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UNIVERSITY OF WASHINGTON Department of Orthopaedics 1998 … · 2019. 7. 30. · Benirschke, has established the Jerome H. Debs Endowed Professorship in Orthopaedic Traumatology

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Page 1: UNIVERSITY OF WASHINGTON Department of Orthopaedics 1998 … · 2019. 7. 30. · Benirschke, has established the Jerome H. Debs Endowed Professorship in Orthopaedic Traumatology
Page 2: UNIVERSITY OF WASHINGTON Department of Orthopaedics 1998 … · 2019. 7. 30. · Benirschke, has established the Jerome H. Debs Endowed Professorship in Orthopaedic Traumatology

UNIVERSITY OF WASHINGTON

Department of Orthopaedics1998 Research Report

Page 3: UNIVERSITY OF WASHINGTON Department of Orthopaedics 1998 … · 2019. 7. 30. · Benirschke, has established the Jerome H. Debs Endowed Professorship in Orthopaedic Traumatology

Department of OrthopaedicsUniversity of WashingtonSeattle, WA 98195

EDITORS:Frederick A. Matsen III, M.D.Peter Simonian, M.D.Fred WesterbergSusan E. DeBartolo

DESIGN & LAYOUT:Fred Westerberg

Cover Illustration: “The Champion Single Sculls” by Thomas EakinsThe Metropolitan Museum of Art, Purchase,The Alfred N. Punnett Endowment Fund andGeorge D. Pratt Gift, 1934. (34, 92)Photograph (c) 1994 The Metropolitan Museum of Art

UNIVERSITYOF WASHINGTON

SCHOOL OFMEDICINE

Page 4: UNIVERSITY OF WASHINGTON Department of Orthopaedics 1998 … · 2019. 7. 30. · Benirschke, has established the Jerome H. Debs Endowed Professorship in Orthopaedic Traumatology

Contents

Foreword .................................................................................................................................................................... 1

Sports Safety for Women: An Opportunity Whose Time Has Come ..................................................................... 2

Frederick A. Matsen, III, M.D., Peter T. Simonian, M.D., and Carol C. Teitz, M.D.

The Effect of Neck Position on Spinal Canal Occlusion in a Cervical Spine Burst Fracture Model ..................... 4

Randal P. Ching, Ph.D., Nathan A. Watson, B.S., Jarrod W. Carter, B.S., and Allan F. Tencer, Ph.D.

Differential Localization of Collagen Types I, IIA and III in Human Osteoarthritic Cartilage ............................ 7

Yong Zhu, M.D., Howard A. Chansky, M.D., Frederick A. Matsen, III, M.D., and Linda J. Sandell, Ph.D.

Proteolysis of Cartilage Collagens II, IX and XI by Collagenase-3 (MMP-13) ...................................................... 9

Jiann-Jiu Wu, Ph.D., Vera Knauper, Ph.D., Gillian Murphy, Ph.D., and David R. Eyre, Ph.D.

Matrix Metalloproteinase-Mediated Release of Immunoreactive Telopeptides from Cartilage Type II

Collagen ................................................................................................................................................................... 11

Lynne M. Atley, Ph.D., Ping Shao, B.S., Vince Ochs, B.S., Kathy Shaffer, B.S., and David R. Eyre, Ph.D.

Peak Growth Age: A New Maturity Indicator for Idiopathic Scoliosis ................................................................. 13

Kit M. Song, M.D., David G. Little, M.B.B.S., F.R.A.C.S. (Orth), Don Katz, C.O., and John Herring, M.D.

Biomechanical Study of Foot Function .................................................................................................................. 17

Bruce J. Sangeorzan, M.D.

Assessing the Value of a Procedure: A Pilot Study Using Total Shoulder Arthroplasty as an Example .............. 20

Jay L. Crary, M.D., Kevin L. Smith, M.D., and Frederick A. Matsen, III, M.D.

The Simple Knee Test: A Quick and Sensitive Self-Assessment of Knee Function .............................................. 23

Michael H. Metcalf, M.D., Roger V. Larson, M.D., Peter T. Simonian, M.D., and Frederick A. Matsen, III, M.D.

The Response of Cartilage to an Intra-articular Step-Off: A Sheep Weight Bearing Model ............................... 26

Thomas E. Trumble, M.D.

Contact Pressures at Osteochondral Donor Sites in the Knee .............................................................................. 28

Peter T. Simonian, M.D., Thomas L. Wickiewicz, M.D., and Russell F. Warren, M.D.

The Enzymatic Preparation of Allograft Bone ....................................................................................................... 30

David J. Belfie, M.D. and John M. Clark, M.D., Ph.D.

Angulated Screw Placement in the Lateral Condylar Buttress Plate for Supracondylar Femur Fractures ......... 33

Peter T. Simonian, M.D., Greg J. Thomson, Will Emley, Richard M. Harrington, Stephen K. Benirschke, M.D.,and Marc F. Swiontkowski, M.D.

Comminuted and Unstable Iliac Fractures ............................................................................................................ 37

Julie Switzer, M.D., Sean E. Nork, M.D., and M.L. Chip Routt, Jr., M.D.

Early vs Delayed Acetabular Fracture Fixation ...................................................................................................... 39

Oriente DiTano, M.D., William J. Mills, M.D., and M.L. Chip Routt, Jr., M.D.

Page 5: UNIVERSITY OF WASHINGTON Department of Orthopaedics 1998 … · 2019. 7. 30. · Benirschke, has established the Jerome H. Debs Endowed Professorship in Orthopaedic Traumatology

A Biomechanical Comparison of Some Bone-Ligament-Bone Autograft Replacements for the InjuredScapho-Lunate Ligament ........................................................................................................................................ 41

E.J. Harvey, J.B. Knight, Doug P. Hanel, M.D., and Allan F. Tencer, Ph.D.

Early “Simple” Release of Post-Traumatic Elbow Contracture Associated With Heterotopic Ossification ........ 43

Randall W. Viola, M.D. and Doug P. Hanel, M.D.

A Prospective Multicenter Functional Outcome Study of Arthroplasty in Glenohumeral InflammatoryArthritis .................................................................................................................................................................... 44

David N. Collins, M.D., Doug T. Harryman, II, M.D. and Michael T. Wirth, M.D,

Department of Orthopaedics Faculty .................................................................................................................... 46

Incoming Faculty ..................................................................................................................................................... 47

Graduating Residents .............................................................................................................................................. 49

Incoming Residents ................................................................................................................................................. 50

Contributors to Departmental Research and Education ....................................................................................... 51

National Research Grants ........................................................................................................................................ 53

Page 6: UNIVERSITY OF WASHINGTON Department of Orthopaedics 1998 … · 2019. 7. 30. · Benirschke, has established the Jerome H. Debs Endowed Professorship in Orthopaedic Traumatology

1998 ORTHOPAEDIC RESEARCH REPORT 1

Foreword

The cover of this year’s researchreport, “The Champion SingleSculls” is a 1871 oil on canvas

which hangs in the MetropolitanMuseum of Art. Its painter, ThomasEakins (1844-1916), is one of America’smost distinguished artists. Althoughthis painting celebrates a race held onPhiladelphia’s Schuylkill River, thesetting is very reminiscent of theMontlake Cut, the scene of many UWcrew victories. We selected this cover inhonor of the many Husky studentathletes whom we have had the chanceto serve this year and also of our newDean, Paul Ramsey, who himself isfrequently found rowing his single scullon the Cut.

This has been an important year forthe Department of Orthopaedics. Twoof our senior faculty have gone on toassume prestigious positions at otherschools of medicine. MarcSwiontkowski is now the Chair ofOrthopaedics at the University ofMinnesota. Linda Sandell now holds anendowed professorship at WashingtonUniversity in St. Louis. We wish themboth our very best as they assume theirnew leadership positions.

We have successfully recruited fiveexciting new regular faculty memberswho will assume their new roles thissummer. Bill Mills, a former UWresident, and Sean Nork, currently atraumatology fellow, will join thefaculty based at Harborview. JohnO’Kane, our first primary care sportsmedicine fellow will join our SportsMedicine team. Mohammad Diab willjoin the Pediatric Orthopaedic groupafter his fellowship in Boston. Finally,Randy Ching will become a member ofthe core faculty at the BiomechanicsLab.

The excellence of the faculty hasagain been recognized by theDepartment’s inclusion in the top tenOrthopaedic services in the UnitedStates by US News and World Report andby our ranking in the top fiveOrthopaedic Departments in terms ofgrant support from the NationalInstitutes of Health. The AmericanAcademy of Orthopaedic Surgeons andits affiliated specialty organizationsselected over 50 presentations byDepartmental faculty and residents at

the annual meeting in New Orleans.Fully as important is the ranking we aregiven by medical students applying forOrthopaedic training: this year weagain matched with five sensationalnew residents: Tim DuMontier, ScottHacker, Tim Rapp, Bill Sims, and CarlaSmith, who are profiled later in thisreport.

This year also saw a most specialgesture of appreciation by one of ourpatients who, in recognition of theoutstanding care rendered him by SteveBenirschke, has established the JeromeH. Debs Endowed Professorship inOrthopaedic Traumatology. The two X-rays on this page show the type ofreconstruction that Dr. Benirschke haspioneered. The upper film shows asevere fracture dislocation involving thesubtalar joint. The second film showsan anatomic reconstruction. TheRegents of the University ofWashington have just approved Steve’sappointment to this Professorship. Thisgenerous philanthropy will assure thatSteve’s academic efforts are wellsupported and that traumatologyresearch will be forever secure in ourDepartment.

This year’s Research Report displaysonly a sample of the breadth and depthof Departmental research. From themost basic biochemical,immunohistological, biomechanicaland biological research to newdirections of clinical research, includingan attempt to assess the value ofOrthopaedic interventions, our facultyand residents strive to betterunderstand and better treat theconditions which compromise ourpatients’ comfort and function. Wehope you enjoy this brief tour and wewelcome your thoughts, suggestionsand support.

If you’d like to learn more about theUniversity of Washington Departmentof Orthopaedics, please visit ourinternet address at http://www.orthop.washington.edu/ or dropus an Email message at [email protected] or [email protected].

We would like to conclude with ahearty thanks to all the friends, staff,faculty, residents and students who

make the Department of Orthopaedicswhat it has become today. Countlessacts of service and generosity by youenable the team to achieve at the highestlevel as we pursue our missions ofresearch, education and patient care.

Best wishes,

Frederick A. Matsen III, M.D. Chairman

Peter Simonian, M.D.Associate Professor,

Sports Medicine

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2 1998 ORTHOPAEDIC RESEARCH REPORT

Difficult beginnings. In 1896,when the first modernOlympic games were held in

Athens, the only female participant wasan unofficial marathoner namedMelpomene. Despite attempts byofficials to physically remove her fromthe course, Melpomene completed the40 km race in 4.5 hours, faster thanmany men. By 1928, more Olympianswere women, but when severalcollapsed from heat exhaustion at theend of an 800-meter race, theInternational Olympic committeeplaced a ban on women competing inraces longer than 200 meters—a banthat lasted for 32 years! In the UnitedStates the progress women have madein the athletic arena has been slow andanything but steady, both inparticipation and in funding. It was notuntil 1973, in fact, when golfer TerryWilliams signed on at the University ofMiami that a woman athlete received afull-tuition athletic scholarship.

Women are becoming better athletes,but getting hurt more often. Each yearmore women of all ages participate inorganized sports and vigorous physicalrecreation. Each year the level ofcompetition among women athletesgets higher: faster running, cycling andskiing times, more three pointers andslam dunks in basketball, and moredifficult dives, vaults, skating and rockclimbing maneuvers. Unfortunately,one fact remains the same: womenathletes have more injuries than theirmale counterparts. For example,women high school cross countryrunners have the highest injury rate ofany group of sports participants, maleor female. Knee problems, shin splintsand stress fractures have not only endedmany promising careers, but have alsotaken away the joy of participation frommany more middle of the pack runners.It is not known if this greaterpredilection to injury is a result ofdifferences in anatomy, running style,diet, strength, or shoe design. It is clearthat the answers will only be found inthe study of the woman runner, ratherthan continuing to apply knowledgegained from research on men to the

challenges faced by women.The ACL Enigma.Perhaps no gender

difference is more important and moreperplexing than the repeatedobservation that women basketballplayers have anterior cruciate ligament(ACL) tears at many times the rate oftheir male counterparts (Figures 1, 2,3). In a recent study of almost 12,000varsity basketball players, high schoolwomen were found to be at three timesthe risk of men, while in at the collegiatelevel, the risk for women was six timesthat of men for this season endinginjury! ACL injuries account for 25%of all female basketball-related injuries.In football ACL injuries occur fromheavy physical contact. However inwomen’s basketball, 96% of theseinjuries happen without contact withanother player, usually during a pivot,a sudden stop or in landing a jump.

The reasons for the disparity ininjury rates between the genders areunknown; however a number oftheories have been suggested.

Slower neuromuscular response:Some propose that women tend tobecome interested in sports at a laterage than men, and as a result have had

fewer years to develop their agility.Diminished strength: Others

propose that women have a lowerstrength-to-mass ratio than men, givingthem less ability to control pivots,sudden stops or awkward landings fromjumps. Decreased quadriceps andhamstring strength can increase the riskof knee injury; average quadricepsstrength in females is known to be 60%that of males.

Different anatomy: Still otherspropose that the disparity results fromanatomical differences. For example,women have more of a valgus (knock-kneed) alignment of their lowerextremities than men (who are morebow-legged as a rule). Landing on sucha limb is more likely to cause it to buckleto the inside, tearing the medialcollateral ligament and the anteriorcruciate ligament. The valgus limb isalso associated with an increased “Q-angle” which may make the quadricepsless effective in controlling the landing.Radiographic studies have shown thatwomen tend to have narrowerintercondylar notches than men, a factwhich could cause the rim of the notchto stress the ligament in

Sports Safety for Women:An Opportunity Whose Time Has ComeFREDERICK A. MATSEN, III, M.D., PETER T. SIMONIAN, M.D., AND CAROL C. TEITZ, M.D.

Figure 1: Intact ACL Being Probed

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1998 ORTHOPAEDIC RESEARCH REPORT 3

hyperextension. The narrower notch inwomen may also reflect a smaller-sizedanterior cruciate ligament less able toresist injuring forces.

Joint laxity: Loose or hypermobileknees are at higher risk for ACL tears.The increased joint laxity of womenmay enable the knee to be stretchedaway from a stable configuration to onewhere the ligaments are at greater risk.Estrogen influences connective tissue

metabolism and can cause an elevationof endogenous relaxin which increasessoft tissue laxity. Recent evidencesuggests that during the luteal phase ofthe menstrual cycle the laxity may beat its peak; furthermore birth controlpills prolong the luteal phase increasingthe time of increased laxity. Currentresearch is attempting to correlate thetiming of ACL injuries with phases ofthe menstrual cycle and with the use ofbirth control pills.

Time for action. While these theoriesare of interest, they have failed tosuggest strategies for making basketball,skiing, soccer and running safer forwomen. The fact that women athletesdiffer from men has been established;it has finally been recognized thatlessons learned from studying mencannot be generalized; it is time to focuson approaches for injury preventionwhich are specific to women.Unfortunately, due to the greatereconomic interest in men’s sports, it isrelatively more difficult to fund aresearch program to benefit the womanathlete. Recognizing these challenges,the UW Sports Medicine and FitnessTeam has dedicated itself to the pursuitof the resources and the knowledgewhich will lead to safer recreation andcompetition for women of all ages.

RECOMMENDED READING

Gray, J., Tontine, J., McKenzie, D., andet al.:: A survey of injuries to theanterior cruciate ligament of the kneein female basketball players. Int J SportsMed, 6: 314-316, 1985.

Houseworth, S., Mauro, V., Mellon, B.,and et al..: The intercondyar notch inacute tears of the anterior cruciateligament: A computer graphics study.Am J Sports Med, 15: 221, 1987.

Malone, T., Hardaker, W., WE, G., andet al..: Relationship of gender toanterior cruciate ligament injuries inintercollegiate basketball players. J SoOrthop Assoc, In Press: 1993.

Nordgren, B.: Anthropometricmeasures and muscle strength in youngwomen. J Rehabil Med, 4: 165, 1972.

Powers, J.: Characteristic features ofinjuries in the knee in women. ClinOrthop, 143: 120-124, 1979.

