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Published for the period of July -2025
Balancing Beauty and Biology: Evolving Strategies in Pigment Disorders
Pigmentation disorders remain one of the most common yet challenging concerns in dermatology, particularly in Indian skin, where melanogenesis is influenced by a complex interplay of genetic, environmental, hormonal, and lifestyle factors. The emotional and psychosocial impact of conditions like melasma, post-inflammatory hyperpigmentation, and dyschromias cannot be overstated, especially in skin of color, where treatment must balance efficacy with safety.
This issue brings together a focused collection of clinical cases and expert perspectives that reflect the evolving science and management of facial pigmentation. From the successful use of multimodal therapy in facial pigmentation to a detailed case of refractory melasma treated with a layered depigmentation approach, our contributors highlight the need for personalized, multi-pathway treatment strategies.
We also feature two insightful case reports that contribute to procedural dermatology. The first highlights the use of microneedling combined with platelet-rich plasma (PRP) in the management of acne scars, demonstrating significant clinical improvement through synergistic collagen stimulation. The second presents the effectiveness of radiofrequency (RF) ablation and CO2 laser ablation in the treatment of dermatosis papulosa nigra, showcasing a comparative and patientcentered approach to aesthetic lesion removal. Finally, we explore the broader shift toward personalised aesthetics in Indian skin, advocating for tailored solutions that move beyond the one-size-fits-all paradigm.
We hope this issue adds meaningful value to your pigment management protocols and reinforces the importance of individualized care in dermatology.
HOPE YOU HAVE A GREAT READ
Thanks & Cheers
- Dom Daniel Executive Editor & Publisher
Editorial Board
Dr. Sanjeev Aurangabadkar
MD (Dermatology)
Consultant Dermatologist
Dr. Aurangabadkar's Skin & Laser Clinic Hyderabad
Dr. Nidhi Singh Tandon
MBBS, MD (DVL)
Consultant Dermatologist, Medical Director & Founder
The Skin Art Clinic Lucknow
Dr. Manoj Agarwala
MBBS, MD (CMC Vellore)
Fellowship in Lasers & Aesthetics
Medical Director and Principal
Dermatologist
M A Skin & Hair Superspecialty Clinic
Raipur, Chhattisgarh
Dr. Nandita Rai
MBBS, MD (Dermatology and Clinical Cosmetology)
Cosmetic Dermatologist West Bengal
Dr. Pragathi Sankineni
MBBS, MD, DVL
Consultant Dermatologist & Cosmetologist
Pragathi Skin & Cosmetology Clinic
Nizamabad, Telangana
A Novel Multi-Ingredient Topical Approach for Melasma: A Case Report
Dr. Sanjeev Aurangabadkar
MD (Dermatology)
Consultant Dermatologist
Dr. Aurangabadkar's Skin & Laser Clinic
Hyderabad
Introduction
Melasma is a frequently encountered .......... acquired pigmentary disorder characterized by the development of symmetrical, brownish macules and patches, primarily affecting sun-exposed areas of the face, such as the malar region, forehead, and upper lip. It is more prevalent in women with Fitzpatrick skin types III to V and tends to follow a chronic, relapsing course. The condition carries a significant psychosocial burden due to its aesthetic impact and therapeutic resistance. The pathogenesis of melasma is multifactorial, involving a complex interplay of genetic predisposition, ultraviolet (UV) radiation, hormonal influences, certain medications, inflammation, and oxidative stress. These factors collectively contribute to increased melanogenesis and dysregulation of melanocyte activity. Traditionally, melasma is histologically classified into three types based on the depth and location of melanin deposition: epidermal, dermal, and
mixed. The epidermal type is characterized by increased melanin accumulation within the basal and suprabasal layers of the epidermis. Although the number of melanocytes remains unchanged, these cells often appear hypertrophic, with elongated dendrites and elevated melanosome production, indicating heightened functional activity. This type typically exhibits enhanced contrast under Wood’s lamp examination, which can aid in clinical differentiation. The dermal type, on the other hand, is marked by the presence of melanophages—macrophages that have ingested melanin— distributed throughout the upper and lower dermis. Histologically, this variant is often accompanied by features suggestive of chronic inflammation, including perivascular lymphohistiocytic infiltrates, solar elastosis, and increased dermal vascularity. The mixed type combines characteristics of both epidermal and dermal
pigmentation and is the most frequently encountered variant in clinical practice. This overlap of features can complicate both diagnosis and treatment, often necessitating a multimodal therapeutic approach. Due to its multifaceted etiology and recalcitrant nature, effective management of melasma necessitates a comprehensive, multi-targeted therapeutic approach. Standard treatments include strict photoprotection, topical depigmenting agents, chemical peels, and laserbased modalities. Among topical therapies, combination regimens that incorporate tyrosinase inhibitors, melanogenesis suppressors, antioxidants, and barrier-repair agents have demonstrated enhanced efficacy. Addressing the underlying oxidative stress and inflammatory processes, in addition to pigment reduction, is essential to achieving optimal and sustained results.1,2,3,4
This case highlights the clinical efficacy and tolerability of a multifaceted topical depigmentation formulation delivered via an airless pump system in the management of moderate-to-severe melasma. The formulation included a synergistic blend of active agents: Hydroquinone 2%, Kojic Acid 2%, BetaArbutin 2%, Lactic Acid 0.3%, Tetrahydrocurcumin, Grape Seed Oil 7% combined with Vitamin E, Antipollon HT 1.5%, and Glycerin 4%. These agents collectively target multiple pathogenic pathways of melasma, including melanogenesis, oxidative stress, and inflammation. The treatment was initiated in a
female patient presenting with extensive facial hyperpigmentation. Over the course of 12 weeks, significant improvement was observed in pigmentation density, skin texture, and overall skin tone uniformity, without notable irritation or adverse effects. The outcome underscores the potential of a multi-ingredient, targeted approach in effectively managing melasma while maintaining excellent skin tolerability.
Case Presentation & History
A 39-year-old female patient presented with a twoyear history of gradually worsening facial pigmentation, primarily localized to the malar regions. She reported that the pigmentation had become more pronounced with prolonged sun exposure, particularly during the summer months, and noted no seasonal improvement. Her dermatologic history was unremarkable, and there was no reported use of hormonal medications or relevant systemic illness. Prior to presentation, she had selftreated the condition using various over-the-counter skin-lightening creams, which provided little to no improvement and occasionally caused mild irritation.
Clinical Examination
On clinical examination, the patient was classified as Fitzpatrick skin type IV, with moderately pigmented skin prone to tanning. Prominent findings included dense, irregularly shaped brownish macules symmetrically distributed over both malar regions. The affected areas showed no signs of
inflammation, erythema, or scaling, suggesting a noninflammatory hyperpigmentation disorder. There was no involvement of other facial zones such as the forehead or upper lip.
Diagnosis
Based on the distribution pattern and clinical features, a diagnosis of epidermal melasma was made. Wood’s lamp examination further supported this diagnosis by enhancing the contrast of the pigmented areas, consistent with superficial melanin deposition. In addition, dermoscopy served as a valuable non-invasive diagnostic adjunct, revealing a homogenous light brown pigmentation pattern and accentuation around follicular openings—features characteristic of epidermal melasma. The patient was counselled regarding the chronic nature of melasma and the importance of adherence to a comprehensive treatment and photoprotection plan.
Treatment Protocol
The patient was initiated on a comprehensive topical regimen containing multiple active agents targeting pigmentation, oxidative stress, and skin barrier function:
• Hydroquinone 2% – A goldstandard tyrosinase inhibitor with strong depigmenting properties.
• Kojic Acid 2% – A fungalderived tyrosinase inhibitor that works synergistically with hydroquinone to enhance efficacy.
• Beta-Arbutin 2% – A natural derivative of hydroquinone
offering additional skin-lightening effects with a gentler profile.
• Lactic Acid 0.3% – A mild alpha-hydroxy acid (AHA) that promotes gentle exfoliation and improves penetration of other active ingredients.
• Tetrahydrocurcumin – A powerful antioxidant known for its anti-inflammatory, anti-melanogenic, and skinbrightening properties.
• Grape Seed Oil 7% + Vitamin E – A combination providing antioxidant protection and supporting skin barrier repair.
• Antipollon HT 1.5% – A novel agent offering protection against environmental pollutants and reducing skin inflammation.
• Glycerin 4% – A humectant that maintains skin hydration and helps prevent irritation from active depigmenting agents.
Maintenance Therapy
Following the initial treatment phase, the patient was transitioned to a maintenance regimen incorporating nonhydroquinone (Non-HQ) skinlightening agents. This step was essential to sustain the achieved results, minimize relapse, and reduce the risk of longterm irritation or side effects associated with continuous hydroquinone use.
Adjunctive Measures
• Photoprotection – Broadspectrum sunscreen (SPF 50+ with PA++++) containing iron oxide was recommended, to be applied twice daily and reapplied every 3–4 hours during the day.
• Lifestyle Counseling –The patient was advised to practice strict sun avoidance, ensure adequate hydration, and
minimize exposure to heat and environmental pollutants.
The depigmenting formulation was applied once nightly on cleansed skin, with careful adherence to photoprotection and lifestyle measures stressed throughout the treatment course.
Follow-Up and Treatment Outcome
The patient was evaluated at regular intervals over a 12-week treatment period to assess clinical progress, monitor skin tolerance, and reinforce adherence to the prescribed regimen. By the 4-week follow-up, initial signs of improvement were evident, with visible lightening of the hyperpigmented macules over the malar regions. The patient noted a reduction in the depth and intensity of pigmentation and reported a visibly brighter and more radiant facial complexion. Importantly, there were no signs of erythema, peeling, irritation, or dryness, indicating that the formulation was well tolerated. The presence of Glycerin and antioxidant-rich emollients, such as grape seed oil and vitamin E, likely contributed to maintaining skin hydration and minimizing irritation from depigmenting agents like hydroquinone and kojic acid.
At the 8-week assessment, further improvement was observed, with a substantial decrease in pigmentation density and a more uniform skin tone. The areas affected by melasma appeared lighter, and the skin surface showed a smoother, more refined texture. No adverse cutaneous
reactions were reported during this period, and the patient expressed satisfaction with the ongoing progress.
By the 12-week follow-up, the patient demonstrated remarkable clinical improvement, with an estimated 75–80% reduction in melasma severity, as confirmed through photographic documentation. The pigmentation was significantly diminished, and the overall skin tone appeared more balanced, even, and luminous. The formulation’s comprehensive approach— targeting melanogenesis, oxidative stress, inflammation, and barrier integrity—proved to be highly effective over the extended treatment period. Notably, there was no evidence of post-inflammatory hyperpigmentation, rebound pigmentation, or treatmentrelated irritation, which are common concerns in long-term depigmentation therapies.
