Histology slide of a solar lentigo Differently from the melanotic nevi and the verrucous nevi on the skin, age spots change in color and in shape with time. Michelitsch and Michelitsch propose a hypothesis inspired by their misrepair-accumulation aging theory for the development of age spots. They propose that aged basal cells contain lipofuscin bodies that cannot be removed and might promote the aging of neighboring cells, generating a feedback loop that causes more and more neighbor cells to become aged and contain lipofuscins. Such cells might then aggregate into a spot with an irregular shape. They propose that the protrusion of a flat spot is a result of the death of aged cells in the spot and release of lipofuscin bodies. The aggregating cells would form a capsule, and the dense lipofuscin bodies make the protruding spot soft and dark in color. However, this proposal appeared as a preprint in 2015, has little direct empirical support, and has never been published in a peer reviewed journal. Another group has reported that "age spots" taken from human skin biopsies of patients facial senile lentigo of Fitzpatrick skin type III or IV aged 55–62 are enriched with senescent fibroblasts compared to surrounding skin. The dark coloration appeared to be due to higher melanin levels and activity of tyrosinase in the senescent fibroblasts than in the controls, potentially related to lower SDF1 expression. Patients were then administered six weekly treatments of microneedle fractional radiofrequency aimed at eliminating dermal senescent fibroblasts; this led to a marked decrease in epidermal pigmentation compared to baseline, accompanied by a decrease in the synthesis of collagen and the normalization of suppressed SDF1 expression.
Liver spot
Roth's spot
Forchheimer spots
Biliary sludge
Bitot's spots
Bier spots
Blind spot 
Elschnig spots