Possibilities of intense pulsed light therapy in correcting the post-acne symptom complex (review)

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INTRODUCTION

Acne vulgaris is a chronic inflammatory skin disease caused by increased androgen levels, accelerated keratinocyte proliferation, enhanced sebum secretion, colonization by Cutibacterium acnes, and the development of an inflammatory response [1, 2]. According to epidemiological studies, acne affects up to 85% of the young population and persists in 12%–14% of adults, significantly decreasing patients’ quality of life [3, 4].

A common complication of acne is post-inflammatory hyperpigmentation and post-inflammatory erythema, which further exacerbate the psychological and social discomfort of patients [5]. According to the published data, clinical manifestations of post-acne are observed in 95% of patients with acne vulgaris [6–9]. The combination of acne with post-inflammatory pigmentation and erythema results in a more pronounced reduction in quality of life compared with acne alone [6–9].

PATHOGENESIS OF POST-ACNE SYMPTOM COMPLEX

Post-inflammatory pigmentation occurs as a result of the local effects of inflammatory mediators such as cytokines and arachidonic acid metabolites, which activate melanocytes, promoting melanin transfer to keratinocytes [10]. The pathogenic processes associated with the epidermal inflammatory response underlying post-inflammatory hyperpigmentation include the release and oxidation of arachidonic acid to prostaglandins and leukotrienes. These compounds influence the activity of immune cells and melanocytes, causing increased melanin production and its transfer to keratinocytes, causing epidermal hypermelanosis [11]. Post-inflammatory hyperpigmentation can also be caused by damage to the basal layer of keratinocytes during inflammation, where melanin released from destroyed cells is absorbed by dermal macrophages, clinically manifesting as hyperpigmentation [12].

The scarring process in acne depends on the balance between collagen production and the degradation of the temporary matrix. Depending on how connective tissue responds to inflammation, healing of acne lesions can result in the formation of two types of scars: hypertrophic, sometimes keloid (with excessive tissue), and atrophic (with insufficient tissue) [13].

Atrophic scars, which account for up to 80% of cases, usually form on the face and less often on the body, whereas hypertrophic scars, accounting for 10%–20% of cases, are more common on the back and chest [14].

Inflammation plays a key role in post-acne scar formation. Fibroblasts, keratinocytes, and sebocytes produce numerous enzymes, including matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs), which are essential for the structure of the extracellular matrix. Metalloproteinases such as MMP-1, 2, 9, 13, and their precursors initiate a lytic cascade affecting the intercellular substance. An imbalance between MMPs and TIMPs can lead to the formation of atrophic or hypertrophic scars [15]. Multiple genes are believed to contribute to the development of keloid scars, and their formation is thought to be associated not only with high fibroblast proliferation rates but also with delayed apoptosis. Atrophic scars usually form due to local destruction of protein components of connective tissue, with inflammation and mechanical trauma acting as triggers. Post-acne atrophic scars are classified based on shape and depth into three subtypes: V-shaped (Icepick), M-shaped (Rolling), and U-shaped (Boxcar) [16]. These subtypes can vary in severity, from mild with few scars covering a limited area to severe with multiple scars affecting large areas. Hypertrophic and keloid scars are classified by age: fresh scars exist up to one year (keloids exist up to three years), while mature scars are older than one year (keloids exist more than three years) [17].

The main factors determining the development of post-acne scars include genetic predisposition to a specific type of response to trauma and damage, which is a key factor in scar formation; duration and intensity of the inflammatory process; genes in the C. acnes genome responsible for collagenase production, which degrades collagen; formation of perifollicular abscesses and follicle rupture in acne, which stimulates wound healing and leads to permanent scars due to the inability to restore collagen fibers; and skin sagging due to disruption of collagen structural integrity, resulting in atrophic scar formation [18].

CAUSES OF POST-ACNE SYMPTOM COMPLEX

The development of the post-acne symptom complex may result from the absence of treatment, insufficient cumulative doses of anti-acne drugs, the use of antibiotics inactive against C. acnes (particularly penicillin derivatives), unprofessional extraction of comedones or inflammatory elements, surgical opening of cystic cavities, systemic complications caused by prolonged monotherapy, and patient-induced excoriation of lesions [19, 20]. All of these factors ultimately lead to chronic inflammation [21]. The correlation between the duration of persistent inflammation and the likelihood of pathological scarring reaches 95% [22]. The most common manifestations of the post-acne symptom complex include pigmented and stagnant spots (36% of all cases), scars (26%), enlarged pores and uneven skin texture (30%), vascular changes (6%), and atheromas or milia (2%) [19].

