Vitiligo Update: Pathogenesis, Therapies, and Integrative Approaches

Vitiligo is a chronic autoimmune condition characterized by depigmented white patches due to melanocyte destruction, attributed to genetic factors and environmental triggers. Vitiligo affects between 0.1% and 2% of the population, including children and adults. Patients of all genders and all races/ethnicities are equally affected.¹ There are various subtypes of vitiligo, including non-segmental vitiligo, the most common subtype, and segmental vitiligo, which presents as patches localized to one side of the body. The depigmented patches have a predilection for the face (eg, periocular and perioral areas), hands, and trunk and range in size from millimeters to centimeters.¹^,² Unique vitiligo subtypes include confetti-type vitiligo, which appears as generalized small guttate white patches, and trichrome vitiligo, characterized by three shades, with normal skin tone, a white patch, and an intermediate tone.³^,⁴ In most cases of vitiligo, depigmented patches tend to expand slowly and centrifugally, with confetti-type and trichrome vitiligo experiencing more rapid progression. Koebnerization, or the appearance of vitiligo in areas following trauma, occurs in up to 60% of patients.²

The mechanism of melanocyte destruction is believed to be a result of cell-mediated immunity driven by CD8⁺ T cells. These autoreactive T cells target melanocyte-specific antigens such as tyrosinase, Melan-A, and tyrosinase-related peptides. CD8⁺ T cells secrete cytokines such as IFN-γ, which trigger the release of CXCL9 and CXCL10 from neighboring keratinocytes, perpetuating a feedback loop that leads to further T-cell activation. Additional insight into resident memory T cells has highlighted their suspected role in vitiligo relapses following treatment remission. Resident memory T cells remain in the skin and recruit circulating T cells early in the immune response under the influence of IFN-γ.¹^,⁵ Additionally, the WNT/β-catenin pathway, essential for the proliferation and migration of melanocytes and the production of melanin, was found to be altered in vitiligo.⁶

Though yet to be clearly defined, key gene polymorphisms play a role in the heritability of vitiligo. Studies suggest the risk of a patient’s sibling developing the disease is 6%, and 23% for an identical twin.⁵ Patients with vitiligo also have an increased risk of developing other autoimmune diseases, such as thyroid disease, rheumatoid arthritis, inflammatory bowel disease, type 1 diabetes mellitus, and systemic lupus erythematosus.⁷

Oxidative stress contributes to the destruction of melanocytes. Tetrahydrobiopterin (BH₄) is an endogenous cofactor that plays a crucial role in enzymatic conversions, as well as dopamine, noradrenaline, and serotonin biosynthesis.⁸^,⁹ Defective recycling of BH₄ leads to increased intracellular hydrogen peroxide production within the epidermis of patients with vitiligo. The accumulation of reactive oxidative species (ROS) results in altered protein function, defective apoptosis in melanocytes, and increased cytokines such as TNF-α and TGF-β.⁸ Melanocytes from patients with vitiligo also show a decrease in catalase, an enzyme that converts H₂O₂ into H₂O and O₂. Of note, this deficiency has been found in other skin disorders and may not be specific to vitiligo.⁹^,¹⁰

Accounts describing instances of vitiligo-like chemical leukoderma associated with certain exposures to monobenzone and monobenzyl ether of hydroquinone (MBEH) provide some insight into how environmental factors and other causative agents may be involved in the pathogenesis of vitiligo. Still, there is a paucity of data.¹¹^,¹²

Treatments

There is a wide range of treatments for vitiligo, from topical therapy to phototherapy, surgical intervention, and systemic therapy.

Topical Therapies

A common first-line treatment is topical corticosteroids. The main function of corticosteroids is to locally reduce inflammation and suppress immune responses in the skin. Topical corticosteroids (TCS) are prescribed according to potency, with high-potency TCS (fluocinonide, betamethasone, halobetasol, clobetasol) favored at affected sites on the trunk, extremities, and scalp. Expert guidelines recommend potent TCS application be limited to once daily for 3 to 6 months using an alternating regimen of 2 weeks on and 2 weeks off.¹³ This regimen helps to limit several side effects associated with chronic topical steroid use, including skin atrophy, striae, hypertrichosis, telangiectasia, purpura, and glaucoma (when used near the eye).⁶ TCS should be used with caution on affected sites on the face (particularly eyelids), skin folds, and genitals. Systemic absorption following widespread application has been described and should be taken into consideration when used on large body surface areas and in children.

