicule “essence” with an occlusive mask to intensify penetration and skin benefits. In step 1, a concentrated ampoule containing natural micro‑spicules (Cica Reedle™ based on silica and Centella) is massaged onto cleansed skin, creating temporary microchannels and a characteristic tingling or prickling sensation while priming the surface.

Step 2 is a serum‑soaked sheet mask placed over this prepped skin for 15–30 minutes; it is typically loaded with humectants and barrier‑supporting actives such as hyaluronic acid, hydrolyzed collagen, peptides, niacinamide, centella, propolis, and amino acids, aiming to hydrate, improve elasticity, refine texture, and calm irritation.  Different versions (e.g., Mild 50, 100, 300) reflect increasing spicule density and intensity: lower numbers are gentler and better suited to sensitive or first‑time users, while higher numbers are positioned for concerns like rough texture, post‑acne marks, dullness, and fine lines, used no more than 1–2 times per week.

​Glutathione Vita Glow Spicule Shot
▌Focuses on radiance and tone uniformity, pairing 2,000 ppm glutathione with vitamin C derivatives in a spicule delivery base.
▌The spicule system provides a “microneedling effect” with tingling/micro‑stimulation while driving antioxidants deeper to enhance glow and transparency.
▌Clinical testing is claimed for improvements in brightness and overall skin tone.

Across these products, Genabelle positions spicules as an at‑home, low‑downtime alternative to procedural microneedling, designed mainly to boost delivery of brightening/antioxidant complexes while also addressing texture and early signs of aging, with suitability claims extending even to drier or more sensitive skin types but still with expected tingling on use.

SPICULES + PEPTIDES
Several brands deliberately pair peptides-molecules that typically show poor passive skin penetration with spicule‑based ‘bio‑microneedling’ systems, leveraging the micro‑channels created by spicules to substantially enhance peptide delivery into deeper epidermal and dermal layers, as proven by spicule‑based peptide delivery studies.

In a 2021 study, sponge spicules from Haliclona sp. (SHS) were incorporated into topical formulations containing insulin (hydrophilic peptide) and cyclosporine A (hydrophobic cyclic peptide). SHS increased insulin transdermal flux from 5.0 ± 2.2 ng/cm²/h (passive) to 457.0 ± 32.3 ng/cm²/h (about 90‑fold) and raised its deposition in deeper skin layers from 0.6% to roughly 55%. This enhancement was both spicule‑dose‑dependent and peptide‑dose‑dependent, supporting a true mechanistic effect of the spicules on peptide penetration.

DR.PEPTI Peptide Spicule Pore Solution Serum contains Hydrolyzed Sponge (3,000 ppm) as the spicule source plus an extensive peptide complex: acetyl hexapeptide‑8, acetyl octapeptide‑3, multiple tetra‑, tri‑, and dipeptides, copper tripeptide‑1, palmitoyl peptides, etc., alongside retinol, exosomes, bakuchiol, glutathione, tranexamic acid and sodium DNA. It is positioned for pore care, elasticity and anti‑aging, using spicules to drive the peptide blend deeper.

TONYMOLY Peptide Spicule Firming Ampoule  is described as an elasticity ampoule with peptide + bakuchiol + collagen‑coated spicules for firming sagging skin and fine lines. Here the spicules are directly linked to both collagen and peptide‑driven firming.

ALTUM™ PEPTIDE / PEPTAXEL™ programs (Skinzzo LAB) is a professional bio‑microneedling system where Raphitox™ spicules are bound to tripeptides, then released in the epidermis via glutathione; positioned as “5th‑generation spicules” specifically designed to deliver peptides for collagen stimulation. Altum™ Peptide (Raphitox‑bound tripeptides) compared a peptide‑only cream vs. spicules + peptides vs. Altum’s peptide‑spicule complex; the “spicules + peptides” combo outperforms peptides alone in improving skin density and wrinkles, supporting the delivery advantage.
​
Spicule Serum concept formulas (CTK): OEM “Spicule Serum” bases combine spicules + a 10‑peptide complex + collagen complex + panthenol, marketed for elasticity, lifting and hydration.

