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Letters to the Editor to:

Current Concepts Review:
Michael A. Mont, Lynne C. Jones, and David S. Hungerford
Nontraumatic Osteonecrosis of the Femoral Head: Ten Years Later
J Bone Joint Surg Am 2006; 88: 1117-1132 [Abstract] [Full text] [PDF]
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[Read Letter to the Editor] Detection of Osteonecrosis on MRI Requires Blood Flow.
James K. Brannon, M.D.   (5 July 2006)

Detection of Osteonecrosis on MRI Requires Blood Flow. 5 July 2006
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James K. Brannon, M.D.,
Orthopaedic Surgeon/Director Joint Preservation Center
University of Missouri Kansas City, Department of Orthopaedic Surgery

Send letter to journal:
Re: Detection of Osteonecrosis on MRI Requires Blood Flow.

Phyein{at}aol.com James K. Brannon, M.D.

To The Editor:

After reading the Current Concepts Review (CCR) article, "Nontraumatic Osteonecrosis of the Femoral Head: Ten Years Later" by Mont, et al.(1), I would like to offer some comments. The article is an excellent compilation of existing data on osteonecrosis and a summary of current thinking about this disease and its treatment using an evidence based review of the literature, However, it would have been even more helpful had Mont et al. addressed the fundamental questions that make the treatment of osteonecrosis so controversial.

First, given our reliance on MRI for the staging and treatment of OHFH, does the MRI really reflect the full extent of disease? Second, how do outcomes vary when comparing surgical techniques that thoroughly debride the femoral head, i.e., removing necrotic bone not detected on the preoperative MRI? Third, why is free vascularized fibula grafting, along with other procedures that thoroughly debride the femoral head, the trapdoor of Mont(2) and the lightbulb of Rosenwasser(3), successful for early stage disease? Can the essential elements of these procedures be extracted and safely applied in a minimally invasive way?

Regarding etiology, pathogenesis, and pathology, the associated risk factors for osteonecrosis are well known and accepted. What is not known is how the anoxic death of osteoprogenitor cells results in ONFH. What has been recently suggested is that cell death is likely apoptotic and inflammation is absent(4). Thus, necrotic bone in this regard will go undetected on the MRI until sufficient fluid changes occur to enable detection of necrotic bone. The critical question is what induces these fluid changes? Mont(1) suggests that when fluid changes do occur they are due to attempted incorporation of the necrotic bone (ossification through creeping substitution). However, calcification of necrotic bone producing a serpingenous line of sclerosis may explain why the sclerotic margin remains at the periphery. Irrespective of ossification or calcification, the failure to incorporate the necrotic bone may be considered an intraosseous nonunion, emphasizing the importance of thorough debridement. Additionally, necrotic bone is brittle and its chronic micromotion in a ductile host bed of bone may induce a repetitive fracture repair response (ossification) at the periphery, creating the characteristic wedge shaped lesion on plain x-ray in some cases. The histopathologic diagnosis of osteonecrosis is made when sclerotic trabeculae with acellular lacunae are observed on light microscopy. All of these potential changes observed on x-ray or histopathology require blood flow. Inflammation is the first phase of fracture healing, and its absence will undoubtedly impair the mesenchymal cell recruitment needed for bone repair(5). Mont summarizes the literature in the CCR(1) and supports vascular occlusion as the inciting event, and I agree, yet the removal of cells to make a histologic diagnosis and the changes observed on MRI require blood flow.

Thus, two critical questions arise. Can one rely on the residual blood flow within the femoral head after thorough debridement to support autologous nonvascular bone graft incorporation? And, does one detect disease when insufficient metabolic activity is present to induce changes on the MRI? Further, brittle necrotic bone undetected on MRI may place undue stress on the overlying cartilage causing its expatiation and osteophyte formation (chronic microcollapse) at the osteochondral junction. Does undetected osteonecrosis (dense and brittle sclerotic bone) lead to radiographic osteoarthrosis, as suggested by Pugh, Radin and Rose(6)? This article (1)would have benefited from a discussion of the histopathology and how it relates to the MRI(7).

