review article glenoid bone deﬁciency in recurrent

Glenoid Bone Deficiency inRecurrent Anterior ShoulderInstability: Diagnosis andManagement

Abstract

Recurrent anterior shoulder instability may result from a spectrumof overlapping, often coexistent factors, one of which is glenoidbone loss. Untreated, glenoid bone loss may lead to recurrentinstability and poor patient satisfaction. Recent studies suggest thatthe glenoid rim is altered in up to 90% of shoulders with recurrentinstability, thus underscoring the need for careful diagnosis,quantification, and preoperative evaluation. Biomechanical andclinical studies offer criteria that may be used in both primary andrevision settings to judge whether shoulder stability is compromisedby a bony defect. Along with patient activity level, these criteria canhelp guide the surgeon in selecting treatment options, which rangefrom nonsurgical care to isolated soft-tissue repair as well asvarious means of bony reconstitution.

Stability of the glenohumeral joint re-quires complex musculoskeletal

interactions. Without a constrainingbony articulation, several static and dy-namic mechanisms must act in coordi-nation to maintain consistent centeringof the humeral head on the glenoidfossa.1 Following an initial traumaticanterior shoulder dislocation, severalfactors may contribute to recurrence.The most common lesion is an antero-inferior capsulolabral avulsion from theglenoid rim,2,3 typically with associ-ated capsular attenuation.4 In addi-tion, acute fracture and/or attritionalglenoid bone loss may contribute torecurrent instability by altering theglenohumeral contact area and thefunction of the static glenohumeralrestraints.5,6 Although the critical im-portance of a functional anteriorcapsulolabral complex has been vali-dated by a large body of work, onlyin the past 5 to 10 years has atten-

tion been focused on the role thatglenoid bone deficiency plays in thesuccessful management of recurrentanterior shoulder instability.

Epidemiology

The prevalence of glenoid bone loss inassociation with recurrent anterior in-stability is not consistently reported inthe literature. This inconsistency mayresult from a lack of uniformity in eval-uating the glenoid rim for bone defects.Despite this variability, a certainamount of glenoid bone loss likely ispresent in most cases of recurrent in-stability;6 some degree of osseous de-ficiency has been noted in up to 22%of patients after an initial disloca-tion,7 in 0% to 90% of patients withrecurrent instability,2,6,8-11 and in upto 89% of failed prior stabilizationprocedures.12

Dana P. Piasecki, MD

Nikhil N. Verma, MD

Anthony A. Romeo, MD

William N. Levine, MD

Bernard R. Bach, Jr, MD

LCDR Matthew T. Provencher,MD, MC, USN

Dr. Piasecki is Attending Surgeon,OrthoCarolina Sports Medicine Center,Charlotte, NC. Dr. Verma is AttendingSurgeon, Division of Sports Medicine,Department of Orthopaedics, RushUniversity Medical Center, Chicago, IL.Dr. Romeo is Associate Professor,Department of Orthopaedics, andSection Head, Shoulder and ElbowSurgery, Division of Sports Medicine,Rush University Medical Center.Dr. Levine is Director of SportsMedicine, Department of Orthopaedics,Columbia University, New York, NY.Dr. Bach is Director, Division of SportsMedicine, Department of Orthopaedics,Rush University Medical Center.Dr. Provencher is Director, Shoulderand Sports Surgery, Department ofOrthopaedic Surgery, Naval MedicalCenter San Diego, San Diego, CA.

Reprint requests: Dr. Romeo, RushUniversity Medical Center, SportsMedicine Department, Suite 1063,1725 West Harrison Street, Chicago, IL60612.

J Am Acad Orthop Surg 2009;17:482-493

Copyright 2009 by the AmericanAcademy of Orthopaedic Surgeons.

Review Article

482 Journal of the American Academy of Orthopaedic Surgeons

Nature of Bone Defects

Sugaya et al6 used three-dimensionalCT scans to evaluate the morphologyof the glenoid rim in 100 consecutivecases of recurrent anterior instability.Ten percent of the patients had nor-mal glenoid bone architecture, 50%had a true bony Bankart lesion, and40% had some degree of bony“erosion,” which may represent atrue erosive mechanism or a com-pression fracture (Figure 1). Of theavulsion fractures, most were classi-fied as medium (5% to 20% of theglenoid fossa) or small (<5% of thefossa). In a retrospective review of123 three-dimensional CT scans un-dertaken for recurrent anterior insta-bility, Saito et al13 noted that themost common location of defectswas directly anterior to the glenoidface, ranging in position from 12:08to 6:32 on a clock face created bydrawing a circle around the glenoid;most defects were between 2:30 and4:20.

