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Addressing The Biomechanics Of Stage II Adult-Acquired Flatfoot
July 2014
Given the common presentation of adult-acquired flatfoot in podiatric practice, this author discusses the pathomechanics of the condition, offers diagnostic insights on the spring ligament and the heel raise test, and shares perspectives from the literature on the efficacy of treatment interventions.
Adult-acquired flatfoot represents one of the most challenging clinical conditions facing the podiatric physician. With insights gained from recent biomechanical studies, clinicians can more accurately design and target treatment strategies for a more positive patient outcome.
The adult-acquired flatfoot is a symptomatic, progressive deformity, which is the result of loss of integrity and function of the posterior tibial tendon as well as key supportive ligaments of the ankle and hindfoot.1 While this condition was previously known as posterior tibial tendon dysfunction (PTTD), we now know that simply attributing this deformity to a single anatomic structure is shortsighted and will overlook the more important role of ligamentous disruption, which leads to the true disability of this disorder.
Adult-acquired flatfoot appears to be a common, if not epidemic, condition presenting to podiatric practice. However, few studies have been conducted to verify the true incidence in the general population. In a survey of 1,000 women over the age of 40 in the United Kingdom, 3.3 percent had symptoms and other clinical evidence of adult-acquired flatfoot.2 Many studies have verified that women over the age of 50 are most at risk for developing adult-acquired flatfoot. Other contributing factors include diabetes, hypertension and obesity.3
Staging of the adult-acquired flatfoot deformity has traditionally followed the classification proposed by Johnson and Strom.4 Stage I adult-acquired flatfoot is characterized by symptoms of pain and swelling along the posterior tibial tendon without visible changes of foot alignment. Stage II deformity shows asymmetry of alignment with hindfoot valgus and forefoot abduction exaggerated on the symptomatic foot. Patients with stage II adult-acquired flatfoot have weakness with inversion and difficulty performing a single foot heel raise, indicating attenuation or rupture of the posterior tibial tendon. Stage III adult-acquired flatfoot represents a progression of all the clinical signs of stage II but the deformity has now become rigid. Myerson proposed Stage IV to include a valgus deformity within the ankle joint itself.5
According to Tome and coworkers, patients in stage II AAF will demonstrate the following clinical findings:
• palpable tenderness of the posterior tibial tendon;
• swelling along the distal sheath of the posterior tibial tendon;
• pain or inability to perform the single limb heel rise;
• flexible valgus deformity of the hindfoot in static stance; and
• increased abduction of the forefoot during gait.6
A lifetime of walking on a pronated foot may lead to overload and ultimate failure of key supportive structures. Uchiyama and coworkers were among the first to document an increased gliding resistance of the posterior tibial tendon when the human foot is pronated and a flatfoot deformity is present.8 These same researchers later verified that a pronated foot position uniquely overloads the posterior tibial tendon rather than the other tendons of the ankle.9 They further recommended that orthoses or surgical procedures that realign the hindfoot and ankle can reduce the load on soft tissue structures and prevent further degeneration.
Since we know that certain patients are at risk for developing adult-acquired flatfoot, particularly those with preexisting flatfeet and overweight individuals, it appears that early intervention with foot orthotic therapy may have a protective benefit. While no studies have determined the benefits of early intervention, the biomechanics of soft tissue overload certainly validate any effort to protect certain structures in the human foot that are at risk for rupture later in life.
Several studies have demonstrated the benefit of certain foot orthotic modifications to reduce internal inversion subtalar joint moments. This will theoretically reduce load on the posterior tibial tendon.
