Tag Archives: Osteochondritis dessicans

Fresh Osteochondral Allografting in the Treatment of Osteochondritis Dissecans of the Talus

by Ali Abadi DPM,MS1 , Raymond Ferrara DPM2

The Foot and Ankle Online Journal 3 (7): 3

A 42 year-old female with persistent ankle pain secondary to trauma of the right ankle is presented. Magnetic resonance imaging revealed an osteochondral lesion of the medial equatorial aspect of the talar bone. After exhausting several type of conservative treatments, such as pain management, ice therapy, NSAID, injection and immobilization, surgical intervention was necessary to treat the osteochondritis dissecans.

Key words: Osteochondritis Dissecans, Osteochondral Allograft, Articular cartilage transplantation, talus.

Accepted: June, 2010
Published: July, 2010

ISSN 1941-6806
doi: 10.3827/faoj.2010.0307.0003

Osteochondritis Dissecans (OCD) was initially described by Alexander Monro (primus) in 1738. [1] In 1870, James Paget described the disease process for the first time, but it was not until 1887 that Franz König published a paper on the cause of loose bodies in the joint. [2] König named the disease “osteochondritis dissecans”, [3] describing it as a subchondral inflammatory process of the knee, resulting in a loose fragment of cartilage from the femoral condyle. In 1922, Kappis described this process in the ankle joint. [4] On review of all literature describing transchondral fractures of the talus, Berndt and Harty developed a classification system for staging of osteochondral lesions of the talus (OLTs). [5]

In 2001, Scranton and McDermott added a fifth stage to the Berndt and Harty classification system in order to describe the cases of patient in whom the cartilage cap is intact with the lesion involving a subchondral cyst within the talar dome. [6] The term osteochondritis dissecans has persisted, and has since been broadened to describe a similar process occurring in many other joints, including the knee, hip, elbow, and metatarsophalangeal joints.

Case Report

A 42 year-old female presented with history of sever right ankle pain. The patient stated that she has deep ankle pain and repeatedly “twists her ankle”. On physical examination the region of pain was localized along the anteromedial aspect of the right talus. The area was tender to direct pressure. There was evidence of swelling at the right medial malleolar, but no signs of acute trauma, or bruising were noted. The ankle range of motion is preserved. Weight bearing radiographs of the ankle revealed osteochondral lesions.

Magnetic resonance imaging (MRI) of the right ankle revealed an osteochondral defect involving the medial talar dome, without associated subchondral collapse. There is a T2 hyperintense and T1 hypointense osteochondral defect, measures 5 mm in transverse extent x 6 mm in cranicaudal extent. (Fig.1A and B)


Figure 1A and B Magnetic resonance imaging demonstrating the osteochondral defect. A) The axial view, B) coronal view.

The ankle mortis is symmetric. There is a surrounding bone marrow edema along the superomedial talar dome. It also revealed mild fluid within the retrocalcaneal bursae and minor tenosynovitis of the medial and lateral ankle tendons. Laboratory examination included corpuscular blood count with differential count, white blood cell count, rheumatoid factor, C-reactive protein, erythrocyte sedimentation rate, and serum uric acid are all unremarkable. Osteochondral allograft was obtain from thirteen year old fresh cadaver and supplied by Arthrex Inc. [7]

Surgical Technique

The surgical procedure was performed under Monitored anesthesia care (MAC) combined with local infiltrative nerve block. The patient was positioned supine on the operating table. Pre-operative antibiotic (2 grams Cefazolin ) were given at the beginning of the case. A pneumatic ankle tourniquet is placed on the mid-calf and inflated to 250mmHg. The skin was prepped and draped from toes to mid calf.

A 6 cm longitudinal incision was made directly over the medial malleolus. (Fig. 2) The incision was then carried down through the subcutaneous tissue using sharp and blunt dissection. Care was taken to avoid all vital neurovascular structures. The talar dome and tibial plafond was located and marked on the skin utilizing the intraoperative fluoroscopy. (Fig. 3) The medial malleolus is predrilled with two 0.045 pins at a slightly divergent angles to help prevent proximal slippage of the medial malleolus during screw insertion. These pins are overdrilled with Arthrex 3.4 mm cannulated Trim-It Drill Bit across the medial malleolus and into the tibial plafond. The holes are then tapped. (Fig. 4) A V-shaped osteotomy was performed and medial malleolus carefully pulled inferiorly to expose the talus. (Fig. 5)

Figure 2  A 6cm longitudinal incision is made along the medial malleolus.

Figure 3 intraoperative  fluoroscopic view showing the tibial plafond.

Figure 4 The medial malleolus is marked at the tibial plafond and the Arthrex 3.4 mm cannulated Trim-It wire is then placed in the tibia.

Figure 5 An intraoperative photograph demonstrating the V-shaped osteotomy on medial malleolus to gain exposure to the OCD lesion.

The posterior tibialis and the flexor hallucis longus tendons are protected with small retractors. The talar lesion is drilled perpendicularly and centrally with the 2.4 mm guide pin. The guide pin is advanced to a depth of 15-20mm. The guide pin is then overdrilled with the appropriate size cannulated Headed Reamer to a depth of at least 12 mm. (Fig. 6) The cannulated OATS Alignment Rod is introduced over the guide pin, which measures the diameter and depth of the pilot hole. At this point we covered the surgical site with saline soaked gauze and directed our attention to the Allograft bone. (Fig. 7) After matching the defected cartilage site to the donor site the Arthrex OATS 6 mm donor harvester was used.

Figure 6 After placement of guide wire, the defect is then reamed.

Figure 7  Fresh donor cadaver bone of the talus.

We drove the harvester into to the donor talus, at 90 degrees, and twisted it clockwise 90 degrees under pressure and then full counter clockwise revolution. (Fig. 8) The tube and the raft were then withdrawn. Then we inserted the graft into the recipient hole in the talus. We utilized the large end of the tamp for tapping the graft into the graft site and made sure there is no protrusion. (Fig. 9 A – C)

Figure 8  The Arthrex OATS 6 mm donor harvester is being twisted clockwise and counterclockwise to secure the donor graft.


Figure 9A,B and C  The 6 mm donor plug is harvested from the talus (A),  12mm of bone plug is removed (B) and then transferred to the patient’s talus. (C)

The medial malleolus is replaced back to its anatomical position. The Arthrex 0.045 pins re-inserted back into the cannulated holes. Two 4.5mm cannulated screws were driven up the holes while the medial malleolus is held in a position of anatomic reduction. (Fig. 10 A and 10B)


Figure 10A and B  The graft is tapped into the talus. (A)  Intra-operative fluoroscopic view showing the two 4.5mm cannulated screw fixation of medial malleolus after graft implantation. (B)


Articular cartilage disease can eventually lead to debilitating injury because of the body’s inability to repair this important tissue. OCD is a pathologic process in which a fragment of subchondral bone becomes avascular and can separate from the surrounding tissue.

