Neovascularity in chronic posterior tibial tendon insufficiency.

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.