Demodex folliculorum and Demodex brevis are common commensal mites of the human pilosebaceous unit that, under certain conditions, may proliferate excessively and cause demodicosis, generating a broad range of dermatological and/or ocular signs. Diagnosis is usually clinical but can be confirmed by quantifying mites using techniques such as standardized skin surface biopsy. The therapeutic approach to demodicosis includes topical and systemic treatments and, more recently, the use of laser treatments and other light sources. This review explores the pathogenesis, different clinical presentations, and therapeutic alternatives proposed for demodicosis, with special emphasis on therapies using light sources.
Demodicosis is a skin disease caused by excessive proliferation of mites of the genus Demodex, which includes the species Demodex folliculorum and Demodex brevis.1–3 These mites, first described in 1841,4 are common commensals on human skin, colonizing the pilosebaceous unit and feeding on sebum by using lipase enzymes for digestion. D. folliculorum is mainly located in the follicular infundibulum, whereas D. brevis is found in deeper areas, such as the sebaceous glands and their ducts.3 Both species can mainly be found on the face, paranasal area, eyelashes, or eyebrows, although D. brevis may also colonize other areas.2Demodex colonization is common in the population, with rates ranging from 20% to 80% and reaching 100% in older individuals, although these rates may vary greatly depending on the detection method.3 In children and adolescents, Demodex colonization is significantly lower, since sebaceous follicles are colonized during late childhood and adolescence through transmission by direct contact.2 Although these mites are saprophytes and generally do not cause clinical manifestations, under certain conditions they can become pathogenic, causing a variety of cutaneous and ocular clinical signs.
This review analyzes the known pathogenic mechanisms, the different clinical presentations, and the treatments proposed for demodicosis, including laser and intense pulsed light therapies.
Materials and methodsWe conducted a literature search was in the PubMed database. The search period ranged from January 2000 through September 2025. The following search formula was used: “Demodicosis [Title/Abstract] OR Demodicidosis [Title/Abstract]”. The inclusion criteria were clinical studies or review articles evaluating pharmacological treatments or light-source-based treatments for demodicosis, or diseases related to Demodex, provided they analyzed the reduction in the mite population after the intervention. The exclusion criteria were basic or preclinical research, studies not performed in humans, articles not written in English or Spanish, and publications whose full text was not available.
The certainty of the evidence was assessed according to the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system guidelines, using the online GRADEpro tool.5 The quality of evidence was classified as very low, low, moderate, or high.
PathogenesisDemodex infestation in the pilosebaceous unit is usually asymptomatic in most individuals. However, certain factors may trigger excessive proliferation and transform this colonization into a pathological condition, altering the balance between the skin microenvironment, the cutaneous flora, and the human immune system.2 These factors include damage to the immune system, infections such as HIV, prolonged use of corticosteroids, and damage to the skin microbiome. In addition, a higher prevalence of diseases caused by Demodex has been observed in patients with obesity, kidney failure, diabetes mellitus,2 use of biologic drugs for atopic dermatitis, such as dupilumab,6 and HLA-Cw2 and HLA-Cw4 haplotypes.7
The pathogenesis of demodicosis involves several mechanisms, such as blockage of follicles and sebaceous ducts by the mite itself and its role as a vector for transmitting bacteria such as Bacillus oleronius, which intensifies the inflammatory response. Some studies have suggested that Demodex can evade the immune response by inhibiting neutrophil phagocytic activity. In addition, hyperstimulation of humoral and innate immunity may be triggered in response to increased mite density per follicular unit or to mite penetration into the dermis, culminating in perifollicular inflammation, destruction of the follicular epithelium, reactive hyperkeratosis, and alteration of the skin barrier. Granulomatous reactions may also occur in response to mite particles. In cases of massive infestation, dead mites release chitinous exoskeletons and bacterial antigens, which may increase TLR-2 expression, triggering an inflammatory cascade and a more intense immune response.1,2
Clinical signsThe clinical signs of demodicosis are varied and depend on mite density, the host immune response, and other factors. It usually presents in individuals >40 years, with periorificial facial involvement and asymmetric distribution, with minimal associated symptoms, such as pruritus, or no symptoms.4
It can be associated with prolonged previous use of topical corticosteroid therapy and may worsen with topical calcineurin inhibitors, such as pimecrolimus or tacrolimus, as well as with occlusive makeup.
