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Freibergs Disease

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Other Names

  • Avascular Necrosis of the Second Metatarsal
  • Avascular Necrosis of the Third Metatarsal
  • Osteochondrosis of the Second Metatarsal
  • Osteochondrosis of the Third Metatarsal
  • AVN of the Second Metatarsal
  • AVN of the Third Metatarsal
  • Osteonecrosis of the Metatarsal Head
  • Avascular Necrosis of the Metatarsal Head
  • Freiberg's Disease
  • Freiberg's Infraction
  • Egg Shell Fracture
  • Peculiar Characteristic Metatarsal Disease
  • Metatarsal Epiphysitis
  • Osteochondritis Deformans Metatarsojuvenilis
  • Malakopathie[1]
  • Kohler’s Second Disease


  • This page refers to avascular necrosis of the metatarsal head, commonly termed Freiberg's Disease (FD)


  • Initially described by Freiberg in 1914, where he published a case series of 6 patients[2]
  • In 1920, Kohler described osteonecrosis of the metatarsal head[3]


  • Demographic
    • Predominantly occurs in teenagers with a 5:1 female preference[4]
    • Manifests between the 11-17 years of age
  • Represents the 4th most common osteochondrosis[5]


  • General
    • See: Avascular Necrosis (Main)
    • Although it can affect any metatarsal, the 2nd is most common
    • The disease is generally self limited and responds well to conservative therapy
    • Etiology is typically multifactorial
  • Locations[6]
    • Second metatarsal head (68%)
    • Third (27%)
    • Fourth (3%)
    • Fifth (rare)
    • Case reports of multiple[7] or bilateral[8] involvement exist
    • The dominant foot is involved 36% of the time[9]


  • Often considered multifactorial and idiopathic, likely a contribution of
    • Trauma
    • Impaired vascularity
    • Systemic disorders
  • Trauma
    • Chronic repetitive micro trauma has been postulated as a contributing factor[10]
    • Because the second metatarsal is the longest, it may increase stress on the metatarsal head distally
    • High heeled shoes have been implicated as causing repetitive forced dorsiflexion, impingement of 2nd MTPJ[11]
  • Skeletal maturity
    • Adolescence is typical time of onset of symptoms
    • Biomechanical experiments suggest a relative weakness of the metatarsal epiphysis at a certain stage of epiphyseal maturation[12]
    • Ossification center appears between ages 5 and 8, final fusion occurring between age 18 and 20
    • Injury at a critical stage of development when the epiphyseal blood supply is jeopardized could lead to failure of revascularization and initiation of the disease process
  • Vascular supply
    • Aberrant anatomy may form a watershed around the second metatarsal head, however this is not proven in anatomical studies
    • Following injury, vascular injury occurs in 5 phases[13]
      • 1: Arterial spasm
      • 2: Resulting in ischemia of the epiphysis
      • 3: Eventual vascular occlusion
      • 4: Granulation tissue brings new blood supply to the epiphysis
      • 5: The bone resorbs, remodels, collapses and results in arthrosis of the joint.
    • This process may cease spontaneously, however time may be required to reverse ischemic changes
  • Systemic Disorders
    • Multiple systemic illnesses have been presumed risk factors or predisposing for development of FD
    • There is little evidence to support these theories
    • This includes
    • Reports in identical twins suggests an underlying congenital component (need citation)


  • General
    • AVN divided into phases: ischemia, infarction, necrosis, subchondral fracture with collapse of the articular surface, resorption, and remodeling
    • Smillie et al categorized the macroscopic appearance of the metatarsal head in Freiberg’s disease[15]
  • Stage I
    • Fissure develops in the ischemic epiphysis
    • Opposing cancellous bone on either side of the fissure appears sclerotic
  • Stage II
    • Central resorption of bone within the metatarsal head causes the subchondral bone to subside
    • Hyaline cartilage hinges at the edge of defect resulting in an alteration of the articular surface
  • Stage III
    • The subchondal bone sink further centrally into the head, creating irregularities of the intact joint surface
    • These projections may fracture but maintain their attachments to the surrounding soft tissues
    • An isthmus of the articular cartilage on the plantar aspect of the metatarsal head remains intact.
  • Stage IV
    • Fractures of the peripheral projections, plantar isthmus of articular cartilage occur
    • Continuity of the articular surface is disrupted
    • Subsided central portion of the articular surface becomes an osteochondral loose body
    • The epiphysis is probably closed at this stage
  • Stage V
    • Flattening deformity and arthrosis
    • Only the plantar aspect of the metatarsal head retains its original contour
    • The loose body has much reduced in size and may have completely resorbed

Associated Conditions

  • Hallux Valgus
    • Seen in about half of cases, transferring weight to other metatarsal heads[6]


