Khushdeep S. Vig

Marlon J. Murasko

Hamza Murtaza


Ankle arthritis causes a substantial socioeconomic burden to the society, and it has significant effects on function, with similar morbidity, pain, and loss of function as hip arthritis. The incidence, however, is significantly lower than that of hip or knee arthritis due to a combination of biomechanical and anatomical factors that protect the ankle joint from developing primary degenerative arthritis. These include differences in articular cartilage, joint motion, and the susceptibility of cartilage to inflammatory mediators. Anatomically, studies suggest that even though the ankle joint has thinner cartilage compared to that of the hip or knee, the cartilage is more uniform, stiffer, and resistant to indentation.1

The ankle bears up to 5 times the body weight with normal walking and has the highest load per surface area of any joint in the body. Yet, it has a smaller surface contact area compared to the hip and knee. However, the ankle joint is highly congruent, and its cartilage is uniform and stiff, allowing it to withstand high forces. In the normal situation, this congruency keeps the contact pressures at an acceptable level. But if the surface area of the joint is decreased or the congruency is lost, alteration of ankle biomechanics ensues, and the pressures rise quickly. The mechanical loading of the joint is altered, which then subsequently leads to arthritis.2

Unlike the arthritides of the hip and knee, ankle arthritis is primarily posttraumatic and most often from rotational ankle fractures. Tibial plafond fractures, malleolar fractures, fracture-dislocations of the ankle, inadequate fracture reduction, and ligamentous injury have been consistently implicated in the development of ankle arthritis. In pilon fractures, the energy of the injury, articular comminution, and displacement are associated with poorer outcomes.3 Other less common causes include chronic ligamentous instability, malalignment, inflammatory conditions, neuropathy, systemic medical conditions such as hemophilia, or idiopathic disease.1 Osteochondral injuries have also been linked to the development of ankle arthritis. However, the risk of developing arthritis following an osteochondral injury may be associated with the depth and location of cartilage damage at the time of injury.

Patients with ankle arthritis usually present with pain around the ankle joint that is worse with movements, often causing them to discontinue sports. In the later stages of the disease, they then develop nocturnal inflammatory pain, which may be associated with symptoms of ankle instability, locking, and stiffness.4 On examining the ankle, the examiner should clarify the patient’s specific discomfort because it often indicates whether the patient has global or focal disease. A history of diffuse ankle pain with activities is more commonly seen with global disease, whereas a more activity-specific complaint suggests focal disease. Pain with activities requiring maximal plantar flexion, such as descending stairs or downhill walking, often suggests posterior ankle pathology. When discomfort is anterior and occurs with activities of ankle dorsiflexion, anterior joint disease is a possibility. Subfibular pain may be suggestive
of either subtalar (ST) or ankle pathology, and posteromedial ankle pain often has a soft-tissue origin.5 Patients generally tend to seek medical help when their symptoms start affecting their ability to perform simple everyday tasks, such as walking and climbing stairs and ladders, especially if they are manual laborers.


Midfoot arthritis is a challenging problem causing chronic foot pain and significant impairment of daily activity. The exact incidence of
midfoot arthritis is unknown, as many patients may never develop symptoms that require formal evaluation. Causes of midfoot arthritis include degenerative, posttraumatic, inflammatory, neuropathic, and post hindfoot fusion.

Posttraumatic arthritis is common in midfoot following both fractures and the more subtle ligamentous Lisfranc injuries. Primary degenerative arthritis can appear spontaneously, but most patients may still describe an injury that has been overlooked. Inflammatory arthritis typically affects multiple joints and so does neuropathic Charcot osteoarthropathy. Ankle or hindfoot fusion can transfer stresses to the midfoot subsequently leading to secondary arthritis.7 Posttraumatic arthritis, however, remains the most common identified etiology of midfoot arthritis. In a Lisfranc injury, primary disruption of the weak dorsal ligaments may lead to instability of the TMT (tarsometatarsal) and intercuneiform joints. In more severe injuries, the stronger plantar and interosseous Lisfranc ligaments may tear, resulting in TMT joint subluxation and/or dislocation with dorsal displacement of the metatarsals. Even after early identification and anatomic reduction, the cartilage and ligament damage sustained at the time of injury may lead to abnormal joint loading, progressive and eccentric wear patterns, and subsequent degenerative joint disease. The severity of injury and anatomic reduction are still, however, critical factors in limiting the development of posttraumatic degenerative changes.8

Most patients with midfoot arthritis present with pain localized to the dorsum of the foot. Activity, especially that involving inversion and adduction of the midtarsal joint, worsens the pain, whereas rest and heat may provide some relief. The pain is constant and is characterized as aching; it may interfere with sleep. Some patients complain of a grating or popping sensation with the use of the joints, and crepitus may be present on physical examination.9 Pain typically gets worse when using stairs or on uneven grounds. Symptoms are due to the lack of stability, altered mechanics, and loading on the inflamed joint. Eventually, midfoot collapse occurs leading to a rigid flatfoot deformity, forefoot abduction and varus, longitudinal arch collapse, and osteophyte formation. Patients also complain of shoe wear difficulty secondary to residual deformity.