SOME NOTEWORTHY LESSER KNOWN BRANDS WHICH INCORPORATED SPICULE DELIVERY SYSTEMS:

▌Pepticule pairs spicules with acetyl hexapeptide-8 for “botulinumtoxin-like”anti-wrinkle effects via deep delivery. 
▌Pestlo Spicule Reborn Peeling Mask combines spicules with green tea and mugwort for brightening and even tone.
▌9wishes Pine Perfect Ampule Serum uses spicules alongside pine, licorice, and green tea extracts to target acne and renewal.
▌Isomers Diamond Peptide Spicule Body Cream blends spicules, diamond powder, alp rose stem cells, caffeine, and peptides to address body stretch marks, sagging, and texture.

REPRESENTATIVE SPICULE SKINCARE PRODUCTS OVERVIEW

VERDICT

“Do spicules work?”: yes, as a micro‑delivery technology, there is evidence that spicules enhance dermal delivery and can improve clinical skin parameters when paired with effective actives and when spicule length and density are sufficient. They likely also provide to some degree of mechanical exfoliation on application. Studies indicate that spicules can also help larger molecules, such as peptides and other macromolecules that usually penetrate the skin poorly in standard skincare, reach deeper skin layers more effectively when they are formulated together. 

“Are spicules a miracle?”: no; current scientific evidence is sparse, short‑term, and often industry‑linked, so they should be viewed as an adjunct delivery tool with potential, not a stand‑alone, clinically proven game‑changer. 

Worth a try”?: Alternative, more controlled options exist (e.g., microneedling, microstamping) that can provide similar or superior penetration or textural benefits without persistent mineral needles in the skin. Products containing “longer” spicules are potentially worth trying only for people with very resilient skin who are highly motivated and comfortable with discomfort and some uncertainty. For sensitive skin or risk-averse users, maybe the very short coated spicules are an option.

​Personally, I would recommend spicule‑based products only with caution at this stage, and limit use to a single product at a time whose active ingredients clearly match your main skin need r concern. The technology is exciting and promising, however more robust human safety data are needed before fully endorsing it, even though there is roughly 10–15 years of user experience without serious adverse effects reported. Daily use is not advisable. Spicules persist in the skin up to 72 hours, with no data on long-term accumulation, which could theoretically trigger granuloma formation from silica persistence as biogenic spicules may trigger foreign body reactions in long-term use, cause subclinical inflammation, or barrier impairment, changes that ultimately accelerate skin ageing.

Take care!
Anne-Marie

REFERENCES

▌Kim TG, Lee Y, Kim MS, Lim J. A novel dermal delivery system using natural spicules for cosmetics and therapeutics. J Cosmet Dermatol. 2022 Oct;21(10):4754-4764. doi: 10.1111/jocd.14771. Epub 2022 Feb 1. PMID: 35034416. 
▌Ha JM, Lim CA, Han K, Ha JC, Lee HE, Lee Y, Seo YJ, Kim CD, Lee JH, Im M. The Effect of Micro-Spicule Containing Epidermal Growth Factor on Periocular Wrinkles. Ann Dermatol. 2017 Apr;29(2):187-193. doi: 10.5021/ad.2017.29.2.187. Epub 2017 Mar 24. Erratum in: Ann Dermatol. 2017 Dec;29(6):828. PMID: 28392646; PMCID: PMC5383744.
▌Kim, H., Lee, H. J., Lee, H., Kim, S. N., & Park, E. S. (2021). Enhanced skin delivery of therapeutic peptides using sponge spicules in combination with flexible liposomes. Biomolecules & Therapeutics, 29(6), 707–716. https://doi.org/10.4062/biomolther.2021.166
▌Lee, N.E.; Kim, J.E.; Bang, C.Y.; Bang, O.Y. Nano-Encapsulated Spicule System Enhances Delivery of Wharton’s Jelly MSC Secretome and Promotes Skin Rejuvenation: Preclinical and Clinical Evaluation. Int. J. Mol. Sci. 2025, 26, 10024. https://doi.org/10.3390/ijms262010024
▌Udompataikul, M., Wongniraspai, M., Showpittapornchai, U., & Jariyapongsakul, A. (Year). The study on effects and safety of Spongilla lacustris in 3% hydrogen peroxide solution on rat skin. Journal Name, Volume(Issue), pages.
▌The Ultimate Guide To Spicules SkinCare: A Revolutionary Approach To Skincare https://spongespicule.com/the-ultimate-guide-to-spicule-skincare/