Risk Factors

  • Unknown

Differential Diagnosis

Clinical Features

  • History
    • The typical patient is a female adolescent
    • Patients report pain, swelling around the MTP joint and second metatarsal head
    • Worse with bearing weight and walking
  • Physical Exam: Physical Exam Foot
    • Second metatarsophalangeal joint may be swollen
    • Hyperkeratosis (callous) can be seen on the plantar surface in the plantar fat pad
    • 2nd MTPJ may be tender, firm from effusion, crepitus felt (from loose bodies)
    • Range of motion is often restricted in more chronic cases
    • More severe cases can present with sagittal or coronal plane malalignment, or crossover deformities
  • Special Tests
    • MTP Drawer Test: stabilize metatarsal, proximal phalanx and attempt to dorsally dislocate proximal phalanx


Thickened and irregularity of the second metatarsal head with secondary degenerative changes at the second metatarsophalangeal joint.[16]


  • Standard Radiograph Foot
  • Early findings
    • Joint space widening appears 3 to 6 weeks after onset of symptoms
    • Increased bone density present as disease progresses
    • Flattening of metatarsal head
  • Findings seen in later stages of the disease
  • Central joint depression of metatarsal head
    • Rarefaction of metatarsal head
    • Loose bodies of metatarsal head
    • Sclerosis of metatarsal head
    • Thickening of the metatarsal shaft
    • Joint space narrowing
    • Arthrosis


  • General[17]
    • Provides early detection
    • Allows for classification, management
  • Findings
    • Increased signal intensity in the metatarsal head (T2 weighted)
    • Marked distension of the second metatarsal head demonstrated as a hypointense signal (T1 weighted)
    • Flattening of the metatarsal head

Bone Scintography

  • General
    • Rarely used, unlikely to be needed diagnostically
    • Positive case reports required special technique
  • Potential findings[18]
    • Increased signal density within the metatarsal head
    • Pinhole collimation: Photopenic infarcted area surrounded by a very hyperactive revascularized collar
    • Blood pool: diffuse increased uptake of the second metatarsal head signifying hyperemia, accelerated bone turnover


Gauthier and Elbaz Classification

  • General[6]
    • Based upon the vascular influence of osteonecrosis and subsequent healing
  • Stage I: consolidation can occur without sequelae
  • Stage II: consolidation leaves the head flattened
  • Stage III: the damage is irreparable
  • Stage IV: finally becomes arthrosis

Thompson and Hamilton Classification

Type Features Treatment
I No degenerative joint disease, Intact articular cartilage NWB with metatarsal pad, Low heel
II Periarticular spurs, Articular cartilageintact Stop sports, Cheilectomy, Debridement
III Severe degenerative joint disease, Loss articularcartilage Du Vries arthroplasty, +/− Debridementphalanx, +/− Volar soft tissue interposition
IV Epiphyseal dysplasia, Multiple head involvement As indicated for types I, II and III



  • Goals
    • Alleviation of symptoms
    • Prevention of deformity
  • Indications
    • Most cases as the disease is generally considered self limited
    • Early pre-deformation stages
  • Relative rest from activity
  • Immobilization
  • Weight bearing status
    • Protected weight bearing should be considered
    • Achieved with hard-soled shoe, boot, or a cast
    • Crutches and non weight bearing may be required in severe cases
  • Shoe modification or inserts
    • Incorporation of a rocker into the sole of the shoe together with a stiffer, thicker sole
  • Orthotics
    • Addition of metatarsal bar helps minimize loading on the painful metatarsal head
    • Sproul et al: provide little benefit for relief of pressure over the metatarsal head[19]
    • Palamarchuk et al case report: allowed an athlete to return to their previous international standard of competition[20]
  • Medications
    • NSAIDS
    • Alendronate
      • Shown to prevent early collapse of the femoral head in patients with non-traumatic AVN of the femoral head[21]
      • Not yet studied in Freiberg's Disease
  • Continuous skeletal traction
    • Objective: prevent impaction on the metatarsal head during development
    • Achieved with a metal arch extending beyond the toes supported from a below knee plaster cast which could make mobilization difficult
    • Case report showed rapid regression of pain within 42 days[22]


  • Indications
    • Rare but usually due to failure of conservative therapy
  • Technique
    • Metatarsal neck osteotomy
    • Open joint debridement
    • Arthroscopic joint debridement
    • Metatarsal osteotomy
    • Core decompression
    • Perichondral grafting
    • Arthroplasty

Rehab and Return to Play


  • Needs to be updated

Return to Play

  • Immobilization for 4-6 weeks or until symptoms resolve with gradual return to activity [23]
  • Patients who received surgery were relieved of symptoms and returned to their daily activities [24]

Complications & Prognosis


  • Unknown


  • Osteoarthritis
  • Chronic pain
  • Surgical Complications
    • Metatarsal head excision can lead to pressure metatarsalgia, progressive hallux vagus, and shortening of the toe
    • Metatarsal osteotomy can disrupt the tenuous blood supply which can aggravate the condition further
    • Replacement arthroplasty can potentially lead to bone erosion, infection, and a stiff, flattening toe
    • Arthrofibrosis and surgical wound infection.

