Plantar Fasciitis is an inflammatory condition causing pain on the underside of the foot near the heel. The pain is commonly intense in the morning and reduces to a dull achy pain as the day progresses. This is commonly caused by abnormal gait, excessive supination or pronation, leg-length inequality, obesity, bad shoes, running on irregular surfaces, standing for long periods, or a shortened calf muscle.

Active Release Technique is extremely effective in treating this condition and restoring the normal function of the foot. In addition, chiropractic adjustments help to restore the proper biomechanics of the foot and leg. Rehab and orthotics are also recommended in treating this condition. Plantar fascia mobilization may be performed at home by rolling a golf ball or frozen water bottle beneath the plantar fascia.

Stretching exercises are appropriate for the gastroc, soleus, hamstring, and plantar fascia.

Ankle joint mobilization and manipulation can help restore normal motion, particularly dorsiflexion.

Patients who hyperpronate and those with fallen arches will benefit from arch supports or orthotics. 

Strengthening exercises are appropriate for the gastroc, soleus, posterior tibialis, and intrinsic muscles of the foot. (82) Examples include marble and towel gripping exercises. Strengthening exercises for the posterior tibialis should be implemented to help arch support. Strengthening of the flexor digitorum brevis is an important component of treatment and may be accomplished by performing toe flexion with an exercise band. (36) Eccentric heel raises with the great toe positioned in passive dorsiflexion (i.e. great toe propped up with a towel) have shown benefit for plantar fasciitis patients.

The Achilles tendon is the largest and strongest tendon in the human body, but is simultaneously a vulnerable link in the locomotion chain. (1) The tendons’ structural prowess is relentlessly confronted by functional demands, that can be up to 12 ½ times body weight while running. (2) 

The Achilles tendon may be acutely strained or ruptured as the result of an excessive stretch or eccentric force. Consistent with other types of acute strains, Achilles tendon injuries may occur when the musculotendonous unit transitions from eccentric deceleration to concentric propulsion. This happens during the “mid-stance” phase of gait. (3) Strains occur when collagen fibers are stretched by more than 4%. Ruptures occur when stretch exceeds 8%. (4,5)

Unlike acute injuries that cause inflammation, tendinopathy is characterized by repeated overloading, microtearing, failed healing, and subsequent tendon degeneration. (3,4,6,7). The process begins with collagen fiber disruption and ends in a disorganized healing process that fails to regenerate a “normal” tendon. Failed healing is blamed on a hyperplastic, but ineffective, microvascular system. (8,9)  

An appreciation of gait mechanics is germane to understanding Achilles tendon injuries. During normal gait, the foot approaches the ground with 3-4 degrees of supination, allowing ground contact to occur on the lateral portion of the calcaneus. As a shock-absorbing mechanism, the foot initially relaxes into subtalar pronation. At mid-stance, the foot converts into a rigid lever and begins to supinate in anticipation of propulsion. Tibial external rotation accompanies ankle supination. Inefficient conversion from shock absorber to rigid lever results in hyperpronation which stresses the medial calcaneotendinous attachment of the Achilles tendon. (10)

Injuries to the Achilles tendon may be classified as “insertional” or “non-insertional.” Insertional tendinopathy, as its name implies, describes damage to tendon fibers at their insertion on the posterior calcaneus. This process may result in calcification and bony exostosis producing a prominent enlargement of the posterior calcaneus, also called a “Haglund deformity” or “pump bump.” Non-insertional Achilles tendinitis most commonly involves the vulnerable “watershed area”, 2-6 cm proximal to the calcaneal insertion. (11) This region of the tendon has a smaller cross-sectional area, is relatively hypovacular, and is subject to a repetitive “wringing” motion during supination/ pronation. This susceptible mid section is the most common site for degeneration and rupture. (12,13) 

Achilles tendon injuries affect between 250,000 and 1 million people per year in the United States. (14,15) Most are middle-aged males in their third or fourth decade of life. (14,16) Interestingly, Achilles tendon injuries occur more frequently on the left side. (16) Patients who have suffered prior Achilles tendon rupture are at significantly higher risk for contralateral tendon rupture. (17)