This post is based on my own, independently purchased products and personal research. It is intended for educational and informational purposes only, does not replace individual medical advice, and is not intended to diagnose, treat, cure, or prevent any disease. All opinions are my own; this content is not sponsored, and no affiliate links are used.

Next‑generation photo‑protection, which I prefer to call “DNA-care”, begins where classic UV-filers stop: at the level of DNA repair, antioxidant defence, and selective interaction with the full light spectrum. Instead of simply blocking radiation, advanced strategies aim to pair DNA repair technologies with powerful antioxidants to neutralise reactive oxygen species from both UV and visible light, while still allowing beneficial wavelengths such as infrared and near‑infrared to support the skin’s intrinsic vitality. Within this context, the concept of the skin interactome offers a powerful framework, revealing how genome, microbiome, and exposome dynamically interact to shape not only current skin health, but also the trajectory of skin ageing over time.

​The skin interactome is an integrative framework that captures the complex and dynamic interactions between the genome, microbiome, and exposome to provide a comprehensive understanding of skin biology and health. Unlike traditional approaches focusing on single factors, the interactome highlights how genetic predispositions, resident microbial communities, and environmental and lifestyle exposures collectively influence skin function, health, and needs. This holistic concept provides an excellent framework for skin research as it guides the development of personalised, next-generation sunscreens (or DNA-care) and skincare products that do so much more for skin health than hydrate or block UV rays as they optimise the skin’s protective, reparative, and homeostatic functions. 

GENOME, EPIGENOME, MICROBIOME, PROTEOME, INFLAMMASOME, AND EXPOSOME INTERPLAY

The genome includes the individual's genetic makeup like skin type, skin tone and the regulatory pathways that dictate responses to UV radiation, DNA repair mechanisms, pigmentation synthesis, and inflammation. Gene activity is dynamically regulated by epigenetic mechanisms such as DNA methylation and histone modifications which are reversible and sensitive to environmental (exposome) and microbial (microbiome) stimuli. Epigenetic modifications mediate how external factors like UV exposure, pollution, and lifestyle and skincare routines influence gene expression without altering the DNA sequence itself. 

The skin microbiome is made up of many different bacteria, fungi, and viruses living on our skin. It plays an important role in regulating immune responses, protecting the skin barrier, and managing oxidative stress. The makeup of these microorganisms varies depending on skin type, like oily or dry skin, and this balance influences overall skin health.
The microbiome interacts closely with the skin’s epigenetic system or epigenome. Microbes produce metabolites and signals that can change epigenetic markers; chemical tags on DNA or proteins that control how genes are switched on or off. At the same time, changes in the skin’s epigenetic landscape shape the environment where microbes live, affecting which microorganisms thrive. This two-way interaction is essential for maintaining healthy skin and affects the likelihood of developing skin diseases.

