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Function of the plantar fascia
The Foot (1999) 9, 73–78 © 1999 Harcourt Brace & Co. Ltd
ORIGINAL ARTICLE
Function of the plantar fascia A. Aquino, C. Payne Department of Podiatry, School of Human Biosciences, LaTrobe University Bundoora, Vic. 3083, Australia SUMMARY. The plantar fascia has long been considered to have a significant purpose in the weightbearing foot, both in static stance and in dynamic function. Various functional and structural roles have been indicated by virtue of its anatomical attachments. This paper aims to review the anatomy and biomechanical considerations of the plantar fascia and, in particular, its central component known as the plantar aponeurosis. Static and dynamic roles of the plantar aponeurosis will be discussed with emphasis placed on the dynamic ‘windlass mechanism’ phenomenon exhibited on first metatarsophalangeal joint dorsiflexion, leading to further indications for research on its role in plantar fascial injury and the pronated or pes planus foot.
thinner as it progresses towards the forefoot. Its mostly longitudinally oriented fibres attach to the flexor digitorum brevis muscle lying underneath. It divides into five slips just below the metatarsal shafts, with each slip generating a superficial and deep tract proximal to the metatarsal heads and inserting into a complex network in the plantar forefoot area. BojsenMoller and Flagstad12 conducted a detailed anatomic study of the plantar aponeurosis and its insertions, using dissections of cadaver specimens. Their data showed that two of the superficial tracts course to the medial and lateral components while the medial three proceed longitudinally in concordance with the digits. Some fibres of these medial tracts form a transverse network just distal to the metatarsal heads and contribute to the plantar interdigital ligament. Most of the superficial tract fibres progress vertically to insert into the dermis. The deep tracts each divide into two sagittal septae, forming the walls of the flexor tunnel for the tendons of flexor hallucis and digitorum longus. The most medial pair of septae insert into the sesamoids and the two heads of flexor hallucis brevis. The rest insert into the flexor tendon sheath, interosseous fascia, the fascia of the transverse head of adductor hallucis, the deep transverse metatarsal ligament and the plantar plate of the metatarsophalangeal joints (MPJs), to firmly attach to the base of the proximal phalanges. Histologically, the bulk of the composition of the plantar aponeurosis is made up of strong collagen fibres.9 There are numerous elastic fibres, varying in thickness and arranged in longitudinal strands and wavy bundled network.13 These elastic fibres were capable of changing their orientation from wavy to straight under a progressively increased load, producing a gradual increase in stiffness. Kitaoka et al. measured fascial
ANATOMY The plantar fascia has been defined as the investing, fibrous layer of the foot’s plantar aspect, located subcutaneously and originating from the calcaneus to insert into the deep soft tissues of the forefoot, the proximal phalanges and the skin via superficial extension.1 Marieb2 considers that the purpose of fascia is to bind muscles into functional groups, hold down tendons and facilitate their movement, by reason of its external attachments to the outer covering of skeletal muscle called the epimysium. The configuration of the plantar fascia is generally considered3 as that of a dense, longitudinally arranged band of fibres divided into medial, central and lateral components. According to Kogler et al.4 and Sarrafian5 the term ‘plantar fascia’ is synonymous with ‘plantar aponeurosis’, encompassing all three parts of the deep fascia of the sole. However, in Moore6 and Pontious et al.3 only the denser central portion is considered truly aponeurotic in composition, structure and function, suggesting that the thinner medial and lateral parts merely serve as fascial coverings for abductor hallucis and abductor digiti minimi, respectively. This paper will thus refer to the central portion only as the plantar aponeurosis, focussing anatomical and biomechanical discussion on the thickest and strongest segment,7,8 which is the usual site for pathology.9,10 Salman11 describes the plantar aponeurosis as the intermediary structure between the skin and osteoligamentous framework of the foot, originating from the medial calcaneal tubercle, where it is at its narrowest and thickest, and becoming broader and Correspondence to C. Payne, Tel: +61 3 9479 5820; Fax: +61 3 9479 5784; e-mail [email protected]
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stiffness in cadaver’s under different loading rates and found that the plantar fascia ruptured or failed on average at 1189 N. This indicates a structure equipped to resist deformation under considerable tensile stress, comparable to approximately one and a half times the body weight of a 70 kg person, thus implying the plantar fascia’s significance in the normal weightbearing of the foot.
BIOMECHANICAL CONSIDERATIONS For conceptual purposes, to help understand the effect of loading on the plantar aponeurosis, the literature often refers to the popular analogy of the foot being an arch-like triangular structure or truss, comprising two beams or struts depicting the osseous longitudinal arches and a tie-rod representing the aponeurosis. This concept was first advanced by Hicks,14 where he considered that a weight on an arch-shaped structure tends to thrust the ends apart. The strength that is peculiar to a true arch or truss is only required when the ends are prevented from becoming further apart. Using cadaver specimens it was demonstrated that tension in the aponeurosis upon dorsiflexion of the toes at the MPJs made the foot act like a truss during different periods of the gait cycle. Applying the same concept, Arangio et al.15 investigated the foot’s loadbearing characteristics using a two-dimensional biomechanical model, consisting of a two-bar linkage and a Kelvin body or spring depicting the plantar aponeurosis, which mathematically predicted and simulated a 17% decrease in arch height without the spring. This alludes to the plantar aponeurosis’s role in augmenting the truss mechanism when placed under tension. Both studies only examined the foot in a static situation using models rather than a dynamic human foot, but they were able to objectively illustrate that tension exists in the aponeurosis when the foot is weightbearing to maintain arch integrity, thereby acting like a ‘tie-rod’. Several other in vitro studies support the notion of the plantar aponeurosis as a significant contributor to arch integrity during simulations of static stance. Huang et al.16 found that the plantar fascia gave the most substantial contribution to arch stability, reporting that its division decreased arch stiffness by 25%. Specimens were vertically loaded and structures presumed to give significant support (such as long and short plantar ligaments, spring ligament and plantar fascia) were sequentially sectioned and displacement directly measured with a potentiometer. Thordarson17 evaluated the effects of sectioning the plantar fascia alone and observed a consistent decrease in arch height, an increase in arch length and forefoot abduction with internal rotation of the navicular after sectioning; suggesting that an element of foot instability would accompany plantar fascia sectioning. Murphy18 discovered that a complete release The Foot (1999) 9, 73–78