Mechanism

There is little more than speculationto suggest a distinct mechanism forglenoid osseous lesions. It is likelythat several factors are responsible.Burkhart and De Beer12 reported asubstantial frequency of acute gle-

noid rim fractures among South Afri-can rugby players compared withAmerican football players (9.4% ver-sus 0%, respectively) and suggestedthat, in the typical rugby dislocation,a greater axial load may be impartedto the glenoid. This mechanism is incontrast with the more common ro-tational mechanism of American

football, in which the inferior gleno-humeral ligament may avulse off asmall fragment of glenoid rim.9,12 Asmooth-appearing, blunted lesionmay be explained by an acute butlower-energy initial event (eg, com-pression fracture) and/or a morechronic, erosive process secondary torecurrent instability.

Bone defects typically occur in one or two possible forms, fracture fragmentand attritional bone loss, or in a combination of both. A, Fracture fragment. Athree-dimensional CT reconstruction image demonstrates anterior glenoidbone loss in the form of a fracture, with a clearly recognizable bonefragment. B, Attritional bone loss. A sagittal MR image demonstrates anteriorglenoid bone loss with a smooth, almost erosive pattern of deficiency and noidentifiable fracture fragment (arrow).

Figure 1

Dr. Verma or a member of his immediate family is a member of a speakers’ bureau or has made paid presentations on behalf ofSmith & Nephew and Arthrosurface; serves as a paid consultant to or is an employee of Smith & Nephew; has received research orinstitutional support from Smith & Nephew, DJ Orthopedics, and Arthrex; and has stock or stock options held in Omeros. Dr. Romeoor a member of his immediate family has received royalties from, is a member of a speakers’ bureau or has made paid presentationson behalf of, serves as a paid consultant to or is an employee of, has received research or institutional support from, has stock orstock options held in, and has received nonincome support (such as equipment or services), commercially derived honoraria, or othernon–research-related funding (such as paid travel) from Arthrex. Dr. Levine or a member of his immediate family serves as an unpaidconsultant to Acumed and Stryker; has received research or institutional support from Arthrex, Arthrotek, Smith & Nephew, Stryker,and Zimmer; and has received nonincome support (such as equipment or services), commercially derived honoraria, or othernon–research-related funding (such as paid travel) from Marcel-Dekker. Dr. Bach or a member of his immediate family has receivedresearch or institutional support from Smith & Nephew, DJ Orthopedics, MioMed Orthopaedics, and Athletico. Dr. Provencher or amember of his immediate family serves as a board member, owner, officer, or committee member of American Orthopaedic Societyfor Sports Medicine, Society of Military Orthopaedic Surgeons, American Academy of Orthopaedic Surgeons, and InternationalSociety of Arthroscopy, Knee Surgery, and Orthopaedic Sports Medicine, and has received research or institutional support fromArthroscopy Association of North America and American Orthopaedic Society for Sports Medicine. Neither Dr. Piasecki nor a memberof his immediate family has received anything of value from or owns stock in a commercial company or institution related directly orindirectly to the subject of this article.

Dana P. Piasecki, MD, et al

August 2009, Vol 17, No 8 483

Natural History

Many individuals with bone losslikely suffer some bony involvementat the time of initial dislocation, thussetting the stage for the developmentof subsequent chronic attritionalchanges. In cases of acute (<3months) recurrent instability, identi-fiable fracture fragments are fre-quently reported.14,15 By contrast, amore attritional pattern was reportedin the series of Mologne et al,16 inwhich, at a mean of 15 months afterthe first dislocation, 50% of glenoidsexhibited erosive bone loss withoutan identifiable fracture fragment.Fracture fragments in chronic cases(>6 months) often show signs of par-tial resorption.17 Rim defects havealso been noted to enlarge overtime.9 These findings suggest thatsome lesions occur at the time of theinitial dislocation, whereas othersmay develop, progress, or remodel asa consequence of repeated instabilityepisodes.

Pathoanatomy andBiomechanics

Loss of bone in the anteroinferiorglenoid decreases the available artic-ular arc, resulting in a mismatch be-tween the glenoid and humerus. Thatis, the glenoid articular area and theconcavity that contains the humerusand can prevent dislocation are bothdiminished. A smaller articular arclength also represents a smaller sur-face area by which the glenoid canresist axial forces, thus increasing therelative shear forces imparted to a re-paired capsulolabral interface.12

Loss of bone along the glenoid rimalso decreases the depth of articularconformity. This decrease resultsfrom loss of a portion of the joint’snormal concavity-compression andthe buttress-type restraint to anteriorinstability.12,18 These mechanisms are

amplified when associated Hill-Sachslesions are present on the humeralside.19 Several authors have demon-strated both small and large glenoiddefects frequently accompanying,6,8

and contributing directly to,12 recur-rent instability, such as osseous frag-ment, obtuse morphology, invertedpear shape, Hill-Sachs lesion, dislo-cation, and subluxation.

