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Evaluating Plantar Fascia Strain in Hyperpronating Cadaveric Feet Following an Extra-osseous Talotarsal Stabilization Procedure
The Journal of Foot & Ankle Surgery 50 (2011) 682–686
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Evaluating Plantar Fascia Strain in Hyperpronating Cadaveric Feet Following an Extra-osseous Talotarsal Stabilization Procedure Michael E. Graham, DPM, FACFAS 1, Nikhil T. Jawrani, MS 2, Vijay K. Goel, PhD 3 1
Director, Graham International Implant Institute, Macomb, MI Research Assistant, Graham International Implant Institute, Macomb, MI 3 Distinguished University Professor, Endowed Chair and McMaster-Gardner Professor of Orthopaedic Bioengineering, Co-Director, Engineering Center for Orthopaedic Research Excellence (E-CORE), Departments of Bioengineering and Orthopaedic Surgery, University of Toledo Colleges of Engineering and Medicine, Toledo, OH 2
a r t i c l e i n f o
a b s t r a c t
Level of Clinical Evidence: 5 Keywords: biomechanics hyperpronation plantar fasciitis strain talotarsal instability
Abnormal talotarsal joint mechanics leading to hyperpronation is implicated as one of the most common causes of plantar fasciopathy. In patients with hyperpronating feet, the plantar fascia experiences excessive tensile forces during static and dynamic weight-bearing activities because of excessive medial longitudinal arch depression. For the purposes of this study, we hypothesized that plantar fascia strain in hyperpronating cadaveric feet would decrease after intervention with an extra-osseous talotarsal stabilization (EOTTS) device. A miniature differential variable reluctance transducer was used to quantify the plantar fascia strain in 6 freshfrozen cadaver foot specimens exhibiting flexible instability of the talotarsal joint complex (i.e., hyperpronation). The strain was measured as the foot was moved from its neutral to maximally pronated position, before and after intervention using the HyProCureÒ EOTTS device. The mean plantar fascia elongation was 0.83 0.27 mm (strain 3.62% 1.17%) and 0.56 0.2 mm (strain 2.42% 0.88%) before and after intervention, respectively (N ¼ 18, variation reported is 1 SD). The average plantar fascia strain decreased by 33%, and the difference was statistically significant with p < .001. From this cadaveric experiment, the reduction in plantar fascia strain suggests that an EOTTS device might be effective in stabilizing the pathologic talotarsal joint complex and the medial longitudinal arch and in eliminating hyperpronation. An EOTTS procedure might offer a possible treatment option for plantar fasciopathy in cases in which the underlying etiology is abnormal talotarsal biomechanics. Ó 2011 by the American College of Foot and Ankle Surgeons. All rights reserved.
Plantar fasciitis, or plantar fasciopathy, is one of the most common causes of pain along the plantar aspect of the foot. The etiology of plantar fasciopathy is broadly classified under the following 3 categories: mechanical, degenerative, and systemic (1–5). It is generally accepted by the medical community that plantar fasciopathy is most often caused by an underlying mechanical etiology (1,2). However, this remains open to debate, as mentioned by Wearing et al (6). Theoretically, abnormal talotarsal joint mechanics leading to hyperpronation results in lowering of the medial longitudinal arch, which places excessive tensile strain on the plantar fascia, eventually leading to microscopic tears and inflammation (7–14). Thus, patients with Financial Disclosure: This research study was funded by GraMedica, LLC (Macomb, MI). Conflict of Interest: Michael E. Graham is the inventor of HyProCureÒ. He is the Founder and President of GraMedica, LLC, the company that manufactures and distributes HyProCureÒ. He is also the Founder of Graham International Implant Institute. Address correspondence to: Michael E. Graham, DPM, FACFAS, Graham International Implant Institute, 16137 Leone Drive, Macomb, MI 48042. E-mail address: [email protected] (M.E. Graham).
hyperpronating feet are at a high risk of acquiring plantar fasciopathy because with each weight-bearing step the plantar fascia experiences excessive abnormal tensile strain (2,15–22). Depending on the underlying etiology, different treatment options have been suggested for managing plantar fasciopathy. In cases in which mechanical etiology is identified as the main cause, it is recommended that the treatment should focus on both a short- and long-term solution (2). The short-term goals should primarily focus on reducing plantar fascia inflammation and the long-term goals should focus on reducing excessive plantar fascia strain caused by hyperpronation, considered 1 of the most common causes of plantar fasciopathy (1,2). Nonoperative treatment modalities such as modified footwear, foot orthoses, foot strapping, orthotic wedges, and so forth have been used to reduce the amount of hyperpronation and have been indicated for the long-term treatment of plantar fasciopathy (2,10,12,23–26). The basic premise for the use of these modalities has been that they provide support to the medial longitudinal arch in the hyperpronated foot and hence reduce plantar fascia strain during static and dynamic weight-bearing activities (27). To evaluate the efficacy of various types of foot orthoses and orthotic wedge
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M.E. Graham et al. / The Journal of Foot & Ankle Surgery 50 (2011) 682–686
combinations for the treatment of plantar fasciitis, Kogler et al (28– 30) measured plantar fascia strain in human adult cadaver foot specimens before and after treatment with various combinations of orthotic support devices and under different load bearing conditions. They concluded that certain types of foot orthoses and orthotic wedge combinations were more effective than others in supporting the foot’s medial longitudinal arch and reducing plantar fascia strain (28–30). The extra-osseous talotarsal stabilization (EOTTS) procedure involves the placement of a device into the sinus tarsi for the treatment of hyperpronation and its associated pathologic features. Clinical research studies, in the pediatric and adult population, have shown that EOTTS devices are successful in the treatment of flatfeet and posterior tibial tendon dysfunction, both of which are associated with hyperpronation (31–35). However, limited scientific studies have been conducted to evaluate the biomechanical effects of these devices on the soft tissue structures supporting the foot and ankle joint complex. Because hyperpronation causes excessive tensile strain to the plantar fascia, and EOTTS devices are indicated for the treatment of hyperpronation, our goal was to experimentally evaluate the efficacy of such devices in reducing plantar fascia strain. For the purposes of this study, we hypothesized that strain on the plantar fascia in hyperpronating cadaveric feet would decrease after placement of the HyProCureÒ (GraMedica, Macomb, MI) EOTTS device. It is our ultimate goal to understand the biomechanics of EOTTS devices in the treatment of pathologies related to flexible talotarsal joint instability and hyperpronation. A complete