of the plantar fascia caused a 62–100% collapse in the medial and lateral longitudinal arches, compared with a partial release. This indicates a greatly diminished tie-rod function of the aponeurosis after sectioning. An axial loading system was used to measure displacement in transverse, sagittal and frontal planes after 16 metal markers were embedded in each specimen allowing radiographic imaging and monitoring of displacement. The testing techniques in all of the in vitro studies presented permit a more controlled setting in which to study the mechanical behaviour of the foot under simulated conditions found in static stance. However, these factors obviously still fail to address the contribution of other elements to arch integrity in the living, dynamic foot, elements such as intrinsic or extrinsic muscular activity. The foot in gait presents an entirely different picture of the amount and timing of aponeurosis tension.19 The tie-rod function of the plantar aponeurosis may be greatly altered in the preserved cadaver specimen compared with the living foot. Other authors have regarded the plantar aponeurosis’s role in a similar fashion to the tie-rod component in an arciform structure. Viel and Esnault20 likened the aponeurosis to the central cable or hypozomata of a Greek boat, which served to create compression forces on parts of the hull upon cable tightening to ensure solidity. They mimicked this action by passively dorsiflexing live subjects’ toes and noting a visual tightening of the plantar aponeurosis. Bartold10 and Schepsis et al.21 compared the foot’s medial longitudinal arch to an archer’s bow and the aponeurosis as the bowstring, explaining that vertical loading (as that which occurs in quiet standing) ‘straightens’ the bow and ‘tightens’ the bowstring, which aims to preserve the bow’s structure. Perry22 describes the aponeurosis as a simple, broad, nonelastic strap that is able to immediately transfer tension from one end to the other, especially upon MPJ dorsiflexion, by virtue of its attachments and its dense composition. All of the conceptualizations mentioned above are based on Hicks14 in expressing the foot as being constructed in a truss-like arciform manner and responding accordingly with aponeurotic tension upon loading to sustain arch integrity. Sarrafian23 instead compared the foot to a twisted rectangular plate, demonstrating that the ‘the transition induced by the twist creates the transverse and longitudinal arches’. This analogy allows for the activation of the ‘truss’ mechanism, hence aponeurosis tightening, at different periods during the gait cycle, augmented or hindered by the foot ‘twisting’ and ‘untwisting’ which represents forefoot pronation and supination to elevate or depress the medial longitudinal arch. The foot is thus capable of remodeling itself throughout gait because of the added element of torque not previously accounted for in the ‘truss’ and ‘tie-rod’ analogy. © 1999 Harcourt Brace & Co. Ltd
Function of the plantar fascia Kogler et al.19 quantified the strain in the plantar aponeurosis using cadaver specimens and five different foot orthotic devices, including the functional foot orthosis (FFO) pioneered by Root et al.24 (1977) and the University of California Biomechanics Laboratory Shoe Insert (UCBL). Their aim was to discover which device significantly decreased aponeurotic strain upon vertical loading. The hypothesis was that if an orthotic device serves to effectively support the longitudinal arches of the foot, soft tissue strain would be minimized. If the plantar aponeurosis does function as a tie-rod to a truss, the authors state that tension would increase as the shorter posterior strut, consisting of the talus and calcaneus, is elevated as this would shorten the distance between the ends of the struts. However, the UCBL device (with its noticeably higher medial arch height and deeper heel cup compared to the FFO) contributed the most significant decrease in aponeurotic strain, while elevating the medial longitudinal arch. Kogler et al.19 suggest that this result came about because of the ‘deactivation’ of the truss mechanism and a redirection of load from the aponeurosis to the osseous structures, located at the apex of the medial longitudinal arch, due to the UCBL’s ability to stabilize these apical structures. This was considered to be in concordance with the ‘twisted plate’ analogy of Sarrafian,23 in that the arch support region of the orthosis resembles the twisted plate model and the orthosis allowed for the deactivation of the ‘truss’ mechanism in decreasing aponeurotic strain. The authors19 concede that the study’s static conditions did not account for the changes in amount and timing of aponeurotic tension present in the live, dynamic foot and how an orthosis might respond to these changes and thus the usefulness of their results may be questioned in a clinical setting. The mechanism whereby a foot orthosis serves to alleviate foot symptoms is still a controversial area of debate.25–27 A recent clinical study supports the findings of decreased plantar aponeurosis strain with the suppression of the truss mechanism and a change in the foot’s load transmission patterns. Bartold28 evaluated the outcome of using FFOs, taping, medial rearfoot wedging to invert the calcaneus or lateral forefoot wedging on relieving clinical symptoms in plantar fascial injury, with only taping and lateral wedging groups to report significantly reduced pain scores. Similar findings were reported in Kogler et al.29 with the use of lateral forefoot wedging found to significantly reduce aponeurotic strain in cadaver specimens. Both studies contend that the alteration in load transmission, from soft tissue to bony structures, is brought about by the initiation of different support mechanisms attributed to the inclined plane introduced by lateral wedging. Kogler et al.29 go further into suggesting that calcaneocuboid joint locking enabled a greater proportion of load to be shifted away from the aponeurosis. Relatively few studies have investigated the dynamic role of the plantar aponeurosis in vivo due to the © 1999 Harcourt Brace & Co. Ltd
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comparative difficulty in acquiring accurate, reproducible, quantitative data due to the invasive nature of the methodology used to obtain it.30 Thordarson et al.31 point out that no in vivo data depicting tension in musculo-tendinous structures during normal gait existed, so reports have sought to infer conclusions from the in vitro methods. Thordarson et al.31 employed this methodology in evaluating the effect of the plantar aponeurosis and other structures during stance and their contribution to dynamic support. They reported that the aponeurosis contributed the most significant arch support in the sagittal plane, demonstrated by maximally dorsiflexing the digits at the MPJs and presupposedly eliciting tension in the aponeurosis (which wasn’t measured) to resist sagittal plane displacement. Kitaoka et al.30 investigated the change in position of the calcaneus, talus, navicular and first metatarsal in three body planes after fasciotomy in intact and ‘destabilized’ feet, with more ligamentous structures sectioned in the latter. They found that displacement changes were more prominent in the ‘destabilized’ feet, implying that the plantar fascia has a significant role as an arch stabilizer. A slightly more recent study by Kitaoka et al.32 defined the contribution of the plantar fascia to arch stability, among other ligamentous structures, as significant in terms of affecting talar-tibial position when sectioned. All of these studies support the contention that the plantar fascia is important for arch integrity and dynamic support. This holds clinical relevance to the assessment of plantar aponeurosis function and pathology in that surgical intervention may lead to further static and dynamic dysfunction, alluded to by several authors.1,15,16,33,34 In spite of the paucity of recent research concerning the plantar aponeurosis’s role in vivo, viewpoints from a clinical perspective have been made with regard to its role during gait. Payne and Dananberg35 proposed a theory of foot function with clinical implications in which the foot is modelled as a sagittal plane pivotal site which the body’s centre of mass is permitted to move forward over during the single support phase of gait. The centre of sagittal plane motion is defined as the first MPJ, for it is directly associated with forward propulsion, being at the interface between the body and the ground. Motion enhancement and a subsequent transfer of normal weight flow is facilitated by three autosupportive mechanisms, activated at certain periods in gait, that serve to resist the forces applied during gait. These mechanisms are thought to rely heavily on adequate first MPJ dorsiflexion, earlier confirmed to have an arch-augmenting effect in static and dynamic roles, and associated secondary tension in the aponeurosis. The first autosupportive mechanism, calcaneocuboid locking,36,37 depends on a transfer of weight flow from the lateral aspect of the forefoot to the medial aspect which induces aponeurotic tension just prior to heel lift. Compressive forces applied across the foot, from activation of the ‘truss’ mechanism upon The Foot (1999) 9, 73–78
