Minoxidil is a vasodilator initially used orally to treat high blood pressure. It was approved by the US Food and Drug Administration (FDA) for this purpose in 1979. Minoxidil activates the ATP-sensitive potassium channel (K+ ATP channel) causing hyperpolarization, efflux of K++ ions, and vessel smooth muscle relaxation.7

When used to treat high blood pressure, approximately 80% of the patients develop hypertrichosis. It was described as effective in improving male AGA in 1980.8 After the first observations, minoxidil started to be studied as a topical solution for the treatment of AGA, initially in men and later in women.

The mechanism of action of minoxidil in the treatment of AGA has yet to be fully elucidated.9 In addition to its vasodilator action, minoxidil increases proliferation in cultured cells of the dermal papilla and may act on gene expression and activation of signaling pathways, leading to the upregulation of genes encoding keratin-associated proteins.10

Most clinical studies with topical minoxidil in women have been carried out with a 2% solution applied twice daily.11 A meta-analysis of these studies showed a mean difference of 12.4 hairs/cm2 in the 2% minoxidil group when compared with the placebo after 24 weeks of treatment.11 The use of 5% minoxidil solution twice daily and 5% minoxidil foam used once daily showed no significant difference in response when compared to the 2% solution applied twice daily.12,13

In Brazil, minoxidil is only marketed as a 5% solution. Due to cosmetic issues and as a matter of practical use, 5% minoxidil once daily is preferred over 2% minoxidil twice daily for the treatment of FPHL, although the 5% solution is not recognized by the regulatory organizations (FDA in the United States or ANVISA in Brazil), for use in females. In 2014, the FDA approved the use of 5% minoxidil in foam vehicles for the treatment of FPHL (Fig. 1).

Figure 1.

Clinical improvement in a patient with FPHL using minoxidil 5% solution 1× a day. (A) Before treatment. (B) After six months of treatment.

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Minoxidil is a prodrug. Thus, to exert its effect (both vasodilator and follicle-stimulating), the minoxidil base needs to be converted to its sulfated form by the enzyme minoxidil sulfotransferase.7,14,15 Sulfotransferase is present in several tissues and is highly expressed in the liver.16 It can also be found in the outer root sheath of the hair follicle.14 There is an interindividual variation in follicular sulfotransferase activity, and patients with higher enzyme activity have been found to show a better therapeutic response.17

When obtained from compounding pharmacies, minoxidil sulfate is often used instead of minoxidil base due to its easier solubilization. Apparently, this alternative could even be advantageous due to the lack of need for metabolization, but minoxidil sulfate has a high molecular weight and low skin penetration. Therefore, it is important that, when choosing a compounded product, the clinician specifies in the prescription that minoxidil base should be used.15

The most common adverse effects of topical minoxidil are hypertrichosis in the facial region and local reactions on the scalp, such as pruritus, burning sensation, erythema, papules, or pustules. The frequency of these manifestations depends on the concentration of minoxidil and the type of vehicle, ranging from 1.9% to 5.7% in different studies.9 Although minoxidil can cause contact dermatitis, the active agent that most frequently leads to this condition is propylene glycol, a substance often present in the vehicle.18 In these cases, symptoms will resolve with the change to propylene glycol-free topical minoxidil.

About 18% of patients using topical minoxidil experience a transient increase in hair loss in the first few weeks of treatment (shedding); this occurs due to the shortening of the telogen phase.19 It is important that patients be advised of this possibility to avoid early treatment discontinuation.

Adherence is essential for a successful treatment. The first results are seen after four to six months, and to maintain them, minoxidil must be continued indefinitely.20,21 In addition to adverse effects, premature discontinuation may occur due to perceived unsatisfactory results or problems with the daily use of the topical treatment, due to changes in hair texture and difficulty to style them.

Topical minoxidil is the therapy with the highest level of evidence for the treatment of FPHL and, although it has been in use for a long time, it remains the first-line treatment.