Although most lesions are thought to have a traumatic origin, other possible causes include defect of ossification, repetitive mechanical stress, and ischemia. [8,9] The main indication for allografting includes talar defects that are 10 mm or greater. The lesions are often missing articular cartilage, or the remaining cartilage is soft and fibrillated. In the Brendt and Harty classification, these are usually stage III or IV leisons. [10] Surgery is offered when the pain is unresponsive to non-operative treatment that includes medication, cast immobilization, bracing and physiotherapy. Contraindications to allografting are few in number. The major reasons are osteoarthritis of tibiotalar joint, reflex sympathetic dystrophy and avascular necrosis of the talus. [11]

There is extensive evidence in support of autograph and allograft replacement of osteochondritis dissecans. Hangody, et al., were the first to report their early and intermediate results. They used the ipsilateral knee as a donor site and found good to excellent long term success in 34 out of 36 patients at an average of 4.2 years. [12] Al-Shaikh, et al., reports their results using the OATS procedure for treatment of the large OCD lesions of talus. Seventeen out of nineteen patients (89%) were satisfied with their results. [13]

Gross, et al., were the first to use fresh osteochondral allografts in the treatment of large OCD lesions of talus. They had 9 patients who underwent fresh osteochondral allograft transplantation from the tali of fresh human cadaver. Six grafts remain in situ with a mean survival of 11 years. [14] According to Gross, et al., the most common complication of fresh osteochondral allografting is resorption and failure of the graft to incorporate, which results in subchondral collapse and fragmentation of the graft.

Post operative management includes non-weight bearing for period of 12 weeks, but range of motion exercises are started once the incision is healed. After three months, patients begin protected weight bearing in a cam boot for 1 month. Full activity is allowed by 6 months.


1. Munro A. Part of the cartilage of the joint separated and ossified. Medical Essays and Observations 1973 4: 19. Cited in Burns RC. Osteochondritis dissecans. CMAJ 1939 41 (3): 232-235.
2. Garrett JC (July 1991). Osteochondritis dissecans. Clin J Sports Med 10 (3): 569-593.
3. Barrie HJ. Osteochondritis dissecans 1887-1987. A centennial look at König’s memorable phrase. JBJS 1987 69B (5): 693-695.
4. Kappis M. Weitere beitrage zur traumatisch-mechanischen entstehung der “spontanen” knorpela biosungen (German). Deutsche Zeitschrift für Chirurgie 1922 171: 13-29.
5. Berndt AL, Harty M. (June 2004). Transchondral fractures (osteochondritis dissecans) of the talus. JBJS 2004 86A (6): 1336.
6. Scranton PE Jr, McDermott JE. Treatment of type V osteochondral lesions of the talus with ipsilateral knee osteochondral autograft. Foot ankle Int 2001 22: 380-384.
7. Arthrex Med. Inst. GmbH. Single use osteochondral Autograft Transfer System (OATS) and Small Joint OATS Sets, www.artherax.com (accessed 28th June 2010).
8. Obedian RS, Grelsamer RP. Osteochondritis dissecans of the distal femur and patella. Clin Sports Med 1997 16:1 57-174.
9. Steadman JR, Rodkey WG,Rodrigo JJ. Microfracture :surgical technique and rehabilitation to treat chondral defects. Clin Ortho Relat Res 2001 391: 362-336
10. Brendt AL, Harry M. Transchondral fractures of the talus. JBJS 1959 41A: 988-1018.
11. Meehan RE, Brage ME. Fresh osteochondral allografting for osteochondral defect of the talus. Techniques Foot Ankle Surg 2004 54: 53-61.
12. Hangody L. Kish G, Kárpáti Z, Szerb I, Eberhardt R. Treatment of osteochondritis dissecans of the talus: use of the mosaicplasty technique. Foot Ankle Int 1997 18: 628-634.
13. Al-sheikh RA, Chou LB, Mann JA, Dreeben SM, Prieskorn D. Autologous osteochondral grafting for talar cartilage defect. Foot Ankle Int 2002 23: 381-389.
14. Gross AE, Agnidis Z, Hutchinson CR. Osteochondral defect of the talus treated with fresh osteochondral allograft transplantation. Foot Ankle Int 2001 22: 385-391.

Address correspondence to: Dr. Ali Abadi , Virtua hospital ,West jersey, 101 Carnie Blvd. Voorhees NJ 08043 Email:aa78@Georgetown.edu .

Dr. Ali Abadi , Virtua hospital ,West jersey, 101 Carnie Blvd. Voorhees NJ 08043.
Dr Raymonfd Ferrera attending at Virtua Hosital, West jersey, 101 Carnie Blvd. Voorhees NJ 08043.

© The Foot and Ankle Online Journal, 2010

Freiberg’s Infraction of the Second Metatarsal Head with Bioorthologic Repair using the NEXA Osteocure™ Bone Graft: A case report

by Al Kline, DPM1

The Foot & Ankle Journal 1 (11): 4

Freiberg’s infraction is a relatively common osteochondritis of the second metatarsal head. It appears to affect young women who are active in sports. Its etiology is thought to be traumatic in nature causing a painful alteration, subchondral disruption and collapse of the articular cartilage. A case report is presented describing this disorder in a young female runner. The use of a bioorthologic bone plug to surgically treat this condition is discussed and presented. It appears that the use of bioorthologic materials provide a promising alternative to surgical osteotomies. It has been shown that bioorthologic materials will provide a porous scaffold allowing blood, marrow and progenitor cells to wick into the pores and provide a stable environment for tissue in-growth and cellular development. Between six and twelve months, the polymer is resorbed and replaces the natural hyaline cartilage of the joint surface.

Key words: Freiberg’s infraction, osteochondritis, osteochondritis dessicans, bioorthologic bone graft

This is an Open Access article distributed under the terms of the Creative Commons Attribution License. It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org)

Accepted: October , 2008
Published: November, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0111.0004

In 1914, Alfred H. Freiberg was the first to describe a painful collapse to the articular surface of the second metatarsal head. [1] The etiology of injury can be attributed to trauma and subchondral disruption of the vascular supply to the articular cartilage. The incidence of injury appears to be most commonly found in young women and girls, although the overall incidence of osteochondroses is higher in men. [2] On occasion, the third metatarsal head may also be involved. Osteochondritis, in effect, can involve any of the five metatarsal heads of the foot. However, the incidence is highest involving the second metatarsal head. [1]

There does not appear to be a genetic link to Freiberg’s infraction, although a recent report of Freiberg’s infraction in twins may suggest an underlying genetic predisposition. [8]

In Freiberg’s original article, he described six women with a painful limp and pain isolated to the second metatarsal head. Radiographs revealed collapse of the articular surface of the second metatarsal head with intra-articular loose bodies seen in three of the six patients. He noted that four of the six patients were under 18 years of age and postulated that a long second metatarsal combined with an ineffective first ray complex attributed to overload of the second metatarsal phalangeal (MTP) joint and subsequent articular collapse. [2]

Patients usually present with a painful and often swollen joint. A history of trauma may or may not exist. There is usually point tenderness to the dorsal aspect of the second metatarsophalangeal joint and associated limitation of joint motion. Diagnosis is often confirmed by simple radiographs which show varying stages of metatarsal head injury and articular depression.