Munderman and colleagues showed that varus posting significantly reduced the inversion moment of the ankle and hindfoot.10 Williams and co-workers studied the effects of the inverted cast correction for custom foot orthoses and found that this modification can reduce the peak inversion moment of the rearfoot by 54 percent in comparison to not wearing orthoses.11 Bonanno and colleagues showed that 4 mm and 6 mm medial heel skive modifications to custom foot orthosis fabrication could increase pressure on the medial calcaneus, and speculated that this may improve pronation control of the subtalar joint in flat, pronated feet.12 Murley and co-workers showed that various foot orthotic designs could reduce peak electromyographic activity in the tibialis posterior, a finding that could validate the use of these devices as a protective mechanism for adult-acquired flatfoot.13
With overload of the posterior tibial tendon, gradual attenuation and eventual rupture occur. Researchers have demonstrated that in early stage II adult-acquired flatfoot deformity, measurable weakness of the foot occurs with these tendon changes.14 The remaining medial ankle flexors, the flexor digitorum longus (FDL) and flexor hallucis longus (FHL), are unable to compensate for weakness of the tibialis posterior in providing necessary hindfoot inversion and forefoot adduction during gait.15,16 Before significant ligamentous rupture occurs, strengthening and rehabilitation of the weakened posterior tibial muscle/tendon unit can be of significant benefit to prevent the progression of deformity. Kulig and colleagues demonstrated this in a prospective study in which patients with stage II adult-acquired flatfoot deformity had significantly decreased pain and improved function after a 12-week program of progressive eccentric resistance exercise of the tibialis posterior muscle combined with custom functional foot orthotic therapy.17
The clinician can gain appreciation for the biomechanical changes by asking the patient with stage II adult-acquired flatfoot to perform a single foot heel rise test. The heel rise test is recommended for individuals with posterior tibial tendon dysfunction (PTTD) to detect a partial or complete rupture of the posterior tibial tendon.31,32 Weakness of the posterior tibialis muscle theoretically contributes to the inability to perform a heel rise task or abnormal kinematics during a heel rise task.33 Clinically, one would observe an abnormal heel rise test when the individual cannot perform a heel rise or performs the heel rise with hindfoot eversion (fails to invert on rising), suggesting that the posterior tibialis muscle no longer is acting to invert the hindfoot.5,34
The normal combined action of the posterior tibialis and triceps surae muscles in theory produces ankle plantarflexion with inversion during a heel rise task.16,35,36 The failure of a patient with stage II adult-acquired flatfoot to perform the heel rise is not directly attributed to ankle plantarflexion weakness. The tibialis posterior is not an effective plantarflexor of the ankle, even in healthy patients. Instead, the heel rise test requires a stable arch and midfoot in order for the triceps to actively plantarflex the ankle and the entire foot across the metatarsal heads. Houck and co-workers demonstrated that patients with stage II adult-acquired flatfoot show greater ankle joint plantarflexion at midstance and reciprocal dorsiflexion of the first ray, indicating breakdown of the midfoot.30 Researchers have shown increased flexibility of the forefoot on the rearfoot in other studies of patients with stage II adult-acquired flatfoot, suggesting that this demonstrates loss of ligamentous stability.31,32
Most clinicians favor AFOs (ankle braces) over foot orthoses to address the severe biomechanical forces they see with stage II adult-acquired flatfoot.38 In another study focusing on three different designs of ankle braces to treat stage II adult-acquired flatfoot, Houck and coworkers found that controlling hindfoot eversion was the most insignificant treatment effect.39 They noted that improvements in medial longitudinal arch alignment and correction of forefoot abduction were the most significant measureable treatment effects, but only found these improvements with certain designs of ankle braces. The custom articulated AFO provided the best improvement of the height of the medial longitudinal arch and correction of forefoot abduction in comparison to a custom solid AFO. The researchers concluded that “The consistent finding in this patient of improved kinematics with the articulated versus solid ankle design underscored the importance of allowing ankle movement for foot function.”39
One dilemma when treating stage II adult-acquired flatfoot is the presence of muscle weakness. Studies have demonstrated not only weakness of the tibialis posterior but overall general weakness of all of the ankle plantarflexors in patients with adult-acquired flatfoot.37,38 This is why Flemister and Houck concluded that “ankle plantarflexion weakness may account for functional impairments and gait disturbances reported by patients with PTTD. Orthoses that restrict ankle motion (solid AFO), while very popular, may induce plantarflexor weakness and increase dependence on the orthosis for support.”39
With rupture of the spring ligament, excessive adduction and plantarflexion of the talus occur across the talonavicular joint. While foot orthoses may be able to provide some support to this joint, the patient often does not tolerate the pressure of the device against the skin of the foot in this region. Since the talus is locked within the ankle mortise, one can best accomplish control of adduction by controlling tibial rotation via an ankle-foot orthosis. This is why the most significant change measured with ankle bracing in a patient with stage II adult-acquired flatfoot was improved alignment of the medial longitudinal arch.37
To this date, there are seven studies published in the medical literature that validate positive treatment effects for stage II adult-acquired flatfoot.17,40-45 The most impressive of these studies utilized a combination of strengthening exercises with AFO therapy. In both the studies by Alvarez and Lin, over 80 percent of the patients treated with articulating AFOs and exercise were able to avoid surgery and remain brace-free with a follow up of one to eight years.42,43
Both strengthening exercise programs and surgical reconstruction of the tibialis posterior tendon have demonstrated recovery of muscle function in patients with stage II adult-acquired flatfoot.17,46 To this date, there are no studies documenting healing of ruptured ligaments when one uses bracing to treat stage II adult-acquired flatfoot. However, the fact that studies have shown that a majority of patients treated with bracing of stage II adult-acquired flatfoot are able to discontinue using their AFOs after a period of use suggests that ligament integrity must have been restored to achieve this level of function.