Although topical minoxidil is effective for treating FPHL, 30% to 60% of patients who use it do not show improvement.6,22 Even for patients without side effects, adherence to the topical treatment can be a problem. The use of oral minoxidil for FPHL aims to increase the potency and improve adherence to treatment due to its greater convenience when compared to topical application.

The main limitation of using oral minoxidil for the treatment of FPHL is its possible side effects. When used for the treatment of arterial hypertension, at doses of 10 to 40 mg/day, the main adverse effects are tachycardia, edema, and hypertrichosis.7 Considering that the effects are dose-dependent, the use of oral minoxidil at low doses minimizes adverse effects, preserving a certain stimulatory action on the hair follicle.

The first study on oral minoxidil for the treatment of FPHL was a prospective evaluation of 100 patients who used it at a dose of 0.25 mg plus spironolactone 25 mg/day, published by Sinclair in 2018.23 The study reported an improvement in the clinical scale and in hair loss.

An Iranian study that included 72 patients compared this same dose of 0.25 mg/day of oral minoxidil versus 2% topical minoxidil in FPHL. An improvement in hair density and hair shaft thickness was observed in both groups, and there was no difference between them.24

In 2019, Ramos et al. published an open-label randomized clinical trial comparing oral minoxidil 1 mg/day vs. 5% topical minoxidil once a day in 52 Brazilian women with FPHL. Both groups showed improvement in hair density and in the photographic evaluation, with no difference between them. However, there was a trend towards superiority of the oral minoxidil group in relation to the topical group, which perhaps might have been better demonstrated in a larger sample25 (Fig. 2).

Figure 2.

Clinical improvement of a patient with FPHL using oral minoxidil 1 mg/day. (A) Before treatment. (B) After six months of treatment.

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The clinical effect of oral minoxidil seems to correlate with its dose. In a randomized double-blind clinical trial of 30 patients with FPHL, Silva et al. found that oral minoxidil 1 mg was superior to oral minoxidil 0.25 mg daily.26 In the first study, patients using oral minoxidil 1 mg showed an increase in hair density of 20.1 hairs/cm2 and in the second study, 27 hairs/cm2.25,26

There are no published series of women with FPHL using daily doses higher than 2 mg of oral minoxidil, despite anecdotal reports of individuals using up to 2.5 mg daily. There are also no data on the combination of topical and oral minoxidil for the treatment of FPHL.27

Recently, the sublingual route has been proposed as an alternative to the oral route to improve the bioavailability of minoxidil to the hair follicle and minimize possible adverse cardiovascular effects. 28 There are still no comparative studies between the two administration routes.

A recent retrospective study evaluated the adverse effects of oral minoxidil in 220 men and 215 women with AGA.29 Among women, the most frequent adverse effects were hypertrichosis (54%), headache (10%), lower limb edema (9%), dizziness (7%), insomnia (7%), and palpitations (4%). Forty-four percent of female patients experienced a temporary increase in hair loss at the start of the treatment. Although frequent, adverse effects were mild and well tolerated and only 13% of the patients discontinued treatment.29 Episodes of hypotension are infrequent with the use of oral minoxidil for AGA, as despite its potent antihypertensive effect it has little hypotensive effect in normotensive individuals.30

The use of oral minoxidil for treatment of AGA, both in men and women, has become increasingly frequent in recent years. This rapid increase was due to the fact that minoxidil is easily used and shows good adherence, as well as the perception of good clinical results. Despite the rapid growth in popularity, larger clinical trials comparing different doses and their outcomes versus traditional topical therapy are still necessary.

The action of testosterone and, mainly, of dihydrotestosterone (DHT), its metabolite produced by the action of the 5α -reductase (5αR) enzyme is crucial in the development and evolution of AGA in man.

Although the evidence showing the participation of androgens in the pathophysiology of AGA has been clearly demonstrated only in men, it has been assumed that they also play a role in women.