MR (magnetic resonance) imaging has been definitively shown to aid in the diagnosis of Freiberg’s infraction before joint changes occur on radiograph. [4] This may be particularly useful in the early stage of the disorder when joint pain is present without observed changes to the joint surface.

In the patient with a normal or even wide joint space, MR imaging allows for early identification of Freiberg’s infraction through low signal intensity changes of subchondral sclerosis. (Fig. 1)

Figure 1 Early flattening (small arrows) with low signal intensity osteochondrosis of the second metatarsal head on a T-1 axial image.  (Courtesy David W. Stoller, MD: Magnetic Resonance Imaging in Orthopaedics & Sports Medicine, pp.488-489, 1993.)

In his original article, Freiberg described his treatment which included simple removal of the loose bodies in the joint. Historically, there have been a number of surgical approaches to the treatment of Freiberg’s infraction. The use of bioorthologics is a relatively new approach to the treatment of osteochondral defects and injury. A case report is presented describing the use of the NEXA Osteocure™ bone graft for repair of a stage II Freiberg’s infraction of the second metatarsal head.

Case Report

An active fifteen year old female runner began having pain and discomfort to the second MTP joint. She did not recall any injury. She is very active in track and basketball. She has been running daily and relates to pain while running. She was using a silicone sleeve over the second toe and takes Tylenol and Motrin for pain and swelling. Her pain began to interfere with her running and she began seeking medical attention.

Her clinical examination revealed a swollen second metatarsophalangeal joint with pain upon dorsiflexion of the second toe. Joint range of motion was limited to about 5 to 10 degrees of dorsiflexion with extreme pain. Radiographic evaluation confirmed second metatarsal head changes consistent with Freiberg’s infraction and a long second ray with Morton’s toe. (Fig. 2)

Figure 2   Initial radiograph shows subchondral disruption of the articular surface of cartilage involving the second metatarsal head.  Note the long second metatarsal and Morton’s toe. 

She underwent MR imaging which revealed diffuse increased signal intensity with local tissue edema and hemorrhage. There was joint effusion with fragmentation of the metatarsal head consistent with Freiberg’s infraction, stage II.

The patient had a track meet within three weeks of our visit and returned about four weeks later and underwent casting and immobilization. After cast immobilization, she was placed in accommodative metatarsal padding and shoes and was asked not to return to running for an additional month. However, she continued to re-develop pain and swelling to the joint and was scheduled for surgery to include osteochondral bone repair with bioorthologic graft using the NEXA Osteocure™ bone graft.

Surgical Technique

The patient was brought to surgery. A local second ray block was performed under intravenous sedation. A small incision was made directly over the second MTP joint. A dorsal capsular incision was performed and upon entry of the joint, we noticed a cartilaginous loose body at the dorsal aspect of the metatarsal head. (Fig. 3)

Figure 3 Once the joint is entered surgically, a dorsal linear capsulotomy reveals a loose joint body.

The soft tissue capsule is delicately reflected to expose the cartilaginous surface of the metatarsal head. A large defect along the dorsal half of the metatarsal head is identified. The cartilage was actually separated from the underlying subchondral bone.

Using a small scalpel, the defect is lifted from the subchondral bone. It is important to identify the loose margin of cartilage and the point of firm attachment of the cartilage cap plantarly in order to preserve the plantar cartilage. (Figs. 4 and 5) Once this margin is identified, the loose cartilage is then excised in a semi-circular fashion. This is done to facilitate the bone plug, which is round in its shape. (Figs. 6 and 7)


Figures 4 and 5  The loose cartilage is identified and demarcated from the subchondral bone.  Care is taken to identify the plantar cartilaginous attachment.


Figures 6 and 7  The loose cartilage is removed and the  plantar cartilaginous attachment is identified.  A semi-circular excision of the cartilage flap has been performed.

A curette is then used to remove the soft, unhealthy subchondral bone. (Fig. 8) Preparation of the site is probably the most crucial aspect of this surgery. In particular, joint range of motion needs to be unimpeded dorsally and requires the removal of joint spurring, loose bodies and bone defects. Using the NEXA Osteocure™ Implant Kit, a corresponding set of color-coded sizers allows for determination of the bone graft size.

Figure 8   A curette is used to remove any diseased subchondral bone.  The diseased portion of bone is usually softer than the underlying cancellous bone.

Color coded sizers of 5, 7, 9 and 11mm diameter correspond to the respective graft size plugs. (Figs. 9,10) Once the graft size is determined, a reaming drill is used to prepare the graft site for implantation. (Figs. 11,12 and 13) The graft is then measured for depth, inserted and tapped within the newly prepared host site. (Figs. 14,15 and 16) The graft is then firmly placed into the host site. The joint can also be placed through its proper range of motion. This will ensure that the graft is articulating with the proximal phalanx. (Figs. 17 and 18)


Figures 9 and 10  The bone plug sizer is used to determine the size diameter of the graft.  Again, the inferior, semi-circular portion of healthy cartilage should fit directly to the sizer.


Figures 11,12 and 13  The drill corresponding to the sizer is used to prepare the host site for the graft plug.


Figures 14,15 and 16  The graft is measured for depth and then inserted into the host site.  A small tap is used to secure the graft into the host site.


Figures 17 and 18  The graft is seated in the defect.  The Osteocure™ graft provides a press fit to the defect with close approximation to the surrounding bone and tissue causing migration of tissue into the scaffolding.  This surface will provide scaffolding for hyaline-like cartilage in 6 to 12 months.

The surgical site is then closed in the customary manner. The patient was then placed non-weight-bearing in a posterior splint and kept on crutches for 4 weeks. This was followed by 2 weeks of partial weight-bearing in a walking shoe. She was able to wear her athletic shoes within 8 weeks after surgery.

The patient was pain free with an increase in joint range of motion. At last visit, she was playing volleyball without pain. (Figs. 19 and 20), however, the patient has been advised not run for six months after surgery to allow the graft to resorb.