Adult-acquired flatfoot represents one of the most challenging clinical conditions facing the podiatric physician. With insights gained from recent biomechanical studies, clinicians can more accurately design and target treatment strategies for a more positive patient outcome.
The adult-acquired flatfoot is a symptomatic, progressive deformity, which is the result of loss of integrity and function of the posterior tibial tendon as well as key supportive ligaments of the ankle and hindfoot.1 While this condition was previously known as posterior tibial tendon dysfunction (PTTD), we now know that simply attributing this deformity to a single anatomic structure is shortsighted and will overlook the more important role of ligamentous disruption, which leads to the true disability of this disorder.
Adult-acquired flatfoot appears to be a common, if not epidemic, condition presenting to podiatric practice. However, few studies have been conducted to verify the true incidence in the general population. In a survey of 1,000 women over the age of 40 in the United Kingdom, 3.3 percent had symptoms and other clinical evidence of adult-acquired flatfoot.2 Many studies have verified that women over the age of 50 are most at risk for developing adult-acquired flatfoot. Other contributing factors include diabetes, hypertension and obesity.3
Staging of the adult-acquired flatfoot deformity has traditionally followed the classification proposed by Johnson and Strom.4 Stage I adult-acquired flatfoot is characterized by symptoms of pain and swelling along the posterior tibial tendon without visible changes of foot alignment. Stage II deformity shows asymmetry of alignment with hindfoot valgus and forefoot abduction exaggerated on the symptomatic foot. Patients with stage II adult-acquired flatfoot have weakness with inversion and difficulty performing a single foot heel raise, indicating attenuation or rupture of the posterior tibial tendon. Stage III adult-acquired flatfoot represents a progression of all the clinical signs of stage II but the deformity has now become rigid. Myerson proposed Stage IV to include a valgus deformity within the ankle joint itself.5
According to Tome and coworkers, patients in stage II AAF will demonstrate the following clinical findings:
• palpable tenderness of the posterior tibial tendon;
• swelling along the distal sheath of the posterior tibial tendon;
• pain or inability to perform the single limb heel rise;
• flexible valgus deformity of the hindfoot in static stance; and
• increased abduction of the forefoot during gait.6
Can Orthotic Interventions And Modifications Help Address The Pathomechanics Of Adult-Acquired Flatfoot?
A sequence of events in the development and evolution of adult-acquired flatfoot is presented in the table “Understanding The Progression Of The Adult-Acquired Flatfoot Deformity” at right. As we evaluate each of the steps in this pathomechanics scheme, I will discuss the biomechanics and treatment interventions along with supportive references from the medical literature. Authors have commonly reported that most patients presenting with stage II adult-acquired flatfoot deformity have a history of preexisting flat feet for most of their life.7 In many cases, the patient has already had treatment for symptoms of flat feet and is already wearing foot orthoses. The significant change that causes the patient to seek treatment is the fact that in one foot, the symptoms and deformity have changed and the level of disability has worsened. At the present time, there is no evidence that any intervention earlier in life will prevent eventual rupture of the posterior tibial tendon. However, researchers have suggested that foot orthotic intervention may have a protective benefit in patients with pronated feet.