The efficacy of 5αR inhibitors (finasteride and dutasteride) in the treatment of male AGA corroborates the importance of DHT in its physiopathogenesis. However, finasteride 1 mg/day (standard dose for treating male AGA) has not been effective for treating FPHL in postmenopausal women.31

In an uncontrolled prospective study, 37 patients used finasteride 2.5 mg/day for 12 months. Twenty-three patients (62%) showed improvement in the photographic assessment and 12 (32%) showed improvement in the hair density score.32

Another prospective uncontrolled study evaluated finasteride at a dose of 5 mg in 87 women. After one year of treatment, 81% of patients showed improvement in the photographic assessment and there was an increase in hair density of 17 hairs/cm2.33 Randomized clinical trials evaluating doses ranging from 2.5 to 5 mg/day of finasteride in women have not yet been performed.34

Finasteride is a type 2 5αR inhibitor and a dose of 1 mg/day leads to a reduction of about 70% in serum DHT levels. Dutasteride inhibits 5αR type 1 and 2 and a dose of 0.5 mg/day reduces DHT levels by about 90%. Due to its greater potency, dutasteride may be an interesting alternative, but evidence supporting its use in FPHL is still scarce.34

The lower response of women to 5αR inhibitors probably occurs due to the involvement of non-hormonal mechanisms in the pathophysiology of FPHL, which are still not fully understood.

Finasteride 1 mg/day and dutasteride 0.5 mg/day have a package insert indicationin Brazil just for the treatment of male AGA. Its use in women is off-label and it should be used with caution in women of childbearing age due to its teratogenic potential (feminization of the male fetus). 34 There are no elements that clearly indicate a greater risk of breast cancer in users of 5αR inhibitors, yet caution remains necessary regarding their use in women at high risk for breast cancer.

There are no studies evaluating the performance of the combination of 5αR inhibitors and minoxidil (topical or oral) in FPHL.

Androgen receptor antagonists are frequently used in the treatment of FPHL, especially when the patient shows signs of hyperandrogenism. Despite their routine use, there is still no high-quality evidence to support the use of these drugs, and their performance associated with minoxidil (oral or topical) remains unknown.

Prostaglandin analogues are important modulators of follicular activity. They stimulate both keratinocyte and melanocyte activity, promoting hair growth and pigmentation.46,47

Latanoprost, a prostaglandin F2α (PGF2α) analog, is used in the treatment of open-angle glaucoma as a 0.005% ophthalmic solution. The side effects include increased length, thickness, and pigmentation of eyelashes.46 In a double-blind, randomized study including 16 male patients with mild AGA, there was a significant increase in hair density (terminal and vellus hair) after eight weeks using 0.1% topical latanoprost, when compared to the baseline picture and placebo group, (an increase of 32 hairs/cm2 over the placebo).47

Bimatoprost is a synthetic prostamide, a PGF2α analogue, originally used in the treatment of ocular hypertension and open-angle glaucoma. Its daily 0.03% topical use has been approved by the FDA for patients with eyelash hypotrichosis.46

Despite their interesting follicular action, the use of prostaglandin analogues is still limited in the treatment of FPHL due to the lack of clinical evidence and the high cost for use in large areas of the scalp.

Micronutrients may play an important role in alopecia by acting on hair follicle development and immune cell function.48 Moreover, nutritional alterations are associated with telogen effluvium, which affects the outcome of FPHL treatment.

Several vitamin supplements and natural products such as saw palmetto, caffeine, melatonin, marine extracts, rosemary oil, procyanidin, pumpkin seed oil, and cannabidiol oil have been described in the treatment of AGA and telogen effluvium.48,49

Lower serum levels of vitamin D and ferritin have been observed in patients with non-cicatricial alopecias compared to the healthy population.50,51 Nevertheless, there is yet no evidence of FPHL improvement with the supplementation of these substances. There is also no evidence of the benefit of biotin and zinc supplementation in healthy patients with FPHL.49

Despite being very frequently used, both by spontaneous patient demand and medical advice, there are still no clinical studies demonstrating consistent evidence of the benefit of using nutraceuticals or specific supplements in the treatment of FPHL.