understanding of the biomechanical functioning of these devices is required to appreciate their advantages and understand any possible adverse effects. Materials and Methods Plantar fascia elongation (strain) was measured in 6 fresh-frozen human adult cadaver foot specimens (all female). Each specimen consisted of the foot, ankle, and distal segment of the leg (approximately 20 cm proximal to the ankle joint). All specimens were inspected for their range of motion at the ankle joint complex. The investigating surgeon clinically determined that each of these specimens exhibited hyperpronation (i.e., flexible instability of the talotarsal joint complex). The exclusion criteria for the specimens included previous operative intervention, fracture or pathologic conditions in the ankle-hindfoot complex such as tarsal coalition, or arthritic degeneration of the midfoot and hindfoot joints. The specimens were adequately thawed to room temperature before testing. Each specimen was dissected free of the soft tissue at the proximal tibial and fibular segment. The proximal segment of the leg was potted using polymethylmethacryalte for mounting in the testing fixture. Care was taken to avoid damage to the soft tissue structures of the foot and ankle joint complex. The plantar fascia was exposed by blunt dissection on the medial plantar aspect of the foot for placement of an elongation measuring device (Fig. 1). The technique and instrumentation described previously by Kogler et al (28) and Alshami et al (36) were used in the present study to measure elongation of the plantar fascia. A differential variable reluctance transducer (DVRTÒ, Microstrain, Williston, VT) with a 9-mm linear stroke range and a resolution of 1.5 mm was used. The output voltage of the DVRTÒ was amplified using a DEMOD-DVRT signal processor (Microstrain) and recorded using the MB-SMT 4 motherboard with data acquisition software (Microstrain). Using the calibration equation provided by the manufacturer, the output voltage (in volts) was converted to displacement (in millimeters). With the foot in the neutral position (neither pronated nor supinated), the DVRTÒ was inserted in the plantar fascia with the help of a needle and barbed pins (Fig. 1). In contrast to the study by Kogler et al (28–30) in which the DVRTÒ was placed in the central band of the plantar fascia, in the present investigation, we placed the DVRTÒ just distal to the origin of the plantar fascia (i.e., the medial calcaneal tuberosity). We chose this setup because the most frequently reported site of pain and failure is the origin of the plantar fascia on the calcaneus (1,2). With the foot held in a neutral position, the DVRTÒ output voltage was recorded to calculate the length between the needle and barbed pin; this was denoted as the reference or the initial length (Lo). Next, the investigator pronated the foot maximally by applying a vertical and abductory force under the fourth and fifth metatarsal head. The foot was held in this position, and the change in the DVRTÒ voltage was recorded after allowing the reading to equilibrate for approximately 15 seconds. This voltage change was converted to a change in length (DL, elongation of the plantar fascia) to yield the final length between the 2 pins (L ¼ Lo þ DL). The percentage of strain was calculated as (DL/ Lo 100). The foot was then unloaded
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Fig. 1. Plantar fascia with differential variable reluctance transducer. Image of left footed specimen mounted on the materials testing system (not shown) with foot in neutral position and differential variable reluctance transducer mounted on plantar fascia, as described in “Materials and Methods” section. Output of differential variable reluctance transducer was recorded in this position to give initial or reference length, after which the foot was maximally pronated and the differential variable reluctance transducer output was recorded to calculate the elongation (strain) of the plantar fascia.
back to its neutral position, and the procedure was repeated 3 times (i.e., N ¼ 3 for each foot without intervention). Note, that the strain or elongation measured is a relative value (i.e., relative with respect to the foot in a neutral position, neither pronated nor supinated). After these measurements, the appropriate size EOTTS device was placed into the sinus tarsi of the cadaveric foot to stabilize the talus on the tarsal mechanism while also ensuring that the normal range of pronation and supination was possible. Trial sizing was performed to determine which size would give the best correction. The 5-mm trial sizer (smallest) was inserted into both the canalis and the sinus portions of the sinus tarsi. The talotarsal joint was then placed through a full range of motion to determine the amount of correction achieved. The goal was to restore the normal range of hindfoot pronation (i.e., 3 to 5 ). If excessive hindfoot motion was present with the 5-mm size, the next incremental trial sizer (available in 1-mm increments 10 mm) was used, and the new range of hindfoot motion was determined. This procedure was repeated until the desired trial sizer achieved the required amount of correction, after which the corresponding size EOTTS device was implanted. Next, elongation of the plantar fascia was measured after maximally pronating the foot, as described (again, N ¼ 3 for each foot with intervention). Throughout the experiment, the investigator was unaware of the output of the DVRTÒ.
Statistical Analysis The data are reported as the mean, median, range, standard deviation ( 1 SD), and 95% confidence interval of the mean of the elongation (in millimeters) and strain (in percentages) for each experimental condition (i.e., without and with intervention) and for each of the 6 foot specimens. The hypothesis tested was that in cadaveric feet exhibiting flexible talotarsal joint instability, elongation (strain) of the plantar fascia would decrease after an EOTTS procedure (Ha: mEOTTS Device < mNo Treatment). Because of the small sample size and assuming a non-normally distributed data set, a one-tailed Wilcoxon signed rank test for 2 groups was computed to test for significance at the 95% confidence level. The null hypothesis of no difference was rejected for p values .05.
Results As previously reported, a consistent load was applied by the investigator under the fourth and fifth metatarsal head while maximally pronating the foot (37). For each of the 6 foot specimens, the relative elongation measured in the plantar fascia as the foot was moved from its neutral to its maximally pronated position, without and with intervention, is listed in the Table 1. The mean elongation of the plantar fascia was 0.83 0.27 mm (strain 3.62%) and 0.56 0.2 mm (strain 2.42%) without and with intervention, respectively (N ¼ 18). The corresponding median values of plantar fascia elongation were 0.78 (range 0.41 to 1.4) mm and 0.51 (range 0.17 to 0.85) mm, without and with intervention, respectively. The 2 groups were significantly different statistically, with p < .001 (Fig. 2).
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Table 1 Plantar fascia strain data (N ¼ 3 for each reported data value) Specimen No.