Factors Affecting Treatment: Most would agree that the larger the lesion, the worse the prognosis. Patient outcomes are predictable when substantial femoral head collapse is present and joint preservation is considered. Thus, total joint arthroplasty is a better alternative in this group(1). Controversy regarding treatment relates to symptomatic spherical femoral heads with lesions that are small, medium, and large. The suggested preferred method of treatment, as described in the CCR, in these groups of patients is clear as is that of Urbaniak(8). Agreement regarding the definition of a large lesion using the methods of Kerboul does not address the controversy around vascular or nonvascular bone grafting(9). More importantly, one must consider the clinical impact of the individual community surgeon’s expertise with surgical dislocation of the hip (Mont-trapdoor (2)/Rosenwasser-lightbulb(3) for nonvascularized bone grafting) and FVFG of Urbaniak(8). Additionally, many patients don’t have access to centers where such expertise exists. Thus, the least invasive procedure, i.e., core decompression is often considered when thorough debridement may be more efficacious, thus outcomes will continue to vary as will the controversy about how to treat precollapse disease. It must be emphasized that thorough debridement is the common feature in Mont’s(2), Rosenwasser’s(3) and Urbaniak’s(8) procedures and that decreasing the necrotic burden in the precollapsed femoral head may portend good clinical outcomes. This type of critical comparison should have been included in the CCR, as it will encourage discussions on how to simplify these complex approaches, making them more universally available.

Mont suggests that an anterior surgical dislocation of the hip allows one to assess the cartilage of the femoral head, potentially changing a treatment plan from a lightbulb procedure (implying pre-collapse disease) to a surface replacement(1). This particular suggestion in the CCR is counterintuitive because one would think that if a direct visual assessment of the femoral head cartilage is necessary to decide to preserve the joint in pre-collapse disease, than the joint is worth preserving. A real concern with an anterior surgical dislocation for post-collapse disease is that femoral head sphericity and acetabular congruence is not easily restored once the hip is dislocated, and this should be discussed. It is important to note that in Mont’s series of thirty surface replacements, 20% had persistent groin pain(10), likely due to the continued necrotic burden within the femoral head. Mont suggests that a surface replacement is a good choice for post-collapse disease(1), yet osteonecrosis is a primary bone disease. Magnussen et al(11) evaluated the mechanical properties of thirteen fresh femoral heads in patients with Stage IV and V osteonecrosis, and suggested that arthroscopy may provide a minimally invasive way to evaluate the articular cartilage in anticipation of RETROGRADE joint surface elevation as described by Urbaniak(8). Magnussen’s(11) intent at Duke seems to suggest a role for hip arthroscopy prior to FVFG by Urbaniak(8), which is far less invasive than the surgical dislocation suggested by Mont(2).

Operative Treatment: The thorough debridement accompanying nonvascularized bone grafting as characterized by Mont(2) and Rosenwasser(3) must be emphasized. Removal of the necrotic burden within the femoral head allows autologous cancellous bone to be stabilized against a bleeding host bed. In Mont’s(2) approach, the femoral head is relocated to its naturally constrained environment (three degrees of freedom) providing sufficient limitation of micromotion to promote primary graft incorporation. It is interesting that Mont et al(1) in the CCR conclude that FVFG provides superior results when compared to NVFG (implying that the vascular anastomosis leads to a good clinical outcome) when a true head to head comparison of FVFG to NVFG has NOT been studied, i.e., the performance of identical surgical procedures in both groups, with only the addition of a vascular anastomosis in the FVFG group. Even when a comparison was attempted and described by Kim et al., the NVFG group in their study (23 hips with post-collapse disease) only had a minimal amount of debridement, as appreciated on a careful review of their surgical techniques(12). Mont et al(1) further developed a system of Grades of Recommendation for treatment of osteonecrosis, and assigned FVFG a grade A recommendation (the highest level recommendation), yet FVFG is probably not performed by the authors and was recently discouraged at the academy by Hungerford as being associated with significant morbidity(13). Thorough debridement of the femoral head to a bleeding host bed will likely provide residual blood flow to nonvascular autologous bone packed into the resultant cavity, and it is this residual blood flow that Mont(2), Rosenwasser(3), and Urbaniak(8) rely on for graft incorporation. Graft stability is achieved in Mont(2)/Rosenwasser’s(3) approach through returning the femoral head to its constrained environment, while that of Urbaniak(8) is achieved with the fibula and prolonged protected weight-bearing. Without addressing WHY FVFG works, it should NOT receive a Grade A recommendation.