There is controversy surrounding the diagnostic boundaries of demodicosis. Some authors propose integrating certain forms of rosacea, such as erythematotelangiectatic and papulopustular rosacea, and demodicosis as different phenotypes or stages of the same entity, in which Demodex plays an essential role and shared inflammatory mechanisms are present.8–10 In this review, however, we present the classification proposed by Chen et al., which distinguishes the following clinical forms4 (Table 1):
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Pityriasis folliculorum or spinulate demodicosis (Fig. 1). This form predominantly affects women and presents as mild diffuse facial erythema, pruritus, burning sensation, fine follicular scales, and follicular plugs. It may be associated with poor hygiene and excessive application of cosmetics.1
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Rosacea-like demodicidosis or Demodex folliculitis (Figs. 2 and 3). This form is characterized by erythema, scaling, and papulopustules similar to rosacea.3 It may be subclassified as papulopustular, nodulocystic, or conglobate. As mentioned above, papulopustular rosacea and rosacea-like demodicosis share many clinical features,8 such as a higher density of Demodex compared with healthy skin. Nevertheless, demodicosis is usually associated with follicular scaling, more superficial involvement, occasionally sudden onset and rapid progression, and absence of symptoms such as flushing and photosensitivity.
Fig. 2.Papulopustular rosacea-like demodicosis. (A and B) Papulopustular rosacea-like demodicosis on the cheeks. Dermoscopy shows Demodex tails in follicular openings with the presence of an isolated pustule. (C and D) Therapeutic response after 1% ivermectin cream for 6 weeks and one PDL laser session – parameters: 10mm, 0.5ms, 6–7J/cm2.
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Demodicidosis gravis. Similar to severe granulomatous rosacea, with formation of granulomas containing phagocytosed Demodex remnants and caseous necrosis.1
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Ocular demodicosis. At the ocular level, it has different forms of presentation, most notably chronic blepharitis, chalazion, or, less frequently, keratoconjunctivitis.4,11
Clinical forms of demodicosis according to the classification by Chen et al.4
| Classification | Complementary nomenclature | Clinical description |
|---|---|---|
| Primary demodicosis | ||
| Pityriasis folliculorum | Spinulate demodicosis | Predominantly affects women and presents with mild diffuse facial erythema, pruritus, burning sensation, fine follicular scales, and follicular plugs. It may be associated with poor hygiene and excessive use of occlusive cosmetics. |
| Rosacea-like demodicosis | Papulopustular demodicosis, nodulocystic demodicosis, conglobate demodicosis | Characterized by erythema, scaling, and rosacea-like papulopustules, and may present as nodulocystic forms.No flushing. |
| Demodicidosis gravis | Granulomatous demodicosis | Similar to severe granulomatous rosacea, with formation of granulomas containing phagocytosed Demodex remnants and caseous necrosis. |
| Ocular demodicosis | Presents as chronic blepharitis, chalazion, or keratoconjunctivitis. | |
| Other primary demodicoses | Perioral demodicosis, scalp demodicosis, auricular demodicosis | |
| Secondary demodicosis | Associated with systemic diseases – immunosuppression, HIV, transplantation, chronic kidney disease – treatments – EGFR inhibitors, phototherapy – or pre-existing dermatoses – acne, rosacea, seborrheic dermatitis. | |
EGFR, epidermal growth factor receptor.
Other primary forms of demodicosis include perioral demodicosis, scalp demodicosis – mostly in older individuals with advanced alopecia – crusted demodicosis, and auricular demodicosis, affecting the external auditory canal or the external tympanic membrane.4
When the increase in the number of Demodex mites is associated with systemic diseases, such as immunosuppression12 due to HIV or transplantation, chronic kidney disease, and so forth; previous treatments, such as EGFR inhibitors or phototherapy; skin tumors, such as melanocytic nevi, basal cell carcinoma, or mycosis fungoides; or other dermatoses, such as acne, papulopustular rosacea, seborrheic dermatitis, perioral dermatitis, and androgenetic alopecia,13 it is classified as secondary demodicosis.4,14
DiagnosisThe diagnosis of demodicosis is established by identifying an abnormally high density of Demodex mites (Dd; >5mites/cm2), together with compatible clinical findings and a favorable response to treatment, with subsequent eradication of the mites.15
The diagnostic methods most widely used to quantify the presence of Demodex are standardized skin surface biopsy (SSSB) and direct microscopic examination (DME).16 SSSB involves the use of cyanoacrylate glue on a glass slide that is adhered to lesional skin, whereas DME is performed using a comedone extractor and examining the extracted material under the microscope.1,2 Because most mites are located deep within the hair follicles, SSSB can be performed consecutively on2 occasions to reach greater depth, thereby allowing a larger number of mites to be obtained. In that case, the cutoff is still considered to be Dd >5/cm2 in the first biopsy, but Dd >10/cm2 in the second.17 However, in routine practice, diagnosis is primarily clinical, and biopsies and histological studies are usually not necessary.