Inflammasomes are multi-protein immune complexes within keratinocytes and immune cells, act as sensors for endogenous and exogenous danger signals including microbial components and environmental insults such as UV-induced oxidative stress. Activation of inflammasomes like NLRP3 triggers the release of pro-inflammatory cytokines (e.g., IL-1β), orchestrating innate immune responses. Dysregulated inflammasome activity driven by microbial imbalance or exposomic factors can lead to chronic inflammatory skin conditions, accelerates photoaging and skin cancer development.
​
The proteome is the full set of proteins expressed by the genome at a given time, executing critical skin functions, including barrier formation, antioxidative defense, DNA repair, and signaling. Proteome composition and activity are tightly controlled by epigenetic regulation and can be modulated by inflammasome-induced inflammatory pathways. Consequently, the exposome’s influence permeates through genome, epigenome, microbiome, inflammasome activation, and proteome dynamics to collectively shape skin phenotype and responses.

SKIN INTERACTOME COMPONENTS AND INTERACTIONS 

​Next-generation photo-protection should consider the broader impact of the skin interactome including genome, microbiome, inflammasome, proteome, and exposome factors.
​
​COLLAGEN EXAMPLE

KEY EXAMPLES
​
▌Visible light protection: Visible light (VL), particularly blue light, penetrates deeper into the skin and can induce pigmentation changes (especially in darker phototypes), oxidative stress, and inflammation. Standard sunscreens often lack effective VL protection. Innovations such as tinted sunscreens containing iron oxides and pigmentary titanium dioxide are being developed to protect the skin from visible light-induced damage and pigmentation. VL defense can be offered by a specific anti-oxidant (licorich root extra) which has proven to effectively reduce ROS from VL, thus reducing the damage.

▌Genetic and molecular photoprotection: Genetic variants, such as those affecting melanocortin 1 receptor (MC1R) signaling, which not only determine pigmentation but also regulate antioxidant defences and DNA repair in melanocytes, critical for photoprotection. Understanding these genomic determinants enables personalised formulation development to enhance antioxidant defences and DNA repair mechanisms crucial for healthy skin.

▌Microbiome-targeted sunscreens: The skin microbiome contributes to skin homeostasis and immune regulation, modulating inflammation and barrier function. Next-generation sunscreens or DNA-care should aim to protect or even positively modulate the microbiota, reducing microbial imbalance (dysbiosis) and associated inflammation. 
In oily skin, increased sebum production creates an environment favorable to Cutibacterium acnes strains that produce elevated levels of porphyrins, bacterial metabolites linked to skin inflammation. Specific acne-associated strains, such as IA-2, IB-1, and IC, enhance porphyrin production, which promotes inflammatory responses. UV-B radiation suppresses porphyrin synthesis, contributing to antibacterial effects, while violet-blue light excites porphyrins to generate reactive oxygen species, useful for photodynamic therapy but potentially causing skin damage and hyperpigmentation, especially in darker phototypes. This example illustrates how exposome factors (light exposure) interact with the microbiome and genome-driven sebum secretion to influence skin inflammation and photoprotection needs in oily skin.

▌Inflammasome modulation: Environmental triggers and microbial dysbiosis can activate inflammasomes, promoting chronic inflammation and accelerating photoaging and carcinogenesis. Photoprotection is evolving to include ingredients that reduce inflammasome activation, thus addressing immune-mediated skin damage.

▌The exposome induces activation of the proteome components matrix metalloproteinases (MMPs), including collagenase, hyaluronidase, and elastase, which collectively degrade key extracellular matrix (ECM) proteins such as collagen, elastin, and hyaluronic acid, leading to disruption of ECM integrity and impaired skin structural homeostasis and cause premature skin aging.​

▌Lifestyle and environmental interventions: Factors like diet, sleep quality, and pollution exposure also influence skin inflammation, oxidative status and cause microbial shifts. Integrated skincare strategies supporting antioxidant capacity complement physical photoprotection.
​
▌In oily skin (genome), increased sebum production leads to elevated levels of lipids susceptible to oxidative damage. Exposure to UV and visible light (exposome) promotes reactive oxygen species (ROS) formation, which initiates lipid peroxidation predominantly targeting sebum components like squalene. This lipid peroxidation disrupts the integrity of skin cell membranes (proteome effect), increases inflammation, and contributes to accelerated skin aging. The resulting oxidative stress can overwhelm antioxidant defenses (epigenetics), creating a vicious cycle that further impairs skin health.

