Ankle Arthritis: Part I. Joint Preservation Techniques and Arthrodesis
Samuel B. Adams, MD
David N. Garras, MD
Simon Lee, MD
Dr. Adams or an immediate family member is a member of a speakers’ bureau or has made paid presentations on behalf of Arthrex, Inc.; serves as a paid consultant to or is an employee of 4web, Medshape, Regeneration Technologies, Inc., Sonoma Orthopaedics, and Stryker; has stock or stock options held in Medshape; and serves as a board member, owner, officer, or committee member of American Orthopaedic Foot and Ankle Society. Dr. Garras or an immediate family member has received royalties from WRS; is a member of a speakers’ bureau or has made paid presentations on behalf of Amniox and Sonoma; serves as a paid consultant to or is an employee of Amniox, Sonoma, and Stryker; has stock or stock options held in AK Spinal Instuments; and serves as a board member, owner, officer, or committee member of American Orthopaedic Foot and Ankle Society. Dr. Lee or an immediate family member serves as a board member, owner, officer, or committee member of American Orthopaedic Foot and Ankle Society.
ABSTRACT
The ankle is a highly congruent joint that experiences large forces through a small surface area. Ankle arthritis can have a substantial impact on patient quality of life. Patients with ankle arthritis present with pain, dysfunction, activity limitations, swelling, and limited ankle motion. The majority of ankle arthritis is caused by prior trauma. If a patient’s nonsurgical management fails, surgical intervention is indicated. Surgical treatment includes a wide variety of procedures and can be subdivided into joint-sparing and joint-sacrificing options based on the amount of arthrosis, deformity present, and patient expectations. Localized arthritis can be treated with anterior débridement or varus or valgus producing supramalleolar osteotomies. Diffuse mild to moderate arthritis can be treated with distraction arthroplasty whereas severe arthritis can be treated with bipolar allograft replacement or arthrodesis.
Introduction
The ankle joint is unusual relative to other weight-bearing joints in the body. For example, primary osteoarthritis (OA) is much less likely to develop and the ankle joint is more capable of resisting degradation compared with the hip or knee joints.1,2 Ankle arthritis can have a substantial impact on patient quality of life. In fact, ankle arthritis causes patients to take fewer total steps per day, take fewer high-intensity steps, and walk at a slower walking speed compared with patients without ankle arthritis.3 Most arthritis seen in the ankle is posttraumatic in nature.4,5,6 This posttraumatic osteoarthritis (PTOA) is typically attributed to the severity of the initial injury and the reduction quality of original fractures.7 Inflammatory arthropathies, neuroarthropathies, primary OA, septic arthritis, hemophilia, and hemochromatosis are other nontraumatic etiologies of ankle arthritis cases.5 Most of those with PTOA of the ankle are relatively young, active, high-demand patients. They may have multiple previous incisions about the ankle, which creates a difficult treatment situation. Patients with PTOA are an average of 7 years younger (58 versus 65 years) than those with primary OA, and PTOA is responsible for 78% of ankle arthritis cases compared with 9% for primary OA.6
Initial treatment of ankle arthritis is typically nonsurgical. Anti-inflammatory and analgesic medications, variable levels of immobilization, intra-articular injections (corticosteroids, viscosupplementation, and platelet-rich plasma [PRP]), dietary supplementation, and orthotic/brace devices are the most commonly used nonsurgical treatment options. If a patient’s nonsurgical management fails, surgical intervention is indicated. Surgical treatment includes a wide variety of procedures and can be subdivided into joint-sparing and joint-sacrificing options based on the amount of arthrosis, deformity present, and patient expectations. Joint-sparing procedures are listed in Table 1. Joint-sacrificing procedures such as allograft transplantation, ankle arthrodesis, or arthroplasty are usually reserved as the last line of treatment. This chapter explores joint preserving techniques, allograft arthroplasty, and arthrodesis as treatments for ankle arthritis.
