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The American Journal of Sports Medicine ajs.sagepub.com
Published online before print November 22, 2005, doi: 10.1177/0363546505281813 Am J Sports Med April 2006 vol. 34 no. 4 612-620
Ligamentous Posttraumatic Ankle Osteoarthritis Victor Valderrabano, MD*,†,‡, Beat Hintermann, MD‡, Monika Horisberger‡, and Tak Shing Fung, PhD§ +
Author Affiliations
Address correspondence to Victor Valderrabano, MD, Human Performance Laboratory & Orthopaedic Department, University of Calgary, 2500 University Drive N.W., Calgary, Alberta, Canada, T2N 1N4 (e-mail:
[email protected]).
Abstract Background: Ankle sprains are the most common injuries in sports and recreational activities. Hypothesis: Ankle osteoarthritis can be caused by ankle ligament lesions. Latency time between injury and osteoarthritis is influenced by the type and side of the injured ligaments. The side of the ligamentous lesion correlates with the hindfoot alignment. Study Design: Case series; Level of evidence, 4. Methods: Of a cohort of 247 patients with ankle arthritis, we reviewed data from 30 patients (33 ankles; mean age, 58.6 years) with ligamentous end-stage ankle osteoarthritis. The patients were evaluated etiologically, clinically, and radiologically. Results: Etiologic analysis: 55% had a ligamentous lesion from sports injuries (soccer, 33%); 85% injured the lateral ankle ligaments, and 15% injured the medial and medial-lateral ligaments. The mean latency time between injury and osteoarthritis was 34.3 years. The survivorship rate for single severe ankle sprains was worse than that for chronic recurrent ligamentous lesions (mean latency time, 25.7 vs 38.0 years; P < .05), and the rate for medial sprains was worse than for lateral sprains (mean latency time, 27.5 vs 35.0 years; P < .05). At follow-up, the American Orthopaedic Foot and Ankle Society hindfoot score was 23.0 points, 52% had varus malalignment, 52% had persistent instability, and the mean ankle arthritis grade was 2.6 points. There was a correlation between chronic lateral ankle instability and varus malalignment. Conclusion: Lateral ankle sprains in sports are the main cause of ligamentous posttraumatic ankle osteoarthritis and correlate with varus malalignment. At the time of end-stage ligamentous ankle osteoarthritis, persistent instability may be encountered. Keywords: ankle
arthritis
ligament
sports
trauma
Approximately 50 million adults in the United States and 15% of the world’s adult population are affected by joint pain and disability that result from osteoarthritis.11 Many of these cases involve osteoarthritis of the ankle. It has been stated that ankle fractures are more common in young adults and that the prevalence of osteoarthritis in the ankle is increasing because of large numbers of sports injuries and increased life expectancy.7,22,33 Although there are several causes for ankle arthritis, including primary osteoarthrosis and systemic arthritis (rheumatoid arthritis and other systemic diseases), posttraumatic osteoarthritis is the cause of more than 70% of ankle arthritis.20,32 Arthritis-predisposing traumatic ankle injuries include fractures of the malleoli, tibial plafond, and talus, as well as isolated osteochondral damage of the talar dome, and ligamentous lesions.10,25 Ankle ligament lesions are the most common injuries sustained in sports and recreational activities13,35 and account for about 25% of the injuries that occur in running and jumping sports.26 Because of functional and biomechanical factors, the stabilizing lateral ligament complex is the most often injured structure, usually as a result of inversion ankle sprain.13,14,21 Despite the efficacy of nonoperative treatment and physical rehabilitation management of ankle sprains, 10% to 30% of patients with these injuries experience chronic ankle instability.19,23 In 1979, Harrington15 reported on 36 patients with chronic lateral ankle instability and found ankle osteoarthritis (particularly varus osteoarthritis) in as many as 78% of the cases after at least 10 years. In a study of 29 patients who sustained an ankle trauma causing an osteochondral lesion of the talus, Canale and Belding3 found after 11 years of follow-up that 48% of the patients showed radiologic evidence of degenerative ankle osteoarthritis. In a retrospective study, Lofvenberg et al25 reported on 37 patients who suffered from nonoperatively treated chronic ankle instability and found a 13% rate of radiologic osteoarthritis changes after 20 years. Methodologically, however, all these previous studies had a nonhomogeneous group based on cause of injury, and none showed an exact analysis of the anatomical type of lesion: medial, lateral, or rotational (combined medial-lateral). Furthermore, to our knowledge, there is no long-term analysis that focuses on sports injuries