A lifetime of walking on a pronated foot may lead to overload and ultimate failure of key supportive structures. Uchiyama and coworkers were among the first to document an increased gliding resistance of the posterior tibial tendon when the human foot is pronated and a flatfoot deformity is present.8 These same researchers later verified that a pronated foot position uniquely overloads the posterior tibial tendon rather than the other tendons of the ankle.9 They further recommended that orthoses or surgical procedures that realign the hindfoot and ankle can reduce the load on soft tissue structures and prevent further degeneration.
Since we know that certain patients are at risk for developing adult-acquired flatfoot, particularly those with preexisting flatfeet and overweight individuals, it appears that early intervention with foot orthotic therapy may have a protective benefit. While no studies have determined the benefits of early intervention, the biomechanics of soft tissue overload certainly validate any effort to protect certain structures in the human foot that are at risk for rupture later in life.
Several studies have demonstrated the benefit of certain foot orthotic modifications to reduce internal inversion subtalar joint moments. This will theoretically reduce load on the posterior tibial tendon.
Munderman and colleagues showed that varus posting significantly reduced the inversion moment of the ankle and hindfoot.10 Williams and co-workers studied the effects of the inverted cast correction for custom foot orthoses and found that this modification can reduce the peak inversion moment of the rearfoot by 54 percent in comparison to not wearing orthoses.11 Bonanno and colleagues showed that 4 mm and 6 mm medial heel skive modifications to custom foot orthosis fabrication could increase pressure on the medial calcaneus, and speculated that this may improve pronation control of the subtalar joint in flat, pronated feet.12 Murley and co-workers showed that various foot orthotic designs could reduce peak electromyographic activity in the tibialis posterior, a finding that could validate the use of these devices as a protective mechanism for adult-acquired flatfoot.13
With overload of the posterior tibial tendon, gradual attenuation and eventual rupture occur. Researchers have demonstrated that in early stage II adult-acquired flatfoot deformity, measurable weakness of the foot occurs with these tendon changes.14 The remaining medial ankle flexors, the flexor digitorum longus (FDL) and flexor hallucis longus (FHL), are unable to compensate for weakness of the tibialis posterior in providing necessary hindfoot inversion and forefoot adduction during gait.15,16 Before significant ligamentous rupture occurs, strengthening and rehabilitation of the weakened posterior tibial muscle/tendon unit can be of significant benefit to prevent the progression of deformity. Kulig and colleagues demonstrated this in a prospective study in which patients with stage II adult-acquired flatfoot deformity had significantly decreased pain and improved function after a 12-week program of progressive eccentric resistance exercise of the tibialis posterior muscle combined with custom functional foot orthotic therapy.17
What Emerging Research Reveals About The Role Of The Spring Ligament
Progressive weakness and attenuation of the posterior tibial tendon will place overload on the ligamentous structures supporting the ankle and hindfoot. Detailed magnetic resonance imaging studies have documented the critical role of ligament rupture with the progression of adult-acquired flatfoot through stage II and III deformity.18,19 The most important structural failure attributed to progression of deformity involves the spring ligament. Early on, clinicians suspected that deformity in the adult-acquired flatfoot could not be attributed solely to rupture of the posterior tibial tendon.7,20,21 Other cadaver studies revealed the importance of the spring ligament in the creation of the flatfoot deformity.22,23 Jennings and Christensen elegantly demonstrated the fact that rupture of the spring ligament cannot be overcome by the posterior tibial tendon, and evaluation of the adult-acquired flatfoot must take the integrity of this structure into account.24 Deland and co-workers have also identified the superficial deltoid ligament as well as the plantar tarsometatarsal ligaments as other key ligaments that sequentially rupture in the progression of adult-acquired flatfoot.18 However, rupture of the spring ligament has gained considerable consensus as the key structure which, when ruptured, leads to the significant postural change of alignment one sees with adult-acquired flatfoot.25Where Forefoot Supination Comes Into Play
