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Scientific Articles   |    
Stabilizing Mechanism in Bone-Grafting of a Large Glenoid Defect
Nobuyuki Yamamoto, MD1; Takayuki Muraki, PhD1; John W. Sperling, MD1; Scott P. Steinmann, MD1; Robert H. Cofield, MD1; Eiji Itoi, MD2; Kai-Nan An, PhD1
1 Biomechanics Laboratory, Division of Orthopedic Research (N.Y., T.M., and K.-N.A.) and Department of Orthopedic Surgery (J.W.S., S.P.S., and R.H.C.), Mayo Clinic, 200 First Street S.W., Rochester, MN 55905. E-mail address for K.-N. An: an.kainan@mayo.edu
2 Department of Orthopaedic Surgery, Tohoku University School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan
View Disclosures and Other Information
Disclosure: In support of their research for or preparation of this work, one or more of the authors received, in any one year, outside funding or grants in excess of $10,000 from the Uehara Memorial Foundation. Neither they nor a member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity.

Investigation performed at the Mayo Clinic, Rochester, Minnesota

Copyright © 2010 by The Journal of Bone and Joint Surgery, Inc.
J Bone Joint Surg Am, 2010 Sep 01;92(11):2059-2066. doi: 10.2106/JBJS.I.00261
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Abstract

Background: 

Conventional wisdom suggests that the glenoid defect after a shoulder dislocation is anteroinferior. However, recent studies have found that the defect is located anteriorly. The purposes of this study were (1) to clarify the critical size of the anterior defect and (2) to demonstrate the stabilizing mechanism of bone-grafting.

Methods: 

Thirteen cadaver shoulders were investigated. With use of a custom testing machine with a 50-N compression force, the peak translational force that was needed to move the humeral head and lateral humeral displacement were measured. The force was used to evaluate the joint stability. An osseous defect was created stepwise in 2-mm increments of the defect width. The bone graft was harvested from the coracoid process. The defect size was expressed as the estimated defect size divided by the measured glenoid length. Testing was performed with (1) the glenoid intact, (2) a simulated Bankart lesion, (3) the Bankart lesion repaired, (4) a 2-mm defect, (5) the Bankart lesion repaired, (6) the defect bone-grafted, (7) a 4-mm defect, (8) the Bankart lesion repaired, (9) the defect bone-grafted, (10) a 6-mm defect, (11) the Bankart lesion repaired, (12) the defect bone-grafted, (13) an 8-mm defect, (14) the Bankart lesion repaired, and (15) the defect bone-grafted.

Results: 

Force and displacement decreased as the size of the osseous defect increased. The mean force after the formation of a defect of =6 mm (19% of the glenoid length) with the Bankart lesion repaired (22 ± 7 N) was significantly decreased compared with the baseline force (52 ± 11 N). Both the mean force (and standard deviation) and displacement returned to the levels of the intact condition (68 ± 3 N and 2.6 ± 0.4 mm, respectively) after bone-grafting (72 ± 12 N and 2.7 ± 0.3 mm, respectively).

Conclusions: 

An osseous defect with a width that is =19% of the glenoid length remains unstable even after Bankart lesion repair. The stabilizing mechanism of bone-grafting was the restoration of the glenoid concavity.

Clinical Relevance: 

Reconstruction of the glenoid concavity may be necessary in shoulders with an anterior glenoid defect that is =19% of the glenoid length.

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    References

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    These activities have been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the American Academy of Orthopaedic Surgeons and The Journal of Bone and Joint Surgery, Inc. The American Academy of Orthopaedic Surgeons is accredited by the ACCME to provide continuing medical education for physicians.
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    Philipp Moroder MD, Mark Tauber MD, Herbert Resch MD
    Posted on December 13, 2012
    When glenoid bone loss becomes significant
    Department of Traumatology and Sports Injuries, Paracelsus Medical University, Salzburg, Austria

    In literature there is a lack of consensus on the extent glenoid bone loss has to exceed before being deemed significant and thus indicating bone grafting instead of capsulo-labral repair.(1) The study “Stabilizing Mechanism in Bone-Grafting of a Large Glenoid Defect“ by Yamamoto et al.(2) represents one of the main biomechanical reference studies in the above-mentioned discussion. The role of glenoid bone loss in recurrent anterior shoulder instability has been recognized and gained rising scientific interest over the last few years as documented by the increasing number of clinical, radiological and biomechanical studies focusing on this topical issue.