as a cause of ligamentous ankle osteoarthritis, particularly using this 3-step path: sports injury causes ligamentous lesion causes posttraumatic ankle osteoarthritis. In addition, no study addresses the issue of whether single severe ankle sprains differ from recurrent ankle sprains in their survivorship and whether the treatment, either nonoperative or operative, may play a role in the long-term development of osteoarthritis. Consequently, the purposes of our retrospective investigation were (1) to analyze the rate and latency time of ligamentous posttraumatic ankle osteoarthritis among a cohort of end-stage ankle arthritis patients; (2) to determine the etiologic factors, especially the involvement of sports injuries and other influencing factors (such as age and gender) in developing this entity; (3) to prove the hypothesis that single severe ankle sprains have a worse survivorship rate than chronic recurrent ligamentous sprains; (4) to assess the effect of the performed ankle ligament treatment on the development of osteoarthritis; and (5) to quantify the clinical findings (for example, malalignment, instability, and osteoarthritis grade) in ligamentous posttraumatic ankle osteoarthritis on a long-term follow-up.
METHODS Of the 247 patients (261 ankles) who were referred to our ankle arthritis center between 1996 and 2003 because of painful end-stage ankle arthritis, 182 patients (185 ankles; 71%) suffered from symptomatic posttraumatic ankle osteoarthritis (Table 1). Of these, 30 patients (33 ankles; 23 men, 7 women), with a mean age of 58.6 years (range, 33–78 years), met the criteria of having sustained 1 or more ligamentous lesions but no other injury, for example, fracture, to the same ankle or lower leg and were included in the study (Figure 1). The following data (as taken from history charts or reported by the patients if charts were not available) were recorded: time of the sustained sprain(s), the underlying pathomechanism(s), and the applied treatment modalities (2 groups; nonoperative and surgical). The time between the documented or reported initial ankle sprain and the date of the patient’s first ankle arthritis consultation with us was defined as latency time (the time span for developing ligamentous posttraumatic ankle osteoarthritis). Ligamentous lesions were classified based on anatomical side (3 groups: medial, lateral, and combined medial-lateral) and frequency (2 groups: single and recurrent).
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lesions were classified based on anatomical side (3 groups: medial, lateral, and combined medial-lateral) and frequency (2 groups: single and recurrent). Pain level was quantified using a visual analog scale, with 0 representing no pain and 10 representing maximum pain. The American Orthopaedic Foot and Ankle Society (AOFAS) hindfoot score,24 which includes pain, function, and alignment evaluations, was used to assess overall functional level (minimum score, 0 points; maximum score, 100 points). Each patient’s level of sports activity was documented using the following scale: none, moderate, normal, high, and elite (Table 2). Total range of motion was measured in degrees for plantar flexion and dorsiflexion, and as a percentage of either the uninvolved contralateral leg or of the healthy population for inversion/eversion, as is required for the AOFAS hindfoot score.24 Hindfoot alignment was defined as follows: normal, valgus, or varus (Table 2). Ankle joint stability was documented using a grading12 and anatomical scale (medial, lateral, or combined medial-lateral) (Table 2). Possible symptomatic distal tibiofibular syndesmosis was assessed by direct palpation and squeeze test as a part of each patient’s standard examination. The patients were examined radiologically using standard weightbearing radiographs in 2 planes. The grade of ankle osteoarthritis was then quantified and evaluated based on the Morrey and Wiedeman classification27 (minimum score, 0 points; maximum score, 3 points) (Table 3).
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TABLE 1 Ankle Arthritis Cohort
TABLE 2 Clinical Grading Scales
TABLE 3
Radiological Osteoarthritis Gradea
Figure 1. Varus ankle osteoarthritis from chronic lateral ankle instability. This patient (case 13 in Table 4) has lateral instability of the left ankle after sustaining recurrent lateral ligamentous injuries as an orienteering runner. The radiographs (A, lateral; B, anteroposterior) show a varus malalignment of the hindfoot, which can also be seen in the clinical picture (C). The radiographs also show flattening of the tibial plafond and anterior protrusion of the talus, which are typical of varus ankle arthritis. The left foot in the dynamic pedobarography (D) shows a lateralization of the center of pressure line and forefoot overcharge compared with the right foot.
