Posterior Tibial Tendon Dysfunction

Original Editor - Brian Duffy

Top Contributors - Max Louis, Lien Hennebel, Nele Postal, Rachael Lowe and Brian Duffy  



The posterior tibial tendon(PTT) functions mainly as a dynamic support of the medial arch. It also inverts the foot and aids in ankle plantar flexion. Dysfunction of the posterior tibial tendon usually manifests early with pain and swelling along the medial aspect of the foot and behind the medial malleolus. The pain is worse with prolonged standing and activities, and usually is associated with tenderness along the length of the tendon. In advanced posterior tibial tendon dysfunction, collapse of the medial arch occurs, leading to the characteristic pes planus deformity with hindfoot valgus; initially, this deformity is flexible, but in more-advanced stages it can become fixed and associated with forefoot abduction[1].Although there are no large-scale of studies that have been performed about the overall incidence of this disease, it is thought that the prevalence is anywhere from 3.3 to 10%, depending on the sex and age of the patient. This disorder is associated with adult-acquired flatfoot deficiency which can cause it to be misdiagnosed, meaning the actual prevalence may be much higher than shown in the literature[2]

Posterior tibial tendon dysfunction (PTTD) is a progressive condition that can be classified into four stages[3].

  • In the early stages there may be pain, the area may be red, warm and swollen.  There are not usually symptoms during gait but symptoms may be present in running.
  • Later as the arch begins to flatten, there may still be pain on the inside of the foot and ankle but at this point, the foot and toes begin to turn outward and the ankle rolls inward.
  • As PTTD becomes more advanced, the arch flattens even more and the pain often shifts to the outside of the foot, below the ankle. The tendon has deteriorated considerably and arthritis often develops in the foot. In more severe cases, arthritis may also develop in the ankle. [4]

Melissa Rabbito., et al: investigated how arch structure may play a role in the progressive nature of PTTD. Runners with PTTD were compared with healthy runners. Runners with PTTD had an increased rearfoot pronation compared to the healthy runners, this pronation places greater strain on the tibialis posterior muscle which explains the progressive nature of PTTD[5].

Edwards., et al: state that PTTD is considered to be the main cause of adult acquired flat foot. [6] Posterior tibial tendon dysfunction (PTTD) is according to some authors a synonym to adult acquired flatfoot deformity (AAFD). The treatment for both conditions is therefore similar.

Clinically Relevant Anatomy:

The posterior tibial tendon runs posterior to the medial malleolus inserting into the navicular tuberosity and the plantar aspect of the tarsus. It is the primary stabilizer of the medial longitudinal arch, aiding in mid and hind foot locking during ambulation. If compromised, a resulting pes planus foot may develop and place greater stress on the surrounding ligaments and soft tissue[7]


The Posterior Tibial Tendon During Gait:

The functions of a healthy tendon are plantar flexion of the ankle, inversion of the foot and elevating the medial longitudinal arch of the foot (it appears as the primary stabilizer of this arch). This elevating of the medial longitudinal arch causes a locked entire of the mid-tarsal bones, so the midfoot and hindfoot are stiff. All of this allows the muscle gastrocnemius to act more efficiently during gait. When the tibial posterior tendon isn't in health anymore and he doesn't do his work, the other joint capsules and ligaments become weak. There is an eversion of the subtalar joint, abduction of the foot (talonavicular joint) and valgus of the heel. Also a flattened arch develops what can cause an adult  acquired flatfoot. And the muscle gastrocnemius is unable to act without the posterior tibial tendon what results in affected balance and gait.

In this figure, they use 'tibialis posterior intramuscular EMG' to quantify the tibial posterior activation during walking. They used participants (female) with acute stage II PTTD. Differences in muscle activation: the participants with PTTD shows a significantly greater tibialis posterior EMG amplitude during the second half of stance phase. They walk with a pronated foot and exhibit an increased tibialis posterior activity compared to the participants without PTTD. [9] 


Epidemiology /Etiology:

Once thought to be a tendonitis, it is now commonly accepted the process is one of tendon degeneration or tendopathy. A poor blood supply has been identified as well as mechanical factors such as peroneal brevis overactivity or a pes planus foot. The latter will gradually place increased stress to the posterior tibial tendon causing early degeneration. Trauma ( ankle sprain, fracture) may also initiate the process[7]

Risk factors to get PTTD are:

  1. Elderly: especially middle aged women [10][11]
  2. Young athletes [10]
  3. Hypertension [10][11]
  4. Obesity [10][11]
  5. Diabetes mellitus [10][11]
  6. Seronegative arthropathies [10]
  7. Accessory navicular bone [10]
  8. Ligamentous laxity [11]
  9. Pes planus (flatfeet) [11]
  10. Steroid therapy [10][11]
  11. Accesory navicular: may interfere with posterior tibial tendon function [10]
  12. Overuse [4] [12]
  13. Previous trauma (certain types of ankle fracture)  [13]
  14. Steroid injections[13]
  15. Psoriatic arthritis / Rheumatoid arthritis[13]

Characteristics / Clinical Presentation:

  • Pain/swelling behind medial malleolus and along medial longitudinal arch
  • Change in static/dynamic foot ( pes planus)
  • Limited walking ability
  • Impaired balance
  • Impaired MMT PF/IV
  • Difficulty/inability to perform unilateral heel raise. Limited calcaneal inversion upon ascent
  • Impaired subtalar mobility 
  • Lateral ankle pain due to subfibular impingement is a late symptom

Differential Diagnosis:

  1. Degenerative arthritis of the ankle, talonavicular or tarsometatarsal joint [10][14]
  2. Neuropathies of the foot caused by diabetes mellitus or peripheral neuropathies (or leprosy) [10]
  3. Spring ligament dysfunction [10]
  4. Rupture of anterior tibial tendon [10]
  5. Tarsal coalition [10]
  6. Congenital vertical talus [10]
  7. Kholers disease [10]
  8. Tarsal tunnel syndrome [10]

Diagnostic Procedures:

Besides the clinical diagnosis, radiographic evaluation can be used to asses deformity and the possible presence of degenerative arthritis or other causes of pes planus. MRI has the highest sensitivity, specificity and accuracy, but ultrasound is less expensive and almost as sensitive and specific as MRI.

Clinical tests for PTTD (more information in Examination)[15]:

  • Too many toes sign [16]
  • Single leg heel raise
  • First metatarsal rise sign[17]
  • Plantar flexion and inversion of the foot against resistance

Extra tests to classify stage of AAFD:

  • Mobility of TN and CC joints
  • Weightbearing X-Rays

Stages of PTTD:

As per Johnson and Strom[4][12][16] [16]:

  1. Stage I: Posterior tibial tendon intact and inflammed, no deformity, mild swelling
  2. Stage II: Posterior tibial tendon dysfunctional, acquired pes planus but passively correctable, commonly unable to perform a heel raise
  3. Stage III: Degenerative changes in the subtalar joint and the deformity is fixed
  4. Stage IV ( Myerson): Valgus tilt of talus leading to lateral tibiotalar degeneration

Stage I:

  • Deformity: tenosynovitis
  • physical exam: single-leg toe raise test (+)
  • radiography: normal

Stage IIA:

  • Deformity: Flatfoot deformity, flexible hindfoot, normal forefoot
  • Physical exam: single-leg heel raise (-), mild sinus tarsi pain
  • radiography: arch collapse deformity

Stage IIB:

  • Deformity: Flatfoot deformity, flexible hindfoot/rear foot, forefoot abduction
  • physical exam: Same stage IIA
  • radiography: same stage IIA

Stage III:

  • deformity in stage II becomes fixed, rigid or inflexible
  • Deformity: flatfoot deformity, rigid forefoot abduction, rigid hindfoot/rearfoot valgus
  • physical exam: sever sinus tarsi pain, single-leg heel raise test (-)
  • radiography: arch collapse deformity (subtalar arthritis)

Stage IV :

  • deformity: flatfoot deformity, rigid forefoot abductin, rigid hindfoot/rearfoot valgus, deltoid ligament compromise
  • physical exam: single-leg heel raise test (-), severe sinus tarsi pain, ankle pain
  • radiography, arch collapse deformity, subtalar arthritis, talar tilt ankle mortise


The diagnosis of posterior tibial tendon dysfunction can be made clinically based on history and objective testing.


Before a clinical examination is performed, the patient should be asked a series of questions to rule out other disorders. It is essential to diagnose posterior tibial tendon dysfunction (PTTD) in an early phase to prevent permanent deformities of the foot/ankle, a physical examination is therefore essential [10].


The physiotherapist can palpate the posterior tibial tendon from above the medial malleolus to its insertion, to control the integrity and assess possible pain and swelling that are common for the first stages of PTTD. In the later stages the deformity can progress and pes planus may be visible. It is important to examine the whole lower body and not just the foot, as valgus in the knees can accentuate the appearance of pes planus. A healthy person has a 5° valgus in his hindfoot, in patients with PTTD the valgus is increased and the abduction in the forefoot is also more pronounced[18] The physiotherapist can determine the severity of the pes planus by checking how many fingers can be passed underneath the midfoot[10].

Special tests for PTTD/AAFD include:[19] 

  • the too many toes sign: the foot should be inspected from behind and above. The too many toes sign is a manner of inspection from behind. At this manner they can establish if there is an abduction of the forefoot and a valgus angulation of the hindfoot. It is based on how many toes you can see from behind. By an affected foot it will be more than one and a half to two toes;
  • double leg heel rise: to go with both feet from a flatfoot stance to standing on the toes. Patients in stage I dysfunction can do this, but it's painfull. Patients with stage II, III or IV dysfunction are unable to do an heel rise. When a patients stands on tiptoes the heel of the affected foot will not bend inwards; the normal foot will stay into inversion while the affected hindfoot will stay in valgus.
  • a single leg heel rise: patients can't do a single heel rise with the affected foot; 
  • the first metatarsal rise sign[17]: the patients stands on his both feet, the shin of the affected foot is taken with a hand and rotated externally. When the patient has PTTD, the head of metatarsal I is lifted, while normal metatarsal I stays on the ground;
  • plantar flexion and inversion of the foot against resistance: to test the power of the tibialis posterior.