In addition, dermoscopy may be useful, as Demodex tails can be observed, visible as whitish filaments measuring 1–3mm that protrude from the follicle, as well as follicular openings infiltrated with yellowish amorphous material, indicating the presence of mites.15 The use of ex vivo dermoscopy has also been described to facilitate visualization.18
On the other hand, advances in diagnostic techniques, such as Demodex DNA analysis by next-generation sequencing (NGS) or confocal microscopy, are being evaluated with promising results.19–21
Differential diagnosis of demodicosis includes conditions such as papulopustular rosacea, erythematotelangiectatic rosacea, cutaneous lupus erythematosus, seborrheic dermatitis, folliculitis, perioral dermatitis, contact dermatitis, and acne. Occasionally, demodicosis may present as a localized facial plaque that can be confused with actinic damage, actinic keratoses, among others. In many of the entities included in the differential diagnosis, abnormally high Demodex densities have been demonstrated – papulopustular and erythematotelangiectatic rosacea, seborrheic dermatitis, periorificial dermatitis, acne, blepharitis, and Meibomian gland dysfunction.7–9,12,20,24–26 Nevertheless, a high Demodex density is not by itself diagnostic of demodicosis and should therefore be interpreted together with the clinical findings, dermoscopy, and response to treatment in order to guide the diagnosis appropriately.
TreatmentTreatment of demodicosis is mainly based on reducing the density of Demodex mites on the skin and improving the associated inflammatory symptoms. Favorable responses have been reported with both various pharmacological treatments and light sources.
Pharmacological treatmentPharmacological treatments for demodicosis are aimed at reducing the Demodex mite population and decreasing associated skin symptoms.4,14,22
Topical treatments (Table 2)These include salicylic acid, selenium, metronidazole, benzyl benzoate, crotamiton, lindane, sulfide, sulfur, tea tree oil, permethrin, retinoids, and topical ivermectin.1,7,21–29 A meta-analysis of 5 clinical studies (n=180)27 reported a mean decrease of 70.01mites/cm2 and an 80% reduction in the number of Demodex-positive patients (≥5mites/cm2) after 16 weeks of treatment with 1% topical ivermectin, with good tolerability. Another meta-analysis highlighted ivermectin, both topical and systemic, the combination of topical ivermectin and metronidazole, and tea tree oil as the treatments with the best combination of efficacy and favorable safety profile.30
Topical treatment for demodicosis.
| Drug | Mechanism of action | Dose | Dosage regimen | Level of evidence |
|---|---|---|---|---|
| Metronidazole25 | Reduces the number of Demodex mites. Anti-inflammatory properties through inhibition of ROS release in neutrophils. | 0.75%–2% gel or cream | Apply 1–2 times daily for 3–270 days | Low |
| Ivermectin27,28 | Antiparasitic; reduces the number of Demodex mites and inflammation. | 1% cream | Apply once daily for 8–12 weeks | Moderate |
| Permethrin25 | Insecticide; interferes with sodium channels in parasites. | 1%–5% cream or lotion | Apply once daily for 3–12 weeks | Low |
| Crotamiton26 | Antipruritic and anti-inflammatory. Reduces the Demodex population. | 10% cream or lotion | Apply once daily for 3–45 days | Low |
| Tea tree oil32,29 | Anti-inflammatory, antiparasitic, antibacterial, antifungal, and antiviral. Anti-inflammatory and re-epithelializing properties. | 50% tea tree oil solution | Apply once weekly for 4–6 weeks | Moderate |
| Benzyl benzoate23 | Neurotoxic to mites. | 10%–25% cream or lotion | Apply twice daily for 45 days* | Low |
ROS, reactive oxygen species.