Figures 19 and 20  Two months following surgery, incorportation of the graft is already seen.  A thin articular margin is also appreciated.  Although, there is still some flattening of the metatarsal head, the patient is now asymptomatic.  A close up of the radiograph (Fig. 20) reveals new subchondral bone formation in a cancellous pattern with metatarsal head resurfacing.


Several synonyms have been used to described Freiberg’s infraction including Freiberg’s infarction, osteochondrosis of the second metatarsal head, eggshell fracture, Koehler second disease, peculiar metatarsal disease, Panner disease of the metatarsal, osteochondritis deformans metatarso-juvenilis, malacopathia, subchondral bone fatigue fracture of the second metatarsal head and dorsal fatigue stress injury of the second metatarsal head. [2,7]

In the majority of cases, the defect is usually dorsally located to the upper half of the articular surface of the metatarsal head. This would also lend support to the etiology of trauma causing this defect. In observing a number of these cases, mechanical changes appear to cause a dorsal articular jamming and trauma to the joint surface. These include a Morton’s toe or long second digit, a short first metatarsal or elongated second ray and instability of the first ray. Limitation of dorsiflexory motion of the second MTP joint will lead to progressive joint damage and eventual articular shear. This will cause an actual lifting and separation of the articular cartilage from the subchondral bone disrupting the vascular supply to the articular cartilage.

Once the articular cartilage separates, the cartilage can fragment. The fragments that separate from the articular cartilage are called joint bodies or joint ‘mice’.

As previously stated, ‘infraction’ is sometimes called Freiberg’s ‘infarction’. Infarction would suggest a vascular event leading to osteonecrosis. It has been suggested that avascular necrosis from injury will lead to the growth plate or epiphyseal injury in young, growing bone. This may also explain why the incidence is higher in young women and girls.

In 1959, Braddock observed that there is a relative weakness of the second metatarsal epiphysis at a certain stage of epiphyseal maturation. [3] Whatever the etiology, the result appears to cause cartilage lifting and separation from the underlying subchondral bone and vascular osteonecrosis of the joint surface.

The extent of articular damage however, appears to be directly proportional to the extent of joint pain. Treatment, including both conservative and surgical approaches, varies to the extent of injury. In early stages, where the articular cartilage may form a small depression, treatment usually consists of immobilizing the joint.

Conservative treatments should almost always consist of immobilization, offloading and casting irrespective of severity and stage. The goal of non-operative immobilization is to promote a decrease in joint effusion and inflammation including the surrounding soft tissue structures. This may be supplemented with NSAID therapy, joint injections and oral steroids. In patient’s who may not want surgery, shoe modification, metatarsal bars, orthotics and even rocker bottom shoes may provide some temporary relief. In a majority of cases, operative intervention is recommended to provide improved joint mechanics, remove damaged joint spurs and loose joint bodies and treat the osteochondral defect.

Methods of Surgical Treatment

Freiberg initially described removal of the loose bodies to the affected joint. Other treatments have been more aggressive, including the actual removal of the metatarsal head. Unfortunately, this will lead to more complicated conditions of the foot including transfer metatarsalgia, stress fracture and contracture of the corresponding digit.

Some authors have also suggested joint arthroplasty and resecting the base of the proximal phalanx. [6] This may decompress the joint, but joint instability and toe shortening or dorsiflexory rotation of the digit is a major complication.

In 1991, Smith, et al., described simple decompression osteotomy using a T-plate in 15 patients with Freiberg’s infraction of the second metatarsal head. They reported good results and relief of pain within 12 months, although all patients had limited motion of the joint post-operatively. [5]

Dorsiflexory osteotomies have also been described in order to rotate the healthy plantar cartilage dorsally. This is commonly performed by a v-osteotomy and use of cross K-wire technique or screw fixation. However, rotational osteotomies are only indicated in Freiberg’s stages I-III where the plantar hinge of the cartilage is still intact. Implants have also been used including silastic and titanium total implants and titanium hemi-implants. Shih, et al., described the successful use of a titanium hemi-implant in the treatment of Freiberg’s infraction. They reported a successful increase in range of motion of the joint from 15 degrees to 45 degrees, with no pain or activity limitation. [6]

The advantage of using bioorthologics in the treatment of osteochondral defects

Newer techniques are now being introduced in an attempt to actually repair the damaged cartilage and subchondral bone in Freiberg’s infraction. Orthobiologic materials, particularly PolyGraft™ materials, provide a scaffolding for regeneration of tissue and have demonstrated evidence of resurfacing the articular cartilage with hyaline-like cartilage. This is different than resurfacing of the joint with fibrocartilage after damage. Fibrocartilage is primarily Type I collagen and is less desirable than Hyaline cartilage, which is primarily comprised of type II collagen. In a recent land-mark study, Cascio, et al., reported exciting chondral repair with observed hyaline cartilage in a goat model using an injectable hydrogel bone graft. [8]

Critical size chondral defects were created on the stifle joint of adult goats. Experimental defects underwent marrow stimulation to recruit reparative stem cells and were primed with a chondroitin-sulfate based adhesive to anchor the scaffold. Controls received marrow stimulation alone.

The operative goat legs were cast for two weeks and after 13 weeks, cartilage fill and repair quality was assessed by histomorphometry evaluation. Results revealed evidence of hyaline-like repair with a 12% increase in total tissue fill in scaffold-treated defects on histomorphometry. Remodeling and articular cartilage bridging was seen up to twelve months after implantation.

This is an exciting development in the treatment of osteochondral defects by actually healing the cartilage defect with desirable hyaline cartilage and will maintain the joints normal cartilaginous properties. The Osteocure™ bone plug is a porous PolyGraft™ and is the first 100% resorbable composite scaffold material designed to fill osteochondral defects. Its properties include a three dimensional scaffolding structure for tissue incorporation and remodeling. Resorbable polymers and bioactive ceramics are combined to produce the desired strength, stiffness and bone growth characteristics. It also withstands mechanical loads and compression without crushing the material. The Osteocure™ graft provides a press fit to the defect with close approximation to the surrounding bone and tissue causing migration of tissue into the scaffolding. The hydrophilic properties of the porous scaffolding allow blood, marrow and progenitor cells to wick into the pores and provide a stable environment for tissue in-growth and cellular development. Between six and twelve months, the polymer graft is resorbed and replaced with living tissue. [9]


Although there is no one consensus on the best surgical treatment for this condition, the use of orthobiologics provides a promising new attempt to restoring the cartilaginous surface of the joint and eliminating joint destruction and pain. More importantly, these products appear to heal and replace the natural hyaline cartilage of the joint surface.