Mesotherapy or intradermotherapy is a minimally-invasive technique that consists of infusing a mixture of active pharmaceutical agents in diluted doses intradermally.52 Once administered, the substances apparently achieve a more intense and lasting effect due to greater local bioavailability, in addition to potentially reducing systemic adverse effects.53

The active agents delivered through multiple injections directly to the affected sites comprise molecules already used through other routes of administration, such as minoxidil, finasteride, dutasteride, growth factors, panthenol, biotin, and steroids.52

Uzel et al. conducted a clinical trial comparing intradermal injections of sterile 0.5% minoxidil solution with injections of 0.9% saline solution. Fifty-four patients were divided into two groups and received weekly applications for ten weeks. In the treatment group, there was an increase in the ratio terminal to vellus hairs (p < 0.001). However, the increase in density in the treatment group was not statistically greater than that of the placebo group (p = 0.54).54

A comparative study evaluated 126 women with FPHL who were divided into two groups. The first group received injections of 0.05% dutasteride associated with biotin, panthenol, and pyridoxine and the second received saline solution. The patients received 12 injections over an interval of 18 weeks. On the photographic assessment, improvement was observed in 62.8% of the patients in the treatment group and 17.5% in the control group (p < 0.05).55

The weekly frequency and discomfort of the infiltration may limit the adherence of some patients to mesotherapy treatment. One alternative would be the use of quarterly dutasteride intradermal injections, due to their longer half-life, but controlled studies are still necessary to evaluate the performance of this therapeutic regimen. 56

The main criticisms related to mesotherapy concern the lack of standardization regarding the form of application, the active agents used, and the frequency of sessions.52 Pain can be a limitation of this complementary therapeutic modality. To reduce pain in patients undergoing scalp mesotherapy, non-pharmacological options such as vibration anesthesia devices were considered safe, effective, and simple to handle, providing tactile distraction at the application site and, therefore, comfort during the procedure.57

In addition to local pain caused by punctures and mild headaches, some complications such as persistent edema, micro bacterial infection, urticaria, skin necrosis, panniculitis, achromia, and cicatricial alopecia have already been reported. However, it is believed that part of these adverse effects is more often related to inadequate clinical indication, inadequate asepsis, use of non-sterile material, and even the performance of the procedure by a non-medical professional, than to mesotherapy itself.53

Special attention should be paid to the use of synthetic growth factors in the mesotherapy mixture. The literature supporting its use is very scarce, and there are reports of cases of melanoma arising after injections of growth factors as a therapy for telogen effluvium.58 Another reported complication was temporary frontal edema after mesotherapy for AGA. The authors have correlated edema with the use of injectable lidocaine, which is one of the formula components, and higher injected volumes are related to this side effect. All patients had a favorable outcome after one to four days with the use of cold packs alone.59

Mesotherapy can be considered an adjuvant option for the treatment of FPHL, although more studies are necessary to standardize the active agents, their concentrations, the periodicity of applications, and the number of sessions indicated. Although it is minimally invasive, it is essential that it be performed by a medical professional with clinical and pharmacological experience, following aseptic regulations consistent with the procedure, aiming to prevent the aforementioned complications.60

The performance of injectable procedures in association with minoxidil (oral or topical) is not known, nor with other antiandrogenic drugs in the treatment of FPHL. Finally, in addition to the fact that the active agents are not approved by the FDA or ANVISA for this route of administration, they contain products with questionable sterilization.

Microneedling is a minimally-invasive technique that consists in using sterile microneedles for repetitive skin punctures that create micro-channels in the skin.52,61 The proposed action mechanism to increase hair growth is due to the release of platelet growth factors (TGF-alpha, TGF-beta, platelet-derived and vascular endothelium-derived growth factor), which would subsequently result in neovascularization, increased collagen, and elastin production, and stimulation of the expression of genes related to hair growth.52,61

There are several devices that can be used to perform the procedure. The most traditional are rollers, stamps, and electric pens, containing needles that vary in number and length.61

Microneedling is a low-cost, quick-to-perform procedure with a simple learning curve. It can be done under topical anesthesia or anesthetic block for greater patient comfort.52,62,63

After anesthesia, the area to be treated must be washed with saline solution and ethanol to ensure an aseptic field. The pen has adjustable penetration speed and depth and must be moved linearly, lifting the device after each application, in a total of up to three applications per location.

