We appreciate Dr. Brannon's comments and questions. He raises several necessary points of clarification.

First, he correctly emphasizes the limitations of citing the article by Gregosiewicz and Wosko(1) pertaining to causation of osteonecrosis in children with known congenital hip dislocation. His mention of the discrepancy regarding the patient age of that series and that of our current paper is indeed accurate. We referenced this article to demonstrate the paucity of literature regarding the relationship between osteonecrosis and developmental dysplasia of the hip (DDH). The primary utility that we found from this article related to its postulation that osteonecrosis tended to be more severe in hips with DDH when commpared to hips without dysplasia. Clearly, any additional extrapolation from the Gregosiewicz and Wosko article(1) would be inaccurate due to the age and disease differences between their series of patients and ours. The article by Hadley and Brown(2),which also was cited in our manuscript was instead, a more appropriate validation of our hypothesis as it emphasized the increased contact stresses on the femoral head in DDH.

The second point raised by Dr. Brannon pertained to the causative agent of the poor outcomes cited in our paper in dysplastic hips. We certainly believe now that the dysplastic acetabulum in itself portends a worse outcome in hips with osteonecrosis when treated with free-vascularized fibular grafting (FVFG). We are not in a position to attribute the poor results to the FVFG treatment chosen as every patient in our study had that same procedure, and those patients with increased CE angles tended to do quite well after the procedure. Furthermore, as Drs. Steinberg and Steinberg(3) point out, the 39% overall rate of progressive collapse of the femoral head and conversion to total hip arthroplasty that we found in our series compares favorably with the existing literature regarding non-arthroplasty treatments of osteonecrosis of the femoral head. This is particularly striking because 30% (60/200) of hips in our series demonstrated some degree of DDH (CE angle less than or equal to 25 degrees). To investigate this issue further, we would need to compare the DDH rates of other series, which are not accessible since these values have not been routinely recorded. It is our hope that some degree of DDH assessment be employed and recorded in the future to further elucidate its role in osteonecrosis treatment outcome, and to perhaps devise a more refined treatment strategy for these patients.

Dr. Brannon also questlioned whether the core tract made during the FVFG surgery may potentiate collapse in the setting of dysplastic hips. This is a distinct possibility, though we did not address this in our study. Perhaps a lower diameter threshold of core tract exists when the presumed increase in contact force from a dysplastic acetabulum is at work? By this rationale, smaller core tracts, such as those made during non- vascularized fibular grafting, porous tantalum implants,(4) or core decompression may play a larger role in the treatment of those patients. Before these techniques can be recommended in this setting, however, basic science studies evaluating the diameter threshold of core tracts in the setting of DDH would need to be better understood.

A further point of desired clarification regarded our statement concluding the abstract: “An estimation of the degree of hip dysplasia should be included in the preoperative assessment of patients with osteonecrosis of the femoral head for prognostic and possibly surgical planning purposes.” Rather than planning a variation of the FVFG procedure, our intent with this statement is to challenge future research and investigations to consider alternative procedures in the setting of DDH and osteonecrosis. In particular, this pertains to procedures addressing the deficient acetabulum.

Finally, Dr. Brannon questioned whether femoral heads may be better saved using avascular techniques that provide better subchondral support after thorough debridement. This concern is quite valid and, though theoretically accurate, will require further elucidation by obtaining a more accurate assessment of critical thresholds of core tract and graft strength in the setting of DDH.

In conclusion, we appreciate the insightful questions and comments expressed by Dr. Brannon regarding our study. After proposing that a relationship exists between (lack of) acetabular coverage and the outcomes of FVFG treatment for ONFH, our results pose many more questions regarding the optimal treatment for these patients. We look forward to further research that addresses this important problem.

References:

1. Gregosiewicz A, Wosko I. Risk factors of avascular necrosis in the treatment of congenital dislocation of the hip. J Pediatr Orthop. 1988;8:17-9.

2. Hadley NA, Brown TD, Weinstein SL. The effects of contact pressure elevations and aseptic necrosis on the long-term outcome of congenital hip dislocation. J Orthop Res. 1990;8:504-13.

