International Journal of Trichology

: 2022  |  Volume : 14  |  Issue : 6  |  Page : 191--196

Hair aging and hair disorders in elderly patients

Alessia Villani1, Maria Ferrillo1, Gabriella Fabbrocini1, Sonia Sofía Ocampo-Garza2, Massimiliano Scalvenzi1, Angelo Ruggiero1,  
1 Department of Clinical Medicine and Surgery, Section of Dermatology, University of Naples Federico II, Naples, Italy
2 Department of Clinical Medicine and Surgery, Section of Dermatology, University of Naples Federico II, Naples, Italy; Department of Dermatology, University Hospital “Dr. José Eleuterio González”, Universidad Autónoma de Nuevo León, Monterrey, Mexico

Correspondence Address:
Sonia Sofía Ocampo-Garza
Autonomous University of Nuevo León, University Hospital Dr. José Eleuterio González, Dermatology Department, Monterrey, Nuevo León


Hair loss in elderly patients is a common complaint. It can be related to different conditions that affect patients' quality of life and represents a challenge for dermatologists. It affects both men and women during the aging process with an estimated percentage of balding after 65 years of age of 53% and 37%, respectively. Androgenetic alopecia, frontal fibrosing alopecia, senile alopecia, and erosive pustular dermatosis of the scalp are the hair diseases most frequently described in this age group. The objective of this review is to summarize the current knowledge about alopecia affecting elderly patients, differentiating between chronological hair aging signs and pathological changes, to help clinicians, offer an adequate management of these disorders to their patients.

How to cite this article:
Villani A, Ferrillo M, Fabbrocini G, Ocampo-Garza SS, Scalvenzi M, Ruggiero A. Hair aging and hair disorders in elderly patients.Int J Trichol 2022;14:191-196

How to cite this URL:
Villani A, Ferrillo M, Fabbrocini G, Ocampo-Garza SS, Scalvenzi M, Ruggiero A. Hair aging and hair disorders in elderly patients. Int J Trichol [serial online] 2022 [cited 2023 May 31 ];14:191-196
Available from:

Full Text


Hair graying and hair loss are two typical aging signs that highly affect patients' quality of life and which represent a challenge for dermatologists.[1],[2] The hair is subject to intrinsic and extrinsic factors that influence hair follicle changes and clinically results in hair alterations such as graying and hair loss, which are commonly described in elderly patients.[3] Hair loss may highly impact patients' quality of life, increasing daily stress and reducing self-esteem.[4]

Hair loss typically affects both men and women during the aging process with an estimated percentage of balding after 65 years of age of 53% and 37%, respectively.[5],[6] It is the result of several pathogenetic factors, including the alteration of pilosebaceous units, hair follicle injuries, or a normal hair cycle disruption.[5] It is important to differentiate between chronological hair aging signs and pathological changes to offer our patients a prompt treatment.[7]

The objective of this article is to review the current understanding and knowledge about alopecia affecting elderly patients, focusing on hair aging changes, and describing the most common hair disorders presenting in elderly patients.

 Hair Aging

As with cutaneous aging, chronological hair aging modifications are related to both intrinsic and extrinsic factors.[8] Intrinsic factors that affect hair follicles include racial and gender features, patients' metabolism, nutritional status, hormone responsiveness, and hair cycle-dependent changes. Not only alterations of hair fibers' growth and pigmentation are seen but also changes in sebum production, fiber diameter, and hair density. These factors may result in the hair looking dull, gray, thin, and frizzy. Extrinsic factors affecting the hair shaft include ultraviolet (UV) light, water, dust, friction, hair combing, cosmetic treatments, and cigarette smoking. These environmental factors may cause hair to appear dry and rough, with breaking or splitting ends.[9],[10] Interestingly, several effects related to cigarette smoking have been linked with induction and acceleration of senile hair changes.[9] It has been shown that cigarette smoking may cause changes in the microvasculature of the dermal hair papilla, thus inducing an imbalance in the follicular protease-antiprotease system, increasing local pro-inflammatory cytokines and resulting in follicular inflammation, fibrosis, and inhibition of aromatase enzyme, causing a relative hypo-estrogenic state.[10] Recent studies showed an increased risk of hair graying in smokers (1.99 times higher) than nonsmokers.[11] Regarding UV effects on hair, UV-B and UV-A exposure may increase free radicals release, damaging structural hair proteins and causing oxidative hair damage which results in increased and accelerated hair loss and hair pigment alteration. Similarly, chemical factors, such as products to straighten the hair, can cause hair damage and reduce hair density and diameter.[9]

