AUTHOR AND EDITOR INFORMATION

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• Indications
• Contraindications
• Workup
• Treatment
• Future and Controversies
• Multimedia
• References

INTRODUCTION

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• Future and Controversies
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• References

In 1914, Alfred H. Freiberg first described the painful collapse of the articular surface of the second metatarsal head. 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.

History of the Procedure

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 1:5.¹ 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.

Etiology

In his original description, Freiberg favored a traumatic etiology; however, he later admitted that trauma itself could not reliably explain all cases. 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 (see Synonyms).

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. (See the eMedicine article 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 (see the eMedicine article Sever Disease). 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.² 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.² 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.³ 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.⁴ 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.⁵ 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.⁶ 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.

Clinical

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.

INDICATIONS

Section 3 of 9  

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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.

CONTRAINDICATIONS

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No true contraindications to treatment of Freiberg infraction exist.

WORKUP

Section 5 of 9  

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Imaging Studies

• Radiographs
• • Depending on the stage of the disease, radiographs may show only sclerosis and widening of the joint space (early), with complete collapse of the metatarsal head and fragmentation later.
  • Oblique views may be especially useful to fully appreciate subtle changes early in the disease.
  • Osteochondral loose bodies may be seen late in the disease as well.
• The use of bone scintigraphy has been described with photopenia in the early stages of the disease, with intense uptake later as the head is reconstituted or revascularized. Although bone scintigraphy has been used in the study of Freiberg disease, its value as a diagnostic or prognostic tool is unknown.
• Magnetic resonance imaging (MRI) has been advocated by some physicians as helpful for preoperative evaluation, especially if an osteotomy is planned.

Histologic Findings

Histologic examination of tissue from resected specimens has produced varied findings. Different studies have found bone resorption and new bone formation, depending on the stage of the disease. Interestingly, Young and colleagues described separation of the deeper layers of the hyaline cartilage in a 55-year-old man with Freiberg disease.⁷ The separation had occurred in close proximity to the zone of mineralization, and avascularity was not evident. The authors concluded that in this 1 case, a traumatic shear or compression-type injury was likely to have been responsible, as opposed to some type of vascular insult (avascular necrosis).

Staging

Several staging systems have been described. Most are based on radiographic appearance, including the amount of collapse and the presence or absence of secondary degenerative changes. The classification scheme developed by Smillie in 1967 is the most often quoted system and divides the radiographic changes into the following 5 stages⁸:

• Stage I - The earliest sign is fissuring of the epiphysis. Radiographic changes at this stage may be so subtle that they are missed with routine radiographs.
• Stage II - Later central depression of the articular surface becomes evident as subchondral cancellous bone is resorbed. The articular cartilage hinges on an intact plantar bridge.
• Stage III - The central depression is seen to be resulting in medial and lateral projections at the margins. The plantar hinge remains intact at its plantar isthmus.
• Stage IV - This stage demonstrates that the central portion has sunk below the surface and is free of the plantar hinge, thus becoming a loose body. Fractures of the medial and lateral projections are present, with folding of the projections over the central loose body.
• Stage V - The final stage shows marked flattening and deformity of the metatarsal head with secondary degenerative changes. The central loose body may have been resorbed at this stage. The shaft of the metatarsal becomes thickened and dense.

TREATMENT

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Medical Therapy

Various suggestions regarding medical therapy for Freiberg disease have been put forth in the literature, depending on the stage and the acuteness of the onset of pain. A period of appropriate nonoperative conservative management is indicated for all patients presenting with Freiberg disease. Regardless of the treatment method chosen, the goal of therapy is to rest the joint to allow inflammation and mechanical irritation to resolve. In patients presenting with severe pain of an acute nature, a non–weight-bearing cast may provide sufficient relief during the acute phase. In other persons, a short leg walking cast may be more appropriate. In patients with chronic complaints, less restrictive options, such as shoe modifications in the form of inserts with metatarsal bars or pads, rigid shanks, or a rocker bottom, may be helpful. Activity modification during  exacerbations  may  help  to  prevent the  aggravating  symptoms  of  pain  and  swelling. Some physicians have advocated steroid injection as an option.

