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Glenohumeral Joint Preservation: Current Options for ManagingArticular Cartilage Lesions in Young, Active Patients

Florian Elser, M.D., Sepp Braun, M.D., Christopher B. Dewing, M.D.,and Peter J. Millett, M.D., M.Sc.

Abstract: This is a review of joint-preservation techniques for the shoulder. Whereas the management ofdiffuse articular cartilage loss in the glenohumeral joints of elderly and less active patients by totalshoulder arthroplasty is well accepted, significant controversy persists in selecting and refining successfuloperative techniques to repair symptomatic glenohumeral cartilage lesions in the shoulders of young,active patients. The principal causes of focal and diffuse articular cartilage damage in the glenohumeraljoint, including previous surgery, trauma, acute or recurrent dislocation, osteonecrosis, infection, chon-drolysis, osteochondritis dissecans, inflammatory arthritides, rotator cuff arthropathy, and osteoarthritis,are discussed. Focal cartilage lesions of the glenohumeral joint are often difficult to diagnose and requirea refined and focused physical examination as well as carefully selected imaging studies. This reviewoffers a concise guide to surgical decision making and up-to-date summaries of the current techniquesavailable to treat both focal chondral defects and more massive structural osteochondral defects. Thesetechniques include microfracture, osteoarticular transplantation (OATS [Osteochondral Autograft Trans-fer System]; Arthrex, Naples, FL), autologous chondrocyte implantation, bulk allograft reconstruction,and biologic resurfacing. As new approaches to glenohumeral cartilage repair and shoulder joint preser-vation evolve, there continues to be a heightened need for collaborative research and well-designedoutcomes analysis to facilitate successful patient care.

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ith an increasingly active population and withimprovements in medical technology and sur-

ical technique, there is both a need and an opportu-ity for joint-preserving surgery for the glenohumeraloint. Focal cartilage lesions of the glenoid and hu-erus have historically been underdiagnosed by clin-

cal examination and by imaging techniques, predis-

From the Steadman Hawkins Research Foundation, Vail, Colo-ado, U.S.A.

F.E., S.B., P.J.M. have received support from Arthrex, Naples,L, exceeding US $500 related to this research.Received August 27, 2009; accepted October 21, 2009.Address correspondence and reprint requests to Peter J. Millett,.D., M.Sc., Steadman Hawkins Research Foundation, 181 Weadow Dr, Ste 100, Vail, CO 81657, U.S.A. E-mail: drmillett@

teadman-hawkins.com© 2010 by the Arthroscopy Association of North America

a0749-8063/10/2605-9498$36.00/0doi:10.1016/j.arthro.2009.10.017

Arthroscopy: The Journal of Arthroscopic and Related

osing them to incidental discovery at the time ofurgery. The incidence of symptomatic Outerbridgerade II to IV lesions of the shoulder has been re-orted to be as high as 5% to 17% in patients withotator cuff tears1 or overhead athletes.2

Cartilage injury in the shoulder may be caused by orssociated with a myriad of factors that include pre-ious surgery, trauma, acute or recurrent dislocation,steonecrosis, infection, chondrolysis, osteochondritisissecans (OCD), inflammatory arthritides, rotatoruff arthropathy, and osteoarthritis. Though symptom-tic osteoarthritis of the shoulder can be successfullyreated with shoulder arthroplasty, focal cartilage le-ions in the younger, active patient population demandlternative treatment strategies that preserve the joint.urvival rates of total shoulder arthroplasty in youngeratients are not as good as in older, less active pa-ients, with survivorship being reported as low as 61%

t 10 years in a series of 33 patients with a mean age

685Surgery, Vol 26, No 5 (May), 2010: pp 685-696

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f 46 years at the time of surgery.3 This review willxplore joint-preserving techniques for cartilage le-ions of the glenohumeral joint that can be used whenreating young, active patients.