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aponeurotic tension, packs the cuboid closely into calcaneus, thus ‘locking’ creating stability in the midtarsal joint complex. This mechanism was implicated by Kogler et al.29 as the maneouvre responsible for redirecting load away from the aponeurosis, substituting a lateral forefoot wedge for the action of the plantar aponeurosis. The second autosupportive mechanism, the locking wedge effect, relies on activation of the ‘truss’ mechanism to maintain internal stability when weight flow is transferred from the heel to the forefoot.37 Compressive loading of the bones occurs as a response from the opposing ground reaction forces, specifically when the metatarsal shafts begin to change their orientation from horizontal to vertical, during single support phase. The tie-rod function of the aponeurosis thus helps to stabilize the central midfoot structures in preparation for propulsion. Hicks38 first described the third autosupportive mechanism, the windlass mechanism. Passive dorsiflexion of the hallux caused the medial longitudinal arch to rise, the rearfoot to supinate, the leg to externally rotate and the plantar aponeurosis to become more tense. This was verified by several authors demonstrating passive hallux dorsiflexion on live subjects in static stance.23,39,40 This phenomenon was likened to the winding of a cable (plantar aponeurosis) around the drum of a windlass (first MPJ) by pulling a handle (proximal phalanx of the hallux). Hicks38 tested this mechanism on a living foot and a cadaver specimen and found that all the effects were present on both, verifying that the windlass mechanism operated independently of muscular activity. In addition, an in vitro study by Thordarson et al.41 confirmed the loss of the windlass mechanism after complete plantar fascial release, indicating the significance of the plantar aponeurosis in establishing this mechanism. The windlass mechanism occurs in gait during toeoff,37 as the last component of sagittal plane motion enhancement. Upon hallux dorsiflexion, the distance between the origin and insertion of the aponeurosis is shortened, thus creating aponeurotic tension and osseous compression, resulting in supination of the foot and external rotation of the leg enabling the foot’s progression to swing phase. The function of the windlass mechanism, apart from augmenting medial arch height and creating stability, is to coordinate the external rotation of the lower leg with external rotation of the pelvis and upper thigh.35,37 Only one in vivo study was found to have investigated the role of the windlass mechanism in normal gait. Kappel-Bargas et al.40 investigated the effect of passive hallux dorsiflexion and rearfoot motion during gait on the height of the medial longitudinal arch in subjects without lower extremity pathology and with greater than 90° of first MPJ range of motion. After placing reflective markers on osseous landmarks in the right foot only, passively dorsiflexing the hallux and visually recording their subjects’ gait, The Foot (1999) 9, 73–78
Kappel-Bargas et al.40 were able to quantitatively conclude that arch height increased with hallux dorsiflexion. In addition, they identified two distinct subject populations, labelled immediate-onset and delayedonset, according to the timing of first MPJ dorsiflexion representing the initiation of the windlass mechanism. The delayed-onset group was found to exhibit more rearfoot inversion at heel strike and a greater, more prolonged rearfoot eversion for the rest of the gait cycle. Muscular activity that may potentially augment arch height was accounted for, with monitoring using electrodes and compulsory repetition of hallux dorsiflexion or gait carried out when muscle contraction was evident, in an attempt to independently analyse the windlass mechanism.
INDICATIONS FOR FURTHER RESEARCH Excessive rearfoot eversion has been linked to pathology in the lower extremity,42 particularly overuse injuries such as plantar fasciitis.8 The aetiology of plantar fasciitis has traditionally been attributed to excessive strain in the plantar aponeurosis, producing symptoms of pain on the medial calcaneal tubercle and medial longitudinal arch, especially upon dorsiflexion of the toes at the MPJs. But plantar fasciitis is also observed to occur in those with high-arched feet and obviously less rearfoot eversion. Understanding the role of the plantar aponeurosis during gait in those with plantar fascial injury is therefore essential to determine appropriate, conservative treatment interventions with regards to plantar fascial injury and may help to elucidate the mechanism of how orthotic devices work in pathological feet to relieve symptoms. Other indications for further research include the role of the windlass mechanism in those with pes planus or a higher degree of rearfoot and/or forefoot pronation. Traditionally,24 excessive subtalar joint pronation has been associated with an ineffective windlass mechanism. The pronated foot is unable to resist the forces applied during gait and therefore unable to create compressive midfoot stability through aponeurotic tightening, which may result in hypermobility and pathology associated with a pronated foot. A recent theoretical approach35,37 suggests that a limitation of motion (structural or functional) at the first MPJ will prevent the windlass mechanism being established and subsequently cause an excessively pronated foot. Further research is necessary to definitively apply biomechanical theory to the clinical setting with regards to the role of the windlass mechanism in normal and pathological feet.
CONCLUSIONS A review of the anatomy and biomechanical considerations pertaining to the plantar aponeurosis has © 1999 Harcourt Brace & Co. Ltd
Function of the plantar fascia been presented and its role in static stance and dynamic function explored in cadaver specimens and in vivo. The plantar aponeurosis can be said to have a ‘tie-rod’ function to the foot’s twisted osteoligamentous plate structure, activating a ‘truss’ mechanism upon tightening to generate compressive forces for greater internal osseous stability. It can be seen that there exists a necessity for research of the aponeurosis in all aspects of dynamic function, to complement the theoretical implications made on studies using in vitro methodology. Based on the evaluation of literature presented, the role of the aponeurosis in the weightbearing foot would be greatly clarified when research can conclusively demonstrate the foot’s response to a given load, both in static and dynamic situations. The mechanism whereby orthotic devices give symptomatic relief, whether by motion control or facilitation of load transmission, would also shed light on the function of the aponeurosis. The importance of the windlass mechanism as an arch-augmenting phenomenon to encourage foot stability in gait, its relationship to rearfoot eversion and its role in the pronated or planus foot would also benefit from further research. REFERENCES 1. Kitaoka HB, Luo ZP, Growney ES, Berglund BS, An KN: Material properties of the plantar aponeurosis. Foot and Ankle International 1994; 15(10): 557–560. 2. Marieb EN: Human Anatomy and Physiology. 3rd ed. California, The Benjamin/Cummings Publishing Company, Inc. 1995 3. Pontious J, Flanigan KP, Hillstrom HJ: Role of the plantar fascia in digital stabilization: a case report. Journal of the American Podiatric Association 1995; 86(1): 43–47. 4. Kogler GF, Solomonidis SE, Paul JP: Biomechanics of longitudinal arch support mechanisms in foot orthoses and their effect on plantar aponeurosis strain. Clinical Biomechanics 1996; 11(5): 243–252. 5. Sarrafian SK: Retaining Systems and Compartments. In: Sarrafian S K (ed) Anatomy of the Foot and Ankle: Descriptive, Topographic, Functional. 3rd ed. Philadelphia, J.B. Lipincott Company, 1993; 113–158. 6. Moore KL: Clinically Oriented Anatomy. 3rd ed. Baltimore, Williams & Wilkins, 1992 7. Schepsis AA, Leach RE, Gorzyca J: Plantar fasciitis: etiology, treatment, surgical results and review of the literature. Clinical Orthopaedics and Related Research 1991; 266: 185–196. 8. Wernick J: Plantar fasciitis: a different time and a different place. Podiatry Management 1998; 17(3) 129–134. 9. Mitchell IR, Meyer C, Krueger WA: Deep fascia of the foot: anatomical and clinical considerations. Journal of the American Podiatric Association 1991; 81(7): 373–378. 10. Bartold S: Conservative management of plantar fasciitis. Australian Podiatrist 1993; 27: 46–50 11. Salman S: Muscles. In: Williams P L (ed) Gray’s Anatomy 38th ed. Edinburgh, Churchill Livingstone, 1995; 891–892. 12. Bojsen-Moller F, Flagstad KE: Plantar aponeurosis and internal architecture of the ball of the foot. Journal of Anatomy 1976; 121(3): 599–611. 13. Wright DG, Rennels DC: A study of the elastic properties of plantar fascia. Journal of Bone and Joint Surgery 1964; 46-A (3): 482–492. 14. Hicks JH: The foot as a support. Acta Anatomica 1955; 25: 34–45. 15. Arangio GA, Chen C, Kim W: Effect of cutting the plantar fascia on mechanical properties of the foot. Clinical Orthopaedics and Related Research 1997; 339: 227–231.
