Freiberg Infraction 

In 1914, Alfred H. Freiberg first described the painful collapse of the articular surface of the second metatarsal head.^[1] He described 6 cases of young women presenting with a painful limp and discomfort localized to the second metatarsal. All 6 patients had similar radiographic findings, which showed collapse of the articular surface of the second metatarsal head. In 3 patients, intra-articular loose bodies also were seen. Of the 6 women, 4 were younger than 18 years. Freiberg believed that the etiology most likely was trauma; hence, he used the term infraction. He postulated that the condition was partially caused by excessive length of the second metatarsal. He believed that a long second metatarsal combined with an ineffective first ray complex led to an overload of the second metatarsal and subsequent articular collapse.

Since Freiberg's original description, several authors have written about this uncommon condition, which has since come to be known as Freiberg infraction or Freiberg disease.

See images below depicting Freiberg infraction:

See the Surgical Therapy section.

Frequency

The true incidence of Freiberg disease has not been established. Some cases are asymptomatic, and others may resolve spontaneously prior to seeking treatment. Freiberg disease appears to be an uncommon condition, as evidenced by the small number of patients in most series that are reported in the literature.

Consistent with Freiberg's original description, the disease most commonly is seen in young women. In a review of 275 reported cases, Katcherian found an overall male-to-female ratio of approximately 1:5.^[2] This female preponderance is unusual among the osteochondroses as a whole, as males typically are more affected.

In more than 95% of cases, the lesion is found in the second or third metatarsal, with the second metatarsal being affected more often. However, any of the metatarsals may be involved, although the first and fifth metatarsals are rarely affected. Almost always, there is a single lesion in 1 foot. Bilateral involvement has been reported to occur in less than 10% of patients.

The individuals most commonly affected range in age from adolescence through the second decade of life. However, Freiberg disease can occur at any age, with ages 8-77 years reported in the literature.

In his original description, Freiberg favored a traumatic etiology; however, he later admitted that trauma itself could not reliably explain all cases.^[3] Despite several thoughtful investigations into the etiology of Freiberg disease, no consensus exists as to what type of disease process this peculiar affliction represents. This lack of consensus is reflected in the numerous terms used in the literature to describe this process.

Freiberg disease in adolescents is thought to belong to a group of related diseases involving growth disturbances of the epiphysis or apophysis, collectively termed the osteochondroses. Of all the osteochondroses, Freiberg disease is reported to be the fourth most common, exceeded by Köhler disease of the tarsal navicular, Panner disease of the capitellum, and Sever disease of the calcaneus. Radiographic changes among the osteochondroses are similar, regardless of location; they show subchondral collapse and fragmentation of the joint surface. Although considered to represent an interruption of normal growth processes, the specific events or factors that incite the cascade leading to articular collapse are unclear.

Although considering Freiberg disease to be a form of osteochondrosis makes sense, it does not fully explain the adult onset form of the disease, which may represent a different process altogether, albeit one with a similar radiographic appearance. While some authors consider the cause to be multifactorial, with no single etiology responsible for all cases, current theories are centered on whether the initial insult is predominantly traumatic or vascular. Infection, once thought to play a role, has essentially been eliminated as a significant factor.

Vascular insult

Radiographic changes that are consistent with avascular necrosis have led some authors to suggest that the inciting event is an injury to the blood supply to the metatarsal head. Whether this is the result of a direct vascular injury or of repetitive injury to an area that has an inherently poor blood supply is unknown. Freiberg disease is seldom associated with other systemically related factors or processes, such as steroid use, alcoholism, or blood dyscrasias, making it different from avascular necrosis that occurs in other parts of the body.

To better understand the blood supply to the metatarsal heads, several cadaveric investigations have been performed. Huber described the variability of the dorsal arteries in 200 feet, finding that 65% of those feet exhibited limited collateral anastomosis. Zollinger similarly demonstrated a lack of anastomosis at the subchondral level. Leung and Wong described as many as 7 different patterns of supply originating from the first webspace dorsal artery. Wiley and Thurston noted variation, finding that 33% of specimens studied lacked a second metatarsal artery, with collaterals from the first and third metatarsal arteries supplying the second metatarsal head.

These studies demonstrated that the vascular supply to the metatarsal heads can be quite variable. Overall, there appears to be a trend in which the second and third metatarsals receive a less consistent blood supply than do the other metatarsals. These studies may suggest that some patients may have a greater risk for the development of Freiberg disease based on their anatomic variances. Others have cited reports of iatrogenic avascular necrosis of the second and third metatarsal heads following elective forefoot surgery as indirect evidence that a disturbed blood supply may be at least partially responsible for the development of Freiberg disease.

Traumatic insult

Some authors, however, favor trauma as the predominant etiologic agent in the development of Freiberg disease. This may be in the form of a single acute injury or multiple repetitive microinjuries. Various authors have suggested that altered kinematics around the forefoot may predispose some patients to injury as a result of abnormal loading and may ultimately contribute to the development of Freiberg disease. Several different local mechanical factors have been implicated.

One anatomic variant often implicated in Freiberg disease is a long second metatarsal. In his original description, Freiberg postulated that a long second metatarsal in combination with altered first ray mechanics eventually leads to overload of the second metatarsophalangeal (MTP) joint. He theorized that with forcible impact in feet predisposed by weakness of the toe flexors (especially the first toe), the longer second toe would be susceptible to injury. However, he did note that only 4 of his 6 original cases had a discrete history of trauma. Similarly, in their evaluation of various etiologic factors implicated in Freiberg disease, Stanley and colleagues found that, as measured from standing radiographs, the affected ray was the longest in 85% of the feet.^[4] The authors believed this finding to be important. They noted that only 5 of 33 feet (15%) in their study had a discrete history of trauma.

