Overuse injuries are defined as tissue damage due to repetitive microtrauma.1 Typically overuse injuries develop without an identifiable event associated with symptom onset. Some of the most common overuse injures of the foot and ankle are tendinopathies, stress reaction, and stress fractures; however, ligamentous injury, plantar fasciitis, and impingement syndromes can also occur.33
The etiology of overuse injuries of the foot and ankle is multifactorial and dependent on the affected structure. Generally, overuse injuries involve exposure to repetitive activity in conjunction with insufficient training or recovery, and/or poor biomechanics. Modifiable factors such as training regimen and conditions, nutrition, and footwear contribute to overuse injury. Additionally, a patient’s anatomy, range of motion, underlying health conditions, and strength may play a role as well.
Epidemiology including risk factors and primary prevention
Overuse injuries comprise about 7% of physician office visits.1 Approximately half of sports related injuries are due to overuse rather than acute injury. Similarly, amongst the injuries that are evaluated by a healthcare provider, overuse is more common than acute etiology.1,30
In general, risk factors for development of tendinopathy include extrinsic factors such as acute on chronic training load (drastic increase in intensity, frequency, and duration of exercise), biomechanical variables such as poor exercise technique, improper equipment (e.g., ill-fitting or old shoes), among others.21,43 Intrinsic factors are those inherent to the patient and include foot alignment, joint laxity, anatomic variations, and history of previous injury.20,48 Medical comorbidities such as diabetes mellitus, gout, rheumatoid arthritis, and obesity may also confer increased risk of tendon injury.4
Specific risk factors for posterior tibial tendinopathy include age greater than 40 years, female sex, hypertension, obesity, diabetes, steroid exposure, excessive pronation, shallow malleolar groove, and accessory navicular bone.49,52,73 Estimates of prevalence of posterior tibial tendon dysfunction range from 3.3-10%.49
Peroneal tendon injury often occurs in young, active patients. While the exact prevalence is unknown, peroneal pathology has been seen in 35% of patients without any corresponding symptoms.50 The peroneus brevis tendon is more often torn in isolation when compared with the peroneus longus.51 Risk factors include varus hindfoot alignment, convex as opposed to concave retromalleolar groove, poorly fitting footwear (notably ski boots and hockey skates), and forefoot strike with running as this leads to increased stress on the ankle.53,73 If swelling and tenderness are observed in the absence of increased activity or inciting event, consideration of rheumatoid arthritis or seronegative arthritis should be made.48
Achilles tendon injury is common in runners (6-17% of running injuries) and gymnasts, as well as middle aged, overweight patients without a history of increased physical activity, and patients with seronegative arthropathy.55,56 Risk factors include tendon hypervascularity, older age, obesity, pes cavus, forefoot varus, poor flexibility of the gastrocnemius, lateral ankle instability, training on hard or slanting surfaces, training in cold weather, decreased plantarflexion strength, and fluoroquinolone usage.48,54,55,74
Flexor hallucis longus tendon injury is commonly seen in athletes who participate in sports requiring repetitive push-off maneuvers such as ballet dancers. Anterior tibial tendon injury is less common but occurs in patients older than 45 years and in distance runners and soccer players.48
Other Soft Tissue Injuries:
Morton’s neuroma, or interdigital neuromas of the foot, typically affects middle aged women with ill-fitting footwear. An estimated 30% of the population is affected.59 Patients typically note burning pain on the plantar surface of the foot between the metatarsal heads.58,76 First metatarsophalangeal joint sprain, otherwise known as ‘turf toe’, is caused by hyperextension of the great toe with axial loading, and is rare, accounting for 0.062 injuries per 1000 athletes.61 Incidence is higher in contact sports, at higher levels of play, and on artificial playing surfaces.62 Injuries are graded based on the extent of injury to the plantar capsular ligament complex.60,61,62,79 Plantar fasciitis is one of the most common causes of heel pain in middle aged women, with an estimated lifetime incidence of 10%. There are several postulated risk factors for development of plantar fasciitis including obesity, flat feet, and prolonged walking or standing on hard surfaces. Please see PM&R Knowledge Now article on plantar fasciitis for a more in-depth review.