The patient reported high levels of satisfaction, citing both the visible results and the comfort of use. She noted improved self-esteem and greater ease in social interactions. The airless pump delivery system was also wellreceived, as it ensured hygienic application, preserved the potency of active ingredients, and facilitated controlled dispensing. Overall, the 12week treatment regimen was well tolerated and delivered consistent, progressive, and sustainable improvement, reinforcing its role as a safe and effective therapeutic option for the management of moderateto-severe epidermal melasma.
1: Clinical outcome after 12 weeks of treatment showing remarkable reduction in pigmentation and significant improvement in overall skin tone and texture
Discussion
The successful outcome in this case underscores the importance of a multimodal approach in melasma therapy. Hydroquinonebased triple combination therapies remain first-line treatments, but the inclusion of additional agents such as kojic acid, arbutin, tetrahydrocurcumin, and antioxidants provided synergistic benefits. Lactic acid likely enhanced the bioavailability of actives, while Antipollon HT offered novel environmental protection.
The favorable outcome observed in this case highlights the efficacy of a comprehensive, multi-targeted approach in the management of melasma—a condition known for its complex pathophysiology and chronic, relapsing nature. While hydroquinone (HQ)-based triple combination therapies remain the gold standard and firstline treatment for melasma. Central to the formulation used in this case was Hydroquinone 2%, a dihydric phenol that exerts its depigmenting effect by inhibiting tyrosinase, the rate-limiting enzyme in melanin synthesis. It also interferes with DNA and RNA synthesis and may selectively affect melanocyte viability, thereby reducing pigment production. Though highly effective, HQ shows the best results when combined with synergistic agents that enhance both efficacy and tolerability. The inclusion of Kojic Acid, Beta-Arbutin, and Tetrahydrocurcumin provided multiple complementary mechanisms. Kojic acid, a fungal metabolite, inhibits tyrosinase activity through copper chelation and has shown enhanced performance in combination regimens. BetaArbutin, a plant-derived glycosylated hydroquinone, acts as a milder tyrosinase inhibitor with a lower risk of irritation, offering added pigment control. Tetrahydrocurcumin, a stable and colorless metabolite of curcumin, delivers strong antioxidant and anti-inflammatory benefits, modulating oxidative stress and downregulating melanogenic signaling pathways.1,5,6,7,8
Antioxidant support in the form of Grape Seed Oil and Vitamin E further enhanced the formulation’s ability to neutralize reactive oxygen species and protect against oxidative damage, which is
increasingly recognized as a central contributor to persistent hyperpigmentation. Vitamin E inhibits lipid peroxidation within melanocyte membranes and enhances intracellular glutathione levels, while grape seed extract contains proanthocyanidins known to reduce melanin synthesis and provide environmental defense. Lactic Acid (0.3%), a mild alpha-hydroxy acid (AHA), played a dual role in this formulation: it promoted gentle exfoliation and enhanced epidermal turnover, while also acting as a humectant to support skin hydration. Its keratolytic action facilitates deeper penetration of active depigmenting agents and contributes to improved skin texture. A unique and forwardthinking addition to the regimen was Antipollon HT (1.5%), a novel anti-pollution ingredient. This component is designed to adsorb environmental pollutants, thereby preventing particulate matter-induced oxidative damage and pigmentation flare-ups. Given the increasing recognition of environmental stressors— especially urban pollution—as aggravating factors in melasma, the inclusion of such protective agents is both timely and clinically relevant.1,5,6,7,8
An important technical advantage in this case was the airless pump delivery system used to dispense the formulation. Airless packaging not only ensures hygienic, controlled dosing but also helps maintain the chemical stability and potency of sensitive active ingredients by minimizing exposure to air, light, and microbial contamination.
Figure
Before treatment
After treatment
A
This contributes to better patient adherence, consistent therapeutic results, and enhanced user satisfaction— critical factors in the long-term management of a chronic condition like melasma.
Notably, oral tranexamic acid—a systemic agent with established efficacy in melasma—was deliberately not included in this case. This decision was made to specifically assess the
References
1. Sarkar, R., Arora, P., Garg, V. K., Sonthalia, S., & Gokhale, N. (2014). Melasma update. Indian dermatology online journal, 5(4), 426–435. https:// doi.org/10.4103/2229-5178.142484
2. Ogbechie-Godec, O. A., & Elbuluk, N. (2017). Melasma: an Up-to-Date Comprehensive Review. Dermatology and therapy, 7(3), 305–318. https://doi. org/10.1007/s13555-017-0194-1
3. Grimes PE. "Management of hyperpigmentation." Dermatol Clin. 2007.
4. Draelos ZD. "Skin lightening preparations and the hydroquinone controversy." Dermatol Ther. 2007.
standalone effectiveness of the topical combination regimen. The favourable clinical outcome achieved without systemic intervention further supports the potential of a well-structured, multi-targeted topical therapy in managing moderate-to-severe melasma.
Conclusion
This case highlights the effectiveness of a multi-targeted topical regimen in managing moderate-to-severe melasma by addressing melanogenesis, oxidative stress, and barrier dysfunction. The use of a stable, airless pump delivery system supported consistent application and patient compliance. Combined with strict photoprotection, this approach reinforces the value of combination therapy as the cornerstone for achieving and maintaining long-term pigment control.
5. Keen, M. A., & Hassan, I. (2016). Vitamin E in dermatology. Indian dermatology online journal, 7(4), 311–315. https://doi. org/10.4103/2229-5178.185494
6. Cristiane C. Silva, Rogério B. Benati, Taís N. C. Massaro, Karina C. Pereira, Lorena R. Gaspar & Priscyla D. Marcato. (2023) Antioxidant and anti-tyrosinase activities of quercetin-loaded olive oil nanoemulsion as potential formulation for skin hyperpigmentation. Journal of Dispersion Science and Technology 44:14, pages 2628-2638.
7. Singh, R., Goyal, S., Ahmed, Q. R., Gupta, N., & Singh, S. (2014). Effect of 82% Lactic Acid in Treatment of Melasma. International
scholarly research notices, 2014, 407142. https://doi.org/10.1155/2014/407142
8. Tantanasrigul, P., Sripha, A., & Chongmelaxme, B. (2025). The Efficacy of Topical Cosmetic Containing AlphaArbutin 5% and Kojic Acid 2% Compared With Triple Combination Cream for the Treatment of Melasma: A Split-Face, Evaluator-Blinded Randomized Pilot Study. Journal of cosmetic dermatology, 24(1), e16562. https://doi.org/10.1111/ jocd.16562
How Four Botulinum Toxin A Formulations Vary in Treating Frown Lines
A recent randomized clinical trial has demonstrated distinct pharmacodynamic profiles among four botulinum toxin A formulations—onabotulinumtoxinA, abobotulinumtoxinA, prabotulinumtoxinA, and incobotulinumtoxinA—when administered for the treatment of glabellar lines in adult female patients. AbobotulinumtoxinA and prabotulinumtoxinA exhibited the most rapid onset of action, with visible clinical effects emerging within the first few days. At extended follow-up, sustained efficacy was most notable with prabotulinumtoxinA and incobotulinumtoxinA, with prabotulinumtoxinA showing greater longevity of effect compared to onabotulinumtoxinA. All four agents demonstrated significant efficacy in reducing glabellar strain and improving patient-reported outcomes during the initial months following treatment. Additionally, the study identified a relationship between baseline wrinkle severity and the degree of clinical improvement, and observed a compensatory increase in lateral canthal strain, suggesting dynamic muscular adaptation. These findings highlight the importance of selecting botulinum toxin A formulations based on individual patient profiles and aesthetic treatment goals.
New Peptide-Based Body Lotion Reduces Inflammation and Enhances Skin Barrier Function
A randomized, double-blind clinical trial involving older female participants demonstrated significant improvements in skin barrier function, hydration, and systemic inflammation following weeks of topical treatment with a novel senotherapeutic peptide formulation. The study included adults who applied the product twice daily and were assessed for transepidermal water loss, skin hydration, pH levels, inflammatory biomarkers, and biological age. Compared to a control moisturizer, the treatment group showed greater reductions in water loss and improvements in skin hydration, texture, elasticity, and firmness. Notably, inflammatory markers such as IL-8 decreased significantly, while TNF-α and IFN-γ remained stable, contrasting with increases observed in controls. Biological age analysis indicated a slowing of systemic aging in the treated group. These findings support the potential of targeting cellular senescence to enhance skin health and longevity, though further studies with larger, more diverse populations and longer follow-up are warranted to confirm these effects.
Personalised Aesthetics –Moving Beyond “One Size Fits All” in Indian Skin
Dr. Nidhi Singh Tandon
MBBS, MD (DVL)
Consultant Dermatologist, Medical Director & Founder
The Skin Art Clinic
Lucknow Introduction
Aesthetic medicine in India is evolving. What was once seen as a luxury for cosmetic enhancement is now shifting toward holistic well-being. But even as technology advances and new procedures emerge, a large portion of aesthetic protocols still follow a one-sizefits-all model—often built around data and standards set for lighter, Caucasian skin types.
In a country like India, where skin tones, structures, and cultural ideals are incredibly diverse, this approach falls short. Indian skin has different needs. It reacts differently, heals differently, and ages differently. So why should it be treated the same way?
The answer lies in personalised aesthetics. With the help of artificial intelligence (AI), biometric analysis, and more informed clinical insight, we can now tailor treatments to match individual physiology, lifestyle, and goals, offering safer, more effective results that truly respect the uniqueness of Indian skin.1
Understanding the Diversity of Indian Skin
Indian skin spans Fitzpatrick skin types III to VI and includes a spectrum of undertones olive, yellow, red, and neutral. High melanin content confers photoprotection but also predisposes the skin to postinflammatory hyperpigmentation (PIH), melasma, and persistent scarring. Furthermore, climatic variations, genetic predispositions, and lifestyle differences across regions further increase the complexity of designing a universal aesthetic protocol.
In this context, standardised treatments such as aggressive chemical peels, lasers, or even off-the-shelf skincare products may produce suboptimal results or even cause harm. The need of the hour is personalisation not just in treatments, but in diagnostics, follow-ups, and outcomes.
Limitations of the One-SizeFits-All Model
Global aesthetic practices have
traditionally been designed around lighter phototypes with lower melanin density. This approach fails to account for:
• Greater melanocyte activity and the risk of pigmentation disorders.
• Variations in barrier function, hydration levels, and sebaceous activity.
• Sociocultural expectations: fairness is no longer the universal goal—glow, health, and texture are increasingly preferred.
• High variability in treatment response depending on stress, hormones, lifestyle, and comorbidities.
This model, when applied to Indian skin, often leads to either poor efficacy or adverse effects. As a result, patients lose confidence in treatments, and practitioners are forced into trialand-error protocols.
AI and Clinical Personalisation
A recent study (Campanella et al., Cosmetics 2025) evaluated aesthetic treatments using biometric data (e.g., BMI, fat mass, lean mass) across different body types and employed clustering algorithms to understand individual responses.2 One of the key insights was that treatment efficacy and patient satisfaction were heavily influenced by individual physiological and behavioural factors, such as exercise, stress and hormonal changes.