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The study was approved by the medical sciences ethical institutional review board at our university, and all subjects signed informed consent forms to participate. The study was performed in accordance with the World Medical Association Declaration of Helsinki. Statistical analysis of the data was performed by an independent biostatistics expert, who used SPSS software (version 12.0, SPSS Science Inc, Chicago, Ill) to perform Fisher exact tests, Pearson correlation analysis (r), independent sample t tests, and statistics for equality of survival distributions. The significance level was set at α = .05.
RESULTS The rate of ligamentous posttraumatic ankle osteoarthritis within the retrospective ankle arthritis cohort used in this study was 13% (33 of 261 patients) (Table 1). Ligamentous lesions sustained during sports activities were the most frequent cause (55%; n = 18), followed by ankle sprains that occurred during conventional daily activities (36%; n = 12) and ankle ligamentous injuries at work (9%; n = 3) (Table 4). In this study, soccer was the sport that most frequently gave rise to injuries causing ankle ligamentous lesions and consequent posttraumatic ankle arthritis (33%). Evaluation of the pathomechanisms at the time of injury revealed a lesion of the lateral ankle ligaments in 28 ankles (85%), of the medial ligaments in 4 ankles (12%), and of the medial-lateral ligaments combined in 1 ankle (3%). Then, taking into consideration the type of pathomechanism, the following constellation was observed: recurrent lateral ligament lesion in 20 ankles (61%), single lateral ankle sprain in 8 ankles (24%), recurrent medial ligament lesion in 2 ankles (6%), single medial ankle sprain in 2 ankles (6%), and recurrent combined medial-lateral ligament injury in 1 ankle (3%) (Table 4). A cohistory of a syndesmotic injury was found in 1 patient (case 14). Neither this patient nor any of the other patients showed a symptomatic distal tibiofibular syndesmosis at examination. During the period between the ligamentous injury and symptomatic osteoarthritis, 21 ankles (64%) underwent nonoperative ligament treatment, and 12 ankles (36%) had surgical ligament repair of the involved side (Table 4).
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TABLE 4 Cohort Data I
The overall mean latency time for the development of ligamentous posttraumatic ankle osteoarthritis was 34.3 years (range, 6–57 years). Although the 20 ankles that sustained recurrent lateral ankle sprains took 38.4 years (range, 21–57 years) to develop end-stage osteoarthritis, the 8 ankles that sustained a single severe lateral ankle sprain took 26.9 years (range, 6–57 years). By comparison, the 2 ankles that sustained recurrent medial ankle sprains had a mean latency time of 34.0 years (range, 13–55 years), and the 2 ankles having a single severe medial ankle sprain had a mean latency time of 21.0 years (range, 21 years). The single ankle with recurrent lateral and medial ankle sprains had a mean latency time of 40.0 years. In general, the single severe ankle sprain group exhibited an overall shorter mean latency time (25.7 years; range, 6–57 years; n = 10) than did the recurrent ankle sprains group (38.0 years; range, 13–57 years; n = 23) (P < .05). The survivorship rate of the single severe ankle sprain group was shown to be similar to the ankle fractures group of the posttraumatic ankle arthritis cohort (P < .05) (Figure 2). Last, the medial ankle sprains group showed a worse survivorship rate (mean latency time, 27.5 years; range, 13–55 years; n = 4) than did the lateral ankle sprains group (mean latency time, 35.0 years; range, 6–57 years; n = 28) (P < .05). Figure 2. Survivorship rate of ankle ligamentous lesions. This graph shows survivorship rate curves for the following groups: patients with a history of single severe ankle sprain, patients with a history of recurrent ankle sprains, and for comparison patients with an ankle fracture (Table 1). The statistical test for equality of survival distributions indicates a significant difference between the single severe ankle sprain group and the recurrent sprains group (P < .05); however, there was no significant difference between the single severe ankle sprain group and the ankle fractures group (P > .05). View larger version: In this page