Development of any stress fracture in the foot or ankle results from abnormal load on a normal bone or normal load on demineralized bone. Participation in activities which involve repetitive submaximal stress on the bone, such as running or jumping, or improper footwear, lead to development of stress fracture. Additional risk factors include decreased bone mineral density, female sex, relative energy deficiency in sport (RED-S), low vitamin D levels, and history of previous stress fractures.39,75,81
Stress fractures occurring in metatarsal bones account for 20-38% of lower extremity stress injuries. The 2nd and 3rd metatarsals are affected most commonly.39,57 Stress fracture of 5th metatarsal accounts for only 2% of all metatarsal stress fractures; however, it requires specific attention due to its poor vascular supply increasing the risk of non-union.41 Calcaneal stress fractures are common and noted to be the most frequently diagnosed stress fracture in women, and the second most common in men behind metatarsal injury.39 Navicular stress fractures account for 14-25% of all stress fractures and affect young male athletes. These fractures pose a high risk of nonunion.81 6.6% of lower limb stress fractures affect the fibula, most commonly in the distal third of the bone.39,57. Talar stress fractures typically present with calcaneal or navicular fractures. About 80% of talus injuries are classified as stress reaction with the remainder being true stress fractures.81 Medial malleolar fractures are rare (0.6-4.1% of all lower extremity stress fractures).57,41,81 Cuboid and cuneiform stress fractures have been reported in the literature but are significantly less common.39
Sesamoid disorders are estimated to comprise about 9% of foot and ankle injuries.60 Sesamoid bones, especially medial, can develop stress fractures.57 Sesamoiditis typically affects young adults and risk factors include pes cavus, abnormal rotation or size of the sesamoids, and chronic repetitive stress.60 Patients typically report pain on the plantar surface of the first metatarsophalangeal joint (MTP) joint. Barefoot walking may reproduce or exacerbate symptoms.
Metatarsalgia, characterized by pain localized to the plantar aspect of the distal metatarsals, is estimated to have an incidence of 5-36%.59 It is typically seen in middle aged women. Risk factors include anatomic anomalies such as first ray insufficiency due to hallux valgus or pes planus, or long second metatarsal. Other risk factors include increased metatarsal loading through chronic synovitis seen in rheumatoid arthritis, gout, or psoriasis.77 Iatrogenic factors such as forefoot surgery can alter foot mechanics and increase risk.
Heel pain can be due to Haglund deformity, a bony prominence at the posterosuperior aspect of the calcaneus. This condition is often seen in patients with concomitant insertional Achilles tendinopathy and retrocalcaneal bursitis.64 Middle aged women are most commonly affected.65,66 Os trigonum, a common accessory ossicle incidentally seen on imaging posterior to the talus and lateral to the FHL tendon, can also lead to chronic posterior ankle pain. Prevalence estimates range from 1-25%.70
In younger (pediatric and adolescent) patients, Sever’s disease, or calcaneal traction apophysitis by the Achilles tendon, is a cause of heel pain with an estimated incidence of 0.36 per 100 young athletes.72 Pain is typically associated with activity or a growth spurt and resolved after the apophysis closes.65,72 Tarsal coalition, the abnormal connection between two tarsal bones with talocalcaneal and calcaneonavicular being the most prevalent subtypes, has an incidence of 1-13%.66 Typically symptoms present in adolescence; however, not all patients with tarsal coalition will be symptomatic.66 Other young athletes may complain of medial arch pain due to accessory ossicles, most commonly accessory navicular. The incidence is 2-14%.68, 70
Overuse injuries result from repetitive microtrauma which over time cumulatively results in tissue damage. A disparity between overload and recovery leads to breakdown on a cellular, extracellular, and systemic level.1 Tendinopathy is caused by excess tensile loading force which leads to a localized inflammatory response and disruption of the tendon.22 With repetitive insult and insufficient healing time, the tendon develops neovascularization, decreased collagen density and disruption of the parallel orientation of collagen fibers. These are the hallmarks of tendinopathy which ultimately leads to decreased resistive strength and increased vulnerability for further injury.1,23