I commend Mont et al(1) for their extensive review of the literature, but would like to emphasize that elucidation of the common features between vascular and nonvascular bone grafting and a critical analysis of the pathophysiology of disease will facilitate a better understanding of the role of the MRI and its limitations and encourage simplification of these procedures to techniques that are more universally available.

The author(s) of this letter to the editor received 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. Mont MA, Jones LC, and Hungerford DS. Nontraumatic Osteonecrosis of the Femoral Head: Ten Years Later. J Bone Joint Surg. Am., May 2006; 88: 1117 - 1132.

2. 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 Joint Surg. 1998; 80-B: 56-62.

3. Rosenwasser MP, Garino JP, Kiernan HA, Michelsen CB. Long term followup of thorough debridement and cancellous bone grafting of the femoral head for a vascular necrosis. Clin Orthop, 1994; 306: 17-27.

4. Weinstein RS, Jilka RL, Parfitt AM, and Manologas SC. Inhibition of osteoblastgenesis and promotion of apoptosis of osteoblast and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone. J Clin Invest. 1998 July 15; 102(2): 274-282.

5. Day SM, Ostrum RF, Chao EYS, Clinton RT, Aro HT, Einhorn TA: Bone injury, regeneration, and repair. In: JA Buckwalter, TA Einhorn, SR Simon editors. Orthopaedic basic sciences: Biology and biomechanics of the musculoskeletal system, 2nd edition. Rosemont, American Academy of Orthopaedic Surgeons, 2000; p. 388.

6. Pugh JW, Radin EL, and Rose RM. Quantitative studies of human subchondral cancellous bone. Its relationship to the state of its overlying cartilage. J Bone Joint Surg. Am., Mar 1974; 56: 313-321.

7. Plenk H, Gstettner M, Grossschmidt K, Breitenseher M, Urban M, and Hofmann S. Magnetic resonance imaging and the histology of repair in femoral head osteonecrosis. Clinical Ortho, Volume (386) May 2001 pp. 42-53.

8. J. Mack Aldridge MIII, Berend KR, Gunneson EE, and Urbaniak JR. Free Vascularized Fibular Grafting for the Treatment of Postcollapse Osteonecrosis of the Femoral Head. Surgical Technique. J Bone Joint Surg. Am., Mar 2004; 86: 87 - 101.

9. Kerboul M, Thomine J, Postel M, Merle d’Aubigne R. The conservative surgical treatment of idiopathic aseptic necrosis of the femoral head. J Bone Joint Surg Br. 1974;56:291-6.

10. Mont MA, Rajadhyaksha AD, Hungerford DS. Outcomes if limited femoral resurfacing arthroplasty compared with total hip arthroplasty for osteonecrosis of the femoral head. J Arthroplasty, 2001;16(8Suppl 1):134-9.

11. Magnussen RA, Guilak F, and Vail T. Articular cartilage degeneration in post-collapse osteonecrosis of the femoral head. Radiographic staging, macroscopic grading, and histologic changes. J Bone Joint Surg. Am., June 1005; 87: 1272-1277.

12. Kim S, Kim Y, Kim P, Ihn J, Cho B, and Koo K. Vascularized Compared with Nonvascularized Fibular Grafts for Large Osteonecrotic Lesions of the Femoral Head. J Bone Joint Surg. Am., Sep 2005; 87: 2012 -2018.

13. Hungerford DS. AAOS 2006 Annual Meeting, March 22-26, Chicago, Illinois.