An os tibiale externum—commonly referred to as an accessory navicular, prehallux, or os naviculare secundarium—is one of the most frequent congenital accessory ossicles found in the human skeleton. Occurring in roughly 4% to 21% of the population, this extra osseous center arises along the medial border of the midfoot, situated adjacent to the tarsal navicular tuberosity and intimately associated with the insertion of the posterior tibial tendon (PTT). While often an incidental asymptomatic finding on routine foot radiographs, the os tibiale externum can become a primary driver of chronic medial foot pain, localized inflammation, dynamic flatfoot deformity, and functional disability.
Anatomical Origins and Etiology
During normal embryonic and childhood skeletal development, the tarsal navicular ossifies from a primary ossification center. In individuals with an os tibiale externum, a secondary, anomalous center of ossification develops adjacent to the main body of the navicular. This secondary center typically appears during early adolescence, coinciding with the broader growth spurt and skeletal maturation phase between ages 10 and 14.
The failure of this secondary ossification center to completely coalesce and fuse with the primary navicular mass gives rise to the persistent accessory ossicle. Genetic factors play a significant role, as the presence of an os tibiale externum frequently exhibits an autosomal dominant pattern of inheritance with incomplete penetrance. Additionally, the condition presents bilaterally in up to 50% to 90% of affected individuals.
Structural Classification: The Geist System
To standardize clinical evaluation and surgical planning, the os tibiale externum is categorized using the Geist classification system, which divides the anomaly into three distinct morphological types based on size, shape, and relationship to the tarsal navicular:
| Classification | Morphological Description | Structural Attachment | Clinical Characteristics |
| Type I | Small (2–3 mm), round or oval sesamoid bone | Embedded entirely within the distal posterior tibial tendon; no direct contact with the navicular | Rarely symptomatic; functions as a true sesamoid; accounts for ~30% of cases. |
| Type II | Triangular or heart-shaped ossicle (up to 12 mm) | Connected to navicular tuberosity via a fibrocartilaginous or hyaline synchondrosis bridge | Most commonly symptomatic; highly susceptible to shear stress, microtrauma, and nonunion. |
| Type III | Large, prominent “cornuate” or hooked navicular tuberosity | Fully fused to the main navicular body via a continuous bony bridge | Pain stems from direct mechanical pressure and friction against footwear rather than synchondrosis disruption. |
Biomechanical Implications and Pathophysiology
The presence of an os tibiale externum profoundly alters the mechanical environment of the medial longitudinal arch. Under normal anatomical conditions, the posterior tibial tendon serves as the primary dynamic stabilizer of the midfoot arch, inserting broadly onto the navicular tuberosity, cuneiforms, and metatarsal bases to invert the hindfoot and support the foot during gait.
When a Type II os tibiale externum is present, a major portion of the posterior tibial tendon inserts directly onto the accessory ossicle rather than the main body of the navicular. This alters the vector of pull and shortens the effective moment arm of the tendon. Consequently, the tendon must exert greater force to maintain the medial longitudinal arch, predisposing the individual to posterior tibial tendon dysfunction (PTTD) and dynamic flatfoot (pes planovalgus) deformities.
Symptoms typically arise through two main mechanisms:
- Synchondrosis Disruption: In Type II ossicles, repetitive walking, athletic activities involving rapid directional changes, or acute inversion injuries introduce high shear stresses across the fragile fibrocartilaginous synchondrosis interface. This leads to chronic micro-fractures, localized hypervascularity, bone marrow edema, and painful nonunion or pseudarthrosis.
- Mechanical Irritation: The medial bony prominence characteristic of Type II and Type III structures projects excessively inward. Rigid or narrow footwear exerts direct compression against this prominence, leading to local adventitial bursitis, subcutaneous tissue thickening, and overlying skin breakdown.
Clinical Presentation and Diagnostic Evaluation
Clinical symptoms often surface during adolescence when the secondary center begins to ossify, or in adulthood following a minor sprain or changes in activity level. Patients typically report localized, aching pain along the medial aspect of the midfoot, exacerbated by prolonged standing, running, or wearing narrow shoes.
