For decades, medical treatments have focused on symptom relief, with cortisone injections, shockwave therapy, physiotherapy, and orthotics dominating the market. However, these approaches often fail to address the underlying biomechanical dysfunctions responsible for plantar fasciitis and heel spurs. For the first time, groundbreaking research has identified the primary culprit: the flexor hallucis longus (FHL) tendon.
The FHL tendon is a critical component of foot biomechanics. It originates in the back of the leg, runs through the ankle, and inserts at the base of the big toe’s distal phalanx. During walking and running, the FHL stabilizes the medial arch and controls the downward movement of the big toe. More importantly, it generates over 60% of the propulsion force during the push-off phase of the gait cycle.
Research shows that the FHL tendon endures 40–60% more tension than the tendons connected to the other toes. This high load explains why the FHL plays a dominant role in straining the plantar fascia. When the big toe flexes during propulsion, the FHL tightens, transferring significant force to the plantar fascia. This repeated tension leads to microtears and inflammation at the fascia’s attachment point on the heel bone.
Unlike the tendons supporting the smaller toes, which distribute forces more evenly, the FHL’s alignment and biomechanical role concentrate pressure on the medial plantar region. This unique dynamic explains why the FHL tendon is at the core of plantar fasciitis and heel spur development.
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