Ankle impingement includes a broad spectrum of pathology with varying etiologies, anatomic features, and presentations. It originates as a sequela from acute macrotrauma or microtrauma from repetitive movements at extreme ranges of motion and is characterized by limitations in range of motion and pain due to pathological contact between structures. This abutment can be among bone, soft tissue, or both. Impingement pathologies in the ankle are generally defined by the particular anatomic area involved. However, for simplicity, they are grouped into anterior and posterior impingement.

Anterior Impingement

Anterior ankle impingement is most often described as anterior ankle pain with restricted dorsiflexion as a result of either tibiotalar osteophytes and/or soft-tissue impingement. It is a common cause of chronic ankle pain and is particularly common in athletes who sustain repetitive dorsiflexion movements. It is thought to be the result of mechanical factors, traction, trauma, recurrent microtrauma, and chronic ankle instability.11 Characteristic spurs or exostoses at the anterior distal tibia and dorsal talar neck have been observed in athletes with anterior ankle pain and limited motion, and the morphology of these exostoses has been found to be intra-articular, well within the distal tibial and dorsal talar capsular attachments.12 Anterior intra-articular soft tissues may also contribute to impingement in isolation or in conjunction with bony lesions. A triangular, soft-tissue mass composed primarily of adipose and synovial tissues exists in the anterior joint space.11 These tissues are compressed after 15° of dorsiflexion in asymptomatic individuals. Anterior osteophytes may limit the space available for this soft tissue and exacerbate its entrapment, resulting in chronic inflammation, synovitis, and capsuloligamentous hypertrophy.

Anterior impingement typically presents as anterior ankle pain during terminal dorsiflexion. Patients are typically young and athletic and present with chronic ankle pain, limited dorsiflexion, and swelling, thereby reducing activity. The patient may also have a history of recurrent ankle inversion injuries.13 In the later stages, dorsiflexion may be limited secondary to mechanical block or pain, creating a cycle of progressive joint stiffness and loss of function. In isolated soft-tissue lesions, the patient may report a subjective popping or snapping sensation.

Posterior Impingement

Posterior ankle impingement results from compression of structures posterior to the tibiotalar and talocalcaneal articulations during terminal plantar flexion. Similar to anterior impingement, this can be caused by multiple osseous and soft-tissue etiologies in isolation or in combination. Pathology associated with the os trigonum of the posterior talus is the most common cause of posterior impingement. Less commonly, posterior symptoms may result from tibiotalar or ST degenerative joint disease due to osteophyte impingement or associated reactive hypertrophic capsule and synovium.14 Various soft-tissue structures may cause posterior impingement symptoms as well. Posterior capsuloligamentous injury due to repetitive or acute hyperflexion can lead to inflammation, scarring, and thickening of the capsule, posterior inferior tibiofibular ligament, and posterior fibers of the deltoid ligament. The flexor hallucis longus tendon, running between the medial and lateral posterior processes of the talus, is commonly affected by tenosynovitis and tendinosis. The tendinopathy may result from overuse or secondary to irritation from surrounding abnormal bony anatomy.12

In the acute injury, a forced hyper plantar flexion is usually described. In chronic cases of overuse and os trigonum syndrome, pain is
frequently noted to the posterolateral aspect of the ankle but can also be seen posteromedial and diffusely to the posterior aspect of the ankle joint. Symptoms may be worsened by activities involving plantar flexion and repetitive push-off maneuvers, including downhill running and walking, descending stairs, and high-heeled shoe wear. Posterior impingement classically presents in ballet dancers and soccer players.


Hindfoot arthritis is a pain and debilitating condition that arises in a similar way to arthritic conditions that affect the surrounding joints. It results from acute microtrauma to cartilage, repetitive microtrauma, abnormal weight-bearing stress from joint malalignment or incongruity, adjacent joint arthritis, or shear stress from ligamentous instability.15

Posttraumatic arthritis in the hindfoot most commonly occurs secondary to intra-articular fractures of the calcaneus, especially if these fractures are managed nonoperatively, which can lead to up to a 5-fold increase in the incidence of ST fusion.16 The intra-articular injury can lead to damage of the articular surface and joint malalignment. Over time, this leads to increased stress along the ST joint causing uneven loading patterns and progressive cartilage wear.16 Inflammatory arthritis also targets the hindfoot, and foot ankle pain is common in the patients with rheumatoid arthritis.17,18 In this condition, synovial inflammation leads to cartilage erosion and periarticular bony resorption, which is exacerbated by ligamentous laxity and attritional tendon rupture. These lead to joint deformity causing cartilage damage and accelerated damage to the joint surfaces.17,18 Neurovascular and neurotraumatic pathophysiology causes loss of protective sensation and proprioception and can result in Charcot arthropathy, which commonly affects the hindfoot. Continued insensate weight bearing causes rapid ST joint destruction via either repetitive microtrauma or increased osteoclastic resorption and fracture.19 Chronic planovalgus deformity seen in the late stages of posterior tibial tendon deficiency increases the load on the ST joint leading to cartilage damage.20 Iatrogenic causes of hindfoot arthritis occur due to increased load on the ST joint as a result of adjacent joint arthrodesis, especially tibiotalar arthrodesis, which has been shown to lead to 90% incidence of ST arthritis.21 A rare pathology leading to hindfoot arthritis is Müller-Weiss disease, or spontaneous osteonecrosis of the navicular leading to planovalgus deformity increasing the stresses seen in the ST joint.22

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Sep 8, 2022 | Posted by in ORTHOPEDIC | Comments Off on Bone
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