Hair graying is frequently reported as one of the first signs of aging.[12],[13],[14] Epidemiologic studies suggest that 6% to 23% of people have 50% gray hair at the age of 50 years. However, the age of onset is influenced by genetic factors including ethnicity and geographic location of origin. Asian and African people present later onset and less gray hair than Caucasians (43.9 ± 10.3 years and 34 ± 9.6 years, respectively).[13] Hair follicle pigmentation is the result of complex interactions between follicular melanocytes, matrix keratinocytes, and fibroblasts.[15] In the hair, in contrast to the continuous melanogenesis of epidermal pigmentation, follicular melanogenesis depends on follicular cycling, being not produced during telogen, which has a longer duration in older age.[16] Hair graying results from a decrease of both follicular melanocyte population and melanin content. Moreover, another important involved mechanism is the decreased ability to handle oxidative damage, which may result from smoking and UV exposure.[6],[16],[17],[18] Although hair loss and hair graying are the most frequently reported visible changes of hair aging, other hair modifications have also been reported, hair diameter reduction is another important factor in the process. Several articles have reported that the age of maximum diameter for females is near the age of 40, while in men, this occurs around the age of 18 and tends to decrease relatively rapidly with increasing age.[19],[20] The decline of sebum production and hair luster due in part to an increase in fiber curvature have also been described.[21],[22] For women, this decline occurs after menopause, whereas for men, it emerges much later, around the age of 80.[21],[22]

 Hair Disorders in Elderlies

While most reported hair aging changes are considered as physiological and para-physiological signs of aging, many hair disorders causing hair loss and scarring have been described in elderly patients. These disorders should be always considered for differential diagnosis of hair aging in order to reach a correct diagnosis and to start a prompt treatment. Androgenetic alopecia (AGA), frontal fibrosing alopecia (FFA), senile alopecia, and erosive pustular dermatosis of the scalp (EPDS) are the most frequently described hair diseases in elderlies.

 Androgenetic Alopecia

Male pattern baldness, or AGA, represents the most common hair loss disorder, affecting both male and female patients at any age. It is characterized by a nonscarring progressive miniaturization of the hair follicle with a specific pattern distribution in genetically predisposed individuals.[23] AGA affects up to 80% of men and 50% of women during their life, with an increasing prevalence according to the age.[23],[24] It is characterized by progressive hair follicle miniaturization which results from an alteration in normal hair cycle.[25] Particularly, the duration of anagen phase, which determines hair length, progressively decreases while the telogen phase increases, resulting in shorter hair and bald appearance.[26] These hair follicle alterations are driven by androgen influence on genetically susceptible hair follicles in androgen-dependent area.[27]