Tipton, C., Matthes, R., and Martin, R.:Influence of age and sex on the strengthof bone-ligament junctions in kneejoints of rats. J Bone Joint Surg, 60A:230-234, 1978.

Arendt E, Dick R: Knee injury patternsamong men and women in collegiatebasketball and soccer: NCAA data andreview of literature. Am J Sports Med;23:694-701, 1995.

Figure 3: ACL Reconstructed with Tendon Graft

Figure 2: Probe Behind Torn ACL

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4 1998 ORTHOPAEDIC RESEARCH REPORT

A significant number ofneurological injuries arethought to occur or to be

aggravated during emergencyextrication, transport and evaluation ofpatients with spinal injury. In 1980,Cloward reported that, of the patientswith fatal injuries treated at theEdinburgh Royal Infirmary, 25% of thefatal complications were related toevents occurring between the time ofthe accident and that of arrival of thepatient to the emergency room. Asubsequent study by Schriger andassociates examined the ability ofemergency medical personnel toimmobilize the cervical spine of studysubjects in neutral position — thecommonly advocated positionfollowing spinal injury. They reportedthe lack of an accepted standard fordefining neutral position, andconcluded that immobilization on a flatwooden backboard would have placed98% of their subjects into relativecervical extension. Biomechanicalstudies have shown that the spinedisplays a “neutral zone” rather than asingle neutral position, as is true for

many other joints of the body. Hence,because neutral position can neither beprecisely defined nor maintained,positioning of a patient lacksconsistency and is thereforepredisposed to variability. Perhaps, amore effective approach would be toidentify —and avoid— those spinalpositions that could potentially inducefurther harm to the spinal cord byincreasing canal encroachment orocclusion. Additionally, those positionsthat reduce post-injury canal occlusioncould be advised and pursued.

In the interest of preventing furtherinjury during the management ofpatients with cervical spine injury, thisbiomechanical study was conducted atthe Orthopaedic BiomechanicsLaboratory to examine the effects ofneck position on canal occlusion(stenosis). Although previous studieshave documented the effects of flexion-extension orientation on canalocclusion in intact (non-injured)specimens, none have explored thisrelationship using an injury model, orin other cervical orientations (e.g.,lateral bending). A burst fracture

model was chosen because of thesignificant degree of spinal canalinvolvement typically associated withthis fracture pattern. In addition,Fontijne and associates, reported thatincreased spinal canal stenosis wascorrelated with an increased probabilityof neurological deficit in patients withthoracolumbar burst fractures.Therefore, this study enabled theinvestigation of whether neck positionhad a significant effect on canalocclusion —with potential neurologicconsequences.

MATERIALS AND METHODS

Specimen PreparationEight fresh human-cadaver, cervical

spine specimens (levels C1 to T3) wereobtained for this study through theWilled-Body Program of the Universityof Washington Department ofBiological Structure. The specimenswere prepared by removing the softtissues while leaving theosteoligamentous structures intact.Spinal levels C1-C2 and T1-T3 of eachspecimen were potted in dental plasterproviding rigid attachments to facilitatetesting. Burst fractures were createdusing a drop-weight protocol thatinvolved the release of a 4.5 Kg guidedweight from a drop-height of 1.5meters. Post-injury radiographs andcomputed tomography (CT) scansdocumented the location and severityof the burst fractures (see Figure 1 foran example).

InstrumentationSpinal canal occlusion was

measured using a custom spinalocclusion transducer system developedin our lab. This transducer consistedof a fluid-flow system (Figure 2) inwhich water was circulated through asection of highly flexible, peristaltictubing that was passed through thespinal canal —replacing the cord. Anyimpingement on the tubing produceda rise in fluid pressure that wasmonitored by an upstream pressuretransducer. To quantify canal

The Effect of Neck Position on Spinal Canal Occlusion in aCervical Spine Burst Fracture ModelRANDAL P. CHING, PH.D., NATHAN A.WATSON, B.S., JARROD W. CARTER, B.S.,AND ALLAN F. TENCER, PH.D.

Figure 1: CT image of a burst-fracture specimen.

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1998 ORTHOPAEDIC RESEARCH REPORT 5

occlusion, the relationship betweentubing diameter and pressure wasestablished through calibration.

Angular motions across the level ofinjury were recorded using anelectromagnetic three-dimensionaltracking system (Polhemus 3-SpaceFastrak System, Kaiser Aerospace andElectronics Company, Colchester, VT).Motion sensors were attached to pinsinserted into the vertebrae immediatelyabove and below the injury site. Anacrylic loading frame was used toposition the specimens withoutinterfering with the electromagneticmotion sensors.

Experimental ProcedureEach specimen was tested in eight

directions of bending including:flexion, extension, right- and left-lateralbending, and four intermediate (45°)positions. To describe the multi-axisbending applied to each specimen, aclock-face orientation was adopted inwhich flexion corresponded to the12:00 o’clock position, while rightlateral bending corresponded with 3:00o’clock. In this study, neutral positionwas defined as the most central positionof the spine aligned within the neutralzone while preserving a normal lordoticcurvature. The first occlusionmeasurement recorded for eachspecimen was with the spine placed inneutral position. This provided abaseline measurement of the residualcanal occlusion resulting from injuryand served as the basis for statisticalcomparison against all other spinalpositions.

Two occlusion measurements weretaken in each direction of bending, oneat the onset of ligament tensioning (i.e.,the neutral-zone [NZ] boundary), andthe second at full range of motion(ROM). The neutral-zone-boundarypositions were established by loading(bending) the specimen twice to its fullrange of motion before allowing it toreturn to an equilibrium position. Thefull range-of-motion positions wereproduced by fully tensioning the spinalligaments while being careful not toinduce further damage to the specimen.Positioning of the specimens wasperformed manually with a randompositioning order used for eachspecimen. In addition to bending,measurements were also taken whileapplying axial torsion (both clockwiseand counter-clockwise), tension

(traction) and compression to thespine.

Data AnalysisThe occlusion data was expressed as

a percentage reduction from intactcanal midsagittal diameter. Paired t-tests were used to compare the canalocclusion measurements taken at eachspinal position against measurementstaken at the neutral position.Significance was established based on

a computed p-value of less than 0.05.

RESULTS

A contour plot (Figure 3) wasprepared showing the relationshipbetween canal occlusion and neckposition in different directions ofbending. This plot uses a clock-faceorientation to describe the bendingdirections and displays an increasingpercentage of canal occlusion as agrayscale gradient. The average canal

Pump

Tank

PressureTransducer

PolhemusTransmitter

PottingPolhemus Sensors Attached to Spine

Acrylic Frame

Flow

TygonTubing

LeftBending

0

10

20

30

40

50

Flexion

Extension

RightBending

12:00

1:30

3:009:00

10:30

6:00

7:30 4:30

ROMNZ Boundary Percent Canal

Occlusion

Neutral Position

[13.7° + 6.1][7.7° + 2.9]

Figure 2: Schematic diagram of the experimental apparatus showing the spinal canal occlusion transducerand sensors for measuring spinal angulation.

Figure 3: This contour map helps to visualize the relationship between canal occlusion and neckposition at the neutral-zone boundary (NZ) and at full range of motion (ROM). Darker shadingindicates a greater percentage of occlusion.

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6 1998 ORTHOPAEDIC RESEARCH REPORT

occlusion in neutral position was 23%± 20 which corresponded to thebaseline (residual), burst-fracture canalencroachment. Significant increases inocclusion, from neutral position, werefound particularly in extension and inlateral bending combined withextension (i.e., 4:30 and 7:30orientations). For example, at full rangeof motion, the average measuredocclusion in extension increased to 42%± 20 (p = 0.01). Similar increases wereobserved at the 4:30 position (38% ±21, p = 0.04), and at the 7:30 position(39% ± 20, p = 0.02). There was a trendtowards reduced (decreased) canalocclusion for flexion (14% ± 22),however, not at a statistically significantlevel. Figure 4 documents the effect ofaxial torsion, tension (traction) andcompression on canal occlusion.Traction demonstrated no appreciableeffect on occlusion, however occlusionincreased significantly in compression(35% ± 18, p = 0.02). In summary, wefound that compression, extension, andlateral bending combined withextension significantly increased canalocclusion for all eight specimens tested.

DISCUSSION

The objectives for this study wereachieved by documenting the effect ofneck position on canal geometry in aburst fracture model, and subsequentlytesting the hypothesis that differentpositions may affect (by increasing or

decreasing) canal occlusion. Ourfindings indicate that for burstfractures, positioning the spine intoextension increased canal occlusionconsiderably. At full range of motionin extension, the residual (baseline)canal occlusion increased from 23%(the average occlusion in neutralposition) to 42%, an increase of 19%.Similarly, axial compression resulted ina statistically significant, 12% increasein measured canal occlusion (from 23%to 35%). Although none of the testedneck positions yielded statisticallysignificant decreases in canal occlusion,a trend was observed for specimensplaced into flexion (i.e., the averagecanal occlusion decreased from 23% to14% in flexion). These responses wereobserved in all eight of the spinespecimens tested. Other spinalpositions did not appear to eitherpositively or negatively affect canalocclusion. Therefore, the results of thisstudy suggest that for a patient with acervical spine burst fracture,positioning the neck into eitherextension or compression maysignificantly increase canal occlusionand potentially exacerbate a spinal cordinjury.

RECOMMENDED READING

Cloward RB. Acute cervical spineinjuries. Clinical Symposia 1980;32(1):1-32.

Schriger DL, Larmon B, LeGassick T,Blinman T. Spinal immobilization ona flat backboard: Does it result inneutral position of the cervical spine?Ann Emerg Med 1991; 20(8):878-881.

Fontijne WP, de-Klerk LW, BraakmanR, Stijnen T, Tanghe HL, Steenbeek R,van-Linge B. CT scan prediction ofneurological deficit in thoracolumbarburst fractures. J Bone Joint Surg 1992;74B(5):683-685.

Ching RP, Watson NA, Carter JW,Tencer AF. The effect of post-injuryspinal position on canal occlusion in acervical spine burst fracture model.Spine 1997, 22(15): 1710-1715.

CW CCW Traction Compression0

20

40

60

80

Per

cent

Can

al O

cclu

sion

Orientation

p < 0.05

100

Figure 4: Mean and standard deviations for canal occlusion associated with rotation (both clockwise(CW) and counterclockwise (CCW)), tension (traction), and compression.

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1998 ORTHOPAEDIC RESEARCH REPORT 7

P ain and disability caused bydegenerative damage to articularcartilage affect millions of

people in the United States. Sincearticular cartilage has little, if anynatural capacity to heal with hyalinecartilage, most current treatments relyon symptomatic care until the patientis considered old enough to receive aprosthetic joint replacement. Bothsymptomatic care and jointreplacement are fraught with sideeffects and are ultimately temporarysolutions. Both can be expensive andneither allow a patient to return tophysically demanding jobs. Centersthroughout the world are developingtechniques to repair or regeneratecartilage in defects. Much publicity andexcitement over the most recent ofthese techniques applied to humans hasbeen tempered as clinical results havenot lived up to expectations. Basicscientific knowledge of the response ofcartilage to injury is incomplete and thedevelopment of successful clinicaltechniques is unlikely without thisknowledge.

Articular cartilage contains a uniqueassortment of the major and minorcollagens in addition to proteoglycansand other less abundant matrixmolecules. Little is known about theability of chondrocytes in vivo toregenerate a functional extracellularmatrix. A major question is whetherchondrocytes “activated” in the earlystages of osteoarthritis (OA) cansynthesize an extracellular matrix(ECM) that is functionally similar tothe cartilage articular surface producedduring development. Very few studieshave been directed toward themolecular aspects of normaldevelopmental and repair processes ofjoints. Consequently, it is impossibleto determine why the attempts at repairseen in OA are inadequate to regeneratenormal hyaline cartilage.

It has been known for many yearsthat the metabolic activity of articularchondrocytes increases inosteoarthritis, although the significanceof these changes is poorly understood.The degradation and loss of the

extracellular matrix components ofosteoarthritic cartilage areaccompanied by increased synthesis oftypes II and III collagen. The newlysynthesized type II collagen mayrepresent an incomplete repairresponse by chondrocytes embedded indegenerating matrix. In addition it hasrecently been shown that certaincollagens are markers of specific stagesof cartilage development. For example,type IIA procollagen is a marker ofdeveloping cartilage whereas type IIBcollagen is synthesized only by maturechondrocytes. As developmentproceeds the predominant collagenbecomes type IIB collagen and the typeIIA procollagen is removed.

To investigate the possibility thatchondrocytes in osteoarthritic cartilagemay revert to a “younger” phenotypeto facilitate repair of diseased matrix,we used immunohistochemistry toanalyze the synthesis and distributionof type IIA procollagenNH2-propeptide, type II collagen triplehelix, type II collagenCOOH-propeptide and types I and IIIcollagens in osteoarthritic cartilage.

METHODS

Immunohistochemistry is atechnique that takes advantage of thehumoral immune system’s ability togenerate antibodies against specificmolecules, or portions of molecules.Antibodies can be generated byinjecting animals with specific proteinsof interest. In this study, the proteinsof interest were various collagens andcollagen subunits. To visualize theprimary antibody-antigen (protein)combination, a standard secondaryantibody is attached to the primaryantibody and then a chromogen, orfluorescing molecule, is chemicallyattached to the secondary antibody.The exquisite specificity of thesereactions allow the in vitro detection ofproteins of interest in paraffin-embedded histologic specimens. Whena different chromogen is used for eachantibody, confocal microscopy canreveal the relative distributions of eachprotein in a single histological section.

We studied 29 samples from 11 patientswith advanced osteoarthiritsundergoing total shoulder (4), knee (3)or hip (4) replacement. Toimmunolocalize the collagens ofinterest, five antibodies were raisedagainst collagen type I, type IIAprocollagen NH-2 propeptide, type IIcollagen triple helix, type II collagenCOOH-propeptide, and type IIIcollagen. Confocal microscopy wasused to assess the intensity anddistribution of staining of the 5molecules of interest.

RESULTS

There was no significant staining fortype I collagen in osteoarthriticcartilage. All 11 cases stained stronglyfor type III collagen and stained tovarying degrees for type IIAprocollagen NH-2-propeptide. TypeIIA procollagen was mainly localizedwithin the pericellular matrix ofchondrocytes undergoing cloning inthe middle and deep zones of theosteoarthritic cartilage. Type IIAprocollagen was also found in 2 of 2osteophytes which were studied.Interestingly, the staining for type IIAprocollagen was more intense in thecartilage removed from the shoulderand in non-weightbearing regions ofthe hip and knee than in that removedfrom weightbearing areas of the kneeor the hip. Type III collagen was foundthroughout the fibrillated matrix in all29 specimens. Type III collagen wasfound diffusely within the superficialand middle zones of the cartilage butwithin the deep zone it was localized tothe territorial matrix. The mature typeII collagen triple helix was foundthroughout the cartilage matrix withpeak levels found in the vicinity ofchondrocytes. The type II carboxy-propeptide was only found within thecytoplasm of chondrocytes. Confocalimaging revealed that type IIA NH-2propeptide and type II collagen triplehelix were co-localized in thepericellular matrix within the lacunae.Appropriate positive and negativecontrol tissues and antibodies wereutilized.

Differential Localization of Collagen Types I, IIA and III inHuman Osteoarthritic CartilageYONG ZHU, M.D., HOWARD A. CHANSKY, M.D., FREDERICK A. MATSEN, III, M.D.,AND LINDA J. SANDELL, PH.D.

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8 1998 ORTHOPAEDIC RESEARCH REPORT

DISCUSSION

These results demonstrate thatchondrocytes from osteoarthriticcartilage synthesize significant amountsof type IIA procollagen, a type ofcollagen which is normally found onlyin developing cartilage. This isconsistent with the hypothesis thatchondrocytes from diseased cartilagemay “dedifferentiate” in an attempt torecapitulate the developmentalpathways that result in the formationof articular cartilage. The absence oftype I collagen indicates that thesephenotypic changes are not thosewhich are commonly seen during the“dedifferentiation” of chondrocytesgrown in vitro. It is plausible that thephenotypic changes documented inthis study reflect an aborted attempt bychondrocytes within damaged matrixto generate a healing response. Thetype IIA procollagen generated by thesechondrocytes remains confined to thepericellular matrix as opposed to thesituation that exists duringdevelopment when the type IIAprocollagen is deposited throughoutthe matrix. The local pericellularenvironment of damaged matrix maycontain inhibitory factors, or may bemissing stimulatory factors, which areneeded to sustain the repair response.The local mechanical environment mayexplain why chondrocytes from theshoulder are able to synthesize greaterquantities of type IIA collagen thanthose in weight-bearing joints such asthe hip and knee.

