The documented incidence of hallux abducto valgus was as high as approximately 50% in one study of South Africans (1) and as low as 2% in one study of a barefoot population (2). Female patients have been found to have a much higher incidence of the deformity (2, 3, 4). Whether these studies indicate a true increased incidence of hallux abducto valgus in the female population or merely represent a reflection of the effects different shoe gear remains an unsettled issue.

Controversy exists regarding the effects of heredity and shoe gear on the development of a bunion deformity. Shine cited faulty shoe gear as a contributing factor in the progression of deformity (2). Sin-Fook and Hodgson found a 31% greater incidence of hallux valgus in a Chinese population who wore shoes versus those who did not (5). In the Japanese population, an anecdotal increase in the number of bunion deformities was noted after the 1970s when Western-influenced shoe gear began to replace the traditional “clog” (6). On the contrary, Root and associates countered that no evidence indicates that shoes can cause this deformity in a foot that functions normally (7). However, even if shoes do not play a direct role in the development of a bunion, they certainly can act as an aggravating factor in the symptoms and possibly serve to enhance progression of deformity.

Heredity and genetic factors undoubtedly play a role in the formation of a bunion. The exact type and extent of involvement are unknown. A positive family history of 63% (3) and 68% (8) was noted in two studies involving hallux abducto valgus deformity. Juvenile bunion deformities do seem to have a higher familial tendency. Johnston went as far as to say that the condition was transferred as an autosomal dominant trait with incomplete penetration (9). In one study, 94% of children with juvenile hallux valgus had mothers who also had the deformity (10).

Aside from the tendency to inherit a bunion deformity, genetics can also play a role in the overall structure and function of the foot. A person may have a genetically induced structural deformity that results in functional instability along the medial column and thus increases the risk of developing hallux abducto valgus. Genetic disorders such as Down’s syndrome, Ehlers-Danlos syndrome, and Marfan’s syndrome can lead to ligamentous laxity and subsequent poor mechanics. This laxity has been shown to lead to increased intermetatarsal and hallux abductus angles (11,12).

Root and associates described four types of conditions that may lead to a hallux valgus deformity (7): biomechanical abnormalities, arthritic conditions, neuromuscular disease, and traumatic compromise. A suggested causative factor in the formation of bunions is excessive pronation throughout the stance phase of gait. Sgarlato and Root et al. adequately defined the biomechanical relationships and functional sequences that can result in first ray disorders (7,13). Functional aberrations include compensated forefoot and rearfoot varus, pes valgus deformity, hypermobile first ray, pronation secondary to equinus (osseous or soft tissue), torsional malalignments, and rotational deformities of the lower extremity. All these disorders, and any other condition that results in an excessive amount of pronatory motion, can predispose one to develop bunions.

Hypermobility of the medial column can also lead to the development of a hallux abducto valgus deformity. Although it is difficult to quantify, the oblique axis of motion about the first ray typically allows for motion in the dorsal medial
to plantar lateral direction. When hypermobility is present, abnormal amounts of motion at this joint can produce more complex symptom patterns. First ray hypermobility not only can cause increased motion and friction between shoe gear and the first metatarsal head, but also can result in stress transfer to the adjacent second metatarsal. This added pressure can produce a variety of pathologic conditions about the second metatarsophalangeal joint, including callus formation, capsulitis, flexor plate disruption, hammer toe formation, and metatarsal stress fractures.

The association between pes valgus and hallux abducto valgus deformities has been appreciated for years. McGlamry and Full believed that the influence of equinus and pes valgus can be detrimental and can negatively affect outcomes after bunion repair (14). Inman noted a close relationship between pronated feet and bunion deformities (15), and other investigators have predicted failure of hallux valgus repair in feet that had coexistent severe pes valgo planus deformity with or without a tight heel cord (16,17). Hodman delivered the most absolute opinion when he asserted that hallux valgus was always combined with pes planus (18). Electromyographic studies have demonstrated that dynamic imbalance of the intrinsic musculature about the first ray is involved in the evolution of hallux valgus deformities (19). This imbalance was believed to be secondary to structural change and pronated function of the hindfoot. Radiographs of juvenile patients with hallux abducto valgus have demonstrated a much higher incidence of pes valgus deformity than would otherwise be anticipated (20). However, some difference of opinion does exist regarding this relationship. In a study involving adults with acquired pes valgus deformity secondary to posterior tibial tendon dysfunction, no increase in hallux valgus was noted (21). However, this would not appear to represent an accurate corollary with a patient who has possessed pes valgus deformity for their entire life. Others have concluded that the incidence of pes planus in the normal population and in those with a hallux valgus deformity was essentially the same (22), although pes planus is not necessarily a pathologic condition as compared with pes valgus deformity.

The terminology regarding pes valgus deformity and simple pes planus has not been well delineated in some instances. Therefore, these studies may be evaluating patients with an entirely different condition. Two studies found no correlation between pes planus and the success rate of hallux valgus repair (22,23). However, simple measurements of arch height do not adequately denote the type of foot or the biomechanical imbalances that are present.

Neuromuscular diseases such as cerebral palsy can also result in muscle imbalance with possible structural changes in the foot, including hallux abducto valgus. Arthritic disease, specifically the inflammatory arthritides, can also produce secondary structural changes in the foot with pathomechanical consequences. Biomechanical control may be particularly important in these patients both preoperatively and postoperatively.

Traumatic conditions around the first metatarsophalangeal joint have been associated with the development of symptoms, notably hallux limitus and hallux rigidus. These injuries range from crush injuries with intraarticular damage to soft tissue sprains and dislocations that damage the periarticular structures. These latter impairments can lead to progressive muscle-tendon imbalance at the first metatarsophalangeal and eventual structural adaptation of the metatarsal and phalanx. Injuries such as Lisfranc’s fracture-dislocation can result in residual instability along the medial column that increases the potential for bunion formation (24).

The simultaneous presence of hallux abducto valgus and metatarsus primus varus has been noted (3,25). Hardy and Clapham reported a correlation between the degree of hallux valgus and the size of the intermetatarsal angle (3). Hardy and Clapham believed that metatarsus primus varus is secondary to the hallux valgus deformity (3), whereas Truslow believed that when metatarsus primus varus existed, hallux valgus was inevitable (26). The question of which condition develops initially, the hallux abductus or the metatarsus primus varus, is still unanswered. Metatarsus adductus is another factor that has been associated with an increasing degree of hallux abductus (27), and it is recognized as a predisposing factor to the development of hallux abducto valgus deformity (28,29).

Although the exact sequence of events that occur in the development of a bunion deformity continues to be debated, a few points are understood and agreed on by most authorities. In cases of hallux valgus, as the great toe deviates laterally, the once stabilizing forces of the adductor hallucis and flexor hallucis brevis become deforming forces as their pull now lies lateral to the long axis of the metatarsophalangeal joint. With progression of the deformity, the soft tissue structures along the lateral side of the joint become contracted, whereas those medially become weakened. This process may eventually result in loss of the medial buttressing effect of the soft tissues and may allow for progressive medial displacement of the first metatarsal head. With continued movement of the metatarsal medially and lateral deviation of the sesamoid apparatus, the integrity of the cristae may be jeopardized by the altered articulation between the sesamoids and the metatarsal head, with resulting permanent articular damage. The combination of dynamic and structural disorders makes treatment of symptomatic hallux valgus deformities challenging to even the most skilled surgeon.