The etiology of alopecia areata is complex, and the correct diagnosis of alopecia areata requires a combination of the patient’s clinical presentation, medical history, physical examination and laboratory tests. The literature reports that the rate of alopecia areata in patients with stage II syphilis is 2.9%-7%, but many patients lack the typical skin lesions of stage II syphilis and are easily misdiagnosed by omission. Clinically, syphilitic alopecia is divided into two types. The first type is symptomatic alopecia, accompanied by an acute phase II syphilis rash (usually papulosquamous) on the patient’s scalp, which is rare; the second type is called substantial syphilis alopecia, where the patient’s scalp has no visible syphilis lesions. There are currently 3 subtypes: classic worm-like alopecia, diffuse hair thinning, and a mixture of both. The worm-like syphilitic alopecia is more common and is easily confused with plucking fetish, pulling alopecia and baldness. It usually begins to appear 6 months to 1 year after infection. The diagnosis is not difficult when coexisting with typical skin lesions. In a few severe cases, eyebrow hair, axillary hair, beard and pubic hair are also lost, which can easily be misdiagnosed as alopecia universalis. The histopathological similarities between alopecia areata and baldness require a syphilis serologic test. Early scholars believed that syphilitic alopecia may be caused by indirect damage from anti-syphilis spirochete serum antibodies. Most scholars now believe that alopecia areata is caused by the invasion of syphilis spirochetes around the hair follicles. Syphilis spirochetes invade the hair follicles from the lower part of the funnel to the outer hair root sheath slightly above the isthmus, without invading the hair papillae, so there is incomplete and reversible hair loss. A recent study in an HIV-positive patient showed the presence of syphilis spirochetes around the hair bulb and invasion of the hair matrix by immunohistochemistry.