Two-thirds of all Achilles tendon injuries involve athletes. (18) Runners are up to 10 times more likely to suffer Achilles tendon injuries compared to age-matched controls. (18) The Achilles is the most common site of tendinopathy in runners. (77) Athletes are at greater risk during speed training or sprinting. (19) Runners who assume a midfoot or forefoot strike pattern may be at even greater risk of injury. (20) Not surprisingly, a higher risk has been identified in other sports that involve running or jumping. The estimated incidence of Achilles tendinopathy is: running sports, 53%; soccer, 11%; dance, 9%; gymnastics, 5%; racquet sports, 2%; football, 1%. (14,21) 

Extrinsic risk factors for Achilles injury include improper warm up, overtraining, running on hard surfaces, excessive stair or hill climbing, improper arch support/ footwear, poor conditioning and abruptly returning to activity after a period of inactivity. (19,22-26) Wearing high-heeled shoes may lead to shortening of the gastroc/soleus, predisposing women to Achilles tendinopathy. (27) Intrinsic factors include hyperpronation, pes planus, cavus foot, gastroc/soleus inflexibility or weakness, limited ankle dorsiflexion, and limited subtalar motion. (14,22-26) Systemic risk factors include diabetes, hypertension, inflammatory arthropathy, gout, obesity, and the use of corticosteroids or quinolones (broad spectrum antibiotics). (28,81,84)

Patients may present with symptoms from an acute strain or a more gradual onset repetitive irritation. Complaints include pain or tenderness in the tendon or heel that intensifies with activity, especially walking or running. Patients may report difficulty when attempting to stand on their toes or walking steps- particularly down stairs. Morning pain and stiffness are common. Patients may report warmth and swelling that increases throughout the day, related to activity. Symptoms may be tracked using the VISA-A questionnaire. (29)  

Palpating the point of maximum tenderness can help localize the site of injury to either the “water shed area,” or the calcaneal insertion. Mid tendon pain suggests non-insertional tendinitis, whereas posterior calcaneal pain suggests insertional tendinitis. Fusiform swelling and tendinous or bony enlargement are common in cases of chronic tendinopathy. Those with insertional tendinopathy may demonstrate evidence of bony enlargement or spurring on the posterior calcaneus. 

Range of motion testing will likely reveal deficits in passive dorsiflexion with pain on resisted plantarflexion. In some patients, single leg heel raises will elicit pain, while in others, repetitive hopping may be needed to elicit complaints. The Silfverskiold test can help differentiate Achilles vs. gastroc tightness in patients with limited dorsiflexion. Clinicians may perform the “calf squeeze test” (Thompson test) to exclude tendon rupture in those who have difficulty ambulating. The test has excellent validity and is performed by squeezing the calf of a prone patient and observing for passive plantar flexion of the foot. (30) Clinicians should perform motion palpation of the subtalar joint to assess mobility and identify restrictions.

Plantaris tendon pathology is associated with chronic mid-portion Achilles tendinopathy. (87-89) The plantaris tendon typically resides deep and adjacent to the Achilles medial border. Repetitive irritation of either tendon may lead to inflammation, scar tissue formation, and adhesion. This restricts gliding and leads to painful tethering when load is applied. (90) In some cases, the plantaris tendon has been known to thicken or even invaginate into the Achilles tendon, thereby thwarting traditional conservative management of Achilles tendinopathy. Tenderness on the medial mid-tendon is suggestive of plantaris involvement, while ultrasound or MRI may be necessary for a definitive diagnosis.

