Accessory Navicular Syndrome (Adult)

1. Clinical Overview

Summary

Accessory Navicular Syndrome (ANS) is a common musculoskeletal entity characterized by medial midfoot pain associated with an accessory ossicle (os tibiale externum) adjacent to the navicular tuberosity. Present in approximately 10–14% of the population, the ossicle is usually an asymptomatic anatomical variant. However, it becomes "syndromic" when mechanical stress disrupts the synchondrosis (the cartilaginous bridge) or creates a mechanical disadvantage for the Tibialis Posterior Tendon (TPT). [1,2]

The hallmark is a painful, palpable prominence on the medial arch. Biomechanically, the syndrome is significant because the TPT's insertion is displaced medially, reducing its lever arm for inversion and arch support. This often leads to secondary Adult Acquired Flatfoot Deformity (AAFD). Management is primarily conservative (orthotics, activity modification), but recalcitrant cases require the Kidner Procedure—excision of the ossicle and re-routing of the TPT to restore its mechanical advantage. [3,4]

Historical Context

• 1914: Geist published the first radiographic classification of the three accessory navicular types. [2]
• 1929: F.C. Kidner described the "prehallux" and proposed surgical transposition of the TPT to the plantar aspect of the navicular to improve its "hoisting" power. [1]
• 1987: Sella and Lawson refined the understanding of the synchondrosis as a site of chronic "pseudoarthrosis" rather than simple bony presence. [5]
• Modern Era: Introduction of suture anchors and MRI-based bone marrow oedema markers has improved surgical outcomes and patient selection.

Key Facts

• Prevalence: 10–14%; bilateral in 50–90% of cases.
• The "Lever Arm" Problem: The accessory bone shifts the TPT insertion medial to the subtalar joint axis, converting an inverter into a weak adductor.
• Geist Type II: The most common symptomatic variant; an articulated ossicle with a fibrocartilaginous bridge.
• Gold Standard Investigation: Weight-bearing X-rays (including external oblique) and MRI for marrow oedema.

The "N-Spot" vs. Prominence Distinction: Tenderness exactly over the medial prominence suggests ANS. Tenderness over the dorsal N-spot (the high point of the navicular) is more suggestive of a navicular stress fracture. This is a critical distinction in high-impact athletes.

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2. Epidemiology & Risk Factors

Incidence & Distribution

• Demographics: Strong female predilection (3:1 ratio). [6]
• Age Peaks: Two primary presentations: adolescence (10–15 years) during ossification, and early adulthood (20–40 years) following trauma or flatfoot onset.
• Athletics: High prevalence in ballet dancers (extreme eversion), court sports (rapid changes of direction), and distance runners.

Risk Factors Table

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3. Pathophysiology: Molecular & Biomechanical Mechanics

A. The Synchondrosis Transition (Pseudoarthrosis)

In symptomatic Geist Type II variants, the interface between the accessory ossicle and the navicular body is not a stable union but a synchondrosis composed of hyaline cartilage, fibrocartilage, and dense connective tissue. [5,8]

1. Shear Stress Dynamics: During gait, the Tibialis Posterior pulls the ossicle superiorly and medially, while the talus drives the navicular inferiorly and laterally.
2. Micro-trauma: These opposing forces create repetitive shear stress. Unlike hyaline cartilage (designed for compression), fibrocartilage is poorly equipped to handle shear, leading to micro-tears and "marrow oedema."
3. Healing Failure: The constant TPT tension prevents the "fracture" from uniting, resulting in a state of chronic pseudoarthrosis.

B. Molecular Pathway of Degradation

Analysis of symptomatic ossicles shows a specific molecular profile similar to early-stage osteoarthritis:

• Matrix Metalloproteinases (MMP-1, MMP-13): Elevated levels within the cartilaginous bridge lead to collagen matrix degradation. [8]
• ADAMTS Enzymes: Responsible for proteoglycan (aggrecan) cleavage, further weakening the synchondrosis.
• Inflammatory Cytokines: IL-1, TNF-α, and PGE2 are upregulated, sensitizing local nerve endings and causing the characteristic localized pain.
• Osteoclast Activation: RANKL expression increases, contributing to the subchondral bone resorption and oedema seen on MRI.

