INTRODUCTION
Androgenetic alopecia (AGA) is a chronic, progressive disorder and the most common cause of non-scarring hair loss, accounting for approximately 38% of all alopecia cases. Although epidemiologic data remain limited, its prevalence increases with age: AGA affects approximately 30% of white men by the age of 30, 50% by the age of 50, and up to 80% by the age of 70. AGA is reported less frequently in Chinese, Japanese, and African American men than in white men [1].
Patients typically seek medical advice around at the mean age of 33 years among men and 45 years among women [2]. Beyond its clinical presentation, AGA may substantially affect psychological well-being, often contributing to reduced quality of life, anxiety, and depression. Therefore, early diagnosis and intervention are crucial to slow disease progression and reduce its emotional burden [3].
CLINICAL FEATURES AND DIAGNOSIS
In men, AGA is characterized by frontotemporal recession, progressive thinning, and reduced hairdensity and shaft diameter. These changes typically affect the temples, vertex, and mid-frontal scalp, and their severity is commonly assessed using the Hamilton-Norwood scale [4].
In women, AGA typically presents as diffuse thinning over the crown and mid-frontal scalp. Unlike male-pattern hair loss, the frontal hairline is usually preserved [5]. The Ludwig and Sinclair scales are commonly used to grade pattern [4].
Although these clinical features are often sufficient for diagnosis, early-stage disease may require additional assessment with noninvasive or invasive techniques, such as trichoscopy, scalp and hair evaluation, the pull test, trichogram, or scalp biopsy [6].
Trichoscopy typically reveals a significant increase in yellow dots, single-hair pilosebaceous units, and perifollicular hyperpigmentation. The percentage of thin hairs (< 0.03 mm) is also higher than in unaffected individuals [7].
In AGA, scalp biopsy in transverse sections presents follicle miniaturization, increased number of vellus and telogen hairs, reduced terminal follicles in the subcutaneous fat, and mild perifollicular inflammation with collagen deposition. A terminal-to-vellus hair ratio of 3 : 1 or lower may support the diagnosis [8].
Additionally, basic laboratory tests, including thyroid-stimulating hormone (TSH), complete blood count (CBC), serum iron, ferritin, and vitamin D, together with gynecologic history in women, may rule out other causes of hair loss [9].
ETIOPATHOGENESIS
Genetics play a major role in AGA [1], accounting for approximately 80% of individual risk. Several genes contribute to disease onset and severity, particularly the androgen receptor (AR) gene, which is associated with increased follicular sensitivity to dihydrotestosterone (DHT). When DHT binds to androgen receptors in susceptible scalp follicles, it may promote pro-inflammatory cytokine release, leading to premature termination of the anagen phase. Chronic, low-grade perifollicular inflammation, often associated with oxidative stress, ultraviolet radiation, or pollution, may result in perifollicular fibrosis and progressive follicle dysfunction [10].
In both women and men with androgenetic alopecia, frontal scalp follicles show higher 5a-reductase activity compared to those in the occipital region. Conversely, occipital follicles have higher aromatase levels. Studies suggest that aromatase reduces follicular sensitivity to androgens and may therefore play a protective role [11].
Several modifiable factors, including cigarette smoking, high body mass index, unhealthy dietary habits, and alcohol consumption, have been proven to exacerbate the symptoms and cause early onset of the disease [12–14].
Although female and male AGA both result in progressive hair follicle miniaturization, their underlying mechanism may differ. In female pattern hair loss (FPHL), the disease may also occur in patients lacking functional androgen receptors, suggesting that androgen-independent pathways could be involved [15].
In women, hair loss is also associated with menopause and endocrine disorders involving hyperandrogenism, polycystic ovary syndrome (PCOS), hyperprolactinemia, congenital adrenal hyperplasia, and, less commonly, ovarian or adrenal tumors [16].