In the case of Demodex blepharitis, in addition to tea tree oil, which seems to be the most effective treatment in a meta-analysis published in 2020,31,32 lotilaner ophthalmic solution (0.25%) is an ectoparasiticide that represents an effective therapeutic alternative with less local irritation.33 However, there are no standardized clinical practice guidelines on the therapeutic regimen or dosage.14 More recently, a multicenter retrospective study of 2157 patients treated with topical ivermectin in a 1% compounded ointment, applied once daily for 2 months, showed a significant reduction in the degree of cylindrical sleeves, or collarettes, conjunctival erythema, and Ocular Surface Disease Index (OSDI) score, with good tolerability, after a mean follow-up of 26 months.28
Systemic treatments (Table 3)In severe cases or in immunocompromised patients, the use of oral metronidazole or ivermectin may be considered.1,12,22 However, evidence on the efficacy of oral metronidazole in demodicosis is limited and heterogeneous. Some studies have shown significant clinical improvement, possibly due to an anti-inflammatory effect, without a parallel reduction in the Demodex population, whereas others describe a rapid and sustained response with regimens of 250mg 3 times daily for 2 weeks.34,35 Recently, in a prospective study including 40 patients with facial demodicosis, after administration of oral ivermectin (200μg/kg/week) for 8 weeks, 75% of patients achieved clinical and acarological remission, with no relevant adverse effects.36 A randomized clinical trial including 120 patients showed superior Demodex clearance with combined ivermectin and metronidazole compared with ivermectin monotherapy.35
Systemic treatment for demodicosis.
| Drug | Mechanism of action | Dose | Dosage regimen | Level of evidence |
|---|---|---|---|---|
| Metronidazole35 | Anti-inflammatory and antiparasitic; reduces ROS. | 250mg orally | 3 times daily for 1–8 weeks | Very low |
| Ivermectin36 | Reduces the number of Demodex mites and inflammation. | 200–250μg/kg orally | Two doses, 1–2 weeks apart | Moderate |
| Isotretinoin37 | Decreases sebum production, reducing mite proliferation. | 0.1mg/kg, low dose | 20mg/day | Low |
ROS, reactive oxygen species.
Furthermore, isotretinoin may be used as an adjunct to reduce sebum production and, consequently, Demodex density.37 In a rare case of ivermectin-refractory demodicosis, complete clinical resolution and mite eradication were observed with combined treatment using low-dose isotretinoin (0.1mg/kg 4 times weekly) and 1% permethrin cream.38
Laser and other light sources (Table 4)Various light sources, including vascular lasers, IPL, photodynamic therapy, and photobiomodulation, have been evaluated in facial and ocular demodicosis. Their role appears to be due both to a possible thermal acaricidal effect and to anti-inflammatory mechanisms and improvement of glandular function.
Treatment with laser and other light sources for demodicosis.
| Treatment | Indication | Parameters | Treatment regimen | No. of studies(No. of patients) | Clinical response | Response in Demodex population |
|---|---|---|---|---|---|---|
| Intense pulsed light (IPL)47–50 | Ocular demodicosis/Meibomian gland dysfunction/blepharitis | 500–1200nm, 9–20J/cm2 | 1–4 sessions, every 2–4 wk | 6 (329) | Significant symptomatic improvement – decrease in erythema, eyelid pruritus, and ocular symptom VAS score. | Mean decrease in Dd of 28.2mites/cm2 (95%CI, −53.6 to −2.8); eradication RR, 1.41 (1.18–1.69). |
| Pulsed dye laser (PDL)39 | Facial rosacea/rosacea-like demodicosis | Fluence, 4–6J/cm2; frequency, 1–2Hz; spot size, 5mm; pulse duration, 0.45ms | 1 session | 1 (31) | – | Decrease in median Dd: 54% at 3 weeks. |
| Yellow laser (577nm)40 | Facial rosacea/rosacea-like demodicosis | Fluence, 20J/cm2; pulse duration, 42–46ms; 80% coverage | 1 session | 1 (34) | Mean clinical improvement VAS: 6.3/10. | Mean decrease in Dd of 44%. |
| Nd:YAG laser41 | Facial telangiectasias/facial erythema | Fluence, 300J/cm2; spot size, 1.5mm; pulse duration, 12ms; frequency, 1Hz | 1 session | 1 (1) | Decrease of 33% in clinical erythema and 67% in telangiectasia grade. | Decrease of 12%–28% in Dd. |
| KTP 532-nm laser | Facial demodicosis | Fluence, 8–10J/cm2; spot size, 10–12mm; pulse duration, 10ms | 1 session | 0 (0) | – | – |
| Photodynamic therapy (ALA-PDT)42,43 | Papulopustular rosacea/rosacea-like demodicosis | Topical 5% ALA; red LED light, 630–635nm; fluence, 37–50J/cm2 | A total of 3–5 sessions. Frequency: every 2–4 wk | 2 (80) | Reduction in inflammatory lesions of 70%–80%; improvement in erythema up to 58%; good/excellent overall responses in 78%. | Significant decrease in Dd (70%; P<.001). |
| Photobiomodulation51 | Meibomian gland dysfunction | Continuous red LED, 630nm, 100mW/cm2, 15min | 4 sessions every 2 wk | 1 (24) | Significant improvement in OSDI (56%) and Meibomian gland function. | No significant changes. |
RR, relative risk; Dd, Demodex density; OSDI, Ocular Surface Disease Index; VAS, Visual Analog Scale.