AGA is the most prevalent form of progressive hair loss disease in adults.[25] However, even if hair changes are firstly driven by androgens, most of the pathophysiological mechanisms involved in androgenic alopecia are still unknown, limiting available treatments. It has different patterns in men and women. In men, it typically starts with bitemporal recession of the frontal hair line, then followed by diffuse thinning of the vertex sometimes producing a bald patch.[21],[27] Instead, women usually have a spared frontal hairline, with diffuse apical hair loss.[28] Although it is usually milder in women than in men, due to the lower expression levels of androgen receptors, up to 50% of women will present androgenic alopecia with an important negative psychological impact, high rate of anxiety, and depression. Hence, early diagnosis and treatments are important to stop hair loss progression and improve clinical and psychological outcomes.[29] Although the significant impact and high demand for treatment, to date, there are only two Food and Drug Administration-approved medications available: topical minoxidil and finasteride, for male AGA and topical minoxidil for female patients.[25],[30] Finasteride is a 5α-reductase inhibitor approved at a dosage of 1 mg/day for the treatment of male patients with AGA between 18 and 40 years. Clinical studies have also showed its efficacy and safety in older men.[25],[30] Dutasteride, an oral type I and II 5a-reductase inhibitor (0.5 mg a day), represents another treatment option.[25] Most frequently reported side effects during 5α-reductase inhibitors treatment are sexual dysfunction and depression, which are also recurring comorbidities in elderlies. Hence, these should be carefully considered before starting treatment. Regarding minoxidil, it is recommended in topical 2%–5% solution 1 mL or half a cap of 5% foam twice daily to improve or to prevent progression of AGA in male patients, while it is recommended in topical 2% solution 1 mL twice daily or half a cap of 5% topical foam once daily in female patients.[31],[32],[33]

 Frontal Fibrosing Alopecia

FFA is a scarring alopecia characterized by selective involvement of the frontotemporal hairline and eyebrows.[34] It may often be misdiagnosed at earlier stages, due to nonspecific and slow-progressive manifestations. However, an early diagnosis is important to prevent disease progression.[35] FFA is commonly found in postmenopausal females, with a mean age of onset of 60 years old.[34],[35],[36] Nonetheless, male cases of FFA have been reported, with younger onset and lower incidence of eyebrow involvement than women.[34],[35],[36],[37] The diagnosis is made with the typical clinical and trichoscopic characteristics, in case of doubt a confirmation with biopsy may be needed. Clinically, patients show a smooth and uniformly pale skin of the alopecic areas, with the presence of lonely hairs.[34] Although its typical clinical presentation, in early stages, a trichoscopic guided biopsy may be needed. Histopathologically, it is characterized by a lichenoid lymphohistiocytic infiltrate around the outer root sheaths in the infundibular and isthmus areas, as well as perifollicular lamellar fibrosis. Findings also consistent with lichen planopilaris (LPP).[37] Indeed, it is considered by some as a variant of LPP, differing from it by the fibrosis and infiltrate of lymphocytes selectively involving the intermediate and vellus-like follicles of the frontal margin and eyebrows.[38] FFA treatment still represents a challenge for dermatologists, with most available treatment outcomes coming from reported cases in literature, due to the lack of randomized clinical trials and official guidelines. Different treatments have been proposed showing variable outcomes.[34],[39],[40],[41] Commonly prescribed topical treatments include minoxidil, calcineurin inhibitors, and corticosteroids, while attempted systemic treatments include corticosteroids, retinoids, finasteride, dutasteride, hydroxychloroquine, pioglitazone, and doxycycline. FFA should always be considered in the differential diagnosis of elderly woman showing a recession of frontal hair line and/or eyebrow loss.

 Senescent Alopecia

Senescent alopecia, also known as senile or late-onset alopecia, is a not well-defined condition. It is characterized by a permanent and diffuse decrease in hair diameter and length.[4],[42] Although it often coexists with AGA, senescent alopecia is characterized by follicle thinning in patients with no history of family balding, and a typical onset over the age of 50. Most common histological findings include a shift to hair fibers of smaller diameter with a normal anagen-telogen ratio.[43] Even if senescent alopecia is a specific and independent hair disorder has long been debated, being sometimes considered as subtype of androgenic alopecia, studies have showed differences in gene expression profiles, suggesting that these conditions may represent two independent hair disorders and that nonandrogen pathways may also contribute to hair loss.[44] However, Whiting et al. reported that treatment with oral finasteride may result in some hair regrowth in elderly patients.[43] Hence, this condition should be further studied.