Effective treatment of post-acne symptoms remains an important challenge in dermatology. Post-acne symptoms following acne therapy have significant social and medical implications owing to their high prevalence [23]. Studies have shown that although acne is not a life-threatening condition, it severely affects the social and psychological well-being of patients. It can lead to decreased self-esteem, psychopathological, anxiety, and depressive disorders, mood deterioration, emotional instability, and even suicidal thoughts, especially due to persistent cosmetic defects on the face and other visible areas, which contribute to distorted body image [24–26]. These issues negatively impact personal and professional relationships, causing embarrassment, inferiority, insecurity, shame, anger, and depression [27].

The degree of psychological discomfort does not always correspond to the severity of post-acne symptoms. Even minor defects can trigger dysmorphophobia and depressive or anxiety disorders, and in some cases, more severe psychiatric problems and suicidal ideation [28]. Excoriated acne may develop in certain patients, which significantly increases the risk of post-acne symptoms. The greater the severity of acne, the more pronounced the depressive symptoms and the lower the quality of life. The most common psychological disturbances affecting the quality of life of patients with acne include anxiety and nervousness (85.2%), insecurity (77.8%), social withdrawal (42.6%), irritability (33.3%), and signs of depression and sleep disturbances (5.6%) [29].

TREATMENT METHODS

The treatment of post-acne skin changes requires analyzing the patient’s individual preferences, assessing the tolerability and expected efficacy of different therapeutic approaches. It is essential to consider erythema, post-inflammatory pigmentation, type, depth, and location of scars, as well as the patient’s skin phototype to minimize adverse effects.

A wide range of topical agents and therapeutic methods are available for the correction of post-acne symptoms. Modern cosmetology offers numerous targeted treatments for skin problem areas, including phototherapy, laser therapy, ultrasound treatment, mesotherapy, biorevitalization, and chemical peels.

Chemical Peels

Chemical peels are recommended for comedonal and papulopustular forms of acne, atrophic scars, and post-inflammatory hyperpigmentation. These procedures effectively address follicular hyperkeratosis—a key factor in acne pathogenesis—through the use of alpha hydroxy acids that promote exfoliation. Medium-superficial and medium-depth chemical peels, including 70% glycolic acid, 30% salicylic acid, 40%–70% pyruvic acid, 20%–35% trichloroacetic acid, and Jessner solution, have demonstrated positive results in correcting macular scars and dyschromia. Superficial peels with alpha hydroxy acids show regression of dyschromia in 92.2% of cases and reduction of pseudoatrophies in 54.4% of cases, though their effect on the total number of scars is limited [30, 31].

Mesotherapy

Mesotherapy is an effective dermatocosmetological approach, particularly in the treatment of comedones, non-purulent inflammatory lesions, atrophic scars, post-acne, stagnant spots and secondary post-inflammatory hyperpigmentation. Mesotherapy products contain trace elements (sulfur, zinc, germanium, etc.), vitamins (riboflavin, folic acid, ascorbic acid), and amino acids (lysine), which collectively enhance local immunity, metabolism, and skin regeneration, and exert keratolytic, depigmenting, and anti-inflammatory effects [32].

Laser Therapy

The CO₂ laser is an ablative device that emits high-energy light to vaporize the surface skin layers (ablation zone). Unlike erbium lasers (Er:YAG, 2940 nm), the CO₂ laser also creates thermal damage zones—carbonization, coagulation, and thermal stimulation—that promote collagen production and skin remodeling over several months post-procedure. Non-ablative lasers, such as Nd:YAG (neodymium), Er:YAG (erbium), Er:Glass (erbium glass solid-state), 1450 nm diode, and PDL (pulsed dye laser), induce thermal injury in the dermis without removing the epidermis. This results in fewer side effects and minimal downtime for the patient, though their efficacy is generally lower than that of ablative lasers [33, 34].

Low-Temperature Argon Plasma

The operation of the Russian Plazmoran device is based on the generation of low-temperature argon plasma: inside the device, argon gas is ionized by an electric field, transforming it into plasma and producing a gas-dynamic flow accompanied by intense optical emission [35, 36]. The clinical efficacy of Plazmoran is attributed to the physical properties of argon plasma, which enhance oxygenation, stimulate immune responses, improve microcirculation, and trigger fibroblast proliferation and migration, thereby accelerating regeneration, which have a positive effect on damaged tissues [37]. Moreover, low-temperature argon plasma exhibits strong antibacterial activity, primarily due to reactive oxygen species, hydrogen peroxide, ultraviolet radiation, and ozone generation [38].