These examples illustrate the complexity of the skin interactome and the necessity of multifunctional, personalized photoprotection products that go beyond UV blocking to comprehensively preserve and restore skin health.

Next-generation sunscreens or DNA-care should offer a comprehensive and personalised approach that integrates the complexity of the skin interactome and real-world lifestyle factors:

15 PILLARS OF ADVANCED SUNSCREEN DNA-CARE TECHNOLOGY

▌Tailored formulations: Customize based on genome and phototype to optimize DNA repair, pigmentation, and barrier function, addressing genetic variations like MC1R and sebum levels linked to skin type.
▌Broad-spectrum environmental defense: Protect against damaging UV, visible light (notably blue light), and pollution using broad-spectrum filters combined with powerful antioxidants that neutralize reactive oxygen species generated by these exposomic factors. However, it should leverage the benefits sun has to offer like infrared and near infrared.
▌Microbiome support: Include prebiotics, postbiotics, and microbiome friendly formulations to maintain a balanced skin microbiota, reduce inflammation, and enhance skin barrier resilience.
▌Inflammasome modulation: Incorporate actives that prevent or reduce inflammasome activation to minimize chronic inflammation, photoaging, and skin carcinogenesis.
▌Proteome protection: Inhibit proteolytic enzymes such as matrix metalloproteinases (MMPs), collagenase, elastase, and hyaluronidase to preserve extracellular matrix proteins (collagen, elastin, hyaluronic acid), maintaining skin structure and preventing premature aging.
▌DNA repair enhancement: Support natural DNA repair pathways with enzymes or boosting actives to repair UV-induced genetic damage.
▌Oxidative stress reduction: Provide an antioxidant-rich composition that targets pollution-induced oxidative damage, supporting skin exposed to urban or high-pollution environments.
▌Nutrient delivery synergy: Combine topical antioxidants with ingredients that complement dietary antioxidants (vitamins C, E, polyphenols), enhancing systemic and topical skin repair.
▌Adaptive and lifestyle-responsive formulations: Formulate variations tailored to pollution levels, climate, user habits, and skin conditions (e.g., more hydration for dry or sleep-deprived skin, lighter textures for oily skin), enabling personalized skincare regimens.
▌Smart usage guidance: Deliver personalized advice on sunscreen reapplication and complementary lifestyle and skincare routines aligned with individual factors such as sleep quality, diet, UV exposure, and pollution levels.
▌Circadian rhythms alignment: Design formulations that respect skin’s biological clock, optimizing sleep, protection and repair cycles for maximal effectiveness.
▌Hydration and barrier strengthening: Incorporate moisturizing, barrier-repair agents customized to skin needs and environmental stressors to support epidermal health.
▌Epigenetic modulation through active ingredients that reactivate protective gene expression by reversing harmful DNA methylation and histone modifications, preventing epigenetic damage from UV and environmental stressors.
▌The product should seamlessly integrate as the final, complementary step in a personalized morning skincare routine tailored to individual skin type and concerns such as pigmentation, photoaging, and skin cancer prevention, offering a pleasant, invisible texture without any pilling.
▌The product should maintain and improve overal skin quality and health.

This holistic, personalized strategy ensures that sunscreens not only prevent sun damage but also actively enhance skin health and quality by addressing molecular, microbial, environmental, and lifestyle complexities. I am confident that as scientific insights and knowledge evolve, I will continue to refine and complement this holistic approach.
​
Take care.
Anne-Marie

ACKNOWLEDGEMENT

▌The key scientific reference and accompanying illustrations used here are adapted from: Khmaladze et al. The Skin Interactome: A Holistic "Genome-Microbiome-Exposome" Approach to Understand and Modulate Skin Health and Aging. Clin Cosmet Investig Dermatol. 2020.pmc.ncbi.nlm.nih