Translating this into the Indian aesthetic space means:
• AI-guided tools can assess skin type, hydration, pigmentation and elasticity to customise skincare routines and
procedural parameters.3
• Bioimpedance analysis (BIA) which includes parameters like BMI, TBW and BMR can help track changes in body composition for body contouring or anti-aging therapies.4
• Clustering and decision support algorithms can be used to predict outcomes and recommend mid-course treatment adjustments.
For example, instead of offering the same laser parameters to all melasma patients, an AIbased tool could classify them into response groups based on prior treatment history, hormonal profile, and PIH risk.
Real-World Implications for Indian Practice
Personalised aesthetic practice could include:
• Digital skin mapping before initiating chemical peels or injectables.
• Tailored protocols for different Indian phenotypes (e.g., North Indian vs. South Indian skin).
• Dynamic treatment plans that evolve with patient lifestyle, menstrual cycles or stress levels.
• Image-based tracking for objective before–after comparisons.
• Custom skincare formulations based on hydration level, pigmentation, sensitivity and barrier status.
Challenges in Implementation
Despite the clear benefits, personalised aesthetics in India faces several hurdles:
• Lack of Indian-specific clinical data in AI algorithm training.
• Limited access to technology in smaller clinics or tier 2 cities.
• Need for standardised imaging
and diagnostic protocols to ensure objective monitoring.
• Inadequate training in both digital tools and ethnic skin science for many practitioners.
Personalisation in Injectable Fillers
Dermal fillers are one of the cornerstones of aesthetic rejuvenation, offering volume restoration, contouring and skin quality improvement. However, the application of fillers in Indian skin demands a fundamentally different approach compared to Western counterparts. The anatomical structure, skin thickness, fat compartment distribution and aesthetic ideals vary significantly across ethnicities.
Ethnic Anatomy and Indian Aesthetics
• Indian faces often feature stronger bony structures, heavier midface fat pads and thicker skin, especially in the lower third of the face.
• There is often a higher baseline pigmentation and vascular reactivity, increasing the risk of bruising and PIH postprocedure.
• Aesthetic goals may lean towards natural enhancement, tear trough correction, jawline refinement and glow restoration, rather than sharp contours or exaggerated lifting.
The Need for Personalisation in Filler Techniques
Standard filler techniques like MD Codes™, while immensely valuable, must be adapted to suit Indian facial characteristics:
• Product choice should be based on skin density, hydration levels and facial dynamics.
• Injection depth and plane must
account for regional variation in facial fat compartments and the tendency for lower-face heaviness.
• Personalised vectoring can guide balanced lifting and harmonious correction, minimising the risk of a “done” look.
Conclusion
The future of aesthetic dermatology lies in moving
References
1. Vatiwutipong P, Vachmanus S, Noraset T, Tuarob S. Artificial intelligence in cosmetic dermatology: a systematic literature review. IEEE Access. 2023 Jul 13;11:71407-25.
2. Campanella S, Palma L. Personalized Beauty: How Clinical Insights Shape Tailored Aesthetic Treatments. Cosmetics. 2025 May 7;12(3):94.
away from generic protocols and embracing an approach that truly honors individual variation. Indian skin, with its unique challenges and strengths, cannot be served by one-size-fits-all solutions. As dermatologists, it is our responsibility to blend clinical expertise with cultural sensitivity and technological tools to offer treatments that are as unique as the patients we care for.
Because in aesthetics, the best outcomes come not from standardisation, but from personalisation.
3. Kania B, Montecinos K, Goldberg DJ. Artificial intelligence in cosmetic dermatology. Journal of Cosmetic Dermatology. 2024 Oct;23(10):3305-11.
4. Figueiredo DM, Duarte RP, Cunha CA. Predictive Model for Estimating Body Weight Based on Artificial Intelligence: An Integrated Approach to Pre-processing and Evaluation. InInternational Conference on
A potent tyrosinase, hyaluronidase, and elastase inhibitor for brighter, firmer, youthful-looking skin.
MELAZERO TREALIX
Reduces hyperpigmentation by erasing existing melanin and inhibiting melanogenesis for even skin tone.
GLOWEVERYDAY GGLOWEVERYDAY LOWEVERYDAY
Delivers deep moisturization and longlasting hydration for smoother, softer, and healthier-looking skin.
Also Fortified with
Tirzepatide:
A Novel Dual Incretin Receptor Modulator Transforming Metabolic Health and Excess Adiposity Management.
Glucagon-like peptide-1 (GLP-1) is a hormone released by the small intestine after meals that plays a crucial role in blood sugar regulation by stimulating insulin secretion, delaying gastric emptying, and suppressing appetite. In individuals with excess adiposity, impaired GLP-1 signaling disrupts appetite control, raises blood glucose levels, and promotes fat accumulation. GLP-1 receptor agonists have become key treatments for managing excess body fat and type 2 diabetes by improving insulin response, reducing calorie intake, and supporting weight loss, with semaglutide exemplifying these benefits and enhancing patients quality of life. Tirzepatide, a novel dual agonist targeting both GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) receptors, extends these effects by simultaneously engaging two incretin pathways, resulting in superior glycemic control and greater fat reduction. Its molecular structure includes a fatty acid
component that prolongs its action, optimizing nutrient metabolism, energy balance, and hormonal regulation. As a dual incretin receptor modulator, tirzepatide represents a significant advance in treating complex metabolic disorders, delivering improved therapeutic outcomes and markedly enhancing patients overall well-being.
Q1. What is tirzepatide, and how does it work?
Tirzepatide is a dual agonist of the GLP-1 and GIP receptors, two key incretin pathways involved in glucose and energy regulation. Unlike traditional therapies that activate only GLP-1, tirzepatide simultaneously targets both, resulting in enhanced insulin secretion, improved insulin sensitivity, delayed gastric emptying, and stronger appetite suppression. This combined mechanism leads to superior blood sugar control, greater reductions in HbA1c, and more effective weight reduction than single-pathway agents.
Q2. How does tirzepatide help reduce appetite and control food intake?
Tirzepatide reduces appetite by acting on central nervous system regions involved in energy balance and appetite regulation, particularly the hypothalamus and brainstem. It activates both GLP-1 and GIP receptors, which play key roles in modulating satiety and caloric intake. One of its notable effects is delayed gastric emptying, which prolongs gastric distension and enhances the sensation of fullness after meals. Additionally, tirzepatide influences reward-related pathways in the brain, helping to reduce cravings and the drive to consume high-calorie, palatable foods. These combined mechanisms contribute to reduced overall energy intake, improved adherence to dietary interventions, and support for sustained weight loss.
Q3. How does tirzepatide help the body manage blood sugar and insulin more effectively?
Tirzepatide improves glycemic control through multiple complementary mechanisms. It stimulates glucose-dependent insulin secretion from pancreatic β-cells, meaning insulin is released primarily when blood glucose levels are elevated, minimizing the risk of hypoglycemia. It also enhances insulin sensitivity in peripheral tissues such as skeletal muscle and adipose tissue, promoting more efficient glucose uptake and utilization. Additionally, tirzepatide suppresses inappropriate hepatic glucose production, a common contributor to hyperglycemia in type 2 diabetes. Collectively, these effects lead to better blood glucose regulation, reduced insulin resistance, and improved metabolic function, supporting both glycemic management and weight reduction.
Q4. How does tirzepatide affect visceral and ectopic fat around organs and tissues?
Tirzepatide preferentially targets and reduces visceral adipose tissue, the metabolically deleterious fat depot surrounding intra-abdominal organs such as the liver and pancreas, which is implicated in insulin resistance, systemic inflammation, and increased cardiovascular risk. It also decreases ectopic lipid accumulation in organs including the liver and skeletal muscle, thereby
mitigating metabolic dysfunction associated with fatty liver disease and impaired glucose metabolism. Through these effects, tirzepatide improves insulin sensitivity, lowers inflammatory mediators, and contributes to favourable adipose tissue redistribution, ultimately reducing the burden of obesity-related metabolic comorbidities.
Q5. Does tirzepatide help maintain muscle mass during weight loss?
Yes, preserving muscle mass during weight loss is essential for maintaining metabolic rate and functional capacity. Tirzepatide supports muscle preservation by enhancing the anabolic effects of insulin, promoting nutrient uptake and protein synthesis within muscle cells. It also activates cellular pathways involved in muscle repair and regeneration, even as adipose tissue is mobilized for energy. By maintaining muscle mass, tirzepatide helps prevent metabolic slowdown and reduces the risk of weight regain, contributing to improved long-term treatment outcomes.
Q6. How does tirzepatide differ from semaglutide in terms of mechanism, effects on adipose tissue, and overall therapeutic benefits?
Semaglutide works by activating only the glucagon-like peptide-1 (GLP-1) receptor, which helps lower blood sugar and reduce appetite. Tirzepatide, on the other hand, activates both GLP1 and glucose-dependent insulinotropic polypeptide (GIP) receptors. This dual action allows tirzepatide to affect more pathways involved in controlling blood sugar, improving how the body responds to insulin, and reducing appetite. Tirzepatide also has a stronger effect on fat tissue, particularly by reducing harmful fat around organs (visceral fat) and fat stored in muscles and the liver. This helps improve metabolism and energy use. Because of these combined effects, tirzepatide generally leads to greater weight loss and better blood sugar control (lower HbA1c) than semaglutide. The enhanced benefits come from how GLP-1 and GIP work together to regulate blood sugar, fat metabolism, and overall energy balance.
Q7. How is tirzepatide given, and what is the dosing schedule?
Tirzepatide is administered by subcutaneous injection once weekly. Treatment begins with a low dose of 2.5 mg to reduce the likelihood and severity of gastrointestinal side effects such as nausea, vomiting, and diarrhoea. Every four weeks, the dose is gradually increased by 2.5 mg increments until reaching a maintenance dose that usually ranges between 5 mg and 15 mg, based on individual patient response and tolerability. This gradual dose escalation helps the body
adjust, optimizes therapeutic effects, and improves patient adherence by minimizing side effects.
Q8. How does tirzepatide influence energy expenditure and metabolic rate in individuals with excess adiposity?
Tirzepatide enhances energy expenditure by promoting beneficial changes in adipose tissue metabolism. It supports the conversion of white adipose tissue into a more thermogenically active form, increasing the body ability to burn calories through heat production. This effect contributes to a higher basal metabolic rate, even at rest. Tirzepatide also improves the efficiency of nutrient utilization and supports greater mitochondrial activity in muscle and fat tissue, helping to regulate energy balance and promote sustainable reduction in excess body fat.
Q9. What additional health benefits does tirzepatide offer beyond weight reduction?