 Erosive Pustular Dermatosis of the Scalp

EPDS is a rare condition typically affecting older patients after local trauma.[45] The condition might be underestimated, with the real incidence being higher than previously thought.[46] Typical clinical findings include superficial progressive erosions with crusts and pustules on atrophic skin which results in secondary cicatricial alopecia.[47],[48] Although the etiology and the exact pathogenesis are still unknown, it is often reported in aged and sun-damaged skin with a history of local trauma or others local triggering factors such as herpes zoster.[49] The histopathology is nonspecific and often inconclusive. Nevertheless, skin biopsy as well as bacterial and mycological cultures are usually necessary to rule out other diagnoses.[21] Most common histopathological findings include sub-corneal pustules, epidermal hypertrophy, or atrophy, erosions, and nonfollicular pustules.[50] Due to the rarity of the disease, treatment guidelines are still lacking. Different treatment options with variable clinical outcomes have been reported, including topical tacrolimus, corticosteroids, calcipotriol, and photodynamic therapy.[49],[50],[51]

 Hair Loss in Neoplastic Conditions

Hair loss is a frequent condition in oncological patients, which may be related to both chemotherapy and skin metastasis. The management of tumor-related hair loss became a major topic in daily dermatological practice, due to the negative impact given by this condition on patients' self-perception and physical appearance, resulting in severe reduction on their quality of life. Scalp may be affected by both primary and metastatic cancers. Indeed, scalp represents a commonly affected site from metastases.[52] Common clinical presentations of cutaneous metastases include solitary or multiple skin nodules with or without ulceration and alopecia neoplastica.[52],[53] Alopecia neoplastica is a pattern of cutaneous metastasis to the scalp that presents as an alopecic patch, being the result of the neoplastic involvement of the hair follicle and the surrounding skin.[53],[54],[55] Typical histological findings are similar to scarring alopecia, showing follicular plugging and dermal fibrosis with an extensive inflammatory infiltrate.[6] Alopecia neoplastica is most frequently found in elderly breast cancer patients. It has been described in several other conditions, including cervical cancer, colon, extramammary Paget's disease, gastric carcinoma, and placental site trophoblastic tumor.[56]

Hair loss is a common, but often distressing, side effect of chemotherapy and radiotherapy. The incidence and severity of this frequent adverse vary depending on the cytotoxic agent, its dose and schedule, route of administration, and whether it is administered alone or in combination with other agents.[57] Chemotherapy-induced alopecia (CIA) may have severe consequences on patients' psychological and social life, resulting in depression, anxiety, negative self-image, and a reduced sense of well-being.[56] It has been reported in three-fifths of patients starting chemotherapy.[58] It typically occurs about 1 week to 2 months after the start of a therapeutic regimen. Different pathological changes of hair can be seen, such as decreased hair diameter, fragmentation, trichorrhexis nodosa, and hair shaft depigmentation. Chemotherapeutic agents affect anagen follicles by causing a sudden cessation of mitotic activity in rapidly dividing hair matrix cells (anagen effluvium). CIA is almost always reversible, showing a regrowth that typically starts several weeks after the end of treatment. However, in rare cases, hair regrowth following intense chemotherapy may be incomplete, resulting in lifelong hair thinning.[58],[59],[60] Available treatment options include topical or oral minoxidil.[32],[61] Scalp hypothermia represents the only available preventive measure. It induces vasoconstriction of hair follicle vessels, reducing blood flow to the hair follicles and consequently the uptake of chemotherapeutic agents, and a reduction of biochemical activity in hair follicle, which results in less susceptibility to the damage induced by chemotherapy.[61] Hair disorders may also occur during oncological targeted therapies. Indeed, tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitor are among the most reported drugs causing hair disorders. TKIs may cause different types of hair disorders, including scarring or non-scarring alopecia, androgen-like frontal alopecia, hair rigidity and curling, or scalp inflammation.[60] These effects might be linked to the high expression of EGFR in hair follicles. Another important tumor treatment with high rate of alopecia is hormonal therapy.[61] A meta-analysis of 35 studies (n = 13,415 patients) reported that the overall incidence of hormone therapy-induced alopecia is 4.4%, ranging from 0% to 25% with anti-androgen therapies and selective estrogen receptor modulators.[62] Although it is often reported as a low-grade alopecia, a recent study evaluating alopecia-related quality of life in patients with breast cancer found that alopecia can adversely impact psychosocial functioning and quality of life.[62]