TABLE 1 Joint-Sparing Procedures | |
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Anatomy and Biomechanics
The ankle is a constrained joint that gains most of its stability from the bony anatomy of the medial malleolus, the distal fibula, and the configuration of the tibiotalar articulation (tibial plafond and talar dome). Additional stability is gained through static ligamentous structures, including the interosseous membrane, tibiofibular and collateral ligaments, and dynamic musculotendinous units. The medial ligamentous structures (deltoid confluence) are the primary stabilizers of the ankle5 but are much less commonly injured than the lateral ligaments (anterior talofibular and calcaneofibular ligaments).
The ankle joint is directly perpendicular to the mechanical axis of the lower extremity. Both the anatomic and mechanical axes are the same in the tibia and should pass through the midpoint of the ankle articulation in the coronal and sagittal planes. In the coronal plane, the tibial plafond forms an angle with the mechanical axis, which is referred to as the distal tibial articular surface (TAS) angle. The tibial lateral surface (TLS) angle is the same measurement in the sagittal plane. The normal TAS angle is 88° to 93°, and a normal TLS angle is 80° to 81°8,9,10 (Figure 1).
The ankle joint is mainly a rolling joint with highly congruent surfaces, particularly during weight bearing.5,6 It is smaller than the knee or hip in surface area and consequently experiences a much higher force per area.5,6,11 When the ankle is not bearing weight, the joint is incongruent. However, when weight bearing, the ankle joint becomes more congruent and allows for more joint surface area contact to dissipate the forces during weight bearing.5 During normal activities, forces in excess of 3.5 times body weight are transmitted across the ankle joint and increase to 9 to 13.3 times body weight during running.12 The primary motion of the tibiotalar joint is in the sagittal plane and averages a 43° to 63° arc in dorsiflexion and plantar flexion, with only 30° required for steady-state walking. There is an average of 10° of rotational movement of the talus within the mortise.5
Incidence and Etiology
Ankle arthritis is estimated to occur in 1% of the population.6 In contrast to other weight-bearing joints of the lower extremity, the ankle joint is much more resistant to the development of primary “wear and tear” OA but is more susceptible to PTOA.5 In fact, 76% to 78% of all ankle arthritis cases can be attributed to trauma whereas primary OA accounts for 7% to 9% of cases.5,6,11 The remainder of ankle arthritis cases (12% to 13%) are attributable to secondary arthritis as a result of rheumatoid arthritis, neuroarthropathy, hemochromatosis, and postinfectious degeneration.5,6,11
Joint motion, cartilage thickness, incidence of fractures or ligamentous trauma, and metabolic and mechanical factors differ between the knee and ankle and help explain the difference in incidence of primary OA and PTOA.2,5,6,11 Whereas knee OA affects more women than men, ankle OA affects more men than women.2
While approximately 80% of ankle arthritis is posttraumatic in nature, not all trauma about the ankle results in PTOA. The overall rate of ankle PTOA is 14% following all ankle fractures; however, arthritis developed in as many as 33% of patients with Weber C fractures in some studies.5,13 Large posterior malleolar fractures with displacement are associated with a higher incidence of arthritis.5,13 Arthritis has been estimated to occur in 13% to 54% of tibial plafond fractures, 40% of bimalleolar fractures, and up to 71% of trimalleolar fractures.9
The exact cause of ankle PTOA is not known. The adequacy of reduction was traditionally believed to be a strong predictor of outcomes5,13 (Figure 2). However, this line of thinking has been disputed in the literature, with different conclusions appearing in various studies.5,13,14 One reason could be the difference in ankle cartilage/chondrocytes. Unlike the knee, the articular cartilage of the ankle is uniform in thickness, measuring 1 to 1.7 mm and displays much higher compressive stiffness than hip or knee cartilage.2,5,6,11 Although ankle cartilage may develop fissures or fibrillations attributable to aging and wear, these conditions do not progress to OA as they would in the knee or hip.2,5,6,11 Ankle cartilage also does not decrease in tensile strength with age.2,3,5,6,11
Additionally, chondrocytes in the ankle respond differently than those in the knee or hip to biochemical and biologic factors and resist degradation. Chondrocytes in human ankle cadavers joints have increased proteoglycan (PG) and rates of collagen rates in comparison with knee chondrocytes.105 The increased turnover may
allow ankle chondrocytes to respond better to subtle atraumatic “wear and tear” arthritis compared with knee chondrocytes. Moreover, ankle chondrocytes are less responsive to inflammatory mediators such as interleukin-1β (IL-1β) and synthesize much less of the collagen breakdown molecule, matrix metalloproteases (MMP) (specifically MMP-8, which is elevated in OA) in response to IL-1 than chondrocytes in the hip or knee.2,5,6,11 This decreased sensitivity is likely attributable to a smaller number of differing types of IL-1 receptors on ankle chondrocytes. As a result, the ankle is potentially less susceptible to damage by inflammatory mediators.