ANATOMY

Recent investigations have deepened our under-tanding of the dimensions of the chondral surfaces ofhe glenohumeral articulation. At the center of theumeral head, the hyaline cartilage on the articularurface is 1.2 to 1.3 mm deep,4 thinning at the periph-ry to 1.0 mm or slightly less. On the glenoid surface,yaline cartilage is thicker at the periphery than in theenter. Bone density in adults is also greater beneathhe cartilage at the center of the glenoid, which haseen attributed to the higher loads that are seen in thisegion.5 The glenohumeral articular surface is congru-nt because of this varying thickness of the cartilage.6

INCIDENCE

The true incidence of focal glenohumeral chondralefects is unknown, because most lesions are discov-red in the setting of treatment for concomitant injury.rthroscopic evaluation of the glenohumeral cartilage

urface in 200 shoulders (195 patients) with full-hickness rotator cuff tears showed a 13% prevalencef articular cartilage pathology.1 Of the patients, 17ad minor lesions (8.5%) and only 9 (4.5%) had majorull-thickness lesions that measured more than 150m2. The prevalence of high-grade articular cartilage

njury in high-level overhead athletes was 17% inhrowers, all located near the insertion of the supraspi-atus tendon.2 Ellman et al.7 found that 6% of patientsmean age, 51 years) who underwent arthroscopicreatment for impingement symptoms had articularartilage lesions, which ranged in size from 15 mm iniameter to comprising 50% of the humeral chondralurface. Other authors have reported a 29% preva-ence of humeral head lesions and 15% prevalence oflenoid cartilage lesions in patients who underwentrthroscopy for subacromial impingement.8 For pa-ients who underwent arthroscopic shoulder surgery atur institution between 1993 and 2008, there was a2.4% prevalence (280 of 2,251) of grade III and IVesions on 1 or both glenohumeral surfaces (unpub-ished data, P.J.M., September 2009).

ETIOLOGY OF CARTILAGE LESIONS

The causes of glenohumeral chondral injury may be

onsidered in a systematic fashion. Injury patterns can be w

roadly considered in relation to acute or recurrent in-tability, high-impact trauma, post-traumatic changes ofsteonecrosis or OCD, and complications or sequelae ofurgery (Table 1).

nstability

There is a well-documented association betweencute and recurrent shoulder dislocation and cartilageesions in the glenohumeral joint. In 1934 Hermods-on9 was the first to describe the ubiquitous compres-ion fracture of the posterolateral humeral head thatccurs with traumatic anterior instability, but it wasill and Sachs for whom the lesion was named.10

tudies have shown a high incidence of 47% to 100%f cartilage compression fractures or shear injury tohe chondral surface in first-time anterior dislocationsnd recurrent dislocations of the shoulder.11-13

Another cause of glenoid articular cartilage defectsay be glenolabral articular disruption (GLAD) le-

ions.14,15 This lesion consists of an anterior-inferiorabral tear associated with an injury to the glenoidrticular cartilage (Fig 1) and is usually caused by aorced adduction injury to the shoulder from an ab-ucted and externally rotated position. They may beifficult to diagnose clinically, although magnetic res-nance imaging (MRI) will usually show them.Chronic instability has been clearly linked to early

lenohumeral osteoarthritis.16,17 The time period ofhoulder instability from first dislocation to surgicalnterior stabilization, glenoid rim impaction fracture,ill-Sachs lesion, age at the time of first dislocation,

ecurrent instability, presence of a rotator cuff tear,nd clearly, any cartilage injury with an index episodef dislocation have all been independently linked toarly glenohumeral osteoarthritis (Table 2).16,18,19

arx et al.18 showed that patients with a history ofrevious shoulder dislocation had a 19 times greaterisk of shoulder arthritis developing than patients

TABLE 1. Etiology of Cartilage Lesions

revious surgeryenetrating or high-impact traumacute or recurrent dislocationsteonecrosis

nfectionhondrolysisCD

nflammatory arthritidesotator cuff arthropathysteoarthritis

ithout such a history. We have shown older age and

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ime from injury to surgery to be independent predic-ors of osteoarthritis, but no correlation between di-ection of instability and osteoarthritis was found.20

e detected no difference between acute and chronicnstability with regard to the prevalence and gradef cartilage injury. In contrast, Brophy and Marx21

howed that chondral damage was associated withhoulder instability that worsened over time, althoughhe relation has yet to be clearly defined.