Beyond its substantial effects on body weight, tirzepatide provides broad improvements in metabolic health. It lowers HbA1c levels, reflecting enhanced long-term glycemic control, and reduces insulin resistance, which plays a key role in preventing diabetes-related complications. Tirzepatide also favourably alters lipid parameters by decreasing LDL cholesterol and triglyceride levels, thereby reducing cardiovascular risk. Additionally, it diminishes systemic inflammation, a major factor in the development of obesity-associated disorders. Collectively, these effects support better metabolic function and help lower the risk of conditions such as cardiovascular disease, non-alcoholic fatty liver disease, and progression of type 2 diabetes.
Q10. How does tirzepatide impact gut hormones beyond GLP-1 and GIP?
In addition to its direct dual agonist activity on GLP1 and GIP receptors, tirzepatide modulates other enteroendocrine signals involved in appetite regulation, particularly peptide YY (PYY) and cholecystokinin (CCK). Both PYY and CCK are anorexigenic gut hormones secreted postprandially from the distal gut and proximal small intestine, respectively, and act on central and peripheral pathways to enhance satiety and decrease meal size. Tirzepatide appears to augment the secretion or activity of these hormones, likely through delayed gastric emptying and enhanced nutrient sensing in the gut. This secondary hormonal modulation reinforces appetite suppression, contributes to reduced energy intake, and may play a role in the agent pronounced effects on weight reduction and maintenance.
Successful Management of Facial Pigmentation with Multimodal Therapeutic Approach
Dr. Manoj Agarwala
MBBS, MD (CMC Vellore)
Fellowship in Lasers & Aesthetics
Medical Director and Principal Dermatologist
M A Skin & Hair Superspecialty Clinic
Raipur, Chhattisgarh
Abstract Introduction
A 32-year-old male presented with a two-month history of progressive facial hyperpigmentation localized to the malar and nasal regions. Dermatoscopic evaluation confirmed predominantly epidermal pigmentation with well-defined borders, indicative of melanin deposition in the basal layer. A multimodal treatment protocol was implemented, integrating topical therapies, oral tranexamic acid, and procedural interventions, including Q-switched Nd:YAG laser therapy, a glycolicmandelic acid peel, and a peel incorporating azelaic acid, kojic acid, phytic acid, and ascorbic acid. At the six-month follow-up, the patient exhibited significant and sustained improvement in pigmentation, with no adverse effects or recurrence. This case highlights the efficacy of a tailored, multimodal therapeutic strategy in managing melanininduced dyschromia and emphasizes the importance of individualized treatment plans in achieving optimal clinical outcomes while prioritizing
patient satisfaction and longterm pigment control.
Facial hyperpigmentation is a prevalent dermatological ......... condition that significantly impacts patients’ aesthetic appearance and psychological well-being. Conditions such as melasma, post-inflammatory hyperpigmentation (PIH), and solar lentigines arise from excessive melanin production or deposition, often triggered by ultraviolet (UV) exposure, hormonal fluctuations, or inflammatory processes. Effective management requires a comprehensive understanding of melanogenesis and a strategic approach that addresses multiple pathways of pigment production and deposition.
This case report details the successful treatment of facial hyperpigmentation in a 32-yearold male using a multimodal approach that combined topical therapies, oral tranexamic acid, and procedural interventions,
including the addition of a peel containing key actives like azelaic acid, kojic acid, phytic acid, and ascorbic acid. The integration of these modalities targeted various aspects of melanogenesis, resulting in significant clinical improvement and high patient satisfaction. This case serves as a model for clinicians aiming to develop effective, patientcentered strategies for managing hyperpigmentation disorders.
Clinical History
Patient Demographics
• Age/Gender: 32-year-old male
• Primary Complaint: Progressive hyperpigmentation over the malar and nasal regions for two months.
• Past Medical History: No significant dermatological or systemic illnesses, including diabetes, thyroid disorders, or autoimmune conditions, were reported.
• Family History: No family history of hyperpigmentation disorders, such as melasma or pigmentary demarcation lines.
• Social and Environmental History: The patient reported moderate sun exposure due to outdoor activities but denied using photosensitizing medications or topical agents that could exacerbate pigmentation. He had no history of smoking or excessive alcohol consumption.
• Previous Treatments: The patient had not sought prior treatment for the condition and had not used over-the-counter products or home remedies before consultation.
Clinical Presentation
The patient presented with symmetrical, dark brown
hyperpigmented patches localized to the malar (cheek) and nasal regions. The lesions were asymptomatic, with no associated itching, pain, or inflammation. The pigmentation had progressively worsened over two months, particularly following unprotected sun exposure, and was reported to cause significant cosmetic concern.
Dermatoscopic Findings
Dermatoscopic examination revealed:
• Predominantly epidermal hyperpigmentation, ............... characterized by a uniform brown pigment network with well-demarcated borders.
• Evidence of melanin deposition in the basal layer of the epidermis, with minimal to no dermal involvement.
• No atypical pigment networks or features suggestive of malignancy, such as asymmetry or irregular borders.
These findings suggested a benign, epidermal form of hyperpigmentation, likely melasma, exacerbated by UV exposure. The absence of significant dermal pigmentation facilitated the use of topical and superficial procedural therapies.
Diagnosis
The clinical and dermatoscopic findings supported a provisional diagnosis of epidermal hyperpigmentation, likely melasma, triggered by UV exposure. Differential diagnoses included post-inflammatory hyperpigmentation and solar lentigines, but the symmetrical distribution, lack of preceding inflammatory events, and localization to sun-exposed
areas favored melasma as the primary diagnosis.
Treatment Plan
A multimodal treatment protocol was designed to target multiple pathways of melanogenesis, incorporating topical therapies, oral systemic therapy, and procedural interventions, including a peel containing key actives like azelaic acid, kojic acid, phytic acid, and ascorbic acid. The plan emphasized patient education and longterm maintenance to prevent recurrence.
Topical Therapy
Topical agents were selected to inhibit melanin synthesis, promote keratinocyte turnover, and protect against UV-induced damage:
• Depigmenting Agents: A combination of kojic acid (2%) and niacinamide (4%) was prescribed for twicedaily application. Kojic acid inhibits tyrosinase, a key enzyme in melanin synthesis, while niacinamide reduces melanosome transfer from melanocytes to keratinocytes, promoting an even skin tone.
• Sun Protection: A broadspectrum sunscreen (SPF 50+ with PA+++) was recommended for daily use, reapplied every three to four hours during sun exposure to prevent UV-induced melanogenesis.
• Cleansing Routine: A benzoyl peroxide-based cleanser (4%) was incorporated to maintain skin hygiene, reduce sebum production, and prevent comedogenesis, which could complicate the clinical picture by causing acne-related inflammation.
Oral Therapy
• Tranexamic Acid: The patient was prescribed tranexamic acid (500 mg once daily at night) for three months. Tranexamic acid inhibits plasminogen activation, reducing the release of melanocyte-stimulating factors such as arachidonic acid and prostaglandins, addressing the vascular and inflammatory components of hyperpigmentation.
Procedural Interventions
Procedural interventions were employed to accelerate pigment clearance and enhance the efficacy of topical and oral therapies:
• Q-switched Nd:YAG Laser
Therapy: Two sessions were performed at four-week intervals using a Q-switched Nd:YAG laser (1064 nm wavelength). This laser delivers short pulses of energy to fragment melanin particles in the epidermis, allowing their clearance by phagocytosis. Fluences were adjusted (2–3 J/cm²) to minimize the risk of post-inflammatory hyperpigmentation, particularly given the patient’s likely Fitzpatrick skin type III.
• Glycolic-Mandelic Acid
Peel: One session of a chemical peel combining glycolic acid (20%) and mandelic acid (10%) was performed. These alpha-hydroxy acids exfoliate the stratum corneum, promote keratinocyte turnover, and facilitate the removal of pigmented cells. The peel was applied for a controlled duration to avoid irritation, followed by post-peel care with soothing agents.
• Combination of Azelaic Acid, Kojic Acid, Phytic Acid and Ascorbic Acid Peel: One session of a this was added to the treatment regimen. This peel is a professional depigmenting treatment containing a combination of active ingredients, including azelaic acid, kojic acid, arbutin, and phytic acid. This peel inhibits tyrosinase activity and disrupts melanin synthesis while promoting gentle exfoliation. This peel was applied in-clinic under controlled conditions, with the mask left on for 8–12 hours as per protocol, followed by a home-care regimen using pigment control solutions maintenance cream to sustain depigmentation. The peel was strategically timed two weeks after the first laser session to complement the procedural sequence and maximize pigment reduction.
Maintenance Therapy
A long-term maintenance regimen was instituted to sustain results and prevent recurrence:
• Depigmenting Kit: A kit containing azelaic acid (10%) and arbutin (5%) was prescribed for nightly use, alongside the pigment control solutions maintenance cream applied as per the peel protocol. These agents continue to inhibit melanin synthesis and provide anti-inflammatory benefits.
• Antioxidants: Topical vitamin C (15%) serum was incorporated into the morning routine to neutralize free radicals, enhance photoprotection, and support collagen synthesis.
• Follow-Up Schedule: Monthly follow-ups were scheduled to monitor progress,
assess for adverse effects, and reinforce adherence to the maintenance protocol. The patient was educated on the importance of consistent sunscreen use and avoiding triggers such as excessive sun exposure.
Outcome
At the six-month followup, the patient demonstrated significant improvement in facial hyperpigmentation:
• A marked reduction in the size and intensity of hyperpigmented patches, with the malar and nasal regions appearing significantly lighter and more uniform in tone.
• No adverse effects, such as irritation, post-inflammatory hyperpigmentation, or scarring, were observed, indicating the safety of the multimodal approach, including the combination of azelaic acid, kojic acid, phytic acid, and ascorbic acid peel.
• No recurrence of pigmentation, attributed to the patient’s adherence to the maintenance regimen, including the pigment control cream and strict sun protection.
• Patient Satisfaction: The patient reported high satisfaction with the aesthetic outcome, noting improved self-confidence and quality of life due to the visible improvement in skin tone.
The addition of the combination of azelaic acid, kojic acid, phytic acid, and ascorbic acid peel likely contributed to the rapid and sustained pigment reduction, as its combination of depigmenting agents complemented the effects of the laser and glycolic-mandelic peel.
Successful
Discussion
Pathophysiology of Hyperpigmentation:
Hyperpigmentation results from excessive melanin production or deposition, driven by melanocyte activation in response to stimuli such as UV radiation, hormonal changes, or inflammation. In melasma, the likely diagnosis in this case, epidermal pigmentation predominates, with melanin accumulating in the basal layer. The symmetrical distribution and UV-related
exacerbation observed in this patient align with melasma’s characteristic features. The absence of significant dermal pigmentation simplified the treatment approach, as epidermal melanin is more responsive to topical and superficial procedural therapies.
Rationale for Multimodal Therapy
The multimodal approach targeted multiple pathways of melanogenesis:
• Topical Therapies: Kojic acid and niacinamide inhibit tyrosinase and melanosome transfer, respectively, while sunscreen prevents UV-induced melanocyte activation. Benzoyl peroxide maintains skin hygiene, reducing the risk of inflammationrelated pigmentation.