Intense Pulsed Light

The principle of Intense Pulsed Light (IPL) technology is based on the ability of light to penetrate biological tissues and selectively act on specific structures (hair follicles, sebaceous glands, abnormal vessels, and pigmented lesions), while stimulating collagen remodeling without damaging the skin surface. IPL sources emit polychromatic light and, if needed, can use specialized filters targeting specific chromophores. IPL is widely used to treat various dermatological conditions. IPL devices employ xenon flash lamps with broad-spectrum filters and are based on selective photothermolysis. Most IPL devices emit light with wavelengths between 400 and 1200 nm, targeting porphyrin, melanin, hemoglobin, and water.

Recent studies have reported successful IPL use in acne treatment [38, 39]. In a study by Mathew et al. [39], 33 patients with post-inflammatory erythema caused by acne underwent IPL treatment using a 560 nm filter with 3–6 sessions. Improvement of erythema by more than 50% was observed in 78.78% of patients. Another study [40] retrospectively analyzed 60 patients (52 women and 8 men) with a mean age of 29 years (range 22–37). Of them, 38 (63.3%) had Fitzpatrick skin type III and 22 (36.7%) had type IV. The duration of post-inflammatory erythema was > 6 but < 12 months in 35 (58.3%) patients, and > 12 months in 25 (41.7%) patients. One (2%) patient received 7 treatment sessions; 2 (4%), 34 (56.7%), 11 (18.3%), and 12 (20%) patients underwent 6, 3, 4, and 5 sessions, respectively. IPL wavelengths in this study ranged from 400 to 1200 nm. During each session, three cutoff filters were used sequentially: 640 nm (8–12 J/cm², 30–35 ms), 590 nm (8–12 J/cm², 15–20 ms), and 560 nm (6–10 J/cm², 12–15 ms) with cooling to 12–15 °C. Treatment involved 3–7 sessions at 4–6-week intervals depending on acne severity in each patient. All patients used sunscreen two weeks before and after the procedure. No local anesthesia was required prior to IPL procedure as a 5–8 mm layer of conductive gel was applied to the face. After each session, the patient were advised to apply ice packs for 15 minutes. Complete or partial resolution of erythema and hyperpigmentation was observed in 49/60 (81.7%) patients, with overall skin tone and texture improvement in all cases.

CONCLUSION

The problem of effective post-acne treatment remains highly relevant in dermatology. The post-acne symptom complex causes cosmetic imperfections and has a significant impact on patients’ psychological well-being, leading to self-esteem issues, depressive and anxiety disorders. Even minor skin defects can provoke serious psychological problems and suicidal ideation.

One of the modern and effective treatment methods for post-acne is IPL therapy—intense pulsed light, which effectively corrects pigmentation and skin texture, reducing the appearance of post-inflammatory spots.

Despite the proven efficacy of IPL therapy, further research in this area is necessary. The primary goal should be to optimize therapeutic approaches to achieve more stable results, reduce recovery time, and improve patients’ overall quality of life.

ADDITIONAL INFORMATION

Author contributions. N.G. Kochergin ― research concept, significant revisions to the manuscript to enhance scientific value; V.V. Romanishko ― collection and analysis of literature sources, preparation and writing of the text. Thereby, all authors provided approval of the version to be published and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Funding sources. No funding.

Disclosure of interests. The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Statement of originality. The authors did not utilize previously published information (text, illustrations, data) in conducting the research and creating this paper.

Data availability statement. Access to the data obtained in this study is not provided.

Generative AI. Generative AI technologies were not used for this article creation.

Provenance and peer-review. This paper was submitted to the journal on an initiative basis and reviewed according to the usual procedure. Two external reviewers and the scientific editor of the publication participated in the review.

About the authors

Nikolay G. Kochergin

I.M. Sechenov First Moscow State Medical University (Sechenov University)

Email: nkocha@yandex.ru
ORCID iD: 0000-0001-7136-4053
SPIN-code: 1403-3031

MD, Dr. Sci. (Medicine), Professor

Russian Federation, 4 Bolshaya Pirogovskaya st, bldg 1, Moscow, 119435

Vlada V. Romanishko

I.M. Sechenov First Moscow State Medical University (Sechenov University)

Author for correspondence.
Email: romanishko.vlada@mail.ru
ORCID iD: 0009-0002-8368-9271
SPIN-code: 9652-3730

graduate student

Russian Federation, 4 Bolshaya Pirogovskaya st, bldg 1, Moscow, 119435

References

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