1 2 3 4 5 6 Grand mean SD Median Range 95% CI
Elongation (mm)
Strain (%)
Reduction in Elongation (%)
Without HyProCureÒ
With HyProCureÒ
Without HyProCureÒ
With HyProCureÒ
0.71 0.64 0.97 1.26 0.72 0.68 0.83 0.27 0.78 0.41–1.4 0.71–0.96
0.64 0.36 0.79 0.73 0.40 0.42 0.56 0.20 0.51 0.17–0.85 0.46–0.65
3.05 2.98 4.28 5.44 2.87 3.07 3.62 1.17 3.44 1.85–6.08 3.08–4.16
2.79 1.67 3.46 3.11 1.60 1.87 2.42 0.88 2.29 0.78–3.76 2.01–2.83
9.5 44.3 18.9 41.9 44.5 38.8 32.5 34.6 9.5–44.5 21.0–53.9
Abbreviations: CI, confidence interval; SD, standard deviation.
Discussion The plantar fascia, also known as the plantar aponeurosis, is a tough, fibrous layer on the plantar aspect of the foot. From a biomechanical perspective, it not only provides support and stability to the medial longitudinal arch, but also plays a very important role during static and dynamic weight-bearing activities of the foot (38,39). During standing and in the initial stance phase of the gait cycle (from heel-strike to mid-stance), the foot assumes a pronated position as it tries to adapt to the underlying surface. As the body weight is transmitted onto the weight-bearing surface below, the medial longitudinal arch is lowered and the plantar fascia experiences tensile forces as it tries to maintain a high arch (40–43). Second, the plantar fascia plays a very important role from the mid stance to the toe off phase of the stance phase of the gait cycle. During terminal stance, the toes passively dorsiflex and lead to shortening (tightening) of the plantar fascia and elevation of the medial longitudinal arch. At this point, the plantar fascia assists in supination of the foot, and this entire mechanism has been compared to a windlass (2,40). Plantar fasciopathy is one of the most common foot and ankle pathologies for which patients seek medical attention (28). Although the etiology of plantar fasciopathy is considered to be multifactorial, it is generally agreed that repetitive trauma to the plantar fascia resulting from excessive tensile forces at its origin is the most common cause of this condition (1,44,45). It is primarily considered an overuse injury and is common among athletes and those with a predisposition to hyperpronate (2,45). Excessive abnormal loading of the plantar fascia resulting from hyperpronation leads to
Fig. 2. Representation of elongation data showing mean plantar fascia elongation of hyperpronated cadaveric feet considered in this study, without and with intervention. Error bars represent 1 standard error of mean. *Significant decrease in elongation of plantar fascia after placement of extra-osseous talotarsal stabilization device.
physiologically intolerable levels of strain, which can lead to microtears, inflammation, and eventual rupture of the plantar fascia (2,7–9,11–13,16,22). The most common treatment options for plantar fasciopathy include the use of oral nonsteroidal anti-inflammatory drugs, ultrasound therapy, physical therapy, ice, and rest (1,2,44). These treatment options are aimed at reducing the pain and inflammation and help to reduce symptoms on a temporary basis. With these treatments alone, recurrence of plantar fasciopathy is a common problem in those with an underlying mechanical etiology. This is because none of these treatments correct the underlying biomechanical defect (i.e., hyperpronation) (1,2,44). Many investigators suggest the use of shoe inserts and orthoses for the long-term management of plantar fasciopathy. The hypothesis supporting the use of orthotic devices is that they reduce excessive plantar fascia strain by supporting the medial longitudinal arch and minimizing excessive and/or prolonged pronation (1,2,46). To test this hypothesis, Kogler et al (28–30) conducted a series of studies in which they evaluated the effect of different orthoses and orthotic wedge combinations on plantar fascia strain in cadaveric feet. In their initial studies, they found that under axial loading of up to 900 N, the University of California Biomechanics Laboratory shoe insert, and 2 other orthoses, significantly reduced the plantar fascia strain compared with the barefoot controls (28,29). In a later study, they also found that under similar loading conditions, orthotic wedges placed under the lateral aspect of the forefoot and rearfoot were significant in reducing plantar fascia strain (30). However, certain shortcomings of the studies by Kogler et al (28–30) are apparent. The basic premise for the use of orthotic devices in the treatment of plantar fasciopathy is that these devices support the medial longitudinal arch in the hyperpronated foot by externally controlling the range of pronation and supination. Because Kogler et al (28–30) used cadaveric specimens that were determined to be clinically and radiographically normal, it remains unclear whether orthotic devices are effective in reducing plantar fascia strain in hyperpronating feet. Additionally, they found that, in normal feet, certain orthotic devices reduce plantar fascia strain compared with the barefoot condition; this suggests that these orthotic devices might be restricting the normal range of joint motion. Limiting the normal range of joint motion has its own consequences and can hinder patients in their daily activities. Another possible area of concern with their study was that they measured strain in the plantar fascia approximately 3 cm distal to its origin. As mentioned previously, most of the cases of plantar fasciopathy report failure at its origin (47). It is, therefore, important to quantify plantar fascia strain near the most frequent location of failure. Kwong et al (2) suggest the use of a semirigid orthosis combined with the use of a firm posterior counter shoe for the longterm treatment of plantar fasciopathy. The success of orthotic treatment depends on the ability of an orthosis to control abnormal pronation. However, traditional orthotic devices fail because most of
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these devices focus only on controlling the position of the calcaneus and are uncomfortable and not well tolerated by the patients. Although the University of California Biomechanics Laboratory shoe insert has been used effectively to control pronation, it is bulkier, restricts foot motion to an extent greater than required, is more difficult to fit properly, and, eventually, results in lower patient compliance. Also, adjustments or changes to the orthotic devices are required from periodically because of changes in the orthotic material properties and loss of adequate support (2). Surgical intervention for the treatment of plantar fasciopathy has been indicated for patients in whom conservative treatments fail to alleviate the pain and symptoms (19–21,48–50). The choice of treatment for such cases has been complete or partial plantar fasciotomy (51,52). However, a number of biomechanical studies have shown that partial or complete plantar fasciotomy can lead to longterm detrimental effects on foot and ankle function (48,51,53). In particular, complete plantar fasciotomy can lead to the loss of medial longitudinal arch stability and abnormalities in the gait pattern (38). It is also speculated that fasciotomy can cause excessive abnormal pronation (48,53). Research has shown that the plantar fascia is the most important structure in terms of supporting the medial longitudinal arch and suggests against the use of plantar fasciotomy (38,48). Plantar fascia release severely affects the windlass mechanism. As mentioned previously, during toe off, the plantar fascia tightens to supinate the foot (making it a rigid structure) and elevates the medial longitudinal arch. This is important for forward propulsion of the body. After plantar fasciotomy, other soft tissue structures such as the posterior tibial tendon have to bear extra load to supinate the foot and support the medial longitudinal arch during the terminal stance phase of the gait cycle. Such excessive loading of the posterior tibial tendon can lead to its degeneration and result in additional complications. Over time, all these factors continue to increase the amount and time that the foot pronates (i.e., hyperpronation). At this point, it is important to remember that pre-existing hyperpronation is the very reason that causes plantar fasciopathy in most cases; thus, by releasing the plantar fascia, the pronation forces are further aggravated. It has been advocated that long-term relief of plantar fasciopathy should be achieved by adequate remedy of the aggravating pronation factors (i.e., stabilization of the talotarsal joint complex) (2). EOTTS devices are indicated for the stabilization of the talotarsal joint complex and have been used for the past 5 decades (33). In the present study, we showed that an EOTTS device reduces plantar fascia strain in hyperpronating cadaveric feet by 33%. This suggests stabilization of the talotarsal joint complex and additional support to the medial longitudinal arch. Furthermore, the HyProCureÒ is an innovative device owing to its design and functional characteristics and requires a minimally invasive procedure for placement in the sinus tarsi. This EOTTS device is indicated for mild to severe hyperpronation, even in cases in which there are no pain or presenting symptoms. In support of this view, Kwong et al (2) reported that patients with a predisposition to overpronate place more strain on the plantar fascia with each weight-bearing step. In such cases, the plantar fascia can adjust to each increased strain level and still be pain free. However, as the pronation deformity progresses, a particular strain level can exceed the plantar fascia’s physiologic tolerance, which is highly variable from one individual to the other. A patient with a less severely pronating foot might present with more pain than a patient with a more severely pronating foot. The pain experienced depends on the ability of the plantar fascia to accommodate physiologically tolerable levels of strain and, hence, is highly variable. Chandler and Kibler (44) also reported that if predisposing maladaptations (e.g., hyperpronation) can be identified and corrected, the initial occurrence of plantar fasciopathy can be prevented.