    Due to the importance of this biomechanical study for the debate about the critical glenoid bone loss extent we would like to make two remarks on the otherwise excellent research by Yamamoto et al.  The first remark is a mathematical correction. According to the published data, Yamamoto deems the significant bone-defect size to correspond to 19% of the glenoid length or 25% of the glenoid width. Both values are drawn from division of the critical 6mm defect created in the biomechanical experiment, after which Bankart repair provided significantly reduced stability, by the corresponding anatomical structure, be it glenoid length or width. Yamamoto adds that according to the 25% width a defect area of 26% of the glenoid surface should be regarded as significant. This statement is mathematically incorrect since the outer segments of a circle always contain less area than the inner ones as can be seen when cutting a tomato into equally thick slices. Therefore, the critical glenoid defect area according to Yamamoto’s data should be 19.6% instead of 26%. This correction becomes important since recently the trend of measuring glenoid bone loss has shifted toward area measurements rather than linear measurements.(3)

    The second remark is an interpretational one. The authors of this biomechanical study created bone-loss situations starting with 0mm defect width and increasing by 2mm steps. With increasing defect extent a decrease of the peak translational force (PTF) despite Bankart repair was noted indicating decreasing shoulder stability. The intact shoulders had a PTF of 68N, shoulders with 0mm defect + Bankart repair 52N, 2mm + Bankart repair 43N, 4mm + Bankart repair 35N, 6mm + Bankart repair 22N, and 8mm + Bankart repair 13N. The authors noted a statistically significant reduction of the PTF in the case of a 6mm defect in comparison to the 0mm defect situation despite Bankart repair in both cases. Biomechanically this comparison is correct because it factors out stability loss due to the repaired but not intact labrum. In reality, however, the goal of surgical shoulder stabilization is not to make a shoulder as stable as a previously repaired one. Obviously, patients expect to re-obtain their normal shoulder stability, especially those with shoulder-demanding work or athletic activities. In that case the comparison of the shoulders with increasing glenoid bone loss should be made with the intact shoulder (PTF of 68N) and not with the one with Bankart lesion and undergone repair (PTF of 52N). If doing so, a 4mm bone loss situation with Bankart repair, which only achieved half the PTF (35N) of an intact shoulder, might render a statistically significant difference yielding critical defect sizes of 13% of the glenoid length, 17% of the glenoid width, and 11% of the glenoid area according to Yamamoto’s data. While probably both interpretations are correct and only offer different views of the same data the possible implications for clinical decision-making are of relevant importance. The cut-off between significant and non-significant glenoid bone loss appears to be found at lower values than determined by Yamamoto et al. However, the clinical threshold value always remains subject to the patient’s individual expectations and need for proper stability.

    References
    1. Bushnell BD, Creighton RA, Herring MM. Bony instability of the shoulder. Arthroscopy. 2008 Sep;24(9):1061-73.
    2. Yamamoto N, Muraki T, Sperling JW, Steinmann SP, Cofield RH, Itoi E, et al. Stabilizing mechanism in bone-grafting of a large glenoid defect. J Bone Joint Surg Am. 2010 Sep;92(11):2059-66.
    3. Bois AJ, Fening SD, Polster J, Jones MH, Miniaci A. Quantifying glenoid bone loss in anterior shoulder instability: reliability and accuracy of 2-dimensional and 3-dimensional computed tomography measurement techniques. Am J Sports Med. 2012 Nov;40(11):2569-77.

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