Solar lentigines (SL) are hyperpigmented lesions generally seen in elderly people. Their pathogenesis has not been completely elucidated. We examined 75 cases of SL using routine histopathology and immunohistochemistry. In addition, seven cases were evaluated by electron microscopy. Histopathologically, we observed vacuolar changes in the dermoepidermal junction in 85% of the cases. Dermal melanophages were seen in 77% of the cases. The immunohistochemical expression rates in the epidermis for cytokeratin (CK)15, CK14, CK10, p63 and nestin were 76%, 100%, 100%, 100% and 17%, respectively. In 58 cases showing dermal melanophages, expression rates of CD163 and factor XIIIa on melanophages were 79% and 83%, respectively. Double positivity for both proteins was identified in 44 cases (75%). Ultrastructurally, vacuolar structures were seen in the cytoplasm of basal cells and upper dermis in all cases examined. We observed elimination processes of damaged basal keratinocytes, which were probably produced by ultraviolet (UV) irradiation, into the papillary dermis. The segregated damaged cell bodies containing melanin granules seemed to be phagocytosed by poorly immunostimulatory macrophages labeled immunohistochemically by CD163 and factor X IIIa, contributing to prolonged pigmentation of SL. In addition, repeated basal keratinocyte damages may be in association with altered CK and p63 expression patterns in the constituent cells of SL.