ABSTRACT
Adipose‐derived exosomes may offer a novel therapeutic approach for lichen planopilaris (LPP) unresponsive to standard treatments, with preliminary evidence suggesting potential benefits in symptom control and hair preservation.
Keywords: adipose tissue, cicatricial alopecia, exosome, lichen planopilaris, regenerative medicine
Abbreviations
- ADSC
Adipose‐Derived Stem Cells
- AT
Adipose Tissue
- CCCA
Central Centrifugal Cicatricial Alopecia
- DLE
Discoid Lupus Erythematosus
- EV
Extracellular Vesicle
- FFA
Frontal Fibrosing Alopecia
- LPP
Lichen Planopilaris
1. Introduction
Lichen planopilaris (LPP) is a primary lymphocytic cicatricial alopecia characterized by perifollicular erythema, hyperkeratosis, and progressive follicular destruction leading to irreversible scarring and hair loss if left untreated [1, 2]. The condition most commonly affects middle‐aged women and is considered a follicular variant of lichen planus, sharing a pathogenesis involving T‐cell‐mediated autoimmune targeting of follicular keratinocytes, especially within the bulge area where epithelial stem cells reside [3, 4]. Histologically, LPP is typified by lichenoid lymphocytic infiltrates surrounding the follicular infundibulum and isthmus, accompanied by basal cell vacuolization and concentric perifollicular fibrosis [5, 6].
Despite its chronic and potentially disfiguring nature, management of LPP remains challenging. Standard therapies such as high‐potency topical corticosteroids, intralesional triamcinolone, hydroxychloroquine, doxycycline, and systemic immunosuppressants—including methotrexate or mycophenolate mofetil—often yield inconsistent results and are frequently limited by side effects or patient intolerance [2, 3, 7]. Disease progression is frequently relentless, and therapeutic responses are often partial or temporary, with limited capacity to induce hair regrowth in late‐stage fibrosed areas.
Recent interest has shifted toward regenerative and cell‐free biologic therapies aimed at restoring immune privilege and promoting follicular regeneration. Among these, autologous adipose‐derived products—including fat grafts, stromal vascular fraction (SVF), and platelet‐rich plasma (PRP)—have demonstrated early promise in alopecia management through immunomodulatory and growth factor‐mediated mechanisms [8, 9, 10, 11]. More recently, exosomes derived from mesenchymal stem cells (MSCs) have garnered attention as acellular, paracrine effectors with potent anti‐inflammatory and regenerative properties [12, 13, 14]. These nanosized extracellular vesicles contain cargo such as microRNAs, proteins, and lipids that can influence cell signaling, inhibit proinflammatory cytokines, and support tissue remodeling [13, 14, 15].
In dermatology, exosome therapies have shown encouraging preliminary results in conditions like androgenetic alopecia, alopecia areata, and plaque psoriasis—disorders that, like LPP, feature immune‐mediated disruption of hair follicle integrity [12, 16, 17, 18]. Their application in cicatricial alopecia, however, remains largely unexplored. Here, we present the case of a 50‐year‐old woman with treatment‐resistant LPP who achieved significant clinical improvement following treatment with autologous adipose tissue‐derived exosomes. To our knowledge, this is one of the first reported cases documenting such an outcome, highlighting the potential role of regenerative cell‐free therapies in managing cicatricial alopecia.
2. Case History/Examination
A 50‐year‐old woman presented with a seven‐year history of progressive scalp hair loss, accompanied by pruritus, burning, and episodic tenderness. The symptoms initially involved the vertex and parietal regions and gradually spread with increasing severity, despite multiple treatment attempts. She reported no significant past medical or autoimmune history and denied the use of hair treatments or traction‐inducing hairstyles. There was no family history of alopecia.
The patient underwent a thorough physical evaluation and dermoscopic examination of the scalp. On examination, well‐demarcated patches of alopecia were noted over the vertex and parietal scalp, with associated perifollicular erythema, perifollicular scale, and loss of follicular openings. The scalp appeared mildly tender on palpation. No signs of frontotemporal recession, eyebrow or eyelash loss, mucosal involvement, or cutaneous lesions elsewhere were noted. The anagen pull test performed was positive.
3. Differential Diagnosis, Investigations, and Treatment
The clinical findings narrowed the differential diagnosis primarily to include both scarring and non‐scarring alopecia. Scarring causes considered were LPP, discoid lupus erythematosus (DLE), frontal fibrosing alopecia (FFA), and central centrifugal cicatricial alopecia (CCCA). DLE was considered unlikely due to the absence of cutaneous lupus stigmata such as dyspigmentation, atrophy, and systemic symptoms [19]. FFA was excluded owing to the lack of frontotemporal recession, eyebrow loss, and its typically postmenopausal onset [6, 7]. CCCA was not supported by the clinical distribution, absence of a relevant family, and ethnic background. Non‐scarring forms, such as female pattern hair loss (FPHL), were considered. However, the presence of perifollicular erythema, perifollicular scaling, scalp discomfort, and histopathological findings of interface dermatitis and perifollicular fibrosis favored a diagnosis of LPP over FPHL.