Clinicians must assess for contributory functional deficits throughout the kinetic chain. 
Runners with non-insertional tendinopathy demonstrate an increased incidence of foot hyperpronation (subtalar eversion). (76) Foot hyperpronation manifests as: loss of the medial longitudinal arch, forefoot abduction (i.e. “too many toes sign”), calcaneal eversion, and navicular drop. Assess for weakness in the posterior tibialis by observing for calcaneal eversion during heel raises. Gastroc/soleus flexibility may be assessed by measuring and comparing passive ankle dorsiflexion. Clinicians should assess knee flexor/hamstring strength, as weakness in this muscle is a known risk factor for Achilles tendon pain. (31) Weakness or delayed activation of the hip abductors (gluteus medius) should be identified and corrected. Functional orthopedic testing for hip abductor weakness would include the Trendelenberg sign, overhead squat test, and single leg squat test. Weakness or delayed activation of the gluteus medius is associated with ankle dysfunction. (32)  

Hallux limitus (limitation in passive dorsiflexion of the first metarsophalangeal joint) disrupts normal foot functional stability and has been associated with Achilles tendon pain. (33) Functional hallux limitus assessment is performed on a long-sitting patient. The clinician places their thumb under the patient’s first metatarsal head and forces the patient’s foot into maximum dorsiflexion and pronation to simulate a ground reaction force. The clinician then pinches the patient’s great toe with their opposite hand and passively moves the toe into dorsiflexion. Dorsiflexion of the great toe should be fluid and produce concurrent plantar flexion of the patient’s metatarsal head into the clinician’s thumb. A sense of “jamming” or “locking” upon dorsiflexion or a lack of concurrent first metatarsal plantar flexion suggests hallux limitis. Assessment of the patient’s shoe insole may help to identify hallux limitus by revealing a lack of wear under the first metatarsal head with disproportionate wear under the second through fifth metatarsal heads and pad of the great toe. (34)  

Radiographs are often unnecessary for the diagnosis of Achilles tendinopathy. (35) The Ottowa Ankle Rules define the appropriateness for imaging patients with ankle or midfoot pain, following trauma. (36-38,74,75) No clearly defined rules exist for imaging non traumatic heel pain. Clinicians may consider radiographs in cases of significant trauma with altered gait or when necessary to rule out other pathology, including calcaneal epiphysitis/ avulsion. Radiographs of Achilles tendonopathy may demonstrate tendon calcifications and spurs/ enthesophytes on the posterior calcaneus. Ultrasound may be an efficient cost-effective means of evaluating the Achilles tendon. (39) Ultrasound or MRI may help identify and define tendon pathology.  

The differential diagnosis for Achilles tendinopathy includes fracture, avulsion, neoplasm, infection, ankle sprain, retrocalcaneal bursitis, posterior ankle impingement, Os-trigonum syndrome, tenosynovitis, tendon dislocation, gastroc musculotendinous strain (tennis leg), sural neuroma, systemic inflammatory disease, and calcaneal apophysitis (Sever’s disease). In children and adolescents, the epiphyseal growth plate is 2 to 5 times weaker than in adults. This group is more likely to suffer epiphyseal injuries in the form of calcaneal apophysitis (Sever’s disease) from stressors that would likely cause Achilles tendinopathy in adults. (40)

Nonoperative treatment is the mainstay for Achilles tendinopathy. (81) “Traditional” treatment plans based solely on rest, therapy modalities, orthotics, and NSAIDs have failed to demonstrate benefit for Achilles tendinopathy patients. (41) Passive modalities including ice, ultrasound, electrical stimulation, and low-level laser also lack support. (42) The current standard of care for Achilles tendinopathy includes a combination of rest, eccentric rehabilitation, and correction of mechanical faults. Studies have demonstrated excellent results in up to 85% of patients undergoing appropriate conservative care. (43) Initially, patients may need to limit or stop activities that cause pain. Significant strains may require the use of crutches or a boot. Runners may need to switch to swimming, cycling, or other activities that limit stress to the Achilles tendon. Patients should avoid shoes with an excessively rigid heel tab to reduce irritation.

Eccentric exercise programs are effective for treating Achilles tendinopathy. (41,44-54) Eccentric training is more effective than concentric training for reducing pain and improving function. (52,55) In fact, research suggests that eccentric strength training programs are more than twice as effective as concentric programs for the treatment of Achilles tendinopathy. (52) A proven program by Alfredson (45) incorporates single leg eccentric heel drops off the edge of a step. Heel drops should be performed with the knee both straight and bent, three sets of 15 repetitions, twice per day for 12 weeks. Heel drops should occur slowly on a 4-10 second count. (56) The patient should use the non-injured leg to return to the “heel up” start position, thereby avoiding concentric contractions. Moderate pain during this exercise is acceptable but if pain is excessive, the patient should assist downward motion with the non-injured leg. 