Hoskinson reported on the long-term results (average 12 years) of conservative treatment on a series of 16 patients.⁵ Eleven of the 16 patients were completely pain free at final follow-up. However, all 16 had restricted ROM. Conversely, James and colleagues reported that of 14 patients initially started on conservative therapy, 7 (50%) required surgery for failure of conservative management to relieve symptoms within the first year.⁹

Surgical Therapy

The progression of Freiberg disease is variable in time course and severity. While some stage I, stage II, and stage III lesions may resolve spontaneously, patients who do not respond to conservative measures and patients with stage IV and stage V lesions may require surgery. Smillie believed that it was possible to restore joint congruity in early lesions (stages I-III) with surgery. Several surgical options have been advocated in the past. Simple debridement and loose body removal were originally described by Freiberg. Other described procedures, including various osteotomies, elevation of the depressed metatarsal head with bone grafting, core decompression, metatarsal head excision, shortening of the metatarsal, proximal phalanx hemiphalangectomy, total joint arthroplasty, and various combinations of the above, have been implemented.

No consensus exists as to which surgical procedure is the most appropriate for patients with symptomatic Freiberg disease. Most series are limited in terms of the number of patients. The relative rarity of the condition makes it difficult to perform prospective analyses.

Simple debridement

Freiberg's original monograph reported that 2 of his 6 patients had good results with debridement. The report only infers that these 2 patients presented with advanced-stage disease based on the presence of loose bodies. Subsequent authors also have advocated simple debridement as an effective treatment for Freiberg disease. However, staging of the lesions, as well as detailed assessment of results, has not commonly been reported, making it difficult to make recommendations based on the currently available data.

Simple debridement can be combined with other procedures. Hoskinson described 12 patients treated with various surgical procedures, including excision of the metatarsal head (3 patients), hemiphalangectomy (3 patients), and debridement with loose body excision (3 patients).⁵ He believed that the best results were seen following simple debridement, but he warned about drawing conclusions from such limited numbers.

Bone grafting

In an attempt to restore joint congruity, Smillie described a procedure in which a cancellous bone graft was used to elevate the depressed metatarsal articular surface.^{8, 10} The technique involved creating a slot in the metatarsal shaft through which the sclerotic bone could be drilled. The metatarsal articular surface was then elevated and supported by a bone graft. The authors recommend this procedure for stage I, II, or III lesions in which an intact cartilage flap is present.

In 1987, Helal and Gibb reported on 25 patients with Freiberg disease; 11 of these patients were treated with a modification of Smillie's original procedure.³ The authors reported 8 patients to be clinically and radiographically normal at 3-8 years following surgery. Three patients demonstrated expanded metatarsal heads radiographically, and 2 of these 3 patients reported pain with running or wearing high-heeled shoes.

Osteotomies

Several different osteotomies have been described. The common goal of all osteotomies is to redirect the loading of the MTP joint away from the damaged area of the articular surface. The 2 basic procedures are dorsal closing wedge osteotomies and shortening osteotomies.

Dorsal closing wedge osteotomies

Gauthier and Elbaz were the first to describe a dorsal closing wedge osteotomy for the treatment of Freiberg disease.¹¹ They reported results from 53 patients who were treated with a dorsiflexion osteotomy of the neck of the metatarsal. As described, the dorsal closing wedge osteotomy reoriented the intact cartilage on the plantar surface to articulate with the base of the proximal phalanx. The authors reported stable results with no complications. In 35 of the 53 cases, the postoperative arc of motion averaged 80°.

Chao and colleagues reported results from 13 patients with all stages of Freiberg disease who were treated with dorsal closing wedge osteotomy combined with synovectomy and debridement.¹² Temporary fixation with Kirschner wires (K-wires) was utilized in all patients. The patients all had follow-up visits at an average of 40 months, and the results, as graded by the American Orthopaedic Foot and Ankle Society (AOFAS) lesser toe metatarsophalangeal-interphalangeal scale, were as follows: 4 excellent, 7 good, and 2 poor or fair. Metatarsal shortening averaged 2.1 mm, with passive ROM decreased by an average of 15° of flexion and 8° of extension. One patient, who underwent 3 mm of shortening, experienced transfer metatarsalgia.

In 1991, Kinnard and Lirette reported on 15 patients who were treated with dorsiflexion osteotomy, including several patients with advanced-stage disease.¹³ They reported complete pain relief, with only 3 patients experiencing mild discomfort with athletic activities. Loss of extension averaged 10°, and flexion loss averaged 15°. Metatarsal shortening averaged 2.5 mm, with no cases of transfer metatarsalgia. No major complications were reported.

Shortening osteotomies

Another osteotomy reported for treatment of Freiberg disease is the shortening osteotomy. The basis for the use of a shortening osteotomy is the observation that when involved, the second metatarsal often is the longest of the metatarsals. Several authors believe that this subjects the involved metatarsal to repetitive injury and abnormal loading. With shortening, overloading of the metatarsal is reduced, as are symptoms.