To confirm the diagnosis, a 4‐mm punch biopsy was performed at the active margin of a lesion. Histopathological examination revealed a perifollicular lichenoid lymphocytic infiltrate, interface dermatitis with basal cell vacuolization, and concentric perifollicular fibrosis with follicular dropout, hallmarks of classic LPP [1, 5].
Initial therapeutic measures included clobetasol 0.05% lotion, hydroxychloroquine (400 mg/day), and a short course of oral doxycycline, yielding minimal clinical stabilization. Topical minoxidil was then prescribed, without a considerable response. To manage her condition, the patient underwent additional therapeutic interventions, including adipose tissue (AT) injection and platelet‐rich plasma therapy. While these procedures initially provided some symptomatic relief, her condition later worsened, prompting her referral to our clinic. Given the disease's refractory course, the patient was offered off‐label treatment with AT‐derived exosomes, supported by emerging evidence suggesting regenerative and immunomodulatory effects in cicatricial alopecias and inflammatory dermatoses [9, 17].
Before the initiation of treatment, the patient underwent comprehensive laboratory testing, including a complete blood count with differential, a comprehensive metabolic panel, a fasting lipid profile, and screening for infectious diseases such as HIV, tuberculosis, and hepatitis B and C. All results were within normal limits. Written informed consent was obtained before proceeding with the therapy. Prior to the treatment, the patient's LPPAI score was 7.83, reflecting high disease activity. This was characterized by notable perifollicular erythema and scaling, as well as subjective symptoms including itching and burning.
Autologous AT was harvested via mini‐liposuction from the periumbilical abdominal region, and exosomes were isolated and purified. The extraction method of AT‐derived exosomes is discussed comprehensively in our previous study [17]. Thirty minutes before the procedure, the treatment area was prepared using sterile gauze and alcohol pads. Local anesthesia was induced with a 2% lidocaine solution. A total of 2 mL of AT‐derived exosomes was then injected intradermally into the affected scalp areas using a 1‐cc syringe with a 27‐gauge needle, with injection points spaced 0.5–1 cm apart. The patient was advised to avoid washing her scalp for the following 24 h to optimize treatment efficacy. No concomitant immunosuppressives were used during this phase. Notably, the patient reported substantial improvement in symptoms after the first session, including reduced pruritus and tenderness. Clinical photography was performed before treatment, 1 and 6 months post‐procedure using a Nikon 10.2‐megapixel camera (Figure 1). At the one‐month follow‐up, the patient exhibited marked improvement in hair growth, a reduction in pruritus, and decreased scalp irritation and tenderness. Hair shedding was significantly reduced, and the hair‐pull test showed a notable decrease in hair fragility. No adverse events, including anaphylactic reactions, fever, nausea, vomiting, pain, or skin irritation, were reported. Laboratory results remained within normal limits throughout the follow‐up period.
FIGURE 1.
The patient's photographs before (A), 1 month (B), and 6 months after (C) the treatment with adipose tissue‐derived exosomes.
4. Conclusion and Results
Following the administration of AT‐derived exosome therapy over one session, at one and 6 months post‐therapy follow‐up, the patient experienced marked clinical improvement. Subjectively, there was a significant reduction in scalp pruritus, burning, and tenderness after the procedure.
One month after treatment, the LPPAI score decreased to 5.33, indicating a moderate level of activity, with a visible reduction in perifollicular inflammation and symptomatic complaints. By 6 months after treatment, the LPPAI score further declined to 1.83, representing minimal disease activity, with almost complete resolution of inflammation and no reported itching or burning.
Hair growth was noted on visual inspection, particularly in the central parietal zone. No adverse effects or signs of disease reactivation were observed during the six‐month follow‐up period. The patient reported high satisfaction with both symptom control and aesthetic improvement.
This case demonstrates the potential of AT‐derived exosome therapy as a regenerative and immunomodulatory treatment modality for refractory LPP. Traditional immunosuppressive and anti‐inflammatory treatments failed to halt disease progression in this patient, whereas exosome‐based intervention provided meaningful symptom relief and even partial hair regrowth—an outcome rarely observed in long‐standing cicatricial alopecia. While these findings are encouraging, large‐scale controlled studies are needed to validate efficacy, optimize dosing, and assess long‐term outcomes relative to other regenerative therapies. Furthermore, future research should focus on the comparative efficacy of exosome therapy versus other regenerative treatments, such as platelet‐rich plasma and adipose‐derived stem cell injections, in LPP and other forms of cicatricial alopecia.