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Although the present biomechanical study showed a significant reduction in plantar fascia strain after an EOTTS procedure, limitations exist. First, the sample size studied was relatively small (N ¼ 6 cadaver specimens). Second, we could not compare the strain measurements obtained in this study with those from previously published work (28–30,36). This was because of the different experimental conditions and definition of the reference position against which the final strain was measured. Although the DVRTÒ technique has been used successfully to measure strain in the plantar fascia, it is limited to uniaxial measurements (28–30,36). Very recently, Clark et al (54) used foil-type microstrain gauges to measure tri-axial plantar fascia strain. However, they mentioned that calibration of these devices is difficult, and they found that plantar fascia strain is mostly longitudinal. Finally, in the present study, we showed that an EOTTS device was successful in eliminating excessive plantar fascia strain in hyperpronating cadaveric feet; however, a well designed prospective study needs to be conducted to evaluate the long-term results of such devices in the treatment of plantar fasciopathy in the adult human population. Acknowledgment We would like to thank Manoj K. Kodigudla and Vikas Kaul at the University of Toledo and Avanthi Chikka at Graham International Implant Institute for their help in arranging the experimental setup and potting of the foot specimens. References 1. Cornwall MW, McPoil TG. Plantar fasciitis: etiology and treatment. J Orthop Sports Phys Ther 29:756–760, 1999. 2. Kwong PK, Kay D, Voner RT, White MW. Plantar fasciitis: mechanics and pathomechanics of treatment. Clin Sports Med 7:119–126, 1988. 3. Bordelon RL. Subcalcaneal pain: a method of evaluation and plan for treatment. Clin Orthop Relat Res 177:49–53, 1983. 4. Leach RE, Dilorio E, Harney RA. Pathologic hindfoot conditions in the athlete. Clin Orthop Relat Res 177:116–121, 1983. 5. McBryde AM. Plantar fasciitis. Instr Course Lect 33:278–282, 1984. 6. Wearing SC, Smeathers JE, Urry SR, Hennig EM, Hills AP. The pathomechanics of plantar fasciitis. Sports Med 36:585–611, 2006. 7. Lutter LD. Pronation biomechanics in runners. Contemp Orthop 2:579, 1980. 8. Waller JF. Physiology of the foot and the biomechanics of the flexible flat foot. J Orthop Nurses Assoc 5:101–103, 1978. 9. Warren BL. Anatomical factors associated with predicting plantar fasciitis in longdistance runners. Med Sci Sports Exerc 16:60–63, 1984. 10. Kosmahl EM, Kosmahl HE. Painful plantar heel, plantar fasciitis, and calcaneal spur: etiology and treatment. J Orthop Sports Phys Ther 9:17–24, 1987. 11. Mann R, Inman VT. Phasic activity of intrinsic muscles of the foot. J Bone Joint Surg Am 46:469–481, 1964. 12. Scherer PR. Heel spur syndrome: pathomechanics and nonsurgical treatment. J Am Podiatr Med Assoc 81:68–72, 1991. 13. Shama SS, Kominsky SJ, Lemont H. Prevalence of non-painful heel spur and its relation to postural foot position. J Am Podiatr Assoc 73:122–123, 1983. 14. Schroeder BM. American College of Foot and Ankle Surgeons: the diagnosis and treatment of heel pain. Am Fam Physician 65:1686–1688, 2002. 15. Stovitz SD, Coetzee JC. Hyperpronation and foot pain: steps towards pain-free feet. Phys Sports Med 32:19–26, 2004. 16. Andrews JR. Overuse syndromes of the lower extremity. Clin Sports Med 2:137– 148, 1983. 17. Campbell JW, Inman VT. Treatment of plantar fasciitis and calcaneal spurs with the UC-BL shoe insert. Clin Orthop Relat Res 103:57–62, 1974. 18. Newell SG. Conservative treatment of plantar fascial strain. Phys Sports Med 5:68– 73, 1977. 19. Leach RE, Seavey MS, Salter DK. Results of surgery in athletes with plantar fasciitis. Foot Ankle 7:156–161, 1986. 20. Lester DK, Buchanan JR. Surgical treatment of plantar fasciitis. Clin Orthop Relat Res 186:202–204, 1984. 21. Lutter LD. Surgical decisions in athletes’ subcalcaneal pain. Am J Sports Med 14:481–485, 1986. 22. Torg JS, Pavlov H, Torg E. Overuse injuries in sport: the foot. Clin Sports Med 8:291–320, 1987. 23. Goulet MJ. Role of soft orthosis treating plantar fasciitis. Phy Ther 64:1544, 1984. 24. Riddle DL, Freeman DB. Management of a patient with a diagnosis of bilateral plantar fasciitis and Achilles tendonitis. Phys Ther 68:1913–1916, 1988.