Hence, alopecia occurring during chemotherapy is often cited as one of the most negative effects on quality of life in patients with cancer. It should always be considered by physicians, teaching patients adaptive self-care strategies, and informing them of available support groups and/or treatments when needed.[63]

 Drug Induced Alopecia

Many drugs may induce hair loss, particularly in those patients with several comorbidities that need many concomitant treatments, such as elderly patients. Hair loss may occur as telogen effluvium, anagen effluvium, or both depending on the type of medication.[64] In telogen effluvium, hair loss becomes evident 2–4 months after starting treatment, being a temporary condition that only requires drug discontinuation. While anagen loss is mostly related to chemotherapy, drug-induced telogen effluvium has been reported as an adverse effect of many drugs. Elderly patients frequently need treatments that have been related to hair loss, including anticoagulants (warfarin, heparinoids, indandiones, and dextran), antiretroviral drugs, anti-thyroid drugs (carbimazole, thiouracils, and iodine), mood stabilizers (lithium, valproic acid, and divalproex), interferons (INF) (IFNα, IFNα-2a), dopaminergic therapy for patients with Parkinson's disease, and many other medications that have been linked to hair loss in single case reports, such as ACE inhibitors (captopril, enalapril, moexipril, ramipril), allopurinol, analgesics-antinflammatories (ibuprofen, indomethacin, naproxen).[61],[64],[65]

Hence, drug-induced hair loss in elderlies may represent a frequent misdiagnosed condition that should always be considered in the differential diagnosis process, contemplating all drugs taken 4 months before the onset of hair loss and confirming, when possible, the causative role of the suspected drug with the normalization of hair loss after 2–3 months of drug discontinuation.

 Adverse Effects Due to Prolonged Use of Hair Cosmetics

The term “weathering” refers to hair breakage from root to tip, related to excessive or repeated use of chemical treatments, grooming habits, or environmental exposures.[66] The results of continuing daily exposure to these factors are more evident with aging, due to cumulative damage. The hair may be damaged by both physical and chemical factors. Physical factors include friction, excessive combing, brushing, or heat. Regarding chemical treatments, bleaching, coloring, perming, and chemical straightening are included. The continued and prolonged exposure to previously cited factors may induce changes in hair texture resulting in hair breakage.[66],[67],[68] Weathering may lead to scaling of the cuticle layers, with cortex exposure and damage, causing hair fiber fracture (trichorrhexis nodosa).[68] Whereas proper hair care techniques are essential to improve hair appearance and to avoid further damages, hair fibers cannot recover their original structure. Nevertheless, if the follicles are not damaged, the hair shafts may be renewed by preventing weathering causes.[68]