Open Bankart reconstructions, as well as nonana-omic reconstructions such as the Bristow, Magnuson-tack, and Putti-Platt procedures, have well-docu-ented associations with degenerative chondral

esions.21-24 In addition to the trauma of the dislo-ations, chondral injury may occur by excessivehear forces from nonanatomic repairs on articularartilage. A single high-impact trauma to the shoul-er may also cause chondral injury.25 In high-en-rgy injuries the subchondral bone is also atisk.26-28 The underlying mechanisms relate to highompressive/shear forces during the impact withisruption of the extracellular matrix and decreasesn chondrocyte metabolism.25

Active patients and athletes are at higher risk forraumatic cartilage lesions.26,27 In overhead athletesost lesions are located near the insertion of the

upraspinatus tendon, superior to the site of a classicill-Sachs lesion. These lesions can be caused by

mpingement between the humeral head and the pos-erosuperior glenoid rim.2 Thus microinstability orhear on the cartilage plays a role in these settings.

Osteonecrosis of the humeral head may result inoth focal and diffuse cartilage lesions of the humeralead. Symptomatic osteonecrosis of the humeral heads not uncommon, second in location only to theemoral head, and it affects patients at younger agesore than other degenerative conditions of the gleno-

umeral joint. Given the diminished weight-bearing

IGURE 1. Right shoulder viewing from posterior. Asterisk, humeith associated labral tear (red arrow). (B) Microfracture of GLAD

C) Early thrombus formation at chondral defect side (blue arrow

ole of the shoulder, however, many cases are notT

etected until advanced stages occur. The articularurface of the humeral head in contact with the gle-oid in midrange levels of motion usually collapsesrst. It is critical to avoid loaded overhead activity toreserve the surrounding cartilage during nonopera-ive or postoperative rehabilitation.

Classification follows a modified Ficat scheme, asescribed by Cruess.29 If detected in early stages,steonecrosis of the humeral head may be surgicallyanaged by core decompression and bone grafting.30

rthroscopic debridement of unstable, focal cartilageaps and lesions has also shown good short-termutcomes at 28 months,20 with significant improve-ent in pain and function in 54 of 61 patients with

rade IV cartilage damage. Other authors have de-cribed good or excellent results in 80% of patients at0 months’ follow-up.31

steochondritis dissecans

OCD is rare in the shoulder and is more commonlyeen in the femoral condyles or the talus. The diseases attributed to fragmentation of the subchondral plateesulting in destabilized chondral flaps and lesions.he precise etiology of OCD remains unclear, but it

ikely results from repetitive microtrauma or isolatedajor trauma.32 Most lesions have been described in

oung male patients in the anterosuperior aspect of theumeral head.32-35

TABLE 2. Predisposing Factors for Early GlenohumeralOsteoarthritis in Chronic Instability

artilage injury with index episode of dislocationlenoid rim impaction fractureill-Sachs lesionge at time of first dislocationecurrent instabilityresence of rotator cuff tear

d. (A) GLAD lesion in right anterior inferior glenoid (blue arrow)(blue arrow, awl) after debridement and labral repair (red arrow).

ral hea

ime period from first dislocation to anterior stabilization

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Treatment options for OCD lesions include debride-ent, removal of loose flaps or bodies, microfracture,

one grafting with or without autologous cartilage im-lants (autologous chondrocyte implantation [ACI]), andransfer of osteochondral plugs.35,36 The optimal ap-roach to surgical management remains controversial.