Diagnosis andQuantification

HistoryA detailed history should be ob-tained from all patients who presentwith recurrent anterior instability.The history should begin with thepatient’s preinjury activity level andthe details surrounding the initialdislocation event. Several factors, ifpresent, may suggest glenoid boneloss. An initial high-energy event,typically involving a mechanism thataxially loads the glenoid, may indi-cate a predisposition for glenoidbone involvement.12 Associated boneloss may be indicated by complaintsof subsequent instability in themidranges of motion (ie, 20° to 60°of abduction)20 and, specifically, bydislocations that occur with lower-energy events and with simple activi-ties of daily living. Any suggestion ofprogressive ease of subluxation mayindicate loss of bony constraints ofthe glenohumeral joint. Prior treat-ments (both surgical and nonsurgi-cal) and their outcomes should be re-viewed. Previous surgical reports andimaging studies should be reassessedto establish the initial injury patternand adequacy of treatment.

Physical ExaminationBoth shoulders should be carefullyinspected for evidence of deformity,scapular dyskinesia, prior surgicalscars, and/or possible rotator cuff at-rophy. A careful neurovascular ex-

amination should be performed,along with standard tests of activeand passive range of motion, rotatorcuff strength, and provocative labralsigns. The surgeon should pay spe-cial attention to subscapularis func-tion, particularly in older patientswith instability, and, because of thepotential for failure of subscapularisrepair, in any patient who has under-gone a previous open stabilization.

An examination of stability shouldbe performed, with comparisonmade to the contralateral shoulder inorder to quantify the direction andmagnitude of laxity. Care should betaken to differentiate these patientsfrom those with multidirectional in-stability. In the case of bony involve-ment, a greater relative degree ofearly and midrange (ie, 20° to 60°)apprehension, which is typically uni-directional, is likely to be seen.1,18 Al-though findings may not readily dif-ferentiate patients with glenoid boneloss from those with soft-tissue–onlylesions, the relative degree of de-tected instability may be greater inpatients with bony defects.16

ImagingIn general, plain radiographs aremoderately accurate at demonstrat-ing glenoid bone loss.9,21 A bonyshadow or displaced bony Bankartfragment may be visualized on astandard AP view or in other projec-tions parallel to the glenoid face,such as the axillary or glenoid profileview.22 The highest-yield projections,however, are angled relative to theglenoid face, such as the apicaloblique,23 Didiée,24 or West Point25

views. The Stryker notch view andAP view with the humerus in internalrotation should also be obtained,given their utility in visualizing po-tential Hill-Sachs lesions on the hu-meral side.24

Beyond standard radiography, MRIor magnetic resonance arthrography

Glenoid Bone Deficiency in Recurrent Anterior Shoulder Instability


(MRA) studies may suggest the degreeof bone loss in the most lateral glenoidcut on the sagittal oblique series. How-ever, the current standard imaging mo-dality for quantifying glenoid bone lossis CT.

Standard CT scans can be used toestimate bone loss and detect rimfracture fragments; more recentthree-dimensionally reconstructedscans can also be performed withdigital subtraction of the humeralhead. By use of this modality, gle-noid osseous deficiency is quantifiedas a percentage of the normal infe-rior glenoid surface area.6,13 A best-fit circle is drawn on the inferior twothirds of the glenoid image, whichhas been shown to be a consistentanatomic configuration.6,26 Theamount of bone missing from the cir-cle, as a percentage of the total sur-face area of the inferior circle, is thendetermined with digital measure-ments. Given the precision withwhich this modality can preopera-tively quantify glenoid bone loss, itsuse should be strongly considered inpatients in whom the history, physi-

cal examination, or standard radio-graphs suggest the possibility of sig-nificant bone deficiency.

Arthroscopic Determinationof Bone LossHuysmans et al26 demonstrated thatthe normal inferior glenoid isbounded by a nearly perfect circlewith an average diameter of 24 mm.A frequently seen bare area inthe center of the glenoid has beenshown to reliably mark the center ofthis circle26-28 (Figure 2). Lo et al8

have described a method of quantify-ing glenoid bone loss by measuringthe anterior-posterior width of thedefect at the level of the bare spot.With the arthroscope in the antero-superior portal (Figure 3), a cali-brated probe is inserted from theposterior portal to measure the dis-tance from the anterior and posteriorrims to the bare spot. The differencebetween the anterior and posteriorradii can then be quickly calculatedand referenced as a percentage of thediameter of the normal inferior gle-

noid. The diameter of the normal in-ferior glenoid is assumed to be twicethe distance of the posterior rim tothe bare spot:

Although the bare spot has beenquestioned as a consistent land-mark,29 the approximate determina-tion of glenoid bone loss by arthro-scopic techniques remains well

Normal glenoid anatomy includes a circular inferior glenoid. Note the barespot in the center of the circle.