In the case of the needled roller, various applications in several directions can be made until blood droplets appear over an area of homogeneous erythema on the scalp, although the ideal endpoint for this procedure remains controversial.62

Although some studies point to favorable results of microneedling in the treatment of AGA, the evidence for the benefit of this treatment is still of poor quality.61 In an open study, Starace et al. evaluated 29 patients with FPHL, who showed an increased density of 19.57 hairs per cm2 in the frontal area after three microneedling sessions four weeks apart.63 There have been reports of tolerable pain and transient lymphadenopathy.

Microneedling can be an adjuvant option for the treatment of refractory FPHL or for those who do not wish to undergo the standard clinical treatment. Its real effectiveness, as well as the ideal frequency of sessions and length of needles, must be established by studies with specific designs. There is some controversy as to whether the puncture should be deep enough to penetrate the barrier and deliver the medication or whether it should be superficial enough to produce minimal damage and little discomfort during the procedure. Needles of 0.5 to 2.5 mm have already been studied, with favorable results.61,64

As an adjunctive treatment for FPHL, microneedling is a relatively new procedure and lacks standardization about the best devices, frequency of applications, endpoint, and the number of sessions.62 Likewise, it is not known whether the fibrosis resulting from several sessions of microneedling can interfere with the technical difficulty of performing follicular transplants later. The topical use of sterile soluble pharmaceutical actives after microneedling with drug delivery intention has not yet been systematically studied regarding additional efficacy, nor are these actives authorized by regulatory organizations (FDA and ANVISA) for use through this route of administration.

The MMP® technique aims to promote drug infusion (drug delivery) and stimulation with needles in the epidermis and superficial dermis. For that purpose, it uses a tattoo machine and appropriate needles, which meet the adequate principles of equipment sterilization and disposal of needles after the procedure, which can be done in an outpatient setting.65 Mixtures with the infused actives are sterile and can be the same as described in the mesotherapy section.

Even when the drug infusion function is not used, at the physician discretion, the punctures produced by the machine can already induce an effect similar to that of using rollers, depending on the depth achieved.65

One study demonstrated that medication delivery through the MMP® technique occurs uniformly in the superficial dermis, requiring only a small volume of actives, in addition to not creating a “mass” effect, which reduces the chance of local adverse reactions. Moreover, the fact that the operator can adjust drug delivery and infusion depth also increase the safety of this technique.66

Pain, which is an undesirable effect of the microneedling technique, can also occur with MMP®.65 The folding technique consists of folding the skin of the area to be treated, between the thumb and index finger of the non-dominant hand of the physician performing the procedure. It may be useful in reducing pain during the procedure, as a result of changing the perception of pain by tactile stimulation and distancing the needles from the galea, which is richly innervated.67 Other more serious side effects have not been reported to date.65

Although apparently promising as adjuvant therapy, the literature on the subject is still scarce, especially with regard to FPHL. Moreover, some important recommendations remain empirical, such as the precise indications for the technique, the number of sessions necessary for the perception of the initial results, the ideal interval between sessions, and the need to recommend maintenance applications. The pharmaceutical actives used still lack authorization from the regulatory organizations (FDA and ANVISA) for use through this route of administration.