▌"Skin Quality – A Holistic 360° View: Consensus Results" Authors include Heather C. Woolery, Martina Kerscher, and others. Published in Clinical, Cosmetic and Investigational Dermatology, 2021. Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8214518/ 

The word “purging” is currently frequently used on social media for almost any breakout after starting a new product and often framed as skin needing to get worse before it gets better.¹ In medicine this is not an official diagnosis, however dermatologists do sometimes see a short phase where acne gets a bit worse in the first weeks of treatment and then clearly improves.¹⁻³ This pattern has been documented mainly for topical prescription retinoids, oral isotretinoin and superficial chemical peels.¹⁻⁵ By contrast, ingredients such as niacinamide, cosmetic strength retinal, retinol and bakuchiol do not show the same clear “purge curve” in controlled studies, even though they are often labelled as “retinoid like” online.⁶⁻¹³ This article explains what purging is, which ingredients truly cause it, how long it tends to last and what the science says about popular actives like niacinamide, vitamin C, retinal, retinol and bakuchiol.

​HOW ACNE FORMS AND WHY PURGING CAN HAPPEN
​
Every acne lesion starts as a tiny blocked pore under the skin, called a microcomedone.¹˒¹⁴ Over time this can develop into a visible whitehead or blackhead and then sometimes into an inflamed papule or pustule.¹˒¹⁴ Treatments that change how skin cells shed inside the pore or that strongly normalise follicular keratinisation can speed up the transition from microcomedone to visible lesion.¹⁻⁴˒¹⁴ This includes retinoic acid strength prescription retinoids and some chemical peels. When they are started, many hidden clogs can surface within a short period, making it look as though “new” acne has appeared.¹⁻⁵

In a true purge, the breakout:
▌Appears in areas where you already get acne
▌Looks like your usual type of acne
▌Starts soon after beginning or increasing a comedolytic treatment
▌Then slowly settles as overall acne improves
In contrast, allergic or strong irritant reactions often bring burning or stinging, marked redness and sometimes bumps in new areas that were not acne prone.

​AGENTS WITH SOLID EVIDENCE FOR EARLY FLARES

Prescription topical retinoids (tretinoin, adapalene, etc.)
Topical retinoids are first line treatments for comedonal and inflammatory acne and act by normalising cell turnover within the follicle.¹˒²˒⁴
In a pooled analysis of phase 3 trials, tretinoin 0.025% gel used in mild acne caused a measurable early flare in some patients, defined as at least a 10% increase in inflammatory lesions at week 2.²
About 15.4% of patients on tretinoin alone met this flare definition compared with 8.7% on vehicle.² In the same analysis, a clindamycin 1.2% and tretinoin 0.025% fixed combination did not show a statistically significant flare at week 2, suggesting that adding an anti inflammatory and antibacterial partner can mitigate this effect.² Clinical reviews summarise that redness, dryness and a small temporary rise in spots are most common in weeks 1 to 3, while overall lesion counts typically fall over 8 to 12 weeks.¹˒²˒⁴

Oral isotretinoin
Oral isotretinoin is reserved for severe, scarring or treatment resistant acne. It reduces sebum production and exerts strong comedolytic and anti inflammatory effects.¹˒⁵ Early flares are well described. They tend to occur in patients with many large comedones and in younger males.⁵
One study found that multiple comedones, male sex and young age were linked to a higher risk of flare, while very severe flares remained uncommon.⁵
Guidelines therefore recommend starting isotretinoin at about 0.5 mg/kg/day and increasing to 1 mg/kg/day as tolerated.¹˒⁵ This gradual approach helps control early worsening and mucocutaneous side effects while preserving long term efficacy.¹˒⁵