Figure 2

Arthroscopic quantification ofglenoid bone loss in a rightshoulder. The arthroscope is placedin the anterosuperior portal, andthe glenoid is viewed from superiorto inferior. A calibrated (3-mmmarks) probe is then insertedthrough the posterior portal andused to measure the anterior andposterior radii of the inferior glenoid(ie, transverse distance at the levelof the bare spot). When an anteriormeasurement is less than theposterior one, anterior bone losswill be apparent. The degree ofbone loss can be quantified as apercentage of the normal diameterof the inferior glenoid (assumed tobe twice the posterior radius).Here, 7 mm of bone remainsanterior to the bare spot,representing a 21% width defect.

Figure 3


August 2009, Vol 17, No 8 485

documented. We believe it should beroutinely performed before any ante-rior stabilization is undertaken toconfirm the appropriateness of thesubsequent procedure.

Critical LimitSeveral investigators have attempted todefine the critical limit at which glenoidbone loss destabilizes the shoulder. Ina classic biomechanical study, Itoiet al5 performed sequential removalof increasingly large portions of theglenoid in 10 cadaveric shoulders.Osteotomies were made at a 45° in-clination to the long axis of the gle-noid, and the degree of bone defi-ciency was quantified by the widthof each sequential resection as a per-centage of the total length of the gle-noid (9%, 21%, 34%, and 46%).Peak forces required to translate thehumeral head a unit distance weremeasured using a multiaxis testing

machine, with and without capsulo-labral repair. Stability decreased pro-gressively as the degree of bone lossincreased, dropping off notably withosseous defects ≥21% (average de-fect width, 6.8 mm). A significantdrop-off in external rotation wasalso seen with defects ≥21%, withcapsular advancement reducing ex-ternal rotation by 25° per centimeterof defect spanned.

Using a similar model, Greis et al30

reported significant increases in gle-nohumeral contact pressures withglenoid bone defects of >30%, fur-ther suggesting that this degree ofbone loss is indeed biomechanicallyrelevant. These results indicate thatwidth defects of the inferior glenoidcircle of 6 to 7 mm are significant(Figure 4). The 21% threshold valuegiven by Itoi et al,5 however, must beinterpreted with care. This percent-age does not correspond to a straight

anterior-posterior width, and itshould not be confused with actualanterior-posterior or surface areameasurements of other studies.

Clinically, Burkhart and De Beer12

appreciated a high rate of failure af-ter isolated capsulolabral repairs per-formed in patients with an inferiorglenoid that narrowed to create aninverted pear appearance whenviewed arthroscopically through ananterosuperior portal. Lo et al8

quantified bone loss in patients withrecurrent instability and an invertedpear glenoid with the arthroscopicmethod described above; they dem-onstrated that patients with an in-verted pear glenoid had a mean ante-rior loss of 8.6 mm of bone,corresponding to 36% loss of the to-tal glenoid width at that level. Con-sistent findings were seen when aninverted pear appearance was artifi-cially created in cadaveric specimens.

Significant bone defects based on biomechanical data.Note that these defects have been created at a 45°inclination to the long axis of the glenoid. Progressiveloss of stability and external rotation are seen as defectsincrease in size, particularly beyond widths ofapproximately 6 to 7 mm. This degree of bone losscorresponds with roughly 5 mm of intact bone beyondthe bare spot.

Figure 4

Significant bone defects based on clinical correlations.The posterior slope of the defect creates a narrowerinferior glenoid width and the so-called inverted pearappearance when viewed superiorly (through theanterosuperior portal).

Figure 5



The inverted pear appearance corre-sponded to 7.5 mm of anterior gle-noid bone loss—a 28% loss of gle-noid width at the level of the barespot (Figure 5).

When the inferior glenoid is viewedas a circle, the anterior-to-posterior gle-noid width loss of a given defect can beconverted to a surface area percentage(as described by Sugaya et al17) bycalculating the corresponding circlesegment area (Table 1). Taken to-gether, these data suggest that signifi-cant instability will accompany ante-rior width losses of >25% to 30% atthe level of the bare spot, or inferiorglenoid surface area losses of >20%to 25% (Figure 6).

However, these thresholds are ap-plicable to the more common sce-nario of isolated glenoid bone loss.In the less common situation of anadditional engaging Hill-Sachs le-sion,12 smaller glenoid defects wouldbe expected to take on greater signif-icance.