Topical calcineurin inhibitors (TCIs) may also be considered first-line treatment and are utilized for monotherapy and combination therapy. TCIs downregulate proinflammatory cytokines, reducing immune-mediated melanocyte destruction and fostering melanocyte migration.¹⁴ The most prescribed TCIs include tacrolimus and pimecrolimus, and adverse effects include burning sensations of the skin, pruritus, and erythema. This treatment is particularly suitable in children and for vitiligo on the face and neck. TCIs can be prescribed for use twice daily for 6 months. Longer courses can be considered depending on response.¹³^,¹⁴ Despite their black box warning, a large multicentered retrospective cohort study of 25,694 patients with vitiligo found no associated long-term risk between the use of TCIs and lymphoma and skin cancer.¹⁵

The Janus kinase (JAK)/signal transducer and activator of transcription (STAT)-1 signaling pathway is a positive feedback loop, mediated by IFN-γ, that recruits CD8⁺ T cells and promotes melanocyte apoptosis. Topical ruxolitinib 1.5% cream, a JAK1/2 inhibitor, is the first FDA-approved treatment for repigmentation of nonsegmental vitiligo. In phase 3 clinical trials, 50.3% of participants achieved a Facial-VASI (F-VASI) 75 at Week 52, and 51.1% of patients achieved a total VASI (T-VASI) of 50 at Week 52.¹⁶ Common side effects include application site reactions, acne, and upper respiratory infections.¹⁷

Phototherapy

Both psoralen–UV-A (PUVA) and narrowband UV-B (NB-UVB) have been used as treatments, with NB-UVB being preferable due to its favorable side effect profile.¹⁸ NB-UVB may be delivered in-office or at home via traditional booths or light panels for widespread involvement or via handheld or targeted therapy for localized patches with the 308-nm light-emitting diode and 308-nm excimer lamp.¹⁹ PUVA is quite limited due to associated adverse effects, including phototoxicity, nausea, and potential risk of skin cancer.¹³^,¹⁸ NB-UVB, however, is well tolerated and can be used on both children and pregnant women. The adverse effects include erythema, dryness, itching, and/or burning. Phototherapy has proven most effective when utilized in combination with topicals but can be used as monotherapy.¹⁸

Surgical Therapy

Surgical intervention is considered a viable treatment option in patients with stable disease (no progression or new active sites for at least 1 year), who have failed more than 6 months of topical treatments and phototherapy.²⁰ Procedures include tattooing, suction blister grafts, miniature punch grafts, split-thickness skin graft, and autologous non-cultured melanocyte–keratinocyte transplantation.²¹

Tattooing is a technique that involves permanent dermal micropigmentation to cover the areas affected by vitiligo.²²^,²³ The areas best suited are small recalcitrant areas such as the lips, hands, hairline, perioral region, and distal digits. Results vary from mild to dramatic repigmentation. A moderate amount of fading is expected within the first 6 weeks post-treatment.²²

Punch skin grafting involves multiple perforations with a small punch measuring 1.5 mm, made 3 to 4 mm apart from each other.²¹^,²⁴ The total number of grafts punched depends on the size of the area. The donor sites for the grafting procedures are most commonly the thighs and upper forearms.²¹^,²⁴ Punch skin grafting is associated with lower rates of depigmentation when compared to split-thickness grafting.²⁴^-²⁶

Split-thickness skin grafting involves harvesting a thin sheet of epidermis and superficial dermis from a pigmented donor site and applying it to dermabraded recipient areas.²⁵^,²⁶ Excellent color match both postoperatively and in long-term follow-up has been reported. The technique can be used over any part of the body, including those with hair. However, it requires good surgical technique.²⁵^,²⁶

Suction blister epidermal grafting (SBEG) is used to treat both resistant and stable vitiligo. In this method, blisters are created using negative pressure by applying suction, leading to a split at the dermoepidermal junction. This results in very thin epidermal grafts, which are then transferred to the recipient site.²⁷ In contrast to mini punch grafting and split-thickness grafting, SBEG yields purely epidermal grafts which take on the characteristics of the recipient site and offer better color match outcomes.²⁷^,²⁸