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Evaluating Plantar Fascia Strain in Hyperpronating Cadaveric Feet Following an Extra-osseous Talotarsal Stabilization Procedure Michael E. Graham, DPM, FACFAS 1, Nikhil T. Jawrani, MS 2, Vijay K. Goel, PhD 3 1
Director, Graham International Implant Institute, Macomb, MI Research Assistant, Graham International Implant Institute, Macomb, MI 3 Distinguished University Professor, Endowed Chair and McMaster-Gardner Professor of Orthopaedic Bioengineering, Co-Director, Engineering Center for Orthopaedic Research Excellence (E-CORE), Departments of Bioengineering and Orthopaedic Surgery, University of Toledo Colleges of Engineering and Medicine, Toledo, OH 2
a r t i c l e i n f o
a b s t r a c t
Level of Clinical Evidence: 5 Keywords: biomechanics hyperpronation plantar fasciitis strain talotarsal instability
Abnormal talotarsal joint mechanics leading to hyperpronation is implicated as one of the most common causes of plantar fasciopathy. In patients with hyperpronating feet, the plantar fascia experiences excessive tensile forces during static and dynamic weight-bearing activities because of excessive medial longitudinal arch depression. For the purposes of this study, we hypothesized that plantar fascia strain in hyperpronating cadaveric feet would decrease after intervention with an extra-osseous talotarsal stabilization (EOTTS) device. A miniature differential variable reluctance transducer was used to quantify the plantar fascia strain in 6 freshfrozen cadaver foot specimens exhibiting flexible instability of the talotarsal joint complex (i.e., hyperpronation). The strain was measured as the foot was moved from its neutral to maximally pronated position, before and after intervention using the HyProCureÒ EOTTS device. The mean plantar fascia elongation was 0.83 0.27 mm (strain 3.62% 1.17%) and 0.56 0.2 mm (strain 2.42% 0.88%) before and after intervention, respectively (N ¼ 18, variation reported is 1 SD). The average plantar fascia strain decreased by 33%, and the difference was statistically significant with p < .001. From this cadaveric experiment, the reduction in plantar fascia strain suggests that an EOTTS device might be effective in stabilizing the pathologic talotarsal joint complex and the medial longitudinal arch and in eliminating hyperpronation. An EOTTS procedure might offer a possible treatment option for plantar fasciopathy in cases in which the underlying etiology is abnormal talotarsal biomechanics. Ó 2011 by the American College of Foot and Ankle Surgeons. All rights reserved.
Plantar fasciitis, or plantar fasciopathy, is one of the most common causes of pain along the plantar aspect of the foot. The etiology of plantar fasciopathy is broadly classified under the following 3 categories: mechanical, degenerative, and systemic (1–5). It is generally accepted by the medical community that plantar fasciopathy is most often caused by an underlying mechanical etiology (1,2). However, this remains open to debate, as mentioned by Wearing et al (6). Theoretically, abnormal talotarsal joint mechanics leading to hyperpronation results in lowering of the medial longitudinal arch, which places excessive tensile strain on the plantar fascia, eventually leading to microscopic tears and inflammation (7–14). Thus, patients with Financial Disclosure: This research study was funded by GraMedica, LLC (Macomb, MI). Conflict of Interest: Michael E. Graham is the inventor of HyProCureÒ. He is the Founder and President of GraMedica, LLC, the company that manufactures and distributes HyProCureÒ. He is also the Founder of Graham International Implant Institute. Address correspondence to: Michael E. Graham, DPM, FACFAS, Graham International Implant Institute, 16137 Leone Drive, Macomb, MI 48042. E-mail address: [email protected] (M.E. Graham).
hyperpronating feet are at a high risk of acquiring plantar fasciopathy because with each weight-bearing step the plantar fascia experiences excessive abnormal tensile strain (2,15–22). Depending on the underlying etiology, different treatment options have been suggested for managing plantar fasciopathy. In cases in which mechanical etiology is identified as the main cause, it is recommended that the treatment should focus on both a short- and long-term solution (2). The short-term goals should primarily focus on reducing plantar fascia inflammation and the long-term goals should focus on reducing excessive plantar fascia strain caused by hyperpronation, considered 1 of the most common causes of plantar fasciopathy (1,2). Nonoperative treatment modalities such as modified footwear, foot orthoses, foot strapping, orthotic wedges, and so forth have been used to reduce the amount of hyperpronation and have been indicated for the long-term treatment of plantar fasciopathy (2,10,12,23–26). The basic premise for the use of these modalities has been that they provide support to the medial longitudinal arch in the hyperpronated foot and hence reduce plantar fascia strain during static and dynamic weight-bearing activities (27). To evaluate the efficacy of various types of foot orthoses and orthotic wedge
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M.E. Graham et al. / The Journal of Foot & Ankle Surgery 50 (2011) 682–686
combinations for the treatment of plantar fasciitis, Kogler et al (28– 30) measured plantar fascia strain in human adult cadaver foot specimens before and after treatment with various combinations of orthotic support devices and under different load bearing conditions. They concluded that certain types of foot orthoses and orthotic wedge combinations were more effective than others in supporting the foot’s medial longitudinal arch and reducing plantar fascia strain (28–30). The extra-osseous talotarsal stabilization (EOTTS) procedure involves the placement of a device into the sinus tarsi for the treatment of hyperpronation and its associated pathologic features. Clinical research studies, in the pediatric and adult population, have shown that EOTTS devices are successful in the treatment of flatfeet and posterior tibial tendon dysfunction, both of which are associated with hyperpronation (31–35). However, limited scientific studies have been conducted to evaluate the biomechanical effects of these devices on the soft tissue structures supporting the foot and ankle joint complex. Because hyperpronation causes excessive tensile strain to the plantar fascia, and EOTTS devices are indicated for the treatment of hyperpronation, our goal was to experimentally evaluate the efficacy of such devices in reducing plantar fascia strain. For the purposes of this study, we hypothesized that strain on the plantar fascia in hyperpronating cadaveric feet would decrease after placement of the HyProCureÒ (GraMedica, Macomb, MI) EOTTS device. It is our ultimate goal to understand the biomechanics of EOTTS devices in the treatment of pathologies related to flexible talotarsal joint instability and hyperpronation. A complete understanding of the biomechanical functioning of these devices is required to appreciate their advantages and understand any possible adverse effects. Materials and Methods Plantar fascia elongation (strain) was measured in 6 fresh-frozen human adult cadaver foot specimens (all female). Each specimen consisted of the foot, ankle, and distal segment of the leg (approximately 20 cm proximal to