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At final follow-up, the patients indicated a pain level represented by a mean score of 6.7 (range, 2–10) (Table 4). Clinically, the mean total range of motion for dorsiflexion/plantar flexion was 27° (range, 5°–50°) (Table 5). The inversion/eversion range of motion was limited, that is, less than 75%, in 20 ankles (61%). The overall functional hindfoot score using the AOFAS hindfoot score was 23.0 points (range, 7–45 points), reflecting substantial functional impairment (Table 4). Although all patients (100%) were participating in a sports activity before the first ankle sprain, once the condition of posttraumatic ankle osteoarthritis was diagnosed, 67% of patients reported participating in a sports activity, with most identifying the level as moderate (Table 4). During the latency time, 82% of patients indicated that they had to reduce their level of involvement in sports activities (Table 4). Clinically, 17 ankles (52%) were unstable: 15 ankles (46%) showed lateral chronic instability, 1 ankle (3%) showed medial chronic instability, and 1 ankle (3%) showed a combined medial and lateral instability (Table 5). Concerning the type of sustained ligamentous lesions, from these 17 unstable ankles, 76% (13 ankles) had a recurrent ankle ligamentous lesion type in the past, and 24% of them (4 ankles) had a severe single ligamentous lesion type. Seventeen ankles (52%) had varus malalignment, whereas 9 ankles (27%) had normal alignment, and 7 ankles (21%) had valgus malalignment (Tables 5 and 6). Of the 15 cases with chronic lateral ankle instability, 10 (66.7%) showed varus malalignment (Table 6, Figure 1). All patients with either chronic medial or combined medial-lateral instability showed valgus malalignment (Table 6). The mean ankle arthritis grade, using the Morrey and Wiedeman classification, was 2.6 (range, 1–3) (Table 6).
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TABLE 5 Cohort Data II
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TABLE 6
Cross-Table: Comparison of Ankle Instability and Hindfoot Alignmenta
Statistically, our analysis of the nonoperative treatment group (21 ankles) versus the surgical ligament repair group (12 ankles) revealed no significant differences between groups for pain score, arthritis grade, and AOFAS hindfoot score (P > .05). There was, however, a significant difference in the mean latency time to develop ankle arthritis (nonoperative treatment group, 40 years [range, 13–57 years]; surgical ligament repair group, 25 years [range, 6–45 years]; P < .05) as well as in the mean age of the patients (nonoperative treatment group, 64 years [range, 47–78 years]; surgical ligament repair group, 50 years [range, 33–60 years]; P < .05). The age correlation analysis showed a high correlation to the latency time (Pearson correlation r = .8, P < .05) but no correlation to the arthritis grade (Pearson correlation r = .07, P > .05) or the AOFAS hindfoot score (Pearson correlation r = .04, P > .05). The female-male comparison analysis showed no significant differences for latency time, pain score, sports activity level, AOFAS hindfoot score, age, or arthritis grade (all P > .05). Women did, however, show a significant tendency toward a higher grade of ankle joint instability than did men (female mean, substantially unstable; male mean, moderately unstable; P < .05).