1. Freiberg, AH. Infraction of the second metatarsal head, a typical injury. Surg Gyn Ob, (19) 163-191, 1914.
2. Boyer, M., DeOrio, J. Freiberg Infraction. E-Medicine, Online article, 2004.
3. Braddock GTF. Experimental epiphyseal injury and Freiberg’s disease. JBJS, 41B (1) February, 1959.
4. Stoller DW. Magnetic Resonance Imaging in Orthopaedics and Sports Medicine. J.B. Lippincott Company, Philadelphia, 1st edition, 1993.
5. Smith TW, Stanley D, Rowley DI. Treatment of Freiberg’s disease: A New Operative Technique. JBJS 73B (1), January, 1991.
6. Shih AT, Quint RE, Armstrong DG, Nixon BP. Treatment of Freiberg’s infraction with the Titanium hemi-implant. JAPMA 94 (6), 590-593, Nov/Dec 2004.
7. Blitz NM, Yu JH. Freiberg’s infraction in identical twins: A case report. JFAS, 44(3), May/June 2005.
8. Cascio B, Sharma, MS, Fermanian, BS, Elisseeff, J: Chondral lesion repair in a critical size defect model using injectable hydrogel scaffold in conjunction with marrow stimulation. AOSSM, Poster #32, 2006.
9. Nexa Orthopaedics: Osteocure: PolyGraft™ Material Technology. [Online PDF]

Address correspondence to: Al Kline, DPM
3130 South Alameda, Corpus Christi, Texas 78404.

1 Adjunct Clinical Faculty, Barry University School of Podiatric Medicine. Private practice, Chief of Podiat ry, Doctors Regional Medical Center. Corpus Christi, Texas, 78411.

© The Foot & Ankle Journal, 2008

Dorsiflexory Wedge Osteotomy to Treat Freiberg’s Infraction of the Second Metatarsal Head: A case report

by Georgeanne Botek, DPM, FACFAS1, Martha A. Anderson, DPM2 , George Balis, MD3

The Foot & Ankle Journal 1 (11): 3

Freiberg’s infraction is an uncommon diagnosis. The incidence of this disorder is unknown. However, it represents the fourth most common intra-articular osteochondrosis. Treatment is based on supportive measures. The underlying pathology is still not well understood. In cases where conservative treatments fail, surgery is indicated to improve patient symptoms. A case of Freiberg’s infraction is presented that is treated with joint debridement and dorsiflexory wedge osteotomy of the second metatarsal. This procedure is not technically difficult and affords the patient symptomatic relief by rotating the healthy plantar cartilage of the joint dorsally and decompressing the joint surface.

Key words: Freiberg’s infraction, osteochondrosis, osteochondritis dessicans

This is an Open Access article distributed under the terms of the Creative Commons Attribution License. It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org)

Accepted: October, 2008
Published: November, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0111.0003

Freiberg’s infraction was first described in 1914. [1] This is the only osteochondrosis that is more common in females and has a ratio of 5:1. [2,3] The typical age range at presentation is between 11-17 years. It was originally termed an infraction because trauma was thought to be the cause of insult to the growing and maturing epiphyseal area. Many other inciting events have been proposed and the etiology of this disease now seems to be multi-factorial. [4-7]

It is suspected that ischemia to the maturing physis plays a part in disease development. [4-7] Some authors have also suggested repetitive microtrauma to the affected part may be the causative agent. [4-8]

The second metatarsal head is the most commonly affected and accounts for approximately 68% of cases. Next is the third metatarsal followed by the fourth and fifth, which are rarely affected. [2,6,8-10]

The most widely used classification system is that of Smillie. [13] This progresses through the stages of deformity from 1 through 5 based on radiographic findings.

Stage 1 of the disease process presents with subchondral epiphyseal fissuring which progresses to collapse of the subchondral plate dorsally with flattening of the articular surface (Stage 3). Late stage disease (4 and 5), there is development of intra-articular loose bodies and degenerative arthrosis with joint space narrowing and metatarsal head flattening. It is also possible to find corresponding degenerative changes at the base of the proximal phalanx in late stage disease. [2,6,8-11] Interestingly, in Europe this infraction is known as Panner’s Disease. [4]

Case Report

An eighteen year old female college student was seen in our department of orthopaedic surgery for right foot pain of eight months duration. She is diagnosed with Freiberg’s infraction of the second metatarsal head. (Figs. 1 and 2)

Figure 1    Pre-operative AP radiograph showing Freiberg’s infraction with subchondral collapse and joint space narrowing.

Figure 2   Pre-operative medial oblique showing large intra-articular loose bodies in the second metatarsophalangeal joint.

Pain is localized over the second metatarsophalangeal joint and worsened with weight bearing and activity. Prior to the onset of pain, she was active in the sport of repelling down large rocks and cliffs.

She had previously been seen by a podiatric physician in her home city and various methods of immobilization were tried. She had minimal improvement with a removable CAM walker. No other immobilization or decrease in activity provided pain relief.

At her initial visit to Cleveland Clinic, she was seen by an orthopaedic surgeon who discussed the case with the collaborating author. The patient underwent a corticosteroid injection. A CAM walker was then worn one week after injection. She was then seen in follow-up and reported approximately one month of pain relief after the injection. Further treatments were then considered and a carbon fiber insert was recommended along with a bone stimulator.

After using the insert over the course of one month, she developed increasing pain to the affected joint. The bone stimulator did not alter the radiographic appearance of her deformity and did not provide any symptomatic relief.

Serial radiographs were taken throughout the course of treatment which remained unchanged. Magnetic resonance imaging (MRI) was also performed prior to surgery. (Figs. 3 and 4)

Figure 3   Pre-operative axial T1 weighted MRI showing the adaptive changes and deformity in the metatarsal head.

Figure 4 Coronal STIR MRI with edema and inflammatory changes at the second metatarsophalangeal joint.

Surgical Technique

A three centimeter incision was placed dorsally over the second metatarsophalangeal joint. Once the capsule was incised and reflected, two large loose bodies were found in the joint measuring approximately three millimeters (mm) each. The dorsal one half to two thirds of the articular cartilage on the metatarsal head was degenerated and atrophic with collapse of the subchondral plate. (Fig. 5)

Figure 5  Post debridement photograph showing extensive loss of the dorsal cartilaginous surface of the metatarsal head.

A dorsiflexory wedge osteotomy of the metatarsal neck was performed to realign the remaining viable plantar articular surface of the metatarsal head. The wedge was taken 1 centimeter proximal to the metatarsal head and was 2-3 mm in width. Temporary fixation was employed using Kirschner wires. The osteotomy was fixated with a 2.0 mm cortical screw using standard AO technique.

Proper positioning was determined using intra-operative fluoroscopy after both the temporary and permanent fixation was in place. (Figs. 6A and B). Soft tissues were approximated and a posterior splint with sugar tong was applied.