allow ankle chondrocytes to respond better to subtle atraumatic “wear and tear” arthritis compared with knee chondrocytes. Moreover, ankle chondrocytes are less responsive to inflammatory mediators such as interleukin-1β (IL-1β) and synthesize much less of the collagen breakdown molecule, matrix metalloproteases (MMP) (specifically MMP-8, which is elevated in OA) in response to IL-1 than chondrocytes in the hip or knee.2,5,6,11 This decreased sensitivity is likely attributable to a smaller number of differing types of IL-1 receptors on ankle chondrocytes. As a result, the ankle is potentially less susceptible to damage by inflammatory mediators.
However, one potential etiology of ankle PTOA is related to inflammation. While inflammation is the
initial step in healing of fractures, intra-articular fractures cause an inflammatory burden on the uninjured cartilage throughout the joint. In fact, it has been shown that the intra-articular environment (synovial fluid) after ankle fracture and at end-stage ankle OA (from traumatic causes) is composed of high numbers of inflammatory mediators.106 In a comparison of 21 patients who sustained intra-articular ankle fractures, Adams et al identified several cytokines and MMPs including GM-CSF, IL-10, IL-1, IL-6, IL-8, TNF, MMP-1, MMP-2, MMP-3, MMP-9, and MMP-10 after intra-articular ankle fractures.15,17 These inflammatory mediators were found to rise acutely after ankle fracture and remained elevated for days to months after injury providing evidence of a persistent inflammatory environment in synovial fluid after injury.
initial step in healing of fractures, intra-articular fractures cause an inflammatory burden on the uninjured cartilage throughout the joint. In fact, it has been shown that the intra-articular environment (synovial fluid) after ankle fracture and at end-stage ankle OA (from traumatic causes) is composed of high numbers of inflammatory mediators.106 In a comparison of 21 patients who sustained intra-articular ankle fractures, Adams et al identified several cytokines and MMPs including GM-CSF, IL-10, IL-1, IL-6, IL-8, TNF, MMP-1, MMP-2, MMP-3, MMP-9, and MMP-10 after intra-articular ankle fractures.15,17 These inflammatory mediators were found to rise acutely after ankle fracture and remained elevated for days to months after injury providing evidence of a persistent inflammatory environment in synovial fluid after injury.
Primary ankle OA may be secondary to asymmetric cartilage wear. Intra-articular deformities with varus tilting occur as a result of impaction, distal tibial osteonecrosis, or chronic cavovarus. However, flatfoot deformity may develop in patients with chronic ankle instability, hindfoot valgus, and peroneal tendon dysfunction.8 This could lead to asymmetric wear and/or progression of degeneration (Figure 3). Degeneration in one area can increase the contact pressures and potentially cause degeneration in another area. Although not in end-stage ankle arthritis, this concept has been demonstrated with even subtle mismatch of articular congruency, such as in the setting of osteochondral grafts in the talus. Latt et al demonstrated that with “recessed” osteochondral grafts there was transfer of pressure to the opposite side of the talus.19 Similarly, ankle instability secondary to incompetent ankle ligaments causes incongruity in the ankle joint. Biguoette et al20 recently compared ground reaction forces in patients with chronic ankle instability to stable controls. The chronic ankle instability group had significantly higher impact peak forces and active peak forces compared with the control group. As this pathology is secondary to an initial traumatic event (ankle sprain), there is debate about whether to arthritis secondary to chronic ankle instability should be considered PTOA.