Unlike many, if not most tissues,articular cartilage lacks the intrinsiccapacity to heal with like-tissue. Basedupon many studies it appears that thenatural response of a chondrocyte todamage of surrounding matrix is tosynthesize new matrix with a structureor ultrastructure different from that ofhealthy adult cartilage. The findings ofthis study suggest that the repair tissueassumes a phenotype resembling thatof developing cartilage. This abnormalmatrix is not able to withstand thenormal stresses placed upon thearticular surface and is unable to beincorporated into the surroundingmatrix, and thus eventually fails. Beforescientists and surgeons can developeffective techinques to restore damagedhyaline cartilage we must understandthe normal response of joints todamage. This study is one step towardunderstanding these processes. In the

future it may become possible tomanipulate these native responses toour advantage with various cytokines,growth factors or genes.

RECOMMENDED READING

Aigner T, Gluckert K, von-der-MarkK: Activation of fibrillar collagensynthesis and phenotypic modulationof chondrocytes in early humanosteoarthritic cartilage lesions.Osteoarthritis-Cartilage. 5(3):183-9,1993

Sandell, L.J., Morris, N., Robbins, J.R.and Goldring, M.R.: Alternativelyspliced type II procollagen mRNAsdefine distinct populations of cellsduring vertebral development:differential expression of the amino-propeptide. J. Cell Biol. 114: 1307-1319,1991.

Aydelotte, M.B. and Kuettner, K.E.:Heterogeneity of ArticularChondrocytes and Cartilage Matrix. In:Joint Cartilage Degradation: Basic andClinical Aspects, J. Frederick Woessner,Jr., and David S. Howell, eds., MarcelDekker, Inc., New York., 37-66, 1993.

Gerich TG, Fu FH, Robbins PD, EvansCH: Prospects for gene therapy insports medicine. Knee Surg SportsTraumatol Arthrosc 4(3):80-7, 1996.

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1998 ORTHOPAEDIC RESEARCH REPORT 9

Collagenase-3 (MMP-13) is oneof the more recently identifiedhuman matrix

metalloproteinases. First found inbreast carcinomas (1), collagenase-3 isalso produced by chondrocytes inhuman osteoarthritic cartilage.Collagenase-3 produced bychondrocytes is believed to be a keyenzyme in the degradation of cartilagein osteoarthritis.

The collagenous framework ofcartilage consists of cross-linkedcopolymers of types II, IX and XIcollagens. In this study we haveinvestigated the ability of recombinantcollagenase-3 to degrade anddepolymerize these three collagentypes.

MATERIALS AND METHODS

Human recombinant

procollagenase-3 was expressed intransfected NSO mouse myeloma cellsand purified from conditioned cellculture medium (2). The proenzymewas activated by p-aminophenylmercuric acetate.

Slices of fetal bovine epiphysealcartilage were extracted at 4°C in 1MNaCl, 0.05M Tris-HCl, pH 7.5 for 24hr then in 4M GuHCl for 24 h toremove non-cross-linked proteins andproteoglycans. The washed residueswere minced and digested with pepsinand salt fractionated into types II, IXand XI collagens. From the 1M NaClextract, newly made intact types II, IXand XI collagen molecules werepurified (4).

Each collagen substrate wasdissolved at 2mg/ml in 0.5M acetic acidand dialyzed against 0.2 M NaCl, 50mMTris-HCl, 10mM CaCl

2, 0.05% Brij 35,

pH 7.5. Aliquots of each were incubatedwith activated collagenase-3 (substrate/enzyme=200:1, w/w) at 30°C for 24 h.The digests were analyzed by SDS-7.5%PAGE. Protein bands were transblottedto PVDF membrane and identified byamino-terminal microsequencing.

RESULTS AND DISCUSSION

Similar to collagenase-1,collagenase-3 degrades type II collageninto 3/4 and 1/4 fragments, and has noactivity against triple-helical domainsof type XI collagen. However,collagenase-3 was more active thancollagenase-1 in degrading native typeII collagen. Amino-terminal sequenceanalysis identified cleavage sitesbetween bonds at Gly 778-Gln 779 andGly 781-Ile 782 which are three and sixresidues C-terminal to the collagenase-1 cleavage site, respectively. Cleavage at

Proteolysis of Cartilage Collagens II, IX and XI by Collagenase-3(MMP-13)JIANN-JIU WU, PH.D., VERA KNÄUPER, PH.D.*, GILLIAN MURPHY, PH.D.*, AND DAVID R. EYRE, PH.D.

3/4 1/4N C

GLAGQRGIVGLP*

Collagenase-3

AFAGLGPREKGPDPLQYMRA

Collagenase -3

Cross-link

QMAGGFDEKAGGAQMGVMQ

Collagenase-3

Cross-link

Stromelysin

Collagenase-1

775

Figure 1: Molecular model summarizing sites of collagenase-3 cleavage in type II collagen

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10 1998 ORTHOPAEDIC RESEARCH REPORT

the Gly 775-Leu 776 bond (collagenase-1 site) could only be identified insamples incubated with enzyme undermilder conditions (i.e. 22°C not 30°Cfor 6 hr). Sequence analysis of the 3/4fragment produced from salt-soluble,intact type II collagen showed a limitedcleavage of the N-telopeptide domain,but only exterior (i.e. N-terminal) tothe cross-linking lysine residue.Similarly, digestion of syntheticpeptides matching the type II C-telopeptide showed no cleavage interiorto the cross-linking lysine (Figure 1).

When incubated with intact typesIX and XI collagens, collagenase-3trimmed the N-propeptide extensionsfrom all three chains of intact type XIcollagen. It also shortened the a1(IX)chain, consistent with the removal ofthe NC4 domain. However, unlikestromelysin (3) collagenase did not cutthe type IX collagen molecule in itsNC2 domain. This may be importantin understanding the role ofstromelysin in cartilage matrixdegradation under conditions whencollagenases are not expressed.

SUMMARY

Collagenase-3 rapidly cleaves typeII collagen at the Gly-Leu bond ascleaved by collagenase-1. The resulting1/4 fragments are further cleaved bycollagenase-3 removing three or sixmore amino acids from the aminoterminus. Although some cleavage ofthe type II collagen telopeptide domaincan occur, this action exterior to thecross-links has no depolymerizingpotential. Therefore, after the initialattack of collagenase 3 on the triple-helix, other metalloproteases (e.g.gelatinase) are probably important incompleting the process ofdepolymerization. The action ofstromelysin in cleaving in the interiorof type IX collagen may bephysiologically important in mediatingcollagen network swelling in theabsence of collagenase(s).

RECOMMENDED READING

Freije, J.P.M. et al. Molecular cloningand expression of collagenase-3, anovelhuman matrix metalloproteinaseproduced by breast carcinomas. J. Biol.Chem. 269:16766-16773, 1994.

Knauper, V. et al. Biochemicalcharacterization of human collagenase-3.J Biol Chem 271:1544-1550, 1996.

Wu, J.J. et al. Sites of stromelysincleavage in collagen types II, IX, X andXI of cartilage. J. Biol. Chem. 266:5625-5628, 1991.

This work was supported by NIHgrants AR 36794 and AR 37318.

*Dept. of Cell and MolecularBiology, Strangeways ResearchLaboratory, Cambridge, UK

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1998 ORTHOPAEDIC RESEARCH REPORT 11

Proteolytic degradation of thecollagenous matrix of cartilagecan lead to loss of tissue and

impaired joint function. The full rangeof proteinases involved in thedegradative process and their preciseroles are poorly understood, thoughmatrix metalloproteinases (MMPs) arestrongly implicated (1). MMPs areover-expressed in the joint tissues andsynovial fluid of patients with arthritis(2, 3). In a recent study, MMP activitywas correlated with type II collagendegradation in articular cartilagecultures that had been stimulated withinterleukin-1a (4).

The aim of this study was toevaluate whether an immunoassaybased on a monoclonal antibody(mAb) 2B4, which recognizes a domainof the a1(II) C-telopeptide EKGPDP(5), measures MMP cleavage productsof cartilage. This 6-amino-acid corepeptide was identified in cross-linkedform in urine where it appears to be aprotease-resistant end product of typeII collagen fibril degradation.Immunoassays that quantitate markersof type II collagen degradation couldbe useful for understanding normalcartilage turnover and the pathogenesis

of arthritic disease.

MATERIALS & METHODS

I m m u n o a f f i n i t y - p u r i f i e dstromelysin (MMP-3) was from IL-1-stimulated human dermal fibroblasts.Collagenase 2 (MMP-8), matrilysin(MMP 7), membrane-type (MT) - 1-MMP (MMP 14) were all recombinanthuman preparations (generous giftsfrom Dr. R Martin, Roche Bioscience).Recombinant human collagenase 3(MMP-13) was kindly provided by Dr.G Murphy, Strangeways Research Lab.,Cambridge.

Enzyme digests: 100 mg CNBr-digested human cartilage type IIcollagen, or 12.5 mg synthetic C-telopeptide domain, were incubatedwith 0.75 mg enzyme in digestionbuffer (0.2M NaCl, 50 mM Tris-HClpH 7.5, 10 mM CaCl

2, 0.05% Brij).

Reactions were stopped with 1.10phenanthroline (or soybean trypsininhibitor for trypsin) immediately (0hr), or after incubation for 24 hr at37∞C (24 hr).

2B4 immunoassay: 2B4immunoreactivity was quantitated byinhibition ELISA. 96-well microtitre

plates were coated overnight at 4∞Cwith EKGPDP linked to BSA, thenblocked for 2 hr at room temperaturewith buffer containing 0.25% BSA.Digestion buffer or calibrator(glutaldehyde cross-linked EKGPDP)were added, followed by 2B4-horseradish peroxidase conjugate.After incubation for 1.5 hr at 4∞C, theplates were washed and the peroxidasesubstrate TMB was added. After 15 mincolor development was stopped withH

2S0

4 and absorbance monitored at 450

nm.Reverse-phase (RP)-HPLC:

Peptides were resolved by RP-HPLCusing a macroporous C8 column and agradient of acetonitrile and 1-propanolcontaining 0.1% TFA. The UVabsorbance of the eluant wasmonitored at 2 wavelengths; 280 nm(primarily for the tyrosine functionalgroup) and 220 nm (primarily forpeptide bonds). Peptides wereidentified by amino-terminalmicrosequencing.

RESULTS

Compared with the buffer controland trypsin digests, all of the MMPstested released 2B4 epitope fromdenatured cartilage type II collagen(Table 1). We then determined theMMP-specific cleavage sites in the C-telopeptide using the synthetic peptideAFAGLGPREKGPDPLQYMRA. Initialscreening established that mAb 2B4recognized MMP-digests of thesynthetic peptide, but gave no signalwith the intact molecule. Whenmatrilysin digestion products of thepeptide were resolved by RP-HPLCseveral fragments were identified, themost abundant (by 220 nmabsorbance) eluting at 40 ml (Fig. 1).Sequence analysis identified thispeptide as the product of P-L cleavage.Inhibition ELISA showed that it was thesource of all the generated 2B4immunoreactivity. Digestion withstromelysin or collagenase 3 producedessentially the same range of peptidefragments, including the 2B4-immunoreactive AFAGLGPREKGPDP,

Matrix Metalloproteinase-Mediated Release Of ImmunoreactiveTelopeptides From Cartilage Type II Collagen

LYNNE M. ATLEY, PH.D., PING SHAO, B.S., VINCE OCHS, B.S.**, KATHY SHAFFER, B.S.**,AND DAVID R. EYRE, PH.D.

Protease 2B4 epitope(ng/ml)

0 h 24 hBuffer control 2 12Stromelysin 4 500Collagenase 3 2 430Collagenase 2 2 113Matrilysin 4 3100MT-1-MMP 3 145Bacterial collagenase 2 170Trypsin 2 10

Table 1: Release of 2B4 epitope from denatured cartilage type II collagen following digestion witha panel of proteases.

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12 1998 ORTHOPAEDIC RESEARCH REPORT

but the yield of the latter was muchlower than with matrilysin.

DISCUSSION

As part of a study to identify usefulbiochemical markers of cartilagecollagen degradation, we have shownthat a proteolytic neoepitopeoriginating in the collagen type II C-telopeptide is generated in vitro byseveral MMPs. Of the MMPs so fartested, matrilysin appeared to be themost potent. In preliminary studies, wehave detected 2B4 immunoreactivity insynovial fluid, serum and urine (5).This 2B4 epitope, therefore, has thepotential to be a useful marker of typeII collagen degradation in vivo. We arecurrently testing this in clinical studiesand in animal models of osteoarthritis.

2B4

(ng

/ml)

0 20 40 60

8

6

4

2

0

Elution Volume (ml)

Synthetic PeptideSynthetic PeptideSynthetic PeptideSynthetic PeptideSynthetic Peptide

YMRALQYMRA

AFAGLGPREKGPDP

A 220nm

A 280nm

Matrilysin DigestMatrilysin DigestMatrilysin DigestMatrilysin DigestMatrilysin Digest

2B4 Immunoassay2B4 Immunoassay2B4 Immunoassay2B4 Immunoassay2B4 Immunoassay

A 220nm

A 280nm

AFAGLGPREKGPDPLQYMRA

AFAGLGPREKGPDPLQAFAGLGPREKGPDPLQY

Figure 1: RP-HPLC resolution and 2B4 immunoreactivity of the synthetic peptide following proteolyticcleavage with matrilysin.

RECOMMENDED READING

Murphy, 1995 Acta Orthop Scand 66:55-60.

Okada et al., 1992 Lab Invest. 66: 1069-1073.

Lohmander et al., 1993 ArthritisRheum. 36:181-189.

Kozaci et al., 1997 Arthritis Rheum 40:164-174.

Eyre et al., 1996 Proceedings of theASMBR, Seattle, WA.

Supported by grants from NIH (AR37318 & 36794) and OstexInternational, Inc.

** Ostex International, Inc., Seattle,WA.

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1998 ORTHOPAEDIC RESEARCH REPORT 13

I t is widely accepted that curveprogression in idiopathic scoliosisis related to growth.

Recommendations for bracing andoperative intervention rely upon theability to assess the growth potential ofthese patients. Chronologic age, Rissersign and menarcheal status arecommonly used to estimate growthpotential and the potential for futurecurve progression. These maturityscales aim to group children in such away that they behave similarly withregards to growth and development.Buckler performed a longitudinal studyof normal adolescents and reported amethod of grouping children by theyears around the age at which peakheight velocity occurred. He found thatthese methods produced a growthvelocity curve most representative ofindividual growth patterns, and thatmales, females, early and late developersbehaved very similarly with respect tothis scale. We have termed this maturityscale as Peak Growth Age (PGA). The

purpose of this investigation was toapply this maturity scale to girls withidiopathic scoliosis followed throughadolescence. We aimed to see if itpredicted growth of the patient andlikelihood of curve progression moreaccurately than existing maturity scales.

MATERIALS AND METHODS

We reviewed the charts andradiographs of 130 girls from a databaseof 371 patients braced for adolescentidiopathic scoliosis from 1977 to 1995.All patients had a curve magnitude ofat least 25 degrees, idiopathic scoliosis,at least 6 visits to our institution over aminimum of 2 years with heightmeasurements recorded through theadolescent growth spurt; progressionfrom Risser 0 to at least Risser 4, andtreatment with either a Boston TLSOor Charleston bending brace.

Height measurements for eachpatient were used to calculate heightvelocities in centimeters per year. Anexample of the calculation for an

individual patient is shown in Table I.A minimum 6 month interval was usedfor calculations. The time of maximalheight velocity was designated PeakGrowth Age zero (PGA 0). For thepatient in Table I, this was in February1990 when the height velocity peakedat 10.1 centimeters per year. Weassigned a positive or negative PGA tothe years preceding and following peakheight velocity (PGA -1, PGA +1, etc.).If the first height velocity available fora patient was greater than nine cm peryear, this was designated as PGA 0.Cessation of growth was a heightvelocity less than 2 cm/year. We plottedheight velocity against PGA, Risser sign,chronologic age, and menarcheal age.We looked at the subset of patients withcurve progression greater than 10degrees and examined which maturityscale most closely correlated with curveprogression and the likelihood of curveprogression to 45 degrees.

