Alopecia is a general medical term meaning loss, reduction or absence of hair and can refer to many different disorders rather than one specific disease. Hair loss may affect the scalp, eyebrows, eyelashes, beard, body hair or multiple regions, and it can be temporary, persistent, scarring or non-scarring. The term therefore encompasses conditions with very different causes, mechanisms, prognoses and treatments. Examples include androgenetic alopecia, alopecia areata, telogen effluvium, anagen effluvium and cicatricial or scarring alopecias. Accurate identification of the type is more important than treating alopecia as a single condition because the therapeutic approach depends on whether follicles remain structurally capable of producing new hair.
Normal hair growth occurs through a cyclical process involving anagen, the active growth phase, catagen, a brief transitional phase, and telogen, the resting phase, followed by shedding and renewed growth. The proportion of follicles in each phase determines the normal pattern of hair density and shedding. Disturbances of the cycle can produce diffuse hair loss without destroying follicles, while inflammatory or autoimmune processes can permanently damage follicles and cause scarring. The visible hair shaft is biologically inert once produced, so disorders of the follicle rather than the shaft itself account for most forms of true alopecia. Factors influencing hair cycling include hormones, genetics, nutrition, systemic illness, medications, inflammation and local tissue conditions.
Androgenetic alopecia is the most common form of progressive patterned hair loss and results from genetically influenced follicular sensitivity to androgen signalling. In susceptible follicles, dihydrotestosterone and related androgen activity contribute to progressive miniaturisation, shortening of the anagen phase and production of increasingly fine hairs. The distribution commonly involves the frontal and vertex scalp in men and diffuse central thinning with relative preservation of the frontal hairline in many women, although patterns overlap. Alopecia areata has a different mechanism, involving autoimmune attack directed at hair follicles and often producing sharply demarcated patches of non-scarring hair loss. It can affect people of any age and may involve nails or other hair-bearing sites.
Diffuse shedding can arise through mechanisms distinct from follicular miniaturisation or autoimmune attack. Telogen effluvium occurs when a greater proportion of follicles prematurely enter the telogen phase, followed by increased shedding several months after a triggering event such as significant illness, major physiological stress, surgery, rapid weight loss or certain medications. Anagen effluvium occurs when actively growing follicles are abruptly damaged, classically by cytotoxic chemotherapy, producing rapid shedding. Traction alopecia results from prolonged mechanical pulling or tension, while hair-pulling disorders involve repetitive removal of hair. Fungal infection of the scalp can also cause alopecia, particularly in children, and requires treatment directed at the infection rather than standard hair-loss therapies.
Scarring alopecias, also called cicatricial alopecias, are especially important because inflammation destroys the follicular unit and replaces it with scar tissue, making spontaneous regrowth from that follicle unlikely. Conditions within this group include several inflammatory disorders with different clinical patterns and pathological findings. Early diagnosis can therefore be critical because treatment aims to suppress active inflammation before irreversible follicular destruction occurs. Clinical assessment may include examination for follicular openings, scaling, erythema, pustules, broken hairs and scarring, while dermoscopy can reveal characteristic structures. In uncertain cases, a scalp biopsy can help distinguish scarring from non-scarring disease and identify the underlying inflammatory pattern.
Evaluation of alopecia begins with the history and examination. Important factors include the timing and speed of loss, distribution, shedding versus thinning, family history, recent illness, nutritional changes, medications, hormonal symptoms, hair-care practices and associated skin or systemic findings. Examination determines whether follicular openings are preserved, whether hairs vary in diameter, whether there is inflammation or scarring and whether the loss follows a recognisable pattern. Laboratory tests are not universally required but may be appropriate when clinical features suggest nutritional deficiency, thyroid dysfunction, hormonal abnormalities or another systemic disorder. Pull tests, hair microscopy, dermoscopy and biopsy can provide additional information in selected cases.
Treatment is highly dependent on the cause. Androgenetic alopecia can be treated with approaches such as topical minoxidil and, in appropriate patients, systemic antiandrogenic or androgen-modifying therapies under medical supervision. Alopecia areata may be treated with corticosteroids, other immunomodulatory therapies or targeted systemic medicines depending on severity and distribution. Telogen effluvium often improves after the precipitating factor resolves, although recovery can take months because hair growth is intrinsically slow. Scarring alopecias require treatment directed at the inflammatory process, and established follicular destruction generally cannot be reversed by ordinary hair-growth stimulants. Hair transplantation may be useful for selected stable forms of non-scarring alopecia but is not a substitute for controlling active inflammatory disease.
Alopecia can have major cosmetic and psychological consequences because hair is closely associated with identity, appearance and social perception. Hair loss does not necessarily indicate poor nutrition, hormonal disease or serious systemic illness, but sudden, extensive or scarring loss warrants appropriate assessment rather than assuming it is ordinary hereditary thinning.
There is also no single treatment that works for all forms, and products marketed broadly for hair growth may be ineffective when follicles have been destroyed or when the underlying diagnosis is different. Distinguishing shedding from miniaturisation, non-scarring from scarring loss and localised from diffuse disease provides the framework for accurate diagnosis. Prognosis ranges from complete spontaneous regrowth to progressive or permanent follicular loss, depending fundamentally on the underlying form of alopecia.