In 2011, a panel of orthopedic surgeons published a detailed classification system of stage II adult-acquired flatfoot deformity, which focused on changes in forefoot alignment that correspond with ligament failure.26 With attenuation of the spring ligament as well as other plantar ligaments of the medial column, forefoot supination or “supinatus” deformity will develop. This is the result of progression of valgus positioning of the hindfoot, which puts reciprocal varus loading against the forefoot. One can visualize this supinatus deformity by correcting the hindfoot to neutral and looking at the alignment of the plantar surface of the metatarsal heads relative to a bisection of the calcaneus. As stage II deformity progresses, supination deformity of the forefoot becomes fixed and rigid. As further ligaments attenuate and rupture along the plantar surface of the midfoot and tarsometatarsal joints, clinicians will note the deformity on standing radiographs along with elevation of the first ray and abduction of the forefoot.A Closer Look At Relevant Gait Studies And The Diagnostic Value Of The Heel Rise Test
Numerous gait studies have been conducted on patients with adult-acquired flatfoot, particularly those with stage II deformity.27-29 These studies have shown postural changes that one would not see in asymptomatic feet that are flat and pronated. Instead, stage II adult-acquired flatfoot deformity consistently shows a combination of excessive hindfoot eversion, lowering of the medial longitudinal arch and significant abduction of the forefoot.6,30
The clinician can gain appreciation for the biomechanical changes by asking the patient with stage II adult-acquired flatfoot to perform a single foot heel rise test. The heel rise test is recommended for individuals with posterior tibial tendon dysfunction (PTTD) to detect a partial or complete rupture of the posterior tibial tendon.31,32 Weakness of the posterior tibialis muscle theoretically contributes to the inability to perform a heel rise task or abnormal kinematics during a heel rise task.33 Clinically, one would observe an abnormal heel rise test when the individual cannot perform a heel rise or performs the heel rise with hindfoot eversion (fails to invert on rising), suggesting that the posterior tibialis muscle no longer is acting to invert the hindfoot.5,34
The normal combined action of the posterior tibialis and triceps surae muscles in theory produces ankle plantarflexion with inversion during a heel rise task.16,35,36 The failure of a patient with stage II adult-acquired flatfoot to perform the heel rise is not directly attributed to ankle plantarflexion weakness. The tibialis posterior is not an effective plantarflexor of the ankle, even in healthy patients. Instead, the heel rise test requires a stable arch and midfoot in order for the triceps to actively plantarflex the ankle and the entire foot across the metatarsal heads. Houck and co-workers demonstrated that patients with stage II adult-acquired flatfoot show greater ankle joint plantarflexion at midstance and reciprocal dorsiflexion of the first ray, indicating breakdown of the midfoot.30 Researchers have shown increased flexibility of the forefoot on the rearfoot in other studies of patients with stage II adult-acquired flatfoot, suggesting that this demonstrates loss of ligamentous stability.31,32
Assessing The Evidence On Treatment Interventions For Stage II Adult-Acquired Flatfoot
Non-operative interventions for adult-acquired flatfoot include longitudinal arch supports, custom foot orthotic devices, ankle braces and custom ankle-foot orthoses (AFOs). To be effective, these devices must offload the supportive ligaments that have been damaged by the progression of deformity and shorten the length of the posterior tibial tendon if it is still intact. How these devices accomplish these treatment goals remains somewhat obscure. Flemister and colleagues speculate that rupture of the spring ligament results in greater hindfoot eversion and plantarflexion of the talus.37 They speculate that foot orthoses that support the medial longitudinal arch while controlling hindfoot valgus may compensate for this ligament failure.37