artilage injury associated with rotator cuff tears

Several studies identify a correlation between rotatoruff pathology and articular cartilage damage in thelenohumeral joint.1,2,35 Focal cartilage lesions haveeen identified in 13% of shoulders in a large series ofull-thickness tears.1 Neer et al.37 described the conceptf rotator cuff arthropathy, which results from the com-ination of massive rotator cuff tears and destructivelenohumeral wear patterns. According to Neer et al., therocess is multifactorial. Both mechanical factors, suchs impingement and instability of the shoulder, and met-bolic considerations, such as malnutrition from inactiv-ty and synovial fluid extravasation in massive rotatoruff tears, have been proposed. Both atrophy and degen-ration of the articular cartilage and osteoporosis of theubchondral bone of the humeral head may result. Aenetic predisposition for increased calcium crystal dep-sition has also been shown to hasten the onset of arthri-is in the setting of massive cuff tears.38

atrogenic injury

Iatrogenic damage to the articular cartilage can beubclassified into chondrolysis (chemical, thermal, id-opathic), infection, and mechanical factors. The de-elopment of glenohumeral chondrolysis after shoul-er arthroscopy is devastating, and some of the moreecent reports in the literature have highlighted somef the potential causes.39 Several case reports havehown extensive glenohumeral chondrolysis aftereemingly routine shoulder arthroscopy, thermal cap-ulorrhaphy, or rotator cuff repairs.40-42 Little hadeen known about the underlying cause of this rare butevastating complication. Ablative thermal energynd intra-articular pain pumps are clearly implicateds causative factors. Thermal ablation in the setting ofittle or no flow may increase arthroscopic fluid tem-eratures above 50°C to 55°C and result in cartilageell death.43 Routine local anesthetics (e.g., bupiva-aine and lidocaine), which have been used for yearss single injections in and around joints, have beenhown to be cytotoxic to chondrocytes in severaltudies.44,45 There are likely to be dose- and time-

ependent effects with these medications, and it is f

urrently our strong recommendation that intra-artic-lar administration through pain pumps be avoided.Postoperative glenohumeral sepsis can also be dev-

stating to articular cartilage. The outcomes of surgeryor septic arthritis are related to timely management,he presence of irreparable rotator cuff tears, and thextent of cartilage loss.46

The risk of cartilage damage due to intra-articularorticosteroid injections remains controversial. Bene-cial results from suppression of local joint inflam-ation are mostly transient. We recommend judicious

nd limited use of intra-articular steroids. Animaltudies have shown that corticosteroids alter tendontructure and weaken collagen, but there are few if anylinical data to support disease progression or chon-ral injury.47

Finally, mechanical factors, such as malpositionedr proud anchors after labral repair or perforatingcrews after osteosynthesis of the humeral head, mayesult in rapid destruction of the chondral surfaces.48

CLINICAL EVALUATION

Symptomatic cartilage lesions rarely appear insolation, and thus concomitant conditions must bearefully and systematically addressed. The clinicalresentation of focal chondral lesions may closelyesemble findings of impingement syndromes.7 Arecise history and clinical examination, especially inoung and active patients, remain pivotal in arriving atn accurate diagnosis.

Focal cartilage lesions should be considered in theetting of

Previous trauma or shoulder surgeryRecent or recurrent shoulder dislocations or sub-luxationsMechanical symptoms (clicking or catching)Discomfort, pain, or interrupted sleepWeakness or loss of range of motion

As part of a comprehensive shoulder examination, theompression-rotation test7 may help in differentiatingetween subacromial impingement and chondral lesions.he patient actively internally and externally rotates therm under axial compression of the glenohumeral joint.ain in the mid ranges of motion has been shown to beoth sensitive and specific for cartilage lesions in thehoulder.7 Subacromial injection can make this test morepecific by eliminating pain provocation from subacro-ial impingement. Crepitation or mechanical symptoms

uring active and passive range of motion may also arise

rom chondral lesions.