Soft tissue manipulation, stretching, and myofascial release techniques are necessary to promote flexibility of the calf muscles. Stretching of the calf muscles should be performed with the knee straight to address the gastroc and with the knee bent to lengthen the soleus. Clinicians should consider the use of IASTM to release adhesions within the Achilles tendon. As an additional benefit, IASTM may accelerate healing, possibly via controlled microtrauma. (57,78-80) Manipulation may be necessary to eliminate restrictions in the kinetic chain, particularly within the ankle. (58) Clinicians may consider the use of a 7-15 mm heel lift (bilaterally) to minimize dorsiflexion stress. Arch supports or orthotics may be necessary to correct hyperpronation. (76) Patients with hallux limitus may benefit from wearing shoe inserts with a “cut out” beneath the first metatarsal head. (59)

The treatments described thus far are directed at a “contractile dysfunction” model. If the patient’s complaints are not resolving as intended, it is important to consider the Mechanical Diagnosis Therapy (MDT) concept of “derangement”. Many cases of “derangement” tendinopathy have responded to end-range plantar flexion, although a recent review of the literature provides no clinical trials of this concept. End range plantar flexion is performed on a regular basis, 10 repetitions every 2-3 hours. A clinical indicator that the patient may respond well to repetitive end-range movements is worsening of their symptoms after dorsiflexion exercises.

Athletes should introduce new activities slowly and avoid increasing activity, particularly running, by more than 10% per week. Runners should begin on smooth, shock-absorbent surfaces and start out at a lower intensity and distance- first increasing distance, then pace. Athletes should avoid training on hard or unlevel surfaces, including hills. Return-to-play criteria for Achilles tendon strains or ruptures include the “Triple 5”:  
1. Ankle dorsiflexion is within 5 degrees of the uninjured side, 
2. Calf circumference (measured 10 cm distal to the tibial tuberosity) is within 5 mm of the uninjured side, and 
3. The patient is able to perform 5 sets of 25 single leg heel raises. (60)  

Patients who fail a trial of conservative care should be referred, but proven alternatives are scarce. Medical co-management is of limited benefit. NSAIDs may relieve symptoms but have little long-term effect on outcome. (61,62) Cortisone injections are unproven for the treatment of Achilles tendinopathy and carry a possible increased risk of tendon rupture. (63,64) Extracorporeal shock-wave therapy (ESWT) or platelet-rich plasma (PRP) injections are controversial alternatives. (65-68) ESWT (originally developed as lithotripsy) is thought to break up calcific deposits and stimulate fibroblast activity to encourage healing. ESWT may be appropriate for recalcitrant cases (81,82). PRP treatments consist of injecting platelet-rich plasma into a tendon to create a concentrated trigger of growth factors and chemoattractants for macrophages and fibroblasts, which gradually repair the damaged collagen. (69) Some clinicians suggest benefit from PRP injections, but others refute its usefulness for Achilles tendinopathy, (81,83) including at least one randomized clinical trial. (70) 

Surgical management is often considered for Achilles tendon ruptures, although several studies, including at least one randomized clinical trial, suggests at least equivalent results between surgical and conservative management. (59,71,72,85)  

Medial tibial stress syndrome (MTSS), aka Medial Tibial Traction Periostitis, describes exercise-induced pain along the posteromedial border of the tibia. The condition is commonly referred to as “Shin splints” and is a familiar malady in athletes and soldiers where it affects up to 1/3 of those populations. (1-4) MTSS is responsible for approximately 15% of all running injuries. (1)

The condition affects the vulnerable insertion points of the tibial fascia and deep ankle flexors along the medial tibial crest. MTSS is believed to result from repetitive eccentric contraction of the deep flexors during running, jumping, or impact loading. (5) Repetitive traction on the medial tibial crest, results in myofascial strain, periosteal inflammation, and bony stress reaction. (6-13) Early etiological theories focused on myofascial strain, but current evidence suggests that a bony stress reaction is the most likely cause of MTSS. (14-20) 