Management

NonsurgicalEvidence exists that immediate exter-nal rotation bracing may somewhatdecrease the risk of recurrence in pa-tients with soft-tissue Bankart le-sions;31 however, no studies have de-termined whether this approach iseffective in patients with significantglenoid bone loss. Therefore, the cur-rent nonsurgical approach focuseson enhancing the dynamic stabilizingrole of the periscapular and rotatorcuff musculature. This compensationmay allow some patients to avoidsurgery; however, as the degree ofbone loss increases, muscular en-hancement via physical therapy willbe increasingly insufficient to main-tain a stable shoulder because of thelack of sufficient bony articulation.Activity level and the degree of boneloss thus are the two most important

Summary of critical bone defects. Losses of <15% width (<3 to 4 mm fromthe anterior rim) may be insignificant in most patients. Width losses of 15%to 30% (between 4 and 9 mm of bone remaining anterior to the bare spot)will be significant in some patients. Losses of >30% (<4 mm of bone leftanterior to the bare spot) will likely be significant in most patients.

Figure 6

Table 1

Conversion of Anterior-posterior Defect Widths to Surface AreaPercentages*

Anterior-posteriorDefectWidth (mm)

Anterior-posteriorWidth (% of

inferior glenoidcircle diameter)

Circular SegmentArea (% of

inferior glenoid circle)

Insignificant2.8† 12 63.6‡ 15 9

Borderline5§ 21 156|| 25 20

Significant6.8¶ 28 237.5# 30 258.6** 36 32

* On a circle, a marginal defect can be described by a width (measured from the outer rim)that corresponds with a circle segment area. When applied to the glenoid, such a segmentdefect represents a percentage of the inferior glenoid circle’s surface area. With thisunderstood, relevant anterior-posterior defect widths can be converted to surface areapercentages.† Corresponds with “9%” resection (anterior-inferior) of Itoi et al5

‡ Corresponds with 15% anterior-posterior width§ Corresponds with 20% anterior-posterior width measurement|| Corresponds with 25% anterior-posterior width of Bigliani et al9

¶ Corresponds with “21%” resection (anterior-inferior) of Itoi et al5

# Corresponds with cadaveric pear glenoids of Lo et al8

** Corresponds with clinical pear glenoids of Lo et al8


August 2009, Vol 17, No 8 487

factors to be considered in decidingon treatment options.

Nonsurgical treatment is best appliedto lower-demand individuals (eg, non-overhead athletes) with smaller defects(ie, <20%). Additionally, voluntary dis-locators, patients with risky comorbid-ities, and those unable to complyadequately with postoperative rehabil-itation are best served by conservativemanagement. The rehabilitation proto-col is generally identical to that used inpatients with soft-tissue–only instabil-ity except that patients with greater de-grees of bone loss, as well as their ther-apists, must remain aware of at-riskpositions in order to prevent disloca-tion. An initial period of immobiliza-tion is generally followed by supervisedrehabilitation, which focuses on pro-gression from passive to active-assistedand active motion as well as eventualrotator cuff and periscapular musclestrengthening. The ultimate goal ismaintenance of the shoulder in a sta-ble arc during functional activities.

SurgicalIn most cases of glenoid bone loss, sur-gical intervention is indicated when aninitial course of nonsurgical manage-ment has failed to restore adequatefunction and quality of life. Surgerymay be recommended as an initial ap-proach in young (aged <25 to 30 years),highly active (eg, overhead, contact)athletes with severe (>25% to 30%)bone loss, given the likelihood that con-servative management will fail in thissetting.12 Most active patients withacute glenoid fractures constituting>30% of the glenoid also should beconsidered for index surgical inter-vention to avoid malunion or non-union. When surgery is indicated,numerous options are available formanaging glenoid bone loss. Thebest procedure is one that considersthe surgeon’s comfort level, the pa-tient’s activity level, and the degreeof bone deficiency (Figure 7).

Bone Loss of Less Than 15%Most patients with recurrent anteriorglenohumeral instability have minorbone loss (ie, <15%), although theoverall incidence is likely underap-preciated.6 Bigliani et al9 reported ona series of 22 patients who had re-current anterior instability after trau-matic dislocations; the authors pre-dominantly noted a small (ie, <10%to 15%) avulsion-type fracture pat-tern of the rim. Most of these frac-tures were treated with direct openanatomic repair of the bonefragment/capsulolabral composite tothe remaining glenoid rim. At amean follow-up of 30 months, Big-liani et al9 noted satisfactory resultsin 86% of patients, 72% with nor-mal postoperative stability. Althoughthe numbers are small, the successrate was much higher in patients inwhom the bone fragment could beanatomically incorporated into therepair. Among fractures repaired inthis manner, 94% remained stablepostoperatively. Among fractures inwhich the bone fragments were ig-nored, 40% of patients sufferedpostoperative recurrent instability.These findings suggest that bonefragment incorporation may be criti-cally important in some cases.