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iagnostic tools

Standard radiographs of the shoulder will easilyetect large osteochondral defects of the humeral headr glenoid and show pathologic subluxation or lockedislocations. Specific views such as the Stryker notchr axillary view offer the best visualization of Hill-achs lesions. Computed tomography with 3-dimen-ional reconstruction will detect even subtle osteo-hondral defects. MRI remains the gold standard iniagnosing focal chondral lesions, although sensitivityf standard MRI is affected by the limited cartilagehickness of only 1.0 to 1.3 mm of the humeral head.27

agnetic resonance arthrography has been shown toe significantly more accurate, correctly identifyingartilage defects in over 70% of patients in 1 studyith follow-up arthroscopy.49 New high-field MRI at.0 T, capable of cartilage matrix assessment withuantitative delayed gadolinium-enhanced MRI ofartilage and T2 and T1 rho mapping techniques, mayrove capable of detecting low-grade, partial-thick-ess lesions with unprecedented sensitivity.50,51 Weecommend MRI for preoperative planning, particu-arly in assessing the size and depth of focal lesions.

lassification of cartilage lesions

There are several classification systems for cartilageamage in current use, and most are based on arthro-copic findings. No recognized classification has beeneveloped from standardized MRI alone, and radiol-gists typically use the Outerbridge classification.52

his lacks precision in differentiating between earlyrade I and II changes, and measures of the depth ofrade III lesions are not reliable.The International Cartilage Repair Society (ICRS)

xpanded the classic Outerbridge grading to the ICRSyaline Cartilage Lesion Classification System pub-

ished in 2003, which—though developed for thenee—is now considered the international standard.53

he ICRS classification is based on the arthroscopicvaluation of the depth and expanse of the debridedefect (Table 3). A comprehensive arthroscopic assess-ent of chondral lesions requires debridement of unsta-

le cartilage flaps and the frayed borders of lesions.

NONOPERATIVE TREATMENT

Treatment demands clear communication betweenurgeon and patient. A clear assessment of the pa-ient’s goals, expectations, and activity level shoulde complemented with an honest description of the

trengths and weaknesses of all management options. e

lder patients, averse to surgery or at high operativeisk because of concomitant diseases, may be betteruited to nonoperative treatment that provides painelief and maintains acceptable shoulder function. Inuch cases the surgeon should prescribe and monitorhysical therapy to maintain or improve strength, mo-ion, and function. The judicious use of intra-articularorticosteroid injections and topical or oral nonster-idal anti-inflammatory drugs are mainstays of non-perative treatment, although their true efficacy is un-nown. Glenohumeral viscosupplementation remains offabel for the shoulder but certainly is worth furthertudy.54,55

OPERATIVE TREATMENT

Operative treatment has been classified as pallia-ive, reparative, restorative, and reconstructive.4 Manyactors influence surgical decision making (Fig 2).he patient’s age, activity level, and willingness toomply with postoperative rehabilitation should beonsidered. Other important factors include the sizend depth of the lesion; unipolar versus bipolar, orkissing,” lesions; loss of structural integrity becausef large bone defects; and concomitant injury patterns.

ocal full-thickness articular cartilage lesions

Focal full-thickness articular cartilage lesions of thehoulder are common and may progress to degenera-ive osteoarthritis. Especially in young patients, symp-omatic, focal full-thickness cartilage lesions shoulde treated surgically. Treatment options are as fol-ows:

DebridementMicrofractureAutologous osteochondral transfers (OATS [Osteo-chondral Autograft Transfer System]; Arthrex, Na-ples, FL)ACI/matrix-induced autologous chondrocyte im-plantation (MACI)

ebridement

For small lesions, simple debridement may suffice.ebridement acts to eliminate mechanical symptoms

hat are caused by edge instability and tends to stabi-ize the lesion, preventing delamination. For lesionshat are at the periphery of the glenoid where loadingay be critical or for small lesions, this may be

dequate treatment. When a small GLAD lesion is

ncountered in the setting of a patient undergoing

690 F. ELSER ET AL.

TABLE 3. ICRS and Outerbridge Cartilage Injury Classification

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urgery for instability, 1 option is to simply debridehe unstable articular flap and then advance the labrumnto the defect when performing the labral repair (Fig). This effectively covers the defect and protects thenderlying bone. When diffuse cartilage loss exists,uch as in the setting of osteoarthritis, debridementay be undertaken to stabilize the remaining articular

urface and to eliminate joint irritation and synovitisrom cartilage detritus.

