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 Table of Contents  
Year : 2020  |  Volume : 8  |  Issue : 1  |  Page : 140-146

Vitiligo with special emphasis on vitiligo surgery

Department of Dermatology, Venereology and Leprology, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, Karnataka, India

Date of Submission07-Apr-2020
Date of Decision15-May-2020
Date of Acceptance19-May-2020
Date of Web Publication20-Jun-2020

Correspondence Address:
Dr. P K Ashwini
Department of Dermatology, Venereology and Leprology, JSS Medical College, JSS Academy of Higher Education and Research, Mysuru, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/amhs.amhs_50_20

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Vitiligo is a common form of localized depigmentation. It is an acquired hypomelanotic condition resulting from the progressive loss of melanocytes. It is characterized by milky white macules. It can be associated with tremendous psychological trauma. A number of medical treatment options exist in the armamentarium of a dermatologist treating vitiligo. However, a significant number of lesions of vitiligo either fail to respond to medical therapy or respond with incomplete repigmentation. Such lesions are considered appropriate for surgical management. Surgical management has provided a very good tool to the management of refractory cases of vitiligo. Hence, in this article, we emphasize on vitiligo and vitiligo surgery.

Keywords: Melanocytes, vitiligo, vitiligo surgery

How to cite this article:
Ashwini P K, Sushmitha D J, Veeranna S. Vitiligo with special emphasis on vitiligo surgery. Arch Med Health Sci 2020;8:140-6

How to cite this URL:
Ashwini P K, Sushmitha D J, Veeranna S. Vitiligo with special emphasis on vitiligo surgery. Arch Med Health Sci [serial online] 2020 [cited 2023 Mar 31];8:140-6. Available from: https://www.amhsjournal.org/text.asp?2020/8/1/140/287366

  Introduction Top

Vitiligo is a very common, acquired, pigmentary disorder of skin and hair characterized by the appearance of white patches on the skin and mucosa.[1] It occurs due to the autoimmune destruction of functional melanocytes (MC). Incidence in the racially pigmented skin is much higher.[2] Vitiligo has been derived from the Latin word “vitium” meaning “blemish.” Alternatively, the Latin derivation may be from the white, glistening flesh of calves.[3] By 1450 BC, white leprosy spots were called as “swetha kushtha” in the Atharva veda and in 1200 BC, Japanese Shinto prayers described the similar condition in the “Amarakosa.” The term 'Vitiligo' was first said to be used by Celsus in his Latin medical classic 'De Medicina in 1st century AD.[4]

The World Vitiligo Day is observed on June 26. This day signifies spreading the knowledge regarding the various treatment options and counseling the public and the patients regarding the stigma associated with the condition. The Indian Association of Dermatologist, Venereologist and Leprologists (IADVL) conducts various public awareness programs on this day such as street plays, seminars, and awareness talks.

  Epidemiology Top

The worldwide prevalence of vitiligo ranges from 0.4% to 2.0%, with the highest incidence being recorded in India, followed by Mexico and Japan.[5],[6] The prevalence of vitiligo has been reported to be between 0.25% and 4% of dermatology outpatients across studies from India. Vitiligo affects both genders, and the mean age of onset is before 20 years in case of childhood vitiligo but varies between 18 and 32 years in adults.[7],[8]

Among the multitude of triggers such as chemicals, allergens, occupation, diet, systemic illness, and sunlight implicated, the physical trauma to the skin perhaps seems to be the most implicated factor, both for onset and development of vitiligo and tendency of the lesions for localizing over trauma-prone sites (Koebner's phenomenon). The presence of Koebner's phenomenon, a very frequent occurrence in 20%–60% vitiligo patients, corroborates with this observation.[9] The proportion of affected patients with positive family history varies in different parts of the world. In India, it ranges from 6.25% to 18%.[3]

  Etiopathogenesis Top

Vitiligo being a multifactorial disease has a relationship with both genetic and acquired factors.[1] Family and twin studies points toward the importance of genetic factors in the development of vitiligo.[10],[11] Many of these genes are involved in melanogenesis, immune regulation, and apoptosis. In vitiligenous skin, there is loss or disappearance of epidermal or follicular MC.[12] The MCs in vitiligo skin are susceptible to environmental triggers or stressors. Ultimately, there is development of autoimmunity which is directed against MC.[13]

Autoimmune hypothesis

Autoimmunity has always been suspected to play a significant role in the pathogenesis of vitiligo. An alteration in immune surveillance has been proposed as the significant primary event leading to dysfunction and destruction of MC.[14]

