Anterior impingement

Anterior ankle impingement generally refers to entrapment of structures along the anterior margin of the tibiotalar joint in terminal dorsiflexion. Multiple osseous and soft tissue anatomic abnormalities have been recognized as causative factors.

Characteristic spurs or “exostoses” at the anterior distal tibia and dorsal talar neck have long been observed in athletes with anterior ankle pain and limited motion. Isolated talofibular lesions have also been described [6]. The morphology of anterior tibiotalar exostoses has been well-studied, and cadaveric dissections have found these lesions to be intra-articular, well within the distal tibial and dorsal talar capsular attachments [7, 8].

Although they are often referred to as “kissing osteophytes”, these tibial and talar spurs surprisingly often do not actually overlap and abut. Evaluation of preoperative CT scans has shown that talar spurs generally lie medial to the midline of the talar dome and tibial spurs are generally located laterally [9]. A distinct trough in the articular talar dome often “accepts” the tibial osteophyte during dorsiflexion. Kim, et al. referred to this as a “tram-track lesion” [10], while Raikin, et al. termed it a “divot sign” [11]. Subsequent studies have confirmed a high rate of corresponding talar cartilage lesions (80.7 %) and loose bodies in patients with distal tibial lesions [12].

Anterior intra-articular soft tissues may 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. These tissues are compressed after 15° of dorsiflexion in asymptomatic individuals [7]. Anterior osteophytes may limit the space available for this soft tissue and exacerbate its entrapment, resulting in chronic inflammation, synovitis, and capsuloligamentous hypertrophy. Post-traumatic fibrous bands [13], thickened anterior tibiofibular ligaments [14, 15], and synovial plica [16], have also been identified as causative factors.

While the impinging anatomic lesions have been well described, their exact etiology is less well understood. Early reports hypothesized spurs to be enthesophytes caused by traction to the anterior capsule during repetitive plantar flexion [3]. However, anatomic studies have demonstrated the chondral margins and lesions to be deep to the joint capsule rather than at its attachment, resulting in the traction, disproving the traction theory [79]. More recent observations of athletic populations commonly affected by anterior impingement have led to hypotheses that pathology occurs due to repetitive impaction injury to the anterior chondral margin from hyper-dorsiflexion or direct impact from an external object such as a soccer ball [17, 18].

Chronic lateral ankle instability has also been hypothesized to contribute to the development of both bony and soft tissue lesions associated with anterior impingement due to abnormal repetitive micromotion [14, 19]. Multiple studies have examined the prevalence of associated anterior impingement lesions at the time of arthroscopy in patients undergoing stabilization procedures for lateral ankle instability. Soft tissue lesions, such as synovitis in the anterior compartment or anterior lateral gutter, have been observed with high frequency (63–100 %), while anterior tibial osteophytes have often been found consistently (12–26.4 %) [2022]. In one study, patients undergoing a Brostrom procedure had 3.37 times the incidence of bone spurs than matched asymptomatic controls [23].