the ankle joint). All specimens were inspected for their range of motion at the ankle joint complex. The investigating surgeon clinically determined that each of these specimens exhibited hyperpronation (i.e., flexible instability of the talotarsal joint complex). The exclusion criteria for the specimens included previous operative intervention, fracture or pathologic conditions in the ankle-hindfoot complex such as tarsal coalition, or arthritic degeneration of the midfoot and hindfoot joints. The specimens were adequately thawed to room temperature before testing. Each specimen was dissected free of the soft tissue at the proximal tibial and fibular segment. The proximal segment of the leg was potted using polymethylmethacryalte for mounting in the testing fixture. Care was taken to avoid damage to the soft tissue structures of the foot and ankle joint complex. The plantar fascia was exposed by blunt dissection on the medial plantar aspect of the foot for placement of an elongation measuring device (Fig. 1). The technique and instrumentation described previously by Kogler et al (28) and Alshami et al (36) were used in the present study to measure elongation of the plantar fascia. A differential variable reluctance transducer (DVRTÒ, Microstrain, Williston, VT) with a 9-mm linear stroke range and a resolution of 1.5 mm was used. The output voltage of the DVRTÒ was amplified using a DEMOD-DVRT signal processor (Microstrain) and recorded using the MB-SMT 4 motherboard with data acquisition software (Microstrain). Using the calibration equation provided by the manufacturer, the output voltage (in volts) was converted to displacement (in millimeters). With the foot in the neutral position (neither pronated nor supinated), the DVRTÒ was inserted in the plantar fascia with the help of a needle and barbed pins (Fig. 1). In contrast to the study by Kogler et al (28–30) in which the DVRTÒ was placed in the central band of the plantar fascia, in the present investigation, we placed the DVRTÒ just distal to the origin of the plantar fascia (i.e., the medial calcaneal tuberosity). We chose this setup because the most frequently reported site of pain and failure is the origin of the plantar fascia on the calcaneus (1,2). With the foot held in a neutral position, the DVRTÒ output voltage was recorded to calculate the length between the needle and barbed pin; this was denoted as the reference or the initial length (Lo). Next, the investigator pronated the foot maximally by applying a vertical and abductory force under the fourth and fifth metatarsal head. The foot was held in this position, and the change in the DVRTÒ voltage was recorded after allowing the reading to equilibrate for approximately 15 seconds. This voltage change was converted to a change in length (DL, elongation of the plantar fascia) to yield the final length between the 2 pins (L ¼ Lo þ DL). The percentage of strain was calculated as (DL/ Lo 100). The foot was then unloaded
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Fig. 1. Plantar fascia with differential variable reluctance transducer. Image of left footed specimen mounted on the materials testing system (not shown) with foot in neutral position and differential variable reluctance transducer mounted on plantar fascia, as described in “Materials and Methods” section. Output of differential variable reluctance transducer was recorded in this position to give initial or reference length, after which the foot was maximally pronated and the differential variable reluctance transducer output was recorded to calculate the elongation (strain) of the plantar fascia.
back to its neutral position, and the procedure was repeated 3 times (i.e., N ¼ 3 for each foot without intervention). Note, that the strain or elongation measured is a relative value (i.e., relative with respect to the foot in a neutral position, neither pronated nor supinated). After these measurements, the appropriate size EOTTS device was placed into the sinus tarsi of the cadaveric foot to stabilize the talus on the tarsal mechanism while also ensuring that the normal range of pronation and supination was possible. Trial sizing was performed to determine which size would give the best correction. The 5-mm trial sizer (smallest) was inserted into both the canalis and the sinus portions of the sinus tarsi. The talotarsal joint was then placed through a full range of motion to determine the amount of correction achieved. The goal was to restore the normal range of hindfoot pronation (i.e., 3 to 5 ). If excessive hindfoot motion was present with the 5-mm size, the next incremental trial sizer (available in 1-mm increments 10 mm) was used, and the new range of hindfoot motion was determined. This procedure was repeated until the desired trial sizer achieved the required amount of correction, after which the corresponding size EOTTS device was implanted. Next, elongation of the plantar fascia was measured after maximally pronating the foot, as described (again, N ¼ 3 for each foot with intervention). Throughout the experiment, the investigator was unaware of the output of the DVRTÒ.
Statistical Analysis The data are reported as the mean, median, range, standard deviation ( 1 SD), and 95% confidence interval of the mean of the elongation (in millimeters) and strain (in percentages) for each experimental condition (i.e., without and with intervention) and for each of the 6 foot specimens. The hypothesis tested was that in cadaveric feet exhibiting flexible talotarsal joint instability, elongation (strain) of the plantar fascia would decrease after an EOTTS procedure (Ha: mEOTTS Device < mNo Treatment). Because of the small sample size and assuming a non-normally distributed data set, a one-tailed Wilcoxon signed rank test for 2 groups was computed to test for significance at the 95% confidence level. The null hypothesis of no difference was rejected for p values .05.
Results As previously reported, a consistent load was applied by the investigator under the fourth and fifth metatarsal head while maximally pronating the foot (37). For each of the 6 foot specimens, the relative elongation measured in the plantar fascia as the foot was moved from its neutral to its maximally pronated position, without and with intervention, is listed in the Table 1. The mean elongation of the plantar fascia was 0.83 0.27 mm (strain 3.62%) and 0.56 0.2 mm (strain 2.42%) without and with intervention, respectively (N ¼ 18). The corresponding median values of plantar fascia elongation were 0.78 (range 0.41 to 1.4) mm and 0.51 (range 0.17 to 0.85) mm, without and with intervention, respectively. The 2 groups were significantly different statistically, with p < .001 (Fig. 2).
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Table 1 Plantar fascia strain data (N ¼ 3 for each reported data value) Specimen No.
1 2 3 4 5 6 Grand mean SD Median Range 95% CI
Elongation (mm)
Strain (%)
Reduction in Elongation (%)
Without HyProCureÒ
With HyProCureÒ
Without HyProCureÒ
With HyProCureÒ
0.71 0.64 0.97 1.26 0.72 0.68 0.83 0.27 0.78 0.41–1.4 0.71–0.96
0.64 0.36 0.79 0.73 0.40 0.42 0.56 0.20 0.51 0.17–0.85 0.46–0.65
3.05 2.98 4.28 5.44 2.87 3.07 3.62 1.17 3.44 1.85–6.08 3.08–4.16
2.79 1.67 3.46 3.11 1.60 1.87 2.42 0.88 2.29 0.78–3.76 2.01–2.83
9.5 44.3 18.9 41.9 44.5 38.8 32.5 34.6 9.5–44.5 21.0–53.9
Abbreviations: CI, confidence interval; SD, standard deviation.