Excellent results have also been re-ported with arthroscopic repair ofthese small defects. Porcellini et al15

treated 25 acute and subacute (ie,within 3 months of injury) rim avul-sion fractures (25 patients) with ar-throscopic mobilization of the frag-ment, followed by reduction andsuture anchor fixation through thelabral interface. Bone loss, whichwas quantified based on a subjectiveassessment of the total glenoid sur-face area involved, was <25% in allcases. At 2-year follow-up, good toexcellent Rowe scores were noted in23 patients, and 92% of patients hadreturned to their previous level ofsport. Two patients returned to sportat a lower level, an outcome that was

attributed to a loss of external rota-tion (mean, 9.7°).

No clinical data suggest a cutoffbelow which outcomes, if ignored,will not suffer. Still, the minimal de-stabilizing effect of the “9%” osteot-omy (12% anteroinferior width loss)of Itoi et al,5 as well as the widely re-ported excellent results in a series ofpresumed soft-tissue–only Bankartlesions (with likely minor unrecog-nized bone deficiencies) reported bySugaya et al,6 suggest that most de-fects of <15% will have minimal im-plications when treated with soundopen or arthroscopic capsulolabralrepair techniques. For these defects,therefore, we feel that a standardBankart repair is indicated.

Bone Loss of 15% to 25%As glenoid bone deficiency nears25%, progressive joint alteration be-comes clinically significant in agreater number of patients. Still, sev-eral series have demonstrated excel-lent outcomes in patients with thisintermediate degree of bone losswhen bone is restored to the glenoidrim. Many suggest that bony restora-tion should be undertaken when pos-sible.

Sugaya et al17 reported outcomes in42 consecutive shoulders with atleast 6 months of recurrent anteriorinstability and recognized glenoidbone deficiency. Rim avulsion frac-tures were arthroscopically reducedand fixed to the glenoid rim with su-ture anchors in the labral interface(Figure 8). As determined by three-dimensional CT scans, the averagepreoperative osseous defect was24.5% of the inferior glenoid sur-face.6 At a mean 34-month follow-up, 93% good to excellent resultswere noted, based on Rowe andUCLA scores; 95% of patients re-turned to sport. Small decreases inexternal rotation (4° to 5°) werenoted, but these did not reach thelevel of statistical significance. Two



patients (5%) suffered recurrent in-stability after contact injury duringsports. Postoperative CT scans wereobtained in 12 patients at final fol-low-up; the scans demonstratedunion in all cases, suggesting thatthese bone fragments retain viabilityand the potential to heal in a re-paired position in most cases, evenup to 6 months after injury.

The literature suggests diminishedoutcomes in these intermediate deficien-cies when bone is not restored to theglenoid rim, as is the case with smallerdefects. Mologne et al16 recently re-ported a single-surgeon experience in23 active military personnel (meanage, 25 years) with recurrent anteriorinstability and associated glenoidbone defects, ranging from 20% to

30% width loss (ie, 5 to 7 mm) atthe level of the bare spot. At a meanof 34 months after arthroscopic sta-bilization, a 14.2% rate of failurewas reported; failure occurred exclu-sively in patients with attritionalbone loss in whom no bony fragmentwas available for incorporation intothe repair. By contrast, no failuresoccurred when a bony fragment was

Treatment algorithm for surgical management of glenoid bone loss. 3D = three-dimensional, ICBG = iliac crest bonegraft, SA = segment area* Possible increased failure rate among contact athletes and limiting loss of external rotation in throwers† Possible long-term arthrosis, implant problems, and/or rare return to play in throwers

Figure 7


August 2009, Vol 17, No 8 489

present and incorporated into the re-pair. Patient-specific factors are alsoimportant to consider in this inter-mediate range of bone loss. Burkhartand De Beer12 noted an 89% failurerate in contact athletes followingsoft-tissue–only repair of defects ofapproximately 25% to 30%.

As bone loss approaches 30% andpatient demands increase, soft-tis-sue–only repair has an increased fail-ure rate. In such situations, availablebone fragments should be incorpo-rated into the capsulolabral repairwhen possible. When no bony frag-ment is available, the surgeon mustconsider open glenoid bone augmen-tation, weighing the potential for in-creased complications against therisk of higher recurrence rates ifbone defects are ignored.