TREATMENT OPTIONS
Managing AGA mainly involves evidence-based pharmacologic and procedural interventions, but lifestyle factors may play a supporting role. Regular aerobic exercise, especially sessions longer than 60 minutes, may be associated with slower progression of hair loss [17]. Smoking cessation is also beneficial, as smokers have a higher risk of more severe androgenetic alopecia [13]. Still, the overall effect of lifestyle changes on AGA is modest, and they should not replace evidence-based medical therapies.
Standard pharmacologic management relies mainly on topical minoxidil, available in 2% and 5% formulations for men and women, and oral finasteride 1 mg/day for men. Low-level laser therapy (LLLT) may be used as a device-based option, whereas hair transplantation can be considered in more advanced or treatment-resistant cases. Regulatory approval varies by region and product type, and should therefore be interpreted separately for drugs, devices, and surgical procedures.
Topical finasteride formulations are authorized in various EU member states to prevent hair loss and stimulate hair growth in men [18]. Other treatments and dosages, including oral minoxidil, dutasteride, or combination therapies, are used off-label, although many are supported by growing clinical evidence and expert consensus [19]. Adjunctive approaches, such as platelet-rich plasma and microneedling are also used; however, current evidence remains insufficient to support routine recommendation [20, 21].
FOOD AND DRUG ADMINISTRATION APPROVED TREATMENTS
Minoxidil
Minoxidil was originally developed as a potent peripheral vasodilator for the treatment of severe, refractory hypertension. During its use, many patients developed hypertrichosis as a side effect [22]. This unexpected observation led to the development of a topical formulation in 1980s for the treatment of AGA, initially in men and later in women. Currently, 5% minoxidil is commonly used once or twice daily in men. In women, 2% minoxidil applied twice daily is recommended and has demonstrated comparable efficacy to 5% minoxidil used once daily [23].
Minoxidil activates potassium channels in smooth muscle cells of peripheral arteries, leading to vasodilation. In the scalp, it increases vascular endothelial growth factor (VEGF) production in dermal papilla cells and stimulates prostaglandin E2 synthesis, which may prolong the anagen phase [24]. It also shortens the telogen phase, resulting in transient shedding during the first 12 weeks of treatment [25].
Clinical response is usually seen after 3–6 months of treatment and approximately 40% of patients experience improvement in hair regrowth [26]. Due to delayed response, limited cosmetic effects, and early telogen shedding, many patients discontinue therapy [27].
Adverse effects of minoxidil include irritant and allergic contact dermatitis, scalp irritation, and facial hypertrichosis [28–30]. Higher-concentration formulations tend to cause more local reactions, likely because of increased propylene glycol content [31]. Foam formulations may improve tolerability in patients with irritation related to propylene glycol-containing solutions.
Low-dose oral minoxidil is increasingly used off-label for the management of hair loss disorders. Clinical studies indicate that it is as effective as topical minoxidil, with potential advantages such as improved adherence, lower cost, and fewer application-related adverse effects [4, 25]. Oral minoxidil appears to be more effective on the vertex, though not on the frontal scalp. Common adverse effects include headache and hypertrichosis. It is contraindicated in patients with pericardial disease, uncontrolled hypertension, and during pregnancy [4, 25].
Finasteride
Finasteride was originally developed for treatment of benign prostatic hyperplasia (BPH). It acts as a competitive and selective inhibitor of 5a-reductase type 2 (SRD5A2) and is approved by the United States Food and Drug Administration (FDA) for the treatment of men with mild to moderate androgenetic alopecia at an oral dose of 1 mg daily [32].
Finasteride works by blocking the conversion of testosterone to DHT, thereby reducing serum, prostate, and scalp DHT levels by 60–70% [33]. The first signs of efficacy may appear within 3 months, although improvements in hair count are typically measurable after 6 months. Continued use beyond 12 months not only increases total hair density but also improves the anagen-to-telogen ratio, promoting the transition of hair follicles into the active growth phase [34]. Long-term therapy may further improve hair quality by increasing hair shaft thickness, pigmentation, length, and growth rate, supporting continued treatment to maintain clinical benefit [35]. Finasteride effectively prevents further progression of androgenetic alopecia in approximately 90% of men, with 37–54% showing partial regrowth after 1 year of treatment [36].