Physical examination reveals a visible and palpable hard bump on the medial side of the foot, directly over the navicular tuberosity. Point tenderness is marked over this prominence. Passive movement of the midfoot or resisted inversion and plantarflexion of the foot reproduces the patient’s pain by stressing the posterior tibial tendon and synchondrosis. Single-leg heel-raise testing may demonstrate weakness or discomfort in the posterior tibial complex.
Diagnostic imaging confirms the condition:
- Plain Radiography: Standard weight-bearing anteroposterior, lateral, and 45-degree medial oblique views clearly visualize the accessory ossicle, assess Geist classification, and evaluate the degree of medial arch collapse.
- Magnetic Resonance Imaging (MRI): MRI is the gold standard for symptomatic evaluation. It reliably demonstrates signal changes indicative of bone marrow edema within the ossicle and parent navicular, fluid accumulation across the synchondrosis, local tenosynovitis, or longitudinal splits within the posterior tibial tendon.
- Nuclear Bone Scan: Shows focal hyperuptake at the synchondrosis, confirming active bone turnover and inflammation.
Non-Surgical Management Strategies
Initial management for a symptomatic os tibiale externum is conservative, focusing on reducing mechanical stress, controlling inflammation, and restoring foot function.
- Immobilization: Severe acute presentations benefit from 4 to 6 weeks of rigid immobilization in a short-leg walking cast or controlled ankle motion (CAM) boot to rest the synchondrosis and tendon.
- Orthotic Therapy: Custom-molded foot orthoses with aggressive medial arch support and a recessed area (or “sweet spot” padding) around the navicular tuberosity redistribute plantigrade pressure away from the tender medial node.
- Footwear Modification: Transitioning to wide toe-box shoes or athletic footwear without rigid medial overlays prevents direct frictional trauma.
- Physical Therapy: Stretching tight gastrocnemius-soleus complexes combined with eccentric strengthening of the posterior tibial tendon and intrinsic foot musculature optimizes dynamic arch stabilization.
- Pharmacotherapy: Short courses of non-steroidal anti-inflammatory drugs (NSAIDs) help manage acute flare-ups. Direct steroid injections into the synchondrosis are used sparingly due to the risk of intratendinous injection and posterior tibial tendon rupture.
Surgical Interventions and Rehabilitation
Surgical treatment is indicated when well-directed conservative measures fail to alleviate pain after 3 to 6 months.
The classic surgical intervention is the Kidner procedure, originally described by F.C. Kidner in 1929. The traditional technique involved complete excision of the accessory navicular, resection of the prominent navicular tuberosity, and transposition of the posterior tibial tendon insertion to the inferior aspect of the remaining navicular bone.
Modern management utilizes a Modified Kidner procedure:
- A medial longitudinal incision is made directly over the navicular tuberosity.
- The posterior tibial tendon is carefully split longitudinally to expose the underlying accessory bone.
- The os tibiale externum is shell-excised, and the remaining navicular tuberosity is osteotomized and recontoured smooth to eliminate mechanical prominence.
- The posterior tibial tendon is reattached securely to the navicular using suture anchors or transosseous sutures, restoring dynamic pull.
Alternatively, for select young patients with large Type II ossicles lacking substantial tendon breakdown, synchondrosis fusion (arthrodesis of the ossicle to the main navicular with internal screw fixation) or percutaneous drilling can be performed to achieve bony union while maintaining native tendon insertion anatomy.
Postoperative protocols generally require 4 to 6 weeks of non-weight-bearing in a cast, followed by progressive weight-bearing in a walking boot and physical therapy to restore range of motion, strength, and proprioception.
Clinical Prognosis
The prognosis for os tibiale externum is generally favorable. Conservative therapy successfully resolves symptoms in a vast majority of pediatric and adult cases. For refractory cases requiring surgical intervention, the modified Kidner procedure yields excellent functional outcomes, with high rates of pain relief and return to baseline athletic performance. Early identification, accurate classification, and targeted biomechanical support remain the cornerstones of effective management.