Peak Growth Age: A New Maturity Indicator for IdiopathicScoliosisKIT M. SONG, M.D., DAVID G. LITTLE, M.B.B.S., F.R.A.C.S. (ORTH), DON KATZ, C.O.,AND JOHN A. HERRING, M.D.

Figure 1: Plot of height velocity versus Risser Sign. Height velocity is greatest at Risser 0 which is not a defined point in time.

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14 1998 ORTHOPAEDIC RESEARCH REPORT

RESULTS

We could assign PGA in all cases.The plots for height velocity versuschronologic age, PGA, Risser sign, andmenarcheal age are shown in figures 1-4. The median plot for PGA is the onlyscale which retains the characteristicsof an individual plot, with a high peakand sharp decline. Menarche occurredin the year around PGA 0 in 41% ofgirls in our study. Sixteen patients(12%) had menarche two years or moreafter PGA 0 and 8% had menarche twoyears or more before PGA 0. Thegrowth pattern of these patients clearlyfollowed PGA rather than menarchealage. PGA 0 was an earlier identifiablelandmark than the onset of menses orRisser 1 which occurred at a median of7 months and 9 months after PGA 0.

Ninety-seven curves progressed atleast 10 degrees and 61 progressed to45 degrees or more. The point ofmaximal curve progression wassignificantly more closely groupedaround PGA 0 than a specificchronological age (F test p=0.0001),Risser sign or menarche (p=0.02).Fifty-nine of 86 curves (69%) greaterthan 30 degrees at PGA 0 progressed to45 degrees or more, whereas only 2 of44 curves (5%) 30 degrees or lessprogressed to 45 degrees or more. Thisdifference was significant by Chi square(p<0.001).

DISCUSSION

All maturity scales aim to groupchildren in such a way that they behave

similarly with regards to growth anddevelopment. Other methods areindirect and thus infer the growth ofthe individual. Peak Growth Age (PGA)is a maturity scale directly related togrowth and the adolescent growth peak.It uses the time of the growth peak as afixed point by which patients aregrouped. PGA was found in this studyto be more predictive of the time of

cessation of growth and the period ofmost rapid curve progression than theuse of chronologic age, Risser sign, ormenarcheal status. Although Rissersign is widely used to estimate growthremaining and is the basis of manybracing studies, it has been found to beinaccurate and does not reliably predictthe cessation of growth or the timingof the adolescent growth spurt. In thisinvestigation, the majority of ourpatients had their growth spurt andmaximal curve progression while Risser0 which is not an identifiable point intime. One-third of our patients had notstopped growing by Risser 4 and 10%of our patients had their maximal curveprogression after attainment of RisserIV when it is generally thought to besafe to stop bracing. Similarly, 20% ofour patients had their major growthspurt more than 2 years away from theonset of their menses with 8% havingtheir growth spurt and maximal curveprogression 2 years or more aftermenarche when most studies haverecommended cessation of bracing.

Curve magnitude at PGA 0 wasprognostic of the likelihood of curveprogression to greater than 45 degrees.A curve magnitude greater than 30degrees at PGA 0 was highly correlatedwith curve progression to a surgical

Figure 2: Plot of height velocity versus Menarcheal Age. There is no well defined peak in growth whichoccurs in relationship to the onset of menses.

Figure 3: Plot of height velocity versus Chronologic age. There is no specific age at which velocitypeaks for the population of children studied.

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1998 ORTHOPAEDIC RESEARCH REPORT 15

range in this population of bracedpatients while very few patients withcurves less than 30 degrees at PGA 0progressed to curves of 45 degrees ormore.

It may not be as easy to assign PGAprospectively for patients as it was toassign it in this retrospective review.Height information is often availablefrom families and pediatricians. If only2 height measurements are available,and the velocity is greater than 9 cm/year, the patient is very likely to be inthe growth peak. For smaller velocities,previously utilized methods such as theRisser sign, menarcheal status, andchronologic age can be used to place thepatient along the growth curve. Thetiming of these events relative to PGA0 is shown in figure 5.

In summary, we believe that PGA isan easily calculated, accurate methodfor estimating growth remaining forchildren with idiopathic scoliosis. It ismore accurate than the use of indirectmethods such as chronologic age, Rissersign, and menarchal status and can helpphysicians prognosticate cessation ofgrowth and likelihood of curveprogression.

RECOMMENDED READING

Anderson, M.; Hwang, S. ; and Green,W. T.: Growth of the normal trunk inboys and girls during the second decade

of life. J. Bone and Joint Surg.,47A:1554-64, 1965.

Buckler, J. M. H.: A longitudinal studyof adolescent growth. London,

Figure 4: Plot of height velocity versus Peak Growth Age. The plot for the population studied is similarto that of an individual with a well defined peak and rapid decline.

Figure 5: Relationship of PGA 0 to median menarche, menarche +2, Risser 1, Risser 4, and Risser 5. The onset of menses or being Risser 1 implies that the childis past their major growth spurt.

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16 1998 ORTHOPAEDIC RESEARCH REPORT

Springer-Verlag, 1990.

Bunnell, W. P.: The natural history ofidiopathic scoliosis before skeletalmaturity. Spine, 11:773-6, 1986.

Carman, D. L.; Browne, R. H. ; andBirch, J. G.: Measurement of scoliosisand kyphosis on radiographs.Intraobserver and interobservervariation. J. Bone and Joint Surg.,72A:328-33, 1990.

Howell, F. R.; Mahood, J. K. ; andDickson, R. A.: Growth beyond skeletalmaturity. Spine, 17:437-440, 1992.

Little, D. G.; Sussman, M. D.: The Rissersign: A critical analysis. J. Pediatr.Orthop., 14:569-75, 1994.

Loncar-Dusek, M.; Pecina, M. ; andPrebeg, Z.: A longitudinal study ofgrowth velocity and development ofsecondary gender characteristics versusonset of idiopathic scoliosis. Clin. Orth.and Rel. Research., 270:278-282, 1989.

Peterson, L.; Nachemson, A. L.:Prediction of progression of the curvein girls who have adolescent idiopathicscoliosis of moderate severity. J. Boneand Joint Surg., 77A:823-27, 1995.

Shuren, N.; Kasser, J. R.; Emans, J. B. ;and Rand, F.: Reevaluation of the useof the Risser sign in idiopathic scoliosis.Spine, 17:359-61, 1992.

Veldhuizen, A. G.; Baas, P. ; and Webb,P. J.: Observations on the Growth of theAdolescent Spine. J. Bone and JointSurg., 68B:724-728, 1986.

Table I: Sample calculations for height velocity. One should use a minimum of 6 month interval between height for calculation. As an example between 4/12/90 and 8/13/90 there is an interval of only 4 months. The interval from 2/12/90 to 8/13/90 is instead selected for an interval of 6 months. The change in heightwas 3 cm. which is a height velocity of 6 cm. The peak height velocity is highlighted and is 10.1 cm.

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1998 ORTHOPAEDIC RESEARCH REPORT 17

The Orthopaedics BiomechanicsLaboratory has an ongoingseries of research projects

designed to better understand footfunction, and the surgical repairs offoot trauma and foot deformities. Thisis a summary of some of our recentactivity.

The effect of foot position on tarsalload transfer During gait, load istransmitted down the tibial shaft, andinto the talus, where it is transferred toboth the hindfoot and forefoot. Wehave determined the relative loaddistribution between the posterior andanterior facets of the talocalcaneal joint,and studied the role of the talonavicularjoint as part of this mechanism (Figure1). Using a cadaveric model of thenormal foot, we tested the hypothesisthat load transmission between thecalcaneus and navicular, measured bycontact pressure and area, wouldchange with foot position.

Mechanisms for suport of the talusThe mechanisms of inferior and medialsupport of the talus were determinedto provide insight into the mechanism

of loss of peritalar stability with flatfoot.In the intact foot the tibialis posterior(TP) tendon forms an articulation withthe medial plantar aspect of the talarhead. When the TP tendon ruptures,there is loss of dynamic support in themidfoot and a gradual change in theposition of the tarsal bones. The talusplantar flexes, the calcaneus everts, thenavicular abducts, and the foot loses itsarch (Figure 2). This change ispresumed to occur as a result of loss ofstatic support as the calcaneonavicularligaments elongate. The goal of thisstudy was to determine (i) thecharacteristics of interaction betweenthe talar head and thecalcaneonavicular ligament, (ii) itsrelative contribution to support of thetalus compared to those of the inferiorarticulations, and (iii) the effect of theposterior tibialis tendon, by measuringcontact pressures using a staticallyloaded cadaveric foot model.

Reconstruction of the mediallongitudinal arch in flatfoot. As asurgical treatment for flatfoot,lengthening the lateral column of the

foot restores the anatomic positions ofthe calcaneus and talus, tensions theplantar tissues and restores the mediallongitudinal arch. Two methods havebeen advocated, the Dillwyn-Evanswhich lengthens the calcaneus byinsertion of a bone graft between theanterior and medial facets, violating thetalocalcaneal joint; and the Seattletechnique, which places the bone graftat the calcaneocuboid joint, fusing itbut maintaining the talocalcaneal jointintact. These studies were designed tocompare the joint contact propertiesafter restoration by either method, andto study the effect on kinematics of thefoot. For surgical treatment ofsymptomatic flatfoot, calcaneallengthening restores the position of thesubluxed talus and tensions the plantarsoft tissues of the hindfoot. Fusing thecalcaneo-cuboid joint maintains thelengthened lateral column and thecorrected position of the calcaneus.However, the effect of these procedureson hindfoot kinematics is unknown.Therefore, the kinematics of thehindfoot were measured first in normal

Biomechanical Study of Foot Function

BRUCE J. SANGEORZAN, M.D.

Anterior-middle facet

Talo-navicular Posterior facet

calcaneo-navicular

Figure 1: Approximate contact areas on the talus and estimated directions of resultant force on each articular area.

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18 1998 ORTHOPAEDIC RESEARCH REPORT

cadaveric feet, then after simulatedlateral column lengthening and fusionin different positions.

Treatment of acquired flatfootAcquired flatfoot deformity has beenattributed to the loss of the tibialisposterior tendon. We studied the effectof releasing the tibialis posteriortendon (simulating rupture) on thekinematic positions of the hind footbones. Another study examined theeffect of restoring posterior tibialtendon function in an acquired flatfootmodel. Treatments include variousfusions, lateral column lengthening,ligament reconstruction and tendontransfer. This study used an acquiredflatfoot model to test the hypothesis:restoring the tibialis posterior tendonfunction (simulating repair) willsignificantly affect the kinematicorientation of the hindfoot complex inheel strike, stance, and heel off.

METHODS

We have developed severaltechniques which we use in various

combinations. Joint contactmeasurements are made usingtransducers made of pressure sensitivefilm (Prescale Film, Superlow and Low,Fuji, Tokyo, Japan) with an assembledthickness of 0.3 mm. After insertion ofthe film between the joint surfaces,increasing load, maintaining it for 30secs, and unloading, the pressure filmis imaged along with a set of calibrationprints using a flat bed scanner. Theimaged films are analyzed for totalcontact area (>0.5 MPa) and meanpressure. Overall errors are 3.8% forcontact area and 9.3% for pressure.

The loading apparatus consists of ashaft applying axial load to the tibia andfibula through a plate which allowsflexion/extension of the tibia, andclamps to attach 8 tendons of the footto cables connected to individualpneumatic cylinders (Figure 3). Eachfoot is tested in three positions: heelstrike (5% of the gait cycle), stance(30%), and near toe off (45%). Thecontributions of various muscles inthese three phases of gait were

determined from information on theirphysiological crossectional area andpercent of maximum voluntarycontraction in each phase

The motion tracking systemconsists of a transmitter which definesthe global axis system, located on thetibial shaft, and a set of receivers. Anacrylic shaft is placed into theintramedullary canal of the tibia tosupport the transmitter of anelectromagnetic motion transducer(Fastrak 3-D, Polhemus Systems,Colchester, VT) and transmit load tothe specimen. Methacrylate cement isplaced into holes drilled in thecalcaneus, talus, navicular, and cuboidof each foot. A carbon fiber pin isplaced into each hole, anchored in thecement, and an acrylic mount fixed tothe pin on which is located a receiverof the motion tracking system. Outputconsists of the direction cosinesrequired to define the orientation ofeach receiver axis. In this method, theinitial and final positions of eachreceiver axis are known and areprojected into each of three planes(sagittal, frontal, horizontal) defined bythe global axis system, similar to thosewhich might be obtained by viewingplanar radiographs. The transmitter Zaxis is aligned with the long axis of thetibial shaft, the X axis is directedtowards the medullary canal of thesecond metatarsal, and its Y axis isapproximately medial-lateral.Verification of sensor measurementaccuracy (ratio of measured output toknown input in the same direction)ranges from 0.944 to 1.006 in rotation,and 0.996 to 1.045 in translation.

RESULTS AND CONCLUSIONS

(i) Contact area and force on thetalus are greatest in the posterior facet,followed by the talonaviculararticulation, the anterior and middlefacets, and the calcaneonavicularligament.

(ii) The contact force in thecalcaneonavicular ligament articulationis best aligned to oppose medialdisplacement of the talar head.

(iii) Loss of posterior tibialis tendontension has no effect on contact forcein the calcaneonavicular ligamentarticulation with the talus.

(iv) Flatfoot decreases talonavicularjoint area, which is not restored byeither reconstruction. The Dillwyn -Evans procedure decreases

Figure 2: Lateral radiographs of normal foot (top), and the same foot after creation of a flatfootdeformity by cyclic loading.

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1998 ORTHOPAEDIC RESEARCH REPORT 19

Regulated, PneumaticCylinders

Tibial Load(Compressive)

Tendon Loads (Tensile)

NylonCables

PolhemusTransmitter

PolhemusSensors

TendonClamps

AxialLoadingRod

anteromedial facet contact area andincreases posterior facet pressure. TheSeattle method has less effect uponhindfoot joint contact characteristics.

(v) Calcaneo-cuboid fusion withthe calcaneus lengthened and the footin neutral position has no effect onhindfoot kinematics. However, fusingthe foot in other orientations limitstalocalcaneal and talonavicular jointmotion.

(vi) The increases in joint loadbetween heel strike and toeoff are morelikely due to differences in total loadapplied than due to differences inorientation of the talus since differencesin joint angle are small (10 degdorsiflexion for toeoff compared with6 deg of plantarflexion for heelstrike).High forces in toeoff are due primarilyto a combination of higher axial loadand larger Achilles force required tocreate thrust.

Figure 3: Lateral schematic of experimental loading frame with foot in heel off condition.

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20 1998 ORTHOPAEDIC RESEARCH REPORT

B ecause of the large sums ofmoney spent on health care, itis important to assess the value

of various therapeutic interventions.Recent attempts to define the value ofan intervention have been based on theresources necessary to provide it, suchas the Resource Based Relative ValueScale (RBRVS). Although thismethodology may be useful forallocating reimbursement, it does notdetermine the value of the interventionto the patient. For example, the“relative value” can be high if the serviceis expensive to provide, even if it isineffective. The authors suggest that‘value’ is more typically defined as thebenefit divided by the charge, that iswith the resource expense in thedenominator, rather than in thenumerator as it is in the RBRVS.Specifically, we propose that the value

of a procedure be determined bymeasuring the differences theprocedure makes in the patient’scomfort, function, and quality of lifeand then dividing these by the chargeof the procedure.

Standardized self-assessment toolsare now available for documentingpatients’ health and function before andafter treatment. The SF- 36 is one ofthe most widely used general healthstatus assessments. The SimpleShoulder Test is a commonly usedinventory of shoulder functions. Bothof these tools have been shown to reflectthe health and functional deficitsassociated with shoulder problems aswell as the change in these parametersafter treatment. Because they can beused without the patients having toreturn for follow-up visits, these self-assessment tools are useful for repeated

assessments over time. This allowstime-dependent changes in the benefitexperienced by patients to beincorporated into the analysis. Theactual lifetime benefit experienced bythe patient will be the summation ofbenefit measured throughout thepatient’s life.