Studies of combined light sources are not included in the table.
The pulsed dye laser (PDL) emits a beam of light with a wavelength of 585–595nm, which can be absorbed by oxyhemoglobin, which is why it is widely used for the treatment of erythematotelangiectatic rosacea.
In a study of 31 patients diagnosed with rosacea, Demodex density (Dd) decreased significantly after a single PDL treatment session (585nm in vascular mode; fluence, 4–6J/cm2; spot size, 5mm; pulse duration, 0.45ms; frequency, 1–2Hz; maximum overlap, 30%): baseline Dd was 13.0 and post-treatment Dd was 6.0 (P=.002). The study did not evaluate whether the decrease in Dd was associated with clinical improvement.39
Yellow laser (577-nm pro-yellow laser)The 577-nm yellow laser can be used for the treatment of certain vascular skin lesions and malformations. A retrospective study (n=34) showed that treatment with a 577-nm laser in scanner mode – parameters of 20J/cm2, 42–46ms, 1.5s, and 80% coverage – significantly reduced Demodex density (baseline Dd, 18.1±10.7/cm2; post-treatment Dd, 10.2±7.9/cm2 after 4 weeks; P=.001). Both clinical improvement, measured using the VAS, and the decrease in Demodex density were significant. However, no direct correlation was observed between mite reduction and clinical improvement.40
Nd:YAG laserThe 1064-nm Nd:YAG laser is mainly used for the treatment of deep vascular lesions and pigmented lesions. In one reported case, a patient with erythematotelangiectatic rosacea experienced an 11.6% to 28.1% reduction in mite density after a single Nd:YAG laser treatment session, with a fluence of 300J/cm2, spot size of 1.5mm, pulse duration of 12ms, and frequency of 1Hz. This was associated with moderate clinical improvement in erythema 1 month after the session.41
KTP 532-nm laserIn our experience, the KTP 532-nm laser – parameters: 10mm, 10ms, 7–10J/cm2 – has proven effective in reducing Demodex density, with associated clinical improvement (Fig. 4).
Other light sources
Photodynamic therapy (PDT) has been used in the context of papulopustular rosacea and rosacea-like demodicosis. In a single-center comparative study, treatment with ALA-PDT (3–5 sessions) was noninferior to oral minocycline 100mg for 8 weeks in reducing papulopustules and improving quality of life, although it was less effective in controlling erythema (35% vs 67%). Demodex density and relapse rates were similar in both groups after 24 weeks of follow-up.42 Other open-label studies have confirmed sustained clinical improvement at 12–24 weeks with ALA-PDT, associated with mild and transient adverse effects, including pain, erythema, and postinflammatory hyperpigmentation.43
The use of phototherapy is not recommended as a therapeutic tool for the treatment of demodicosis. Whereas some studies have failed to find significant differences in Demodex density or in the prevalence of facial demodicosis in patients treated with narrowband UVB (NB-UVB) or UVA-1,44 a cross-sectional study of 45 patients treated with phototherapy (PUVA or NB-UVB) observed a significantly higher prevalence of demodicosis in patients treated with phototherapy (28.9%) than in controls (7%) (P=.01), being especially high among those treated with PUVA (58.3%). The authors attributed this increase to the immunosuppressive effects of UV radiation and to induced sebaceous hyperplasia.45
We did not find any studies evaluating the response to intense pulsed light (IPL) or photobiomodulation in facial demodicosis.
