Ankle Arthritis: Part I. Joint Preservation Techniques and Arthrodesis

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.


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

Arthroscopic or open débridement

Subchondral drilling

Osteochondral allografts for defects

Chondrocyte transplantation (autologous, juvenile particulate)

Periarticular osteotomy

Distraction arthroplasty

Interposition arthroplasty

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.

FIGURE 1 A, AP radiograph demonstrating that the tibial plafond makes an angle with the mechanical axis that is referred to as the distal tibial articular surface (TAS) angle. B, Lateral radiograph demonstrating that the tibial lateral surface (TLS) angle is the same measurement in the sagittal plane. The normal TAS angle is 88° to 93°, and the TLS angle is 80° to 81°.

FIGURE 2 AP (A), mortise (B), and lateral (C) views of the ankle of a 43-year-old man with a 10-year history of an ankle fracture treated nonsurgically. Radiographs show evidence of a midfibular shaft fracture with malunion and unstable syndesmosis with substantial joint space narrowing.

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.

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.

FIGURE 3 AP radiograph of the ankle of a 54-year-old man with a history of chronic ankle instability with multiple ankle inversion injuries reveals substantial varus deformity with medial tibiotalar joint space loss and chronic spurring of the ankle joint.

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.

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.

Feb 27, 2020 | Posted by in ORTHOPEDIC | Comments Off on Ankle Arthritis: Part I. Joint Preservation Techniques and Arthrodesis
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