Clinical Presentation and Imaging
Patients with ankle arthritis present with pain, dysfunction, activity restrictions, swelling, and limited ankle motion. Their primary report is pain in a transverse line across the anterior ankle. Patients often note pain with any weight-bearing activity such as prolonged standing, walking, running, and stair climbing. Most patients also have reduced self-perceived function as determined by functional assessments and questionnaires.3 There is typically a history of ankle trauma or multiple ankle sprains.
Patients often have decreased sagittal plane motion and plantar flexion moment and power.3 Nonarthritic ankle motion primarily occurs in the sagittal plane, with an arc of 30° required for normal walking.5 In the setting of end-stage ankle arthritis, motion is limited.5 As a result, compensation by the hindfoot and forefoot is necessary, which increases the shear forces at the midtarsal joints.5 Ankle arthritis affects various gait pattern parameters such as walking speed, cadence, and stride length.3,5 Patients with arthritis also exhibit antalgic gait patterns with abnormal plantar pressures. Those with ankle arthritis also exhibit increased oxygen consumption and decreased gait efficiency.5 Consequently, sporting activities, prolonged ambulation, fast walking, and running are difficult.5
The first step in the treatment of ankle arthritis is to obtain a thorough history and physical examination. The history should ascertain the etiology of the disease, timing of onset of symptoms, current and prior symptoms, history of traumatic events or recurrent injuries, current level of function, treatment to date, and the desired level of function. Confounding factors, including systemic diseases, current medications (including current opiate use), prior surgeries, history or suspicion of infections or wound healing problems, and a social history that
includes drug abuse and smoking history should be investigated in depth. A referral to a primary care physician or rheumatologist may help delineate the etiology of arthritis in patients with no history of mechanical causes or trauma. A neurology consultation may be required for patients with atypical pain, numbness, dysesthesias, burning, or non-activity-related pain to rule out spinal or neuropathic etiology.
includes drug abuse and smoking history should be investigated in depth. A referral to a primary care physician or rheumatologist may help delineate the etiology of arthritis in patients with no history of mechanical causes or trauma. A neurology consultation may be required for patients with atypical pain, numbness, dysesthesias, burning, or non-activity-related pain to rule out spinal or neuropathic etiology.
Postoperative complications and adverse outcomes must be mitigated preoperatively. Indolent infections and traumatized soft tissues can pose risks for any surgical intervention, especially when surgical implants are to be placed. Any patient with a history of infection or nonunion should be considered for a staged procedure to obtain deep cultures and inflammatory markers (complete blood count with differential, erythrocyte sedimentation rate, and C-reactive protein level) to rule out any indolent infections. Patients with circulatory dysfunction, diabetes mellitus, smoking history, and those with a history of osteonecrosis are at much higher risk for wound complications, infections, and nonunions. Smoking is a well-documented cause of postoperative complications in foot and ankle surgery, increasing risk for nonunion by 16 times versus nonsmokers.21 Smokers should be encouraged to quit smoking; surgeons have advocated withholding surgical intervention until patients are nicotine free in elective cases. There is no consensus as to the required length of time required for the complications of smoking to dissipate to the level experienced by nonsmokers or if the variance ever completely normalizes. Patients with diabetes or peripheral neuropathy will require more rigid fixation and longer periods of immobilization.22
The physical examination should begin with a gait analysis and evaluation of the alignment of the entire extremity to include the hip and knee. Proximal deformities should be addressed before any treatment of the ankle is considered. A complete examination of a patient’s neurovascular status is essential. A patient with any changes in skin color, weak pulses, differences in vascularity compared with the contralateral side, or lymphedema should have a complete vascular workup or referral to a vascular surgeon. The location and condition of all prior incisions and scars should be noted. Range of motion of the ankle, subtalar joint, and transverse tarsal joints should be examined and recorded. Care should be taken to isolate motion to the responsible joints because Chopart joint motion (talonavicular and calcaneocuboid joints) often complicates the examination.