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16. Huang CK, Kitaoka HB, An KN, Chao EYS: Biomechanical evaluation of longitudinal arch stability. Foot and Ankle International 1993; 14(6): 353–357. 17. Thordarson DB, Kumar PJ, Hedman TP, Ebramzadeh E: Effect of partial versus complete plantar fasciotomy on the windlass mechanism. Foot and Ankle International 1997; 18(1): 16–20. 18. Murphy GA, Pneumaticos SG, Kamaric E, Noble PC, Trevino SG, Baxter D E: Biomechanical consequences of plantar fascia release. Foot and Ankle International 1998; 19(3): 149–152. 19. Kogler GF, Solomonidis SE, Paul JP: Biomechanics of longitudinal arch support mechanisms in foot orthoses and their effect on plantar aponeurosis strain. Clinical Biomechanics 1996; 11(5): 243–252. 20. Viel E, Esnault M: The effect of increased tension in the plantar fascia: a biomechanical analysis. Physiotherapy Practice 1989; 5(2): 69–73. 21. Schepsis AA, Leach RE, Gorzyca J: Plantar fasciitis: etiology, treatment, surgical results and review of the literature. Clinical Orthopaedics and Related Research 1991; 266: 185–196. 22. Perry J: Anatomy and biomechanics of the hindfoot. Clinical Orthopaedics and Related Research 1993; 177: 9–15. 23. Sarrafian SK: Functional characteristics of the foot and plantar aponeurosis under tibiotalar loading. Foot and Ankle 1987; 8(1): 4–18. 24. Root ML, Orien WP, Weed JH: Normal and Abnormal Function of the Foot. Vol. II. Los Angeles, Clinical Biomechanics Corporation, 1977 25. Kilmartin TE, Wallace WA: The scientific basis for the use of foot orthoses in the treatment of lower limb sports injuries: a review of the literature. British Journal of Sports Medicine 1994; 28: 180–186. 26. Landorf KB, Keenan AM: Efficacy of foot orthoses: what does the literature tell us? Australasian Journal of Podiatric Medicine 1998; 32(3) 105–113 27. Payne CB: The Past, present, and future of podiatric biomechanics. Journal of the American Podiatric Medical Association 1998; 88(2) 53–63 28. Bartold S: The Biomechanics of Plantar Fascial Injury: Calcaneal Inversion Does Not Reduce Plantar Fascial Strain. Book of Abstracts from the 18th Australian Podiatry Conference, 1998. 29. Kogler GF, Veer FB, Solomonidis SE, Paul JP: The Influence of Medial and Lateral Orthotic Wedges on Loading of the Plantar Aponeurosis. Book of Abstracts from the 9th World Congress of the International Society For Prosthetics And Orthotics 1998; 579–581. 30. Kitaoka HB, Ahn TK, Luo ZP, An KN: Stability of the arch of the foot. Foot and Ankle International 1997; 18(10): 644–648. 31. Thordarson DB, Schmotzer H, Chon J, Peters J: Dynamic support of the human longitudinal arch. Clinical Orthopaedics and Related Research 1995; 316: 165–172. 32. Kitaoka HB, Luo ZP, An KN: Mechanical behaviour of the foot and ankle after plantar fascia release in the unstable foot. Foot and Ankle International 1997; 18(1): 8–15. 33. Daly PJ, Kitaoka HB, Chao EYS: Plantar fasciotomy for intractable plantar fasciitis: clinical results and biomechanical evaluation. Foot and Ankle 1992; 13(4): 188–195. 34. Murphy GA, Pneumaticos SG, Kamaric E, Noble PC, Trevino SG, Baxter DE: Biomechanical consequences of plantar fascia release. Foot and Ankle International 1998; 19(3): 149–152. 35. Payne C, Dananberg H: Sagittal plane facilitation of the foot. Australasian Journal of Podiatric Medicine 1997; 31(1): 7–11. 36. Bojsen-Moller F: Calcaneocuboid joint and stability of the longitudinal arch of the foot at high and low gear push off. Journal of Anatomy 1979; 129(1): 165–176. 37. Dananberg H: Gait style as an etiology to chronic postural pain: part I – functional hallux limitus. Journal of the American Podiatric Medical Association 1993; 83 (8): 433–441. 38. Hicks JH: The mechanics of the foot: part II – the plantar aponeurosis and the arch. Journal of Anatomy 1954; 88: 25–31.
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39. Viel E, Esnault M: The effect of increased tension in the plantar fascia: a biomechanical analysis. Physiotherapy Practice 1989; 5 (2): 69–73. 40. Kappel-Bargas A, Woolf RD, Cornwall MW, McPoil TG: The windlass mechanism during normal walking and passive first metatarsophalangeal joint motion. Clinical Biomechanics 1996; 13 (3): 190–194.
