Müller-Weiss Disease

The navicular is the last tarsal bone to ossify (around age 3, later in girls' relative terms but ossifying earlier in girls chronologically; delayed ossification leaves it vulnerable). Maceira and Rochera proposed that delayed ossification in childhood — from nutritional, socioeconomic or mechanical stress — leaves a soft, cartilaginous lateral navicular exposed to asymmetric compressive load. A short first ray (index minus) or forefoot morphology shifting load laterally concentrates force on the lateral navicular between the talar head and lateral cuneiform. Over decades the lateral pole is compressed and effectively "extruded" medially and dorsally: the bone becomes comma-shaped, the talar head migrates dorsolaterally past the deficient lateral navicular, and the subtalar joint rotates into varus. On this reading Müller-Weiss is a dysplasia with secondary mechanical failure, not a primary vascular event.

The alternative view is primary spontaneous osteonecrosis of the adult navicular. The navicular has a watershed central third supplied peripherally by dorsalis pedis and medial plantar branches, analogous to the vascular vulnerability underlying navicular stress fracture. Sclerosis, fragmentation and MRI signal change resemble osteonecrosis elsewhere. Critics note that histology from fusion specimens often shows viable bone with degenerative and reparative change rather than classic necrosis, and that the stereotyped lateral-compression morphology is better explained mechanically.

Most modern authors accept a combined model: a developmentally vulnerable, dysplastic lateral navicular fails under chronic asymmetric load, with superimposed secondary ischaemic change in the compressed fragmented segments. For the exam, present both theories and credit Maceira's mechanical model for explaining the characteristic pes planovarus.

But do not call the planovarus pathognomonic — Maceira's own paper does not. He writes that the plantar arch "may correspond to that of a normal, cavus, or flat foot". What is constant is the squeezed, laterally compressed navicular and the inverted subtalar joint driven by the laterally protruding talar head; the flat arch is the commonest of three possible consequences, not a diagnostic requirement. A normal-looking arch does not exclude Müller-Weiss, and a foot that is frankly cavus can still be it.

First line in all stages, and frequently durable in Maceira stages 1-3. Published series report the majority of patients achieving acceptable symptom control without surgery.

• Rigid custom orthoses — the prescription is the exam point: medial longitudinal arch support to unload the collapsed medial column, combined with LATERAL hindfoot posting (lateral heel wedge) to accommodate/correct the varus heel and shift load off the compressed lateral navicular. A standard flatfoot orthosis with medial posting drives the heel further into varus and worsens symptoms.
• Rocker-sole, stiff-soled footwear to offload the talonavicular joint during push-off.
• Activity modification (avoid uneven ground, prolonged standing), weight optimisation.
• Simple analgesia/NSAIDs; a period in a walking boot for flares.
• Image-guided talonavicular corticosteroid injection — diagnostic value (confirms the pain generator before fusion) and temporary therapeutic benefit.

Decision threshold for surgery: persistent disabling pain despite at least 6 months of well-executed orthotic management, or progressive collapse with advancing stage — not radiographic stage alone.

Goals: eliminate the painful arthritic articulation(s), restore medial column length and alignment (correct Meary line), and correct hindfoot varus.

Workhorse: talonavicular fusion, usually extended to talonavicular-cuneiform (TNC) fusion.

• Indication: refractory stage 3-5 disease with talonavicular with or without naviculocuneiform arthritis.
• Why extended fusion: the residual navicular is small, fragmented and sclerotic; isolated TN fusion through diseased bone risks non-union and leaves the naviculocuneiform joint (frequently involved) as a persistent pain source. Bridging talus-to-cuneiforms with structural graft restores medial column length reliably.
• Contraindications: active infection, Charcot neuroarthropathy, non-reconstructable soft-tissue envelope, critical ischaemia.

Talonavicular-cuneiform fusion with structural grafting:

• Position: supine, ipsilateral hip bumped to neutral rotation, thigh tourniquet.
• Imaging/equipment: image intensifier; small-fragment and midfoot plating sets, headless/partially threaded compression screws; iliac crest or allograft structural wedge; autograft harvest consent.
• Preparation: confirm pulses; prophylactic antibiotics; plan incisions to respect skin bridges if combining with calcaneal osteotomy.
• Approach: dorsomedial longitudinal incision over the talonavicular joint, interval between tibialis anterior and extensor hallucis longus; protect the medial branch of the superficial peroneal nerve and the dorsalis pedis neurovascular bundle laterally.
• Dissection: capsulotomy of talonavicular and naviculocuneiform joints; excise non-viable fragmented navicular segments; debride sclerotic surfaces back to bleeding cancellous bone — this is the step that determines union. Drill/petal dense surfaces.
• Reduction/Reconstruction: restore medial column length and Meary alignment with a tricortical structural graft in the navicular defect; correct the talar head onto the reconstructed column; supplement with cancellous autograft. Confirm heel in neutral-to-slight valgus; if residual varus, add lateralising calcaneal osteotomy.
• At-risk structures: dorsalis pedis artery and deep peroneal nerve (dorsal), tibialis posterior insertion (medial/plantar), superficial peroneal nerve branches.
• Fixation: compression screws from talus into cuneiforms across graft, augmented with a dorsomedial bridging plate; rigid construct is essential in this biologically hostile bone.
• Closure: layered closure over the capsule; below-knee backslab.
• Aftercare: non-weightbearing 6 to 8 weeks in cast/boot, then progressive protected weightbearing in a boot to roughly 12 weeks; confirm union clinically and radiographically (CT if in doubt) before unrestricted loading. Warn the patient union may be slow.
• Pitfalls: under-débridement of sclerotic bone (non-union), fusing with residual varus (lateral overload, painful gait), under-estimating naviculocuneiform involvement (persistent pain), skipping structural graft (short medial column, recurrent dorsal talar subluxation).
• Salvage of failure: non-union — revision with fresh grafting, more rigid fixation, biologic augmentation, metabolic work-up; malunion in varus — corrective calcaneal osteotomy or extension to triple fusion.

• Non-union: the principal complication given sclerotic avascular bone; mitigated by thorough preparation, compression, grafting and prolonged protection. Rates vary across small series; extended constructs with structural graft report good union in most patients.
• Malalignment/malunion in residual varus — preventable at surgery; symptomatic cases need corrective osteotomy.
• Adjacent joint degeneration (subtalar, cuneiform-metatarsal) after transverse tarsal fusion — counsel pre-operatively.
• Wound problems, superficial peroneal or deep peroneal nerve injury, hardware prominence.
• Outcomes: fusion-based reconstruction gives reliable pain relief and functional improvement in most reported series; patients accept midfoot stiffness readily because the joints were already stiff and painful.