A number of complications are associated with vitiligo surgery. For instance, split-thickness skin grafting can be associated with graft rejection, perigraft halo, milia, and scarring at the donor site.²¹^,²²^,²⁸ Suction blister grafts can lead to ecchymosis and postinflammatory hyperpigmentation, while miniature punch grafts can lead to cobblestoning—a polka dot appearance on the skin—and graft rejection.²⁷^,²⁸^,²⁹

Autologous non-cultured melanocyte–keratinocyte transplantation (MKTP) can be used to treat stable vitiligo cases and is one of the more popular techniques among dermatologists.²¹^,²⁹ MKTP has high repigmentation rates across various vitiligo subtypes. Pre-MKTP phototherapy can be used to prime the skin before transplant to reduce disease activity and improve recipient site results.²⁴^,²⁹ MKTP is a safe and effective treatment.

In 2023, the ReCell (Avita Medical) device was FDA-approved for the repigmentation of stable depigmented vitiligo lesions in patients 18 years of age and older. ReCell offers a more streamlined and safe technique to autologous epidermal suspension through a point-of-care spray-on skin cell preparation. Hamzavi et al reported 36% of treated lesions achieved ≥80% repigmentation at Week 24 compared to 0% for those treated with NB-UVB (P < .025). Repigmentation was sustained through week 52.³⁰^,³¹

Integrative/Complementary Therapies

The literature suggests that a number of alternative therapeutics may offer potential benefits in the treatment and management of vitiligo. This includes Picrorhiza kurroa of Ayurvedic medicine, Ginkgo biloba, L-phenylalanine, Aloe vera, Chinese herbal medicine (CHM), green tea extract, and quercetin. Studies report repigmentation in patients who utilized these treatments either alone or in conjunction with conventional topical medications and light therapy with little to no side effects.^32-37

A randomized, double-blind, placebo-controlled trial of 47 patients showed a statistically significant improvement in active progression of vitiligo in subjects treated with Ginkgo biloba extract versus placebo (P = .006).³³ More subjects receiving G. biloba reported marked to complete repigmentation as compared to placebo. However, this result was not statistically significant. No significant side effects were reported.

A retrospective review of vitiligo patients treated with Aloe vera thrice daily for 6 months in conjunction with sunlight exposure between July 2021 and August 2022 noted substantial rates of repigmentation.³⁴ Mild pruritus, burning, and stinging were reported during the first week of usage.

Similarly, in a meta-analysis of five randomized controlled trials with 513 total participants, oral CHM yielded repigmentation rates of 30% in combination with NB-UVB. The meta-analysis revealed a superior effectiveness in those receiving oral CHM plus NB-UVB when compared to phototherapy alone (P < .00001). Tribulus terrestris and Psoralea corylifolia were identified as the most common herbs found in each formulation.³⁶

Given the role of oxidative stress in vitiligo, other therapies such as green tea extract and quercetin may be useful adjunctive treatments. In vitro studies of green tea extract and quercetin showed antioxidant and cytoprotective abilities against hydrogen peroxide-mediated cell death in melanocytes, and a combination of green tea extract, quercetin, and folic acid showed a synergistic effect in preventing cellular damage.³⁷ In a study of 28 subjects, a combination of alpha-lipoic acid, vitamin C, and vitamin E combined with NB-UVB showed a significant improvement compared to phototherapy alone, with 47% of participants achieving >75% repigmentation (P < .05).³⁸ A topical catalase, pseudocatalase, has been tested in several studies as a treatment for vitiligo, but the results have not been consistent.³⁹

Future Directions/Clinical Trials

Significant advances have been made in therapeutic options for vitiligo in recent years. There are many clinical trials investigating new and emerging therapies. In addition to the approval of topical ruxolitinib, the oral JAK inhibitors baricitinib (a JAK1/2 inhibitor), upadacitinib (JAK1 inhibitor), povorcitinib (JAK1 inhibitor), and ritlecitinib (a JAK3/TEC inhibitor) are currently being tested in ongoing trials, further emphasizing the expanding role of JAK inhibition in vitiligo management. Additionally, there is a phase 3 trial underway evaluating the safety and efficacy of ruxolitinib cream in the treatment of pediatric patients aged 2 to 11 years with nonsegmental vitiligo. A phase 2 trial with 364 patients showed that after 24 weeks, ritlecitinib 50 mg significantly reduced Facial Vitiligo Area Scoring Index (F-VASI) from baseline.⁴⁰

