Foot pain, especially along the medial arch, frequently presents a diagnostic challenge in orthopedic and sports medicine clinics. One of the most common congenital anomalies contributing to this discomfort is the presence of an accessory navicular (AN) bone. Located medially near the main tarsal navicular, this supernumerary bone is present in approximately 10 to 14 percent of the population. While often asymptomatic, symptomatic presentation, known as Accessory Navicular Syndrome (ANS), occurs primarily during adolescence when the synchondrosis (the fibrous or cartilaginous bridge connecting the AN to the navicular) fails to ossify or fuses incompletely under stress. The resulting mechanical disruption and chronic inflammation necessitate a structured and systematic therapeutic response. The effective treatment of Accessory Navicular Syndrome relies fundamentally on a phased protocol, beginning with comprehensive conservative management strategies and escalating to targeted surgical intervention only when non-operative methods fail to provide satisfactory symptomatic relief.
Understanding the classification and biomechanics of the accessory navicular is critical, as it dictates the optimal treatment pathway. The widely accepted classification system divides the anomaly into three types. Type I is a small, typically asymptomatic sesamoid bone embedded within the distal posterior tibial tendon (PTT). Type III, the “cornuate” navicular, represents a fused osseous protrusion, which is usually stable but can cause symptomatic friction. The most common and clinically relevant variant is Type II, which involves a secondary ossification center connected to the main navicular by a synchondrosis. In Type II ANS, the primary source of pain is the repetitive, high-tensile pull of the PTT, which inserts onto the accessory bone. This stress causes chronic irritation and inflammation of the fibrocartilaginous junction, often exacerbated by activities that place load on the medial arch. Diagnosis is typically confirmed radiographically, with lateral and oblique views providing clear visualization of the accessory ossicle. Magnetic resonance imaging (MRI) or bone scintigraphy may be used to confirm inflammation or a stress fracture at the synchondrosis, which reinforces the need for inflammation control as the first step in treatment.
The initial therapeutic phase is universally conservative, focusing on relieving acute symptoms and controlling inflammation. The first step involves relative rest and activity modification to eliminate the provocative mechanical strain. Non-steroidal anti-inflammatory drugs (NSAIDs) are a standard pharmacological intervention used to reduce pain and local inflammation. In cases of severe, debilitating pain, a period of temporary immobilization using a walking boot or a short-leg cast for two to four weeks may be necessary to completely unload the PTT and allow the inflamed synchondrosis to calm down. Furthermore, local injection therapy, typically involving a corticosteroid mixed with a local anesthetic, can provide significant, rapid relief, helping to break the cycle of inflammation and pain. While injections are not a cure, they serve as a powerful tool to transition the patient from the acute phase of pain management into the next critical phase: long-term biomechanical control.
Once acute inflammation subsides, the second phase of conservative treatment focuses on addressing the underlying biomechanical deficiency: the lack of proper medial arch support, which leads to excessive strain on the PTT. This phase is centered on the utilization of custom or prefabricated orthotic devices. The primary goal of the orthotic is to elevate and support the medial longitudinal arch, thereby reducing pronation and minimizing the tension exerted by the PTT on the accessory bone insertion point. The effectiveness of orthotic management is significantly higher when combined with a structured physical therapy regimen. This rehabilitation program should emphasize therapeutic exercises designed to improve ankle and foot stability, strengthen the intrinsic foot muscles, and, most importantly, address any weakness or dysfunction within the posterior tibialis muscle itself. Improving the dynamic control of the arch often stabilizes the symptomatic synchondrosis and allows a return to full, pain-free activity. For the majority of patients, a conservative protocol lasting six to twelve months, combining immobilization, orthotics, and rehabilitation, proves sufficient for achieving satisfactory long-term results.
However, when a rigorous course of conservative care fails to alleviate chronic pain—a persistent condition typically defined as pain lasting six months or longer that impairs daily function—surgical intervention becomes the definitive treatment option. The primary objective of surgery is twofold: to eliminate the source of pain (the accessory bone) and to correct the associated pes planus (flatfoot) deformity caused by the abnormal PTT insertion. The two standard operative procedures are simple excision and the Kidner procedure. Simple excision involves removing the accessory navicular and any surrounding inflamed soft tissue. While effective for less severe, smaller, or Type I lesions, this approach fails to correct the underlying mechanical deficiency caused by the displaced PTT.
The gold standard surgical treatment for symptomatic Type II ANS is the modified Kidner procedure. This technique involves the complete excision of the accessory navicular, the excision of the non-union or synchondrosis, and, crucially, the reattachment of the posterior tibial tendon. Since the PTT’s insertion is typically displaced in Type II ANS, the procedure involves tunneling the tendon into a trough created in the main, anatomical tarsal navicular. This medial and distal advancement effectively shortens the tendon’s lever arm, increases its mechanical efficiency, and provides greater pull to support the medial arch, thereby correcting the often-associated flexible flatfoot deformity. The complexity of the Kidner procedure necessitates a longer post-operative recovery period, typically involving six weeks of non-weight-bearing immobilization followed by gradual progression to protected weight-bearing. Regardless of the surgical technique employed, post-operative rehabilitation is paramount, focusing intensely on PTT strengthening and gait retraining to ensure a successful return to full athletic and daily activities. In conclusion, the successful management of Accessory Navicular Syndrome hinges on a disciplined, phased treatment approach, which systematically progresses from inflammation control and biomechanical support to the ultimate corrective measure of the Kidner procedure for recalcitrant cases.