3. Steinberg DR, and Steinberg ME. Commentary and Perspective: Influence of Acetabular Coverage on Hip Survival After Free Vascularized Fibular Grafting for Femoral Head Osteonecrosis. http://www.ejbjs.org/Comments/2006/cp_oct06_steinberg.shtml

4. Tsao AK, Roberson JA, Christie MJ, Dorr DD, Heck DA, Robertson DD, Poggie RA. Biomechanical and clinical evaluations of a porous tantalum implant for the treatment of early-stage osteonecrosis. J Bone Joint Surg Am. 2005;87 Suppl 2:22-7

To The Editor:

I read with great interest, "Influence of Acetabular Coverage on Hip Survival After Free Vascularized Fibular Grafting for Femoral Head Osteonecrosis," by Roush et al.(1), and the commentary by Steinberg and Steinberg (2). Indeed, this article and the commentary by Marvin Steinberg(2) represent the views and thoughts of two senior authors with opposing opinions on how to treat osteonecrosis. Urbaniak(3) supports vascularized bone grafting, while Steinberg(4) supports avascular cancellous bone grafting. While the intent of the article of Roush et al.(1) was not to document clinical efficacy for either type of bone grafting, the conclusions made therein invariably influence one's ability to recognize a potential limitation of FVFG and it is from this observation that I would like to offer a few comments.

Roush et al.(1) retrospectively reviewed a consecutive series of 200 hips in 160 patients with osteonecrosis of the femoral head who had undergone FVFG. They found that of those hips with a center-edge angle (CEA) of ≤30°, 55% demonstrated progression of collapse, while 45% were converted to a total hip arthroplasty. In contrast, only 10% of hips with a CEA of >30° demonstrated progression of collapse, and only 6% were converted to a total hip arthroplasty. Roush et al.(1) encourage the reader to consider acetabular dysplasia an independent risk factor negatively influencing prognosis and cite a study in children with congenital dislocation of the hip by Gregosiewicz and Wosko(5) to support their position. However, one must carefully consider this conclusion. Gregosiewicz and Wosko(5) reported that children are at the highest risk for osteonecrosis when the following are present: (a) age less than 6 months, (b) severe acetabular dysplasia, (c) use of an abduction apparatus such as the Frejka pillow for outpatients, and (d) "frog-leg" position after reduction. The observation of Gregosiewicz and Wosko(5) implies increased contact forces on a soft, predominantly cartilaginous femoral head after reduction. An age less than 6 months correlates well with the congenital nature of acetabular dysplasia. In contrast, the mean age at the time of surgery in the article by Roush et al. is 33.6 years, with the worse degree of collapse being only 3mm in eleven patients(1). If the intent of Roush et al.(1) was to imply a causative role for acetabular dysplasia, then one would think that the adult hips in their series would have been more arthritic, particularly after 33 years. Clearly, one must contemplate how a dysplastic hip, CEA ≤30°, functioned on average for 33 years, then developed a primary bone disease, i.e., osteonecrosis, with the etiologic associations known in 75% of the 200 hips, only to collapse after FVFG. Roush et al.(1) seem to suggest that the failed femoral heads would have survived had it not been for the acetabular dysplasia. Yet, the acetabular dysplasia was present prior to FVFG. Could these dysplastic hips have benefited from a different joint preservation procedure? Although Steinberg et al.(2) suggest that perhaps the femoral heads with the lower center edge angles were deformed, implying a propensity to collapse, one must recognize how FVFG may potentiate the demise of a femoral head with a dysplastic acetebulum. Thus, is it the dysplastic acetebulum that portends a poor outcome as suggested by Roush et al.(1), or is it the treatment chosen, i.e., FVFG?