Most clinicians favor AFOs (ankle braces) over foot orthoses to address the severe biomechanical forces they see with stage II adult-acquired flatfoot.38 In another study focusing on three different designs of ankle braces to treat stage II adult-acquired flatfoot, Houck and coworkers found that controlling hindfoot eversion was the most insignificant treatment effect.39 They noted that improvements in medial longitudinal arch alignment and correction of forefoot abduction were the most significant measureable treatment effects, but only found these improvements with certain designs of ankle braces. The custom articulated AFO provided the best improvement of the height of the medial longitudinal arch and correction of forefoot abduction in comparison to a custom solid AFO. The researchers concluded that “The consistent finding in this patient of improved kinematics with the articulated versus solid ankle design underscored the importance of allowing ankle movement for foot function.”39
One dilemma when treating stage II adult-acquired flatfoot is the presence of muscle weakness. Studies have demonstrated not only weakness of the tibialis posterior but overall general weakness of all of the ankle plantarflexors in patients with adult-acquired flatfoot.37,38 This is why Flemister and Houck concluded that “ankle plantarflexion weakness may account for functional impairments and gait disturbances reported by patients with PTTD. Orthoses that restrict ankle motion (solid AFO), while very popular, may induce plantarflexor weakness and increase dependence on the orthosis for support.”39
With rupture of the spring ligament, excessive adduction and plantarflexion of the talus occur across the talonavicular joint. While foot orthoses may be able to provide some support to this joint, the patient often does not tolerate the pressure of the device against the skin of the foot in this region. Since the talus is locked within the ankle mortise, one can best accomplish control of adduction by controlling tibial rotation via an ankle-foot orthosis. This is why the most significant change measured with ankle bracing in a patient with stage II adult-acquired flatfoot was improved alignment of the medial longitudinal arch.37
To this date, there are seven studies published in the medical literature that validate positive treatment effects for stage II adult-acquired flatfoot.17,40-45 The most impressive of these studies utilized a combination of strengthening exercises with AFO therapy. In both the studies by Alvarez and Lin, over 80 percent of the patients treated with articulating AFOs and exercise were able to avoid surgery and remain brace-free with a follow up of one to eight years.42,43
Both strengthening exercise programs and surgical reconstruction of the tibialis posterior tendon have demonstrated recovery of muscle function in patients with stage II adult-acquired flatfoot.17,46 To this date, there are no studies documenting healing of ruptured ligaments when one uses bracing to treat stage II adult-acquired flatfoot. However, the fact that studies have shown that a majority of patients treated with bracing of stage II adult-acquired flatfoot are able to discontinue using their AFOs after a period of use suggests that ligament integrity must have been restored to achieve this level of function.
Final Words
The stage II adult-acquired flatfoot deformity represents a failure of the posterior tibial tendon and key supportive ligaments of the ankle and hindfoot. Clinicians can address the early presentation of this deformity with muscle strengthening and foot orthoses with modifications to decrease strain on the medial ankle structures. When the spring ligament ruptures, one can obtain control on talus adduction by controlling tibial rotation with ankle-foot orthoses. When it comes to stage II adult-acquired flatfoot, articulated ankle-foot orthoses are preferred to recruit weakened musculature, which accompanies this deformity. Studies show that the majority of