What about bakuchiol
​
Bakuchiol is a plant derived compound that influences many of the same genes as retinol and is often called a “natural retinol alternative”.²¹⁻²³
In a 12 week randomized, double blind trial, 44 patients applied either bakuchiol 0.5% cream twice daily or retinol 0.5% cream once daily for facial photoageing.²¹ Both groups showed significant reductions in wrinkle surface area and pigmentation, with no statistical difference in efficacy, but retinol users reported more scaling and stinging.²¹ A comprehensive review of topical bakuchiol concluded that it behaves as a functional retinol analogue for photoageing with minimal side effects and better tolerance.²²⁻²³ In vivo and ex vivo work shows multi directional activity on collagen, pigmentation and oxidative stress but does not report early acne worsening as a consistent feature.²²⁻²³
So while bakuchiol is “retinol like” in terms of gene expression and anti ageing, the available data suggest:
▌It is often better tolerated than retinol.²¹
▌It does not show a clear acne purge pattern in clinical studies.²¹⁻²³

Vitamin C and other trendy actives
 
Vitamin C serums are often blamed online for “purging”, but clinical studies of topical ascorbic acid focus mainly on photoageing and pigmentation rather than acne.³˒⁹˒²⁴ These trials sometimes report stinging, burning or erythema as side effects, yet they do not show the characteristic early acne flare with later improvement that is documented for prescription retinoids and isotretinoin.¹˒²˒⁵˒²⁴ Vitamin C is not a proven purging agent, and breakouts after starting a vitamin C product are more likely due to irritation, the vehicle or an underlying acne fluctuation than to a true mechanistic “purge”.¹˒²˒³˒⁵˒²⁴

PURGING VS IRRITATION
​

1. Where purging is documented
   • Prescription strength retinoids such as tretinoin and oral isotretinoin have prospective acne data showing a defined early flare period in some patients, followed by overall improvement.¹˒²˒⁵
   • Superficial chemical peels can also cause temporary flare ups while improving acne over the course of several treatments.³˒¹²⁻¹⁵
2. Where we see irritation, not purging
   • Retinal and retinol can irritate at higher strengths, but the available acne and anti ageing studies do not show the same clear “worse at week 2, better by week 12” acne pattern as tretinoin.¹⁷⁻²⁰
   • Bakuchiol appears comparable to retinol for photoageing and is often better tolerated, again without a defined purge phase.²¹⁻²³
3. Likely explanations when breakouts follow cosmetic retinoids, bakuchiol or niacinamide
   • Underlying acne that is flaring independently
   • Irritant dermatitis with barrier damage leading to non specific breakouts
   • Comedogenic, fragranced or occlusive vehicles
   • Introduction of several strong actives at once, creating cumulative stress on the skin

From a scientific point of view it is misleading to take the documented flaring behaviour of tretinoin and isotretinoin and apply it wholesale to every “retinoid like” or other cosmetic, especially when clinical trials do not support that leap.¹⁻⁵˒¹⁷⁻²³
 
HOW LONG DOES PURGING LAST WHEN IT HAPPENS 

Across agents that truly cause purging, the pattern is broadly similar. Purging, if it occurs, tends to appear in the first 1 to 3 weeks of a new treatment and then settles over the next 4 to 12 weeks as total lesion counts drop.¹⁻⁵˒³˒¹²⁻¹⁵ With topical prescription retinoids, the peak of dryness, redness and extra spots is usually between weeks 1 and 3, with clearer improvements by weeks 8 to 12.²⁻⁴ With isotretinoin, early flares are most common at higher starting doses and in those with many macrocomedones.¹˒⁵ With peels, selective patients may notice a flare after the first or second treatment, while repeated sessions over several weeks show net reductions in lesions.³˒¹²⁻¹⁵ Provided the treatment is continued at a tolerable intensity and there are no signs of severe reaction, purging generally resolves without leaving new scarring.¹˒²˒⁵
 
IS PURGING AN OILY-SKIN TYPE PROBLEM

Clinical data do not support the idea that only oily skin can purge. In the isotretinoin flare study, the main risk factors were multiple comedones, male sex and younger age. Seborrhoea as such was not singled out as a separate predictor.⁵ In the tretinoin flare analysis, flares occurred in some patients with mild acne regardless of skin type.² Peel trials included a mix of Fitzpatrick phototypes and baseline skin characteristics, with flare ups reported across this spectrum.³˒¹²⁻¹⁵ In practice, any person with a significant microcomedone burden can experience purging when a strong comedolytic therapy is started, even if their skin is not very oily.¹˒³
 