Newer research suggests that traction periostitis may be an inflammatory precursor to tibial stress fracture. (21) The stress of exercise can weaken bone. Healthy bone responds to this stress by remodeling itself more densely. Stress reactions occur when the normal adaptive remodeling response is unable to keep pace with the loads of excessive training, i.e. high demands with inadequate recovery times. (22,23) Prolonged insult may lead to tibial stress fracture, and many authors now believe that MTSS and stress fracture represent two different points along a continuum of bony stress reaction. (24,25)  

The leading mechanism of injury is repetitive eccentric contraction from running or jumping on hard surfaces. (26-28) Excessive or improper training is the leading factor for the development of MTSS. (2,3,29-33) Common training errors include the terrible too’s (too much, too fast, too long.) (31-34) Athletes who run more than 20 miles per week are at increased risk of developing MTSS. (35) Inexperienced runners or those with poor technique are at greater risk. (4) Running with a narrow or “crossover” gait increases tibial stress. (87)

Foot hyperpronation is a significant risk factor for the development of MTSS, as a collapsing foot puts additional stress on the suspect tissues. (4,10,12,14,28,36) Interestingly, the use of orthotics is associated with the development of MTSS, although orthotic use should not be viewed as an independent risk factor since those using orthotics are likely to hyperpronate. (4) Females are affected more frequently and have a 1.5-3.5 increased likelihood of progressing to stress fracture. (4,37) Additional risk factors include a prior history of MTSS and increased BMI. (4) 

The clinical presentation of MTSS includes vague, diffuse pain over the middle to distal posteromedial tibia. Athletes often present following an increase in activity intensity or duration. Symptoms are often worse with exertion – particularly at the beginning of a work-out. (38) Initially, symptoms may subside during training, but as the condition progresses, symptoms may linger throughout activity or even at rest. (38) Pain that persists more than five minutes post-activity carries a higher suspicion of stress fracture. (49) Clinicians should be alert for symptoms of numbness or paresthesia, which could suggest exercise-induced compartment syndrome.  

Clinical evaluation demonstrates diffuse tenderness over the posteromedial tibial border. Prolonged stress may generate a periosteal reaction detectable as a “rough” or “bumpy” feel upon palpation. (39)Tenderness from MTSS should involve at least 5 cm of the tibial border. (39) More focal tenderness, the presence of anterior tibial tenderness, or any significant swelling suggests stress fracture. Applying a vibrating tuning fork over the tibia may help detect stress fracture (75% sensitivity). (40) Single leg hopping is painful in about half of MTSS cases (and 70-100% of stress fractures) (41-43) The Talar Bump Test may help differentiate tibial stress fracture from MTSS.

Tenderness over the flexor digitorum longus and tibialis posterior is a clinical hallmark of the condition, although whether this is a primary cause or secondary effect remains uncertain. (44,45) Clinicians should assess for the presence of hypertonicity in the gastroc or soleus, as this finding is commonly associated with MTSS. (46,47) 

The presence of foot hyperpronation may be assessed through the navicular drop test (performed by marking the navicular and measuring the amount of drop from non weight bearing to weight bearing.) (48) Clinicians should assess for other potential risk factors, including inflexibility or imbalance of the hamstring and quadriceps, genu varus or valgus, tibial torsion, femoral anteversion, and leg length discrepancies. (14) Hip abductor weakness is a common culprit of many lower chain overuse injuries and may be assessed through the “hip abductor weakness cluster”. (86) Excessive external rotation of the hip is another known contributor. (4,50)

Assessment of gait or running patterns can identify biomechanical errors. (51,52) Clinicians should assess joint mobility throughout the lower extremity. Neurovascular assessment is typically unremarkable. (38) The presence of sensory or motor loss suggests an alternate diagnosis, including exertional compartment syndrome, peripheral neuropathy, or radiculopathy.  