C. The Biomechanical "Lever Arm" Failure

The Tibialis Posterior is the primary dynamic stabilizer of the medial longitudinal arch.

• Normal Anatomy: TPT inserts on the navicular tuberosity and plantar cuneiforms. Its pull is plantar to the subtalar joint (STJ) axis, acting as a "hoist" for the arch.
• Accessory Patho-anatomy: The TPT inserts onto the medial aspect of the accessory bone.
• The Result: This shifts the vector of pull medial to the STJ axis. Instead of lifting the arch, the TPT "bowstrings" across the medial side.
• Secondary Consequences: This loss of mechanical advantage leads to overloading of the Spring Ligament (calcaneonavicular ligament), resulting in progressive arch collapse and TPT tendinosis. [7]

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4. Classifications: The Geist Roadmap

The Geist classification remains the clinical standard for describing accessory navicular morphology.

Sella and Lawson Refinement (Type II):

• Type IIa: Plane synchondrosis (straight interface). Highest risk of shear-related pain.
• Type IIb: Curved or interlocking interface. More stable but can still become symptomatic under high load. [5]

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5. Clinical Presentation

Symptoms

• Medial Arch Pain: Aching pain localized to the navicular prominence, worse with activity or tight footwear.
• The "Second Ankle": Patients describe a visible, often red, bump on the inner side of the foot.
• Activity Flare: Sudden worsening after an eversion "twist" or high-mileage running.

Physical Signs

• Point Tenderness: Maximum over the medial navicular tuberosity.
• Bursal Swelling: Common in Type III (cornuate) due to footwear friction.
• "Too Many Toes" Sign: Suggests forefoot abduction and associated flatfoot.
• Functional Testing:
  • Single Leg Heel Raise: Pain over the navicular during the "up" phase. Weakness or inability to invert the heel suggests TPT dysfunction.
  • Resisted Inversion: Pain when the patient resists an eversion force.

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6. Investigations

1. X-Ray (Weight-Bearing)

• Standard Views: AP and Lateral.
• The "External Oblique" (45°): This is the most sensitive view for ANS. It profiles the synchondrosis by preventing the ossicle from being obscured by the main body of the navicular. [9]

2. MRI (The Gold Standard)

• STIR/T2-FS Images: The presence of bone marrow oedema in the ossicle and adjacent navicular is the strongest predictor of surgical success. [8,10]
• TPT Assessment: Check for longitudinal split tears or tendinosis.

3. SPECT-CT

• Used if MRI is contraindicated. Shows high uptake ("hot spot") at the synchondrosis, confirming active bone turnover.

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7. Management: The Kidner Protocol

A. Conservative Management (0–6 Months)

Management should be exhaustive before considering surgery, as many cases "cool down" with offloading.

1. Orthotics: Semi-rigid arch supports with a "medial posting" (wedge) and a "navicular cut-out" to relieve direct pressure.
2. Immobilization: 4–6 weeks in a CAM boot for acute synchondrosis flares.
3. Physiotherapy: Focus on Tibialis Posterior eccentric strengthening and calf-pump activation.

B. Surgical Management: The Kidner Procedure

Indication: Failure of ≥6 months of conservative management with MRI-confirmed marrow oedema. [11,12]

Surgical Steps (The Formal Kidner)

1. Approach: Longitudinal incision over the medial navicular prominence.
2. Exposure: The TPT is identified, usually splayed over the accessory bone.
3. Excision: The accessory ossicle and the cartilaginous bridge are excised.
4. Ostectomy: The medial prominence of the navicular (cornuate part) is trimmed until flush with the medial cuneiform.
5. Tendon Advancement (The Kidner Step): The TPT is re-routed from its medial position to a more plantar-distal attachment on the navicular body.
6. Fixation: Modern technique uses a bio-composite suture anchor (4.5mm or 5.5mm) into the plantar-medial navicular.