Neurohumoral hypothesis

According to this hypothesis, destruction of MC occurs due to liberation of some unusual neurochemical mediator or a gross alteration in the ratio of the normal neurotransmitter levels in the lesion. This could be due to the common origin of both the MC and nerves arising from the neural crest cells.[15],[16]

Free radical hypothesis

The oxidative stress theory suggests that the intra -epidermal accumulation of reactive oxygen species, the most notorious one being hydrogen peroxide (H2O2), lead to the destruction of melanocytes.[17]

Other proposed theories include low circulating growth factors, Vitamin D deficiency, and melanocytorrhagy.[18],[19],[20],[21],[22]

  Clinical Features Top

Vitiligo is characterized by the appearance of patchy discoloration of the skin in the form of typical chalky-white or milky skin lesions. The macules are round or oval in shape with sizes ranging to few millimeters to a foot or more. Lesions affect the skin and mucous membranes. They are asymptomatic although itching or burning may precede or accompany the onset of vitiligo.[23],[24],[25],[26]

Sites commonly affected are pretibial area, knees, sides of ankles, elbows, and skin overlying the digits.[14] Periorificial areas such as the circumoral, anogenital and periocular areas are also affected. Leukotrichia (gray hairs) is a common feature of vitiligo lesions, especially on hair-bearing skin. It has diagnostic and prognostic significance. Diagnostic significance implies that it helps in differentiating it from other hypopigmented macules. Prognostic significance indicates a poor repigmenting capacity.[27]

[TAG:2]Classification of Vitiligo [28][/TAG:2]

There is no universally accepted classification available for vitiligo.


  1. Focal vitiligo: One or more macules in one area, but not in a segmental distribution
  2. Unilateral or segmental vitiligo: One or more macules involving a unilateral segment of the body and the lesions stop abruptly at the midline
  3. Mucosal vitiligo: Mucous membranes alone.


  1. Vitiligo vulgaris: Scattered patches that are widely distributed
  2. Vitiligo acrofacialis: Seen on distal extremities and face
  3. Mixed vitiligo: Mixture of acrofacialis and vulgaris.

Vitiligo universalis

Complete or nearly complete depigmentation.[28]

Histopathology [29]

There is complete absence of melanin granules in the vitiligenous skin. Histochemical studies show gross lack of dihydroxy phenylalanine-positive MC in the basal layer. The special stain used for melanin is Mason Fontana stain.

  Associations of Vitiligo Top

Cutaneous associations: Leukotrichia, premature graying of the hair, and other conditions such as lichen planus, alopecia areata, and halo nevus, are frequently reported cutaneous associations.[30],[31]

  Systemic Associations Top

Systemic diseases such as pernicious anemia, thyroid disorders, diabetes mellitus, Addison's disease, and autoimmune polyendocrinopathy are a few of the systemic conditions associated with vitiligo.[3]

  Course of the Disease Top

The course of vitiligo is very unpredictable and uncertain. Lesions might remain static/same for an indefinite period after a certain degree of regional extension. In vitiligo vulgaris, lesions can develop on several different areas in succession. At times, the repigmented spots occur spontaneously. Complete spontaneous cure is extremely rare.[14]

  Management Top

There is no ideal treatment for vitiligo as the exact pathogenesis of the disease is still elusive. Earliest of the therapies or treatment modalities that were available was from various indigenous folk medicines. They were used in different countries. It comprised of an oily extract from the seeds of Psoralea corylifolia.[14]

Current treatment options for vitiligo include medical, surgical, and adjunctive treatments. They range from topical corticosteroids (TCS), topical calcineurin inhibitors (TCIs), ultraviolet (UV)-based therapy (narrowband [NB]-UVB, targeted phototherapy, and psoralen and UVA photochemotherapy), to multiple surgical treatments – punch grafting, suction blister grafting, and melanocyte keratinocyte transplantation.[32] Medical treatment mainly targets the immune system. It helps in arresting the spread of depigmentation.