Bone stress injuries comprise another category of overuse injury and may result from excess force on healthy bone or from typical force on abnormal bone. Stress fractures are defined as a microfracture in the cortical bone tissue and develop when bone fails to adapt to the mechanical load experienced during physical activity. Excess loading leads to increased osteoclast activity, which results in temporary weakening of the bone.24 Bone remodeling cannot maintain the integrity of the normal bone structure and microfracture develops, otherwise known as a stress reaction.25 Over time, with repetitive stress and without a parallel increase in osteoblast activity, the bony architecture further collapses until a true cortical fracture develops.4,5
Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)
Tendinopathies: The affected tendon will typically demonstrate localized pain, swelling, decreased range of motion, and poor exercise tolerance.20 It has been suggested that tendon pathology occurs along a spectrum with stages including reactive tendinopathy, tendon disrepair or failed healing, and degenerative tendinopathy. Briefly, reactive tendinopathy is described as a proliferative response of the tenocyte and extracellular matrix to tensile or compressive overload. In this phase, the tendon exhibits thickening in discrete areas to reduce the stress placed on the tendon via an increase in cross-sectional area.11 During the tendon disrepair stage, the extracellular matrix exhibits an increase in number of cells, namely chondrocytes and myofibroblasts, which increase production of collagen and proteoglycans which leads to disorganization of the matrix. There may also be neovascularization and neuronal ingrowth during this phase.11 Finally with degenerative tendinopathy, apoptosis occurs and areas of acellularity within the tendon may be apparent, the surrounding matrix is disordered and capacity for recovery is minimal. While these proposed stages do not necessarily correlate with pain and tendon dysfunction, tendons which exhibit pathology are more likely to develop symptoms.83
Bone Stress Injuries: Clinically, patients present with an insidious onset of localized bony pain typically towards the end of exercise.24 As the bone stress injury worsens, symptoms may increase with pain present during lower intensity activity such as walking.24 Effective diagnosis and treatment of bone stress injuries is essential to prevent completion of the fracture and nonunion.
Specific secondary or associated conditions and complications
Complications associated with tendinopathy include risk of re-injury, development of chronic pain, and on rare occasions, rupture of the tendon. One database study suggests that approximately 4% of patients diagnosed with Achilles tendinopathy eventually experience rupture.80
Stress fractures are divided into two main categories, low risk and high risk. The low-risk category includes stress fractures of the posteromedial tibia, calcaneus, and second and third metatarsal shafts. While any stress reaction may progress to complete fracture and be complicated by nonunion, this is more typically seen in high-risk fractures.
High risk stress fractures are called such due to risk of delayed recovery, increased risk of progression to true fracture, delayed union or nonunion entirely. Anatomic locations which receive maximal tensile load in conjunction with poor vascular supply are at risk for suboptimal healing. Within the foot and ankle, high risk stress fracture locations include the medial malleolus, talus, navicular, proximal fifth metatarsal and great toe sesamoids. Nonunion is the primary complication of stress fractures, with a 35-50% malunion risk in fifth-metatarsal stress fractures and a 20% risk in navicular fractures.1, 2, 42 Suggestions for referral for surgical fixation include fracture line on radiograph or displacement in medial malleolar injury.81 Surgical fixation for navicular stress fractures is typically considered for elite athletes due to quicker return to play or if type II and II fractures exist.81. Fractures at the proximal fifth metatarsal at the metaphyseal-diaphyseal junction, otherwise known as a Jones fracture, often requires surgical fixation. Surgical referral may also be made for sesamoid fractures if nonresponsive to conservative management.
Essentials of Assessment
Key elements of the history include mechanism of injury, onset, location and character of pain, duration of symptoms, aggravating and alleviating factors. The context in which the current injury developed is important as well. Therefore, it is essential to gather information about the type of activity the patient participates in, frequency and intensity of exercise, equipment used, running surface, weekly mileage, etc.32 History of any previous foot or ankle injury and rehabilitation completed for these injuries is important to note. Questions about footwear, orthotics, or braces should be included. Discussion with the patient regarding goals for functional results can help guide treatment. As always, medical and surgical history should also be included.