DISCUSSION Although a few authors have addressed this topic in the past,3,15,25 our clinical study presents the most prolonged long-term and detailed analysis of causes and characteristics of posttraumatic ankle osteoarthritis after ankle ligament lesions. Although arthritis of the hip and knee is of predominantly degenerative origin and seen in older patients, 70% to 80% of ankle arthritis is posttraumatic in origin and is often seen in younger patients compared with the age of patients with degenerative or systemic ankle arthritis.5,20,32 This finding is consistent with our study (Tables 1 and 4). Our findings indicate that in 13% of posttraumatic osteoarthritis cases, the cause is a ligamentous lesion. Our results also show that lesions of the lateral ankle ligament complex are the main cause for developing ligamentous posttraumatic ankle arthritis (85% lateral ligament lesions, 12% medial ligament lesions, 3% combined medial-lateral ligament lesions). This predominance of lateral ligament injuries is also supported by other authors,13,14,17,18,21 with the most frequent mechanism of injury shown to be the unexpected and rapid hyperinversion of the hindfoot.1,8 In this group of patients with ligamentous posttraumatic ankle arthritis, sports injuries were the underlying cause in 55% of the cases, with soccer injuries being the most likely to cause this entity (33% of all the reported sports injury cases in this arthritis cohort, or 18% of all posttraumatic ankle arthritis after ligamentous damage). In a recent investigation, Drawer and Fuller7 demonstrated that soccer players have a high risk for developing osteoarthritis in the
lower extremities (more in the knee than the ankle); however, they did not report on the underlying etiologic factors. To our knowledge, there are no data available in the literature about the incidence rate of posttraumatic ankle osteoarthritis after a ligamentous lesion from soccer injuries, which may be mainly because there is only a low prevalence as a whole for ankle arthritis, although ankle lateral ligament injuries are very common in soccer. Without commenting on the incidence of ankle arthritis, Woods et al34 reported that ankle ligament sprains account for 11% of the total injuries seen in soccer players. Of this total, 77% involve the lateral ligament complex. Similar results were reported by Ekstrand and Tropp.9 The latency time analysis, that is, the analysis of the time from the moment of ligamentous injury to the moment of developing symptomatic end-stage ankle osteoarthritis, showed a significant difference between those patients who had a single severe ankle sprain (26 years) and those who had recurrent ankle sprains (38 years). The latency time differed even more dramatically when the affected side was taken into account (see results). One may speculate that the latency time for developing ligamentous ankle osteoarthritis may be influenced by the degree of cartilage damage that occurred at the time of injury. Evidence of cartilage damage in ankle sprains has been previously addressed. For example, Taga et al,30 in a report on 9 patients with acute ankle injuries and 22 patients with chronic ankle injuries, found (arthroscopically) chondral lesions in 89% and 95%, respectively. Hintermann et al,17 in a report on 148 patients with chronic ankle instability after 1 or more sprains, found (arthroscopically) that 66% of those with laterally unstable ankles had cartilage lesions, as did 98% of those with medially unstable ankles. Assuming that chronic instability may cause a pathologic amount of talus translation and rotation within the mortise29 and that the higher it is, the higher the shear forces acting on the cartilage surface, these results might suggest that with respect to potential cartilage damage, injury to the medial ankle ligaments is more critical than is injury to the lateral ligaments. In either case, however, the resulting instability of the talus within the mortise may cause slow but efficient damage to the superficial layer of the ankle cartilage, which is believed to play a major role in resisting the development of osteoarthritis.31 Our study shows evidence for a correlation between type of ankle sprain and malalignment. Lateral ankle sprain or chronic lateral ankle instability were predominantly found to be correlated with varus-malaligned ankle osteoarthritis (Table 6). There may be a biomechanical explanation for this finding. Hashimoto and Inokuchi16 found in a kinematic gait analysis that ankles that have sustained an injury to the lateral ligaments abnormally pronate and rotate externally at the time of heel strike and abnormally supinate, that is, varisation of the heel, and rotate internally during the acceleration phase. Furthermore, in a 3D model of the human ankle joint, Noguchi28 found that stress distribution increased on the medial side of the ankle joint when the lateral ligaments were released. In a recent retrospective MRI study of 94 ankle sprains, Brown et al2 reported a 52% incidence of having both distal tibiofibular syndesmosis and lateral ankle ligament lesions. All these kinds of chronic changes in ankle mechanics, together with a potential peroneal muscle dysfunction, may lead to repetitive cartilage damage on the medial ankle and may support the development of varus-malaligned ankle osteoarthritis. Our data support this theory: 67% of the patients with a lateral ankle ligament lesion showed varus-malaligned osteoarthritis. Harrington15 also reported that the majority of chronic lateral ankle osteoarthritis cases were varus arthritis. By contrast, the effect of medial ankle instability on ankle osteoarthritis is not well understood, and only very few clinical and biomechanical reports have been published on the topic. Clarke et al,4 in an in vitro study of sectioning the deltoid ligament, found that the total contact area of the ankle joint was decreased by 15% to 20% in medially unstable ankles. These findings correspond well with those of Hintermann et al19 in a series of 52 arthroscopically investigated ankles with medial ankle instability. Most recently, Deland et al6 concluded from the result on 5 ankles that chronic deltoid failure with valgus malalignment predisposes the ankle to early osteoarthritis. All of these findings support the belief that the medial ligaments are of utmost importance in stabilizing the ankle and, therefore, in preventing ankle osteoarthritis. It is surprising that our study found that there was a shorter mean latency time for the development had been performed after the first ankle sprain compared with the nonoperative treatment. The additionally damaged the ankle and accelerated the development of osteoarthritis, however, should be selected for surgical reconstruction were more unstable or had more severe chondral damage after
of ankle osteoarthritis when ligament reconstruction conclusion that ligament reconstruction may have drawn with caution. First, it may be that those ankles the initial sprain than those treated nonoperatively.