Of the metatarsals, the second and third are the least mobile. This has led some investigators to conclude that the second and third metatarsals, because of their relative inflexibility and increased load transmission, are at increased risk of sustaining repetitive microtrauma. Similarly, Smillie considered Freiberg disease to be a repetitive stress injury, analogous to a march, or stress, fracture. He believed that concentration of stress in the trabecular bone at the dorsal aspect of the metatarsal head eventually leads to collapse. In their summary of various etiologic factors, Stanley and colleagues evaluated pressure under the metatarsals in patients diagnosed with Freiberg disease.^[4] Only 5 of 33 feet showed abnormally high pressures at the affected site. However, in 16 patients (48%), the greatest measured pressure was indeed at the site where Freiberg disease was present.

McMaster proposed 1 possible mechanism of injury for the development of Freiberg disease. He believed that the typical location of the lesions can be explained on the basis of mechanical impingement between the base of the proximal phalanx and the dorsum of the metatarsal head in forced dorsiflexion. His theory was based on similarities between the lesions he observed in hallux rigidus and Freiberg disease. He postulated that the relative lack of flexibility of the second and third metatarsals contributes to the development of lesions seen in these particular locations.

In an attempt to test this hypothesis, Helal and Gibb induced joint incongruity by creating artificial effusions.^[5] Viscous silicone was injected into the MTP joints of cadaveric feet. Joint congruity was then radiographically assessed in varying degrees of dorsiflexion and plantar flexion. The authors observed dorsal impingement of the metatarsal head and the proximal phalanx under these conditions. They attributed the dorsal impingement to joint incongruity induced by the effusion. They believed that the impingement occurred dorsally because the MTP joint capsule is inherently thicker dorsally than it is ventrally. However, whether or not an effusion plays a significant role in the development of Freiberg disease in vivo is unclear.

In an attempt to evaluate trauma in the development of Freiberg disease, Braddock subjected intact cadaveric second MTP joints to axial loads.^[6] In 2 of the 10 specimens, he was able to create lesions closely resembling those seen in Freiberg infraction. The stage of epiphyseal maturation in the 2 specimens was similar to that commonly seen in Freiberg disease of adolescent onset. This led the author to conclude that trauma to the second metatarsal at the proper phase of epiphyseal maturation could produce lesions similar to those of Freiberg disease.

Others have considered the disorder's predilection for women as indirect evidence that trauma plays a role in the development of Freiberg disease. Theories are based on the difference in the selection of shoe wear between men and women. High-heeled shoes presumably subject the metatarsal heads to repetitive injury and increased pressure transmission. Hoskinson reported the development of Freiberg disease in 3 females following initial attempts at wearing high-heeled shoes.^[7] However, other than anecdotal experience, no direct evidence links the wearing of high heels with the development of Freiberg disease.

Nguyen and colleagues observed 7 cases of Freiberg disease occurring in older patients with diabetes.^[8] They questioned whether trauma to the metatarsal heads as an indirect result of a peripheral neuropathy could result in the development of Freiberg disease. They postulated that intrinsic motor weakness, as is often seen with peripheral neuropathy, can lead to extension of the toes at the MTP joint, resulting in an increase in weight bearing by the metatarsal heads, repetitive injury, and subsequent collapse. Of the 7 patients they studied, 3 had a documented neuropathy. The authors did not comment on whether the patients had protective sensation or if changes of Charcot arthropathy were present in the other joints of the foot.

In summary, the exact nature of the etiology of Freiberg disease is unknown. It is most likely a multifactorial etiology that includes vascular and traumatic insults. Certain patients may be anatomically predisposed based on local mechanical, vascular, and developmental factors. Whether or not the process is the same for older patients as it is for adolescents is unknown. The relative infrequency of the disease, as well as the variable presentation regarding age and injury, makes the study of various etiologies challenging. In the future, genetic or other variables that play a role in the development of Freiberg disease may be identified. Further investigation is needed.

Diagnosis

The diagnosis of Freiberg disease is relatively straightforward when patients present with the typical complaints of activity-related forefoot pain with passive motion of the MTP joint and pain with palpation over the metatarsal head. The differential diagnoses may include metatarsalgia, Morton neuroma, stress fracture of the metatarsal, and synovitis.

History

Patients typically present with pain, stiffness, and a limp. History of trauma may or may not exist. The pain is often vague, related to activity, and poorly localized to the forefoot. Patients may describe a chronic history of forefoot pain with episodic exacerbation or a sudden onset of pain related to a specific injury.

Physical examination

Physical examination typically reveals a limited range of motion (ROM), swelling, and tenderness with direct palpation of the MTP joint. A small effusion may be present. A callus may be seen underneath the affected metatarsal head. Occasionally, patients are completely asymptomatic, with changes noted only on radiographs taken for other purposes. Whether these patients later develop symptomatic Freiberg disease is not known.

While some stage I, stage II, and stage III lesions (see Staging) may resolve spontaneously, patients who do not respond to conservative measures may require surgery, as may patients with stage IV and stage V lesions.

No true contraindications to treatment of Freiberg infraction exist.