An effective exam includes inspection of both lower extremities starting at the hips in standing, supine, and prone positions. Note any leg-length discrepancy, local deformity, edema, erythema, ecchymosis, atrophy, tendon asymmetry, or previous scars. Palpation should be performed, examining for tendon thickening, crepitus, tendon nodules or gapping, and areas of point tenderness. Passive and active range of motion of the joints of the foot and ankle should be analyzed. A localized neurologic exam testing range of motion and strength in dorsiflexion, plantarflexion, inversion, eversion as well as foot/ankle sensation is important.1
- Pain with resisted dorsiflexion, eversion of the ankle suggests peroneal tendinopathy.7,48
- Patients with posterior tibialis tendinopathy may have flat foot or collapse of the arch, ‘too many toes’ sign (examiner may see more toes exposed on the lateral side of the affected foot when observing from behind), or hindfoot valgus.48
- FHL tendinopathy symptoms can be reproduced by resisting great toe flexion particularly with the foot in plantarflexion.54
- Anterior tibial tendinopathy related pain can be reproduced by resisted ankle dorsiflexion.
- Crepitus of the Achilles tendon with dorsiflexion and plantarflexion can suggest Achilles tendinopathy. Thompson test, wherein the patient lays prone and the examiner squeezes the gastrocnemius while watching for plantarflexion, is considered positive and suggestive of rupture if no plantarflexion occurs, with a sensitivity of 96% and specificity of 93%.6,82
- Stress fracture: Typically pain can be reproduced with palpation over the bone affected.
- Morton’s neuroma: Axial pressure applied to the intermetatarsal space will reproduce symptoms. Mulder’s sign, a painful clicking sensation when pressure is exerted on the intermetatarsal space while the metatarsals are tightened with the other hand has a sensitivity of 94-98%.76.
- Metatarsalgia: Patients may have abnormal forefoot plantar calluses with tenderness to palpation specifically over the distal diaphysis proximal to the metatarsal head.
- Sesamoiditis: Tenderness to palpation over the plantar surface of the sesamoids is suggestive. Typically range of motion is not provocative unless pressure is applied over the sesamoids.
- Turf toe: Exam may show swelling of the first MTP joint and painful passive flexion and extension of the great toe.
- Plantar fasciitis: Patients generally have point tenderness over the plantar fascia particularly with dorsiflexion of the foot.
- Haglund deformity: Exam will demonstrate tenderness over the superior aspect of the posterior calcaneal tuberosity.
- Irritation of coalitions: On physical exam, patients may present with a ‘double medial malleolus’ over the middle facet which may be indicative of talocalcaneal coalition and should prompt additional investigation with imaging.78 Patients may also present with decrease in subtalar motion.
Evaluation of the hip-knee-foot kinetic chain during single leg stance or squat is helpful for identifying muscular imbalances or biomechanical abnormalities. Analysis of gait during ambulation, running, and jumping is essential for identification of risk factors such as over-striding, foot-strike position, excessive pronation/supination, as well as imbalance of forces during push-off.5,8 Patients with forefoot varus and decreased dorsiflexion may have an increased likelihood of developing metatarsal stress fracture.44 Forefoot strike during running results in increased eccentric loading on the ankle and increases force on the Achilles tendon, which may confer greater risk of development of tendinopathy.45,46 Rearfoot strike, however, increases the impact force through the foot and is correlated with a higher rate of stress injury.41,46
Laboratory studies are usually not necessary for evaluation of foot and ankle overuse injuries. They may play a role in ruling out other conditions; specifically, infection, malignancy, or rheumatologic conditions. In the case of high suspicion for these alternative diagnoses, C-reactive protein, erythrocyte sedimentation rate, complete blood count, metabolic panel, vitamin D and calcium levels should be evaluated.9 In patients with repeated stress injury, a bone metabolic panel may be useful for evaluating bone health. This panel typically evaluates vitamin D, calcium, parathyroid hormone, and thyroid hormone levels.
