Types of Hair Loss and Treatment Options, Including the Novel Low-level Light Therapy and its Proposed Mechanism

Mahyar Ghanaat, MD


South Med J. 2010;103(9):917-921. 

In This Article

Types and Epidemiology of Hair Loss

Male pattern hair loss (MPHL), also known as androgenetic alopecia (AGA), is the most common form of hair loss in men.[1–3] Similarly, female pattern hair loss (FPHL) is the most common form of hair loss in women.[4] The incidence and prevalence of MPHL is dependent on age and race. Chinese, Japanese, and African American people are affected less than Caucasians.[2,5] Its incidence increases by age.[5] Prevalence values have variable ranges from 16–96%, depending on the age group and whether or not mild forms of MPHL are included (Table 1).[2,6,7] Prevalence values for FPHL are comparable to MPHL (Table 2).[8] The severity of MPHL is based on the Norwood Hamilton Classification, which takes into account bitemporal and vertex hair loss (Fig. 1).[2] FPHL is evaluated based on the Ludwig scale, which ranges from I-III (Fig. 2).[4] These classification systems differ based on the fact that hair loss and thinning in men most commonly occurs in an orderly fashion and involves the temporal and vertex region while sparing the occipital region; diffuse thinning and loss of density with a normal distribution and maintenance of the frontal hairline is often seen in women.[2,4,5,9,10]

Figure 1.

Norwood Hamilton classification. Reprinted with permission from Endocrinol Metab Clin North Am 2007;36:381, ©2007 Elsevier Inc. All rights reserved.

Figure 2.

Ludwig classification. Reprinted with permission from Clin Interv Aging 2007;2:190, ©2007 Dove Medical Press Ltd. All rights reserved.

The term AGA pertains to the pathophysiology of MPHL, in which there is an induction of hair loss due to the effects of androgens such as testosterone (T) and its derivative dihydrotestosterone (DHT) in genetically susceptible individuals.[2] Recently, authors have argued against the use of the term AGA in women, as the role of androgens in FPHL is debatable.[4,7,11,12] Testosterone is a lipophilic compound that diffuses the cell membrane. It is converted into its more active form, DHT, by the cytoplasmic enzyme 5-alpha reductase (5-AR).[2,4] There are two types of 5-AR. Type 1 is found in keratinocytes, fibroblasts, sweat glands, and sebocytes, and Type 2 is found in skin and the inner root sheath of hair follicles.[4,13,14] Androgens play an important role in the control of hair. During puberty, due to a surge in T, there is an induction of pubic hair growth and a decrease in follicle size in the bitemporal region.[8] Also, castrated men are not known to develop MPHL.[2,7] However, there is no correlation between T levels and MPHL.[2] The role of DHT was first noticed in pseudohermaphrodites lacking this enzyme, who did not develop MPHL.[2,7] DHT then binds the nuclear androgen receptor (AR) that regulates gene expression.[2,7] Although the exact genes involved in hair loss are not known with certainty, some of the proposed genes responsible for hair growth (mainly studied in knockout and transgenic mice) are desmoglein, activin, epidermal growth factor (EGF), fibroblast growth factor (FGF), lymphoid-enhancer factor-1 (LEF-1), and Sonic Hedgehock.[15]

Besides patterned baldness, there are several other forms of hair loss, which include alopecia areata (AA), telogen effluvium (TE), and several androgen-related female alopecias. AA is an autoimmune inflammatory condition which may affect the hair of the head, face, and body.[16] Although most commonly thought of as an acquired disorder, congenital cases have been described.[17] It has an incidence of 0.1–0.2%, and affects 1–2% of men and women.[16,18] Hair involvement in AA is often patchy. Two variants of AA are alopecia totalis, a total loss of scalp hair, and alopecia universalis, total loss of scalp and body hair.[16] AA is linked to several human leukocyte antigen (HLA) alleles, such as HLA-AI, HLA-HLA-B26, HLA-DQ1, and HLA-DQ3.[16] Although most commonly treated by an injection of intralesional corticosteroids, other treatment modalities are used.[16] These include topical and systemic corticosteroids, minoxidil for moderate cases, anthralin, contact sensitizers (when more than half the scalp is affected), psoralen plus ultraviolet A (PUVA), cyclosporine, tacrolimus, and biologics.[16,18,19] Biologics include agents such as alefacept, efalizumab, etanercept, infliximab, and adalimumab. Of these, alefacept seems to be most promising, while adalimumab and infliximab have been reported to induce AA.[20]

Telogen effluvium (TE) is abnormal hair cycling causing excessive loss of telogen hair.[12] It is likely the most common cause of alopecia in children.[12] Some of the common causes include acute severe illness, surgery, iron deficiency anemia, thyroid disease, malnutrition, chronic illness, and medications such as oral contraceptives, lithium, and cimetidine.[12,19] A good illness and medication history is necessary to make the diagnosis, as well as laboratory studies such as complete blood count (CBC), thyroid function tests, and syphilis titers.[12,19]

Androgen-related female alopecias include a variety of types of hypergonadism. Polycystic ovarian syndrome (PCOS) is a common cause of hypergonadism which could cause amenorrhea, hirsutism, and FPHL.[14] Some antiandrogen medications that may be helpful for FPHL include cyproterone acetate, spironolactone, and flutamide.[10] However, one study argues that 88% of FPHL will not improve with oral antiandrogens.[10]


Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.