C. The "Simple Excision vs. Kidner" Debate

There is ongoing debate regarding whether TPT advancement is necessary.

• Simple Excision: Best for Geist Type II/III without flatfoot. Quicker recovery, lower risk of tendon failure.
• Formal Kidner (Advancement): Mandatory if there is pre-existing Adult Acquired Flatfoot Deformity (AAFD). The advancement restores the "hoisting" lever arm. [13]

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8. Post-Operative Rehabilitation

Recovery from a formal Kidner procedure is prolonged due to the tendon reattachment.

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9. Complications

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10. Prevention & Screening

• Primary Prevention: Use of appropriate arch-supporting footwear in adolescents with visible medial prominences.
• Secondary Prevention: Early orthotic intervention after the first acute "flare" to prevent chronic synchondrosis disruption and TPT tendinosis.
• Screening: In athletes, check for "too many toes" and single-leg heel raise endurance during pre-participation physicals.

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11. Practice SBAs (10 Questions)

Question 1

A 22-year-old female presents with medial midfoot pain. X-ray shows a heart-shaped ossicle with a clear synchondrosis. What is the Geist classification?

• A) Type I
• B) Type II
• C) Type III
• D) Type IV
• E) Type V Answer: B. Type II is the synchondrosis variant.

Question 2

What is the primary mechanical deficit caused by an accessory navicular?

• A) Shortening of the Achilles
• B) Medial shift of the TPT lever arm
• C) Lateral shift of the STJ axis
• D) Overactivity of the Peroneus Longus
• E) Rupture of the Deltoid ligament Answer: B. The TPT pull shifts medial to the STJ axis, losing its inversion power.

Question 3

Which radiographic view is most sensitive for visualizing the synchondrosis?

• A) Weight-bearing AP
• B) Weight-bearing Lateral
• C) 45° External Oblique
• D) Harris Heel View
• E) Saltzman View Answer: C. The external oblique profiles the navicular-accessory interface.

Question 4

What is the "Gold Standard" MRI finding that predicts surgical success?

• A) T1 signal intensity
• B) Cortical thickening
• C) STIR marrow oedema
• D) Presence of a bursa
• E) Fatty infiltration of the TPT Answer: C. Marrow oedema indicates "active" syndrome.

Question 5

Which enzyme is specifically upregulated in the symptomatic synchondrosis?

• A) Caspase-3
• B) MMP-13
• C) Lipase
• D) Creatine Kinase
• E) Amylase Answer: B. MMP-13 is a key matrix-degrading enzyme in the synchondrosis. [8]

Question 6

A patient fails 6 months of orthotics and has severe flatfoot. What is the most appropriate surgery?

• A) Simple excision
• B) Kidner procedure (excision + TPT advancement)
• C) Triple arthrodesis
• D) First metatarsal osteotomy
• E) Gastroc recession only Answer: B. Flatfoot requires the Kidner step (advancement) to restore arch support.

Question 7

During a Kidner procedure, which nerve is most at risk?

• A) Sural nerve
• B) Deep peroneal nerve
• C) Saphenous nerve
• D) Sciatic nerve
• E) Common peroneal nerve Answer: C. The saphenous nerve and its branches run medially over the navicular.

Question 8

What force is primarily responsible for synchondrosis disruption?

• A) Tension
• B) Compression
• C) Shear
• D) Torsion
• E) Axial loading Answer: C. Shear forces occur between the TPT and the downward-moving navicular.

Question 9

In the Sella and Lawson classification, which Type II variant is most prone to shear?

• A) Type IIa (Plane)
• B) Type IIb (Curved)
• C) Type III
• D) Type I
• E) Type IV Answer: A. The straight "plane" interface has the least mechanical stability against shear.

Question 10

What is the typical timeframe for return to sports after a formal Kidner procedure?

• A) 2–4 weeks
• B) 4–6 weeks
• C) 2–3 months
• D) 4–6 months
• E) 12 months Answer: D. Return to high-impact sports usually takes 4–6 months.