Standing foot and ankle x-rays can be useful to supplement the clinical history and physical examination. While more useful for acute injury management, the Ottawa Ankle Rules for imaging can help guide the decision to order an x-ray. For stress fractures, plain radiographs may initially be negative as estimates of sensitivity range from 15-56%.33 Plain radiographs may be repeated after 2-3 weeks, at which point evidence of callus formation may be apparent. Magnetic resonance imaging (MRI), has become the gold standard for evaluation of stress fracture.2 Sensitivity for detection of stress fractures is 88% compared with 42% for bone scan and 74% for computerized tomography (CT).33 A four-stage grading system has been developed to classify stress fractures depending on MRI findings: grade 1 injuries show periosteal edema on fat-suppressed images, grade 2 injuries demonstrate abnormal increased signal intensity on fat-suppressed T-2 weighted images, grade 3 injuries show decreased signal intensity on T-1 weighted images, and grade 4 injuries demonstrate a fracture line on both T-1 and T-2 weighted images.1 CT may be used to differentiate lesions that can mimic stress fracture, such as osteoid osteoma, osteomyelitis and malignancy.10,26 Ultrasound is not routinely utilized in the evaluation for stress fractures although there is some suggestion that periosteal reaction in metatarsal stress fractures can be detected before changes on plain radiographs.33
Both ultrasound and MRI are utilized in the diagnosis of tendon disorders but are not required for diagnosis. Ultrasonography provides an inexpensive, albeit operator-dependent, evaluation of the tendon. Typical observations include size (as measured by diameter or cross-sectional area) and appearance (echogenicity, vascularity), noting any focal findings and correlating pain. Additionally, the presence of bursitis and tenosynovitis can be evaluated. Ultrasound also allows for evaluation of dynamic movement of the tendon as well as easy comparison to the contralateral side.32 MRI provides information on the internal morphology of the tendon and the surrounding structures, usually used for evaluation before surgical intervention or if ultrasound is not diagnostic.1,20
Supplemental assessment tools
Supplemental assessment tools include the use of goniometers for objective measurement of range of motion. Application of a vibrating tuning fork for evaluation of stress fractures may be utilized as mentioned above. Quantitative gait analysis and evaluation of running and jumping technique is helpful to identify biomechanical deficiencies. Nerve conduction and electromyography studies are helpful in the case of neuropathic pain to determine if there is nerve injury.
Early predictions of outcomes
Predictors of poor outcomes include progression of the pain from occurring only with activity to occurring at rest or with low-intensity activity.24 Pain at rest or during daily activities may indicate injury that will have a slower recovery.
Some environmental factors include footwear, running surfaces, lap direction, and training quantity and quality.5 Running with worn-out shoes or on harder surfaces may produce greater stresses on the body.12-14 Also, excess cushioning creates a stiff counter, increasing torque and resultant stress with push-off.15
Social role and social support system
Treatment outcomes are impacted by cooperation of the patient, parents (in young athletes), athletic trainers, and coaches. Providing education about the injury and expectations for recovery to the patient and support system is essential to promote treatment adherence. Sport psychologists can address coping with the natural process of the disease, the timing of recovery, and the treatment expectations.
Return to premorbid activity, such as the return to play in athletes and return to work in professional individuals, presents unique challenges in management of overuse foot and ankle injuries. Professional athletes may require more aggressive treatment with faster return to play protocol. A multidisciplinary approach with input from involved team members is essential to make an informed decision.
In general, treatment and return to play guidelines have been divided into several phases. Phase 1 requires limitation of further injury, control of pain and swelling, and minimization of strength and flexibility loss. In phase 2, athletes should focus on improvement of strength and range of motion while allowing for healing of damaged structures. In phase 3, the goal is achievement of near normal strength and flexibility of injured structure and further maintenance of cardiovascular fitness. In phase 4, athletes can return to play without restriction providing there is no pain of injured structures within 24 hours of activity.32
Rehabilitation Management and Treatments
Available or current treatment guidelines
In large part, there are no specific treatment guidelines for ankle and foot overuse injuries. Midportion Achilles tendinopathy should initially be managed with activity modification and eccentric exercises with a focus on mechanical loading in therapy. Please see the PM&R Knowledge Now section dedicated specifically to Achilles tendinopathy for additional information.