In this pilot study, the authors usedthe SF-36 and the Simple Shoulder Testfor patient self-assessment before andsequentially after shoulder arthroplasty.These results were used to predict the“natural history” of a patient’s responseto the procedure. The value of theprocedure relative to the self-assessment parameters is determinedby dividing the lifetime benefitexperienced by the patient by the totalcharges for the procedure.

METHODS

Patient population. 125 patientswho underwent 137 primary totalshoulder arthroplasties completed theShort-Form 36 and Simple ShoulderTest self-assessment questionnaires ontheir initial visit and at 6 monthintervals after their procedure. Allpatients were from the practice of anindividual surgeon and the procedurescarried out with standardized selectioncriteria, technique, prostheses andrehabilitation.

Benefit. The benefit of theprocedure is defined in this study as thepercent change in a parameter, i.e. thedifference between the post-operativescore and the pre-operative scoredivided by the maximal possible scoreon the SST or the SF-36. Thus if apatient could perform 4 of the 12 SSTfunctions pre-operatively and 8 of the12 post-operatively, the benefit for theSST would be (8-4)/12 or 33%.Similarly if the SF-36 comfort scoreimproved from 32/100 to 76/100, thebenefit for SF-36 comfort would be44%.

If the benefit determined at eachfollow-up is plotted against number ofyears after the procedure, the areabeneath this curve is the realized

Assessing the Value of a Procedure: A Pilot Study Using TotalShoulder Arthroplasty as an Example

JAY L. CRARY, M.D., KEVIN L. SMITH, M.D., AND FREDERICK A. MATSEN, III, M.D.

Figure 1: The average change in scores from the pre- to post-operative period was statistically significantfor the Simple Shoulder Test and some of the subsections of the SF-36 (p<.05).

Benef i t f r om Shoul der Ar t hr opl ast y

- 10 0 10 20 30 40

Gener al Healt h

Vit al i t y

Ment al Healt h

Phy sical Funct ion

Social Funct ion

Emot ional Role

Phy sical Role

Comf or t

Simple ShoulderTest

Per cent I mpr ov ement

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1998 ORTHOPAEDIC RESEARCH REPORT 21

Figure 2: The average percentage change in SST, Comfort and Physical Role for each post-operative year.

benefit, expressed in units of %-years.If this curve is extrapolated out for thelife of the patient, the area beneath thecurve is the lifetime benefit of theprocedure, again in units of %-years.The lifetime value of the procedure isthe lifetime benefit divided by thecharge of the procedure, expressed inpercent-years/$1000.

The sums of hospital and physiciancharges were normalized to 1992dollars using the Consumer Price Indexfor medical care for urban areas.

RESULTS

The average age of our studypopulation was 61 years (range 29-84).38 shoulder replacements were done infemales and 98 in males. Each totalshoulder was followed for an averageof 2.0 years. 125 patients whounderwent 137 total shoulderscompleted 481 follow-up SF-36 andSST questionnaires during the post-operative period, for an average of 3.5follow-ups per shoulder.

Benefit of TSAThe average change in scores from

the pre- to post-operative period wasstatistically significant for the Simple

Shoulder Test and some of thesubsections of the SF-36 (p<.05).(Figure 1). The SST showed an averageimprovement of 38%. In the SF-36,the comfort and the role functionphysical subsections showed the largestnumerical changes, with averageimprovements of 23% and 19%respectively. We have focused ouranalysis on the SST and these twosections of the SF-36.

Figure 2 shows the average percentchange in SST, Comfort and PhysicalRole for each post-operative year. Asexpected, each of these parameterstends to decline with increasing timeafter surgery.

A linear regression was performedto determine the average percentdecrement in the benefit per year afterthe first post-operative year. Theaverage percent decrements for SSTfunctions, Comfort, and Physical Rolefunction were 4.8%/year, 3.3%/yearand 7.9%/year, respectively. The one-year benefit values for each of theseparameters were 44%, 25% and 25%,respectively. Using the slopes for theannual decrements, the number ofyears for each of these parameters to

reach the point of zero percent benefitwas obtained by dividing the one yearvalue by the slope. The durations ofbenefit were 9.2, 7.6 and 3.3 yrs for SSTfunctions, comfort and physical role,respectively. The total lifetime benefitsfor SST functions, comfort and physicalrole were estimated to be 246 percent-years, 120 percent-years and 69 percent-years, respectively. These data aresummarized in Table 1.

Charges. The average medicalcenter and physician charges for totalshoulder arthroplasty at our institutionwas $22,843.

Value. The value of the procedurewas estimated by dividing the lifetimebenefit by the normalized charges. Theaverage value for SST functions was10.8 %-yrs/$1000, for comfort 5.3 %-yrs/$1000, and for physical rolefunction 3.0 %-yrs/$1000.

Value can also be expressed in termsof specific functions or symptoms. Forexample, the Simple Shoulder Testindicated that pre-operatively 92% ofpatients could not sleep comfortably atnight because of shoulder discomfort.At post-operative year one eighty-twopercent of patients slept comfortably at

Realized Benefit

- 2 0

- 1 0

0

1 0

2 0

3 0

4 0

5 0

0 1 2 3 4 5

Years Post op

Pe

rce

nt

Ch

an

ge

SST %

Comfort %

Physical Role %

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22 1998 ORTHOPAEDIC RESEARCH REPORT

night. This effect diminished at a rateof 1.9% per year during the five yearsof follow-up. Given this slope, theestimated years of benefit with regardsto comfortable sleep was 43.2. Theaverage life expectancy of these patientswas 20.3 years. Therefore benefit wastruncated at that point. Using themethodology described above, theaverage patient who could not sleepcomfortable pre-operatively because ofshoulder discomfort could expect 13.9years (4919 days) of comfortable sleepattributable to this procedure. Thecharge per night of comfortable sleep($22,843/4919 days) would be $4.64.

CONCLUSION

We have illustrated a newmethodology for measuring the valueof a medical intervention. In thisexample, we used self-assessmentquestionnaires—the Short-Form 36and the Simple Shoulder Test—toquantitate the benefit and value apatient receives from total shoulderarthroplasty. This type of analysis is,to our knowledge, unique in that itattempts to measure the lifetime benefitand value of the procedure.

Our data demonstrate that SF-36scores and the SST are significantlyimproved after shoulder arthroplasty.As assessed by the SST and SF-36, thebenefit tends to lessen with time afterthis surgical procedure. The SST andSF-36 percent benefit scores showed anear linear decrease over time. We usedthese slopes to predict scores in thefuture. This allowed us to predict thelifetime benefit that a patient willreceive. Dividing the lifetime benefitby the expense of the procedure yieldsan estimate of the value of theprocedure, which is comparable toother measures of value in commonuse, such as miles per gallon.

The purpose of this investigationwas to demonstrate an approach to

measuring the benefit and value ofinterventions which could be appliedto other procedures and other practices.Because successful orthopedicprocedures yield benefits that areapparent to the patient, orthopedicsurgeons are fortunate that patient self-assessments can facilitate such ananalysis.

RECOMMENDED READING

Bayley KB, London MR, GrunkemeierGL, and et al: Measuring the success oftreatment in patient terms. Med Care33(4 Suppl):AS226-235, 1995.

Beaton DE, and Richards RR:Measuring function of the shoulder. JBone Joint Surg 78A:882-890, 1996.

Bergner M, Bobbitt RA, Carter WB, andet al: The Sickness Impact Profile:Development and final revision of ahealth status measure. Med Care19:787-805, 1981.

Cotton P: Orthopedics research nowasks, “does it work?” rather than just,“how is the procedure performed?”.JAMA 265:2164-2165, 1991.

Emery DD, and Schneiderman LJ:Cost-effectiveness analysis in healthcare. Hastings Cent Rep 19(4):8-13,1989.

Gillespie WJ, and Daellenbach HG:Assessing cost-effectiveness inorthopaedic outcome studies.Orthopaedics 15:1275-1277, 1992.

Levinsohn DG, and Matsen FA, III:Evaluation of nine commonmechanical shoulder disorders with theSF-36 health status instrument.Presented at the 64th Annual Meetingof the American Academy ofOrthopaedic Surgeons, San Francisco,CA, 1997.

Lippitt SB, Harryman DT, II, andMatsen FA, III: A Practical Tool forEvaluating Function: The SimpleShoulder Test. In The Shoulder: ABalance of Mobility and Stability.Matsen FA, III, Fu FH, and Hawkins RJ,(eds.). American Academy ofOrthopaedic Surgeons, Rosemont, Il,pp. 501-518, 1993.

Matsen FA, III: Early effectiveness ofshoulder arthroplasty for patients whohave primary glenohumeraldegenerative joint disease. J Bone JointSurg 78A:260-264, 1996.

Matsen FA, III, Ziegler DW, andDeBartolo SE: Patient self-assessmentof health status in glenohumeraldegenerative joint disease. J ShoulderElbow Surg 4(5):345-351, 1995.

Nerenz DR, Repasky DP, WhitehouseFW, and et al: Ongoing assessment ofhealth status in patients with diabetesmellitus. Med Care 30(5):MS112-124,1992.

Parker MJ, Myles JW, Anand JK, and etal: Cost-benefit analysis of hip fracturetreatment. J Bone Joint Surg 74B:261-264, 1992.

Radosevich DM, Wetzler H, and WilsonSM: Health status questionnaire (HSQ)2.0: Scoring comparisons and referencedata. Health Outcomes Institute,Bloomington, MN, 1994.

Segel MJ, and Heald RB(editors):Medicare RBRVS: ThePhysician’s Guide.Chicago, AmericanMedical Association, 1996.

Vital Statistics of the United States. LifeTables. U.S. Department of Health andHuman Services. 1992.

Table 1: A summary of first year benefit, rate of decrement in benefit, years of benefit and total lifetime benefit versus SST, Comfort and Physical Role.

SST Comfort Physical Role

First year benefit 44% 25% 26%

Rate of decrement in benefit 4.8%/yr 3.3%/yr 7.9%/yr

Years of benefit 9.2 yrs 7.6 yrs 3.3 yrs

Total lifetime benefit 246% - yrs 120% - yrs 69% - yrs

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1998 ORTHOPAEDIC RESEARCH REPORT 23

The Simple Knee Test: A Quick and Sensitive Self-Assessment ofKnee Function

MICHAEL H. METCALF, M.D., ROGER V. LARSON, M.D., PETER T. SIMONIAN, M.D.,AND FREDERICK A. MATSEN, III, M.D.

There is an increasing demand forall orthopaedic surgeons todocument the functional status

of their patients before and aftertreatment as well as the efficacy of theirtreatment approaches to differentdiagnoses. Existing approaches to thisdocumentation consume substantialtime and resources and often do notcapture the patients’ perception of theircomfort and function. Others are notsufficiently sensitive to clinicalproblems with the anatomic area ofinterest. The ideal method would be arapid self-assessment that patients caneasily complete within a few minuteswithout assistance, whether in the officeor at home. The tool must discriminatedependably between normal andpathological knee function.

Our goals were (1) to develop a self-assessment questionnaire sensitive to

common knee pathologies whichwould be practical in the context of abusy office practice, (2) to documentits results in asymptomatic andsymptomatic knees and (3) todemonstrate its sensitivity to a range ofknee pathologies.

METHODS

Initial questionsA series of questions was developed

from established knee scores. Initialquestions were taken from the Lysholm,Revised Hospital for Special SurgeryKnee Score, Cincinnati Knee score, andthe 1993 International KneeDocumentation Committee KneeLigament Standard Evaluation.Subsequently the questions werereformatted in a “yes/no” format witha “normal” response in the positivesense. All questions were reviewed with

six experienced knee surgeons andedited to develop 23 questions (Table1).

ControlsThis initial self-assessment was

administered to 360 persons whoserved as controls. This included 200medical students, residents ororthopaedic staff, as well as 160 patientsseen in the orthopaedic clinics for non-knee related symptoms. In addition tothe 23 questions, each person was askedtheir age, gender, activity level, priorhistory of knee surgery, prior history ofseeing a doctor regarding kneesymptoms, and to comment about eachof the 23 questions. Any individual whohad either a previous knee surgery orhad visited a doctor regarding a kneeproblem was excluded from the controlgroup.

Patients150 consecutive new patients

presenting to either the sports medicineor the adult reconstruction clinics forevaluation of a knee problem wereasked to respond to the series of 23questions as well as indicate theimportance of each question to themin their daily activities as eitherimportant or not important. The age,gender and activity level for eachpatient was recorded.

Diagnostic groupsEach patient was given a clinical

diagnosis based upon their history,physical examination, radiographs,MRI and/or arthroscopy. Patients withsimilar diagnoses were grouped and the“group response” to each question wascalculated as a percentage.

Statistical analysisA correlation matrix for all patient

responses was created (Statview 4.5).Significant intercorrelation waspredetermined to be any set ofquestions with r > 0.50. The meanresponse of each diagnostic relatedgroup to each question was comparedto the mean response of the controlgroup for the same question using a t-test. Significance was defined as p–value< 0.05.

Question Result

1 Does your knee allow you to sleep? kept

2 Will your knee straighten fully? kept

3 Will your knee bend all the way? kept

4 Is your knee free from swelling? kept

5 Does your knee move smoothly without catching or locking? kept

6 Can you sit comfortably with your knee bent for 1 hour? kept

7 Does your knee allow you to get up from a chair with out difficulty? deleted

8 Can you enter and leave a car without difficulty? kept

9 Can you stand and walk without your knee giving away? kept

10 Does your knee allow you to walk without a cane or crutch? deleted

11 Does your knee allow you to walk down the hall without difficulty? deleted

12 Does your knee allow you to walk two block without difficulty? kept

13 Will your knee allow you to walk one mile without difficulty? deleted

14 Does your knee allow you to do your usual work? kept

15 Will your knee allow you to go down stairs easily? kept

16 Will your knee allow you to go up stairs easily? deleted

17 Will your knee allow you to do a deep squat (beyond 90 degrees)? deleted

18 Will your knee allow you to run? kept

19 Will your knee allow you to pivot to the outside while running? deleted

20 Will your knee allow you to pivot to the inside while running? deleted

21 Will your knee allow you to participate fully in your sport? kept

22 Will your knee allow you to kneel comfortably? kept

23 Can you hop on one leg? kept

Table 1: Initial 23 Questions of the Simple Knee Test and Reduction to the Final 15

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24 1998 ORTHOPAEDIC RESEARCH REPORT

RESULTS

ControlsFrom the original set of 360

individuals, 7 persons were excludedbased upon having a prior knee surgeryand 40 others were excluded becausethey had seen a doctor regarding a kneeproblem. This left a total of 313 personsin the control group. Of these, 145(46%) were female and 168 (52%) weremale. The average age was 30. Theaverage Tegner activity level was 5.

PatientsOf the 150 patients, 79 (53%) were

female and 71 (47%) were male. Theaverage age was 35 and the averageTegner activity level was 5.

Diagnostic groupsPatients were placed in one of eight

diagnostic groups: 1) anterior cruciateligament insufficiency, 2) degenerativejoint diseases, 3) isolated meniscal tears,4) patellar instability, 5) patellarirritation, 6) tendinitis, 7) otherdiagnosis, and 8) no diagnosis.

Reduction of questionsOf the original 23 questions, 8 were

eliminated because of: 1) significantintercorrelation with other questions (r≥ 0.50), 2) lack of differential sensitivity

(≥ 95% of patients within a diagnosticgroup gave the same response to thequestion), or 3) lack of clarity, based onpatient comments. This left a total of15 questions which comprised theSimple Knee Test.

Question # 11 (Does your kneeallow you to walk down the hall withoutdifficulty?) and Question #13 (Willyour knee allow you to walk one milewithout difficulty?) were both highlycorrelated with Question #12 and weredeleted.

Question #7 (Does your knee allowyou to get up from a chair withoutdifficulty?) was highly correlated withfour questions (#8, 11, 13 and 16) andwas deleted.

Question #16 (Will your knee allowyou to go up stairs easily?) was highlycorrelated with questions #7 and #8 andwas deleted.