In a phase 2b study over 52 weeks, oral povorcitinib led to significant repigmentation of the face and body in subjects with extensive nonsegmental vitiligo. Responses were generally maintained up to 24 weeks after stopping the treatment.⁴¹ In a phase 2, multicenter, randomized, double-blind, placebo-controlled, dose-ranging study, upadacitinib monotherapy significantly improved repigmentation of facial and body vitiligo lesions, prompting an ongoing phase 3 randomized controlled trial evaluating the efficacy of upadacitinib 15 mg in adults and adolescents with nonsegmental vitiligo.⁴²

Another promising investigational therapy is cerdulatinib, a dual JAK and spleen tyrosine kinase (SYK) inhibitor. The inhibition of both JAK and SYK pathways may offer a novel mechanism to modulate immune responses and melanocyte survival, potentially improving repigmentation outcomes. A phase 2a, randomized, double-blind, vehicle-controlled study is currently underway to evaluate the safety and tolerability of cerdulatinib gel, 0.37%, in adults with vitiligo.⁴³

Afamelanotide, a synthetic melanocortin-1 receptor agonist, is currently being investigated as a new treatment modality for vitiligo, including an open-label, phase 2 study to assess the changes in pigmentation and safety of subcutaneous, bioresorbable afamelanotide implants in the treatment of vitiligo on the face. A phase 2b study to compare the efficacy and safety of subcutaneous, bioresorbable afamelanotide implants plus NB-UVB light source in the treatment of nonsegmental vitiligo is also underway.

Conclusion

Topical therapy, particularly in combination with phototherapy, remains a gold standard for many dermatologists when treating vitiligo. However, a wide variety of procedural interventions are available. There are new medications on the horizon that hold much promise, including JAK inhibitors. These emerging therapies have the potential to expand treatment options for both adult and pediatric vitiligo patients, offering more targeted and effective approaches to disease management and improving patient outcomes. Given the complex pathogenesis of vitiligo, including the role of oxidative stress, further research into potential adjunctive therapies is necessary in expanding the arsenal of options available for individualized care. 

References

1. Perez-Bootello J, Cova-Martin R, Naharro-Rodriguez J, Segurado-Miravalles G. Vitiligo: pathogenesis and new and emerging treatments. Int J Mol Sci. 2023;24(24):17306. doi:10.3390/ijms242417306

2. Ahmed Jan N, Masood S. Vitiligo. In: StatPearls. StatPearls Publishing; 2023. Accessed April 4, 2025. https://www.ncbi.nlm.nih.gov/books/NBK519015/

3. Sosa JJ, Currimbhoy SD, Ukoha U, et al. Confetti-like depigmentation: a potential sign of rapidly progressing vitiligo. J Am Acad Dermatol. 2015;73(2):272-275. doi:10.1016/j.jaad.2015.05.014

4. Goh BK, Pandya AG. Presentations, signs of activity, and differential diagnosis of vitiligo. Dermatol Clin. 2017;35(2):135-144. doi:10.1016/j.det.2016.11.004

5. Frisoli ML, Essien K, Harris JE. Vitiligo: mechanisms of pathogenesis and treatment. Annu Rev Immunol. 2020;38:621-648. doi:10.1146/annurev-immunol-100919-023531

6. Cunningham KN, Rosmarin D. Vitiligo treatments: review of current therapeutic modalities and JAK inhibitors. Am J Clin Dermatol. 2023;24(2):165-186. doi:10.1007/s40257-022-00752-6

7. Hu Z, Wang T. Beyond skin white spots: vitiligo and associated comorbidities. Front Med (Lausanne). 2023;10:1072837. doi:10.3389/fmed.2023.1072837

8. Laddha NC, Dwivedi M, Mansuri MS, et al. Vitiligo: interplay between oxidative stress and immune system. Exp Dermatol. 2013;22(4):245-250.