MANAGING AND MINIMISING PURGING

Dose and frequency
For isotretinoin, starting at about 0.5 mg/kg/day and then increasing as tolerated is standard to reduce early flares and mucosal side effects.¹˒⁵
For topical retinoids, beginning with every second night application, or using a lower strength and increasing slowly, is widely used to lower irritation and perceived flares.¹⁻⁴

Combinations and barrier support
Combining tretinoin with clindamycin reduced flare rates compared with tretinoin alone in a phase 3 analysis, showing the value of pairing retinoids with anti inflammatory therapy.² In severe nodulocystic acne at high risk of fulminant flares, short term systemic corticosteroids with isotretinoin can be helpful.¹˒⁵ Barrier supportive skincare also matters. In the split face study, a ceramide and niacinamide moisturizer used with adapalene and benzoyl peroxide improved barrier function and acne outcomes without increasing flares compared with a hydrophilic cream.⁷
Gentle cleansers, non comedogenic moisturizers and sunscreen lower irritation and help patients stay on course through any mild purge.⁶⁻⁸

When to seek medical review
Mild, temporary worsening of usual type acne in usual areas can often be managed with dose or frequency reductions and supportive skincare.¹⁻⁴
Red flags include sudden painful nodules, many new cysts, spread to new body areas or systemic symptoms such as fever or joint pain, which require medical review and often a change in therapy.¹˒⁵
 
CAN PURGING BE PREVENTED

Purging cannot always be avoided, but several steps can reduce the risk and severity.
▌Treat large comedones before starting isotretinoin, for example with extraction. This may reduce the chance of sharp early flares.¹
▌Start both isotretinoin and topical retinoids “low and slow” and increase only as tolerated.¹⁻⁵
▌Add anti inflammatory and barrier supportive partners such as clindamycin with tretinoin or ceramide and niacinamide moisturizers alongside retinoid or benzoyl peroxide regimens.²˒⁷
▌Avoid stacking multiple strong actives at the same time. Peel studies show that even one peel can cause flare ups, so combining peels with strong retinoids and high strength benzoyl peroxide from day one is often unnecessary and risky.³˒¹²⁻¹⁵
Setting realistic expectations is equally important. Patients who know that a short, limited flare is possible and temporary are less likely to abandon effective therapy early.¹⁻⁴

​KEY POINTS
​
▌Purging is a short lived, treatment linked increase in visible acne that happens when potent comedolytic therapies push already clogged pores to the surface faster.¹⁻⁵
▌It has been clearly documented for topical prescription retinoids, oral isotretinoin and superficial chemical peels, and is sometimes seen with benzoyl peroxide; niacinamide, cosmetic retinal or retinol, bakuchiol and vitamin C do not have comparable purge data.¹⁻⁸˒¹²⁻¹⁷˒²¹⁻²⁴
▌Niacinamide does not show a purge pattern in trials and instead often improves inflammation and barrier function.⁶⁻⁸
▌Cosmetic retinal, retinol and bakuchiol can irritate at higher strengths but have not been shown to cause a consistent, quantified acne purge like tretinoin or isotretinoin.¹⁷⁻²³
▌Purging is not limited to oily skin and depends more on comedone load and treatment strength and schedule.¹⁻⁵
▌Smart dosing, thoughtful combinations and barrier support can reduce flares and improve adherence so that patients reach the real benefits of therapy.¹⁻⁵˒⁷

This content is for informational and educational purposes only and is not intended to diagnose, treat, cure, or prevent any disease, nor to replace individual medical advice; always consult a qualified healthcare professional to determine the most appropriate approach for your personal needs and goals.

Take care!
Anne-Marie

​
References ​ 

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