• Oral Tranexamic Acid: By inhibiting plasminogen activation, tranexamic acid reduces vascular and inflammatory triggers of melanogenesis, particularly relevant in melasma.
Figure 1: After 6 month of treatment marked reduction in the size and intensity of hyperpigmented patches
• Procedural Interventions:
The Q-switched Nd:YAG laser fragments melanin for phagocytic clearance, while the glycolic-mandelic peel promotes exfoliation and pigment removal. The combination peel of azelaic acid, kojic acid, phytic acid and ascorbic acid enhances these effects by combining multiple depigmenting agents to inhibit tyrosinase and promote epidermal renewal. Its prolonged contact time and subsequent maintenance cream ensure sustained pigment suppression.
• Maintenance Therapy:
Azelaic acid, arbutin, pigment control cream and vitamin C provide ongoing inhibition of melanin synthesis and protection against environmental triggers, while regular follow-ups ensure adherence.
Role of the combination of Azelaic Acid, Kojic Acid, Phytic Acid and Ascorbic Acid peel
The combination peel of azelaic acid, kojic acid, phytic acid and ascorbic acid is a specialized depigmenting treatment designed to address hyperpigmentation, particularly melasma. Its active ingredients target multiple steps in melanogenesis:
• Azelaic Acid: Inhibits tyrosinase and has antiinflammatory properties, reducing melanocyte stimulation.
The combination of Azelaic Acid, Kojic Acid, Phytic Acid
and Ascorbic Acid peel’s inclinic application, followed by the pigment control solutions maintenance cream, ensures both immediate and long-term depigmentation. In this case, the peel complemented the laser and glycolic-mandelic peel by providing a broader spectrum of depigmenting action, contributing to the rapid and sustained improvement observed.
Clinical and Psychological Benefits
The multimodal approach, enhanced by the combination of Azelaic Acid, Kojic Acid, Phytic Acid and Ascorbic Acid peel, resulted in comprehensive pigment reduction, addressing both aesthetic and psychological concerns. Facial hyperpigmentation can cause significant emotional distress, and the patient’s improved self-confidence underscores the importance of effective treatment in enhancing quality of life.
Challenges and Considerations
Managing hyperpigmentation involves challenges such as recurrence risk, potential side effects, and variability in patient response. The combination of Azelaic Acid, Kojic Acid, Phytic Acid and Ascorbic Acid peel, while effective, requires careful patient selection and post-treatment care to avoid irritation or sensitivity. The patient’s likely Fitzpatrick skin type III and adherence to postpeel protocols minimized these risks. Patient education on sun protection and maintenance therapy was critical to preventing recurrence, as melanogenesis
pathways remain reactive to environmental triggers.
Broader Implications
This case demonstrates the value of a multimodal, individualized approach in dermatology. The addition of the combination of Azelaic Acid, Kojic Acid, Phytic Acid and Ascorbic Acid peel enhanced the efficacy of the treatment protocol, providing a robust option for managing epidermal hyperpigmentation. This paradigm—integrating topical, systemic, and procedural interventions—can serve as a template for treating similar cases, including melasma and mild PIH. Future research should explore optimizing the sequencing of procedural interventions and the longterm efficacy of combination of Azelaic Acid, Kojic Acid, Phytic Acid and Ascorbic Acid peel in diverse skin types.
Conclusion
The successful management of facial hyperpigmentation in this 32-year-old male highlights the efficacy of a multimodal therapeutic approach integrating topical therapies, oral tranexamic acid, Q-switched Nd:YAG laser therapy, a glycolic-mandelic acid peel, and a combination of Azelaic Acid, Kojic Acid, Phytic Acid and Ascorbic Acid peel. The treatment protocol effectively targeted melanogenesis, resulting in significant and sustained pigment reduction without adverse effects. This case underscores the importance of individualized, evidencebased strategies and the critical role of maintenance therapy,
including the pigment control cream, in preventing recurrence. By combining scientific rigor with patient-centered care, clinicians can achieve optimal outcomes in managing complex dermatological conditions.
Conflict of Interest
None declared.
References
1. Ibrahim MI, Abdallah TN, El Husseiny RM, Abdel Fattah NS. Evaluation of microneedling followed by tranexamic acid cream versus solution in melasma: split-face study. QJM. 2023;116(Suppl 1):hcad069.224.
2. Feng X, Su H, Xie J. Efficacy and safety of microneedling with topical TXA for melasma: systematic review and metaanalysis. J Cosmet Dermatol. 2024;15965.
3. Sharaf F, et al. Oral tranexamic acid and microneedling in melasma
management. J Am Acad Dermatol. 2020.
4. Hofny A, et al. Comparative study of fractional CO2, microneedling-assisted TXA delivery in melasma. Arch Dermatol Res. 2025.
5. Pillaiyar T, Manickam M, Namasivayam V. Tyrosinase inhibitors: azelaic acid and kojic acid perspectives. J Enzyme Inhib Med Chem. 2017;32:……
6. Draelos ZD. A review on azelaic acid vs hydroquinone in melasma. Dermatol Ther. 2007;20:……
7. Farhang S. Cosmelan peel: blend of azelaic, kojic, phytic, ascorbic acids for stubborn pigmentation. RealSelf. 2023.
8. Self A. Vitamin C in hyperpigmentation management. Br J Dermatol. 2023;…
9. Allure. Topical TXA for melasma. Allure.com. 2023.
Microneedling and PRP for Acne Scar Eradication: A Case Report
Dr. Nandita Rai
MBBS,
MD (Dermatology and Clinical Cosmetology)
Cosmetic Dermatologist
West Bengal
Introduction
Acne scars arise due to tissue damage during the healing process of severe or untreated acne lesions. They are broadly classified into atrophic scars, characterized by a loss of collagen, and hypertrophic scars, involving excess collagen deposition.1 Atrophic scars, more prevalent than hypertrophic and keloidal scars at a ratio of 3:1, it include distinct subtypes ice pick scars, which are narrow and deep like small punctures; boxcar scars, round to oval depressions with well-defined edges similar to scars from chickenpox, with shallow ones under 3 mm and deep ones 3 mm or larger; and rolling scars, wider depressions with a rolling or undulating appearance due to dermal tethering. Hypertrophic scars manifest as raised, firm lesions within the original injury site, typically appearing pinkish and possibly regressing over time. Keloid scars extend beyond the initial injury boundaries, presenting as reddish-purple papules or nodules, more common in darker skin tones and often on the trunk.2
The pathogenesis of acne
begins with several contributing factors, including increased sebum production, altered sebum lipids, and androgen activity, which collectively lead to follicular hyperkeratinization and proliferation of Propionibacterium acnes (P. acnes). Sebaceous gland lipids, such as neutral and polar lipids, play essential roles in signaling pathways and can exhibit both pro- and anti-inflammatory properties. Fatty acids act as ligands for nuclear receptors like PPARs (Peroxisome proliferatoractivated receptors), influencing sebocyte activity and differentiation. P. acnes further complicates the inflammatory response by activating keratinocytes and sebocytes via Toll-like receptors (TLR), CD14, and CD1 molecules. This activation triggers a cascade of events, including the production of cytokines and chemokines by macrophages expressing TLR2, exacerbating the inflammatory process within pilosebaceous follicles. This inflammatory milieu contributes to follicular rupture and perifollicular abscess formation, which are pivotal in the pathogenesis of acne scars. The wound healing process
in acne scars progresses through distinct stages: inflammation, granulation tissue formation, and matrix remodeling. In the inflammatory stage, vasoconstriction followed by vasodilation and erythema occurs, stimulating melanogenesis and potentially leading to postacne erythema and hyperpigmentation. Activated immune cells such as granulocytes, macrophages, neutrophils, lymphocytes, and platelets release inflammatory mediators that prepare the site for subsequent tissue repair.3
During granulation tissue formation, damaged tissues are repaired, and new capillaries form. Monocytes differentiate into macrophages, releasing growth factors like plateletderived growth factor (PDGF), fibroblast growth factor (FGF), and transforming growth factors α and β, which stimulate fibroblast migration and collagen production. Initially, type III collagen predominates, but over time, the balance shifts towards type I collagen, similar to unwounded skin. However, an imbalance in collagen turnover, mediated by metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs), can lead to abnormal scar formation. Matrix remodeling involves the orchestrated action of fibroblasts and keratinocytes producing MMPs that degrade and remodel the extracellular matrix (ECM). Dysregulation in MMPs and TIMPs (The tissue inhibitors of metalloproteinases) can result in either inadequate collagen deposition and atrophic scars or excessive collagen accumulation leading to hypertrophic scars or keloids.3
Advancements in diagnostic tools and treatment options are continuously improving our ability to manage acne scars. By employing comprehensive assessments and tailored treatment plans, dermatologists can enhance both the aesthetic outcomes and quality of life for individuals affected by this condition.
Case Report
A 34-year-old male patient with a history of acne and acne scars since adolescence presented with oily skin. His lifestyle included smoking one pack of cigarettes daily, stress, insufficient sleep, regular gym attendance, and a good diet. He had no significant family or allergy history. The Initial acne management involved the use of benzoyl peroxide (BPO), adapalene, clindamycin, and an anti-pigmentation cream, along with oral antibiotics, as prescribed by different dermatologists. Laboratory investigations, including complete blood count (CBC), lipid profile, liver function test (LFT), urea, creatinine, fasting blood sugar (FBS), post prandial blood sugar test (PPBS), and tests for hepatitis C and HIV, were all within normal limits. After considering all these points, we decided to treat the patient with microneedling and PRP. Treatment started, followed by 3 sessions at 2-3 month intervals. Within a year, the patient's condition was improved more than 50% along with niacinamide lactic acid and anti-inflammatory cream two times daily along with anti-acne moisturizer and anti-acne sunscreen 2-3 times daily along with multivitamin capsules. And life style management and less smoking and maintenance of sleeping time, were also emphasized.