Finasteride is generally not recommended for use in women, especially those who are or may become pregnant, due to its teratogenic potential. As a 5a-reductase inhibitor, finasteride may interfere with the development of male genitalia during pregnancy [37]. Additionally, its efficacy in women is inconsistent: it may improve hair loss in women with hyperandrogenism but appears less effective in postmenopausal women, suggesting that different forms of female hair loss have distinct underlying mechanism [38].
Finasteride is associated with a range of adverse effects, collectively sometimes referred to as post-finasteride syndrome. These include sexual dysfunction, such as erectile dysfunction, decreased libido, and reduced semen volume, as well as reproductive effects, including epididymal damage [39]. Persistent sexual adverse effects have been reported in approximately 3–5% of users [40].
In addition to sexual symptoms, finasteride has been linked to neurological and psychological effects, including increased rates of depression, anxiety, and suicidal ideation [40, 41]. Some studies suggest that these adverse effects may result from interactions beyond the primary therapeutic target, 5a-reductase type 2 [42].
Recent studies have explored topical finasteride as an alternative to oral therapy. Several European countries have approved spray formulations for men aged 18–41 years with early-stage androgenetic alopecia. A 0.25% topical solution acts locally on the scalp to inhibit 5a-reductase and reduce DHT levels [43]. Phase III clinical trials conducted in Europe demonstrated statistically significant improvements in hair count compared with placebo, with no serious treatment-related adverse events and a favorable safety profile [44].
The efficacy of topical finasteride in promoting hair growth appears comparable to that of oral finasteride, but with markedly lower systemic exposure, reduced peak plasma concentrations, and a smaller, clinically insignificant early reduction in serum DHT levels [18, 44]. Adverse effects are usually limited to the application site and may include scalp pruritus, burning, irritation, contact dermatitis, or erythema [45]. Topical finasteride may therefore be a promising option for patients who do not tolerate oral therapy, although additional high-quality, long-term clinical trials are still needed to further validate its efficacy and safety [45].
Low-level laser/light therapies
LLLT has been shown to stimulate cellular functions through a mechanism known as photobiostimulation. Several low-level laser devices emitting red light, including comb- or cap-based systems, have been evaluated for the treatment of AGA in both men and women [46, 47].
Fractional lasers create microscopic thermal injury zones, triggering a wound-healing response and potentially promoting hair growth. They may also enhance microcirculation and stimulate mitochondrial ATP production, which may contribute to activation of the anagen phase of hair follicles [46]. These mechanisms may increase hair density and reduce hair shedding, although the magnitude of clinical benefit varies across studies [47].
In a randomized controlled study involving 110 patients, use of a low-level laser comb device was associated with a significantly greater increase in hair density compared with placebo after 26 weeks. The treatment was generally well tolerated, with no serious adverse effects reported in that study [48]. The efficacy of LLLT appears broadly comparable to topical minoxidil in some studies, and combination therapy may provide additional benefit; however, the quality and heterogeneity of available evidence should be considered [49].
Adverse effects of LLLT are generally mild and may include scalp tenderness and pruritus. These symptoms typically resolve spontaneously within 2 weeks [50].
Hair transplantation
Hair transplantation involves relocating follicular units from androgen-insensitive donor areas to regions affected by AGA. The transplanted follicles retain their relative resistance to miniaturization and continue to produce terminal hair. In 2009, the FDA approved a robotic device designed to improve the precision and efficiency of follicular unit extraction [6].
Currently, two main micrografting techniques are used: follicular unit strip surgery (FUSS) and follicular unit extraction (FUE). FUE is often preferred in younger patients and in those with short hairstyles because it avoids a linear donor-site scar [51]. In addition to objective changes in hair density, hair transplantation may influent patient-perceived and observer-rated psychosocial outcomes, including perceived attractiveness, age, and social impressions after the procedure [52].