Figures 6A and B Intra-operative fluoroscopy after dorsiflexory closing wedge osteotomy fixated with a 2.0 mm screw.

The patient was seen in follow up one week post-operatively and placed in a fiberglass, below-the-knee cast. At fifteen weeks, post-operative radiographs revealed intact fixation and bony trabeculation across the osteotomy site. (Figs. 7A-C)


Figures 7 A-C  Post-operative radiographs taken fifteen weeks after surgery showing consolidation across the osteotomy site.

The patient has minimal discomfort in the second metatarsophalangeal joint and is healing uneventfully. (Fig. 8)

Figure 8  Clinical photograph taken 15 weeks post-operatively showing rectus alignment of the second digit without significant shortening.


Freiberg’s infraction is a rare diagnosis and the true incidence is unknown. This is because many patients do not experience symptoms and may have incidental radiographic evidence of disease sequelae. Although it is rare, it is the fourth most common intra-articular osteochondrosis. [5,8]

Many methods of treatment have been described. Immobilization and limitation of activity or shoe modification is the most common course of conservative treatment. [2,4-6,11]

Several surgical procedures are also available for patients that fail to improve with conservative means. These include joint debridement, core decompression, metatarsal head resection, joint replacement, bioorthologic grafts and metatarsal osteotomies.

A number of authors have published information on the success of dorsiflexory wedge osteotomies for the treatment of Freiberg’s infraction. This procedure seems to be gaining in popularity due to the successful treatment of all stages in Freiberg’s infraction. Gauthier and Elbaz first reported on the technique in 1979. [10] The osteotomy was intra-articular and excised the devitalized dorsal surface of the metatarsal head. Cerclage wire was employed for fixation. This technique was later modified by Kinnard and Lirette who fixated the osteotomy with absorbable suture. [12]

In 1999, Chao, Lee, and Lin published the extra-articular metaphyseal dorsal closing wedge osteotomy for treatment of Freiberg’s infraction. Crossed Kirschner wires were utilized for fixation and were removed in all patients after radiographic signs of healing. Average shortening of the affected metatarsal was 2.1 mm with this procedure. [11]

The principle behind the dorsiflexory wedge osteotomy is to realign the intact plantar metatarsal cartilage and provide for a more physiologic range of motion. Initially the lesion was excised with an intra-articular osteotomy. This technique is also successful when performing it in an extra-articular fashion. The extra-articular osteotomy has the advantage of being technically less difficult and more stable by the use of compressive screw. It also affords a degree of metatarsal shortening to decompress the involved joint.


The dorsiflexory wedge osteotomy for the treatment of Freiberg’s infraction is a generally successful procedure with good subjective outcomes. It may be performed for all stages of disease. Performing the extra-articular osteotomy allows for ease of fixation compared with the intra-articular osteotomy. This procedure also affords a degree of joint decompression and small amount of metatarsal shortening.


1. Freiberg AH. Infraction of the second metatarsal bone. Surg Gynecol Obstet (19):163 – 191, 1914.
2. Katcherian DA. Treatment of Freiberg’s disease. Orthop Clin N Am 25 (1):69-81, 1994.
3. Duthie RB, Houghton GR. Constitutional aspects of the osteochondroses. Clin Orthop Rel Res (158):19-27, 1981.
4. Ary KR, Turnbo M. Freiberg’s infraction an osteochondritis of the metatarsal head. J Am Podiatr Med Assn 69 (2):131-132, 1979.
5. Miller ML, Lenet MD, Sherman, M. Surgical treatment of Freiberg’s infraction with the use of total joint replacement arthroplasty. J Foot Surg 23 (1):35-40, 1984.
6. Scartozzi G, Schram A, Janigian J. Freiberg’s infraction of the second metatarsal head with formation of multiple loose bodies. J Foot Surg 28 (3): 195-199, 1989.
7. Stanley D, Betts, RP, Rowley DI, Smith TW. Assessment etiologic factors in the development of Freiberg’s disease. J Foot Surg 29 (5):444-447, 1990.
8. Binek R, Levinsohn EM, Bersani F, Rubenstein H. Freiberg disease: Complicating unrelated trauma. Orthopedics 11 (5):753-757, 1988.
9. Nguyen VD, Keh RA, Daehler RW. Freiberg’s disease in diabetes mellitus. Skeletal Radiol (20) (6):425-428, 1991.
10. Gauthier, G and Elbaz, R. Freiberg’s infraction: A subchondral bone fatigue fracture. Clin Orthop Rel Res 142: 93 – 95, 1979.
11. Chao KH, Lee CH, Lin LC. Surgery for symptomatic Freiberg’s disease. Acta Orthop Scand 70: 483-486, 1999.
12. Kinnard, P and Lirette, R. Freiberg’s disease and dorsiflexion osteotomy. J Bone Joint Surg 73B (5): 864-865, 1991.
13. Smillie IS. Treatment of Freiberg’s infraction. Proc R Soc Med. Jan 60(1):29-31, 1967.

Address correspondence to: Martha Anderson, DPM, Kaiser Permanente Department of Podiatry. 12301 Snow Rd. , Parma, OH 44130.

1 Cleveland Clinic, Medical Director of the Diabetic Foot Clinic, Department of Orthopaedic Surgery, Cleveland, OH. 44130
2 Third Year Resident (PGYIII), Cleveland Clinic/Kaiser Permanete Residency Program, Cleveland, OH. 44130
3 Cleveland Clinic, Department of Orthopaedic Surgery, Cleveland, OH. 44130.

© The Foot & Ankle Journal, 2008

Photo Quiz: Bone Lesion to the Neck of the Talus

Vasu Pai MS, D[Orth], National board [Orth], FICMR, FRACS, MCh[Orth]1 , Vishal Pai, M.B., Chb2

The Foot & Ankle Journal 1 (6): 5

ISSN 1941-6806
doi: 10.3827/faoj.2008.0106.0005

Case History

An 8 year old boy presents with history of ankle pain for 4 months. His pain is mainly to the anterior aspect of the ankle joint. He had been limping for last 6 weeks. Clinical evaluation reveals tenderness over the dorsal aspect of the talus. The dorsiflexion of the ankle was terminally limited and extremely painful. The subtalar joint was normal. There is normal heel inversion on standing tip-toe.

Laboratory data was unremarkable. As symptoms did not settle at 6 months, the joint was aspirated under anesthesia. Two milliliter of straw colored fluid was aspirated from the ankle joint. Gram stain was negative and culture did not reveal any growth of organisms. Cell count was less than 2000 and suggestive of non-specific synovitis.