Bone Loss of MoreThan 25% to 30%For bone loss of >25% to 30% (ie,<4 to 5 mm of bone remaining ante-rior to the bare spot and/or an in-verted pear appearance), optimal re-sults typically require reconstitutionof the glenoid bony arc, given thebiomechanical loss of stability5,32 andpoor clinical outcomes when ig-nored.8,12 Ideally, arc reconstitution

would be possible by repairing frac-ture fragments along with the capsu-lolabral tissues. In the more acutesetting, good results have been re-ported for open fracture fixation.Scheibel et al33 reported good to ex-cellent results with no recurrentinstability at a mean 30-monthfollow-up after open fixation of large(>25%) glenoid rim fractures. Expertopinion provides anecdotal examplesof success by addressing a smallnumber of these fractures with ar-throscopic reduction and percutane-ous screw fixation. Regardless of themeans, the important principle ap-pears to be anatomic reconstructionwhenever possible.

In the more common scenario,however, the glenoid is deficient ar-throscopically (ie, inverted pear gle-noid), without an adequate fracturefragment available for reconstruc-tion.12 In these cases, the fragment iseither absent (attritional loss) or haspartially resorbed and is too small toaccommodate screw fixation. Whenbone loss of this nature is >25% to30%, some form of open bone aug-mentation is required in the primarysetting. Several techniques have beendescribed; however, no single bone

augmentation procedure is regardedas being best. The implication acrossseveral different techniques, how-ever, is that, so long as the osseousdeficiency is restored in a near-anatomic fashion, outcomes gener-ally will be very good. Final deci-sions regarding the ideal boneaugmentation procedure, therefore,are left to surgeon preference.

The most popular and well-studiedmethods of glenoid augmentation in-volve transfer of the coracoid processto the anteroinferior glenoid (ie, Bris-tow or Latarjet procedures).34,35 TheLatarjet procedure is preferred bymany surgeons because it uses alonger segment of coracoid than doesthe Bristow, fixing its long axis par-allel to the anterior glenoid rim andproviding a more anatomic restora-tion of the glenoid bony arc12 (Figure9). In the Bristow procedure, thecoracoid is fixed perpendicular to theglenoid at its base. However, goodresults have been reported for both.35

The Latarjet procedure is performedthrough an anterior approach. After re-lease of the pectoralis minor tendon, thecoracoid is osteotomized proximal toits angle, rotated 90°, and passedthrough a split in the midportion of the

Arthroscopic repair of glenoid bone fragments. A, Anterior labral bone fragment attached to the labrum. B, Suturespassed through the fragment-labral interface. C, Final repair construct.

Figure 8



subscapularis tendon. Minor adjust-ments to the bony contour can be madewith a burr and the graft fixed flushwith the glenoid articular surface withscrews, its long axis parallel to the longaxis of the glenoid. A cuff of coraco-acromial ligament may be left on thecoracoid process for attachment to thecapsulolabral complex. The capsule andlabrum are additionally fixed posteriorto the graft at the glenoid margin withsuture anchors—that is, the graft be-comes extra-articular. The Bristow pro-cedure is performed using a similar ap-proach, although the coracoid isosteotomized transversely and fixed tothe glenoid neck at its base, so that thelong axis is directed anteriorly. In theseapproaches, the conjoined tendon is leftintact for potential bone block bloodsupply as well as to act as a theoreticalsoft-tissue sling in abduction. Alterna-tively, the coracoid graft may be re-leased from its tendinous attachmentsand used as a free bone block.

Hovelius et al35 published the clini-cal outcomes of a prospective cohortof 118 patients with recurrent ante-

rior instability treated with aBristow-Latarjet procedure at amean 15.2-year follow-up. Redislo-cation occurred in 3.4% of patientsand subluxation in 10%. Good toexcellent Rowe scores were reportedin 86%; 98% of patients were satis-fied or very satisfied on final follow-up. In a separate publication, how-ever, 14% of the patients in the samecohort reported moderate to severedislocation arthropathy; mild ar-thropathy was reported in another35%.36 Although not statistically sig-nificant, this glenohumeral arthropa-thy occurred more frequently in pa-tients whose grafts were placed at orlateral to the glenoid rim.

Hovelius et al37 also compared aprospective cohort of 30 Bristow-Latarjet procedures with a retrospec-tive cohort of soft-tissue–only Ban-kart repairs at a mean follow-up of>15 years. One in four of theBristow-Latarjet patients reportedsubjective or objective anterior ap-prehension; still, the rates of revision

for recurrent instability, dislocationarthropathy, and overall patient sat-isfaction were similar between thegroups. Most patients in both co-horts resumed their premorbid levelof athletic activity, with a greaternumber of patients in the Latarjetgroup subjectively able to throw nor-mally after surgery.

