Tibialis posterior tendinopathy

Tibialis posterior tendinopathy is a condition of overload and progressive dysfunction of the tendon of the tibialis posterior muscle. It initially presents as pain, most often located on the medial side of the ankle or foot, sometimes associated with mild swelling along the course of the tendon.

The tibialis posterior plays an essential role in supporting the medial arch of the foot and in controlling foot pronation. When its capacity to produce and transmit sufficient force decreases, the foot may gradually lose part of its dynamic support.

This condition is part of a continuum ranging from a painful tendinopathy without significant deformity to a progressive deformity of the foot with collapse of the arch. The historical term “posterior tibial tendon dysfunction” (PTTD) is still widely used in the literature; however, more recent classifications place greater emphasis on the overall deformity of the foot and use the term Progressive Collapsing Foot Deformity (PCFD).

In advanced forms, the damage is no longer confined to the tendon: it gradually extends to the ligaments, joints and bones. Management must therefore be tailored to the stage of the disease, which is why early recognition and treatment are important.

The tibialis posterior is a deep muscle of the posterior compartment of the lower leg. It originates from the posterior surface of the tibia, the posterior surface of the fibula and the interosseous membrane that connects them.

Its tendon runs down behind the medial malleolus before heading towards the medial side of the foot. It inserts mainly on the navicular, with expansions to the cuneiforms, the cuboid and the bases of some metatarsals — an anatomy that explains its major role in supporting the arch of the foot.

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The tendon never works alone: it acts in close association with the plantar calcaneonavicular ligament (“spring ligament”), the plantar fascia, the deltoid ligament, the intrinsic foot muscles, the tibialis anterior and the fibular muscles. It is thus one of the main dynamic stabilisers of the medial arch.

Biomechanics of the tibialis posterior

The tibialis posterior contributes to foot supination, inversion, plantar flexion, hindfoot stabilisation and support of the medial arch. During walking and running, the foot must be mobile enough to absorb stress at foot strike, then rigid enough to transmit forces efficiently during push-off: the tibialis posterior contributes to this transformation by controlling pronation.

During the stance phase, a certain amount of pronation is physiological; the tibialis posterior slows its range and thus works as a true active muscular brake. As push-off approaches, the foot must instead become more rigid: the muscle contributes to foot supination and arch stabilisation, turning the foot into an efficient propulsion lever.

Role in supporting the arch of the foot

Together with the spring ligament, the plantar fascia and the other foot muscles, the tibialis posterior forms a dynamic and passive support system for the arch. When the tendon becomes painful or loses mechanical capacity, a chain of events can gradually develop: reduced tibialis posterior strength → increased pronation → lowering of the arch → increased ligament loading → progressive foot deformity.

This progression is not systematic, however. Early tendinopathy can remain stable for several years without progressing to significant deformity. The aim of early management is precisely to prevent the loss of tendon capacity from becoming great enough to cause this deformity.

Tibialis posterior tendinopathy is particularly common in middle-aged and older adults. It is less common in young athletes than Achilles or patellar tendinopathy, but it can nevertheless occur in athletes exposed to repeated running or walking stresses.

Several factors are associated with this condition: age, excess weight, high blood pressure, diabetes, dyslipidaemia, flat feet, a history of ankle injury and a substantial increase in activity load.

The true prevalence varies depending on the populations studied and the diagnostic criteria used; it is probably underdiagnosed, particularly in the early stage of the disease.

Tibialis posterior tendinopathy is a multifactorial condition, most often resulting from a combination of several mechanical, muscular, metabolic and age-related factors.

Mechanical factors

Several factors increase the stress placed on the tendon: flat feet, overpronation, hindfoot valgus, a sudden increase in activity, prolonged walking, running, prolonged standing at work and excess weight.

Having flat feet does not, however, mean that tendinopathy will necessarily develop: the foot can function perfectly well with a low arch if muscular and ligamentous capacity remains sufficient.

Factors related to muscle strength

Reduced strength of the tibialis posterior and triceps surae reduces the capacity of the lower limb to control the stresses placed on the foot. The intrinsic foot muscles also play an important role in stabilising the arch.

