Although possible, idiopathic, neoplastic,¹ and congenital afflictions of the second and lesser metatarsophalangeal joints (MTPJ) are rare. Degenerative,^2,3 iatrogenic, vascular,^4–9 autoimmune,¹⁰ traumatic,¹¹ and metabolic¹² causes are predominant, although the extent of articular abnormality may vary widely. Degenerative causes are the most common and include predislocation, subluxation, and dislocation of the second MTPJ resulting in the crossover toe deformity,¹³ and chondromalacia resulting from repeated intra-articular corticosteroid injections. The effects of concomitant first ray insufficiency, hallux abductovalgus (HAV) deformity, and aberrant metatarsal parabola are understood as causative factors in the development of the significant portion of second MTPJ abnormality, and the importance of correction of these etiologic factors is assumed.¹⁴ The natural history of the concept of insufficient first ray has been exhaustively described in the literature and are not recapitulated here.

Vascular insufficiency, another common cause of second MTPJ arthritis, was described by Freiberg in 1914 and is recognized to include a component of microtraumatic injury.^4,6,15 Localized osteonecrosis, flattening of the metatarsal head, and subchondral collapse results from interrupted epiphyseal blood flow. In addition, iatrogenically induced vascular insufficiency and capital osteonecrosis of the second metatarsal head during a metatarsal surgical procedure is possible with overly aggressive dissection.

Similarly, autoimmune and rheumatic causes of lesser MTPJ arthropathy can be devastating. Rheumatoid arthritis may affect the second MTPJ directly with fibular deviation and subluxation, and indirectly as a result of concomitant effects on the first MTPJ. Subluxation and dislocation of the second MTPJ is common with severe rheumatoid HAV deformities and is complicated by concurrent rheumatic articular pannus, tissue atrophy, and frequent ongoing prednisone or disease-modifying antirheumatic drug treatment. Furthermore, the incidence of postoperative infection and wound-healing complications in these patients is not insignificant and cannot be understated.¹⁶

Infectious causes of second MTPJ pathology are more prevalent in the insensate population, and the pathomechanic imbalances in the insensate foot frequently predispose to plantar ulceration, infection, and contiguous osteomyelitis of the plantar surface of the lesser metatarsal heads.¹⁷ Less frequently, hematogenous spread of distant pathogens has been reported.^18,19 Furthermore, septic arthritis may occur and potentiate serious cartilage damage if not recognized and treated urgently.

Traumatic instances may include crush injury, gunshot injury, and dislocation of the second MTPJ. Crush and gunshot injuries frequently result in massive bone and soft-tissue loss,¹¹ whereas traumatic dislocations affect soft-tissue collateral structures and vascular supply, and potentiate typical posttraumatic arthritis.^20,21

Metabolic and endocrine causes of second MTPJ abnormality may result from gout or pseudogout and Charcot neuroarthropathy (CN), although the second MTPJ is infrequently the index site of these conditions. Gout primarily affects the first MTPJ in men and postmenopausal women, but may affect any joint or enthesis. Both crystalline arthropathies primarily potentiate severe inflammation and degeneration of the articular surfaces, and atrophy and tophaceous infiltration of the associated capsule and ligaments.²² Although CN is incompletely understood, the natural history of the disease and requisite concomitant neuropathy appear to be metabolically driven and predictably result in subchondral sclerosis, cyst formation, and eventual extensive fragmentation and collapse in weight-bearing joints. CN is most commonly seen in the foot at the tarsometatarsal and midtarsal joints, but has been described in the ankle, calcaneus, subtalar joint, and MTPJ. Surgical treatment is not often warranted for forefoot CN, as the extensive degeneration is often masked by dense neuropathy and is asymptomatic. Instead, primarily conservative treatment is indicated.^12,23

The vascular supply of the second metatarsal head is primarily through capsular arteries and dorsal, medial, and lateral diaphyseal and metaphyseal arteries arising from the associated dorsal and plantar metatarsal arteries. The intraosseous nutrient artery enters the lateral diaphysis proximally and divides into short proximal and long distal branches that anastomose with the metaphyseal arteries. The joint is innervated primarily through the deep peroneal nerve and the plantar first and second common digital branches of the medial plantar nerve. The associated skin is innervated by the branches of the medial and intermediate dorsal cutaneous nerves.²⁴

Medial and lateral collateral ligaments stabilize the joint capsule, and the extensor hood broadens the effective insertion of the long and short extensor tendons to the level of the joint and distally. The deep transverse intermetatarsal ligaments effect static transverse plane stabilization of the joint and the thick, fibrous plantar plate provides dynamic sagittal plane stability.