The minimum radiographic assessment must include three weight-bearing views of the ankle (AP, mortise, and lateral). These images will reveal the radiographic extent of the ankle arthritis including the intra-articular deformity, joint space narrowing, and ankle osteophytes. Kraus et al23 published a radiographic atlas of ankle arthritis changes and associated Kellgren-Lawrence grades. Another study demonstrated that increasing Kellgren-Lawrence grades significantly correlated with increasing pain and decreasing American Orthopaedic Foot and Ankle Society (AOFAS) ankle-hindfoot scores.15
If alignment is questioned at the level of the ankle joint or below then a hindfoot alignment view should be obtained.16 Proximal alignment questions or leg-length discrepancies can be assessed on full-length and limb alignment films. The location and degree of deformity are the most important factors in the decision-making process for surgical treatment. The presence of arthritis in the subtalar joint or the transverse tarsal joints may alter treatment algorithms. If radiographs do not correlate with a patient’s symptoms or examination, MRI or CT may be indicted. CT may identify adjacent joint arthritis, subchondral cysts, and any specific bony deformities, whereas MRI may be indicated to evaluate for suspected osteonecrosis, bone edema, or associated soft-tissue pathology. These advanced imaging modalities are also important for preoperative planning.
Nonsurgical Treatment
Although the literature is limited regarding the success rate of nonsurgical treatment, all patients with ankle arthritis should undergo a trial of nonsurgical management before proceeding with surgical intervention. However, some authors advocate early surgical intervention for patients with congenital or posttraumatic deformity rather than waiting for symptoms to worsen.24 This is especially true for severe deformities with impending skin compromise or when the deformity/arthritis causes altered gait that can lead degeneration of other joints, such as the contralateral hip.
Nonsurgical treatments are aimed at relieving symptoms and prolonging the life and function of the native ankle but at the present do not cure the arthritis. Rest and activity modification may help relieve the initial inflammation, but these interventions generally are not acceptable long-term solutions for active patients.24 Walking aids such as canes or walkers are also helpful, but usually are tolerated only by elderly patients. For patients with reports of instability or weakness, a course of physical therapy that includes strength training, proprioceptive training, stretching, and aerobic nonimpact exercise may be beneficial.1,24
Oral Therapy
Oral NSAIDs and, on occasion, a short course of oral steroids may be beneficial, especially for patients with inflammatory arthropathies (but also are useful for all etiologies).1 NSAIDs exert their function by inhibiting
cyclooxygenase and reducing prostaglandins, which are inflammatory mediators that protect gastric mucosa.25 Corticosteroids also function by inhibiting several inflammatory pathways.25 Care should be taken in long-term use of NSAIDs because they can have deleterious effects on liver and kidney function, which necessitates monitoring. NSAIDs can also lead to gastric or enteric ulcers and carry an increased risk for bleeding. Analgesic medications, whether topical compounding creams or oral acetaminophen or tramadol, may be useful in controlling pain and increasing function and have a safer adverse effect profile than NSAIDs.25
cyclooxygenase and reducing prostaglandins, which are inflammatory mediators that protect gastric mucosa.25 Corticosteroids also function by inhibiting several inflammatory pathways.25 Care should be taken in long-term use of NSAIDs because they can have deleterious effects on liver and kidney function, which necessitates monitoring. NSAIDs can also lead to gastric or enteric ulcers and carry an increased risk for bleeding. Analgesic medications, whether topical compounding creams or oral acetaminophen or tramadol, may be useful in controlling pain and increasing function and have a safer adverse effect profile than NSAIDs.25
Glucosamine is thought to inhibit IL-1 production, prostaglandins, and MMPs. It may increase the native production of hyaluronic acid.26 Chondroitin sulfate inhibits leukocyte elastase and the migration of polymorphonuclear leukocytes, and it may also increase hyaluronic acid production.26 There is no research on the use of glucosamine or chondroitin sulfate in the ankle. Most of the current literature suggests that glucosamine and chondroitin sulfate may provide symptomatic relief of moderate to severe arthritis of the knee with minimal side effects.26
Patients with rheumatoid arthritis and other secondary causes of ankle arthrosis would benefit from treating the underlying condition. Disease-modifying antirheumatic drugs (DMARDs) are medications that halt the progression of the rheumatoid destructive process. These include both biologic (IL-1 and tumor necrosis factor antagonists) and nonbiologic (methotrexate and sulfasalazine) options.25 However, these drugs typically take months to exert their action and should be managed by a rheumatologist.