Schroder et al38 demonstrated long-term durability of the Bristow-Latarjet procedure at 26 years in USNaval Academy midshipmen. How-ever, loss of external rotation andpotential glenohumeral arthrosis re-main a concern.

Others have recommended glenoidreconstruction with structural bonegraft. Most commonly, iliac crest au-tograft or allograft (the so-calledEden-Hybbinette procedure) is used,given the close match of bony con-tour to the glenoid39 (Figure 10). Inthis procedure, the curve of the innertable of the iliac wing is matched tothat of the glenoid, with the concaveinner table facing laterally and the

Latarjet procedure. A, Anterior glenoid bone grafting,sagittal view. The coracoid process is transferred intothe glenoid defect, fixed with its long axis parallel to thatof the glenoid. B, Axial view, with graft anterior. Thecapsule is repaired posterior to the graft, making itextra-articular. The graft itself may be repaired to thecapsule via a stump of the coracoacromial ligament (notshown).

Figure 9

Intra-articular tricortical iliac crest autograftreconstruction. A, Sagittal view of the glenoid en face.The graft is fixed such that the iliac wing’s naturalcontour roughly matches that of the glenoid articular arc.B, Axial view. The capsule is attached anterior to thebone block, making the graft intra-articular.

Figure 10


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cancellous base of the graft securedto the glenoid neck. The biomechani-cal merits of such contoured bone-block reconstruction have been dem-onstrated by Montgomery et al,32

who in their cadaveric study showedthat a well-contoured bone block re-stores glenohumeral stability in sig-nificant defects. However, early clini-cal series demonstrated high rates ofpostoperative arthrosis39 and up to18% recurrent instability.40 As in theLatarjet procedure, the capsule maybe repaired to the native glenoidsuch that the iliac crest bone graftbecomes an extra-articular structure.

Still, Haaker et al41 reported a90% rate of patient satisfaction andno recurrent instability in 24 patientstreated with iliac crest autograftat 42-month follow-up. Likewise,Warner et al20 reported their clinicalresults using tricortical iliac crest au-tograft to reconstruct clinically sig-nificant glenoid bone defects in 11cases of recurrent anterior instability.The grafts were meticulously con-toured to the glenoid and fixed intra-articularly with cannulated screws,followed by an anteroinferior capsu-lar repair (making the graft intra-articular). At a mean 33-monthfollow-up, no recurrent episodes ofinstability were noted, and CT scansobtained 4 to 6 months postopera-tively demonstrated graft incorpora-tion in all patients, with preservationof joint space.

Revision SurgeryRevision surgery is subject to thesame biomechanical principles as issurgery in the primary setting. Signif-icant bone loss will predictably leadto failure if not addressed at the in-dex procedure.12 In addition, thebony deficit may frequently be un-derrecognized.13 It is therefore in-cumbent on the surgeon to considerwhether significant bone loss hascontributed to a failed stabilization.In the presence of adequate capsular

tissue, however, we recommend theuse of the same treatment protocolfor revision cases with bone loss asthat used in the primary setting.

Summary

Although recurrent anterior shoulderinstability can result from a varietyof causes, a high frequency of trau-matic cases involves some degree ofanterior glenoid bone loss that maybe unrecognized at the preoperativepatient evaluation. Proper radio-graphs, advanced imaging techniques(ie, MRI, MRA, three-dimensionalCT), and arthroscopic measurementsprovide the means for determiningthe extent of bone loss. Biomechani-cal and clinical observations havedemonstrated the critical role of anintact glenoid articular arc in main-taining shoulder stability and func-tion. These principles hold true forprimary as well as revision stabiliza-tions; high rates of surgical failurehave been recognized when largerdefects are not appropriately ad-dressed at the time of surgery.

Understanding the significance of thedegree of bone loss helps to guide treat-ment. Defects involving <15% of theanterior or anteroinferior glenoid mar-gin are likely to be insignificant in mostpatients and can be addressed with astraightforward Bankart repair. Defectsof 15% to 30% represent an interme-diate area, within which the level of pa-tient activity dictates the importance ofbone restoration. Toward the high endof this range, greater importance isplaced on glenoid arc reconstitution incontact athletes. Bone defects in thismiddle zone can be managed via openor arthroscopic repair of an availableglenoid rim fragment or, when no suchfragment exists, via open bone aug-mentation techniques. With >30%bone loss, unless a large fracture frag-ment can be anatomically reduced, it isgenerally advisable to proceed with

open bony augmentation procedures.In general, as the degree of bone lossincreases, the ability to ensure predict-able function and return to play dimin-ishes, although attention paid to basicbiomechanical, clinical, and recon-structive principles can provide a sat-isfactory return to function in most pa-tients.

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