icrofracture

Steadman et al.56 popularized the microfractureechnique in the knee, and we have applied it effec-ively to treat chondral injuries in the shoulder.57 Thereat advantage of microfracture in shoulder surgerys that it can be performed arthroscopically in 1 settingFigs 1 and 3). Key technical points include adequateebridement of the calcified chondral layer (untilunctate bleeding is observed) and proper placementf the awl holes perpendicular to the subchondral platet 2- to 3-mm intervals. Protected loading conditionsnd motion are important for healing.4 Cells prolifer-

IGURE 2. Flowchart of operative treatment for chondral lesionsf humeral head. The asterisk indicates that more data are needed.

IGURE 3. Arthroscopic microfracture humeralead. (A) Awl penetrating subchondral bone. (B)unctual bleeding after microfracture.

te and differentiate into a functional fibrocartilageepair tissue.58,59

In the series reported by Millett et al.57 with 25houlders in 24 patients treated by arthroscopic mi-rofracture, there was significant pain reduction andmproved shoulder function. After a mean follow-upf 47 months, mean pain scores decreased from 3.8 to.6 postoperatively (0, no pain; 10, worst pain) andean American Shoulder and Elbow Surgeons scores

mproved significantly from 60 (range, 22 to 80) pre-peratively to 80 (range, 45 to 100) postoperativelyP � .05). We also found significant improvementsostoperatively (P � .05) in patients’ ability to work,ctivities of daily living, and sports activity. Overall,he greatest improvements were seen in patients whoad microfracture of isolated lesions of the humerus.In the knee microfracture yields comparable results

o other techniques. A randomized trial comparingCI with microfracture in the knee showed no differ-

nces at 5 years’ follow-up,60 whereas another studyhowed comparable clinical outcomes but histologi-ally superior tissue regenerate in the ACI group.61

A prospective study in 5 patients evaluating theombination of microfracture and periosteal flap inocal chondral lesions in the glenohumeral jointhowed a significant improvement in the Constantcore from 43.4 preoperatively to 81.8 and signifi-antly less pain at a mean follow-up of at least 24onths.62

ATS

The results of OATS for high-grade humeral headnd glenoid lesions have been reported in a smalleries of patients.63 The study showed a significantonstant score improvement from 73.9 to 88.7 after aean of 32.6 months, but the development of osteo-

rthritis and the progression of pre-existing osteoar-hritic changes were not altered. Although OATS andCI have been studied extensively in the knee show-

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ng their efficacy,64,65 similar trials are needed to de-ermine the relative success of these techniques in thehoulder.

CI and MACI

ACI in the shoulder has only been reported in aingle case study.66 Outcome studies of full-thicknessartilage defects of the knee treated by ACI showood to excellent results, even at long-term follow-p.67 Many surgeons continue to prefer alternate tech-iques that do not require the staged approach anddditional expense of ACI.

MACI, a collagen bio-scaffold that delivers in vitroultured autologous chondrocytes into the defect, is aore recent innovation.68 Studies on MACI showed

5% hyaline-like cartilage regeneration after 6 monthsnd good to excellent outcomes.69 MACI might showromise for the glenohumeral joint, because it is atable cell-based delivery system that enables the re-eneration of hyaline-like cartilage in a high percent-ge.

arge full-thickness articular cartilage lesions

esions With Significant Bone Loss or Partialumeral Head Necrosis

Large full-thickness articular cartilage lesions andesions with significant bone loss and partial humeralead necrosis can be treated by osteochondral allo-rafts or resurfacing procedures.Osteochondral Allografts: Osteochondral allo-

rafts do not impair the overall results for the patientith donor-site morbidity, and thus there is no limi-

ation to size. However, there are also potential dis-dvantages, such as limited chondrocyte viability, lossf matrix viability as shown by cationic staining,mmunogenicity, and possible disease transmission.70

tudies have shown better outcomes in traumatic os-eochondral lesions and younger patients (�50 years)ith success rates between 75% and 85% at a mean of.8 to 7.5 years’ follow-up.71,72 Rigid fixation of hostone to graft bone is important for long-term allografturvival.70