For the remainder of foot and ankle overuse disorders, treatment is based on clinical reports, expert opinion, and review of current scientific literature. The overall goal of treatment for overuse injuries is pain control to allow for adequate rehabilitation of strength, endurance, proprioceptive deficits, and correction of factors leading to load imbalance and repetitive strain.32
Posterior tibial tendinopathy not improving with conservative therapy by three months or those that are diagnosed at advanced stage of injury (i.e. subtalar joint is fixed, notable foot deformity), requires referral to an orthopedic surgeon.48 Peroneal tendinopathy, depending on severity of injury, heals fully between two weeks to six months. The majority of injuries are amenable to nonoperative treatement.51,73 Achilles tendinopathy healing requires 6-8 weeks of adequate treatment and may require several months if there is tendon rupture.55,56 Typically, FHL tendon injuries require two to three weeks of treatment for healing.48,5 Healing of anterior tibial tendinopathy typically requires three to six weeks. Complete rupture is uncommon but requires surgical treatment.48
Successful treatment of stress fractures occurring in metatarsal bones is achieved with rest or immobilization for 4-6 weeks.39,57 Calcaneal stress fracture treatment with exercise modification is often successful.39,57 Navicular stress fractures are typically treated more conservatively due to risk of non-union with non-weight bearing for at least six weeks.81 Fibular stress fractures are treated conservatively for 6-8 week with favorable outcomes. Six weeks of conservative treatment is often sufficient for talar stress fractures.39 Medial malleolar stress fractures have an average time to return to play is 7.6 weeks (range 3-12 weeks) with operative treatment typically allowing for quicker return to play.57,41,81 Sesamoid stress fractures that fail non-operative management after 2-3 months are treated surgically to avoid nonunion.57
Morton’s neuroma typically resolves with pressure relieving footwear.58,76 Metatarsalgia is treated with a metatarsal pad to reduce compression and irritation.59 More than two thirds of patients diagnosed with plantar fasciitis will have improvement in symptoms within one year of conservative management.63 The majority of patients with turf toe sustain mild injury and most typically recover with conservative management after about two weeks.79 With more severe injury, patients may require three to four months for healing and less than 2% of patients require surgery.60,61,62,79
Heel pain secondary to Haglund deformity typically resolves with conservative measures; however, surgical resection of the bony deformity may be required in resistant cases.65,66 Tarsal coalition though initially managed conservatively requires surgery in two thirds of cases.67 Accessory ossicles are generally amenable to conservative management and surgical intervention has shown mixed success.69,70 Os trigonum typically responds well to conservative management.71
At different disease stages
Preventative measures include education about proper fitting and selection of shoes, appropriate increase in training frequency and intensity, as well as medical screening to identify individuals at risk of overuse injuries.8
The goals of treatment for tendinopathies are to minimize pain, prevent further degeneration, and allow return to activity. Conservative management options include rest (complete or relative), cryotherapy, short term use of scheduled anti-inflammatory medications, orthotics (heel lift, change of shoes, corrections of malalignments), and topical glyceryl trinitrate.35 Patients should be referred to physical therapy to guide engagement in progressive exercises, namely eccentric exercise programs, for several weeks and focus on improving flexibility. Eccentric strengthening is postulated to aid in treatment by stimulating tissue remodeling and promoting normalization of the tendon structure.31 Operative treatment is recommended for patients who do not respond adequately to a 3 to 6-month trial of appropriate conservative treatment.1,16
Stress fractures are treated with relative rest, correction of training errors, addressing muscular imbalances, and optimization of mechanical alignment. Treatment of low-risk stress fractures requires relative rest with progression to activity modification on a pain free level within 3-8 weeks. Treatment of high-risk stress fractures, depending on the exact site and grade of the fracture, may require absolute rest (4-12 weeks) or surgery.1,17 Arendt and Griffiths proposed a classification (grade 1-4) for stress fractures with the aim to define the length of resting time (e.g., stage 1; 3.3 weeks and stage 4; 14.3 weeks).40 Non-weight bearing with immobilization in a cast may be necessary depending on the location of the fracture.39 An effective rehabilitation program includes referral to physical therapy for muscle strengthening and guided generalized conditioning, typically through cross-training or aquatic exercise.4,17 Analgesics may be used for pain control and anti-inflammatory medications should be used sparingly and for short periods of time, as they can interfere with bone healing.17 Orthotics may play a role particularly in athletes with hyperpronation. Lastly, further workup to evaluate for underlying bone demineralization or disorder may be required depending on the history.
Coordination of care
Coordination of care includes clear communication between a multidisciplinary healthcare team which may include physiatrists, orthopedic surgeons, family physicians, and physical therapists. In the case of stress fractures, nutrition and sports psychologists may be involved as well.