PRP is a technique that consists of the intradermal injection into the scalp of a concentrated autologous platelet preparation, which releases several growth factors, such as platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-β), vascular endothelial growth factor (VEGF), Epidermal Growth Factor (EGF), and insulin-like growth factor-1 (IGF-1). All of these growth factors play an important role in the hair cycle, as they stimulate stem cells located in the bulge, responsible for the follicular unit growth.68

A randomized controlled clinical trial in women with FPHL evaluated the effect of two monthly sessions of PRP against a placebo. This study found that, after 24 months of follow-up, there was an improvement in the photographic assessment in 57% of patients with PRP, versus 7% of improvement in patients receiving saline solution.69

Recently, a meta-analysis including 15 clinical trials evaluating PRP for AGA described an increase in hair density of 36.8 hairs cm2 (95% CI 22.6–51.1). However, many of these studies are limited by the small sample size and lack of adequate blinding.70

PRP is a promising adjuvant treatment in the management of FPHL; however, there is yet no standardization regarding blood preparation, centrifugation regimens, platelet density, need for platelet activation, and the technique of application.70,71 In a recent review, Stevens J. et al. suggested the following protocol: single centrifugation with platelet enrichment of three to six times the mean concentration of whole blood, proposed session interval of three monthly sessions, followed by quarterly sessions in a year.68

Both PRP and microneedling promote the local release of growth factors and epidermal and upper dermal trauma, but there are no comparative studies between the two treatment methods.

Up to now, the use of PRP for dermatological treatments in Brazil is still vetoed by the Federal Council of Medicine.

Oxidative stress, perifollicular microinflammation, and microvascular insufficiency have been reported as factors associated with AGA.72,73 Goldman et al. observed that in AGA, bald areas have lower oxygen (O2) levels than non-bald ones, suggesting some degree of microvascular insufficiency.74 Moreover, the conversion of testosterone into DHT preferentially occurs in an O2-poor medium, and therefore, an increased blood supply would reduce local hypoxia and thus could be beneficial in the treatment of AGA.75,76

It is known that DHT induces the production of transforming growth factor-β1 (TGF-β1) in the dermal papilla cells, having an important action in follicular epithelial cell growth suppression. Thus, TGF-β1 is a pro-apoptotic factor, with a relevant role in the onset of AGA, and antagonizing it could constitute a way to prevent disease progression.77

Botulinum toxin (BT) is a neurotoxin obtained from the bacterium Clostridium botulinum, which inhibits muscle contraction by blocking acetylcholine. The reasoning for the injectable use of BT in AGA would be to promote relaxation of scalp muscles, reducing muscle pressure on the perforating arteries and potentially increasing blood and O2 flow to the bald areas. Therefore, there would be a reduction in tissue DHT by the effect known as “washout” and, consequently, a lower rate of follicular miniaturization considered the main pathophysiological basis of the disease.75 As an additional mechanism, recently, Shon et al. suggested that intradermal injection of BT may be a possible treatment option for AGA, as it inhibits TGF-β1 secretion from hair follicles, thus contributing to the aforementioned effects.77

A prospective study evaluated 37 men using finasteride and minoxidil for AGA, who underwent application of botulinum toxin in half of the scalp, and the other half was injected with saline solution. After six months, there was a greater increase in hair density, 47.43 (±25.72) in the area treated with botulinum toxin compared to the control side, 21.68 (±11.09; p < 0.05).78 Despite the suggestion of applying the intradermal units 1 cm apart from each other, there is still no consensus on how to apply it and the interval regimen. The proposal to use botulinum toxin for the treatment of AGA is recent, promising, and has a good safety profile. However, systematic studies are required to prove its effectiveness in both men and women.76

Photobiomodulation or low-level laser therapy (LLLT) is a treatment modality used for patients with alopecia approved by the FDA in 2009.79

Photobiomodulation therapy devices typically contain laser diodes or light emitting diodes (LEDs) that emit light continuously (continuous wave) or in short, rapid pulses (pulsed emission). While lasers produce coherent, monochromatic light with a more focused radiation area, LEDs produce incoherent light with a broader emission spectrum and greater radiation field. Coherent laser light has historically been considered more effective than LED light, but it remains controversial whether one light source actually offers a clinical benefit over the other.80

The exact mechanism of action of photobiomodulation in the treatment of AGA is still unknown. It has been suggested that LLLT promotes keratinocyte and fibroblast mitosis through the stimulation of anti-inflammatory and antioxidant cytokines, in addition to a perifollicular vasodilator effect.79 Studies in both sexes showed that LLLT would be a well-tolerated therapy with no reported adverse effects. From an effectiveness point-of-view, most of the time, the results in AGA point to a quantitative increase in hair density and reduction in hair loss when compared to the placebo group.79

There are several devices for home use in the form of caps, helmets, headbands, and combs. Each one has a different amount of laser points and some are associated with LEDs, making it inappropriate to compare results between one device and the other.