Before treatment
Figure 1: Acne scars on cheeks
After treatment
Microneedling and PRP for Acne Scar Eradication:
Diagnosis
The ECCA (Echelle de Evaluation Clinique des Cicatrices d’Acné), or Clinical Evaluation Scale for Acne Scars, is a widely utilized tool for assessing facial acne scarring. It provides a comprehensive and quantitative method for evaluating the severity and characteristics of acne scars. The ECCA scale is designed to objectively measure the extent and impact of acne scarring, focusing on various morphological aspects. ECCA allows for precise measurement of scar severity, incorporating specific criteria to evaluate different scar types and their impact. The scale categorizes scars based on their morphology, including depressed scars often resulting from loss of dermal tissue. Hypertrophic scars raised scars due to excessive collagen production. Keloidal scars a more severe form of raised scars that extends beyond the original wound boundaries. It involves a detailed clinical examination to assess the depth, width, and texture of the scars. The ECCA (Echelle de Evaluation Clinique des Cicatrices d’Acné) employs a detailed scoring system to assess acne scars based on predefined criteria. Each scar is rated according to several key factors which includes severity, which evaluates the degree of scar depression or elevation relative to the surrounding skin; area affected, which measures the size and extent of the scarred region; and texture changes, which assesses the smoothness or roughness of the scar surface. This structured approach allows for a comprehensive evaluation of scar characteristics and severity. The ECCA is useful for evaluating baseline
scar severity and monitoring changes over time following treatments. It helps in comparing the effectiveness of different therapeutic interventions.4
The Global Severity Scale is a comprehensive six-category tool for the overall assessment of acne scars, offering a holistic view of scar severity by evaluating various aspects of scarring. It categorizes scars as follows: No Scarring, indicating an absence of visible scars; Mild Scarring, where scars are barely noticeable and have minimal impact on skin appearance; Moderate Scarring, with noticeable scars that do not significantly alter overall skin texture or appearance; Severe Scarring, characterized by pronounced scarring affecting a substantial portion of the skin, impacting texture and appearance; Very severe scarring, with extensive scarring causing significant texture changes and high visibility; and extreme scarring, involving severe scarring with profound effects on skin texture and appearance, potentially affecting functionality. Key features of this scale include its holistic evaluation of the overall impact on appearance and texture, and its combination of visual inspection with physical evaluation. The scale is essential for treatment planning, helping to determine appropriate strategies based on scar severity, and for outcome measurement, tracking the effectiveness of different treatment modalities over time.4
Morphological evaluation of acne scars focuses on their physical characteristics to assess types and severity. This detailed analysis involves examining scar attributes such as shape, texture,
and depth. Key assessment criteria include identifying scar type (atrophic, hypertrophic, or keloidal), measuring the degree of depression or elevation relative to surrounding skin, evaluating surface texture (smoothness, roughness, or irregularities), and assessing the size and overall affected area. Techniques used in this evaluation include clinical examination through visual and tactile methods, and photography and imaging with high-resolution technology to document and analyze scar characteristics. The application of morphological evaluation is crucial for selecting tailored treatment options based on scar morphology and for monitoring progress by tracking changes in scar characteristics over time, particularly in response to treatment.4
Diagnosing acne scars involves assessing both physical aspects, using standardized tools and considering the patient's history and lifestyle. Early, personalized treatment and lifestyle changes can greatly enhance scar appearance.
Treatment
Managing acne scars requires a systematic, algorithmic approach that targets each type of scar. Treatments should focus on atrophic scarring, tailored to whether scars are generalized or isolated. A personalized combination of therapies offers the best chance for significant improvement.
Keloid scars can be treated with tretinoin 0.05%, which promotes epidermal hyperplasia and collagen production, enhancing skin firmness. For active acne, adapalene/
benzoyl peroxide gel normalizes follicular cell differentiation and reduces inflammation but has limited impact on acne scars.
Tazarotene accelerates skin turnover, improving texture and stimulating collagen production, benefiting superficial scars. Vitamin C aids in healing and treating atrophic scars by enhancing collagen metabolism, promoting fibroblast activity, reducing inflammation, and improving hyperpigmentation. Laser resurfacing, including ablative and fractional types, effectively treats acne scars. Ablative lasers like CO2 and Er:YAG remove damaged tissue and stimulate collagen production, while fractional lasers offer precise treatment with less downtime. Nonablative lasers improve skin texture and color without removing layers. Chemical peels and dermabrasion/ microdermabrasion enhance skin texture and stimulate collagen, with treatment tailored to scar severity. Fractional photothermolysis uses microbeams to create thermal zones, stimulating collagen for minimal downtime. Punch techniques, dermal grafting, fat transplantation, and subcision each offer unique benefits for different scar types and can be combined for optimal results.5,6
Microneedling is a therapeutic technique used to treat acne scars by improving skin texture and reducing their appearance. The procedure involves a device with fine needles that create controlled micro-injuries in the skin's surface layers. These micro-injuries stimulate the skin's natural healing response, triggering the production of
collagen and elastin fibres. This collagen induction therapy is particularly effective for atrophic scars, such as depressions or pits in the skin, by promoting collagen synthesis that fills in these imperfections and smoothest overall skin texture. Multiple sessions of microneedling, spaced several weeks apart, are typically recommended to achieve noticeable improvements in acne scars. Additionally, microneedling enhances the absorption and effectiveness of topical treatments like vitamin C serums or growth factors, which further support skin regeneration and scar remodelling.6
Platelet-Rich Plasma (PRP) therapy uses a concentration of platelets derived from the patient’s own blood to treat acne scars. The procedure involves drawing a small amount of blood, which is then processed in a centrifuge to isolate the PRP, rich in growth factors and proteins. This PRP is injected into the scarred areas, promoting healing and tissue regeneration by stimulating collagen production and improving skin texture. With minimal invasiveness and low risk of side effects, PRP therapy leverages the patient’s own biological material for effective scar reduction. It is often combined with other treatments, such as microneedling or laser therapy, to enhance results and address various aspects of acne scarring.6 Stem cell therapy is an emerging treatment for acne scars that utilizes the regenerative potential of stem cells to enhance skin appearance. The process typically involves isolating stem cells from the patient's own
tissue, such as fat or bone marrow, or using cultured stem cells from a donor source. These stem cells are then injected into scarred areas or applied topically to stimulate healing and tissue regeneration, secrete growth factors that promote collagen production, repair damaged tissue, and improve skin texture.7 Combined therapy for acne scars uses multiple treatments, such as laser resurfacing, chemical peels, dermabrasion, microneedling, and fillers, to address different aspects of scarring. This combined approach enhances skin texture, boosts collagen production, and addresses both superficial and deep scars, offering tailored and effective treatment for the best possible outcomes.7 Intralesional steroid therapy is an effective treatment for hypertrophic and keloid acne scars, involving the direct injection of corticosteroids into the scar tissue. This method works by reducing inflammation and curbing excessive collagen production, which helps flatten and soften raised scars. The procedure is minimally invasive and frequently results in substantial enhancement of scar appearance and texture, while mitigating associated symptoms such as pruritus or sensitivity.2 Early intervention in active acne is crucial to prevent or minimize acne-related scarring. It is essential to ensure that active acne lesions are effectively treated before initiating scar treatment to avoid a cycle where ongoing lesions continue to scar in previously treated areas. This sequential approach ensures comprehensive management and better outcomes in scar reduction therapies.
Microneedling and PRP for Acne Scar Eradication: A
Discussion
Acne scarring typically occurs during the peak period of active acne, which predominantly affects individuals between the ages of 14 and 19. Active acne during adolescence and young adulthood serves as the primary precipitant for psychosocial stressors linked to acne scars. Adolescence represents a critical developmental phase marked by the formation of self and social identities, during which the brain undergoes considerable structural and functional maturation. This developmental stage renders individuals more susceptible to mental health issues. In contrast to congenital disfigurements, acquired disfigurements such as acne scars are more susceptible to the impact of coping mechanisms developed in response to initial appearance changes. Consequently, early and effective management of active acne is the most effective strategy to prevent the formation of acne scars and alleviate the psychological stressors associated with active acne. A survey involving 250 adolescents and young adults aged 13–25 with moderate to severe acne vulgaris demonstrated a significant correlation between acne severity and disturbances in body image. This finding underscores the unique vulnerabilities of adolescents, including ongoing brain development and heightened sensitivity to environmental stressors, which contribute to a higher prevalence of psychiatric conditions during this developmental period. Early intervention addressing dysfunctional body image and low self-esteem is crucial for
mitigating the mental health impacts associated with acne scarring. In addition to physical manifestations, psychological disturbances may arise due to the neuromodulator effects of prescription acne therapies, particularly isotretinoin. As an oral retinoid indicated for severe, treatment-resistant acne, isotretinoin interacts with retinoic acid receptors (RARs) in the central nervous system, potentially disrupting serotonin signalling pathways and predisposing patients to depressive symptoms. These psychological effects can persist beyond the course of treatment. Additionally, isotretinoin may impede the healing process and increase the likelihood of atypical acne scarring, thereby exacerbating patient distress and contributing to a sense of medical disillusionment.8
Patients with acne scarring experience significantly elevated levels of depressive symptoms, anxiety, and suicidal tendencies. These psychiatric comorbidities are characterized by a high likelihood of recurrence, suggesting that the resolution of active acne does not necessarily end concurrent psychopathological issues. Research indicates that individuals with acne scarring often exhibit enduring "cognitive scars," similar to those described by Aaron Beck in depression, which increase the risk of recurrence. Major depressive disorder has a 50% recurrence rate after a single episode and 80% after multiple episodes, while generalized anxiety disorder has a 45% recurrence rate. These high recurrence rates are exacerbated by
maladaptive thought patterns formed through persistent negative self-conceptualizations. Even after overcoming anxiety or depression, individuals with a history of mental illness may have significantly lower self-esteem compared to those without such a history. This underscores the potential for acne scarring to cause lasting emotional stress that contributes to chronic psychiatric dysfunction. Thus, early and consistent mental health management is essential to reframe negative cognitions and prevent the recurrence of psychiatric disorders associated with acne scarring.8
Key challenges in the prevention of acne scarring include time constraints during consultations, insufficient physician-patient communication, and poor adherence to treatment regimens. It is crucial to foster an environment where patients feel comfortable discussing their acne scarring and to instill optimism regarding the prevention of future scarring. Many patients are hesitant to initiate discussions about long-term treatment options, potentially due to a lack of understanding of the pathophysiology of acne scarring. Educating patients on the mechanisms of acne scarring—such as the role of inflammation and bacterial colonization—through visual aids like diagrams can enhance their comprehension and motivation for early and sustained intervention. While knowledge transfer from physicians to patients can be challenging, nurses can play a pivotal role in patient education, especially when consultation time is limited. Additionally, social
media influencers can serve as valuable role models, particularly for younger patients. Recent advances in understanding the pathophysiology of acne scarring, including the impact of bacterial colonization of microcomedones, underscore the need for thorough evaluation and early, continuous treatment of inflammation to prevent scarring. Therefore, incorporating the risk of acne scarring into initial treatment plans and promoting adherence
References
1. Connolly D, Vu HL, Mariwalla K, Saedi N. Acne Scarring-Pathogenesis, Evaluation, and Treatment Options. J Clin Aesthet Dermatol. 2017; 10(9):12-23.
2. Jfri A, Alajmi A, Alazemi M, Ladha MA. Acne Scars: An Update on Management. Skin Therapy Lett. 2022; 27(6):6-9.
3. Fabbrocini G, Annunziata MC, D'Arco V, et al. Acne scars: pathogenesis, classification and treatment. Dermatol Res Pract. 2010; 2010:893080. doi:10.1155/2010/893080.