The plain radiograph of the ankle and foot is normal. The bone scan revealed an increased uptake in the left side of the talus. The CT scan revealed a small lesion which could be identified over the superior border of the talus with surrounding sclerosis. The MRI revealed increase signal intensity in T2 and decrease signal intensity in T1. (Fig. 1) There was increased enhancement with post gadolinium injection. A benign lesion was diagnosed.


Figure 1    T1 and T2 MRI shows signal intensity changes involving the neck of the talus.

The left ankle was surgically explored through an antero-lateral approach. The sensory branch of musculocutaneous nerve was preserved. The neck of the talus superiorly was irregular and was curetted very easily. (Fig. 2) The wound was closed in layers. The ankle was held in a neutral position in a short leg cast.

Figure 2    Irregular, soft, cystic-like material is easily curetted from the neck of the talus.

Histopathological examination showed abundant osteoid in fibrovascular stroma. The trabeculae were rimmed by prominent osteoblasts with no mitotic activity. (Fig. 3) At one year follow up there was no recurrence or the lesion. Patient is now totally asymptomatic.

Figure 3  Trabeculae rimmed by prominent osteoblasts in fibrovascular stroma.

Question: Based on the patient’s clinical history, MRI ,surgical and histologic findings, which of the following is the correct diagnosis?

A. Osteochondritis dessicans (OCD lesion)
B. Atypical Osteoid Osteoma
C. Osteoblastoma
D. Brodie’s Abscess
E. Ewing’s tumor


Address correspondence to: Dr. Vasu Pai, Gisborne Hospital, Ormand Road, Gizborne, New Zealand.
E-mail: vasuchitra@gmail.com

1 Orthopaedic Specialist, Gisborne, Hospital, Ormand Road, Gisborne, New Zealand.

2 House Surgeon, Middlemore Hospital, Auckland, New Zealand.

© The Foot & Ankle Journal, 2008

Talar Osteochondral Defect Grafting with Nexa Orthopedics OsteoCure™ Bone Graft Plug

by Jonathan Sharpe, DPM1, Mark A. Hardy, DPM, FACFAS2

The Foot & Ankle Journal 1 (6): 1

Osteochondritis dessicans of the ankle is a condition often encountered by the foot and ankle physician. Many treatments have been described in the literature including cast immobilization, arthroscopic debridement, open debridement, and autogenous grafting. The NEXA OsteoCure™ bone graft plug allows for immediate lesion excision while avoiding the morbidity associated with obtaining an autograft. The authors provide a brief review of talar dome lesions including staging and classification and their experience and technique involved for utilizing NEXA Orthopedics OsteoCure™ bone graft plugs.

Key words: Osteochondritis dessicans, Talus, Talar dome lesions, NEXA Orthopedics OsteoCure™ bone graft plugs

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org)

Accepted: May 2008
Published: June 1st, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0106.0001

Osteochondral defects of the talar dome, aka osteochondritis dissecans, are common pathological entities encountered by the podiatric physician. Although trauma is thought to play a primary role in the genesis of these lesions, idiopathic osteonecrosis may also be a cause. Subjectively, these patients frequently present complaining of a deep, aching, non-descript pain in the ankle joint that worsens with activity.

Clinical examination may reveal joint line tenderness, effusion, as well as pain upon ankle joint range of motion. Diagnosis is frequently made with imaging after high clinical suspicion, and the lesions are typically seen anterolaterally or posteromedially. (Fig. 1)

Figure 1   Diagnosis of osteochondral defects are often made with CT scans.  The lesions are typcially seen anterolaterally and posteromedially.

Insight into the morphology and mechanism of action of these lesions was illustrated in a retrospective study of thirty-one ankles in twenty-nine patients with osteochondral lesions by Canale, et al. [1] It was found that lateral lesions were associated with inversion or inversion-dorsiflexion trauma and that these lesions are morphologically shallow and anteriorly located on the talar dome. Lateral lesions were more likely to become displaced in the joint and to have persistent symptoms. Medial lesions were both traumatic and atraumatic in origin, morphologically deep, located more posteriorly on the talar dome, and less symptomatic. These typically occurred with a plantarflexion and inversion type of injury. [1]

With an acute injury, the osteochondral lesion may not be visible on the initial radiographs. If there is a high index of suspicion, repeat radiographs in two to four weeks should be obtained or one should consider more advanced imaging. In a study by Anderson, et al., it was found that when plain radiographs of the ankle are relied on for the diagnosis of an osteochondral fracture of the talus, many lesions remain undiagnosed. [2] Stage-I osteochondral fractures show no diagnostic changes on plain radiographs, and Stage-II lesions are usually subtle and, therefore, are often overlooked by both radiologists and clinicians. The most commonly used classification system for these injuries was created by Berndt and Harty. [3]

A type I lesion represents a small area of compression. A type II lesion is a partially detached osteochondral lesion. When the lesion becomes completely detached, but remains in its anatomical location, it is a type III lesion. A detached lesion with any movement or migration is classified as type IV. A CT may offer more accurate staging of the lesion, although classification may not correlate with intraoperative findings. (Fig. 2)

Figure 2   The CT may offer more accurate staging of the lesion, although classification may not correlate with intraoperative findings.  

Pettine, et al., evaluated seventy-one osteochondral fractures of the talus for an average of 7.5 years after the onset of symptoms to determine which factors influenced the final result. It was found that the type of fracture was the most important factor and that delay in treatment also affected the results adversely. [4]

In the study by Canale, et al., using the classification system of Berndt and Harty, it appeared that Stage-I and Stage-II lesions should be treated non-operatively, regardless of location. Stage-III medial lesions should be treated non-operatively initially but if symptoms persist, surgical excision and curettage are indicated. Stage-III lateral lesions and all Stage-IV lesions should be treated surgically and early. Long-term results indicated that few lesions unite when treated non-operatively. Degenerative changes in the ankle joint, whether symptomatic or not, were common regardless of the type of treatment. [1]

Non-operative treatment of these lesions includes casting and immobilization. There is no evidence, however, that these patients need to be immobilized if they are kept non-weight bearing. There is also no evidence that a non-weight bearing cast offers better results than a weight bearing cast.

A retrospective study of 22 ankles in 22 patients with osteochondral talar dome lesions between 1975 and 1983 indicated that surgical treatment yields superior results to conservative therapy. [5] Many of these lesions are treated surgically with arthroscopic joint examination and debridement of the lesion. This process may be aided by an external joint distracting device. Anterolateral lesions are typically more amenable to arthroscopic debridement than posteromedial lesions because of their anatomical location. In a study by Kumai, et al., the authors found good clinical results in arthroscopic debridement and k-wire drilling of lesions in patients who were younger than sixty years old.6 Posteromedial lesions typically necessitate an osteotomy of the medial malleolus for exposure, with open reduction and internal fixation and subsequent prolonged non weight-bearing. (Fig. 3)

Figure 3   Posteromedial lesions typically necessitate an osteotomy of the medial malleolus for exposure.  Here,  ORIF screws are placed through the medial malleolus following the procedure.  