The surgical technique of FVFG as described by Urbaniak(6) comprises thorough debridement of the femoral head. The core tract, ranging in diameter from 16mm to 19mm, is designed to avoid occlusion of the peroneal vessels and to prevent tension on the anastomosis. This large core tract likely destabilizes the femoral head and neck and potentiates collapse where contact forces are greatest, i.e., a dysplastic acetebulum. Although Urbaniak(6) describes passing a guide wire into the necrotic lesion within the femoral head, it is far more important that the starting point of the guide wire along the lateral cortex be situated to prevent tension on the anastomosis once the large core tract is created. This requirement likely determines the position of the fibula and may prevent placing it optimally in view of the acetabular dysplasia. Roush et al.(1) fall short of identifying this potential limitation of FVFG and conclude by asking the reader to preoperatively quantify the extent of dysplasia for prognostic and POSSIBLY surgical planning purposes. One wonders what other surgical plans exist when Roush et al.(1) comment, "the surgical procedure has remained essentially unchanged since the publication of our original reports."

Mont(7) and Rosenwasser(8) have demonstrated that avascular bone grafting combined with thorough debridement can be successfully applied to select patients with osteonecrosis of the femoral head and good outcomes can be achieved. Continued emphasis on the role of the VASCULARIZED fibula in the treatment of osteonecrosis might invariably prevent one from recognizing the features that vascular (FVFG) and avascular (trapdoor- Mont(7), lightbulb-Rosenwasser(8)) bone grafting have in common, namely, thorough debridement. Importantly, the thorough debridement of the trapdoor/lightbulb procedure leaves the femoral neck substantially intact. Thus, when the acetebulum is dysplastic, could more femoral heads be saved using avascular techniques that provide better subchondral support after thorough debridement?

I commend Roush et al.(1) for critically reviewing the failures of FVFG in a series of 200 hips, but strongly believe the article would have been more helpful had the authors discussed how the surgical technique of FVFG, having not changed in nearly 20 years, may have contributed to destabilizing a femoral head with increased contact forces due to acetabular dysplasia. The work of the senior authors, Urbaniak(6) and Steinberg(9), is well recognized in the literature. However, as a new generation of orthopaedists develops interest in this devastating disease, we must recognize that perhaps FVFG cannot be uniformly applied to all hips, as implied by Roush et al.(1) More importantly, treatment protocols should focus on the features vascular and avascular bone grafting techniques have in common, when such features are associated with good clinical outcomes.

The author(s) of this letter to the editor did receive payment or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the author(s) are affiliated or associated.

References:

1. Roush TH, Olson SA, Pietrobon R, Braga L, and Urbaniak JR. Influence of Acetabular Coverage on Hip Survival After Free Vascularized Fibular Grafting for Femoral Head Osteonecrosis J. Bone Joint Surg. Am., Oct 2006; 88: 2152 - 2158.

2. Steinberg DR, and Steinberg ME. Commentary and Perspective: Influence of Acetabular Coverage on Hip Survival After Free Vascularized Fibular Grafting for Femoral Head Osteonecrosis. http://www.ejbjs.org/Comments/2006/cp_oct06_steinberg.shtml

3. Urbaniak JR, Coogan PG, Gunneson EB, Nunley JA: Treatment of osteonecrosis of the femoral head with free vascularized fibular. A long- term follow-up study of one hundred and three hips. J Bone Joint Surg Am, 1995;77:681-94.

4. Steinberg ME. Core decompression. Semin Arthroplasty, 1998;9: 213-20.

5. Gregosiewicz A, Wosko I. Risk factors of avascular necrosis in the treatment of congenital dislocation of the hip. J Pediatr Orthop. 1988;8:17-9.

6. Urbaniak JR, Coogan PG, Gunneson EB, Nunley JA. Treatment of osteonecrosis of the femoral head with free vascularized fibular grafting. A long-term follow-up study of one hundred and three hips. J Bone Joint Surg. Am.1995;77: 681-694.

7. Mont MA, Einhorn TA, Sponseller PD, Hungerford DS: The trapdoor procedure using autogenous cortical and cancellous bone grafts for osteonecrosis of the femoral head. J Bone and Joint Surg Br, 1998;80:56- 62.

8. Rosenwasser MP, Garino JP, Kierman HA, Michelsen CB: Long-term follow-up of thorough debridement and cancellous bone grafting of the femoral head for avascular necrosis. Clin Orthop, 1994;306:17-27.

9. Steinberg ME, Hayken GD, Steinberg DR: A Quantitative system for staging avascular necrosis. J Bone and Joint Surg Br, 1995;77:34-41.