  Topical Corticosteroids Top

These are often used as the first-line therapy for localized disease. When TCS are used over 2–4 months, it yields good results, but side effects may develop such as atrophy, hypertrichosis, and in cases, treatment needs to be interrupted.[33] When applied over eyelids, additional side effects such as increased intraocular pressure and glaucoma call for extra caution.[34]

  Topical Calcineurin Inhibitors Top

Among the various medical treatment options, TCIs such as tacrolimus and pimecrolimus are recommended as one of the first-line treatments for localized forms of vitiligo. Combining TCIs with phototherapy has definitely shown to enhance the treatment response.[35]

  Phototherapy Top

Phototherapy is the use of UV radiation or visible light for therapeutic purposes. UV radiation is a small component of the electromagnetic spectrum with a NB of radiation from 200 to 400 nm.[36]

Psoralen ultraviolet A photochemotherapy

Consumption of psoralen tablets followed by UV A-320–400 nm (PUVA) has shown a beneficial effect in vitiligo. The plant origin widely used is 8-methoxy psoralen. The synthetic drug 4, 5, 8-trimethyl psoralen, which is less phototoxic after oral administration, is primarily used for treatment of vitiligo. In a similar manner, PUVASOL can be given where psoralen with sunlight is used as a source of UVA rays. The disadvantage here is the difficulty in quantifying UV light. It can be used to induce pigmentation over streaks of residual depigmentation left after grafting. Topical application of 8 methoxy psoralen followed by sun exposure is advised for three to four times per week.[32],[36]

Narrow band (311 nm) UVB phototherapy

Just like the PUVA therapy, NB-UVB may exert its effects in vitiligo through a two-step process. First being the stabilization of the depigmenting process and the second being the stimulation of residual follicular MC. Fluorescent bulbs that deliver UVB in the range of 310–315 nm are used.[36]

Targeted phototherapy

It involves application of light energy directly on the lesion through special delivery mechanisms such as fiberoptic cables.[37] The term “targeted phototherapy” includes different technologies such as excimer laser (308 nm), intense pulse light systems, and nonlaser UV light sources with improved hand-held delivery systems.[37]

Systemic therapy

Azathioprine, levimasole, antioxidants, oral corticosteroids are used. Oral minipulse is a type of pulse steroid therapy where oral betamethasone 5 mg daily for 2 consecutive days has also been used to treat resistant and extensive disease with variable results. It helps to control the progression of rapidly spreading disease. The patients need to be monitored for development of steroid-induced side effects like weight gain and acne form eruptions.[14] Also, low-dose oral mini pulse dexamethasone 2.5 mg/day on 2 consecutive days per week is found to be beneficial for arresting progressive unstable vitiligo with minimal adverse effects.[38]

[TAG:2]Surgical Thérapies [39],[40],[41][/TAG:2]

Surgery for vitiligo is useful in resistant areas and residual lesions. The choice of surgical treatment depends on the type of vitiligo; stability, extent, and site of lesions; the availability of equipment; and expertise of the treating surgeon. The various procedures include surgical excision, dermabrasion, punch grafting, micropigmentation, minigrafting, thin thiersch grafting, epidermal grafting, and transplantation of in vitro cultured epidermis bearing MC.

  Principle of Vitiligo Surgery Top

All surgical techniques for vitiligo rely on the one basic principle; when melanocyte reservoir is lost in the epidermis, repopulating with functional MC from normally pigmented epidermis or hair follicles. The MCs which have been introduced will then establish and function as epidermal melanin units.

  Parameter for Patient Selection Top

  1. Duration of stability
  2. Test grafting
  3. Keobner's phenomenon
  4. Longevity of stability
  5. Disease versus lesional stability.

  Stability in Vitiligo Top

It is mandatory that all surgeries are done after establishing stability of the disease. It indicates the absence of development of new patches and absence of increase in size of the existing patches. Absence of Keobner's phenomenon should also be considered for labeling it as stable vitiligo. Though there is lack of agreement regarding duration of stability, a period of 1 year is best followed as per the recommendations by IADVL taskforce for standard guidelines of care for dermatological procedures. Lesional stability can be considered before considering the patient for surgical techniques. A stable patch has well-defined borders in comparison with un stable patch which shows ill-defined borders. Hypomelanotic lesions with poorly defined borders indicate active lesions compared to patches which are amelanotic with sharply defined borders [42]

Scoring system in vitiligo:[14]

  1. Vitiligo Area Severity Index – In this scoring system, the percentage of vitiligo involvement is calculated in terms of hand unit and the degree of pigmentation is estimated to the nearest of percentages [Annexure 1]
  2. Vitiligo Disease Activity Score – It is a 6-point scale for assessing vitiligo activity. The scoring is based on the individual own opinion of present disease activity [Annexure 2].