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41. Thordarson DB, Kumar PJ, Hedman TP, Ebramzadeh E: Effect of partial versus complete plantar fasciotomy on the windlass mechanism. Foot and Ankle International 1997; 18(1): 16–20. 42. Hintermann B, Nigg BM: Pronation in runners – implications for injuries. Sports Medicine 1998; 26(3): 169–176
© 1999 Harcourt Brace & Co. Ltd
ORIGINAL ARTICLE
Function of the plantar fascia A. Aquino, C. Payne Department of Podiatry, School of Human Biosciences, LaTrobe University Bundoora, Vic. 3083, Australia SUMMARY. The plantar fascia has long been considered to have a significant purpose in the weightbearing foot, both in static stance and in dynamic function. Various functional and structural roles have been indicated by virtue of its anatomical attachments. This paper aims to review the anatomy and biomechanical considerations of the plantar fascia and, in particular, its central component known as the plantar aponeurosis. Static and dynamic roles of the plantar aponeurosis will be discussed with emphasis placed on the dynamic ‘windlass mechanism’ phenomenon exhibited on first metatarsophalangeal joint dorsiflexion, leading to further indications for research on its role in plantar fascial injury and the pronated or pes planus foot.
thinner as it progresses towards the forefoot. Its mostly longitudinally oriented fibres attach to the flexor digitorum brevis muscle lying underneath. It divides into five slips just below the metatarsal shafts, with each slip generating a superficial and deep tract proximal to the metatarsal heads and inserting into a complex network in the plantar forefoot area. BojsenMoller and Flagstad12 conducted a detailed anatomic study of the plantar aponeurosis and its insertions, using dissections of cadaver specimens. Their data showed that two of the superficial tracts course to the medial and lateral components while the medial three proceed longitudinally in concordance with the digits. Some fibres of these medial tracts form a transverse network just distal to the metatarsal heads and contribute to the plantar interdigital ligament. Most of the superficial tract fibres progress vertically to insert into the dermis. The deep tracts each divide into two sagittal septae, forming the walls of the flexor tunnel for the tendons of flexor hallucis and digitorum longus. The most medial pair of septae insert into the sesamoids and the two heads of flexor hallucis brevis. The rest insert into the flexor tendon sheath, interosseous fascia, the fascia of the transverse head of adductor hallucis, the deep transverse metatarsal ligament and the plantar plate of the metatarsophalangeal joints (MPJs), to firmly attach to the base of the proximal phalanges. Histologically, the bulk of the composition of the plantar aponeurosis is made up of strong collagen fibres.9 There are numerous elastic fibres, varying in thickness and arranged in longitudinal strands and wavy bundled network.13 These elastic fibres were capable of changing their orientation from wavy to straight under a progressively increased load, producing a gradual increase in stiffness. Kitaoka et al. measured fascial
ANATOMY The plantar fascia has been defined as the investing, fibrous layer of the foot’s plantar aspect, located subcutaneously and originating from the calcaneus to insert into the deep soft tissues of the forefoot, the proximal phalanges and the skin via superficial extension.1 Marieb2 considers that the purpose of fascia is to bind muscles into functional groups, hold down tendons and facilitate their movement, by reason of its external attachments to the outer covering of skeletal muscle called the epimysium. The configuration of the plantar fascia is generally considered3 as that of a dense, longitudinally arranged band of fibres divided into medial, central and lateral components. According to Kogler et al.4 and Sarrafian5 the term ‘plantar fascia’ is synonymous with ‘plantar aponeurosis’, encompassing all three parts of the deep fascia of the sole. However, in Moore6 and Pontious et al.3 only the denser central portion is considered truly aponeurotic in composition, structure and function, suggesting that the thinner medial and lateral parts merely serve as fascial coverings for abductor hallucis and abductor digiti minimi, respectively. This paper will thus refer to the central portion only as the plantar aponeurosis, focussing anatomical and biomechanical discussion on the thickest and strongest segment,7,8 which is the usual site for pathology.9,10 Salman11 describes the plantar aponeurosis as the intermediary structure between the skin and osteoligamentous framework of the foot, originating from the medial calcaneal tubercle, where it is at its narrowest and thickest, and becoming broader and Correspondence to C. Payne, Tel: +61 3 9479 5820; Fax: +61 3 9479 5784; e-mail [email protected]
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stiffness in cadaver’s under different loading rates and found that the plantar fascia ruptured or failed on average at 1189 N. This indicates a structure equipped to resist deformation under considerable tensile stress, comparable to approximately one and a half times the body weight of a 70 kg person, thus implying the plantar fascia’s significance in the normal weightbearing of the foot.
BIOMECHANICAL CONSIDERATIONS For conceptual purposes, to help understand the effect of loading on the plantar aponeurosis, the literature often refers to the popular analogy of the foot being an arch-like triangular structure or truss, comprising two beams or struts depicting the osseous longitudinal arches and a tie-rod representing the aponeurosis. This concept was first advanced by Hicks,14 where he considered that a weight on an arch-shaped structure tends to thrust the ends apart. The strength that is peculiar to a true arch or truss is only required when the ends are prevented from becoming further apart. Using cadaver specimens it was demonstrated that tension in the aponeurosis upon dorsiflexion of the toes at the MPJs made the foot act like a truss during different periods of the gait cycle. Applying the same concept, Arangio et al.15 investigated the foot’s loadbearing characteristics using a two-dimensional biomechanical model, consisting of a two-bar linkage and a Kelvin body or spring depicting the plantar aponeurosis, which mathematically predicted and simulated a 17% decrease in arch height without the spring. This alludes to the plantar aponeurosis’s role in augmenting the truss mechanism when placed under tension. Both studies only examined the foot in a static situation using models rather than a dynamic human foot, but they were able to objectively illustrate that tension exists in the aponeurosis when the foot is weightbearing to maintain arch integrity, thereby acting like a ‘tie-rod’. Several other in vitro studies support the notion of the plantar aponeurosis as a significant contributor to arch integrity during simulations of static stance. Huang et al.16 found that the plantar fascia gave the most substantial contribution to arch stability, reporting that its division decreased arch stiffness by 25%. Specimens were vertically loaded and structures presumed to give significant support (such as long and short plantar ligaments, spring ligament and plantar fascia) were sequentially sectioned and displacement directly measured with a potentiometer. Thordarson17 evaluated the effects of sectioning the plantar fascia alone and observed a consistent decrease in arch height, an increase in arch length and forefoot abduction with internal rotation of the navicular after sectioning; suggesting that an element of foot instability would accompany plantar fascia sectioning. Murphy18 discovered that a complete release The Foot (1999) 9, 73–78