5. Discussion
LPP is a subset of lichen planus that causes scarring alopecia through progressive hair follicle destruction [8]. Although its precise etiology remains unclear, a cytotoxic T‐cell‐mediated immune response targeting follicular antigens is thought to play a key role in disease progression. Due to its chronic, relapsing nature, LPP is notoriously difficult to manage, and current treatment strategies primarily aim to reduce inflammation, alleviate symptoms, and slow disease progression rather than restore lost hair [10, 11]. However, conventional therapies such as corticosteroids, hydroxychloroquine, and immunosuppressants often yield suboptimal results, with many patients experiencing incomplete responses or continued disease activity [10]. Given these challenges, there is growing interest in regenerative therapies that may offer both anti‐inflammatory benefits and follicular repair potential.
Recent studies have highlighted the therapeutic potential of AT‐derived treatments in various forms of hair loss, including androgenetic alopecia, alopecia areata, alopecia universalis, folliculitis decalvans, and traumatic alopecia [20]. Autologous fat grafting has been associated with significant improvements in hair density, follicular health, and symptom relief in LPP patients [11]. However, its clinical application is hindered by challenges such as low cell survival rates, tissue necrosis, and cyst formation due to inadequate vascular integration [15]. Adipose‐derived stem cells (ADSCs) have emerged as a promising alternative, offering enhanced angiogenesis, immunomodulation, and tissue repair capabilities. Given that exosomes serve as key mediators of ADSC function, their therapeutic potential in hair disorders has been an area of active investigation [21].
Exosomes are extracellular vesicles that play a crucial role in intercellular communication, carrying bioactive molecules such as proteins, RNA, and microRNA that influence cellular processes [21]. Studies suggest that exosomes derived from ADSCs can promote hair follicle regeneration through multiple mechanisms, including Wnt/β‐catenin signaling activation, tumor necrosis factor‐α pathway modulation, and increased vascular endothelial growth factor release. In a murine model of alopecia areata, mesenchymal stem cell‐derived exosomes significantly enhanced follicular proliferation and hair regrowth [16]. Similarly, in androgenetic alopecia, exosome therapy has demonstrated efficacy in promoting dermal papilla cell viability and stimulating the hair growth cycle [9, 20]. These findings support the potential role of exosomes in immune‐mediated and scarring alopecia, such as LPP.
In our case, a single session of AT‐derived exosome therapy resulted in notable clinical improvements, including increased hair density, reduced pruritus, and decreased disease activity without adverse effects. While these results align with prior research on exosome therapy in hair disorders, further studies are needed to establish standardized treatment protocols, determine the optimal number of treatment sessions, and evaluate long‐term outcomes in LPP patients. Additionally, comparative studies assessing the efficacy of exosomes versus other regenerative approaches, such as platelet‐rich plasma and adipose‐derived stem cell injections, could provide valuable insights into the most effective therapeutic strategies for cicatricial alopecia.
The primary limitations of this report include the absence of histopathological images, which would have enhanced diagnostic verification. A follow‐up biopsy was not performed after treatment, limiting the ability to assess histologic remission or structural follicular recovery. Although dermoscopic examination was conducted, photographic documentation was not obtained during diagnosis or follow‐up, reducing the availability of objective visual data. As this is a single‐patient case, larger studies are necessary to confirm the efficacy, reproducibility, and long‐term safety of exosome‐based therapies in lichen planopilaris.
Author Contributions
Mohammad Ali Nilforoushzadeh: conceptualization, data curation, investigation, methodology, resources, validation. Ali Ezzatollahi Tanha: data curation, investigation, project administration, validation, writing – original draft, writing – review and editing. Soraya Talebi: data curation, investigation, resources. Yekta Ghane: conceptualization, project administration, supervision, validation, writing – original draft. Niloufar Najar Nobari: conceptualization, data curation, investigation, methodology, supervision, validation.
Ethics Statement
All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1975, as revised in 2000.
Consent
Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor‐in‐Chief of this journal.
Conflicts of Interest
The authors declare no conflicts of interest.
Acknowledgments
The authors have nothing to report.
Nilforoushzadeh M. A., Tanha A. E., Talebi S., Ghane Y., and Nobari N. N., “Adipose Tissue‐Derived Exosomes in the Treatment of Lichen Planopilaris: A Case Report,” Clinical Case Reports 13, no. 10 (2025): e70943, 10.1002/ccr3.70943.
Funding: The authors received no specific funding for this work.
Mohammad Ali Nilforoushzadeh and Ali Ezzatollahi Tanha contributed equally to this manuscript and share first authorship.
Contributor Information
Yekta Ghane, Email: yektaghanemd@gmail.com.
Niloufar Najar Nobari, Email: niloofar.nobari@yahoo.com.
Data Availability Statement
Our data included personal patient data. Additional data is available from the corresponding author upon reasonable request.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
Our data included personal patient data. Additional data is available from the corresponding author upon reasonable request.