The use of osteochondral allografts in shoulder sur-ery is not common. Allografts have been used to fillngaging Hill-Sachs lesions,73 as well as defects fromroximal humeral bone tumor resections, with goodesults.74 There is limited experience with the use ofllografts for treatment of OCD of the glenohumeraloint.36 Osteochondral allografts are a promising alter-ative to resurfacing procedures, particularly in young,

thletic patients (Fig 4). t

Joint Resurfacing: Recently, new partial replace-ents and stem-less implants for shoulder arthroplasty

ave been developed that are particularly attractive forse in young patients. These implants preserve anat-my and leave open various options for subsequentevision surgery (Fig 5). In contrast to older prosthe-es, the new implants provide the ability to adjusthem to the cortical rim of the resected humeral headi.e., reconstruction of the humeral offset) and offer aariety of anatomic head sizes.75 Unfortunately, out-omes analyses are still forthcoming.

steoarthritisPalliative Procedures: Palliative procedures, such

s arthroscopic debridement31,76 and arthroscopic cap-ular release, can be performed in cases of osteoar-hritis, especially in younger patients to delay morenvasive surgery. The goals of the procedure are toiminish pain and increase motion, by reducing jointontact pressures and impingement from engagingsteophytes.76,77 At our institution, 27 young patients,ith a minimum 1-year follow-up, have been treatedith a surgical procedure that we have called theAM procedure—an acronym for “comprehensive ar-

hroscopic management” of shoulder arthritis that in-ludes an extensive debridement, capsular release, andumeral osteoplasty (Fig 6). At short-term follow-up,

IGURE 4. Allograft reconstruction of humeral head. (Courtesy ofon J. P. Warner, M.D.)

he mean patient satisfaction rate with the procedure was

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693GLENOHUMERAL JOINT PRESERVATION

igh and averaged 8.5 of 10 points, and only 1 patientas progressed to an arthroplasty (unpublished data, F.E.,.P.H., and P.J.M., October 2009).78 The long-term

urability is still unknown, but this approach does notreclude total shoulder arthroplasty.Resurfacing Procedures: Diffuse, advanced os-

eoarthritic changes of the glenohumeral joint in

IGURE 5. Partial prosthetic head replacementor focal osteoarticular defect of the humeralead from post-traumatic osteonecrosis in aoung patient. (A) The left picture shows a largeocal osteoarticular defect of the humeral head,B) after preparation of the bone bed and inser-ion of the fixation screw; (C) status post implan-ation of the partial humeral head prosthesis; (D)n this coronal section notice how the radius ofurvature has been restored. This is important torevent erosion of the adjacent humeral articularartilage and the articulating glenoid articularurface.

IGURE 6. Comprehensive arthroscopic man-gement (CAM) for glenohumeral osteoarthritis.A) Resection of inferior spur of humeral headarrow). (B) After resection (circle). (1, arthro-cope; 2, shaver.)

ounger, active patients are difficult to manage. Ide-lly, hemiarthroplasty or total shoulder replacementhould be deferred until the patient is older and lessctive to achieve longer durability of the implant andinimize the necessity of future revision surgery. On

he other hand, the results of total shoulder arthro-lasty are substantially better with an intact rotator

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uff and good bone stock of the glenoid. New stem-ess implants for shoulder arthroplasty are promisingptions if palliative procedures fail. Results after con-entional arthroplasty/hemiarthroplasty in youngeratients performed for the treatment of osteoarthritisfter failed surgical stabilization procedures are rela-ively poor.3 Arthroplasty or hemiarthroplasty pro-ided satisfactory pain relief and improved motion,ut these procedures were associated with high ratesf revision surgery because of component failure,ecurrent instability, and pain.3

Biologic Glenoid Resurfacing/Interposition Ar-hroplasty: Alternative approaches to address unipo-ar glenoid arthritis have been proposed. Krishnan etl.79 recently published a prospective study on bio-ogic glenoid resurfacing using anterior capsule (7houlders), autogenous fascia lata (11 shoulders), andchilles tendon allograft (18 shoulders). The early

esults were comparable to the results of total shoulderrthroplasty without the inherent risks of the nonbio-ogical replacements. Achilles tendon allograft hasvolved as a preferred resurfacing material for thelenoid.79 Other authors, however, have not been ableo reproduce these results.