We have employed the NEXA Orthopedics OsteoCure™ Bone Graft Plug with success for surgical repair of talar osteochondral lesions. The OsteoCure™ Plug is a cylindrical implant ideal for filling defects in bone.

The implant is a resorbable, porous scaffold, which allows the in-growth of new healing tissue. The implant is sized for cylindrical defects with a minimum depth of 5 mm and a maximum depth of 12 mm. Careful pre-operative planning should be taken to ensure adequate visualization of the defect to be grafted. An osteotomy may need to be employed to ensure sufficient access to the lesion.

Surgical Technique

The following described technique has been outlined from NEXA’s surgical technique literature. The OsteoCure™ Plug Implant Kit contains the cylindrical implant, the delivery device, and a trimming knife. This is to be used with the accompanying OsteoCure™ Plus Site Preparation Kit. (Fig. 4)

Figure 4    The OsteoCure™ Plug Implant Kit contains the cylindrical implant, the delivery device and the trimming knife.  This is to be used with the accompanying OsteoCure™ Plus Site Preparation Kit.  

The standard implant depths range from 5 mm to 12 mm, but longer implants are available. The implants also come in a variety of diameters to suit the varying sizes of these lesions. The color-coded instrument set comes in 5, 7, 9, and 11 mm to correspond to the accompanying OsteoCure™ implant sizes. Once adequate visualization and access of the talar lesion has been obtained, a thin walled drill sleeve is introduced to the talar dome, taking care to encompass the entire lesion. (Figs. 5-7)


Figures 5,6,7   Once the osteochondral defect is identified, a thin walled sleeve drill is introduced to the talar dome.

Prior to insertion, an appropriately sized obturator is introduced into the handle of the drill sleeve for ease of insertion. The drill sleeve is then gently introduced through the cartilaginous surface by pronating and supinating the device. Once the drill sleeve has been slightly advanced, remove the obturator from the drill sleeve. The depth can easily be measured on the drill sleeve, which is calibrated in millimeter measurements. Care must be taken to insert the drill sleeve in a manner perpendicular to the articular surface to ensure that the graft lies flush after insertion. Next, the metallic cap is removed while maintaining the drill sleeve at the desired depth. The corresponding drill is then introduced into the drill sleeve and the lesion is drilled to the desired depth. (Fig. 8)

Figure 8   Care is taken to insert the drill sleeve and drill in a manner perpendicular to the articular surface to ensure that the graft will lie flush after insertion.  

Continue drilling until the drill stop contacts the drill sleeve. The drill and drill sleeve are then both removed from the surgical field. (Fig. 9)

Figure 9   The talar dome defect is now drilled and prepared for grafting.

Next, the cylindrical graft is prepared. The graft comes housed in a delivery device. The device has a plunger on the opposite end of the graft. The plunger end should be introduced into the lesion and pressed firmly into place. This will force the graft out of the proximal end of the delivery device, effectively sizing the implant. (Fig. 10)

Figure 10   The plunger end of the device is introduced, effectively sizing the implant.

The delivery device is then removed from the field and the redundant overhanging graft is trimmed with the knife included in the kit. (Fig. 11)


Figures 11,12,13   The redundant portion of graft is trimmed.  (Fig. 11)  The graft is introduced (Fig. 12) and gently tamped into place.  Gently contour the graft as needed with a scalpel. (Fig. 13)

The delivery device is then reintroduced to the lesion with the graft now facing distally toward the lesion. It is helpful to advance the graft a few millimeters to help introduce it into the drilled defect. The plunger on the proximal end of the delivery device is then firmly advanced, seating the graft into the defect. (Fig. 12)

It can be gently tamped with a mallet. The graft should sit flush with the articular surface. If there is a small step-off deformity, gently contour the graft with a scalpel. (Fig. 13)

Once the graft has been placed, commence with ORIF of osteotomy if necessary and standard wound closure. (Fig. 14)

Figure 14   The graft is seated in place.  ORIF of the malleolus is then performed with appropriate closure of the surgical site.

According to NEXA, immediately following implantation the scaffold allows blood, marrow and progenitor cells to be transported into the pores. The scaffold provides a porous and mechanically protected environment for healing, tissue in-growth and cellular development. The calcium sulfate dissolves within 6 weeks to 6 months. New tissue forms within the pores. Between 6 months and 12 months, the polymer undergoes resorbtion and is gradually replaced with tissue as well. After 12 months the polymer is predominantly resorbed and the defect will contain new tissue.

Our post-operative treatment protocol consists of non-weight bearing for 2 weeks, followed by active range-of-motion, usually, once the incisions have healed. Partial weight bearing is then employed for 2 weeks, in a fracture boot, with progression to full weight bearing for an additional 2 weeks.

At 6-8 weeks the patient is then enrolled into a formal physical therapy program.


1. Canale-ST; Belding-RH Osteochondral lesions of the talus JBJS-Am. 62(1): 97-102, Jan. 1980.
2. Anderson IF, et al: Osteochondral fractures of the dome of the talus JBJS – Am. 71(8):1143-52, Sept. 1989.
3. Brendt, AL, Harty, M. Transchondral fractures (osteochondritis dissecans) of the talus. JBJS. Vol 41-A. 988-1020, 1959.
4. Pettine KA. Morrey BF. Osteochondral fractures of the talus. A long-term follow-up. JBJS – British 69(1):89-92, Jan. 1987.
5. Flick AB. Gould N. Foot & Ankle. Osteochondritis dissecans of the talus (transchondral fractures of the talus): review of the literature and new surgical approach for medial dome lesions. [JC:f3x] 5(4):165-85, Jan-Feb 1985.
6. Kumai T, Takakura Y, Higashiyama I, Tamai S. Arthroscopic drilling for the treatment of osteochondral lesions of the talus. J Bone Joint Surg Am. 81(9):1229-35, Sept, 1999.

Address correspondence to: Mark A. Hardy, DPM, FACFAS, Kaiser Permanente Foundation Department of Podiatric Surgery
12301 Snow Road Parma, OH 44130
Email: markhardy@sbcglobal.net

1Senior Resident, Kaiser Permanente/Cleveland Clinic Foundation Residency Program, Cleveland, Ohio.

2Director, Cleveland Clinic/Kaiser Permanente. Foot & Ankle Residency Program. Director, Foot and Ankle Trauma Service. Kaiser Permanente – Ohio Region

© The Foot & Ankle Journal, 2008