The number of weekly applications and the duration of each application varies according to the device. Clinical response, according to studies, begin around four months after starting treatment.79

Regarding the energy provided by the devices, review studies have shown variations between 630 and 808 nanometers. From the biomolecular point of view, LLLT showed an increase in the main extracellular matrix proteins, which corroborates the clinical perception of increased hair diameter in users with AGA. Interestingly, the low-frequency (less than 60 minutes a week) treatment regimen seems to be more effective than the high-frequency one (more than 60 minutes a week).81

LLLT is an option as an adjuvant treatment for FPHL or as an alternative for those who do not wish to undergo clinical or surgical treatments. There is no evidence to support the use of LLLT sporadically prior to minimally invasive hair procedures, such as mesotherapy, microneedling, and MMP®.81

Hair prosthesis is a more specific term than wig to describe the hair piece used in medical conditions, such as advanced stages of FPHL.

Although the medical literature on this subject is still limited, it is crucial for the dermatologist to know the peculiarities of hair prostheses, such as the types of fibers from which they can be made, the characteristics of the bases, their main fixing methods and extension of the prostheses, to better indicate them.84

Sprays, powders, or fibers are methods of hair loss concealing that act as a temporary camouflage to cover areas with less density or absence of hair on the scalp.

Hair fibers, for example, consist of keratin that electrostatically adheres to the hair, giving it an appearance of more volume and, thus, disguising the areas of alopecia. Sprays, on the other hand, are more suitable for covering white hair or attenuating differences in color between hairless areas and those with hair.

The covering effect is natural and obtained immediately after the application. It does not cause any harm to the patient and is compatible with other dermatological treatments. In general, they are resistant to sweat, rain and wind, and can be removed after washing with shampoos. Because they do not have toxicity and are not absorbed, pregnant women and children can use them. Covering with these products promotes a natural and immediate result and should be considered complementary options to clinical treatment.

Trichomicropigmentation, also known as hair micropigmentation, is a non-surgical aesthetic procedure that uses conventional tattooing on the scalp and areas with hair, with the purpose of disguising unsightly scars, deformities, hair loss areas, and other conditions that cause hair thinning.85

The technique includes inserting microdroplets of pigment through the epidermis into the upper dermis (approximately 1.5 mm deep) using a standard tattoo instrument, which holds between one to six needles and cycles between 100 to 150 cycles per second. A tattoo is performed using a dotted pattern imitating the follicular ostia to decrease the contrast between the hair and the skin color. Thus, it produces an effect of increased hair density.85 The size and spacing of the dots will vary according to the professional artistic judgment.

Pigments used in micropigmentation are mainly inert, non-toxic, non-allergenic, stable in tissue and injected with approximately 6-µm gauge needles. The pigment substances differ depending on the required color. Cinnabar and mercuric sulfate are used for red coloring, iron oxide for black and brown, and cadmium sulfide is used for yellow coloring.60 There may be a bluish or greenish color resulting from direct exposure to ultraviolet light on the pigment through the skin. Moreover, prolonged exposure to the sun can accelerate changes in pigment hue. 86

This procedure must be performed by trained professionals. It has risks, such as bacterial infection and allergic reactions, and it can complicate with bleeding followed by loss of pigment when injected too superficially.85

Trichomicropigmentation is an interesting option for patients with FPHL in more advanced stages, with unsatisfactory response to clinical treatment, or with limitations to perform hair restoration surgery. Additionally, it promotes a permanent camouflage of thinning hair areas, promptly restoring self-esteem to affected patients (Fig. 5).

Figure 5.

Hair loss camouflage with trichomicropigmentation.

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