  Dermoscopy Top

Dermoscopy shows white structureless areas and reduced pigment network in Vitiligo. White structureless areas appear to “glow” due to total loss of MC in the epidermis. A vitiligo patch is considered stable in the presence of sharp border, absent pigment network, reticulate pigment network, perilesional hyperpigmentation, and perifollicular pigmentation and in the absence of satellite lesions and micro Keobner's phenomenon. A cutoff score of more than or equal to 1.5 using the “BPLeFoSK criteria” is recommended.[43],[44]

  Surgical Methods Top

The methods of vitiligo grafting are divided into tissue grafting and cellular grafting. Tissues such as epidermal-dermal mini punches, ultra-thin skin layers, epidermal roof of a blister, or hair follicles are used as the sources of MC. Cellular grafts include cultured or noncultured melanocyte grafts.

Tissue graft:

  1. Mini punch grafting
  2. Suction blister grafting
  3. Thin split-thickness grafting
  4. Hair follicle grafts
  5. Smash grafts
  6. Mesh grafts.

Cellular graft:

  1. Noncultured cell suspensions – epidermal cell and follicular cell
  2. Cultured MC/keratinocytes grafts.

[TAG:2]Patient Selection [39][/TAG:2]

Surgery is indicated for patients with stable vitiligo patches. It can be considered in patients who are unresponsive to medical treatment. Younger patients respond better. Concurrent need for medical therapy and phototherapy postsurgery should be emphasized. Patient counseling is of utmost importance. Patients with an unrealistic expectation is not a good candidate for surgery. It is important to assess the psychosocial norms of the patient.

Preprocedural investigations such as complete blood counts, blood sugar estimation, and bleeding and clotting time can be done in most of the cases.

Ideal donor site

The upper outer aspect of thigh, medial aspect of forearm, arm, abdomen, and gluteal area can be considered. For facial lesions, the postauricular area can be considered because color match is important.

The recipient area preparation can be done using manual or motorized derma abrader, ablative CO2, or fractional CO2 laser, or Erbium YAG laser, or micro needling, cryo blistering, or suction blistering. Dermabrasion must be done evenly all over the depigmented area and 2–3 mm of peri lesional normal skin. This is to prevent the development of a peri graft halo postoperatively.

Mini punch grafting [41]

Epidermal mini punches of 1–2 mm sizes are harvested from the normal pigmented donor site using disposable punchesm and they are transplanted into the depigmented recipient area. It is best suited for sites with irregular contours such as nipple-areola complex, palms and soles, acral areas. It is an inexpensive, simple, and easy procedure to perform with minimal requirements. Cobblestoning and polka dot appearance are usual complications causing a cosmetic unacceptability. To minimize the chances of developing a peri graft halo, the initial recipient chambers are made very close to the border of the patch. The three-layered dressing on the recipient area is removed after 4–7 days. Postgraft phototherapy is usually followed. The grafted area is expected to repigment within 3–6 months [Figure 1]. Similarly, hair follicle transplantation can be employed, especially for those patches with leukotrichia.
Figure 1: Miniature punch grafting: Early spread of pigment seen from punch grafts

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Suction blister grafting [45]

Epidermis is harvested from donor site by prolonged negative pressure, using a 50 cc disposable syringe attached to the plunger of 20 cc syringe using a three-way cannula, resulting in a blister formation. Approximate blistering time is from 1 to 3 h. The suction causes a physiological split at dermo-epidermal junction. The roof of the blister is then transplanted on the dermabraded recipient site, leading to transfer of MC. Sites such as lips and eye lids which need thin grafts are the best suited sites. It is an inexpensive and safe procedure. Donor-site scarring is also unusual. It gives a good cosmetic result on lip. The procedure is good to be performed for facial vitiligo. It is time consuming and yields only small-sized grafts.

Ultra-thin skin grafts

They are also called split-thickness skin grafts.[46] Epidermal layers of 0.08–0.15 mm thickness are used as tissue source for MC. A donor skin of 10%–20% larger than the recipient area is harvested using skin harvesting knife [Figure 2]. They are suitable for larger patches and covers large areas over short period of time. Uniform pigmentation can be expected in this technique [Figure 3] and [Figure 4]. Donor area healing may be delayed and postinflammatory hyperpigmentation on recipient area might occur. The initial 72 h after graft placement is crucial for graft uptake. Proper immobilization is essential after grafting. The technique demands good surgical skill. It offers cosmetically better results than mini punch grafting.[47] Moreover, compared to other grafts mentioned above, this procedure can cover larger areas.[48]
Figure 2: Ultra-thin grafts harvested from donor site and placed in saline

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Figure 3: Pre graft – Vitiligo patch on the knee

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Figure 4: Postgraft pigmentation – 6 weeks after split-thickness grafting

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Cellular transplantation [49]

These techniques such as keratinocyte melanocyte grafts offer several advantages over tissue grafts. It has shown to cover larger surface area, better color matching, and uniform repigmentation. The donor recipient area coverage is in the ratio of 1:8 to 1:10. It requires laboratory facilities, involves high cost and is time consuming.