patients with stage II adult-acquired flatfoot treated with articulated AFO devices can avoid surgery and many can eventually ambulate relatively pain-free without the continued use of bracing. Dr. Richie is an Adjunct Associate Professor within the Department of Applied Biomechanics at the California School of Podiatric Medicine at Samuel Merritt University in Oakland, Calif. He is a Fellow and Past President of the American Academy of Podiatric Sports Medicine. Dr. Richie is a Fellow of the American College of Foot and Ankle Surgeons. He is in private practice in Seal Beach, Calif. Dr. Richie writes a monthly blog for Podiatry Today. One can access his blog at www.podiatrytoday.com/blogs/301 . References 1. Richie DH. Pathomechanics of the adult acquired flatfoot. Foot and Ankle Quarterly. 2005;17(4);109-124. 2. Kohls-Gatzoulis J, Woods B, Angel JC, Singh D. The prevalence of symptomatic posterior tibialis tendon dysfunction in women over the age of 40 in England. Foot Ankle Surg. 2009;15(2):75-81. 3. Holmes GB Jr, Mann RA. Possible epidemiological factors associated with rupture of the posterior tibial tendon. Foot Ankle. 1992:13(2):70-79. 4. Johnson KA, Strom DE. Tibialis posterior tendon dysfunction. Clin Orthop. 1989:239:196-206. 5. Myerson MS. Adult acquired flatfoot deformity: treatment of dysfunction of the posterior tibial tendon. Instr Course Lect. 1997;46:393-405. 6. Tome J, Flemister S, Nawoczenski D, Houck J. Comparison of foot kinematics between subjects with posterior tibial tendon dysfunction and healthy controls. J Orthop Sports Phys Ther. 2006;36(9):635–644. 7. Dyal CM, Feder J, Deland JT, Thompson FM. Pes planus in patients with posterior tibial tendon insufficiency: asymptomatic versus symptomatic foot. Foot Ankle Int. 1997:18(2):85–88. 8. Uchiyama E, Kitaoka HB, Fujii T, et al. Gliding resistance of the posterior tibial tendon. Foot Ankle Int. 2006;27(9):723-7. 9. Fujii T, Uchiyama E, Kitaoka HB, Luo ZP, Zhao KD, An KN. The influence of flatfoot deformity on the gliding resistance of tendons about the ankle. Foot Ankle Int. 2009;30(11):1107-10. 10. Mundermann A, Nigg BM, Humble RN, Stefanyshyn DJ. Foot orthotics affect lower extremity mechanics in running. Clin Biomech. 2003;18(3)254-262. 11. Williams DS 3rd, McClay Davis I, Baitch SP. Effect of inverted orthoses on lower-extremity mechanics in runners. Med Sci Sport Exer, 2003, 35(12): 2060-2068 12. Bonanno DR1, Zhang CY, Farrugia RC, et al. The effect of different depths of medial heel skive on plantar pressures. J Foot Ankle Res. 2012;5:20. 13. Murley GS, Landorf KB, Menz HB. Do foot orthoses change lower limb muscle activity in flat-arched feet towards a pattern observed in normal-arched feet? Clin Biomech (Bristol, Avon). 2010;25(7):728-36. 14. Houck JR, Nomides MS, Neville CG, Samuel Flemister A. The effect of stage II posterior tibial tendon dysfunction on deep compartment muscle strength: a new strength test. Foot Ankle Int. 2008;29(9):895-902. 15. Hintermann B, Nigg BM, Sommer C. Foot movement and tendon excursion: an in vitro study. Foot Ankle Int. 1994;15(7):386-395. 16. Niki H, Ching RP, Kiser P, Sangeorzan BJ. The effect of posterior tibial tendon dysfunction on hindfoot kinematics. Foot Ankle Int. 2001;22(4):292-300. 17. Kulig K, Reischl SF, Pomrantz AB, et al. Nonsurgical management of posterior tibial tendon dysfunction with orthoses and resistive exercise: a randomized controlled trial. Phys Ther. 2009;89(1):26-37 18. Deland JT, de Asla RJ, Sung IH, Ernberg LA, Potter HG. Posterior tibial tendon insufficiency: which ligaments are involved? Foot Ankle Int. 2005;26(6):427-35. 19. Balen PF, Helms CA. Association of posterior tibial tendon injury with spring ligament injury, sinus tarsi abnormality, and plantar fasciitis on MR imaging. AJR Am J Roentgenol. 2001;176(5):1137-1143. 20. Gazdag AR, Cracchiolo A. Rupture of the posterior tibial tendon. Evaluation of injury of the spring ligament and clinical assessment of tendon transfer and ligament repair. J Bone Joint Surg Am. 1997;79(5):675-681. 21. Deland JT, Arnoczky P, Thompson FM. Adult acquired flatfoot deformity at the talonavicular joint: Reconstruction of the spring ligament in an in vitro model. Foot Ankle. 1992;13(6):327-32. 22. Kitaoka HB, Luo ZP, An KN. Three-dimensional analysis of flatfoot deformity: cadaver study. Foot Ankle Int. 1998;19(7):447–451. 