Discussion The plantar fascia, also known as the plantar aponeurosis, is a tough, fibrous layer on the plantar aspect of the foot. From a biomechanical perspective, it not only provides support and stability to the medial longitudinal arch, but also plays a very important role during static and dynamic weight-bearing activities of the foot (38,39). During standing and in the initial stance phase of the gait cycle (from heel-strike to mid-stance), the foot assumes a pronated position as it tries to adapt to the underlying surface. As the body weight is transmitted onto the weight-bearing surface below, the medial longitudinal arch is lowered and the plantar fascia experiences tensile forces as it tries to maintain a high arch (40–43). Second, the plantar fascia plays a very important role from the mid stance to the toe off phase of the stance phase of the gait cycle. During terminal stance, the toes passively dorsiflex and lead to shortening (tightening) of the plantar fascia and elevation of the medial longitudinal arch. At this point, the plantar fascia assists in supination of the foot, and this entire mechanism has been compared to a windlass (2,40). Plantar fasciopathy is one of the most common foot and ankle pathologies for which patients seek medical attention (28). Although the etiology of plantar fasciopathy is considered to be multifactorial, it is generally agreed that repetitive trauma to the plantar fascia resulting from excessive tensile forces at its origin is the most common cause of this condition (1,44,45). It is primarily considered an overuse injury and is common among athletes and those with a predisposition to hyperpronate (2,45). Excessive abnormal loading of the plantar fascia resulting from hyperpronation leads to
Fig. 2. Representation of elongation data showing mean plantar fascia elongation of hyperpronated cadaveric feet considered in this study, without and with intervention. Error bars represent 1 standard error of mean. *Significant decrease in elongation of plantar fascia after placement of extra-osseous talotarsal stabilization device.
physiologically intolerable levels of strain, which can lead to microtears, inflammation, and eventual rupture of the plantar fascia (2,7–9,11–13,16,22). The most common treatment options for plantar fasciopathy include the use of oral nonsteroidal anti-inflammatory drugs, ultrasound therapy, physical therapy, ice, and rest (1,2,44). These treatment options are aimed at reducing the pain and inflammation and help to reduce symptoms on a temporary basis. With these treatments alone, recurrence of plantar fasciopathy is a common problem in those with an underlying mechanical etiology. This is because none of these treatments correct the underlying biomechanical defect (i.e., hyperpronation) (1,2,44). Many investigators suggest the use of shoe inserts and orthoses for the long-term management of plantar fasciopathy. The hypothesis supporting the use of orthotic devices is that they reduce excessive plantar fascia strain by supporting the medial longitudinal arch and minimizing excessive and/or prolonged pronation (1,2,46). To test this hypothesis, Kogler et al (28–30) conducted a series of studies in which they evaluated the effect of different orthoses and orthotic wedge combinations on plantar fascia strain in cadaveric feet. In their initial studies, they found that under axial loading of up to 900 N, the University of California Biomechanics Laboratory shoe insert, and 2 other orthoses, significantly reduced the plantar fascia strain compared with the barefoot controls (28,29). In a later study, they also found that under similar loading conditions, orthotic wedges placed under the lateral aspect of the forefoot and rearfoot were significant in reducing plantar fascia strain (30). However, certain shortcomings of the studies by Kogler et al (28–30) are apparent. The basic premise for the use of orthotic devices in the treatment of plantar fasciopathy is that these devices support the medial longitudinal arch in the hyperpronated foot by externally controlling the range of pronation and supination. Because Kogler et al (28–30) used cadaveric specimens that were determined to be clinically and radiographically normal, it remains unclear whether orthotic devices are effective in reducing plantar fascia strain in hyperpronating feet. Additionally, they found that, in normal feet, certain orthotic devices reduce plantar fascia strain compared with the barefoot condition; this suggests that these orthotic devices might be restricting the normal range of joint motion. Limiting the normal range of joint motion has its own consequences and can hinder patients in their daily activities. Another possible area of concern with their study was that they measured strain in the plantar fascia approximately 3 cm distal to its origin. As mentioned previously, most of the cases of plantar fasciopathy report failure at its origin (47). It is, therefore, important to quantify plantar fascia strain near the most frequent location of failure. Kwong et al (2) suggest the use of a semirigid orthosis combined with the use of a firm posterior counter shoe for the longterm treatment of plantar fasciopathy. The success of orthotic treatment depends on the ability of an orthosis to control abnormal pronation. However, traditional orthotic devices fail because most of
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these devices focus only on controlling the position of the calcaneus and are uncomfortable and not well tolerated by the patients. Although the University of California Biomechanics Laboratory shoe insert has been used effectively to control pronation, it is bulkier, restricts foot motion to an extent greater than required, is more difficult to fit properly, and, eventually, results in lower patient compliance. Also, adjustments or changes to the orthotic devices are required from periodically because of changes in the orthotic material properties and loss of adequate support (2). Surgical intervention for the treatment of plantar fasciopathy has been indicated for patients in whom conservative treatments fail to alleviate the pain and symptoms (19–21,48–50). The choice of treatment for such cases has been complete or partial plantar fasciotomy (51,52). However, a number of biomechanical studies have shown that partial or complete plantar fasciotomy can lead to longterm detrimental effects on foot and ankle function (48,51,53). In particular, complete plantar fasciotomy can lead to the loss of medial longitudinal arch stability and abnormalities in the gait pattern (38). It is also speculated that fasciotomy can cause excessive abnormal pronation (48,53). Research has shown that the plantar fascia is the most important structure in terms of supporting the medial longitudinal arch and suggests against the use of plantar fasciotomy (38,48). Plantar fascia release severely affects the windlass mechanism. As mentioned previously, during toe off, the plantar fascia tightens to supinate the foot (making it a rigid structure) and elevates the medial longitudinal arch. This is important for forward propulsion of the body. After plantar fasciotomy, other soft tissue structures such as the posterior tibial tendon have to bear extra load to supinate the foot and support the medial longitudinal arch during the terminal stance phase of the gait cycle. Such excessive loading of the posterior tibial tendon can lead to its degeneration and result in additional complications. Over time, all these factors continue to increase the amount and time that the foot pronates (i.e., hyperpronation). At this point, it is important to remember that pre-existing hyperpronation is the very reason that causes plantar fasciopathy in most cases; thus, by releasing the plantar fascia, the pronation forces are further aggravated. It has been advocated that long-term relief of plantar fasciopathy should be achieved by adequate remedy of the aggravating pronation factors (i.e., stabilization of the talotarsal joint complex) (2). EOTTS devices are indicated for the stabilization of the talotarsal joint complex and have been used for the past 5 decades (33). In the present study, we showed that an EOTTS device reduces plantar fascia strain in hyperpronating cadaveric feet by 33%. This suggests stabilization of the talotarsal joint complex and additional support to the medial longitudinal arch. Furthermore, the HyProCureÒ is an innovative device owing to its design and functional characteristics and requires a minimally invasive procedure for placement in the sinus tarsi. This EOTTS device is indicated for mild to severe hyperpronation, even in cases in which there are no pain or presenting symptoms. In support of this view, Kwong et al (2) reported that patients with a predisposition to overpronate place more strain on the plantar fascia with each weight-bearing step. In such cases, the plantar fascia can adjust to each increased strain level and still be pain free. However, as the pronation deformity progresses, a particular strain level can exceed the plantar fascia’s physiologic tolerance, which is highly variable from one individual to the other. A patient with a less severely pronating foot might present with more pain than a patient with a more severely pronating foot. The pain experienced depends on the ability of the plantar fascia to accommodate physiologically tolerable levels of strain and, hence, is highly variable. Chandler and Kibler (44) also reported that if predisposing maladaptations (e.g., hyperpronation) can be identified and corrected, the initial occurrence of plantar fasciopathy can be prevented.