Intra-articular Injections
Intra-articular corticosteroid injections may limit pain and inflammation and can be safely used sparingly. Repeated injections carry limited risk for skin discoloration, fat necrosis, and soft-tissue destruction and pose increased risk for infection.1,24 There has been no evidence to indicate destructive effects to cartilage resulting from these injections. Oral and injectable corticosteroids should be used with caution and monitoring in patients with diabetes because they can lead to alterations in blood glucose levels.
Hyaluronans have been used with success in the knee as well as in other joints. However, limited literature exists to support their use in the ankle. Hyaluronic acid has been shown to inhibit phagocytosis, decrease synovial fluid inflammatory mediators, and stimulate production of hyaluronic acid by chondrocytes.26 Salk et al27 performed a randomized controlled, double-blinded study on 20 patients using sodium hyaluronate over five weekly injections. At 6-month follow-up, there was a decrease in pain and disability and a trend toward better symptomatic relief in the hyaluronate group. It was also found to be as safe as saline.26,27 This finding was confirmed in other studies that showed a significant decrease in pain and improvement in function with hyaluronate use.28,29
Although PRP has been used in an expanding number of musculoskeletal disorders, there is minimal evidence to support its use in the ankle. The mechanism of action of PRP is thought to involve platelet degranulation with the subsequent release of various growth factors and the stimulation of stem cell lines involved in the healing and reparative process. Fukawa et al17 recently published a study of PRP injections into 20 patients with ankle OA. Three injections were given at 2 week intervals under ultrasonography guidance. Pain was significantly improved even at 24 weeks (study end point) after injection but maximal pain relief occurred 12 weeks after injection.
Stem (stromal) cell injections have also been tried, but as with other injectables, there is little data to support their use. A recent meta-analysis of stromal cell injections into various joints, including the ankle, demonstrated a significant decrease in AOFAS scores in patients who received an ankle injection but no difference in the American Knee Society Knee Score System, the Hospital for Special Surgery Knee Rating Scale and the International Knee Documentation Committee score for patients receiving knee injections. This may indicate that stem cell injections may be better served for ankle arthritis.30
Vannabouathong et al published a systematic review of intra-articular injections of steroids, hyaluronic acid, PRP, and stem cells into the ankle. Unfortunately, the data were quite limited and therefore minimal conclusions can be obtained with regard to one therapeutic injection over another.