Patient & family education
Patients and their support systems, including family, coaches, and trainers, should be involved in care. Education about the diagnosis, treatment options, expectations for recovery, and the return to play decision making process should be provided. Communication with employers outlining appropriate activity is also important.
There are several emerging treatment options for stress fractures, including injection with concentrated bone marrow aspirate, platelet rich plasma (PRP), injectable bone graft substitutes, pulsed parathyroid hormone, electrical osseus stimulation and extracorporeal shock wave therapy (ESWT) have been investigated but the results have been largely inconclusive.18,29 Additional therapies including oxygen supplementation therapy aimed at stimulating osteoblasts, growth factor rich preparations, and application of magnetic fields are being investigated to aid in the treatment of stress fractures. 38,17 Therapeutic ultrasound may decrease healing time in navicular stress injuries.27
With regard to tendinopathy, several therapies have been examined. ESWT has shown promise particularly with treatment of calcific tendinopathy, however additional high quality studies are needed to make definitive determination with regard to overuse tendinopathy.28,47 Injections with hyaluronic acid and corticosteroids may benefit some patients, however the data is largely inconclusive, and the role of steroids remains controversial due to risk of tendon rupture and worsening dysfunction.34,36 Peroneal tendinopathy may be treated with PRP injections however results have been mixed in the medical literature.19 Prolotherapy has shown efficacy in treatment of other tendinopathies such as the rotator cuff but no studies have been done with regard to the foot and ankle specifically.28 Iontophoresis may provide pain relief but there is insufficient evidence to support its regular use.37
Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills
The etiology of ankle and foot overuse injuries is multifactorial, involving intrinsic and extrinsic risk factors. Identification and education concerning these risk factors is necessary to avoid chronicity.
Gathering a comprehensive history of presenting illness including the context in which symptoms developed, with an understanding of the patient’s goals for treatment, is essential to making the correct diagnosis and designing an effective treatment plan.
Thorough physical examination including functional assessment, paying careful attention to any muscular imbalances, can assist with guiding appropriate physical therapy regimen.
Typically standing ankle and foot radiographs are used to evaluate for stress fracture; however, they may initially be negative therefore MRI has become the gold standard in evaluation. Ultrasound is efficacious in diagnosis of tendinopathy and allows for evaluation of functional evaluation of the tendon.3
The goal in treatment of overuse injuries of the foot and ankle is to provide adequate pain control to allow for rehabilitation to prevent further injury and allow healing of damaged structures.
Cutting Edge/ Emerging and Unique Concepts and Practice
Some of the cutting-edge therapies for stress fracture treatment include use of hyperbaric oxygen chambers, injection with PRP and recombinant parathyroid hormone, however evidence to support these strategies is inconclusive. With regard to tendinopathy, emerging biologic therapy using injections with molecular scaffolds to deliver mechanical supports which provide an environment aimed at matrix remodeling and tendon regeneration is on the horizon.34 Gene therapy remains experimental; however, the goal is to provide genetic material that codes for growth factors which promote differentiation of stem cells into fibroblasts thus accelerating tendon healing.34 Lastly, the use of stem cells to promote tendon regeneration is being investigated.
Gaps in the Evidence-Based Knowledge
Stress fracture prophylaxis with calcium or vitamin D supplementation, or bisphosphate therapy, have been theorized however the evidence to support these interventions is inconclusive.17 Emerging treatment strategies for tendon injuries is of high interest as tissue engineering and regenerative medicine concepts continue to evolve. Further research is needed in order to qualify the precise conditions which are successfully treated by these therapies before such interventions can be safely introduced into clinical trials.20 As for stress fractures, few studies using growth factors have reported that when used during surgical treatment of high-risk fractures, they may accelerate and improve recovery.17 As mentioned above, there are many cutting-edge therapies that are being used to treat overuse injuries, however additional high-quality research is needed to delineate how exactly these therapies play into treatment and return to play protocols.
- Wilder, P. and Sethi, S. Overuse injuries: tendinopathies, stress fractures, compartment syndrome, and shin splints. Clin Sports Med. 2004;23:55-81.