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14. Biomechanics of the Kidner Procedure

The Kidner procedure is not just an excision; it is a mechanical realignment.

A. The "Vectored" Advantage

• Problem: The accessory navicular (especially Type II) acts as a "stand-off" that alters the pull of the Tibialis Posterior Tendon (TPT). Instead of pulling the arch "up and in", it pulls it "in" (adduction), causing the arch to collapse.
• Solution: By removing the ossicle and transplanting the TPT more plantarly (lower down) on the navicular, we restore the vertical vector of the tendon, effectively "jacking up" the medial arch.

B. Soft Tissue Tensioning

• The "Gold Standard" Tension: The TPT should be advanced until the foot naturally sits in slight inversion when the patient is under anaesthesia.

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15. Orthotic Design: The "Navicular Wrap"

Standard orthotics often fail because they press directly on the painful bump.

A. The "Sweet Spot" Modification

• Navicular Cut-out: The orthotic shell must have a deep "well" or cut-out at the site of the ossicle to prevent direct pressure.
• Medial Flange: A high medial wall helps to control the "talar drift" that often accompanies the condition.

B. Taping Techniques

• Low-Dye Taping: Can be used to "simulate" the effect of an orthotic. If a patient gets 50% relief from a 3-day tape trial, they are a prime candidate for high-end custom orthotics.

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16. Differential Diagnosis of Medial Foot Pain

A. Tarsal Tunnel Syndrome

• Key Difference: Pain is more "electric" or burning and radiates to the sole of the foot. Positive Tinel's sign behind the medial malleolus.

B. Spring Ligament Tear

• Key Difference: Pain is slightly more plantar and distal to the navicular. Associated with rapid-onset flatfoot (Stage IIB PTTD).

C. Kohler's Disease

• Key Difference: Only seen in children (aged 4-7); looks like a "wafer" navicular on X-ray.

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17. Future Trends: Minimally Invasive Surgery

A. Arthroscopic Excision

• Concept: Using 4mm portals to visualize the synchondrosis and excise the ossicle with a "burr".
• Benefit: Significant reduction in wound complications (which are historically high at the medial foot).

B. Synthetic Augmentation

• InternalBrace: Emerging use of ultra-high-molecular-weight polyethylene tapes to protect the TPT advancement while it heals, allowing for "immediate weight-bearing" post-op.

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18. Patient Explanation

You have a small "extra bone" on the inside of your foot. While many people have this and never know it, in your case, the tendon that supports your arch is pulling on this extra bone, causing pain and a flatter foot. Most of the time, we can manage this with special inserts in your shoes. If these don't work, we can do a "Kidner procedure" where we remove the extra bone and "tighten" the tendon to rebuild your arch.

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19. Examination Focus: Viva & OSCE Points

The "Orthopaedic" Viva

• The "Kidner" Trio: 1. Ossicle excision. 2. Medial navicular prominence trimming. 3. TPT advancement.
• PTTD association: Be prepared to explain how accessory navicular is the "childhood precursor" to adult-acquired flatfoot.
• Muller-Weiss Syndrome: Spontaneous osteonecrosis of the navicular in adults—don't confuse it with accessory navicular!

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20. References

1. Kidner FC. J Bone Joint Surg Am. 1929;11(4):831-837.
2. Geist ES. Am J Orthop Surg. 1914.
3. Kopp FJ, Marcus RE. Foot Ankle Int. 2004. [PMID: 15024031]
4. Harris RI, Beath T. Army Foot Survey. 1947.
5. Sella EJ, et al. Clin Orthop Relat Res. 1986. [PMID: 3769260]
6. Bernasconi A, et al. Foot Ankle Surg. 2019. [PMID: 30424911]
7. Miller TT. AJR Am J Roentgenol. 2001. [PMID: 11418395]
8. Malhotra K, et al. JBJS Essent Surg Tech. 2021.

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Last Updated: 2026-01-05 | MedVellum Editorial Team

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