Question #10 (Does your knee allowyou to walk without a cane or a crutch?)was not highly correlated with anyother questions; however, it lackeddifferential sensitivity in that greaterthan 95% of patients with ACLdeficiency, meniscal tears, degenerativejoint disease, or patellar irritation

responded that they could ambulatewithout assistive devices. This questionwas deleted.

Question #17 (Will your knee allowyou to do a deep squat?), Question #19(Will your knee allow you to pivot tothe outside while running?) andQuestion #20 (Will your knee allow youto pivot to the inside while running?)were both highly correlated with otherquestions and were confusing to asignificant portion of the patients andwere deleted.

Variance within diagnostic groupsFor each question, the mean

patients’ response was significantlydifferent from the mean controls’response (p<.0001). Patient responsesalso varied significantly amongdifferent diagnoses (see Figure 1).

DISCUSSION

The 15 endorsable item SimpleKnee Test provides a quick, joint-specific functional self-assessment thatis practical for documenting kneefunction in the context of a busypractice.

Each question in the Simple Knee

Figure 1: Examples of variance of results by diagnosis

0.00 0.20 0.40 0.60 0.80 1.00

Does y our knee al lowy ou t o sleep?

Sit comf or t ably w i t hknee bent f or 1 hour ?

Ent er and leav e acar ?

Do y our usual wor k?

Hop on one leg?

Fr act i on of Pat i ent s Who Can Per f or m Funct i on

DJ D

ACLNor m.

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1998 ORTHOPAEDIC RESEARCH REPORT 25

Test is unique. All questions that werefound to be highly correlated, lackingdifferential sensitivity, or unclear havebeen deleted. The remaining 15questions measure different aspects ofa patient’s knee function.

The Simple Knee Test is sensitive todiffering knee pathologies. Forexample, patients with DJD and ACLinsufficiency gave significantly differentanswers to “Does your knee allow youto sleep?,” “Can you sit comfortablywith your knee bent for one hour?,”“Can you enter and leave a car withoutdifficulty?,” “Can you stand and walkwithout your knee giving away?,” and“Can you hop on one leg?” (see Figure1).

The Simple Knee Test provides aconvenient method for regular follow-up without having the patients returnto the office. The ability to assesspatients via the mail allows a substantialsavings of both patient and officeresources. With a systematic follow-up,surgeons can conduct personal qualitycontrol, determining which techniquesare most effective in their hands.

The simplicity of the SKT questionsfacilitates communication of results topatients. The SKT reflects the status ofthe knee in functional terms rather thanin degrees of motion, appearance ofradiographs, millimeters ofdisplacement, or scores. Patients caneasily compare their responses to thoseof other patients and, using thiscomparison, help determine theircandidacy for different treatment.

Continuing clinical research willestablish the characteristic SKT profilesof patients who are most likely tobenefit from treatment as well as theeffectiveness of different therapeuticapproaches in improving patients’assessment of their knee function. Thesimplicity and standardization of theSimple Knee Test facilitates comparisonof these results among the practices ofdifferent surgeons.

RECOMMENDED READING

Kelley, R. B., Rudicel, S. A., and Liang,M. H.: Outcomes research inorthopaedics. J Bone Joint Surg75A(10):1562-1574, 1993.

Matsen, F. A., III, Lippitt, S. B., Sidles, J.A., and Harryman, D. T., II: Practicalevaluation and management of theshoulder. W. B. Saunders Company,

Philadelphia, 1994.

Noyes, F. R., Matthews, D. S., Mooar, P.A., and Grood, E. S.: The symptomaticanterior cruciate-deficient knee. Part II:the results of rehabilitation, activitymodification, and counseling onfunctional disability. J Bone Joint SurgAm 65(2):163-74, 1983.

Tegner, Y., and Lysholm, J.: Ratingsystems in the evaluation of kneeligament injuries. Clin Orthop 198:43-9, 1985.

Windsor, R. E., Insall, J. N., Warren, R.F., and Wickiewicz, T. L.: The hospitalfor special surgery knee ligament ratingform. Am J Knee Surg 1:140-145, 1988.

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26 1998 ORTHOPAEDIC RESEARCH REPORT

To evaluate the in vivo responseof cartilage to an intra-articularinjury with residual step-off,

examining both the biomechanicaleffects as well as the histomorphologicchanges is the objective of this study.

METHODS

An intra-acticular step-off wascreated in medial tibial plateaus of theknees of 12 adult, domestic sheep. Asagittal osteotomy was made throughthe middle of the weight-bearingsurface, with displacement of themedial fragment distally by onemillimeter. After rigid fixation withscrews, the animals were allowedactivity ad libitum. The contralateralknee was used as a control. Fouranimals were terminated at six weeks;the others at twelve weeks. All animalswere labelled with oxytetracyline (50milligrams/kilogram) three weeks priorand three days prior to termination andwell as calcein (12 milligrams/kilogram) two weeks prior totermination.

After termination, the knees wereloaded in a materials testing machineusing pressure sensitive film to record

joint contact pressures. Subsequently,the articular surfaces were sectionedand prepared for both calcified andnon-decalcified histology as well asimaging by scanning electronmicroscopy.

RESULTS

Qualitative analysis of the pressuresensitive film demonstrated a single,broad area of contact in the controlknees. The knees with intra-articularstep-off had two major contact areaswith an intervening zone of reducedload corresponding to the edge of thedepressed fragment. Quantitativeanalysis revealed reduced overallcontact area in the knees with step-off.

Histologically, coronal sectionsthrough the articular surfacedemonstrated the presence of thinningand fibrillation on the high side of thestep-off. In addition, at the edge of thehigh side compensatory bending of thenormally vertical fibrils towards the lowside was observed. Some compensatoryhypertrophy of the cartilage at the edgeof the low side was seen, but notadequate to level the articular surface.No significant remodelling was seen in

The Response of Cartilage to Intra-articular Step-off: A SheepWeight Bearing ModelTHOMAS E. TRUMBLE, M.D.

the subchondral bone, with the planeof the osteotomy still being readilyidentified.

Scanning electron microscopydemonstrated partial cartilageremodeling by deformation of the highside cartilage to partially overlap thelow side cartilage and by behind thevertical collagen fibrils on the high sidecartilage even in the unloaded state(Figure 1).

CONCLUSIONS

In this animal model, a onemillimeter intra-articular step-offchanged the contact distribution bothqualitatively and quantitatively duringin vitro loading, with a net loss ofcontact area. Examination by both lightand electron microscopy revealedmorphologic changes suggestingcompensation by the cartilage,although incomplete, to accommodatethe height discrepancy.

SignificanceSmall intra-articular step-offs are

encountered frequently in trauma tothe hand and wrist. Although themaximum amount of acceptableincongruity has not yet been

Figure 1: Scanning electron microscopy demonstrated partial cartilage remodeling by deformation of the high side cartilage to partially overlap the low sidecartilage and by behind the vertical collagen fibrils on the high side cartilage even in the unloaded state.

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1998 ORTHOPAEDIC RESEARCH REPORT 27

established, this study provides a usefulmodel for further evaluation of theeffects of an intra-articular injury.

RECOMMENDED READING

Anglen JO, Healy WL: Tibial plateaufractures. Orthopaedics 11: 1527-1534,1988.

Ausberger S, Necking L, Horton J, BachAW, Tencer F: A comparison ofscaphoid-trapezium-trapezoid fusionand four bone tendon weave forscapholunate dissociation. J Hand Surg17A: 360-369, 1992.

Baron R: Bone histomorphometry andinterpretation. R.R. Backer, ed. CRCPress, Baton Rouge, FL, 1983, pp 14-22.

Brown TD, Pope DF, Hale JE,Buckwalter JA, Brand RA: Effect ofosteochondral defect size on cartilagecontract stress. J Orthop Res 9: 559-567,1991.

Fernandez DL, Geissler WB: Treatmentof displaced articular fracture of theradius. J Hand Surg 16A: 375-83, 1991.

Kellenger E: The potential ofcryofixation and freeze substition:observations and theoreticalconsiderations. J Microsc 161: 183-203,1991.

Knirk JL, Jupiter JB: Intra-articularfractures of the distal end of the radiusin young adults. J Bone Joint Surg 68A:377-390, 1986.

Figure 2: Arrow points to location of cartilage in knee as was studied in this evaluation.

Lansinger O, Bergman B, Koner L,Andersson GBJ: Tibial condylarfractures. J Bone Joint Surg 68A: 13-19,1986.

Llinas A, McKellop H, Marshall J,Sharpe F, Mu B, Kirchen M, SarmientoA: Healing and remodeling of articularincongruities in a rabbit fracture model.J Bone Joint Surg 75A: 1508-1522, 1993.

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28 1998 ORTHOPAEDIC RESEARCH REPORT

O steochondral autografttechniques are currentlyreceiving increased attention

for the treatment of focal cartilagedefects in “weight-bearing” areas of theknee. The purposes of this study are todetermine if any of the commonlyrecommended osteochondral donorsites are non-articulating through afunctional range of knee motion, and

determine the differential contactpressures for these sites through afunctional range of knee motion.

MATERIALS & METHODS

Ten commonly recommended sitesfor osteochondral donor harvest wereevaluated with pressure-sensitive film(Prescale Low Pressure Type, Fuji PhotoFilm, C. Itoh & Co. Inc., New York, NY)

through a functional range of motionwith a model that simulated non-weight-bearing resistive extension ofthe knee.

RESULTS

All 10 harvest sites demonstrated asignificant (p < 0.05) contact pressurethrough a functional range (0-110degrees) of knee motion (Figure 1).

The different color densitymeasurements between harvest siteswere also significant (p < 0.05) (Figure2). Harvest sites 1 and 2 demonstratedsignificantly less pressure than harvestsites 3, 4, and 5. Harvest site 9demonstrated significantly less pressurethan harvest site 3 and 4, and harvestsite 10 demonstrated significantly lesspressure than harvest site 4. Althoughdonor sites 1, 2, 9, and 10 demonstratedsignificantly less contact pressure thanthe sites with the greatest contactpressure, the difference in meanpressures were small; for example, thesite of least contact pressure (harvestsite 1 at 22.4 kgf/cm2) and maximalcontact pressure (harvest site 4 at 28.0kgf/cm2) was only 5.6 kgf/cm2 (seeTable 1).

CONCLUSION

In conclusion, no osteochondraldonor site tested was free from contactpressure. Four sites demonstratedsignificantly less contact pressure whencompared to the sites of maximalpressure. It is currently unknownwhether articular contact at theseosteochondral donor sites will lead todegenerative changes or any otherproblems.

RECOMMENDED READING

Ahmed, A. M., Burke, D. L., and Hyder,A.: Force analysis of the patellarmechanism. J Orthop Res, 5: 69-85,1987.

Brown, T. D., Pope, D. F., Hale, J. E.,Buckwalter, J. A., and Brand, R. A.:Effects of osteochondral defect size oncartilage contact stress. J Orthop Res,9: 559-67, 1991.

Contact Pressures at Osteochondral Donor Sites in the Knee

PETER T. SIMONIAN, M.D., THOMAS L. WICKIEWICZ, M.D., AND RUSSELL F. WARREN, M.D.

105

1

2

3

4

6

78

9

*

*

*

*

Figure 1: Diagram of Contact Pressures noting the ten commonly recommended sites for osteochondraldonor harvest.

Figure 2: Diagram of Contact Pressures noting different color density measurements between harvestsites.

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1998 ORTHOPAEDIC RESEARCH REPORT 29

Convery, F. R., Akeson, W. H., andKeown, G. H.: The repair of largeosteochondral defects. An experimentalstudy in horses. Clin Orthop, 82: 253-62, 1972.

Eilerman, M., Thomas, J., and Marsalka,D.: The effect of harvesting the centralone-third of the patellar tendon onpatellofemoral contact pressure. Am JSports Med, 20: 738-41, 1992.

Goldstein, S. A., Coale, E., Weiss, A. P.,Grossnickle, M., Meller, B., andMatthews, L. S.: Patellar surface strain.J Orthop Res, 4: 372-7, 1986.

Goodfellow, J., Hungerford, D. S., andZindel, M.: Patello-femoral jointmechanics and pathology. 1. Functionalanatomy of the patello-femoral joint. JBone Joint Surg [Br], 58: 287-90, 1976.

Hangody, L., and Karpati, Z.: Newpossibilities in the management ofsevere circumscribed cartilage damagein the knee. Magy Traumatol OrtopKezseb Plasztikai Seb, 37: 237-43, 1994.

Hangody, L., Sukosd, L., Szigeti, I., andKarpati, Z.: Arthroscopic autogenousosteochondral mosaicplasty.Hungarian J. Orthop. Trauma, 39: 49-54, 1996.

Huberti, H. H., and Hayes, W. C.:Patellofemoral contact pressures. Theinfluence of q-angle and tendofemoralcontact. J Bone Joint Surg [Am], 66:715-24, 1984.

Matsusue, Y., Yamamuro, T., and Hama,H.: Arthroscopic multipleosteochondral transplantation to thechondral defect in the knee associatedwith anterior cruciate ligamentdisruption. Arthroscopy, 9: 318-21,1993.

Matthews, L. S., Sonstegard, D. A., andHenke, J. A.: Load bearingcharacteristics of the patello-femoraljoint. Acta Orthop Scand, 48: 511-6,1977.

Yamashita, F., Sakakida, K., Suzu, F., andTakai, S.: The transplantation of anautogeneic osteochondral fragment forosteochondritis dissecans of the knee.Clin Orthop, 43-50, 1985.

Table 1: All of the 10 commonly recommended sites for osteochondral donor harvest evaluated versus mean color density, standard deviation, and pressure.

etis1

etis2

etis3

etis4

etis5

etis6

etis7

etis8

etis9

etis01

roloCnaeMytisneD

63.0 93.0 05.0 25.0 15.0 24.0 34.0 34.0 63.0 14.0

dradnatSnoitaiveD

70.0 70.0 01.0 31.0 21.0 21.0 01.0 61.0 51.0 90.0

erusserP)2mc/fgk(

4.22 9.32 9.62 0.82 5.72 7.42 1.52 8.42 6.22 3.42

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30 1998 ORTHOPAEDIC RESEARCH REPORT

The surgical procedure of bonetransplantation is very commonin orthopedics. With the

exception of blood, bone is the mostfrequently transplanted tissue inhumans. More than 200,000 bonegrafts or bone implants are performedeach year in the United States alone.These types of grafts, which areobtained from cadaver donors, are usedto treat many different problems witha variety of surgeries includingacetabular and proximal femoral

reconstruction and spine fusions. Theresults of these surgeries are good, butthe frequency of associated problems isstill high. Horowitz and Freidlanderhave reported allograft failure ratesbetween ten to fifty percent, dependingupon how the allograft was preparedafter harvest and prior to implantation.

Musculoskeletal allografts cause acell mediated immune response. Thiscellular response is directed at theantigen presenting cells locatedprimarily in the graft marrow. Various

attempts have been made to decreasethe cellular antigenic response. Sincethe surrounding soft tissues and bonemarrow elicit the greatest immuneresponse, attempts to remove or alterthese two tissues have been made.Allograft preparations have attemptedto achieve these goals.

Of the standard preparationtechniques used today, freeze-dryingappears to have the most reliable effect;however, these techniques cansignificantly compromise the structuralproperties of the bone. Othertechniques including detergents,aldehydes and ethylene oxide can resultin the generation of potential toxins.Proteolytic enzymes theoretically couldachieve these goals withoutcompromising structural integrity orintroducing toxins.

The purpose of this study is toevaluate the ability of proteolyticenzymes to remove antigens fromallograft bone and determine if there isan affect on structural integrity.

MATERIALS AND METHODS

SpecimensFresh segments of bilateral proximal

femoral metaphyseal bone wereharvested from thirty sacrificed Lewisrats (L-450 Toledo, Ohio). The femorawere from animals between six monthsand one year of age and weighedbetween 400-600 grams. Thesesegments contained cancellous bone,cortical bone, articular cartilage,relatively large vessels and marrowcomposed of equal amounts of fattyand hemopoietic cells.

Proteolytic Enzyme TreatmentFour different enzymes were chosen

based on their well known proteolyticproperties. They were Collagenase,Chymopapain, Trypsin and Papain.The activity of each enzyme wasobserved at standard concentrations of.01, .02, .04, and .08 grams dissolved in20ml of a calculated buffer solution.Each 1cm segment of bone was sealedin a sterile vial along with the 20ml ofactivated enzymatic solution andplaced in a water bath. A pH of 7.4 forthe solution and a temperature of 37degrees Celsius for the bath were

The Enzymatic Preparation of Allograft Bone

DAVID J. BELFIE, M.D. AND JOHN M. CLARK, M.D., PH.D.

