Posterior tibial tendon dysfunction is a cause of painful acquired flatfoot in adults. It is associated with progressive collapse of the medial longitudinal arch, hindfoot valgus, and forefoot abduction deformities. The clinical manifestations and surgical treatment have been well documented in the literature. Epidemiologic studies have not shown any clear predisposing factors to the disease. Numerous etiologies have been proposed to explain the clinical evidence of tendon degeneration found at the time of surgery including trauma, anatomic, mechanical inflammatory, and ischemic factors. Although previously thought to be secondary to an inflammatory process resulting in acute and chronic tendinitis, more recent histopathologic evidence has revealed a degenerative tendinosis with a nonspecific reparative response to tissue injury characterized by mucinous degeneration, fibroblast hypercellularity, chondroid metaplasia, and neovascularization. These pathologic changes result in marked disruption in collagen bundle structure and orientation. This may compromise the tendon and predispose it to rupture under physiologic loads. However, it cannot be determined whether these changes precede or postdate posterior tibial tendon dysfunction. It seems that there are many contributing factors to the etiology of posterior tibial tendon dysfunction all culminating in a common disease process with resulting tendon degeneration and an insufficient repair response.