9. Telegina TA, Vechtomova YL, Borzova VA, Buglak AA. Tetrahydrobiopterin as a trigger for vitiligo: phototransformation during UV irradiation. Int J Mol Sci. 2023;24(17):13586. doi:10.3390/ijms241713586

10. Marchioro HZ, Silva de Castro CC, Fava VM, et al. Update on the pathogenesis of vitiligo. An Bras Dermatol. 2022;97(4):478-490. doi:10.1016/j.abd.2021.09.008

11. Oliver EA, Schwartz L, Warren LH. Occupational leukoderma: preliminary report. JAMA. 1939;113(10):927-928.

12. Ghosh S. Chemical vitiligo: a subset of vitiligo. Indian J Dermatol. 2020;65(6):443-449.

13. Seneschal J, Speeckaert R, Taïeb A, et al. Worldwide expert recommendations for the diagnosis and management of vitiligo: position statement from the International Vitiligo Task Force—Part 2: specific treatment recommendations. J Eur Acad Dermatol Venereol. 2023;37(11):2185-2195. doi:10.1111/jdv.19450

14. Lee JH, Kwon HS, Jung HM, et al. Treatment outcomes of topical calcineurin inhibitor therapy for patients with vitiligo: a systematic review and meta-analysis. JAMA Dermatol. 2019;155(8):929-938.

15. Ju HJ, Han JH, Kim MS, et al. The long-term risk of lymphoma and skin cancer did not increase after topical calcineurin inhibitor use and phototherapy in a cohort of 25,694 patients with vitiligo. J Am Acad Dermatol. 2021;84(6):1619-1627. doi:10.1016/j.jaad.2021.01.067

16. Rosmarin D, Passeron T, Pandya AG, et al. Two phase 3, randomized, controlled trials of ruxolitinib cream for vitiligo. N Engl J Med. 2022;387(16):1445-1455.

17. U.S. Food and Drug Administration. Opzelura (ruxolitinib) cream, 1.5% prescribing information. 2022. Accessed April 4, 2025. https://www.accessdata.fda.gov/drugsatfda_docs/label/2022/215309s001lbl.pdf

18. Bae JM, Jung HM, Hong BY, et al. Phototherapy for vitiligo: a systematic review and meta-analysis. JAMA Dermatol. 2017;153(7):666-674.

19. Hu Y, Xu Z, Liu L, et al. A randomized prospective study to compare the efficacy of 308-nm light-emitting diode and 308-nm excimer lamp in the treatment of facial vitiligo. Arch Dermatol Res. 2025;317(1):210. doi:10.1007/s00403-024-03721-7

20. Savant SS. Surgical therapy of vitiligo: current status. Indian J Dermatol Venereol Leprol. 2005;71:307.

21. Frączek A, Kasprowicz-Furmańczyk M, Placek W, Owczarczyk-Saczonek A. Surgical treatment of vitiligo. Int J Environ Res Public Health. 2022;19(8):4812. doi:10.3390/ijerph19084812

22. Halder RM, Pham HN, Breadon JY, Johnson BA. Micropigmentation for the treatment of vitiligo. J Dermatol Surg Oncol. 1989;15(10):1092-1098. doi:10.1111/j.1524-4725.1989.tb03129.x

23. Kerure AS, Marwah M, Wagh ND, Udare S. Micropigmentation. Indian Dermatol Online J. 2023;14(5):605-610. doi:10.4103/idoj.idoj_767_21

24. Babu A, Thappa DM, Jaisankar TJ. Punch grafting versus suction blister epidermal grafting in the treatment of stable lip vitiligo. Dermatol Surg. 2008;34(2):166-178.

25. Agrawal K, Agrawal A. Vitiligo: repigmentation with dermabrasion and thin split-thickness skin graft. Dermatol Surg. 1995;21(4):295-300.

26. Khunger N, Kathuria SD, Ramesh V. Tissue grafts in vitiligo surgery: past, present, and future. Indian J Dermatol. 2009;54(2):150-158. doi:10.4103/0019-5154.53196

27. Koga M. Epidermal grafting using the tops of suction blisters in the treatment of vitiligo. Arch Dermatol. 1988;124(11):1656-1658.

28. Chandela M, Khurana VK, Mehta RK, et al. A study of autologous non-cultured epidermal suspension (NCES) transplant in patients with stable vitiligo without the use of NB-UVB. Maedica (Bucur). 2023;18(4):576-585. doi:10.26574/maedica.2023.18.4.576

29. Zhang D, Wei X, Hong W, et al. A retrospective study of long-term follow-up of 2283 vitiligo patients treated by autologous, non-cultured melanocyte-keratinocyte transplantation. Aging (Albany NY). 2021;13(4):5415-5425. doi:10.18632/aging.202472

30. Cervelli V, De Angelis B, Balzani A, et al. Treatment of stable vitiligo by ReCell system. Acta Dermatovenerol Croat. 2009;17(4):273-278.

