title: Stabilizing mechanism in bone-grafting of a large glenoid defect.
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 > or =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 > or =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.
authors.affiliation: Biomechanics Laboratory, Division of Orthopedic Research, Mayo Clinic, 200 First Street S.W., Rochester, MN 55905, USA.
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Yamamoto
authors.forename: Takayuki
authors.initials: T
authors.lastname: Muraki
authors.forename: John W
authors.initials: JW
authors.lastname: Sperling
authors.forename: Scott P
authors.initials: SP
authors.lastname: Steinmann
authors.forename: Robert H
authors.initials: RH
authors.lastname: Cofield
authors.forename: Eiji
authors.initials: E
authors.lastname: Itoi
authors.forename: Kai-Nan
authors.initials: KN
authors.lastname: An
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001696:Biomechanical Phenomena; D016025:Bone Transplantation; D002102:Cadaver; D005260:Female; D006801:Humans; D007593:Joint Instability / Q000503:physiopathology / Q000601:surgery*; D008297:Male; D008875:Middle Aged; D016059:Range of Motion, Articular; D012783:Shoulder Dislocation / Q000503:physiopathology / Q000601:surgery*; D012785:Shoulder Joint / Q000502:physiology / Q000601:surgery*; D016896:Treatment Outcome