Metabolic factors

Several conditions are associated with an increased risk: diabetes, high blood pressure, obesity and dyslipidaemia. A combination of several of these metabolic factors appears to be particularly unfavourable.

Age-related factors

The tendon’s capacity to adapt to mechanical stress gradually decreases with age, which explains why this condition is much more common in middle-aged and older adults.

The main symptom is pain on the medial side of the ankle or foot, generally following the course of the tendon: behind the medial malleolus, along the medial border of the foot, down to its insertion on the navicular.

At first, pain appears only during activities that place heavy demands on the tendon: prolonged walking, running, climbing stairs, hiking or prolonged standing. Swelling along the tendon may also be observed. As the condition progresses, pain may appear during everyday activities.

The gradual loss of tibialis posterior capacity may also show up as difficulty standing on tiptoe on one foot, foot fatigue, a feeling that the arch is collapsing, a gradual increase in pronation or difficulty with prolonged walking. A particularly telling sign is the onset of difficulty performing a single-leg heel raise: the patient may at first manage it with pain or with reduced heel height, then become unable to perform the movement properly in more advanced forms.

Clinical examination

The examination should assess the state of the tendon, muscle strength, foot alignment, mobility and function all at once. Inspection looks for reduced medial arch height, hindfoot valgus, forefoot abduction, a change in the axis of the calcaneus and asymmetry between the two feet. Viewed from behind, increased visibility of the lateral toes on the affected side (“too many toes sign”) may indicate forefoot abduction; this sign is classically looked for in advanced forms.

The Single Leg Heel Rise Test is one of the most important functional tests: the patient raises the heel while standing on one foot, which should normally be accompanied by progressive inversion of the calcaneus. Pain, reduced heel height, rapid fatigue, an inability to repeat the movement or a lack of calcaneal inversion suggest tibialis posterior dysfunction. This test simultaneously assesses triceps surae strength, tibialis posterior function and the capacity of the arch to withstand stress; it is also an excellent tool for monitoring rehabilitation.

Assessment of ankle and foot mobility looks for limited dorsiflexion or supination, hindfoot stiffness, or limited mobility of the midtarsal joints and the first ray. An essential distinction must be made between a flexible deformity (still passively correctable) and a rigid deformity (not correctable), which is of major importance for prognosis and treatment strategy. Finally, the muscle assessment looks for weakness of the tibialis posterior, triceps surae, intrinsic foot muscles, tibialis anterior and fibular muscles — ideally assessed under load, in a functional situation, which is more informative than a simple isolated test.

The surgical strategy depends mainly on the stage of the disease. In early forms, conservative treatment remains the preferred option. In forms with flexible deformity, reconstructive surgery may be considered when several months of well-conducted conservative treatment have not produced sufficient improvement. In advanced forms with rigid deformity or joint involvement, surgery may become necessary.

Depending on the situation, procedures may combine tendon repair or debridement, tendon transfer, calcaneal osteotomy, correction of midfoot deformity, ligament reconstruction or, in advanced arthritic forms, arthrodesis. The strategy therefore depends far more on the stage of the deformity than on the mere presence of tendinopathy.

A specialist opinion is particularly recommended in cases of persistent pain despite properly conducted management, suspected tendon rupture, inability to perform a single-leg heel raise, progressive or rigid deformity, newly developed flat foot in an adult, associated joint pain or suspected spring ligament involvement.

Recovery time depends heavily on the stage of the disease. Early tendinopathy can begin to improve within a few weeks with proper load adjustment and progressive rehabilitation. More advanced forms, particularly when a foot deformity is already present, may require several months of management.

The earlier management begins, the more it is possible to favour a conservative strategy and avoid progression to a structural deformity of the foot.

Prevention relies on maintaining good functional capacity of the foot: regular strengthening of the tibialis posterior and triceps surae, work on the intrinsic foot muscles, balance training, pronation control and maintaining good ankle mobility.

In athletes, periods of returning to sport after a break should be particularly gradual, with a carefully planned increase in training load. In people with flat feet, monitoring for the onset of medial pain or a gradual decrease in the ability to stand on tiptoe makes it possible to intervene early, before a deformity sets in.