31. Hamzavi IH, Ganesan AK, Mahmoud BH, et al. Effective and durable repigmentation for stable vitiligo: a randomized within-subject controlled trial assessing treatment with autologous skin cell suspension transplantation. J Am Acad Dermatol. 2024;91(6):1104-1112. doi:10.1016/j.jaad.2024.08.027

32. Gianfaldoni S, Wollina U, Tirant M, et al. Herbal compounds for the treatment of vitiligo: a review. Open Access Maced J Med Sci. 2018;6(1):203.

33. Parsad D, Pandhi R, Juneja A. Effectiveness of oral Ginkgo biloba in treating limited, slowly spreading vitiligo. Clin Exp Dermatol. 2003;28(3):285-287. doi:10.1046/j.1365-2230.2003.01207.x

34. Padmakar S, Kumar GA, Khurana N, et al. Efficacy and safety of natural Aloe Vera gel in the treatment of stable vitiligo. Clin Epidemiol Glob Health. 2023;22:101332. doi:10.1016/j.cegh.2023.101332

35. Lotti T, Buggiani G, Troiano M, et al. Targeted and combination treatments for vitiligo: comparative evaluation of different current modalities in 458 subjects. Dermatol Ther. 2008;21(Suppl 1):S20-S26.

36. Chen YJ, Chen YY, Wu CY, Chi CC. Oral Chinese herbal medicine in combination with phototherapy for vitiligo: a systematic review and meta-analysis of randomized controlled trials. Complement Ther Med. 2016;26:21-27.

37. Jeong YM, Choi YG, Kim DS, et al. Cytoprotective effect of green tea extract and quercetin against hydrogen peroxide-induced oxidative stress. Arch Pharm Res. 2005;28:1251-1256.

38. Dell’Anna ML, Mastrofrancesco A, Sala R, et al. Antioxidants and narrow band-UVB in the treatment of vitiligo: a double-blind placebo-controlled trial. Clin Exp Dermatol. 2007;32(6):631-636. doi:10.1111/j.1365-2230.2007.02514.x

39. Białczyk A, Wełniak A, Kamińska B, Czajkowski R. Oxidative stress and potential antioxidant therapies in vitiligo: a narrative review. Mol Diagn Ther. 2023;27(6):723-739. doi:10.1007/s40291-023-00672-z

40. Ezzedine K, Peeva E, Yamaguchi Y, et al. Efficacy and safety of oral ritlecitinib for the treatment of active nonsegmental vitiligo: a randomized phase 2b clinical trial. J Am Acad Dermatol. 2023;88:395-403. doi:10.1016/j.jaad.2022.11.005

41. Pandya A, Ezzedine K, Passeron T, et al. Efficacy and safety of povorcitinib for extensive vitiligo: 52-week results from a double-blinded, placebo-controlled, dose-ranging phase 2b study. Br J Dermatol. 2024;191(Suppl 2).

42. Passeron T, Ezzedine K, Hamzavi I, et al. Once-daily upadacitinib versus placebo in adults with extensive non-segmental vitiligo: a phase 2, multicentre, randomised, double-blind, placebo-controlled, dose-ranging study. EClinicalMedicine. 2024;73:102655. doi:10.1016/j.eclinm.2024.102655

43. Horwitz SM, Feldman TA, Ye JC, et al. Results from an open-label phase 2a study of cerdulatinib, a dual spleen tyrosine kinase/janus kinase inhibitor, in relapsed/refractory peripheral T-cell lymphoma. Leuk Lymphoma. Published online February 8, 2025. doi:10.1080/10428194.2025.2455489

44. U.S. National Library of Medicine. ClinicalTrials.gov. Accessed February 20, 2025. https://clinicaltrials.gov/search?cond=Vitiligo&term=afamelanotide&checkSpell=

Pranja A. Sahadeo

• Doctoral Candidate, Howard University College of Medicine
  Washington, DC

Raveena Khanna, MD

• PGY-3 Dermatology Resident, Howard University College of Medicine
  Washington, DC

Rawn Bosley, MD

• Dermatologist and Dermatologic Surgeon, Private Practice
  Carrollton, TX

Cheri Frey, MD

• Assistant Professor of Dermatology
• Residency Program Director, Howard University College of Medicine
  Washington, DC