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Second, it is possible that the surgical reconstruction technique used was not appropriate to restore physiologic function of the ankle in a long-term sense. Another important finding from our study is that 52% of the ligamentous osteoarthritic ankles exhibited persistent mechanical lateral instability, which could be found by classic examination tests, such as the inversion stress test and anterior drawer test (Table 2). This persistent instability may have important implications for clinicians treating such a posttraumatic ankle arthritis cohort. Patients with ankle arthritis and persistent lateral instability may profit, at least temporarily, from an intensive physical rehabilitation program, for example, addressing peroneal muscle dysfunction and functional instability patterns. Furthermore, the persistent lateral instability may be considered by surgeons using total ankle replacement: the instability should be addressed before total ankle replacement to restore physiologic ligament balance. The obtained AOFAS hindfoot score and arthritis grade determined by our study are consistent with other studies of patients with symptomatic ankle osteoarthritis.20,32 The impairment of functional ability that results during the gradual development of ankle osteoarthritis may explain the reported reduction in personal sports activity level in 82% of the cases. Our study does have certain limitations. First, because of its retrospective design, this study includes only those patients from the original cohort who manifested posttraumatic ankle osteoarthritis after suffering ligamentous lesions of the ankle, which may affect the evaluation of the prevalence and latency time of this entity. A prospective study of young patients with ankle ligamentous injuries would make it possible to evaluate the exact prevalence rate of osteoarthritis after ligamentous lesions. As the latency time range of our study shows, however, a study follow-up of as long as 60 years would be necessary. Furthermore, from an ethical point of view, because the overall incidence of secondary osteoarthritis is unknown, a tremendous number of patients would have to be observed during a period of years. Another limitation is the small and unequal number of patients in the different groups of ankle ligament lesion types. This limitation might be difficult to rectify, even in a prospective study, given the low incidence of medial ankle sprain. A final limitation is the nonrandomized assignment of patients to either the nonoperative treatment group or the surgical ligament repair group. Again, to address this limitation, an enormous number of patients would have to be randomized and treated either nonoperatively or surgically using the same surgical technique (and, if possible, the same surgeon) and observed prospectively for decades.
CONCLUSION Although the ankle joint is known to have an overall low incidence of ankle arthritis, there is evidence that the ankle joint is more susceptible to arthritic changes after a severe ligamentous trauma than is generally believed. The mean latency time of 34.3 years to develop symptomatic end-stage ligamentous ankle osteoarthritis differed substantially by the type of ligamentous injury (single severe sprain, recurrent ankle sprain) and the side (medial, mediallateral, lateral). Epidemiologically, sports injuries (particularly soccer injuries) caused the main factor, that is, ligamentous lesions of the ankle, that led to the development of ligamentous ankle osteoarthritis. Single ankle sprains showed a worse survivorship rate than did chronic recurrent ligamentous lesions. The type of treatment did not affect the outcome of clinical and radiologic variables, but it did change the arthritis latency time: surgically treated ankles had a shorter mean latency time than did nonoperatively treated ankles. There was an important correlation between chronic lateral ankle instability and varus malalignment. Finally, when considering treatment of ligamentous ankle osteoarthritis, it may benefit clinicians and surgeons to be aware that there could be persistent instability in 52% of the cases.
Acknowledgments The authors acknowledge the Swiss Federal Council of Sports (Magglingen, Switzerland) for the financial support of this study within the research concept “Sport and Motion 2004 – 2007.”
Footnotes No potential conflict of interest declared. Copyright 2006 by American Orthopaedic Society for Sports Medicine
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