4. Tanizaki H, Tanioka M, Yamashita Y, Hayashi N. Quantitative evaluation
to treatment regimens are essential for optimizing patient outcomes.9
Conclusion
Acne scarring is a prevalent complication affecting numerous patients with acne vulgaris, prompting many to pursue various therapeutic interventions for enhanced cosmetic outcomes. Treatment should start with addressing residual erythema, followed by targeted interventions for atrophic scars based on their type. Solitary scars may benefit from surgical techniques or fillers, while extensive scarring often requires lasers and resurfacing treatments. Integrating multiple modalities, guided by ongoing research and tailored to individual needs, ensures optimal cosmetic outcomes and patient satisfaction. A thorough understanding of scar types and a personalized treatment strategy are essential for success.
of atrophic acne scars using 3D image analysis with reflected LED light. Skin Res Technol. 2020; 26(1):20-24. doi:10.1111/ srt.12756.
5. Bikash C, Sarkar R. Topical management of acne scars: The uncharted terrain. J Cosmet Dermatol. 2023; 22(4):1191-1196. doi:10.1111/jocd.15584.
6. Chilicka K, Rusztowicz M, Szyguła R, Nowicka D. Methods for the Improvement of Acne Scars Used in Dermatology and Cosmetology: A Review. J Clin Med. 2022;11(10):2744. Published 2022 May 12. doi:10.3390/jcm11102744.
7. Gozali MV, Zhou B. Effective treatments of atrophic acne scars. J Clin Aesthet Dermatol. 2015; 8(5):33-40.
8. Zhou C, Vempati A, Tam C, et al. Beyond the Surface: A Deeper Look at the Psychosocial Impacts of Acne Scarring. Clin Cosmet Investig Dermatol. 2023; 16:731-738. Published 2023 Mar 25. doi:10.2147/CCID.S406235.
9. Dréno B, Stein Gold L. Acne Scarring: Why We Should Act Sooner Rather Than Later. Dermatol Ther (Heidelb). 2021; 11(4):1075-1078. Doi: 10.1007/s13555021-00562-4 Microneedling and PRP for Acne Scar Eradication: A Case Report
Five Clinical Subtypes Identified in Vitiligo Cohort
An observational study has applied advanced factor analysis and clustering techniques to classify individuals with nonsegmental vitiligo into five distinct clinical phenotypes, moving beyond traditional lesion-based groupings. The identified clusters include highly active disease with trichrome and confetti patterns, mild disease, widespread chronic depigmentation, and two types associated with Koebner phenomenon. Notably, the "highly active" group, characterized by rapid progression and pruritus, may benefit from early systemic intervention, while patients with extensive, longstanding disease and leukotrichia may require intensified therapeutic strategies despite limited current options. This refined phenotype-based classification promises to guide more personalized treatment approaches, although further validation using patient-reported outcomes and molecular profiling is needed to optimize clinical utility.
Innovative Stem Cell Hair Serum Enhances Hair Loss Treatment When Used with Minoxidil.
A real-world study suggests that combining a stem cell–based hair serum with topical minoxidil may significantly improve outcomes in patients with mild to moderate androgenetic alopecia and female pattern hair loss. The multicenter, prospective, parallel-arm observational study included adult patients diagnosed with progressive hair loss for more than six months. Participants were randomized to receive either minoxidil alone or minoxidil combined with the botanical peptide-rich serum. After a course of twice-daily topical application over several weeks, those using the combination therapy showed greater improvement, with a noticeable reduction in hair shedding, lower scores in the Hair Pull Test, and better photographic hair density outcomes compared to minoxidil alone. No adverse effects were reported, indicating a favourable safety and tolerability profile. Though limited by a small sample size and short duration, the findings suggest that adding a plant-based, peptide-enhanced serum to minoxidil therapy may enhance efficacy, reduce side effects, and offer a safer, more holistic treatment approach for hair loss.
Three-Component Topical Therapy Proven Effective and Safe for Long-Term Acne Treatment
A recent study presented at a dermatologic conference evaluated the long-term safety and efficacy of a triple-combination fixeddose topical therapy containing clindamycin phosphate, adapalene, and benzoyl peroxide for the treatment of moderate to severe acne vulgaris. This open-label, single-center trial included adolescent and adult patients with a baseline Investigator Global Assessment (IGA) score indicating moderate to severe disease. Participants applied the topical therapy once daily over an extended treatment period representative of real-world use. The results demonstrated significant and sustained improvements in both inflammatory and noninflammatory lesion counts, beginning early in the course of therapy and continuing throughout the treatment period. Improvements were also noted in acne-related sequelae, including scarring, postinflammatory hyperpigmentation, and erythema. Notably, postinflammatory pigmentation and erythema were substantially reduced, and facial scarring improved over time. Skin dryness remained stable, and no adverse events or issues with tolerability were observed, with minimal scores reported for redness, burning, itching, and swelling. These findings affirm the extended safety and efficacy of this triplecombination topical agent, supporting its use as an effective long-term treatment option for patients with acne vulgaris.
LED daylight photodynamic combination therapy shows strong efficacy in treating actinic keratosis among immunocompromised patients.
A prospective, randomized study evaluated the efficacy of combining LED illumination with daylight photodynamic therapy in immunocompromised patients with actinic keratosis, particularly solid organ transplant recipients. Conducted on patients with multiple facial or scalp lesions, the trial demonstrated greater lesion reduction in the group receiving combined therapy compared to daylight therapy alone. At follow-up, the combined group showed notably higher lesion clearance. Local skin reactions were slightly more pronounced in the dual-modality group but remained well-tolerated, with pain levels considered minimal. Patient satisfaction was high across both groups, though most expressed no strong preference between the two approaches. The findings suggest that residual photosensitizers following daylight exposure may be further activated by subsequent LED illumination, enhancing therapeutic outcomes. Future, more controlled studies can gather additional data to support the use of this therapy in a patient population that can often be challenging to treat.
Effectiveness of Radiofrequency (RF)
Ablation and CO2 Laser
Ablation
Therapy for Dermatosis Papulosa Nigra: A Case Report
Dr. Pragathi Sankineni
MBBS, MD, DVL
Consultant Dermatologist & Cosmetologist
Pragathi Skin & Cosmetology Clinic
Nizamabad, Telangana
Introduction
Dermatosis Papulosa Nigra (DPN) is a benign, hyper pigmented skin condition predominantly observed in individuals with darker skin tones. It is characterized by the presence of multiple small, dark papules that typically appear on the face and neck. Although DPN is generally harmless, it can be cosmetically concerning for those affected, leading to a demand for aesthetic interventions. Dermatosis Papulosa Nigra presents as multiple, small, asymptomatic papules ranging from 1 to 5 mm in diameter. These papules are usually smooth, dome-shaped, and have a dark brown to black coloration. They are most commonly found on the cheeks, periorbital areas, and the neck. In some cases, lesions may also appear on the upper back and chest. The condition typically emerges during early adulthood, and the number of papules often increases with age.1
The exact etiology of DPN
remains partially understood, but it is believed to involve a combination of genetic and environmental factors. There be an abnormal proliferation of melanocytes or other epidermal cells contributing to the formation of these papules. Genetic predisposition plays a significant role, as DPN is more prevalent in individuals with darker skin types, particularly those of African descent, and familial patterns suggest a possible autosomal dominant inheritance with variable expressivity. Additionally, a somatic activating mutation in the FGFR3 gene has been identified in DPN lesions, supporting the notion of shared genetic pathways between DPN and other skin conditions. The lesions often appear in photo exposed areas such as the head, neck, and upper trunk, leading to hypotheses about the role of cumulative ultraviolet (UV) exposure in their development. FGFR3 mutations are more frequent in sun-exposed regions and with age, and evidence
suggests that darker-skinned individuals who use topical depigmentation treatments may experience exacerbation of DPN, possibly due to decreased UV protection. These observations suggest that UV exposure may contribute to the pathogenesis of DPN.2 Studies indicate that individuals with lighter skin types within the population exhibit a lower frequency of DPN compared to those with Fitzpatrick skin type VI. There is a strong familial component to DPN, with positive family histories reported in 77% to 93% of cases. This condition shows a higher prevalence in women, who are twice as likely to be affected as men. DPN typically presents during adolescence, unlike seborrhoea keratosis (SKs), and can occasionally be observed in children as young as three years old. The number and size of DPN lesions tend to increase with age, with a peak incidence in the sixth decade of life. Although DPN is not associated with systemic diseases or syndromes, an eruptive form has been reported in conjunction with adenocarcinoma of the colon.2
Although the condition poses no significant health risks, individuals seeking aesthetic improvement may benefit from consultation with a dermatologist to discuss potential treatment options.
Case Report
A 50-year-old female patient presented with multiple firm, smooth, dark brown to black papules that were both flattened and elevated. These lesions, along with some skin tags, were predominantly located on the malar areas of her face. Based on these clinical findings, a
diagnosis of Dermatosis Papulosa Nigra (DPN) was confirmed. To treat the DPN, two advanced therapeutic options were considered: radiofrequency (RF) ablation and CO2 laser ablation therapy. RF ablation works by using high-frequency electrical currents to generate heat, effectively destroying the abnormal tissue without damaging the surrounding skin. This method offers precision and control, making it an ideal choice for treating small, raised lesions like those seen in DPN. On the other hand, CO2 laser ablation therapy uses a concentrated beam of carbon dioxide laser light to vaporize the upper layers of the skin, removing the papules with high accuracy. The CO2 laser's ability to target specific areas ensures minimal damage to the surrounding tissue and promotes faster healing. The patient underwent the chosen treatment and experienced significant improvement. The DPN lesions showed marked recovery, with a noticeable reduction in their appearance. This outcome highlights the effectiveness of both RF and CO2 laser ablation therapies in managing DPN, providing patients with smoother, clearer skin. The success of the treatment also underscores the importance of using advanced laser technologies in dermatological practice to achieve optimal results for skin conditions like DPN.
Before treatment
After treatment
Figure 1: Multiple firm, smooth, dark brown to black papules on face
Effectiveness
Diagnosis
The diagnosis of DPN is primarily based on clinical evaluation, with supplementary diagnostic tools used as needed to ensure accuracy and exclude other conditions.
