**1. Introduction**

Alopecia areata (AA) may cause significant cosmetic and psychological distress in affected persons due to the unpredictable course of the disease. The management of patients with AA is challenging, with no definite cure established. Corticosteroids have been the mainstay treatment used *via* topical, systemic, or intralesional routes. Other various treatment options have been tried, including systemic immunosuppressants such as methotrexate, azathioprine, and sulfasalazine and contact sensitizers such as dinitrochlorobenzene (DNCP), diphencyprone (DPCB), and squaric acid dibutyl ester (SADBE) [1, 2].

Phototherapies including psoralen plus ultraviolet (PUVA), UVA-1, and narrowband UVB (NB-UVB) were used to treat AA with some success rates. However, the disadvantage of these modalities is the exposure of a large area of normal skin to irradiation along with the alopecia area, making the increment of irradiation dose limited. Despite that, this method could be an effective alternative for patients who are resistant to systemic and topical therapy. Topical PUVA or phototoxic PUVA consists of a solution containing 8-methoxypsoralen that was administered to the affected areas of the scalp around 20 minutes before exposure to ultraviolet radiation. The dose was based on the patient's skin phototype [3]. UVA-1 (340–400 nm) was superior to narrowband-UVB (NB-UVB; 311 nm), as it can penetrate the deep layer of the skin where the hair follicle is situated.

Recently, 308 excimer laser/light therapy has been used for treating AA with the significant results and fewer adverse reactions. This technology has the ability to induce apoptosis of affected T-cells. The advantages of excimer therapy include a lower cumulative UV dose involved, a shorter time of treatment, and the option of targeting individual lesions without affecting the surrounding healthy skin [4]. It is now considered a good option in treating different immune-mediated skin diseases. Moreover, excimer can be emitted as coherent (laser) or non-coherent light, both seem compelling, with the cost-effectiveness ratio more favorable to light.

### **2. What is excimer?**

Excimer, also known as "excited dimer," is a class of diatomic molecules composed of atoms that are electronically excited and associated with the second atom in its ground (thermally unstable) state. The molecular ground state is unbound or weakly bound (by van der Waals forces). This means that a population inversion can be established automatically when the excited state occurs. Excimer lasers are capable of producing powerful and efficient broadband emissions at various spectral regions throughout the ultraviolet region. The most common types of excimer laser are the rare gas halides, which exhibit high power, average power, and single pulse energy. These include ArF, KrF, XeC1, and XeF. The last two types of excimers with weak ground states exhibit the most structured spectrums of overlapping remission transitions [5].

Formerly, excited dimers were represented only by homonuclear diatomic molecules with a steady excited state but repulsive ground states. Subsequently, excimer was extended to include any polyatomic molecule with a repulsive or weakly bound ground state—excimer molecule with heteronuclear dimer known as "exciplex" or exciting complex. For instance, Xe2\* is an excimer molecule, while XeCl\* and KrCl\* are exciplex molecules.

The new ultraviolet B ray source, exciplex "xenon chloride lamp," emits monochromatic 308 nm light representing the natural evolution of the excimer laser (**Table 1**). The monochromatic excimer light (MEL) produces 50 mW/cm2 power density at a distance of 15 cm from the source and has a maximum irradiating area of 504 cm2 [6].

#### **2.1 Historical aspect**

The excimer laser was proposed in 1960 by Fritz Houtermans. Incidentally, in 1967, Mester et al. noted that using low-level laser therapy (LLLT) to treat cancer in mice with shaved backs could induce hair regrowth [7]. Later, the use of noble gas halides (originally Xe Br and then Xe Cl) was developed by many groups in 1975. These groups include the Avco Everett Research Laboratory and Sandia Laboratories [8, 9].

*Overview of the Role of 308 Monochromatic Excimer Phototherapy for the Treatment of Alopecia… DOI: http://dx.doi.org/10.5772/intechopen.108531*


#### **Table 1.**

*Comparison between excimer light and excimer lamp.*

It was used for the first time in medical applications in 1997 when Bónis *et al*. tested its effect on psoriasis [10]. The study reported that excimer lasers might allow targeted, rapid phototherapy superior to conventional UV phototherapy with incoherent light. In 2001, Baltas et al. reported using the excimer laser to treat vitiligo [11]. Several studies have investigated the efficacy of 308 excimer on various dermatological disorders such as atopic eczema, mycoses fungoides, and AA [12–17]. All AA (single, multiple, and totalis) were identified and treated in those studies. Various protocols regarding the initial dose, increment dose, number of sessions per week, and complete course of treatment were applied.

#### **2.2 Mechanism of action of 308 excimer in alopecia areata**

AA is a T-cell-mediated autoimmune disease. It was believed that the immune system attacks the hair in the anagen phase, which leads to a rapid transition to catagen and telogen, resulting in hair loss. This process is triggered by the activation of the JAK/STAT cytokines, including IL-15 and interferon-gamma pathways [18].

The significant character of the hair follicle lies in its relative immune privilege, established by the suppression of surface molecules needed for presenting autoantigens to CD+ T lymphocytes and by the generation of an inhibitory local signaling environment. AA has been thought to develop due to cell death of protein 1 ligand (PD-L1), which leads to the collapse of immune privilege in the hair follicle [19].

Several triggers have been suggested to induce AA, including infection, drugs, trauma, and stress. Others such as autoimmune thyroid disease, atopy, and vitiligo are commonly associated. Psychological and physical insults may trigger the episodes of AA, but there is no evidence that they influence prognosis.

The high-dose monochromatic UV radiation of 308 excimer phototherapy can induce immunological suppression by altering cytokine production such as IL-4, IL-10, prostaglandin E2, platelet-activating factor, cis-urocanic acid, and trigger apoptosis. A study that used an excimer laser to treat AA in mice evaluated the number of perifollicular CD4+ and CD8+ in the treated patches before and after 12 weeks [20]. Results showed a significant decrease in the perifollicular infiltration of CD4+ and CD8+ with gross hair regrowth in the treated area.

It was suggested that the laser's effect on the activity and maintenance of T-cells could be mediated by the exertion of soluble mediators. The short wavelength of the excimer laser cannot penetrate human hair follicles, which means that the soluble mediators could potentially be utilized in inhibiting the activation of autoimmune reactions [20].