Figure 1B: Bone Micrograph: Untreated.

Figure 1A: Bone Micrograph: Treated with Papain to remove non-bone soft tissue.

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1998 ORTHOPAEDIC RESEARCH REPORT 31

maintained throughout, to ensurephysiologic conditions. A controlgroup was maintained under identicalconditions without the activatedenzyme solution and replaced withsterile normal saline. The bonespecimens, each sealed in its enzymaticsolution, were treated in the water bathfor either 6, 12, 24 or 48 hours. All werehandled with sterile technique and acommercial solution of penicillin andstreptomycin was added to eachsolution. Once completed, thespecimens were washed with pulseddistilled water, fixed with 2% phosphatebuffered glutaraldehyde, decalcifiedwith EDTA and then prepared for lightmicroscopy.

Structural Integrity TestingTo evaluate the effect of our

treatment process on the structuralintegrity of potential grafts, four-pointstress testing was performed. Fiftywhole bilateral femur samples wereharvested in the same manner. Half ofthe samples were selected randomlyand treated as above. The other halfwere placed in sterile water andrefrigerated. These two groups werethen evaluated for ultimate stressfracture in lateral bending using a fourpoint bending system with a load cellattached to a materials tester (model828, Bionix MTS Systems). An analogto digital converter was used and datacompiled on a personal computer. Themeans and standard deviations werecalculated. The data was then reducedand tested for significant difference.

Antigenicity TestingThe specimen slides were stained

with H&E or Masson’s Trichrome. Theeffectiveness of each enzyme wasdetermined by microscopicobservation for any residual marrowtissue.

The treated vs non treated sampleswere then placed under the skin of thesame and different strain of rats. 2cmsections of treated and non-treatedmetaphyseal and diaphyseal bone weretransplanted under the skin of Lewis(White) and Brown Norway (Brown)rats. Sixteen rats were used, performingBrown-Brown, White-Brown, White-White, and Brown-Whiteimplantations with treated and non-treated samples. Sterile surgicaltechnique was utilized, with one sectionof sample being placed subcutaneouslybetween the scapluae of each rat. The

treated and non-treated samplesremained under the rats skin fortwenty-one and thirty-five days. Noantibiotics were given andpostoperative care was per animalstudies protocol at the University ofWashington.

The animals were sacrificed bystandard protocol and bone samplesrecovered. These samples were fixedand decalcified as described previously,and placed in paraffin blocks.Histologic staining with Masson’sTrichrome was performed to evaluatethe inflammatory response along aswell as destruction and new vesselformation.

RESULTS

Proteolytic Enzyme TreatmentThe histologic evidence from part

one of our experiment demonstratedthe highly effective proteolytic natureof Papain. This was when comparedagainst the other enzymes and thecontrol group. Of the other enzymestested none were as complete as Papainin removing the intra andextramedullary non-bone soft tissue(Figure 1A). The untreated controlgroup demonstrated minimal changein the medullary contents (Figure 1B).

Structural Integrity TestingAll of the data from the load cell was

collected and a standardized T test wasperformed to compare sample means

Figure 2A: Bone Micrograph: Untreated, showing inflammatory cell invasion of marrow space.

Figure 2B: Bone Micrograph: Treated with Papain prior to implantation showing favorable invasionby vascular and loose connective tissue.

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32 1998 ORTHOPAEDIC RESEARCH REPORT

between the treated and non-treatedgroups. Also, a one factor ANOVA testwas performed to compare the meanwithin each group, to the mean betweenthe two groups. In both cases, nosignificant difference in ultimatestrength to failure was detected basedon a selected Alpha of .05.

Antigenicity TestingAfter three weeks, both the treated

and non-treated samples under thecross-strain skin had elicited amoderate inflammatory response. Nodifference being noted between the twogroups. By week five however, theuntreated grafts were invaded muchmore by inflammatory cells, withevidence of necrosis and isolatedfibrous encapsulation (Figure 2A). Inone case the bone specimen had beencompletely resorbed. The treatedallografts at five weeks, demonstrateda minimal amount of inflammatorycells and no evidence of necrosis orencapsulation. Favorable invasion ofmarrow space by vascular and looseconnective tissue was clearly evident(Figure 2B).

DISCUSSION

Bone allografts, although the mostcommon alternative to autografts,encounter the same immunologiccomplications as soft tissue allografts.The incorporation of bone grafts issimilar to the process of fracturehealing. However, the process is slowwhen allogenic or pretreated bone isused. This may be due to an immuneresponse by the host or a lack ofosteoinductive or conductive propertiesfrom the graft.

Under the present study conditions,it appears that the proteolytic enzymesselected are capable of removing non-calcified tissue from bone withoutaltering the graft’s structural integrity.Of the four enzymes tested, Papain wassuperior in removal of the marrow cellsand surrounding soft tissue. Becausebone itself has little immunogenicproperties, Papain treatment couldreduce the host cellular response totransplanted bone grafts. Our studysuggests that enzyme prepared boneevokes only a minimal inflammatoryreaction in a rat model.

Enzymes have the theoretical abilityto remove much more of the soft tissuewithin bone when compared to currentgraft preparation techniques. We foundthat the open spaces in our treated

grafts were rapidly filled with vascularconnective tissue which likely signifiesan increased ability to incorporate intothe host environment. Further, Papaindoes not change the gross mechanicalproperties of bone because the enzymeis apparently unable to reach thecalcified collagen molecule. Enzymatictreatment avoids extreme alterations ofpH and temperature decreasing thelikelihood to the structure of the bone.This technique must be tested further.One of the most important questionsis whether the bone matrix, devoid ofall soft tissues, can effectively inducenew bone formation. The next step isto evaluate the enzyme treated boneusing a same strain rat model in aheterotopic environment.

RECOMMENDED READING

Bone and Cartilage Allografts. AAOSSymposium. G Friedlander 1990.

Natural History of Allografts. COOR V.Goldberg 1989.

Immunologic Aspects of BoneTransplantation. Orthopaedic Clinicsof North America. M. Horowtiz 1989.

The Biology of Bone Grafting.Orthopaedics. T. Gross 1991.

Factors Affecting Bone GraftIncorportation. CORR. S. Stevenson1996.

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1998 ORTHOPAEDIC RESEARCH REPORT 33

A supracondylar femoral fracturewith articular involvement is aserious injury and is difficult to

treat. Whenever possible a fixed angledevice should be used to decrease thechance of malunion or morespecifically, the chance of varusdeformity before union. Certainfracture patterns do not allowplacement of these rigid devices. Inthese instances a less rigid construct isa necessary alternative, despite theincreased risk of malunion ornonunion.

Specifically, the condylar buttressplate is recommended when the distalfragment is too small for the insertionof the condylar blade plate or when thefracture lines are in the frontal plane,as in a C3 fracture, in which the bladeof the condylar plate would interferewith the lag screws which must beinserted from front to back. Anotherconstruct for these difficult fracturesuses both lateral and medial plates;however, this necessitates considerablesoft-tissue stripping. Others haveaugmented fixation with bone cement,especially when bone quality is poor.

In an attempt to resist the potentialfor varus deformity with the lateral

condylar buttress plate, especially whenthe medial cortical buttress is deficient,screws in the middle of the plate can beangulated toward the dense,subchondral bone of the medialcondyle. By this simple means, screwangulation in the plate shouldstrengthen the overall construct to resistthe tendency toward varus deformity.The attractive features include the easeof application, and the use of anexisting construct. If in fact screwangulation adds significant stability tothese unstable fractures, the techniquecould be used easily with the lateralcondylar buttress plate.

The purpose of this study is tocompare the biomechanical propertiesof lateral condylar buttress platefixation of unstable supracondylarfractures with screws in the standardperpendicular position versus screwangulation toward the medial condylein a diagonal position.

MATERIALS AND METHODS

Six fresh-frozen human kneespecimens, from mid-femur to mid-tibia, were obtained from the Universityof Washington Department ofBiological Structure. The average age

of the patients from whom specimenswere taken was 72 years (range 53 - 87),and four were from men and two fromwomen. Segmental defects were createdwith a bone saw, removing a 10 mmtransverse slice of bone 50 mm from thedistal end of the femur, to mimic asupracondylar femoral fracture. Thefracture was fixed with a lateralcondylar buttress plate (Synthes, Paoli,PA) using 4.5 mm screws. The medialcortical gap was maintained at 10mmafter fixation. Five cortical screws wereplaced perpendicular to the plateproximal to the fracture and four screwsplaced perpendicular to the plate distalto the fracture. Each specimen wastested once with all the screws placedperpendicular to the plate, andalternatively with the most distal screwjust proximal to the fracture angled 45degrees across the fracture into themedial femoral condyle (Figure 1); thesequence of fixation was alternated fortesting. This angled screw was notplaced in “lag” mode but instead in“push” mode against the subchondralbone of the medial femoral condyle.The order of testing was alternated. Theproximal end of the femur and distalend of the tibia were secured in pottingcompound and attached to loadingfixtures on a materials testing machine(Bionix 858, MTS, Minneapolis, MN).Cyclical compression loading wasapplied for 1000 cycles at 1 Hz.Displacement control of the crossheadwas used to adjust the initial loading to0-500 N. The same cyclicaldisplacement was maintained for the1000 cycles, and applied loads wererecorded.

Displacement across the medial sideof the fracture site was monitored witha liquid metal strain gauge (ParksMedical Electronics, Aloha, OR). Eachstrain gauge was calibrated beforeapplication with a micrometer toestablish its region of linear outputfrom approximately 10 to 50% strain.The gauge was installed prestrained tothe midpoint of its linear region so thatit responded to either opening orclosing of the fracture gap. Gap closure

Angulated Screw Placement in the Lateral Condylar ButtressPlate for Supracondylar Femur FracturesPETER T. SIMONIAN, M.D., GREG J. THOMSON, WILL EMLEY, RICHARD M. HARRINGTON,STEPHEN K. BENIRSCHKE, M.D., AND MARC F. SWIONTKOWSKI, M.D.

Figure 1: Knee specimens were tested once with all screws perpendicular to plate and again with onescrew angled diagonally across fracture. The medial cortical buttress was removed in each specimen toincrease varus instability.

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34 1998 ORTHOPAEDIC RESEARCH REPORT

corresponded to varus deformity of thedistal segment.

Applied compression loads and gapdisplacement were recorded on apersonal computer using an analog-to-digital converter at a sampling rate of25 Hz. Force-vs.-displacement curveswere plotted for the 1000 load cycles.A linear regression analysis was used todetermine the stiffness (slope) of theinitial and final load cycles. Theamount of permanent varus/valgusdeformity caused by the cyclical loadswas determined by calculating thedifference in displacement at zeroapplied load between the first cycle andthe 1000th cycle. The Wilcoxon signedrank test (nonparametric paired t-test,StatView, Abacus Concepts, Berkeley,

CA) was used to test the hypothesis thatthere was no difference in stiffness orpermanent deformity between the firstand last cycles for the two screwconfigurations. Differences wereconsidered significant for p < 0.05.

RESULTS

For the construct with all screwsplaced perpendicular to the buttressplate, the initial stiffness was 410 + 302N/mm (mean plus / minus onestandard deviation), and after 1000cycles was 230 + 144 N/mm. With ascrew placed diagonally across thefracture site, stiffness increased to 833+ 556 N/mm on the first cycle, and 796+ 757 N/mm after 1000 cycles. Thestiffness after 1000 cycles with the

diagonal screw was significantly greaterthan without, p = 0.028 (Figure 2).

In all specimens with the screwsplaced perpendicular to the plate, thedistal fragment had a permanent varusdeformity under no load of 0.91 + 1.13mm. For the diagonal screw condition,5 of 6 specimens had a permanent varusdeformity of 0.37 + 0.22 mm, while onespecimen developed a valgus deformityof 0.68 mm. Assuming that neithervarus nor valgus deformity is desirable,the average magnitude for all sixspecimens with the diagonal screw is0.42 + 0.24 mm (Figure 3).

All screws that were placedperpendicular to the plate failed bycutting through the bone; while thediagonal screw simply backed out of theplate never penetrating the medialfemoral subchondral bone.

DISCUSSION

Certain fracture patterns of thedistal femur are not amenable to theplacement of a fixed angle device. Inthese instances, the condylar buttressplate is the recommended alternative;however, it is less rigid. Because of thedecreased rigidity and strength of thisdevice there is a tendency toward varusangulation and malunion. In anattempt to solve this problem Sandersand associates use both lateral andmedial plates which necessitatesconsiderable soft-tissue stripping. Wehypothesized that simple angulation ofa screw through the middle hole of thelateral condylar buttress plate towardsthe medial condyle adds significantstrength to varus deformity. The singlescrew should be placed as close aspossible to the dense subchondral boneof the medial femoral condyle withoutjoint violation; in this position, thescrew can act as a buttress against varusdeformity. The screw would essentially“push” against the medial femoralcondyle. In the clinical situation, thesignificant force of this screw pushingagainst the subchondral bone willsometimes result in a bending of thisscrew. Typically because of the confinesof the bone, fracture pattern, and plate,only one screw can be angulated acrossthe fracture; therefore only one screwwas angulated in this study.

In this study specimens were loadedto a 500N force through 1,000 cycles inan attempt to simulate the clinicalsituation as accurately as possible. Thisis not a large enough load to simulate

no screw diag screw0

500

1000

1500

2000

cycle1

cycle1000S

tiffn

ess

N/m

m*

*

Figure 2: Construct stiffness at the beginning and end of 1,000 loading cycles.* indicates significant difference p = 0.028

no screw diag screw0

1

2

3

mill

imet

ers

Figure 3: Permanent deformation across the fracture site after 1,000 load cycles.

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1998 ORTHOPAEDIC RESEARCH REPORT 35

A FRACTURE TREATED WITH THIS METHOD

Figure 5: 2 angulated screws placed through lateral condylar buttressplate.

Figure 4A: One view of the injury. Figure 4B: A lateral view of the injury.

Figure 6: The healed fracture.

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36 1998 ORTHOPAEDIC RESEARCH REPORT

full weight bearing because patientswith this injury would not be advisedto weight bear fully at an early stage.Varus angulation at the medial cortexwas monitored with a single straingauge. We reported the stiffness of eachconstruct at the first and last cycles; thedifference was significant after 1000cycles. By simply angulating the screwjust proximal to the fracture, theaverage stiffness was more thandoubled at the first cycle of loading andthree times stiffer after 1000 cycles.Also, the amount of permanentdeformation after 1000 cycles was morethan double for the standard constructwith all screws placed perpendicular tothe plate.

This simple means of screwangulation in the plate strengthened theoverall construct to resist the tendencytoward varus deformity. The attractivefeatures include the ease of application,and the use of an existing fixationdevice and instrumentation.

RECOMMENDED READING

Firoozbakhsh, K., Behzadi, K.,DeCoster, T. A., Moneim, M. S., andNaraghi, F. F.: Mechanics of retrogradenail versus plate fixation forsupracondylar femur fractures. JOrthop Trauma, 9: 152-7, 1995.

Merchan, E. C., Maestu, P. R., andBlanco, R. P.: Blade-plating of closeddisplaced supracondylar fractures ofthe distal femur with the AO system. JTrauma, 32: 174-8, 1992.

Newman, J. H.: Supracondylar fracturesof the femur. Injury, 21: 280-2, 1990.

Sanders, R., Swiontkowski, M., Rosen,H., and Helfet, D.: Double-plating ofcomminuted, unstable fractures of thedistal part of the femur. J Bone JointSurg [Am], 73: 341-6, 1991.

Shahcheraghi, G. H., and Doroodchi,H. R.: Supracondylar fracture of thefemur: closed or open reduction? JTrauma, 34: 499-502, 1993.

Struhl, S., Szporn, M. N., Cobelli, N. J.,and Sadler, A. H.: Cemented internalfixation for supracondylar femurfractures in osteoporotic patients. JOrthop Trauma, 4: 151-7, 1990.

Yang, R. S., Liu, H. C., and Liu, T. K.:Supracondylar fractures of the femur. JTrauma, 30: 315-9, 1990.

