The Science of Posterior Tibial Tendon Dysfunction
Posterior tibial tendon dysfunction (PTTD), now commonly termed Progressive Collapsing Foot Deformity (PCFD), represents a complex, progressive condition involving failure of the posterior tibial tendon and associated ligamentous structures. The posterior tibial tendon serves as the primary dynamic stabilizer of the medial longitudinal arch and controls hindfoot motion during the stance phase of walking. The condition begins with inflammation and degenerative changes within the tendon substance (tendinosis), often triggered by repetitive microtrauma or acute overload. As the tendon's structural integrity compromises, its eccentric strength diminishes, particularly during the loading response and terminal stance phases of gait. This leads to progressive loss of the tendon's ability to resist pronation forces and maintain arch integrity. Secondary to tendon failure, supporting ligamentous structures become progressively incompetent. The spring ligament complex (calcaneonavicular ligament) stretches and eventually fails, followed by attenuation of the superficial deltoid ligament, long and short plantar ligaments, and plantar fascia. This cascade creates a characteristic pattern of deformity: hindfoot valgus, forefoot abduction, midfoot collapse, and eventual ankle valgus in advanced cases. The condition progresses through distinct stages: Stage I involves tendinosis without deformity, Stage II presents flexible deformity that corrects with non-weight bearing, Stage III shows fixed deformity with subtalar joint arthritis, and Stage IV involves ankle valgus and deltoid ligament failure. Understanding this progression is crucial as treatment options and prognosis differ significantly between stages.
Contributing Factors
The posterior tibial tendon functions as part of an integrated system that maintains the medial longitudinal arch and controls foot mechanics during weight-bearing activities. During normal gait, the tendon contracts eccentrically from heel strike through midstance to resist excessive pronation, then concentrically during heel rise to invert the hindfoot and lock the midfoot for efficient push-off.
When the posterior tibial tendon fails, the foot loses its primary mechanism for arch support and supination. The talus adducts and plantarflexes, the navicular drops medially, and the calcaneus moves into valgus. This creates a "too many toes" sign when viewed from behind, as the laterally deviated forefoot becomes visible.
The biomechanical changes extend beyond the foot. Hindfoot valgus causes compensatory external rotation of the tibia, affecting knee mechanics and potentially contributing to patellofemoral dysfunction. The inability to achieve a rigid lever arm during push-off reduces propulsive efficiency and increases energy expenditure during walking.
Weight-bearing forces that normally distribute across the entire foot concentrate on the medial structures, accelerating ligamentous failure. The loss of the windlass mechanism due to midfoot collapse further compromises the foot's ability to become a rigid lever, perpetuating the cycle of dysfunction.
Risk factors that predispose to biomechanical failure include obesity (increasing load), diabetes (affecting tendon quality), previous ankle trauma disrupting normal mechanics, inflammatory arthritis causing tendon degeneration, and congenital flatfoot creating chronic overload of compensatory structures.