Posterior tibial tendonitis, often referred to as posterior tibial tendon dysfunction (PTTD), is a condition involving the inflammation or degeneration of a tendon in the lower leg and ankle. This disorder is widely recognized as the most common underlying cause of acquired adult flatfoot deformity. The condition rarely arises from a single traumatic event, but rather from a complex combination of mechanical overload, tissue breakdown, and underlying health factors that weaken the tendon over time.
The Crucial Function of the Posterior Tibial Tendon
The posterior tibial tendon (PTT) originates from a muscle deep within the calf, traveling down the inner side of the ankle and attaching to several bones in the midfoot. The tendon must curve sharply around the bony prominence of the inner ankle, the medial malleolus, before spreading its attachments across the arch. Its primary function is to maintain the medial longitudinal arch, which is the structure commonly called the arch of the foot.
The PTT acts as a dynamic stabilizer, actively supporting the arch during weight-bearing activities like walking and running. It also assists with foot inversion, which is the motion of turning the sole of the foot inward, and plantarflexion, or pointing the toes downward. This action is particularly important for controlling the foot’s natural inward roll, known as pronation, during the midstance phase of walking.
Biomechanical Stressors Leading to Tendon Overload
The most direct causes of PTTD involve physical mechanisms that place excessive strain on the tendon, leading to micro-tears and a breakdown of the tendon fibers. This repetitive microtrauma is considered the most common pathway to failure.
High-impact and repetitive activities significantly contribute to this overload. Sports that involve sudden, repeated impacts, such as running, jumping, court sports like basketball and tennis, or even extensive walking, force the tendon to work harder and for longer periods. Over-training or using poor technique in these activities increases the frequency and magnitude of the strain, exceeding the tendon’s capacity for repair.
A pre-existing foot structure, particularly one with excessive pronation or a flexible flatfoot, also forces the PTT to work against an inherent mechanical disadvantage. When the foot rolls too far inward (overpronation) during the gait cycle, the PTT is placed under greater tension as it attempts to stabilize the collapsing arch. This continuous, heightened effort during every step leads to chronic overuse and eventual degeneration of the tendon tissue. Less commonly, PTTD can be initiated by a direct traumatic event, such as a severe ankle sprain or a fall that causes an acute tear or significant damage to the tendon.
Systemic and Health Predisposing Factors
While mechanical forces cause the overload, several internal health factors can weaken the PTT tissue itself, lowering its tolerance threshold for strain. Age-related changes are a prominent factor, with the condition most often affecting individuals over 40. As people age, the tendon’s blood supply can diminish, and the tissue undergoes natural degeneration, a process often termed tendinosis, which makes it less elastic and more susceptible to damage from normal activity.
Increased body weight from obesity multiplies the load placed on the PTT during every weight-bearing activity. This constant, elevated force accelerates the degenerative process, making the tendon more vulnerable to failure.
Underlying medical conditions further compromise the tendon’s integrity and healing capacity. Diabetes is a significant risk factor because it impairs blood flow and general tissue healing throughout the body, including the tendons. Inflammatory conditions, such as rheumatoid arthritis, can directly attack and degrade the tendon tissue, leading to inflammation and structural breakdown. Other factors that predispose individuals to PTTD include hypertension and the use of corticosteroid medications, both of which are associated with reduced tendon resilience.
The Path from Strain to Acquired Flatfoot
Untreated or chronic strain on the posterior tibial tendon initiates a progressive cycle of dysfunction that culminates in acquired flatfoot. As the PTT becomes damaged and inflamed, it loses its ability to contract effectively and begins to elongate. Once the tendon can no longer support the arch, the foot structure begins to collapse under body weight. The medial longitudinal arch flattens, and the heel bone often rolls outward into a valgus alignment. This collapse places secondary stress on the surrounding ligaments, particularly the plantar ligaments, which then also begin to fail. The ultimate result is a progressive collapsing foot deformity, the most common form of adult-acquired flatfoot. This structural change alters the entire biomechanics of the foot and ankle, leading to difficulty with walking and pushing off the ground.