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Freibergs Disease
From WikiSM
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
Background
- This page refers to avascular necrosis of the metatarsal head, commonly termed Freiberg's Disease (FD)
History
- 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]
Epidemiology
- 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]
Pathophysiology
- 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]
Etiology
- Often considered multifactorial and idiopathic, likely a contribution of
- Trauma
- Impaired vascularity
- Systemic disorders
- Trauma
- 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
- Systemic Lupus Erythematosus
- Hypercoagulability
- Conditions causing increase osseous pressure
- Case reports in Diabetes Mellitus[14]
- Reports in identical twins suggests an underlying congenital component (need citation)
Histopathology
- 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]
Pathoanatomy
Risk Factors
- Unknown
Differential Diagnosis
- Fractures & Osseous Disease
- Traumatic/ Acute
- Stress Fractures
- Other Osseous
- Dislocations & Subluxations
- Muscle and Tendon Injuries
- Ligament Injuries
- Plantar Fasciopathy (Plantar Fasciitis)
- Turf Toe
- Plantar Plate Tear
- Spring Ligament Injury
- Neuropathies
- Mortons Neuroma
- Tarsal Tunnel Syndrome
- Joggers Foot (Medial Plantar Nerve)
- Baxters Neuropathy (Lateral Plantar Nerve)
- Arthropathies
- Hallux Rigidus (1st MTPJ OA)
- Gout
- Toenail
- Pediatrics
- Fifth Metatarsal Apophysitis (Iselin's Disease)
- Calcaneal Apophysitis (Sever's Disease)
- Freibergs Disease (Avascular Necrosis of the Metatarsal Head)
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
Evaluation

Thickened and irregularity of the second metatarsal head with secondary degenerative changes at the second metatarsophalangeal joint.[16]
Radiographs
- 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
MRI
- 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
Classification
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 |
Management
Nonoperative
- 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
- 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]
Operative
- 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
Rehabilitation
- 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
Prognosis
- Unknown
Complications
- 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
- Internal
- External
- Sports Medicine Review Foot Pain: https://www.sportsmedreview.com/by-joint/foot/
References
- ↑ Bragard, G: Berlag zim malakopathie der metatarsal kopichen Koehlerersce Krankeit. Ztsce Orthop Clinic 46:49, 1924.
- ↑ Frieberg, AH: Infraction of second metatarsal bone, atypical injury. Surg Gynaecol Obstet 19:191, 1914.
- ↑ Kohler, A: Eine typische erkrankug des.2 metatarsophalangeal gelekes. MMW 67:1289 – 1290, 1920.
- ↑ Katcherian, DA: Treatment of Freiberg’s disease. Orthop Clin North Am 25:69, 1994.
- ↑ Omer, GE: Primary articular osteochondroses. Clin Orthop 158:33, 1981.
- ↑ 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.
- ↑ 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
- ↑ 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
- ↑ 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
- ↑ Smillie, IS; Freiberg’s infarction (Kohler’s second disease). J Bone Joint Surg Br 39:580, 1957.
- ↑ Katcherian, DA: Treatment of Freiberg’s disease. Orthop Clin North Am 25:69, 1994.
- ↑ Braddock, GTF: Experimental epiphyseal injury and Freiberg’s disease. J Bone Joint Surg Br 41:154 – 159, 1959.
- ↑ 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.
- ↑ 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
- ↑ Smillie, IS; Treatment of Freiberg’s infraction. Proc R Soc Med 60(1):29 – 31, 1967.
- ↑ Case courtesy of Dr Domenico Nicoletti, Radiopaedia.org, rID: 44376
- ↑ 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
- ↑ Mandell, JA, Harcke, HT: Scintigraphic manifestations of infarction of the second metatarsal (Freiberg’s disease). J Nucl Med 28(2):249 – 251, 1987.
- ↑ 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
- ↑ Palamarchuk, HJ; Oehrlein, CR: Freiberg’s infraction in a collegiate heptathlete. J Am Pod Med Assn 90(2):77 – 80, 2000.
- ↑ 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
- ↑ 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.
- ↑ 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).
- ↑ 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
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Last edited:
4 October 2022 12:45:26
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