Hair loss in elderly patient is a common complaint in dermatological practices, which may be related to different conditions. Due to the high impact on patient's quality of life, an early diagnosis and correct management are fundamental. Physiological aging changes, induced by intrinsic and extrinsic factors, as well as pathological or drug-induced hair loss should always be considered at this age group.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Santos Z, Avci P, Hamblin MR. Drug discovery for alopecia: Gone today, hair tomorrow. Expert Opin Drug Discov 2015;10:269-92.
2Conic RR, Juhasz M, Rambhia P, Damiani G, Atanaskova-Mesinkovska N, Piliang M, et al. Characterizing hair loss in the elderly: An observational study of 163 patients. J Eur Acad Dermatol Venereol 2019;33:e226-8.
3Ji J, Ho BS, Qian G, Xie XM, Bigliardi PL, Bigliardi-Qi M. Aging in hair follicle stem cells and niche microenvironment. J Dermatol 2017;44:1097-104.
4Torres F. Androgenetic, diffuse and senescent alopecia in men: Practical evaluation and management. Curr Probl Dermatol 2015;47:33-44.
5Hordinsky M, Sawaya M, Roberts JL. Hair loss and hirsutism in the elderly. Clin Geriatr Med 2002;18:121-33, vii.
6Chen W, Yang CC, Todorova A, Al Khuzaei S, Chiu HC, Worret WI, et al. Hair loss in elderly women. Eur J Dermatol 2010;20:145-51.
7Mandt N, Blume-Peytavi U. Aging of hair and nails. Hautarzt 2005;56:340-6.
8Lee WS. Photoaggravation of hair aging. Int J Trichology 2009;1:94-9.
9Trüeb RM. Association between smoking and hair loss: Another opportunity for health education against smoking? Dermatology 2003;206:189-91.
10Lu Z, Fischer TW, Hasse S, Sugawara K, Kamenisch Y, Krengel S, et al. Profiling the response of human hair follicles to ultraviolet radiation. J Invest Dermatol 2009;129:1790-804.
11Jo SJ, Paik SH, Choi JW, Lee JH, Cho S, Kim KH, et al. Hair graying pattern depends on gender, onset age and smoking habits. Acta Derm Venereol 2012;92:160-1.
12Santos Nogueira AC, Joekes I. Hair color changes and protein damage caused by ultraviolet radiation. J Photochem Photobiol B 2004;74:109-17.
13Trüeb RM. Aging of hair. J Cosmet Dermatol 2005;4:60-72.
14Panhard S, Lozano I, Loussouarn G. Greying of the human hair: A worldwide survey, revisiting the '50' rule of thumb. Br J Dermatol 2012;167:865-73.
15Slominski A, Paus R. Melanogenesis is coupled to murine anagen: Toward new concepts for the role of melanocytes and the regulation of melanogenesis in hair growth. J Invest Dermatol 1993;101:90S-7S.
16Slominski A, Wortsman J, Plonka PM, Schallreuter KU, Paus R, Tobin DJ. Hair follicle pigmentation. J Invest Dermatol 2005;124:13-21.
17Trüeb RM, Rezende HD, Dias MF. A comment on the science of hair aging. Int J Trichology 2018;10:245-54.
18Goodier M, Hordinsky M. Normal and aging hair biology and structure 'aging and hair'. Curr Probl Dermatol 2015;47:1-9.
19Robbins C, Mirmirani P, Messenger AG, Birch MP, Youngquist RS, Tamura M, et al. What women want – Quantifying the perception of hair amount: An analysis of hair diameter and density changes with age in Caucasian women. Br J Dermatol 2012;167:324-32.
20Otsuka H, Nemoto T. Study on Japanese hair. J Jon Cosmet Sci Soc 1988;12:192-7.
21Maddy AJ, Tosti A. Hair and nail diseases in the mature patient. Clin Dermatol 2018;36:159-66.
22Mirmirani P. Age-related hair changes in men: Mechanisms and management of alopecia and graying. Maturitas 2015;80:58-62.