Imaging of early and uncomplicated MTSS is often unnecessary. (53) Imaging is appropriate in the presence of: red flags, focal tenderness, pain at rest, or when the patient fails to improve with a reasonable trial of conservative care. (53) Radiographs taken within the first 2-3weeks are not likely to show any change; however, patients with longstanding MTSS may demonstrate periosteal reaction indicating callus formation and stress fracture. (55)  

Clinicians should be vigilant for the possibility of stress fracture. Plain films frequently do not demonstrate the signs of tibial stress fracture (periosteal elevation/callus formation or cortical lucency ). (42,56,57) Unresponsive patients or those with a higher likelihood of stress fracture (runners) may benefit from advanced imaging, including MRI or bone scan. (58) MRI is highly sensitive (74-100%) and is best able to grade the progression of stress reaction from periosteal edema (Grade 1), to progressive bone marrow edema (Grade 2-3), to cortical stress fracture (Grade 4). (59-61)  

In addition to stress fracture, the differential diagnosis of MTSS includes: exertional compartment syndrome, peripheral vascular disease, muscle strain, occult fracture, infection, neoplasm, DVT, peripheral neuropathy, popliteal artery entrapment syndrome, lumbosacral radiculopathy, and vascular claudication. (62-64)

The successful management of MTSS requires the removal of risk factors, and rest. Clinicians must identify the combination of training errors and biomechanical risk factors that led to the development of the patient’s condition. (65) No intervention has proven more successful than rest for the management of MTSS. (4) Unfortunately, patients often are affected by MTSS during a time when they are training for a sport or upcoming event. Continuance of the offending activity will often lead to undue chronicity, frustration for patient and clinician, and decreased performance capabilities. Athletes may need to decrease frequency, intensity, and duration of impact activities, including running and jumping. Athletes may need to consider non-weight bearing cross-training like stationary cycling or pool running. Initially, anti-inflammatory modalities, including ultrasound or e-stim may provide relief. (67) Ice or home ice massage may provide an anti-inflammatory or palliative benefit.  

Resolution of MTSS requires correction of any associated kinetic chain dysfunction. (68-70) Stretching exercises and myofascial release are appropriate for the gastroc, soleus, hip external rotators, tibialis posterior, and tibialis anterior muscles. (71) Strengthening exercises may be appropriate for the tibialis posterior and hip abductors. Manipulation may be employed to resolve joint restrictions in the spine, sacroiliac joint, pelvis, and lower extremity. (69,70,74) 

Arch supports or custom orthotics may be appropriate for patients with fallen arches (75), although at least one contradictory systematic review suggests that orthotics may be causative and are not useful for prevention. (76) The use of compressive taping, bracing, or stockings is thought to enhance bone remodeling and is used by some providers although supporting evidence is inconclusive. (77-79) Additional possibilities for the management of MTSS include dry needling, autologus blood injection, platlet rich plasma (PRP) injections, prolotherapy, and acupuncture. (74,80) Extracorporeal shock wave therapy (ECST) may speed recovery times. (81)

Return to activity should start slowly with a graded running program, beginning with a 1/4 mile run and progressing by 1/4 mile each time the athlete has no pain for two consecutive workouts. (82) Athletes should initially avoid running on hard or uneven surfaces and begin at a lower intensity and distance, increasing by no more than 10-15% per week. Runners should first increase distance, then pace, and avoid hard or unlevel surfaces, including hills. Runners with a narrow gait may benefit from incorporating a wider step width. (87) Clinicians should assess shoes for excessive wear and match the patient to the most appropriate show. (i.e. stability, neutral, cushioning) Running shoes lose half of their shock absorption capacity after 300-500 miles and should be replaced within that range. (83-85)

Surgical intervention, including posterior fasciotomy, is rarely indicated. (74)

Posterior tibial tendon dysfunction (PTTD) is the most common cause of adult-acquired flat foot. (1) Symptoms begin with pain and may progress to degeneration and deformity if left untreated. (1,3) Early recognition and management can lead to significantly improved outcomes. (1)