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Although the present biomechanical study showed a significant reduction in plantar fascia strain after an EOTTS procedure, limitations exist. First, the sample size studied was relatively small (N ¼ 6 cadaver specimens). Second, we could not compare the strain measurements obtained in this study with those from previously published work (28–30,36). This was because of the different experimental conditions and definition of the reference position against which the final strain was measured. Although the DVRTÒ technique has been used successfully to measure strain in the plantar fascia, it is limited to uniaxial measurements (28–30,36). Very recently, Clark et al (54) used foil-type microstrain gauges to measure tri-axial plantar fascia strain. However, they mentioned that calibration of these devices is difficult, and they found that plantar fascia strain is mostly longitudinal. Finally, in the present study, we showed that an EOTTS device was successful in eliminating excessive plantar fascia strain in hyperpronating cadaveric feet; however, a well designed prospective study needs to be conducted to evaluate the long-term results of such devices in the treatment of plantar fasciopathy in the adult human population. Acknowledgment We would like to thank Manoj K. Kodigudla and Vikas Kaul at the University of Toledo and Avanthi Chikka at Graham International Implant Institute for their help in arranging the experimental setup and potting of the foot specimens. References 1. Cornwall MW, McPoil TG. Plantar fasciitis: etiology and treatment. J Orthop Sports Phys Ther 29:756–760, 1999. 2. Kwong PK, Kay D, Voner RT, White MW. Plantar fasciitis: mechanics and pathomechanics of treatment. Clin Sports Med 7:119–126, 1988. 3. Bordelon RL. Subcalcaneal pain: a method of evaluation and plan for treatment. Clin Orthop Relat Res 177:49–53, 1983. 4. Leach RE, Dilorio E, Harney RA. Pathologic hindfoot conditions in the athlete. Clin Orthop Relat Res 177:116–121, 1983. 5. McBryde AM. Plantar fasciitis. Instr Course Lect 33:278–282, 1984. 6. Wearing SC, Smeathers JE, Urry SR, Hennig EM, Hills AP. The pathomechanics of plantar fasciitis. Sports Med 36:585–611, 2006. 7. Lutter LD. Pronation biomechanics in runners. Contemp Orthop 2:579, 1980. 8. Waller JF. Physiology of the foot and the biomechanics of the flexible flat foot. J Orthop Nurses Assoc 5:101–103, 1978. 9. Warren BL. Anatomical factors associated with predicting plantar fasciitis in longdistance runners. Med Sci Sports Exerc 16:60–63, 1984. 10. Kosmahl EM, Kosmahl HE. Painful plantar heel, plantar fasciitis, and calcaneal spur: etiology and treatment. J Orthop Sports Phys Ther 9:17–24, 1987. 11. Mann R, Inman VT. Phasic activity of intrinsic muscles of the foot. J Bone Joint Surg Am 46:469–481, 1964. 12. Scherer PR. Heel spur syndrome: pathomechanics and nonsurgical treatment. J Am Podiatr Med Assoc 81:68–72, 1991. 13. Shama SS, Kominsky SJ, Lemont H. Prevalence of non-painful heel spur and its relation to postural foot position. J Am Podiatr Assoc 73:122–123, 1983. 14. Schroeder BM. American College of Foot and Ankle Surgeons: the diagnosis and treatment of heel pain. Am Fam Physician 65:1686–1688, 2002. 15. Stovitz SD, Coetzee JC. Hyperpronation and foot pain: steps towards pain-free feet. Phys Sports Med 32:19–26, 2004. 16. Andrews JR. Overuse syndromes of the lower extremity. Clin Sports Med 2:137– 148, 1983. 17. Campbell JW, Inman VT. Treatment of plantar fasciitis and calcaneal spurs with the UC-BL shoe insert. Clin Orthop Relat Res 103:57–62, 1974. 18. Newell SG. Conservative treatment of plantar fascial strain. Phys Sports Med 5:68– 73, 1977. 19. Leach RE, Seavey MS, Salter DK. Results of surgery in athletes with plantar fasciitis. Foot Ankle 7:156–161, 1986. 20. Lester DK, Buchanan JR. Surgical treatment of plantar fasciitis. Clin Orthop Relat Res 186:202–204, 1984. 21. Lutter LD. Surgical decisions in athletes’ subcalcaneal pain. Am J Sports Med 14:481–485, 1986. 22. Torg JS, Pavlov H, Torg E. Overuse injuries in sport: the foot. Clin Sports Med 8:291–320, 1987. 23. Goulet MJ. Role of soft orthosis treating plantar fasciitis. Phy Ther 64:1544, 1984. 24. Riddle DL, Freeman DB. Management of a patient with a diagnosis of bilateral plantar fasciitis and Achilles tendonitis. Phys Ther 68:1913–1916, 1988.
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