23Blumeyer A, Tosti A, Messenger A, Reygagne P, Del Marmol V, Spuls PI, Trakatelli M, Finner A, Kiesewetter F, Trüeb R, Rzany B, Blume-Peytavi U; European Dermatology Forum (EDF). Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men. J Dtsch Dermatol Ges 2011;9 Suppl 6:S1-57. doi: 10.1111/j.1610-0379.2011.07802.x.
24Piraccini BM, Alessandrini A. Androgenetic alopecia. G Ital Dermatol Venereol 2014;149:15-24.
25Lolli F, Pallotti F, Rossi A, Fortuna MC, Caro G, Lenzi A, et al. Androgenetic alopecia: A review. Endocrine 2017;57:9-17.
26Piérard-Franchimont C, Piérard GE. Teloptosis, a turning point in hair shedding biorhythms. Dermatology 2001;203:115-7.
27Gan DC, Sinclair RD. Prevalence of male and female pattern hair loss in Maryborough. J Investig Dermatol Symp Proc 2005;10:184-9.
28Ho CH, Sood T, Zito PM. Androgenetic alopecia. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2022.
29Starace M, Orlando G, Alessandrini A, Piraccini BM. Female androgenetic alopecia: An update on diagnosis and management. Am J Clin Dermatol 2020;21:69-84.
30Kelly Y, Blanco A, Tosti A. Androgenetic alopecia: An update of treatment options. Drugs 2016;76:1349-64.
31Olsen EA, Whiting DA, Savin R, Rodgers A, Johnson-Levonas AO, Round E, et al. Global photographic assessment of men aged 18 to 60 years with male pattern hair loss receiving finasteride 1 mg or placebo. J Am Acad Dermatol 2012;67:379-86.
32Villani A, Fabbrocini G, Ocampo-Candiani J, Ruggiero A, Ocampo-Garza SS. Review of oral minoxidil as treatment of hair disorders: In search of the perfect dose. J Eur Acad Dermatol Venereol 2021;35:1485-92.
33Kanti V, Messenger A, Dobos G, Reygagne P, Finner A, Blumeyer A, et al. Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men – Short version. J Eur Acad Dermatol Venereol 2018;32:11-22.
34Iorizzo M, Tosti A. Frontal fibrosing alopecia: An update on pathogenesis, diagnosis, and treatment. Am J Clin Dermatol 2019;20:379-90.
35Alegre-Sánchez A, Saceda-Corralo D, Bernárdez C, Molina-Ruiz AM, Arias-Santiago S, Vañó-Galván S. Frontal fibrosing alopecia in male patients: A report of 12 cases. J Eur Acad Dermatol Venereol 2017;31:e112-4.
36Tosti A, Piraccini BM, Iorizzo M, Misciali C. Frontal fibrosing alopecia in postmenopausal women. J Am Acad Dermatol 2005;52:55-60.
37Kossard S, Lee MS, Wilkinson B. Postmenopausal frontal fibrosing alopecia: A frontal variant of lichen planopilaris. J Am Acad Dermatol 1997;36:59-66.
38Mirmirani P, Zimmerman B. Cocking the eyebrows to find the missing hairline in frontal fibrosing alopecia: A useful clinical maneuver. J Am Acad Dermatol 2016;75:e63-4.
39Moreno-Ramírez D, Ferrándiz L, Camacho FM. Diagnostic and therapeutic assessment of frontal fibrosing alopecia. Actas Dermosifiliogr 2007;98:594-602.
40Saceda-Corralo D, Moreno-Arrones ÓM, Fonda-Pascual P, Pindado-Ortega C, Hermosa-Gelbard Á, Rodrigues-Barata AR, et al. Steroid-induced changes noted on trichoscopy of patients with frontal fibrosing alopecia. J Am Acad Dermatol 2018;79:956-7.
41Strazzulla LC, Avila L, Li X, Lo Sicco K, Shapiro J. Prognosis, treatment, and disease outcomes in frontal fibrosing alopecia: A retrospective review of 92 cases. J Am Acad Dermatol 2018;78:203-5.
42Kligman AM. The comparative histopathology of male-pattern baldness and senescent baldness. Clin Dermatol 1988;6:108-18.
43Whiting DA. How real is senescent alopecia? A histopathologic approach. Clin Dermatol 2011;29:49-53.
44Karnik P, Shah S, Dvorkin-Wininger Y, Oshtory S, Mirmirani P. Microarray analysis of androgenetic and senescent alopecia: Comparison of gene expression shows two distinct profiles. J Dermatol Sci 2013;72:183-6.