of the plantar fascia caused a 62–100% collapse in the medial and lateral longitudinal arches, compared with a partial release. This indicates a greatly diminished tie-rod function of the aponeurosis after sectioning. An axial loading system was used to measure displacement in transverse, sagittal and frontal planes after 16 metal markers were embedded in each specimen allowing radiographic imaging and monitoring of displacement. The testing techniques in all of the in vitro studies presented permit a more controlled setting in which to study the mechanical behaviour of the foot under simulated conditions found in static stance. However, these factors obviously still fail to address the contribution of other elements to arch integrity in the living, dynamic foot, elements such as intrinsic or extrinsic muscular activity. The foot in gait presents an entirely different picture of the amount and timing of aponeurosis tension.19 The tie-rod function of the plantar aponeurosis may be greatly altered in the preserved cadaver specimen compared with the living foot. Other authors have regarded the plantar aponeurosis’s role in a similar fashion to the tie-rod component in an arciform structure. Viel and Esnault20 likened the aponeurosis to the central cable or hypozomata of a Greek boat, which served to create compression forces on parts of the hull upon cable tightening to ensure solidity. They mimicked this action by passively dorsiflexing live subjects’ toes and noting a visual tightening of the plantar aponeurosis. Bartold10 and Schepsis et al.21 compared the foot’s medial longitudinal arch to an archer’s bow and the aponeurosis as the bowstring, explaining that vertical loading (as that which occurs in quiet standing) ‘straightens’ the bow and ‘tightens’ the bowstring, which aims to preserve the bow’s structure. Perry22 describes the aponeurosis as a simple, broad, nonelastic strap that is able to immediately transfer tension from one end to the other, especially upon MPJ dorsiflexion, by virtue of its attachments and its dense composition. All of the conceptualizations mentioned above are based on Hicks14 in expressing the foot as being constructed in a truss-like arciform manner and responding accordingly with aponeurotic tension upon loading to sustain arch integrity. Sarrafian23 instead compared the foot to a twisted rectangular plate, demonstrating that the ‘the transition induced by the twist creates the transverse and longitudinal arches’. This analogy allows for the activation of the ‘truss’ mechanism, hence aponeurosis tightening, at different periods during the gait cycle, augmented or hindered by the foot ‘twisting’ and ‘untwisting’ which represents forefoot pronation and supination to elevate or depress the medial longitudinal arch. The foot is thus capable of remodeling itself throughout gait because of the added element of torque not previously accounted for in the ‘truss’ and ‘tie-rod’ analogy. © 1999 Harcourt Brace & Co. Ltd
Function of the plantar fascia Kogler et al.19 quantified the strain in the plantar aponeurosis using cadaver specimens and five different foot orthotic devices, including the functional foot orthosis (FFO) pioneered by Root et al.24 (1977) and the University of California Biomechanics Laboratory Shoe Insert (UCBL). Their aim was to discover which device significantly decreased aponeurotic strain upon vertical loading. The hypothesis was that if an orthotic device serves to effectively support the longitudinal arches of the foot, soft tissue strain would be minimized. If the plantar aponeurosis does function as a tie-rod to a truss, the authors state that tension would increase as the shorter posterior strut, consisting of the talus and calcaneus, is elevated as this would shorten the distance between the ends of the struts. However, the UCBL device (with its noticeably higher medial arch height and deeper heel cup compared to the FFO) contributed the most significant decrease in aponeurotic strain, while elevating the medial longitudinal arch. Kogler et al.19 suggest that this result came about because of the ‘deactivation’ of the truss mechanism and a redirection of load from the aponeurosis to the osseous structures, located at the apex of the medial longitudinal arch, due to the UCBL’s ability to stabilize these apical structures. This was considered to be in concordance with the ‘twisted plate’ analogy of Sarrafian,23 in that the arch support region of the orthosis resembles the twisted plate model and the orthosis allowed for the deactivation of the ‘truss’ mechanism in decreasing aponeurotic strain. The authors19 concede that the study’s static conditions did not account for the changes in amount and timing of aponeurotic tension present in the live, dynamic foot and how an orthosis might respond to these changes and thus the usefulness of their results may be questioned in a clinical setting. The mechanism whereby a foot orthosis serves to alleviate foot symptoms is still a controversial area of debate.25–27 A recent clinical study supports the findings of decreased plantar aponeurosis strain with the suppression of the truss mechanism and a change in the foot’s load transmission patterns. Bartold28 evaluated the outcome of using FFOs, taping, medial rearfoot wedging to invert the calcaneus or lateral forefoot wedging on relieving clinical symptoms in plantar fascial injury, with only taping and lateral wedging groups to report significantly reduced pain scores. Similar findings were reported in Kogler et al.29 with the use of lateral forefoot wedging found to significantly reduce aponeurotic strain in cadaver specimens. Both studies contend that the alteration in load transmission, from soft tissue to bony structures, is brought about by the initiation of different support mechanisms attributed to the inclined plane introduced by lateral wedging. Kogler et al.29 go further into suggesting that calcaneocuboid joint locking enabled a greater proportion of load to be shifted away from the aponeurosis. Relatively few studies have investigated the dynamic role of the plantar aponeurosis in vivo due to the © 1999 Harcourt Brace & Co. Ltd
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comparative difficulty in acquiring accurate, reproducible, quantitative data due to the invasive nature of the methodology used to obtain it.30 Thordarson et al.31 point out that no in vivo data depicting tension in musculo-tendinous structures during normal gait existed, so reports have sought to infer conclusions from the in vitro methods. Thordarson et al.31 employed this methodology in evaluating the effect of the plantar aponeurosis and other structures during stance and their contribution to dynamic support. They reported that the aponeurosis contributed the most significant arch support in the sagittal plane, demonstrated by maximally dorsiflexing the digits at the MPJs and presupposedly eliciting tension in the aponeurosis (which wasn’t measured) to resist sagittal plane displacement. Kitaoka et al.30 investigated the change in position of the calcaneus, talus, navicular and first metatarsal in three body planes after fasciotomy in intact and ‘destabilized’ feet, with more ligamentous structures sectioned in the latter. They found that displacement changes were more prominent in the ‘destabilized’ feet, implying that the plantar fascia has a significant role as an arch stabilizer. A slightly more recent study by Kitaoka et al.32 defined the contribution of the plantar fascia to arch stability, among other ligamentous structures, as significant in terms of affecting talar-tibial position when sectioned. All of these studies support the contention that the plantar fascia is important for arch integrity and dynamic support. This holds clinical relevance to the assessment of plantar aponeurosis function and pathology in that surgical intervention may lead to further static and dynamic dysfunction, alluded to by several authors.1,15,16,33,34 In spite of the paucity of recent research concerning the plantar aponeurosis’s role in vivo, viewpoints from a clinical perspective have been made with regard to its role during gait. Payne and Dananberg35 proposed a theory of foot function with clinical implications in which the foot is modelled as a sagittal plane pivotal site which the body’s centre of mass is permitted to move forward over during the single support phase of gait. The centre of sagittal plane motion is defined as the first MPJ, for it is directly associated with forward propulsion, being at the interface between the body and the ground. Motion enhancement and a subsequent transfer of normal weight flow is facilitated by three autosupportive mechanisms, activated at certain periods in gait, that serve to resist the forces applied during gait. These mechanisms are thought to rely heavily on adequate first MPJ dorsiflexion, earlier confirmed to have an arch-augmenting effect in static and dynamic roles, and associated secondary tension in the aponeurosis. The first autosupportive mechanism, calcaneocuboid locking,36,37 depends on a transfer of weight flow from the lateral aspect of the forefoot to the medial aspect which induces aponeurotic tension just prior to heel lift. Compressive forces applied across the foot, from activation of the ‘truss’ mechanism upon The Foot (1999) 9, 73–78
