People with GA usually notice a ring of small, firm bumps (papules) more commonly over the backs of the forearms, hands or feet, often centered on joints or knuckles.

In 1977, Dahl et al. proposed that since the lesions of GA often display a thickening of, occlusion of, or other trauma to blood vessels, blood vessels may be responsible for GA. From their study of 58 patients, they found that immunoglobin M (IgM), complement, and fibrinogen were in the blood vessels of GA areas, suggesting that GA may share similarities with an immune-mediated, type 3 reaction or that chronic immune vasculitis may be involved in the pathogenesis.

Their data suggests that lymphokines, such as macrophage-inhibiting factor (MIF), leads to sequestration of macrophages and histiocytes in the dermis.

Then, upon lysosomal enzyme release by these sequestered cells, connective tissue damage ensues, which results in GA.[10] Later, these authors found data suggesting that activation of macrophages and fibroblasts are involved in the pathogenesis of GA and that fibrin and the rare IgM and C3 deposition around vessels were more likely a delayed-type hypersensitivity with resulting tissue and vessel changes rather than an immune-complex mediated disease.

[7][12][13] Granuloma annulare may be divided into the following types:[14]: 703–5 Because granuloma annulare is usually asymptomatic and self-limiting with a course of about two years, initial treatment is generally topical steroids or calcineurin inhibitors; if unimproved with topical treatments, it may be treated with intradermal injections of steroids or phototherapy.

[17] The disease was first described in 1895 by Thomas Colcott Fox as a "ringed eruption of the fingers",[3] and it was named granuloma annulare by Henry Radcliffe Crocker in 1902.