Patient history is integral to diagnosing DPN, as it provides context that complements physical and dermatoscopic evaluations. Although the diagnosis primarily relies on the characteristic appearance of the lesions, a comprehensive patient history offers valuable insights. For instance, understanding when the lesions first appeared and their progression helps identify typical patterns of DPN, which usually begins in adulthood and may gradually increase in number or size. Furthermore, patients often describe DPN lesions as asymptomatic, consistent with the condition's benign nature. Information about previous skin conditions and treatments can also aid in distinguishing DPN from other similar lesions.2
Dermoscopy is an essential diagnostic tool for assessing dermatosis DPN. Through dermoscopic evaluation, DPN lesions typically exhibit uniform pigmentation, with a consistent dark brown to black colour and evenly distributed melanin within the epidermis, contributing to their dark appearance. The lesions have well-defined, sharp borders that distinguish them from those with irregular edges and usually feature a smooth surface, though some may appear slightly raised or verrucous. DPN lesions generally show minimal to no visible vascular structures, differentiating them from other
vascular or pigmented skin conditions. They are free of crusts or scales, maintaining a homogeneous appearance without internal variations in pigmentation. Dermoscopy does not reveal specific patterns like the "stellate" or "reticular" patterns seen in melanoma, and there are typically no significant changes in pigmentation or structure over time within the same lesion.2
Histopathological examination of DPN offers a detailed microscopic view of the lesion, revealing key findings that confirm the diagnosis and differentiate it from other skin conditions. Typically, DPN lesions exhibit increased melanin deposition in the basal layer of the epidermis, leading to dark pigmentation due to heightened melanocyte activity, while maintaining a normal epidermal structure without significant distortion or atypical changes. Some lesions may show mild to moderate acanthosis or papillomatosis, presenting a verrucous appearance, though this is usually benign. The dermis generally shows minimal involvement, with normal collagen and no atypical features or significant inflammation. DPN lesions typically lack prominent vascular structures, distinguishing them from other conditions with notable vascular patterns. Histopathological findings confirm the benign nature of DPN by revealing no atypical cells, malignancy, or invasive behaviour, and by not showing patterns associated with malignancy. Overall, these findings support the diagnosis of DPN and help exclude other conditions with similar clinical presentations.3
DPN is diagnosed as a typically benign condition. Treatment may be pursued for cosmetic or symptomatic reasons. The aim of the diagnosis is to confirm the benign nature of the lesions, ensuring accurate treatment planning and effective management tailored to patient needs.
Treatment
Scissor excision is a precise surgical modality employed for the management of DPN. This technique involves the utilization of small, curved scissors to meticulously excise individual DPN lesions and it allows for targeted removal of the papules, ensuring complete excision while preserving surrounding healthy tissue and minimizing potential damage. Cryotherapy is a prevalent therapeutic approach for dermatosis DPN, utilizing cryogenic agents, such as liquid nitrogen, to induce localized tissue destruction.4 This involves direct application of liquid nitrogen to the DPN lesions, resulting in their crystallization and subsequent necrosis. The application method may involve a spray device or a cotton-tipped applicator, with the duration of freezing ranging from a few seconds to several minutes, tailored to the size and depth of the lesions. Cryotherapy provides effective ablation of the targeted lesions through cryo-induced cellular damage, often resulting in complete lesion eradication. Electrodessication is an effective treatment modality for dermatosis papulosa nigra (DPN), employing highfrequency electrical currents to destroy unwanted skin lesions. The technique involves using
electrical currents to generate heat, which is applied to the DPN lesions, causing them to dry out and coagulate, leading to necrosis of the tissue. This procedure is carried out using an electrosurgical device with a fine electrode that makes contact with the lesion, delivering the electrical current. It is minimally invasive, often not requiring sutures, which reduces the risk of scarring and allows for a relatively quick recovery.4
The 532-nm potassium-titanylphosphate (KTP) laser and the 532-nm diode laser are effective treatments for DPN. The KTP laser uses green light to selectively target melanin in DPN lesions, causing photothermolysis and destroying pigmented cells while sparing surrounding tissue. It is applied in pulsed or continuous wave modes for a few minutes based on lesion size and number. Similarly, the 532-nm diode laser also targets melanin with green light, leading to precise destruction of pigmented cells with minimal tissue damage. Both lasers are minimally invasive, offer effective treatment with minimal downtime, and have a reduced risk of scarring, making those excellent options for managing DPN.4 The pulsed dye laser (PDL) effectively treats DPN by emitting light at 585–595 nm, which targets melanin in lesions, causing selective destruction of pigmented cells. The laser is applied in short pulses, customized to the lesion's characteristics, and the procedure usually takes just a few minutes. Q-switched and picosecond lasers with wavelengths like 532-nm, 694-nm, 755-nm, and 1064-
nm are also used for DPN. Their short pulse durations create photomechanical effects, which may help minimize post-inflammatory hyperpigmentation.5
Radiofrequency (RF) ablation is a technique used in the treatment of DPN. This method utilizes radiofrequency energy to heat and destroy targeted skin lesions. The procedure involves using RF energy to generate heat, delivered through a specialized electrode, which heats and vaporizes the pigmented cells within the DPN lesions, leading to their destruction. The RF ablation device is applied directly to the lesions, with settings such as power and duration adjusted according to the lesion’s size and depth. This approach ensures precise and tailored treatment for individual lesions.4
The Carbon Dioxide (CO2) laser is a well-established ablative technology used in the treatment of DPN, effective for various dermatologic conditions, including pigmented lesions. This laser emits a wavelength highly absorbed by water in the skin, leading to vaporization of the tissue. For DPN, the CO2 laser targets pigmented lesions by ablating the epidermis and part of the dermis, effectively removing melanin-containing cells and the lesion itself. The procedure involves using the CO2 laser with settings typically including a spot size of around 0.7 mm, power ranges of 0.50.7 W, and a pulse frequency of 10 Hz. The laser is applied in a controlled manner to the lesions, with treatment duration and intensity adjusted based on the size and depth of the lesions.4
The Neodymium-Doped Yttrium Aluminium Garnet (Nd-YAG) laser, emitting at 1064 nm, is used to treat dermatosis papulosa nigra (DPN) by targeting melanin in pigmented lesions. It works through selective photothermolysis, where the laser's heat causes coagulation and necrosis of melanincontaining cells. Typical settings include a 3 mm spot size, 145155 J/cm² energy levels, and a 20 ms pulse duration. The NdYAG laser is effective in pigment removal, minimally invasive, generally requires no anesthesia, and has a short recovery period. The Erbium-Doped 1550-nm Fractionated Laser is a nonablative resurfacing tool for DPN. It targets water in the skin with a 1550 nm wavelength, delivering fractional laser energy to create microthermal zones that stimulate collagen production and promote gradual removal of pigmented lesions. The treatment involves multiple passes (8-10) with energy levels of 60-70 mJ and a total energy range of 2.42-2.94 kJ over 3 sessions, preserving the epidermis and facilitating skin healing.4
Each of these modalities presents distinct advantages for the management of DPN, offering a spectrum of treatment approaches from minimally invasive to more aggressive interventions. These options can be customized based on patientspecific requirements and lesion attributes.
Discussion
DPN is a benign skin condition categorized as a variant of seborrheic keratoses. It is particularly prevalent among individuals of African descent
and is also commonly observed in Asian populations. Studies have reported that the incidence of DPN in populations with darker pigmentation ranges from 10% to 75%, reflecting its significant occurrence in these demographic groups.2
The differential diagnosis for DPN encompasses several conditions with overlapping features. Seborrheic keratoses, which are common benign skin tumors, can resemble DPN in appearance. Acrochordons, or skin tags, are small, benign growths that might be mistaken for DPN. Verrucae, or warts caused by human papillomavirus (HPV), can sometimes mimic DPN. Melanocytic nevi (moles) are pigmented lesions that differ from DPN in their distinct appearance and histological features. Angiofibromas, which present as reddishbrown papules, can also be confused with DPN. Additionally, adnexal tumors such as trichoepitheliomas, fibrofolliculomas, tricholemmomas, basaloid follicular hamartomas, and syringomas are rare skin appendage tumors that may present diagnostic challenges due to their similarity to DPN.2
Topical hydroquinone, a common agent in treating DPN, is typically used in concentrations of 2% to 4%. It functions as a skin-lightening agent by inhibiting tyrosinase, an enzyme essential for melanin production, thus reducing the hyperpigmentation of DPN lesions. Hydroquinone can be applied alone or in combination with other agents. When used alone, it is applied to the affected areas once or twice daily, with
care taken to prevent irritation such as erythema, peeling, or dryness. Hydroquinone is often combined with tretinoin, a retinoid that enhances skin cell turnover and improves hydroquinone penetration, facilitating the shedding of pigmented cells and stimulating the production of new, less pigmented cells. This combination addresses both pigmentation and skin texture. Azelaic acid provides antiinflammatory and skin-lightening effects, complementing hydroquinone’s action. It also offers antimicrobial properties, beneficial for treating any underlying inflammation or bacterial involvement. Kojic acid, another melanin production inhibitor, can be combined with hydroquinone to enhance treatment efficacy through different biochemical pathways. It may also mitigate the risk of hydroquinone-induced irritation. Adjustments to hydroquinone concentration or addition of other agents may be required based on patient response. Patients should use broadspectrum sunscreen daily, as hydroquinone increases sensitivity to sunlight, potentially leading to further pigmentation if not adequately protected.4
Similar to seborrheic keratoses, DPN lesions may become inflamed or irritated. Potential complications related to the removal of DPN lesions include infection risk of microbial infection at the site of lesion removal. Scarring which is potential for permanent alterations in skin texture or appearance post-removal. Dyspigmentation which involve changes in skin pigmentation at the site of treatment.
Primary care providers should consider referring patients to a dermatologist if there is diagnostic uncertainty regarding DPN or concerns about the potential for cutaneous malignancy. Dermatologists offer specialized assessment and management, ensuring precise diagnosis and appropriate therapeutic interventions. DPN presents as hyperpigmented or skincolored papules predominantly on the face and neck, commonly initiating in adolescence.2 Given that many healthcare professionals, including nurse practitioners, may not be wellversed in this condition, referral to a dermatologist is advised for accurate diagnosis and treatment. Patients often seek medical consultation primarily for cosmetic reasons, underscoring the need for effective management of aesthetic concerns.
Conclusion
DPN presents several challenges including significant cosmetic impact, diverse treatment options, and the need for patient education and compliance. Addressing these challenges requires careful treatment selection from among various modalities. Future research should focus on enhancing treatment efficacy with novel agents and optimized protocols, understanding the condition’s molecular and genetic underpinnings, evaluating longterm outcomes, and developing patient-centered approaches that consider individual preferences and skin types. Balancing cosmetic outcomes with safety and long-term efficacy remains essential for
Effectiveness
management of DPN.
References
1. Uwakwe LN, Souza B, Subash J, McMichael AJ. Dermatosis Papulosa Nigra: A Quality of Life Survey Study. J Clin Aesthet Dermatol. 2020; 13(2):17-19.
2. Xiao A, Muse ME, Ettefagh L. Dermatosis Papulosa Nigra. In: StatPearls. Treasure Island (FL): StatPearls Publishing; August 7, 2023.
3. Metin SA, Lee BW, Lambert WC, Parish LC. Dermatosis papulosa nigra: a clinically and histopathologically distinct entity. Clin Dermatol. 2017; 35(5):491-496. doi:10.1016/j.clindermatol.2017.06.001
4. Tran M, Richer V. Elective Treatment of Dermatosis Papulosa Nigra: A Review of Treatment Modalities. Skin Therapy Lett. 2020; 25(4):1-5.
5. Karadag AS, Ozkanli Ş, Mansuroglu C, Ozlu E, Zemheri E. Effectiveness of the Pulse Dye Laser Treatment in a Caucasian Women With Dermatosis Papulosa Nigra. Indian J Dermatol. 2015; 60(3):321. doi:10.4103/0019-5154.156447.