Successful hair transplantation deepens on sufficient donor hair density, particularly in the posterior scalp. Higher donor density allows a greater number of grafts to be harvested; however, donor density does not always correlate with the severity of frontal hair loss [53]. Therefore, careful patient selection and preoperative assessment of donor capacity are essential.
Adverse effects of hair transplant are usually mild and, in many cases, preventable. The most common include bleeding, crusting, frontal edema, hypertrophic scarring or keloid formation, and sterile folliculitis [54].
OFF-LABEL THERAPIES
Spironolactone
Spironolactone is a potassium-sparing diuretic structurally related to aldosterone. It is not approved for the treatment of AGA but is commonly used off-label in women for androgen-related conditions, such as hirsutism [5].
Its therapeutic potential in alopecia is attributed to its antiandrogenic properties. Spironolactone lowers circulating androgen levels and blocks androgen receptors in the hair follicle, thereby potentially slowing or partially reversing follicular miniaturization [5].
Several studies have supported its efficacy in female pattern hair loss, either as monotherapy or as adjunctive therapy. The best results have been reported after at least 12 months of continuous treatment, particularly in patients with more advanced stages of alopecia [55].
In a retrospective study of 67 women treated with spironolactone only, 49.3% experienced visible improvement in hair density and reduced hair shedding. However, treatment was largely ineffective at doses below 100 mg/day. Clinical benefit was observed more consistently at doses of 100–200 mg daily, especially when treatment was maintained for at least 1 year [56].
Potential adverse effects in men include gynecomastia, decreased libido, and erectile dysfunction, which limit its use in this population. Due to its antiandrogenic and feminizing effects, spironolactone is not used in male AGA [5].
Spironolactone should not be used for the treatment of AGA during pregnancy or breast-feeding [4].
Dutasteride
Dutasteride is used off-label for the treatment of AGA. It inhibits both type I and type II 5a-reductase enzymes and may therefore provide stronger suppression of DHT than finasteride, which primarily inhibits type II 5a-reductase. Like finasteride, dutasteride blocks the conversion of testosterone to DHT, a key mediator of hair follicle miniaturization in AGA [4, 57, 58].
Although dutasteride is not approved for the treatment of AGA in the United States or Europe, it has been approved in countries such as Japan, South Korea, and Taiwan at a dose of 0.5 mg/day for male pattern hair loss [57].
The daily dose of 0.5 mg dutasteride reduces serum DHT levels by approximately 92%, compared with approximately 73% reduction observed with finasteride at 5 mg/day, indicating stronger systemic DHT suppression [59]. Despite its greater pharmacological potency, the adverse-effect profile of dutasteride spears broadly similar to that of finasteride [58].
Platelet-rich plasma
Platelet-rich plasma (PRP) is an autologous platelet concentrate containing various growth factors that may support hair growth and follicular activity. These growth factors include platelet-derived growth factor (PDGF), insulin-like growth factor (IGF), and vascular endothelial growth factor (VEGF). PRP may stimulate follicular activity, promote neovascularization, and prolong the anagen phase by reducing apoptosis [4, 60].
In some studies, PRP was associated with more favorable clinical outcomes than 5% topical minoxidil, including a higher rate of negative hair-pull tests (91.7% vs. 69.4%) [60].
PRP appears to be more effective in early-stage AGA and in patients with miniaturized hairs < 0.03 mm in diameter [4].
PRP has been reported to increase hair density and reduce hair shedding. However, it did not significantly affect hair shaft thickness, and further high-quality, standardized trials are needed to confirm these findings and optimize treatment protocols.
Microneedling
Microneedling is a procedure that involves creating small percutaneous wounds using fine needles. In AGA, its proposed mechanism of action involves stimulation of stem cells, induction of regenerative processes, and release of PDGF [4, 61].