The use of meniscal allografts to resurface the gle-oid in conjunction with hemiarthroplasty has alsoeen proposed. Nicholson et al.80 published a series of0 young patients (mean age, 42 years) using lateraleniscus allograft for glenoid resurfacing during

TABLE 4. Key Points and Current Concepts in TreatingCartilage Lesions in Young, Active Patients

t the center of the humeral head, the hyaline cartilage thicknessis 1.2 to 1.3 mm, thinning at the periphery to 1.0 mm.

hronic instability has been clearly linked to early glenohumeralosteoarthritis.

ctive patients and athletes are at higher risk for traumaticcartilage lesions.

iven the diminished weight-bearing role of the shoulder, manycases of glenohumeral cartilage defects are not detected untiladvanced stages occur.

ntra-articular administration of local anesthetics (bupivacaine,lidocaine) through pain pumps should be avoided because ofthe risk of chondrolysis.

arly treatment of cartilage lesions is recommended in young,active patients to avoid the premature onset of osteoarthritis.

nnovative strategies for the treatment of cartilage lesions suchas ACI/MACI, OATS, and microfracture show excellentpromise, but they must still be established as effectivetechniques in the shoulder.icrofracture has the best evidence for treating focal cartilagelesions in the glenohumeral joint to date. Furthermore, it iscost-effective and can be performed arthroscopically in 1

ssetting.

emiarthroplasty. Their overall results were good,ocumenting significant improvements in outcomecores, but they found a moderate complication rate of7% requiring reoperation. Longer-term data, how-ver, have shown deterioration of the procedure, andhe initial enthusiasm for this technique seems to haveaded somewhat.

Arthroplasty: For older patients with severeymptomatic osteoarthritis, total shoulder arthroplastyemains the gold standard. The number of shouldereplacement surgeries performed in the United Statesoubled from 10,000 to 20,000 per year over the lastecade,81 and it is now estimated to be closer to0,000 per year. There is a clear correlation betweenhe surgeon’s volume and the outcome after surgery.81

ortality rates, rates of postoperative complications,nd inpatient days have been shown to be significantlyigher for operations that are performed by surgeonserforming fewer than 5 procedures per year.81 Theres a role for shoulder replacement surgery in the treat-ent of young, active patients with diffuse cartilage

oss, but given the high rates of revision surgery,on-arthroplasty options should be carefully consid-red and used if appropriate.

CONCLUSIONS

The key points of this article are summarized inable 4. Evolving innovative strategies for the treat-ent of cartilage lesions in the knee joint have been

ollowed by good short- to intermediate-term resultsut are yet to be established as effective techniques forimilar lesions in the shoulder. Investigators mustontinue to evaluate the safety and efficacy of newartilage repair and restorative strategies in the shoul-er. There is a preponderance of evidence to supporthe early treatment of cartilage lesions of the gleno-umeral joint in young, active patients to avoid theremature onset of osteoarthritis. Surgeons shouldaintain a heightened awareness of chondral injuries

n the glenohumeral joint and should be more aggres-ive in early diagnostic and therapeutic interventions.here is growing evidence to support the claim that

he progression of chondral injury may be slowed ifhe time between injury and surgery is minimized inatients with traumatic, recurrent shoulder instability.lthough the next decade is certain to bring excitingew technologies to bear on the treatment of focal andiffuse cartilage injury, successful intervention willtill depend on the sensitive diagnostic skills andound, principled decision making of the shoulder

urgeon.

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