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aponeurotic tension, packs the cuboid closely into calcaneus, thus ‘locking’ creating stability in the midtarsal joint complex. This mechanism was implicated by Kogler et al.29 as the maneouvre responsible for redirecting load away from the aponeurosis, substituting a lateral forefoot wedge for the action of the plantar aponeurosis. The second autosupportive mechanism, the locking wedge effect, relies on activation of the ‘truss’ mechanism to maintain internal stability when weight flow is transferred from the heel to the forefoot.37 Compressive loading of the bones occurs as a response from the opposing ground reaction forces, specifically when the metatarsal shafts begin to change their orientation from horizontal to vertical, during single support phase. The tie-rod function of the aponeurosis thus helps to stabilize the central midfoot structures in preparation for propulsion. Hicks38 first described the third autosupportive mechanism, the windlass mechanism. Passive dorsiflexion of the hallux caused the medial longitudinal arch to rise, the rearfoot to supinate, the leg to externally rotate and the plantar aponeurosis to become more tense. This was verified by several authors demonstrating passive hallux dorsiflexion on live subjects in static stance.23,39,40 This phenomenon was likened to the winding of a cable (plantar aponeurosis) around the drum of a windlass (first MPJ) by pulling a handle (proximal phalanx of the hallux). Hicks38 tested this mechanism on a living foot and a cadaver specimen and found that all the effects were present on both, verifying that the windlass mechanism operated independently of muscular activity. In addition, an in vitro study by Thordarson et al.41 confirmed the loss of the windlass mechanism after complete plantar fascial release, indicating the significance of the plantar aponeurosis in establishing this mechanism. The windlass mechanism occurs in gait during toeoff,37 as the last component of sagittal plane motion enhancement. Upon hallux dorsiflexion, the distance between the origin and insertion of the aponeurosis is shortened, thus creating aponeurotic tension and osseous compression, resulting in supination of the foot and external rotation of the leg enabling the foot’s progression to swing phase. The function of the windlass mechanism, apart from augmenting medial arch height and creating stability, is to coordinate the external rotation of the lower leg with external rotation of the pelvis and upper thigh.35,37 Only one in vivo study was found to have investigated the role of the windlass mechanism in normal gait. Kappel-Bargas et al.40 investigated the effect of passive hallux dorsiflexion and rearfoot motion during gait on the height of the medial longitudinal arch in subjects without lower extremity pathology and with greater than 90° of first MPJ range of motion. After placing reflective markers on osseous landmarks in the right foot only, passively dorsiflexing the hallux and visually recording their subjects’ gait, The Foot (1999) 9, 73–78
Kappel-Bargas et al.40 were able to quantitatively conclude that arch height increased with hallux dorsiflexion. In addition, they identified two distinct subject populations, labelled immediate-onset and delayedonset, according to the timing of first MPJ dorsiflexion representing the initiation of the windlass mechanism. The delayed-onset group was found to exhibit more rearfoot inversion at heel strike and a greater, more prolonged rearfoot eversion for the rest of the gait cycle. Muscular activity that may potentially augment arch height was accounted for, with monitoring using electrodes and compulsory repetition of hallux dorsiflexion or gait carried out when muscle contraction was evident, in an attempt to independently analyse the windlass mechanism.
INDICATIONS FOR FURTHER RESEARCH Excessive rearfoot eversion has been linked to pathology in the lower extremity,42 particularly overuse injuries such as plantar fasciitis.8 The aetiology of plantar fasciitis has traditionally been attributed to excessive strain in the plantar aponeurosis, producing symptoms of pain on the medial calcaneal tubercle and medial longitudinal arch, especially upon dorsiflexion of the toes at the MPJs. But plantar fasciitis is also observed to occur in those with high-arched feet and obviously less rearfoot eversion. Understanding the role of the plantar aponeurosis during gait in those with plantar fascial injury is therefore essential to determine appropriate, conservative treatment interventions with regards to plantar fascial injury and may help to elucidate the mechanism of how orthotic devices work in pathological feet to relieve symptoms. Other indications for further research include the role of the windlass mechanism in those with pes planus or a higher degree of rearfoot and/or forefoot pronation. Traditionally,24 excessive subtalar joint pronation has been associated with an ineffective windlass mechanism. The pronated foot is unable to resist the forces applied during gait and therefore unable to create compressive midfoot stability through aponeurotic tightening, which may result in hypermobility and pathology associated with a pronated foot. A recent theoretical approach35,37 suggests that a limitation of motion (structural or functional) at the first MPJ will prevent the windlass mechanism being established and subsequently cause an excessively pronated foot. Further research is necessary to definitively apply biomechanical theory to the clinical setting with regards to the role of the windlass mechanism in normal and pathological feet.
CONCLUSIONS A review of the anatomy and biomechanical considerations pertaining to the plantar aponeurosis has © 1999 Harcourt Brace & Co. Ltd
Function of the plantar fascia been presented and its role in static stance and dynamic function explored in cadaver specimens and in vivo. The plantar aponeurosis can be said to have a ‘tie-rod’ function to the foot’s twisted osteoligamentous plate structure, activating a ‘truss’ mechanism upon tightening to generate compressive forces for greater internal osseous stability. It can be seen that there exists a necessity for research of the aponeurosis in all aspects of dynamic function, to complement the theoretical implications made on studies using in vitro methodology. Based on the evaluation of literature presented, the role of the aponeurosis in the weightbearing foot would be greatly clarified when research can conclusively demonstrate the foot’s response to a given load, both in static and dynamic situations. The mechanism whereby orthotic devices give symptomatic relief, whether by motion control or facilitation of load transmission, would also shed light on the function of the aponeurosis. The importance of the windlass mechanism as an arch-augmenting phenomenon to encourage foot stability in gait, its relationship to rearfoot eversion and its role in the pronated or planus foot would also benefit from further research. REFERENCES 1. Kitaoka HB, Luo ZP, Growney ES, Berglund BS, An KN: Material properties of the plantar aponeurosis. Foot and Ankle International 1994; 15(10): 557–560. 2. Marieb EN: Human Anatomy and Physiology. 3rd ed. California, The Benjamin/Cummings Publishing Company, Inc. 1995 3. Pontious J, Flanigan KP, Hillstrom HJ: Role of the plantar fascia in digital stabilization: a case report. Journal of the American Podiatric Association 1995; 86(1): 43–47. 4. Kogler GF, Solomonidis SE, Paul JP: Biomechanics of longitudinal arch support mechanisms in foot orthoses and their effect on plantar aponeurosis strain. Clinical Biomechanics 1996; 11(5): 243–252. 5. Sarrafian SK: Retaining Systems and Compartments. In: Sarrafian S K (ed) Anatomy of the Foot and Ankle: Descriptive, Topographic, Functional. 3rd ed. Philadelphia, J.B. Lipincott Company, 1993; 113–158. 6. Moore KL: Clinically Oriented Anatomy. 3rd ed. Baltimore, Williams & Wilkins, 1992 7. Schepsis AA, Leach RE, Gorzyca J: Plantar fasciitis: etiology, treatment, surgical results and review of the literature. Clinical Orthopaedics and Related Research 1991; 266: 185–196. 8. Wernick J: Plantar fasciitis: a different time and a different place. Podiatry Management 1998; 17(3) 129–134. 9. Mitchell IR, Meyer C, Krueger WA: Deep fascia of the foot: anatomical and clinical considerations. Journal of the American Podiatric Association 1991; 81(7): 373–378. 10. Bartold S: Conservative management of plantar fasciitis. Australian Podiatrist 1993; 27: 46–50 11. Salman S: Muscles. In: Williams P L (ed) Gray’s Anatomy 38th ed. Edinburgh, Churchill Livingstone, 1995; 891–892. 12. Bojsen-Moller F, Flagstad KE: Plantar aponeurosis and internal architecture of the ball of the foot. Journal of Anatomy 1976; 121(3): 599–611. 13. Wright DG, Rennels DC: A study of the elastic properties of plantar fascia. Journal of Bone and Joint Surgery 1964; 46-A (3): 482–492. 14. Hicks JH: The foot as a support. Acta Anatomica 1955; 25: 34–45. 15. Arangio GA, Chen C, Kim W: Effect of cutting the plantar fascia on mechanical properties of the foot. Clinical Orthopaedics and Related Research 1997; 339: 227–231.