James and colleagues described a shortening osteotomy in which the metatarsal is shortened through a dorsal incision and is fixed with a small T plate.⁹ Pedobarographic evaluation was performed on 7 patients who were treated with a shortening osteotomy, and results showed a mean decrease in pressure under the second metatarsal from 7 kg/cm² to 4 kg/cm². Of these patients, 4 were available for review; 2 had no symptoms, and 2 were much improved.

Smith and coauthors described a similar procedure in which the metatarsal was shortened approximately 4 mm.¹⁴ In the 16 patients who were treated in their series, all but 1 had complete pain relief. However, 7 of the 16 patients experienced stiffness of the involved ray, with 4 patients unable to place the toe flat when standing. Five patients graded their result as excellent, 9 patients said that they were very pleased with the outcome, 1 was satisfied with it, and 1 was unhappy with the result. Two minor complications occurred, with 1 sinus requiring reexploration and 1 hardware failure occurring despite union. Advantages cited by the authors included the ease of the procedure, avoidance of damage to the metatarsal head, and apparent remodeling of the articular surface, as seen radiographically in most cases.

Resection arthroplasty

Resection arthroplasty, although advocated in the past, has fallen out of favor for the initial treatment of Freiberg disease. Various methods have been described, including resection of the base of the proximal phalanx or of the metatarsal head. Resection can be combined with soft-tissue interposition arthroplasty or even syndactylization of the toes, or it can be performed without these other procedures. Hoskinson reported on 8 patients treated with resection arthroplasty, both hemiphalangectomy and resection of the metatarsal head. He found that only 3 of the 8 patients had a satisfactory result, with residual symptoms and deformity limiting the remaining 5 patients. Resection arthroplasty is an inherently destructive procedure. With these procedures, several authors have expressed concerns about the development of transfer lesions as a result of rendering the affected metatarsal incompetent. Additionally, potential complications  from  any  of  the  resection techniques  include  progressive  hallux  valgus  and excessive shortening.

Total small joint arthroplasty

Total small joint arthroplasty utilizing a silicone prosthesis also has been described for the treatment of Freiberg disease. Potential complications are similar to those for resection arthroplasty; other potential problems, inherent in the implants themselves, include synovitis, infection, and dislocation. Several implants are available commercially. Most of these implants originally were developed for use in the hand. Potential advantages over resection arthroplasty include maintenance of length, improved joint motion, and better weight distribution if condyles are preserved. Newer implants, such as the Swanson total flexible-hinge lesser MTP joint implant, which is specifically designed for the foot, may prove to be better than previous implants, but long-term data are lacking.

Other procedures

Freiberg and Freiberg described core decompression for the treatment of early stage lesions.¹⁵ They reported on a procedure in which the metatarsal head is drilled multiple times with a .045-inch K-wire, with satisfactory results (somewhat analogous to drilling for osteochondritis dissecans). Maresca and colleagues described arthroscopic drilling in a patient with bilateral stage II disease, with evidence of restoration of the joint surface and satisfactory results at 2 years.¹⁶ Although encouraging, further investigation is warranted into the potential usefulness of such procedures.

Algorithm

Common to all of these procedures is the goal of diminishing pain and restoring joint function. However, most studies have included small numbers of patients and have not been stratified by age or stage of the disease, making it difficult to draw conclusions about the potential effectiveness of these procedures. Different authors have suggested treatment algorithms based on the stage of the disease and the presenting symptoms. Daniels suggested 1 such algorithm. He recommended grafting and joint elevation as per Smillie for patients with stage II disease, grafting or dorsiflexion osteotomy as per Gauthier and Elbaz for patients with stage III disease, and metatarsal shortening for patients with stage IV or stage V disease.¹¹ Daniels cautioned against the use of resection or joint arthroplasty, to avoid potential problems with transfer lesions.

Helal and Gibb suggested a pattern for management of Freiberg disease as well. Similar to Daniels, they suggested grafting and elevation of the collapsed articular surface for patients with stage I or stage II disease. For later-stage lesions (stages III-V), these authors suggested tailoring the treatment to the patient's symptoms. They recommended using an osteotomy to treat patients with pressure metatarsalgia and using replacement arthroplasty to treat patients suffering from arthritic symptoms of pain with joint motion. However, it is important to recognize that, currently, no consensus exists as to which procedure works best for all patients. In general, if conservative treatment fails, the least destructive and invasive procedures should be considered first for patients with early stage disease, with the more invasive, joint-altering procedures reserved for advanced cases or for patients in whom other forms of treatment have failed.

FUTURE AND CONTROVERSIES

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• Future and Controversies
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• References

Although originally described over 85 years ago, Freiberg disease remains controversial as to its cause and most appropriate treatment. The disorder's relative rarity and varied presentation have made it difficult to obtain a sufficient population for study purposes. Current recommendations have been based on small series of patients treated by various methods, and no clear consensus as to the most appropriate management exists. A trial of conservative treatment can be implemented for most patients presenting with Freiberg disease. If conservative treatment fails, several surgical options exist. Further investigation through prospective or multicenter analysis is needed to guide future treatment options.