See Also


  1. Bragard, G: Berlag zim malakopathie der metatarsal kopichen Koehlerersce Krankeit. Ztsce Orthop Clinic 46:49, 1924.
  2. Frieberg, AH: Infraction of second metatarsal bone, atypical injury. Surg Gynaecol Obstet 19:191, 1914.
  3. Kohler, A: Eine typische erkrankug des.2 metatarsophalangeal gelekes. MMW 67:1289 – 1290, 1920.
  4. Katcherian, DA: Treatment of Freiberg’s disease. Orthop Clin North Am 25:69, 1994.
  5. Omer, GE: Primary articular osteochondroses. Clin Orthop 158:33, 1981.
  6. 6.0 6.1 6.2 Gauthier, G; Elbaz, R: Freiberg’s infraction: a subchondral bone fatigue fracture. A new surgical treatment Clin Orth Rel Res 142:93 – 95, 1979.
  7. Rafee, A; Chougle, A; Sulaiman, M; McEvoy, A: Unilateral sequential Freiberg’s Disease: an atypical presentation. Foot Ankle Surg 12:153 – 155, 2006. http://dx.doi.org/10.1016/j.fas.2006.02.002
  8. Maresca, G; Adriani, E; Falez, F; Mariani, PP: Arthroscopic treatment of Freiberg’s infarction Arthroscopy 12(1):103 – 108, 1996. http://dx.doi.org/10.1016/S0749-8063(96)90229-7
  9. Stanley, D; Betts, RP; Rowley, DI; Smith, TWD: Assessment of etiological factors in the development of Freiberg’s disease. J Foot Surg 29(5):444 – 447, 1990
  10. Smillie, IS; Freiberg’s infarction (Kohler’s second disease). J Bone Joint Surg Br 39:580, 1957.
  11. Katcherian, DA: Treatment of Freiberg’s disease. Orthop Clin North Am 25:69, 1994.
  12. Braddock, GTF: Experimental epiphyseal injury and Freiberg’s disease. J Bone Joint Surg Br 41:154 – 159, 1959.
  13. Viladot, Beito Lavery, LA: Freiberg’s disease and dislocation of the second metatarsophalangeal joint: aetiology and treatment. Clin Pod Med Surg 7(4):619 – 631, 1990.
  14. Nguyen, VD; Keh, RA: Daehler RW. Freiberg’s disease in Diabetes Mellitus. Skelet Radiol 20:425 – 428, 1991. http://dx.doi.org/10.1007/ BF00191084
  15. Smillie, IS; Treatment of Freiberg’s infraction. Proc R Soc Med 60(1):29 – 31, 1967.
  16. Case courtesy of Dr Domenico Nicoletti, Radiopaedia.org, rID: 44376
  17. Steinberg, ME; Steinberg, DR: Classification systems for osteonecrosis: an overview. Ortho Clin North Am 35(3):273 – 83, 2004. http://dx.doi.org/10.1016/j.ocl.2004.02.005
  18. Mandell, JA, Harcke, HT: Scintigraphic manifestations of infarction of the second metatarsal (Freiberg’s disease). J Nucl Med 28(2):249 – 251, 1987.
  19. Sproul, J; Klaaren, H; Mannarino, F: Surgical treatment of Freiberg’s Infraction in athletes. Am J Sports Med 21:381 – 384, 1993. http://dx.doi.org/10.1177/036354659302100309
  20. Palamarchuk, HJ; Oehrlein, CR: Freiberg’s infraction in a collegiate heptathlete. J Am Pod Med Assn 90(2):77 – 80, 2000.
  21. Lai, KA; Shen, WJ; Yang, CY; Shao, CJ; Hsu, JT; Lin, RM: The use of alendronate to prevent early collapse of the femoral head in patients with non traumatic osteonecrosis. A Randomised clinical study. J Bone Joint Surg Am 87(10):2155 – 9, 2005. http://dx.doi.org/10.2106/JBJS.D.02959
  22. Morandi, A; Prina, A; Verdoni, F: Treatment of Kohler’s second syndrome by continuous skeletal traction. Ital J Orthop Traumatol 16(3):363 – 368, 1990.
  23. Ferit, D., Mustafa Turgut, Y. and Pelin Zeynep Bekin, S., 2017. Freiberg Disease Presenting as Forefoot Pain. International Journal of Foot and Ankle, 1(1).
  24. Baravarian, B., 2014. Key Insights On Treating Freiberg’s Infraction. podiatrytoday, 27(3), p.1
Created by:
John Kiel on 30 June 2019 20:55:03
Last edited:
4 October 2022 12:45:26