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16. Huang CK, Kitaoka HB, An KN, Chao EYS: Biomechanical evaluation of longitudinal arch stability. Foot and Ankle International 1993; 14(6): 353–357. 17. Thordarson DB, Kumar PJ, Hedman TP, Ebramzadeh E: Effect of partial versus complete plantar fasciotomy on the windlass mechanism. Foot and Ankle International 1997; 18(1): 16–20. 18. Murphy GA, Pneumaticos SG, Kamaric E, Noble PC, Trevino SG, Baxter D E: Biomechanical consequences of plantar fascia release. Foot and Ankle International 1998; 19(3): 149–152. 19. Kogler GF, Solomonidis SE, Paul JP: Biomechanics of longitudinal arch support mechanisms in foot orthoses and their effect on plantar aponeurosis strain. Clinical Biomechanics 1996; 11(5): 243–252. 20. Viel E, Esnault M: The effect of increased tension in the plantar fascia: a biomechanical analysis. Physiotherapy Practice 1989; 5(2): 69–73. 21. Schepsis AA, Leach RE, Gorzyca J: Plantar fasciitis: etiology, treatment, surgical results and review of the literature. Clinical Orthopaedics and Related Research 1991; 266: 185–196. 22. Perry J: Anatomy and biomechanics of the hindfoot. Clinical Orthopaedics and Related Research 1993; 177: 9–15. 23. Sarrafian SK: Functional characteristics of the foot and plantar aponeurosis under tibiotalar loading. Foot and Ankle 1987; 8(1): 4–18. 24. Root ML, Orien WP, Weed JH: Normal and Abnormal Function of the Foot. Vol. II. Los Angeles, Clinical Biomechanics Corporation, 1977 25. Kilmartin TE, Wallace WA: The scientific basis for the use of foot orthoses in the treatment of lower limb sports injuries: a review of the literature. British Journal of Sports Medicine 1994; 28: 180–186. 26. Landorf KB, Keenan AM: Efficacy of foot orthoses: what does the literature tell us? Australasian Journal of Podiatric Medicine 1998; 32(3) 105–113 27. Payne CB: The Past, present, and future of podiatric biomechanics. Journal of the American Podiatric Medical Association 1998; 88(2) 53–63 28. Bartold S: The Biomechanics of Plantar Fascial Injury: Calcaneal Inversion Does Not Reduce Plantar Fascial Strain. Book of Abstracts from the 18th Australian Podiatry Conference, 1998. 29. Kogler GF, Veer FB, Solomonidis SE, Paul JP: The Influence of Medial and Lateral Orthotic Wedges on Loading of the Plantar Aponeurosis. Book of Abstracts from the 9th World Congress of the International Society For Prosthetics And Orthotics 1998; 579–581. 30. Kitaoka HB, Ahn TK, Luo ZP, An KN: Stability of the arch of the foot. Foot and Ankle International 1997; 18(10): 644–648. 31. Thordarson DB, Schmotzer H, Chon J, Peters J: Dynamic support of the human longitudinal arch. Clinical Orthopaedics and Related Research 1995; 316: 165–172. 32. Kitaoka HB, Luo ZP, An KN: Mechanical behaviour of the foot and ankle after plantar fascia release in the unstable foot. Foot and Ankle International 1997; 18(1): 8–15. 33. Daly PJ, Kitaoka HB, Chao EYS: Plantar fasciotomy for intractable plantar fasciitis: clinical results and biomechanical evaluation. Foot and Ankle 1992; 13(4): 188–195. 34. Murphy GA, Pneumaticos SG, Kamaric E, Noble PC, Trevino SG, Baxter DE: Biomechanical consequences of plantar fascia release. Foot and Ankle International 1998; 19(3): 149–152. 35. Payne C, Dananberg H: Sagittal plane facilitation of the foot. Australasian Journal of Podiatric Medicine 1997; 31(1): 7–11. 36. Bojsen-Moller F: Calcaneocuboid joint and stability of the longitudinal arch of the foot at high and low gear push off. Journal of Anatomy 1979; 129(1): 165–176. 37. Dananberg H: Gait style as an etiology to chronic postural pain: part I – functional hallux limitus. Journal of the American Podiatric Medical Association 1993; 83 (8): 433–441. 38. Hicks JH: The mechanics of the foot: part II – the plantar aponeurosis and the arch. Journal of Anatomy 1954; 88: 25–31.
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39. Viel E, Esnault M: The effect of increased tension in the plantar fascia: a biomechanical analysis. Physiotherapy Practice 1989; 5 (2): 69–73. 40. Kappel-Bargas A, Woolf RD, Cornwall MW, McPoil TG: The windlass mechanism during normal walking and passive first metatarsophalangeal joint motion. Clinical Biomechanics 1996; 13 (3): 190–194.
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41. Thordarson DB, Kumar PJ, Hedman TP, Ebramzadeh E: Effect of partial versus complete plantar fasciotomy on the windlass mechanism. Foot and Ankle International 1997; 18(1): 16–20. 42. Hintermann B, Nigg BM: Pronation in runners – implications for injuries. Sports Medicine 1998; 26(3): 169–176
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