23. Chu IT, Myerson MS, Nyska M, Parks BG. Experimental flatfoot model: the contribution of dynamic loading. Foot Ankle Int. 2001;22(3):220–225. 24. Jennings MM, Christensen JC. The effects of sectioning the spring ligament on rearfoot stability and posterior tibial tendon efficiency. J Foot Ankle Surg. 2008;47(3):219–24. 25. Williams G, Widnall J, Evans P, Platt S. Could failure of the spring ligament complex be the driving force behind the development of the adult flatfoot deformity? J Foot Ankle Surg. 2014;53(2):152-5. 26. Haddad SL, Myerson MS, Younger A, Anderson RB, Davis WH, Manoli II A. Adult acquired flatfoot deformity. Foot Ankle Int. 2011;32(1):95-111. 27. Ness ME, Long J, Marks R, Harris GF. Foot and ankle kinematics in subjects with posterior tibial tendon dysfunction. Gait & Posture. 2008;27(2):331–339. 28. Rattanaprasert U, Smith R, Sullivan M, Gilleard W. Three-dimensional kinematics of the forefoot, rearfoot, and leg without the function of tibialis posterior in comparison with normal during stance phase of walking. Clin Biomech (Bristol, Avon). 1999;14(1):14-23. 29. Ringleb SI, Kavros SJ, Kotajarvi BR, Hansen DK, Kitaoka HB, Kaufman KR. Changes in gait associated with acute stage II posterior tibial tendon dysfunction. Gait Posture. 2007;25(4):555–64. 30. Houck JR, Neville CG, Tome J, Flemister AS. Ankle and foot kinematics associated with stage II PTTD during stance. Foot Ankle Int. 2009;30(6):530-9. 31. Myerson MS, Badekas A, Schon LC. Treatment of stage II posterior tibial tendon deficiency with flexor digitorum longus tendon transfer and calcaneal osteotomy. Foot Ankle Int. 2004;25(7):445–450. 32. Otis JC, Gage T. Function of the posterior tibial tendon muscle. Foot Ankle Clin. 2001;6(1):1–14. 33. Wacker J, Calder JD, Engstrom CM, Saxby TS. MR morphometry of posterior tibialis muscle in adult acquired flat foot. Foot Ankle Int. 2003;24(4):354–357. 34. Kohls-Gatzoulis J, Angel JC, Singh D, Haddad F, Livingstone J, Berry G. Tibialis posterior dysfunction: a common and treatable cause of adult acquired flatfoot. BMJ. 2004;329(7478):1328–1333. 35. Hansen ML, Otis JC, Kenneally SM, Deland JT. A closed-loop cadaveric foot and ankle loading model. J Biomech. 2001;34(4):551–555. 36. Kulig K, Burnfield JM, Requejo SM, Sperry M, Terk M. Selective activation of tibialis posterior: evaluation by magnetic resonance imaging. Med Sci Sports Exerc. 2004;36(5):862–867. 37. Flemister AS, Neville CG, Houck J. The relationship between ankle, hindfoot, and forefoot position and posterior tibial muscle excursion. Foot Ankle Int. 2007;28(4):448–55. 38. Neville C, Flemister A, Tome J, Houck J. Comparison of changes in posterior tibialis muscle length between subjects with posterior tibial tendon dysfunction and healthy controls during walking. J Orthop Sports Phys Ther. 2007;37(11):661-9. 39. Neville C, Houck J. Choosing among 3 ankle-foot orthoses for a patient with stage II posterior tibial tendon dysfunction. J Orthop Sports Phys Ther. 2009;39(11):816–824. 40. Chao W, Wapner KL, Lee TH, Adams J, Hecht PJ. Non-operative management of posterior tibial tendon dysfunction. Foot Ankle Int. 1996;17(12):736–41. 41. Augustin JF, Lin SS, Berberian WS, Johnson JE. Non-operative treatment of adult acquired flat foot with the Arizona brace. Foot Ankle Clin. 2003;8(3):491 –502. 42. Alvarez RG, Marini A, Schmitt C, Saltzman CL. Stage I and II posterior tibial tendon dysfunction treated by a structured non-operative management protocol: an orthosis and exercise program. Foot Ankle Int. 2006;27(1):2–8. 43. Lin JL, Balbas J, Richardson G. Results of non-surgical treatment of stage II posterior tibial tendon dysfunction: a 7- to 10-year followup. Foot Ankle Int. 2008;29(8):781-6. 44. Krause F, Bosshard A, Lehmann O, Weber M. Shell brace for stage II posterior tibial tendon insufficiency. Foot Ankle Int. 2008;29(11):1095-1100. 45. Nielsen MD, Dodson EE, Shadrick DL, Catanzariti AR, Mendicino RW, Malay DS. Non-operative care for the treatment of adult-acquired flatfoot deformity. J Foot Ankle Surg. 2011;50(3):311-314. 46. Valderrabano V, Hintermann B, Wischer T, et al. Recovery of the posterior tibial muscle after late reconstruction following tendon rupture. Foot Ankle Int. 2004;25(2):85–95.
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