Insufficient posterior tibial tendons in 28 specimens from patients with clinical Stage II or III disease were examined to clarify the etiology of adult-acquired flatfoot deformity. Hematoxylin and eosin and Masson trichrome-stained sections of formalin-fixed tissue were viewed in plain and polarized light. We performed a qualitative analysis for abnormalities in collagen orientation, degree of vascularization, tenocyte cellularity, mucinous change, and chondroid metaplasia. Tendons were divided into three zones: tenosynovial lining cell layer, subtenosynovial lining cell layer, and tendon proper. All tendons showed neovascular infiltration causing collagen fibril disruption; 50% of specimens had diffuse involvement. Increased mucin content and chondroid metaplasia occurred in 28% and 36% of specimens, respectively. The tenosynovial lining cell layer showed hyperplasia in 28% of specimens. The subtenosynovial lining cell layer showed thickening and neovascularization in 79% of specimens, which appeared to be the source for the diffuse neovascular infiltrative process. There is little histopathologic evidence to support an inflammatory etiology to the posterior tibial tendons in acquired-adult flatfoot deformity. Neoangiogenesis, the prominent histologic finding, is consistent with an obscure insult. We postulate that overuse, tension, or stretching may activate the tenosynovial lining cells and incite angiogenesis.