The deep compartment of the leg consists of three muscles: the posterior tibialis (PT), flexor digitorum longus (FDL), and flexor hallucis longus (FHL). The posterior tibialis is the deepest and largest muscle of the trio – typically comprising almost 60% of the cross sectional area of the entire deep compartment. (4-7) The posterior tibialis originates on the interosseous membrane and the posterior surfaces of the tibia and fibula. (4) The muscle’s tendon begins several centimeters above the ankle then courses through the deep posterior compartment of the leg behind the medial malleolus before turning toward its main attachment on the navicular tuberosity. (4) Ancillary attachments include the second and third cuneiform, cuboid, bases of the second, third, & fourth metatarsals, and sustentaculum tali of the calcaneous. (4,8-10) 

Actions of the posterior tibialis muscle include inversion and plantar flexion of the foot. Because of its size and moment arm, the posterior tibialis is the primary elevator and dynamic stabilizer of the medial longitudinal arch of the foot. (5,11-15) During the normal gait cycle, the posterior tibialis lifts the medial longitudinal arch, thereby interlocking the tarsals (calcaneous, cuboid, talus, and navicular) into a rigid lever for propulsion. (12,17) The role of the posterior tibialis is most significant during push off. (18,19)

Early literature suggested that up to 50% of PTTD cases arose from trauma. (20,21) More recent literature suggests that the majority of cases begin from repeated micro trauma. (22) Repetitive stressors initiate a cascade of dysfunction that begins with “normal” inflammation but regresses to “failed healing”, fibrosis, and tendon degeneration. Degeneration affects the gliding resistance of the tendon and progressively diminishes the tendon’s ability to support the foot. (22) As the tendon becomes less effective, the longitudinal arch of the foot is allowed to collapse; thereby, increasing strain on the posterior tibialis. (22,25,26) The most common site for injury is a zone of relative hypovasulcarity directly posterior to the medial malleolus. (22,27,28)

The continuum of PTTD progresses through the following stages: (29) 
I Tenosynovitis without deformity 
IIA Flat foot deformity  
IIB Flat foot deformity with excessive forefoot abduction 
III Rigid forefoot abduction and hindfoot valgus 
IV Deltoid ligament compromise  

Like most cumulative trauma disorders, the etiology of posterior tibial tendon dysfunction is multi factoral. Problems typically arise when repetitive strain exceeds the tendon’s threshold for injury. Extrinsic factors that contribute to the development of posterior tibial tendinopathy include training errors- particularly those related to intensity, duration, and/or training on excessively hard surfaces. (30) In addition to the obvious contribution from hyperpronation, other intrinsic factors that increase the likelihood of developing PTTD include a history of obesity, diabetes, hypertension, seronegative arthropathy, steroid injection, surgery, or trauma. (1,31-33) A recent prescription of fluoroquinolones may increase the risk of tendon rupture. (35)  

The stereotypical PTTD patient is an obese, middle-aged female. (1) Some researchers estimate that PTTD may be present in up to 10% of this population. (37) PTTD is typically unilateral- bilateral disease is rare. (1) Common presenting complaints of an irritated (but intact) posterior tibial tendon include insidious onset unilateral pain and swelling along the course of the tendon – most notably behind the medial malleolus. (38-41) Symptoms often begin following an increase in training intensity or duration. (42) Symptoms may be exacerbated by weight bearing activity, particularly, standing tiptoe and walking stairs or on uneven surfaces. (39,43) Loss of arch height and other associated biomechanical deformities may become evident as the condition progresses however, tendon degeneration begins long before physical deformity. (44) Patients who have altered gait may demonstrate abnormal shoe wear. (39) As the condition nears end-stage, patients may describe the feeling that they are walking on the inside of their ankle, and pain may transfer to the lateral ankle due to incursion of the distal fibula and calcaneous. (46) 

Clinical evaluation will typically demonstrate tenderness and swelling posterior and inferior to the medial malleolus. (38,43,47-49) A significantly fallen arch with minimal pain and swelling over the posterior tibial tendon could indicate rupture. (50) Patients with PTTD demonstrate hind foot eversion proportionate to the degree of posterior tibialis weakness (48) Isometric strength testing may reproduce pain or weakness during resisted inversion (supination), and/or plantar flexion (43,49,50) Motion assessment may demonstrate a rigid hindfoot valgus deformity in later stages. (47) Clinicians should assess for pain and/or weakness of toe flexion to help differentiate tendinopathies involving the adjacent flexor digitorum longus and flexor hallucis longus. 