- Patel, D., Matt, R., and Kapil, N. Stress Fractures: Diagnosis, Treatment, and Prevention. American Family Physician. 2011; 83(1).
- Khoury, V., Guillin, R., Dhanju, J., and Cardinal, E. Ultrasound of Ankle and Foot: Overuse and Sports Injuries. Seminars in Musculoskeletal Radiology. 2007;11(2).
- Mayer, S., Joyner, P. Almekinders, L., and Parekh, G. Stress Fractures of the Foot and Ankle in Athletes. Sports Health. 2013;6(6);481-491.
- Strakowski J, Jamil T. Management of common running injuries. Phys Med Rehabil Clin N Am.2006;17(3):537-552.
- Saglimbeni, A. (2016, August 18). Achilles Tendon Injuries Clinical Presentation. Retrieved from https://emedicine.medscape.com/article/309393-clinical.
- Malhotra, R. (2016, May 10). Peroneal Tendon Pathology Clinical Presentation. Retrived from https://emedicine.medscape.com/article/1236405-clinical.
- Hreljac A. Etiology, prevention, and early intervention of overuse injuries in runners: a biomechanical perspective. Phys Med Rehab Clin North Am.2005;16(3):651-667.
- Brukner P, Bennell K. Stress fractures. In: O’Connor F, Wilder R, eds. The Textbook of Running Medicine. New York,NY:McGraw-Hill; 2001:227-256.
- Balint GP. Best Practice and Research Clinical Rheumathology. 2003;17(1):87-111.
- Cook, J. L., and Craig R. Purdam. “Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy.” British journal of sports medicine 43.6 (2009): 409-416.
- Nigg BM. Biomechanical aspects of running. In: Nigg BM, ed. Biomechanics of Running Shoes. Champaign,IL (IL): Human Kinetics; 1986:1-25.
- Frederick EC, Hagy JL. Factors affecting peak vertical ground reaction forces in running.Int J Sports Biomech. 1986;2:41-49.
- Stacoff A, Denoth J, Kaelin X, et al. Running injuries and shoe construction: some possible relationships. Int J Sports Biomech. 1988;4:342-357.
- Cavanagh PR, Lafortune MA. Ground reaction forces in distance running. J Biomech. 1980;13:397-406.
- Alfredson, H., and Cook, J.A treatment algorithm for managing Achilles tendinopathy: new treatment options. Br J Sports Med. 2007;41:211–216.
- Astur, D., Zanatta, F. , Goncalves, G., Moraes, E., De Castro, A., and Ejnisman, B. Stress fractures: definition, diagnosis and treatment. Rev Bras Ortop. 2016;52(1):3-10.
- Vannini F, DiMatteo B, Filardo G, Kon E, Marcacci M, Giannini S. Platelet-rich plasma for foot and ankle pathologies: a systemic review. Foot Ankle Surg. 2014;20(1):2-9.
- Ho, J., Sawadkar, P., and Mudera, V. A review on the use of cell therapy in the treatment of tendon disease and injuries.J Tissue Eng.2014.5:1-18.
- Aicale, R., D. Tarantino, and N. Maffulli. “Overuse injuries in sport: a comprehensive overview.” Journal of orthopaedic surgery and research 13.1 (2018): 1-11.
- Johanson, Marie A. “Contributing factors in microtrauma injuries of the lower extremity.” Journal of back and musculoskeletal rehabilitation 2.4 (1992): 12-25.
- Albers, Iris Sophie, et al. “Incidence and prevalence of lower extremity tendinopathy in a Dutch general practice population: a cross sectional study.” BMC musculoskeletal disorders 17.1 (2016): 1-6.
- Aicale, R., D. Tarantino, and N. Maffulli. “Bio-orthopaedics [Internet].” (2017): 249-73.
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Original Version of the Topic
Alexandra Rivera-Vega, MD, Stephanie P. Joseph, MD, William F. Micheo, MD. Ankle and foot overuse disorders. 9/20/2014
Previous Revision(s) of the Topic
William Micheo, MD, Brenda Castillo, MD, Alexandra Rivera, MD, Odrick Rosas, MD. Ankle and foot overuse disorders. 2/13/2018
Lindsay Burke, MD
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Kristina Barber, MD
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Malia Cali, MD
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Adele Meron, MD
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