Bracing Treatment
Bracing treatment is a valuable option with which to control pain and improve function in ankle arthrosis. Ankle motion occurs mainly in the sagittal plane; however, there is coronal plane motion as well. Therefore, brace options must be able to control both sagittal and frontal plane motion to effectively alleviate symptoms.31 A custom-made ankle-foot orthosis (AFO) will help decrease symptoms and increase endurance.24 A leather gauntlet (Arizona type) brace has similar properties as the AFO but is usually much better tolerated.31 When all weight-bearing activities cause pain, a patella tendon-bearing AFO may be used to immobilize and off-load the forces across the ankle. Shoe modifications such as a heel lift, solid ankle cushioned heel, and stiff rocker-bottom sole are also useful (Figure 4). Heel lifts are used to limit ankle dorsiflexion reducing the pain from anterior impingement.24,31 Stiff-shanks, rocker-bottom shoes/soles can limit ankle
motion and normalize gait.24 They can be effective in the treatment of ankle arthritis but are more efficacious for midfoot arthritis. A solid ankle cushioned heel dampens heel strike and lessens rapid ankle plantar flexion during heel strike. Additionally, all of these modifications can be combined, such as a heel lift or a solid ankle cushioned heel and an Arizona or AFO brace.31
motion and normalize gait.24 They can be effective in the treatment of ankle arthritis but are more efficacious for midfoot arthritis. A solid ankle cushioned heel dampens heel strike and lessens rapid ankle plantar flexion during heel strike. Additionally, all of these modifications can be combined, such as a heel lift or a solid ankle cushioned heel and an Arizona or AFO brace.31
Surgical Treatment
When obtaining a patient’s history, information about their current symptoms and level of function, their desired level of function, and current radiographic studies may help direct treatment. Decisions regarding joint preservation or sacrifice are dependent on many factors, including the patient’s age, predisease functional status, current and desired functional level, history of infections, osteonecrosis, systemic diseases such as diabetes or rheumatoid arthritis, vascular status, and radiographic findings. There should be an individualized plan that is agreeable to both the patient and surgeon that provides maximal relief and function from a single procedure and does not preclude salvage options.
Joint Preservation Surgery
Synovectomy and Débridement
Patients recalcitrant to nonsurgical treatment who have localized anterior ankle pain and painful dorsiflexion are defined as having anterior ankle impingement. Patients can present with radiographic evidence of a distal anterior tibial osteophyte and a bony block or limited ankle range of motion (ROM), or they may have anterior ankle pain with terminal dorsiflexion and may benefit from a simple arthroscopic or open anterior decompression. Débridement for mild to moderate arthrosis with osteophytes, synovitis, loose bodies, and mechanical impingement is effective for pain relief and improvements in terminal dorsiflexion ROM1,24 (Figure 5). Patients with rheumatoid arthritis, hemophilia, pigmented villonodular synovitis, and other soft-tissue pathologies may benefit from a simple synovectomy.24 However, a 5-year survival analysis indicates that débridement is most effective in patients with predominately anterior ankle impingement and minimal global arthritic changes.32 In a 2007 study of outcomes after anterior débridement, investigators found that none of the patients treated for anterior impingement required further surgery at 5-year follow-up compared with 28%
of those with degenerative changes.32 This finding was independent of patient age. If there is any anterior talus translation then this technique should not be used because removal of the anterior tibial lip can cause further anterior talus translation.
of those with degenerative changes.32 This finding was independent of patient age. If there is any anterior talus translation then this technique should not be used because removal of the anterior tibial lip can cause further anterior talus translation.
Distraction Arthroplasty
Background. While once popular, distraction arthroplasty is falling out of favor due to cost and mixed outcomes. It is an alternative option to ankle arthrodesis or arthroplasty in younger patients with arthritis. Ankle distraction arthroplasty was first popularized in 1995.33 Distraction has been used in other joints with relative success.34,35,36 This technique uses an Ilizarov-type external fixator to distract the ankle joint and relies on ligamentotaxis to restore normal joint space, off-load the joint, and allow cartilage to recover.34,35,36 The exact mechanism of its action is not known. Theories involve mechanical stress relief, continued intermittent intra-articular fluid pressure changes, and increased synovial fluid (believed to enhance chondrocyte reparative activity).33,35,36,37 Other theories include a positive stretch effect on nerve endings, decreased synovial inflammation, intra-articular fibrous tissue formation, stretching of the joint capsule, and decreased joint reactive forces.35,36,38 Distraction likely allows for fibrocartilage formation, which may seal cartilage defects and decrease pain from hydrostatic pressure on the subchondral bone.33,34,35,39 Maintenance in the fixator for 3 months allows for a reduction of subchondral bone sclerosis, which has been linked to improved clinical outcomes.34,35,36