Osteoarthritis (OA), the most common form of arthritis globally, is frequently associated with weight-bearing joints like the knee and hip. However, its occurrence in the complex architecture of the midfoot represents a significant yet often under-recognised source of chronic pain and disability. Midfoot osteoarthritis is a degenerative condition characterised by the progressive loss of articular cartilage, synovitis, and reactive bone changes within the tarsometatarsal (TMT) and naviculocuneiform joints. Its impact is profound, altering foundational biomechanics, challenging diagnosis, and demanding a nuanced approach to management.

The midfoot, comprising the five tarsometatarsal joints (Lisfranc’s joint complex) and the naviculocuneiform joints, serves as the critical keystone of the medial longitudinal arch. It functions as a rigid lever during the propulsive phase of gait, translating force from the hindfoot to the forefoot. This very role makes it susceptible to OA. The primary aetiology is often post-traumatic, accounting for the majority of cases. High-energy injuries like Lisfranc fracture-dislocations, even when treated appropriately, frequently result in post-traumatic arthrosis due to the difficulty in restoring perfect articular congruence. More insidiously, low-energy repetitive microtrauma, often seen in athletes or individuals with pes planus (flat feet), can lead to chronic ligamentous laxity, joint instability, and subsequent degenerative change. Primary osteoarthritis, without a clear inciting event, is less common but occurs, with a higher prevalence in women and with advancing age. Systemic inflammatory arthritides like rheumatoid arthritis can also affect the midfoot, but the pathology and management differ from mechanical OA. Key risk factors include obesity, which exponentially increases load through the joints, familial history, and specific foot morphologies such as a long second metatarsal or a pronated foot posture that alters stress distribution.

Clinically, midfoot OA presents with a distinct but often misinterpreted constellation of symptoms. The hallmark is a deep, aching pain localised to the dorsal and medial aspect of the foot, exacerbated by weight-bearing activities, particularly during the push-off phase of walking. Patients often describe difficulty on uneven ground, climbing stairs, or rising onto their toes. Characteristically, they may report a sensation of instability or a “collapsing” arch. Stiffness, especially after periods of rest (gel phenomenon), is common. On examination, there is often palpable dorsal osteophytic hypertrophy, described as a “bony ridge,” along the affected TMT joints. Weight-bearing may reveal midfoot collapse, forefoot abduction, and a planovalgus (flat and rolled out) deformity in advanced cases. Direct compression of the midfoot or a forced pronation-supination stress test typically elicits sharp pain. A careful gait analysis often shows an antalgic pattern with a shortened stance phase and an early heel rise to minimise midfoot motion.

Diagnosis is a critical challenge, as midfoot OA is frequently missed or attributed to other conditions like plantar fasciitis or peripheral neuropathy. The cornerstone of diagnosis is a detailed history and clinical examination, supported by appropriate imaging. Weight-bearing plain radiographs of the foot are indispensable. They reveal the pathognomonic signs: joint space narrowing, subchondral sclerosis, and dorsal osteophyte formation. The medial cuneiform-first metatarsal joint is most commonly affected, followed by the second and third TMT joints. A weight-bearing lateral view may show sag at the TMT joints and loss of the longitudinal arch. However, radiographs can underestimate the severity, as early cartilage loss may not be apparent. Advanced imaging, particularly Weight-Bearing CT (WBCT), is revolutionising the assessment. It provides three-dimensional, load-bearing views of bone alignment and joint congruity, uncovering subtle instabilities and arthritic changes invisible on plain films. MRI is useful for evaluating soft tissue structures, oedema, and early chondral damage but is typically reserved for atypical presentations. Differential diagnosis must include inflammatory arthritis, midfoot sprain, Charcot neuroarthropathy (in diabetic patients), stress fractures, and tendinopathies.

The management of midfoot OA is tailored to the severity of symptoms, the degree of deformity, and the patient’s functional demands. There is no disease-modifying drug for OA; therefore, treatment focuses on symptom relief and functional restoration. The first-line approach is always non-operative. Patient education and activity modification to avoid high-impact exercises are foundational. Weight loss is emphasised as a potent modifiable factor. Footwear modification is arguably the most effective conservative measure. Stiff-soled, rocker-bottom shoes transfer stress away from the midfoot during gait, while wide, deep-toebox shoes accommodate dorsal osteophytes. Custom-moulded, full-length rigid orthotics or carbon fibre footplates are designed to restrict midfoot motion, support the arch, and redistribute pressure. Physiotherapy aims to strengthen the intrinsic foot muscles and the peroneal tendons to improve dynamic stability. Analgesia, typically with paracetamol or oral/topical NSAIDs, provides supplementary relief. For persistent focal pain, ultrasound-guided corticosteroid injections can offer significant, though often temporary, respite.

When a comprehensive non-operative regimen spanning 3-6 months fails to provide adequate quality of life, surgical intervention is considered. The choice of procedure hinges on the joints involved, the presence of deformity, and joint mobility. For isolated, painful arthritis without significant deformity, an arthrodesis (fusion) of the affected joints is the gold standard. This procedure, most commonly performed on the medial two or three TMT joints, eliminates painful motion, corrects alignment, and creates a stable, plantigrade foot. The trade-off is permanent stiffness in the fused segments, but adjacent joints often compensate well. In cases of fixed, severe planovalgus deformity with collapse, a more extensive fusion involving the naviculocuneiform joint or a medial column stabilisation may be required. Newer techniques, such as interpositional arthroplasty using tendon or synthetic spacers, are considered for lower-demand patients to preserve some motion, but long-term outcomes are less predictable than fusion. The recovery from arthrodesis is protracted, involving 6-12 weeks of non-weight-bearing in a cast, but patient satisfaction rates are generally high, with most reporting substantial pain relief and improved function.

Osteoarthritis of the midfoot is a disabling condition that silently undermines the structural and functional integrity of the foot. Its aetiology is rooted in trauma and biomechanical stress, and its clinical presentation, while distinctive, requires a high index of suspicion for accurate diagnosis. The diagnostic journey, increasingly aided by weight-bearing CT, must differentiate it from a host of other pedal pathologies. Management is a graduated process, demanding a patient-centred approach that progresses from intelligent footwear and orthotics to expertly executed surgical fusion when necessary. As our population ages and remains active, awareness of midfoot OA as a significant cause of chronic foot pain must increase. Recognising its silent burden is the first step towards restoring the firm foundation upon which mobility and independence are built.