Ocular demodicosisIntense pulsed light (IPL)Intense pulsed light (IPL) uses a range of visible-light wavelengths that can be absorbed by different chromophores located in the skin and transformed into heat energy in the treated areas. Several mechanisms have been proposed by which IPL could target Demodex mites, including coagulative necrosis and reproductive suppression.46–49
A recent meta-analysis including 6 studies – 5 randomized clinical trials and 1 nonrandomized study – with a total of 329 patients analyzed the efficacy and safety of IPL alone or combined with glandular massage or tea tree oil. The fluences used ranged from 9 to 20J/cm2, with 1–4 sessions separated by intervals of 2–4 weeks. Treatment was associated with a higher Demodex eradication rate compared with controls (RR, 1.41; 95%CI, 1.18–1.69; P<.01) and with a significant reduction in mite density, with a pooled mean difference of −28.2mites/cm2 (95%CI, −53.6 to −2.8). Clinical improvement was also significant in most studies, with decreases in pruritus, eyelid erythema, and inflammatory ocular signs. No serious adverse effects were reported, and only 3% of patients reported a mild, transient burning sensation.50
Other light sourcesA randomized trial of 24 patients assessed the efficacy of photobiomodulation – continuous red LED, 630nm, 100mW/cm2, 15min – in patients with Meibomian gland dysfunction, either alone or in combination with intense pulsed light (IPL, 580–1200nm, 12–14J/cm2). Both groups showed significant symptom improvement after 4 sessions, although the reduction in Demodex did not reach statistical significance.51 Another retrospective study also evaluated the combination of IPL with photobiomodulation – blue and red light using LED masks, 12min per color, mean of 7.6 sessions – in 17 patients with Demodex-associated blepharitis. Significant improvement was observed in clinical signs, including reduction of cylindrical sleeves, or collarettes, saponification, conjunctival hyperemia, corneal staining, and dry-eye symptoms. Demodex density was not quantified.52
No studies were found on other light sources – lasers, phototherapy, or photodynamic therapy – used in ocular demodicosis.
DiscussionDemodicosis is a cutaneous and ocular disease caused by overpopulation of the Demodex mite, which induces a local inflammatory response in the pilosebaceous unit or eyelid margin. The therapeutic arsenal includes topical or systemic acaricidal treatments, drugs aimed at sebaceous control, such as isotretinoin, and, in recent years, several light sources that have shown potential both in reducing parasitic burden and in controlling associated inflammation.
The light-based therapies evaluated include vascular lasers – PDL, KTP, yellow laser, and Nd:YAG – intense pulsed light (IPL), photodynamic therapy (ALA-PDT), and photobiomodulation. Overall, the evaluated studies describe significant clinical improvement and a reduction in Demodex density in most cases treated with laser or IPL, usually after one or a few sessions. In addition, in our experience, KTP and PDL vascular lasers may be particularly useful, especially when combined with topical ivermectin. In many cases, a single session is sufficient to observe clear clinical improvement.
At the ocular level, IPL shows ocular eradication rates >80% in Demodex-associated blepharitis, with parallel improvement in Meibomian gland function and ocular symptoms. However, as occurs with other light-based therapies in dermatology, the methodological quality of the evidence is limited: retrospective studies predominate, with small sample sizes and follow-up periods shorter than 6 months, and with no data on recurrence or duration of effect.
Regarding other light sources, photodynamic therapy (ALA-PDT) and photobiomodulation appear to act mainly through anti-inflammatory mechanisms, with good clinical results but without a demonstrated acaricidal effect.
The main advantages of light sources are their safety, low rate of adverse effects, and the possibility of considering them as an alternative in patients in whom systemic treatments are contraindicated – for example, during pregnancy or breastfeeding – provided that their use is individualized. Conversely, their limitations are relevant: costly equipment, low availability, and still limited evidence.
Ultimately, light-based therapies open a promising therapeutic pathway in the comprehensive management of demodicosis, but their role should be defined as higher-quality evidence and longer follow-up become available.
ConclusionsDemodicosis is a common entity in dermatological and ophthalmological practice. It is difficult to diagnose because of clinical overlap with other similar diseases and has multiple therapeutic options.
Topical and systemic acaricidal treatments, especially ivermectin, constitute one of the main pillars of current treatment. However, light-source-based therapies – including vascular lasers, IPL, and ALA-PDT – represent safe and potentially effective alternatives, with results in some studies comparable to topical or oral pharmacotherapy.
The available evidence remains limited and heterogeneous, supported by small series and short follow-up periods. Prospective randomized trials with prolonged follow-up and joint assessment of clinical and acarological response will be necessary to define the duration of effects, recurrence rates, and the exact place that each light-based modality should occupy within the therapeutic algorithm for demodicosis.
Conflict of interestThe authors declare no conflict of interest.