Clinical evaluation should seek to classify the stage of the disease – collapse of the medial longitudinal arch corresponds to Stage IIA, while excessive forefoot abduction, (“too many toes” sign) signifies progression to Stage IIB. Hindfoot valgus that has progressed from flexible to rigid signifies Stage III. Tenderness below the lateral malleolus from bony incursion is a sign of Stage IV disease. 

The single limb heel rise is a sensitive test to detect PTTD. (47,48) The test is performed by allowing the single leg standing patient to balance with one hand on the wall while attempting to rise on the toes of the affected foot for 8-10 repetitions. The inability to complete this test correlates to the degree of PTTD. (1,47)  

PTTD is primarily a clinical diagnosis. (53) In general, plain films have little diagnostic value for soft tissue lesions. (53) Nonetheless, radiographs may be needed to exclude other possibilities from the differential diagnosis. Plain films would include weight bearing, AP and lateral views of the foot and ankle. (55) Collapse of the medial longitudinal arch is a classic radiographic finding associated with PTTD. As the disease progresses, films may demonstrate valgus mal-alignment of the talus and sub talar degeneration. (55-57) MRI may better demonstrate soft tissue lesions as well as the sub-tendinous bone marrow edema that often accompanies the condition. (55,57) Diagnostic ultrasound is a useful, low cost alternative for the diagnosis of PTTD. (55,58) Studies have shown that diagnostic ultrasound is only slightly less sensitive than MRI for defining PTTD. (59)  

The differential diagnosis for PTTD includes flexor hallucis longus or flexor digitorum longus tendinopathy, posterior impingement, stress fracture, deltoid ligament injury, osteoarthritis, Lisfranc injury, and tarsal tunnel syndrome. (60,61)  

Early identification of PTTD is essential to limit progression of the disease. (1) Conditions that advance may ultimately require surgery for the resultant instability, impingement, degeneration, and deformity. (1,3,79) Optimal management is partially dependent upon the stage of the disease. (1) Patients with acute tendon irritation (Stage I) may benefit from anti-inflamatory modalities and NSAIDs. (62-65) NSAIDS may not be a good choice for more chronic “tendinopathies” (66) 

Arch supports and orthotics are mainstays of management, but have shown varying degrees of success. (67,68) The intended purpose of orthotics is to correct “flexible” deformities, i.e. maintain the medial arch and correct hind foot position, thus decreasing stress on the posterior tibial tendon. (69,70) Orthotics may help patients in the early stages of PTTD, but may be less beneficial once the foot has lost stability or has developed a rigid deformity. (69) Studies have shown that for unstable feet, orthotics do not consistently improve alignment or gliding resistance of the posterior tibialis. (69,73) 

Active rehab should be directed at strengthening the posterior tibialis tendon as well as the peroneals, anterior tibialis, and gastroc/soleus. (84) Specific exercises would include resisted plantar flexion, heel rises, toe walking, inversion and adduction. (84) Strengthening the posterior tibialis via eccentric exercise leads to more rapid improvements in symptoms and function. (80) Stretching of the gastroc/ soleus is appropriate. (84) Exercises should be performed while wearing shoes and arch supports or orthotics. (62,74,75) Soft tissue manipulation and myofascial release should address the posterior tibialis and associated musculature. IASTM may be appropriate to stimulate healing of degenerated tendons.

Conservative care (including stretching, strengthening, modalities, NSAIDS and support ranging from orthotics to a rigid boot) has shown success rates ranging from 67-90%. (81-84) PTTD patients who do not respond to four weeks of conservative care may benefit from a walking cast or cam boot to immobilize the foot. (62,76) Those who have failed four months of conservative care and those with advanced disease (i.e. beyond Stage II, with non-correctable deformity and joint degeneration) may benefit from orthopedic or podiatric referral. (62,77,78)