The process involves harvesting of skin similar to ultra-thin grafting, which is later trypsinized using 0.25% trypsin-EDTA solution. The vital steps in epidermal noncultured suspension include donor harvesting, trypsinization to separate the cells, anti-trypsinization to remove excess trypsin, centrifugation to make a cell suspension, and finally transplanting the obtained suspension over the dermabraded recipient area. In 1998, Olsson and Juhlin [50] introduced rapid trypsinization method within 60 min under 37°C (hot trypsinization) and transplanting the cell suspension, nourished with melanocyte culture medium, directly on the dermabraded recipient site. Addition of hyaluronic acid to the cell suspension to increase viscosity and adherence to the recipient site was proposed by van Geel et al.[51] Holla et al. modified the steps to reduce the cost of the procedure by introducing phosphate-buffered saline, as a way to circumvent the use of trypsin inhibitor.[52]

After the procedure, the onset of pigmentation can take 3 weeks and 6 months [Figure 5] and [Figure 6]. Adjuvant therapies such as phototherapy help. Proper counseling of the patients is important as to what can be expected and also about the possible progression of the disease process.[39]
Figure 5: Patchy pigmentation postmedical therapy – recalcitrant patch without even repigmentation

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Figure 6: Even repigmentation seen 8 weeks postgraft-noncultured epidermal suspension

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Autologous noncultured epidermal cell suspension is also simplified using a four-compartment method compared to the laboratory-based method. The results are comparable to the conventional method of vitiligo surgery.[53] Combination of noncultured epidermal and dermal suspension is a novel technique. The combination technique is said to give excellent results in patients with vitiligo with shorter duration of clinical stability.[54]

  Future Prospects in Vitiligo Therapy Top

The discovery of melanocyte specific T memory cells leads to bringing vitiligo under memory skin disease. Future therapies should goal at blocking the differentiation and/or their accumulation in vitiligo skin. It is suggested to use TCIs as maintenance therapy in repigmented patches to prevent their loss of pigmentation. Systemic immunomodulating agents could be another strategy for patients with higher body surface area. In addition, steroid-sparing immunomodulating agents that could be used for mid and/or long-term period, such as methotrexate or JAK inhibitors, have to be considered in future, to avoid steroid systemic side effects.[55]

Significant repigmentation has been noted with use of two JAK kinase inhibitors tofacitinib and ruxolitinib. Afamelanotide, a synthetic alpha melanocyte-stimulating hormone which requires the presence of melanocortin 1 receptor and supplementation with NB-UVB to stimulate melanoblast differentiation, may be an effective new vitiligo therapy.[56]

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  Annexures Top

Annexure 1: Vitiligo Area Severity Index

The percentage of vitiligo involvement is calculated in terms of hand units. One hand unit (which encompasses the palm plus the volar surface of all digits) is approximately equivalent to 1% of the total body surface area. The degree of pigmentation is estimated to the nearest of one of the following percentages: 100% – complete depigmentation, no pigment is present; 90% – specks of pigment present; 75% – depigmented area exceeds the pigmented area; 50% – pigmented and depigmented areas are equal; 25% – pigmented area exceeds depigmented area; and 10% – only specks of depigmentation present.

The VASI for each body region is determined by the product of the area of vitiligo in hand units and the extent of depigmentation within each hand unit measured patch.

The total VASI, with a score ranging from 0 to 100, is calculated using the formula: VASI = S (all body sites) (hand units) × (residual depigmentation).

Annexure 2: Vitiligo Disease Activity Score (VIDA)

The VIDA is a 6-point scale for assessing vitiligo activity. Scoring is based on the individual's own opinion of the present disease activity over time. Active vitiligo involves either expansion of existing lesions or appearance of new lesions. Grading is as follows: VIDA Score +4 – Activity of 6 weeks or less duration; +3 – Activity of 6 weeks to 3 months; +2 – Activity of 3–6 months; +1 – Activity of 6–12 months; 0 – Stable for 1 year or more; and - 1 – Stable with spontaneous repigmentation since 1 year or more. A low VIDA score indicates less activity.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]

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