Outcome Measures:

Medical Management:

To decide whether patients need operative or non-operative treatment, different variables have to be taken into account by the attending physician. [21] According to Alvarez et al. non-invasive therapy, such as orthosis and physical therapy [22] are preferable for they do not damage healthy surrounding tissue, but only when non-operative treatment fails, surgical treatment is required. [21] [23] Clear evidence exists that suggests that the quality of life for patients with posterior tibial tendon dysfunction is significantly affected. Furthermore, evidence suggests that early conservative intervention can significantly improve quality of life regarding disability, function, and pain[24].

Surgical treatment can be used according to the stage in which PTTD is present.

Stage I:

  • Decompression of tendon [10][25]
  • Open synovectomy [10]
  • Some suggest an augmentation of the abnormal tendon with flexor digitorum longus (FDL) tendon.[10]

Stage II: Not yet a preference to which technique should be used. Several interventions possible:

  • FDL Transfer and medial displacement calcaneal osteotomy [10][25]
  • Lateral column lengthening (e.g. calcaneo-cuboid distraction arthrodesis) [10][26]
  • Medial column fusion (navicular-cuneiform or/or metatarsal- cuneiform joint) [10]
  • Isolated hindfoot fusions [10]
  • Arthroereisis [10][25][26]

Stage III:

  • Triple arthrodesis (subtalar, calcaneocuboid and talonavicular fusion) [10]
  • Isolated hindfoot fusions (eg. subtalar fusion) or medial column fusion [10]

Stage IV:

  • Pan-talar arthrodesis [10]

Physical Therapy Management:

The key to a successful outcome is early detection of the dysfunction and conservative management to prevent chronicity.  The goals of nonoperative treatment include the elimination of clinical symptoms, improvement of hindfoot alignment, and the prevention of progressive foot deformity. Conservative management with physiotherapy and orthotics is preferable to surgical management and should always be the first option. Stage I and II comprise a still flexible foot structure and is considered to be appropriate for non-surgical treatment. Stage III and IV contain already rigid longitudinal arch flattening with a tear of the spring ligament complex and talar valgus tilt in the ankle mortise, here, active compensation is not able to take place[27].

As long as PTTD and the foot deformity demonstrate no symptoms, treatments are basically considered unnecessary. If patients do have symptoms, however, a variety of therapy options may be administered: foot orthoses, ankle foot orthoses, stabilising tape, exercise (training therapy with, for example, eccentric exercise), pain medication and/or anti-inflammatory medication and patient education[27]

  • Orthotic devices or bracing: to support the arch.
  • Immobilization: a short-leg cast or boot, it allows the tendon to heal, or avoid all weight-bearing.
  • Physical therapy: exercises help rehabilitate the tendon and muscle including static stretching of gastrocnemius and soleus muscle, concentric/eccentric training of the posterior tibialis 
  • Medications: non steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, help reduce the pain and inflammation.
  • Shoe modifications: advise changes such as special inserts designed to improve the arch support. [4]


Optimisation of foot loading management by means of foot orthoses and adequate footwear is the most important aspect in therapy. Depending on the progression of the pathology, this can be progressively managed with over-the-counter non-individualised foot orthoses, then with individualised foot orthoses and finally with semi-rigid ankle foot orthoses[27].  For stage I disease, nonsurgical treatment should be tried for at least 3 to 4 months. A short walking cast or removable cast boot immobilization is indicated for patients with acute tenosynovitis. If symptoms are improved after immobilization, then a custom orthotic or ankle foot orthosis (AFO) may be fitted to the patient. The orthotic should be a full-length, semirigid, totalcontact insert with medial posting. The primary function of the orthotic is to provide arch support and correct the flexible component of the deformity.

Treatment options per stages of PTTD are determined on the basis of whether there is an acute inflammation and whether the foot deformity is fixed or flexible:

  1. Stage I: Acute: 4-8 weeks immobilisation, RICE; Chronic: flat footwear and corrective orthose or ankle foot orthosis, lace-up
  2. Stage II: Acute 4-8 weeks immobilisation, RICE; Chronic: lace-up, corrective orthosis and flat footwear
  3. Stage III: Lace-up, customised footwear or semirigid shoes and accommodative orthosis
  4. Stage IV: Lace-up, customised footwear or semirigid shoes and accommodative orthosis

Clinical Bottom Line:

Posterior tibial tendon dysfunction (PTTD) is one of the most common problems of the foot and ankle and it is one of the leading causes of acquired flatfoot deformity in the adults.  The tendon provides stability for the medial longitudinal arch of the foot, chronic dysfunction may result in a flatfoot (stage II, III and IV).  Management of PTTD includes orthosis use, concentric and eccentric training of the tibialis posterior muscle, stretching of the soleus muscle and gastrocnemius muscle. Surgical treatment is only needed when the conservative treatment fails.


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