Obesity, hypertension, and steroids have as their end-organ effect a diminution of local microvascularity. The significant correlation of these factors with Achilles tendinopathy suggests the importance of their effect on microvascularity in the development of Achilles tendinopathy.
Rupture of the posterior tibial tendon has been postulated to occur, in part, as a result of degenerative changes to the tendon. This possibility was examined by a review of 67 patients (average age 57 years) diagnosed with rupture of the posterior tibial tendon. Forty-five of the 67 patients (60%) had one or more of the following positive medical histories: (1) hypertension, (2) obesity, (3) diabetes mellitus, (4) previous surgery or trauma about the medial aspect of the foot, or (5) steroid exposure. Thirty-five patients (52%) had either hypertension, diabetes mellitus, or obesity. A statistical correlation was demonstrated between rupture of the posterior tibial tendon and obesity (P = .005) and to a lesser extent hypertension (P = .025). These disorders have been uniformly associated with an acceleration of the degenerative processes associated with aging, commonly via an acceleration of microvascular and macrovascular diseases. An additional vascular risk is implicated by the known zone of hypovascularity of the posterior tibial tendon and risk of rupture secondary to systemic or local injections of corticosteroids. The prevalence of posterior tibial tendon rupture parallels the degenerative processes of aging, hypertension, diabetes mellitus, and obesity. Additionally, the effects of corticosteroids and local surgical procedures may further be associated with local vascular impairment and eventual rupture.
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