MULTIMEDIA

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• References

Media file 1:  Early stage I-II lesion, best seen on an oblique radiograph
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Media file 2:  Stage III lesion with advanced flattening
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Media file 3:  Stage IV lesion with articular collapse and loose body formation
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Media file 4:  Stage V lesion with advanced degenerative changes involving the metatarsal head and proximal phalanx
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Media type:  X-RAY

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Indications
• Contraindications
• Workup
• Treatment
• Future and Controversies
• Multimedia
• References

1. Katcherian DA. Treatment of Freiberg's disease. Orthop Clin North Am. Jan 1994;25(1):69-81. [Medline].
2. Stanley D, Betts RP, Rowley DI, et al. Assessment of etiologic factors in the development of Freiberg's disease. J Foot Surg. Sep-Oct 1990;29(5):444-7. [Medline].
3. Helal B, Gibb P. Freiberg's disease: a suggested pattern of management. Foot Ankle. Oct 1987;8(2):94-102. [Medline].
4. Braddock GT. Experimental epiphyseal injury and Freiberg's disease. J Bone Joint Surg. 1959;41B:154-9.
5. Hoskinson J. Freiberg's disease: a review of the long-term results. Proc Roy Soc Med. 1974;67:106-7.
6. Nguyen VD, Keh RA, Daehler RW. Freiberg's disease in diabetes mellitus. Skeletal Radiol. 1991;20(6):425-8. [Medline].
7. Young MC, Fornasier VL, Cameron HU. Osteochondral disruption of the second metatarsal: a variant of Freiberg's infraction?. Foot Ankle. Oct 1987;8(2):103-9. [Medline].
8. Smillie IS. Treatment of Freiberg's infraction. Proc R Soc Med. Jan 1967;60(1):29-31. [Medline]. [Full Text].
9. James MR, Rowley DI, Betts RP. An operation for Freiberg's disease. J Bone Joint Surg. 1985;67B:671.
10. Smillie IS. Freiberg's infraction (Kohler's second disease). J Bone Joint Surg. 1957;39B:580.
11. Gauthier G, Elbaz R. Freiberg's infraction: a subchondral bone fatigue fracture. A new surgical treatment. Clin Orthop Relat Res. Jul-Aug 1979;(142):93-5. [Medline].
12. Chao KH, Lee CH, Lin LC. Surgery for symptomatic Freiberg's disease: extraarticular dorsal closing-wedge osteotomy in 13 patients followed for 2-4 years. Acta Orthop Scand. Oct 1999;70(5):483-6. [Medline].
13. Kinnard P, Lirette R. Freiberg's disease and dorsiflexion osteotomy. J Bone Joint Surg Br. Sep 1991;73(5):864-5. [Medline]. [Full Text].
14. Smith TW, Stanley D, Rowley DI. Treatment of Freiberg's disease. A new operative technique. J Bone Joint Surg Br. Jan 1991;73(1):129-30. [Medline]. [Full Text].
15. Freiberg AA, Freiberg RA. Core decompression as a novel treatment for early Freiberg's infraction of the second metatarsal head. Orthopedics. Dec 1995;18(12):1177-8. [Medline].
16. Maresca G, Adriani E, Falez F, et al. Arthroscopic treatment of bilateral Freiberg's infraction. Arthroscopy. Feb 1996;12(1):103-8. [Medline].
17. Ary KR, Turnbo M. Freiberg's infraction: an osteochondritis of the metatarsal head. J Am Podiatry Assoc. Feb 1979;69(2):131-2. [Medline].
18. Bayliss NC, Klenerman L. Avascular necrosis of lesser metatarsal heads following forefoot surgery. Foot Ankle. Dec 1989;10(3):124-8. [Medline].
19. Binek R, Levinsohn EM, Bersani F, et al. Freiberg disease complicating unrelated trauma. Orthopedics. May 1988;11(5):753-7. [Medline].
20. Bordelon RL. Silicone implant for Freiberg's disease. South Med J. Aug 1977;70(8):1002-4. [Medline].
21. Campbell WC. Infraction of the head of the second and third metatarsal bones: report of cases. Am J Orthop Surg. 1917;15:721.
22. Douglas G, Rang M. The role of trauma in the pathogenesis of the osteochondroses. Clin Orthop Relat Res. Jul-Aug 1981;(158):28-32. [Medline].
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Article Last Updated: Sep 25, 2007