The wound-healing microenvironment created by microneedling may also facilitate the delivery and absorption of various topical agents [61].
In one study, microneedling monotherapy increased total hair count more than topical 5% minoxidil alone, while combination therapy provided greater improvement than either treatment alone [62]. Clinical studies suggest that microneedling with a 1.5 mm dermaroller may provide additional benefit [4].
Despite these promising early results, the available evidence is still limited. Larger, well-designed randomized controlled trials are needed to confirm the efficacy, optimal treatment protocols, and long-term safety of microneedling for AGA [20].
Pulsed electromagnetic field therapy
Pulsed electromagnetic field therapy (PEMF) may stimulate cellular activity by modulating calcium channels and activating signaling pathways, including the Wnt/beta-catenin one involved in hair follicle cycling. Low-frequency electromagnetic fields have been reported to increase the expression of anagen-associated molecules in dermal papilla cells and may support follicular activity through stem-cell-related mechanisms [63, 64].
Wearable or motion-activated PEMF devices have been investigated as potential adjunctive treatments for AGA. Available studies suggest that PEMF may increase hair follicle density and could complement other therapies, such as PRP or hair transplantation. It may also exert anti-inflammatory effects and influence hormonal pathways potentially involved in AGA progression [63, 64].
Although PEMF shows biological plausibility, clinical evidence remains limited. Most available studies have evaluated PEMF in combination with other therapies; therefore, further research is needed to clarify its independent efficacy, optimal treatment parameters, and long-term safety [63, 64].
COMBINATION THERAPY
Multiple studies have reported improved outcomes with combination therapies for AGA compared with monotherapy.
Topical minoxidil and oral finasteride: a 12-month study showed that combining low-dose oral finasteride with topical minoxidil significantly improved hair growth compared with either treatment alone [65].
Microneedling and minoxidil: combination therapy with microneedling and topical minoxidil was associated with significantly greater and earlier hair regrowth than minoxidil alone [66].
Botulinum toxin A and minoxidil: combining botulinum toxin A injections with topical minoxidil led to greater scalp symptoms alleviation, improvement in hair growth, and quality of life at 4 and 6 months, without additional adverse effects compared to minoxidil alone [67].
PRP and minoxidil: studies have reported improved hair density and hair shaft diameter in patients treated with both PRP and minoxidil compared with either therapy alone [68].
These findings suggest that combination therapies may improve outcomes in patients with AGA. However, treatment protocols remain heterogeneous, and further standardized studies are needed to determine the most effective combinations, treatment intervals, and patient groups most likely to benefit.
CONCLUSIONS
AGA is a multifactorial, progressive condition driven primarily by genetic predisposition and androgen activity, especially DHT. Although it is not life-threatening, it may significantly affect quality of life and psychological well-being, particularly in younger individuals. Early diagnosis, supported by clinical evaluation and family history, is essential to limit further progression and implement individualized treatment strategies.
Currently, topical minoxidil, oral finasteride, and LLLT remain among the most commonly used treatments for AGA, with substantial evidence supporting their efficacy. However, their limitations, including delayed response, variable outcomes, and potential adverse effects, have prompted the exploration of alternative and adjunctive therapies. Among these, topical finasteride and low-dose oral minoxidil appear particularly promising because of their favorable efficacy and tolerability profiles. Other options under investigation include dutasteride, PRP, spironolactone, and lifestyle modifications. Evidence remains limited for microneedling, PEMF, and botulinum toxin, highlighting the need for further high-quality studies.
Despite promising results, no single treatment provides a universal cure. Long-term success often depends on patient adherence and appropriately selected combination approaches.
As understanding of the underlying pathophysiology continues to evolve, particularly with regard to inflammatory and androgen-independent mechanisms, further research is necessary to develop more targeted, effective, and better-tolerated treatments. Ongoing studies and a personalized, evidence-based approach are essential to improving clinical outcomes and patient satisfaction in the management of AGA.