45Karanfilian KM, Wassef C. Erosive pustular dermatosis of the scalp: Causes and treatments. Int J Dermatol 2021;60:25-32.
46Broussard KC, Berger TG, Rosenblum M, Murase JE. Erosive pustular dermatosis of the scalp: A review with a focus on Dapsone therapy. J Am Acad Dermatol 2012;66:680-6.
47Patton D, Lynch PJ, Fung MA, Fazel N. Chronic atrophic erosive dermatosis of the scalp and extremities: A recharacterization of erosive pustular dermatosis. J Am Acad Dermatol 2007;57:421-7.
48Pye RJ, Peachey RD, Burton JL. Erosive pustular dermatosis of the scalp. Br J Dermatol 1979;100:559-66.
49Kim KR, Lee JY, Kim MK, Yoon TY. Erosive pustular dermatosis of the scalp following herpes zoster: Successful treatment with topical tacrolimus. Ann Dermatol 2010;22:232-4.
50Semkova K, Tchernev G, Wollina U. Erosive pustular dermatosis (chronic atrophic dermatosis of the scalp and extremities). Clin Cosmet Investig Dermatol 2013;6:177-82.
51Yang CS, Kuhn H, Cohen LM, Kroumpouzos G. Aminolevulinic acid photodynamic therapy in the treatment of erosive pustular dermatosis of the scalp: A case series. JAMA Dermatol 2016;152:694-7.
52Pathak S, Joshi SR, Jaison J, Kendre D. Cutaneous metastasis from carcinoma of lung. Indian Dermatol Online J 2013;4:185-7.
53Cohen PR. Primary alopecia neoplastica versus secondary alopecia neoplastica: A new classification for neoplasm-associated scalp hair loss. J Cutan Pathol 2009;36:917-8.
54Archer CB, Smith NP. Alopecia neoplastica responsive to tamoxifen. J R Soc Med 1990;83:647-8.
55Gül U, Kiliç A, Akbaş A, Aslan E, Demiriz M. Alopecia neoplastica due to metastatic colon adenocarcinoma. Acta Derm Venereol 2007;87:93-4.
56Hesketh PJ, Batchelor D, Golant M, Lyman GH, Rhodes N, Yardley D. Chemotherapy-induced alopecia: Psychosocial impact and therapeutic approaches. Support Care Cancer 2004;12:543-9.
57Batchelor D. Hair and cancer chemotherapy: Consequences and nursing care – A literature study. Eur J Cancer Care (Engl) 2001;10:147-63.
58Pai GS, Vimala AM, Dinesh M. Occurrence and severity of alopecia in patients on combination chemotherapy. Indian J Cancer 2000;37:95-104.
59Wiwanitkit S, Wiwanitkit V. Alopecia due to cancer. Indian J Med Paediatr Oncol 2013;34:141-2.
60Annunziata MC, Ferrillo M, Cinelli E, Panariello L, Rocco D, Fabbrocini G. Retrospective analysis of skin toxicity in patients under anti-EGFR tyrosine kinase inhibitors: Our experience in lung cancer. Open Access Maced J Med Sci 2019;7:973-7.
61Tosti A, Pazzaglia M. Drug reactions affecting hair: Diagnosis. Dermatol Clin 2007;25:223-31, vii.
62Saggar V, Wu S, Dickler MN, Lacouture ME. Alopecia with endocrine therapies in patients with cancer. Oncologist 2013;18:1126-34.
63Freites-Martinez A, Shapiro J, Chan D, Fornier M, Modi S, Gajria D, et al. Endocrine therapy-induced alopecia in patients with breast cancer. JAMA Dermatol 2018;154:670-5.
64Piraccini BM, Iorizzo M, Rech G, Tosti A. Drug-induced hair disorders. Curr Drug Saf 2006;1:301-5.
65Tosi A, Misciali C, Piraccini BM, Peluso AM, Bardazzi F. Drug-induced hair loss and hair growth. Incidence, management and avoidance. Drug Saf 1994;10:310-7.
66Gavazzoni Dias MF. Hair cosmetics: An overview. Int J Trichology 2015;7:2-15.
67Dawber R. Hair: Its structure and response to cosmetic preparations. Clin Dermatol 1996;14:105-12.
68Tosti A, Piraccini BM. Diagnosis and Treatment of Hair Disorders: An Evidence Based Atlas. Abingdon, Oxon, England: Taylor & Francis; 2006.