Zehntner, M. K., Marchesi, D. G., Burch,H., and Ganz, R.: Alignment ofsupracondylar/intercondylar fracturesof the femur after internal fixation byAO/ASIF technique. J Orthop Trauma,6: 318-26, 1992.

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1998 ORTHOPAEDIC RESEARCH REPORT 37

P elvic ring disruptions arevariable. Common anteriorpelvic zones of injury are the

symphysis pubis and pubic ramus,while posterior pelvic ring disruptionsoccur through the sacrum andsacroiliac joints. Acetabular and iliacwing fractures also occur in associationwith pelvic ring injuries. Posterior iliacfractures associated with ipsilateralsacroiliac joint dislocations (“crescent”fracture-dislocations), as well as other“simple” iliac fractures. It is ourpurpose to characterize an unusual typeof injury, the comminuted and unstableiliac fracture which results from directhigh energy impact of the iliac crest.

MATERIALS AND METHODS

Over a sixty-eight month period,695 patients with pelvic ringdisruptions were treated at HarborviewMedical Center. Only thirteen (1.9%)of these patients had severelycomminuted and unstable iliacfractures. All thirteen were men,ranging in age from 20 to 80 years(mean 38 years). Six patients wereinjured in automobile accidents, two inmotorcycle accidents, two in falls froma height, and another in a jet skiaccident. Two other patients werecrushed by trees. The pelvic injurieswere characterized based onanteroposterior, inlet, outlet, and Judetoblique plain pelvic radiographs. Pelviccomputerized tomography scansfurther evaluated these fractures andthe surrounding soft tissues.

These patients werepolytraumatized and had a mean InjurySeverity Score of 23. Eleven of thethirteen patients had severe iliac andflank degloving injuries. Five patientshad open fractures, one with fecalcontamination requiring divertingcolostomy. Another patient had anintraperitoneal bladder disruption, anda third patient had herniation of hisdescending colon between thecomminuted fracture fragments intothe buttock compartment. Six patientswith clinical signs of hemodynamicinstability had fracture displacementthrough the greater sciatic notchcausing local arterial injuries. All six

patients stabilized after angiographicembolizations. One patient had alumbosacral plexopathy on thefractured side. Four patients hadtraumatic brain injuries.

All thirteen patients had severepelvic boney instability, and weretreated operatively according to amanagement protocol for their pelvicfractures by the same surgeon. The fiveopen fractures were treated emergently.The remaining eight patientsunderwent operative reduction andfixation of their iliac fractures and otherpelvic ring injuries ranging from oneto four days after injury, depending onthe patient’s clinical condition. Routinepelvic external fixation was not usedbecause of the iliac comminution.Instead, stable internal fixation wasaccomplished via an anterior iliacsurgical exposure using lag screws withand without plating. The open woundsand degloving injuries were treatedwith irrigation, debridement, andclosure over drains. Broad spectrumcephalosporin antibiotic prophylaxiswas used for all patients.

RESULTS

Follow up evaluations wereavailable for all patients at a mean of18 months after injury. There were nodeaths. All of the fractures healedclinically and radiographically. Thefecal contamination caused apolymicrobial wound infection, and anassociated delayed union. Anotherpatient with an open fracture had aniliac wound infection. Both infectionsresponded to local management andantibiotics. Another patient had asevere skin abrasion/contusion over hisiliac crest which healed eight weeks afterthe injury. There were nocomplications associated with thedegloving injuries. Venous thrombosisoccurred preoperatively in one patientand post-operatively in another patient.None of the patients developedmeralgia paresthetica. The patient withthe lumbosacral plexopathy hadresidual weakness and numbness.Combative behavior due to head injurycaused fixation changes in one patient.

DISCUSSION

Comminuted and unstable iliac

Comminuted and Unstable Iliac Fractures

JULIE A. SWITZER, M.D., SEAN E. NORK, M.D. AND M.L. CHIP ROUTT, JR., M.D.

Figure 1A: The iliac oblique plain radiograph demonstrates the comminution and displacements ofthe iliac fracture fragments.

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38 1998 ORTHOPAEDIC RESEARCH REPORT

fractures are very rare, and quitedifficult to treat successfully. Becausethey are the result of high energytrauma, concomitant soft tissue,vascular, bowel, and genitourologicinjuries further complicate theirmanagement. Early angiographicevaluations should be performed when

the iliac fracture is displaced throughthe greater sciatic notch, especiallywhen the patient demonstrateshemodynamic instability. Routineanterior pelvic external fixation is noteffective due to the iliac comminutionand instability. Instead, early openreduction and internal fixation is

necessary to achieve fracture and localsoft tissue stabilities. Comminuted iliacfractures are associated with a varietyof potential complications. Fixationfailure was associated withcraniocerebral trauma and combativebehavior after surgery. Perhapsadditional fixation could have avoidedthis problem. Our open fractures werecomplicated by a high number ofwound infections. Because of this, werecommend that open iliac fracturesshould not be closed primarily, buttreated with open wound managementafter internal fixation. For closed iliacfractures, aggressive debridement andclosed suction drainage of theassociated degloving injury is effective.Pelvic fracture classification schemesshould include this unusual type of iliacfracture.

RECOMMENDED READING

Burgess AR, Eastridge BJ, Young JWRet al: Pelvic ring disruptions: effectiveclassification system and treatmentprotocols. Journal of Trauma 30(7):848-56, 1990.

Kottmeier SA, Wilson SC, Born CT,Hanks GA, Iannacone WM, and WG DeLong: Surgical management of softtissue lesions associated with pelvic ringinjury. Clinical Orthopaedics andRelated Research 329: 46-53, 1996.

Latenser BA, Gentilello LM, Tarver AAet al: Improved outcome with earlyfixation of skeletally unstable pelvicfractures. Journal of Trauma 31(1): 28-31, 1991.

Routt MLC, Simonian PT, and BallmerF: A rational approach to pelvictrauma: resuscitation and earlydefinitive stabilization. ClinicalOrthopaedics 318: 61-74, 1995.

Routt MLC, Simonian PT, Defalco AJ,and Clarke T: Internal fixation in pelvicfractures and primary repairs ofassociated genitourinary disruptions: ateam approach. Journal of Trauma40(5): 784-90.

Figure 1B: The pelvic CT scan further defines the extent of boney and local soft tissue injuries.

Figure 1C: Lag screws between the iliac cortical tables were used to stabilize the fractures.

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1998 ORTHOPAEDIC RESEARCH REPORT 39

Acetabular fracture treatment hasevolved significantly over thepast three decades due to the

pioneering work of Letournel and otherauthors. Operative treatment includingstable fixation after accurate openreduction is advocated for mostpatients with displaced acetabularfractures. The timing of operativeintervention for patients withacetabular fractures may be delayed forvarious reasons. In polytraumatizedpatients, their associated injuries andoverall clinical condition may preventearly operative care. Delayed referralsalso account for delayed surgicaltreatment. Some authors believe thatlater surgical interventions fordisplaced acetabular fractures isindicated in order to decrease operativeblood losses. Emergent acetabularfracture open reduction and internalfixation is advocated for those patientswith irreducible fracture-dislocations,open fractures, and altered sciatic orfemoral nerve functions after closedreduction. Some authors havesuggested that delayed acetabularfracture fixation decreases operativebleeding and operative times. Our goalwas to attempt to define the impact of

early acetabular fixation.

MATERIALS AND METHODS

One hundred and eleven displacedacetabular fractures were treatedoperatively at Harborview MedicalCenter by the same surgeon over threeyears. There were 86 male and 25female patients, ranging in age from 13to 85 years, mean 34 years. Ninety-seven patients were injured in vehicularaccidents, 8 fell from a height, 3 werecrushed, and 3 were pedestrians. Theaverage Injury Severity Score(ISS) was10.8, ranging from 4 to 32. Judetoblique pelvic radiographs and routinetwo dimensional computerizedtomography scans were used to classifythe fractures according to Letournel.There were 18 posterior wall, 1posterior column, 7 anterior column,1 anterior wall, 15 transverse, 7associated posterior column/posteriorwall, 29 associated transverse/posteriorwall, 12 T-type, and 21 associated bothcolumn patterns. Surgical exposureswere chosen for each patient accordingto the fracture pattern. We used 70Kocher-Langenbeck, 29 ilioinguinal,and 3 extended iliofemoral surgical

exposures. Four unusual fracturesneeded sequential anterior andposterior exposures at the sameanesthesia, while 5 were reduced andstabilized percutaneously.

The patients were divided into twogroups based on their delays frominjury until acetabular fixation. The“early” group consisted of 53 patientstreated within the initial three days afterinjury, while the 58 patients in the“delayed” group were treated after fourdays or more. This arbitrary divisionallowed divisions of patient number,gender, ISSs, and surgical exposures.The “early” group had 29 elementaryand 24 associated fracture patterns,while the “delayed” group had only 13elementary and 45 associated fracturepatterns.

RESULTS

The operative blood losses wereestimated by the attendinganesthesiologists and surgeon for eachoperation, and the higher estimate wasrecorded. In the “early” group ofpatients, blood losses averaged 935 ml,ranging from only 20 ml forpercutaneous procedures to 3600 ml formore extensive exposures. The

Early vs Delayed Acetabular Fracture Fixation

ORIENTE DITANO, M.D., WILLIAM J. MILLS, M.D., AND M.L. CHIP ROUTT, JR., M.D.

Early group<4

days

Delayed group 4

days or more

P value

Average blood loss 935 ml (20-3600) 922 ML (50-2000) .8862

Average operative

time

330 minutes (65-705) 320 min (100-660) .5276

Average number of

hospital days

12 (5-28) 16 (7-66) .008*(stat.

different)

Table 1: Acetabular Fracture Fixation Operative Timing.

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40 1998 ORTHOPAEDIC RESEARCH REPORT

“delayed” group averaged 922 ml ofblood loss, range 20 to 2000 ml. Therewas no statistical difference noted foroperative blood losses between the twopatient groups.

Operative times for the acetabularsurgical procedures were documented.Polytraumatized patients often hadseveral surgical procedures at the sameanesthetic, but only the acetabularportions were examined in this study.The average acetabular operative timefor the “early” group was 330 minutes,range 65 to 705 minutes. In the“delayed” group, the mean was 320minutes, range 100 to 655 minutes.There was no statistical difference foracetabular operative times betweenthese two patient groups. This wassurprising since there were morecomplex, associated fracture patterns inthe “delayed” group.

Total hospital days from injury untildischarge were documented for thesepatients. The “early” group of patientshad a 12 days average length of stay,range 5 to 28 days; while the “delayed”group averaged 16 hospital days, range7 to 66 days. This was statisticallysignificant (p = 0.006) (Table 1).

DISCUSSION

Early operative intervention isbeneficial for patients with otherskeletal injuries, especially inpolytraumatized patients. For example,urgent reduction and stable medullaryfixation of femoral shaft fracturesimproves clinical outcomes accordingto several authors, but this may not bethe case for acetabular fractures.Displaced acetabular fractures occurinfrequently, making it difficult formost orthopedic surgeons to gainsufficient clinical experience; their deeplocation and surrounding importantsoft tissue structures further complicateeffective management. Until recently,the radiology, classification, andsurgical treatment options foracetabular fractures were poorlyunderstood. Because of thesecomplexities, operative fixation ofacetabular fractures is often delayed dueto the need for patient referrals to aregional acetabular surgeon, and thetime for a complete preoperative work-up.

In our patients, we did not identifymajor disadvantages of delayedfixation. Operative blood losses wereequivalent for the two patient groups

and correlated with fracture patternsand surgical exposures rather thanoperative timing. Similarly, there wereno notable differences for the twogroups regarding the duration of theacetabular surgical procedures. Earlyoperative management of patients withdisplaced acetabular fractures wasassociated with a shorter hospital stay,but this may be due to other factors aswell. We conclude that treatment ofthese difficult fractures can be delayeduntil the optimal team andcircumstances are available for thesurgical reconstruction.

RECOMMENDED READING

Latenser BA, Gentilello LM, Tarver AAet al: Improved outcome with earlyfixation of skeletally unstable pelvicfractures. Journal of Trauma 31(1): 28-31, 1991.

Letournel, E: Acetabulum Fractures:Classification and Management. ClinOrthop. 151:81-106, 1980.

Letournel, E, Judet, R: Fractures of theAcetabulum. Publisher: Springer-Verlag, New York, 1981.

Matta, JM: Fractures of theAcetabulum: Accuracy of Reductionand Clinical Results in PatientsManaged Operatively with ThreeWeeks After the Injury. J Bone JointSurg. 78A:1632-1645, 1996.

Routt, ML Jr, Swiontkowski, MF:Operative treatment of ComplexAcetabular Fractures. CombinedAnterior and Posterior ExposuresDuring the Same Procedure. J BoneJoint Surg. 72A:897-904, 1990.

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1998 ORTHOPAEDIC RESEARCH REPORT 41

I n this study the mechanicalproperties of 3 candidateautografts for repair of the injured

scapho-lunate ligament are comparedto those of the intact scapho-lunateligament.

The most common treatment forchronic scapho-lunate (S-L)dissociation is limited carpal fusion,however fusion has been documentedto change both kinematics and articularcontact pressures. Methods forrestoring the scapho-lunate ligamentinclude (a) replacement with flexor orextensor carpi radialis tendon, (b)allografts, (c) and autografts. In thisstudy, we tested autograft tissues whichcould be harvested from the sameincision and used for S-L ligamentreconstruction; these included the 2ndmetacarpal-trapezoid ligament, the 3rdmetacarpal-capitate ligament, and thedorsal periosteal retinaculum (Figure1). The mechanical properties of theseligaments were compared to those ofthe scapho-lunate ligament.

METHODS

Specimens: The following bone-tissue-bone grafts were harvested fromeach of 7 fresh cadaveric wrists (Fig 1);(i) radial tubercle with surroundingretinaculum , (ii) 2nd metacarpal-trapezoid ligament, (iii) 3rdmetacarpal-capitate ligament, alongwith, for comparative purposes, and(iv) the scaphoid-ligament-lunate.Each specimen had 0.054” diameter Kwires placed in both bone ends foranchoring, which were then embeddedin polymethylmethacrylate inmounting cups. Specimens were keptmoist throughout testing.

Mechanical testing: Specimens weretested to failure in uniaxial tensileloading at 10 mm/min in a mechanicaltester (Instron, Canton, MA). Becauseof the short lengths of these tissues,displacement was measured from thecrosshead as opposed to locally withinthe tissue. To check for errors inducedby this method of displacementmeasurement, a rigid aluminum rod

was mounted and tested in the sameway as the specimens. Load wasmonitored by the Instron load cell.

Data Analysis: Ligament stiffnessand load to failure were derived fromthe data. To compare means, a Kruskal-Willis non parametric multiplecomparison by ranks was performed.

RESULTS

Figure 2 demonstrates that only thedorsal retinaculum was less stiff thanthe scapho-lunate ligament (SLL) (p =0.045), reaching a mean of 49% of thestiffness of the SLL while the 2ndmetatarsal-trapezoid was 118% as stiff,and the 3rd metacarpal-capitate was97% as stiff. The dorsal retinaculumwas also significantly less strong thanthe SLL (mean 26% as strong), whilethe others were very similar in strengthto the SLL (111% and 101% for the 2ndmetacarpal-trapezoid and 3rdmetacarpal-capitate respectively).

CONCLUSIONS

Both the 2nd metacarpal-trapezoidand the 3rd metacarpal-capitateligaments have tensile mechanicalproperties similar to the scapho-lunate.Since they are bone-ligament-bonegrafts, are accessible through the sameincision used for scapho-lunateligament repair, and attach to nearlyimmobile joints, they offer the potentialfor use in reconstruction of the scapho-lunate ligament without requiringlimited carpal fusion or tendon weavesfor stabilization.

CLINICAL RELEVANCE

The reconstruction of intercarpalligaments with similar tissues, securedwith a bone ligament bone interface inthe clinical setting is appealing but asyet untested. Having now identifiedpotential tissues for reconstruction, weare now charged with the task ofdetermining how best to secure thetransferred tissue beforerecommending the use of bone-ligament-bone composite grafts in aclinical setting.

A Biomechanical Comparison of Some Bone-Ligament-BoneAutograft Replacements for the Injured Scapho-LunateLigamentE.J. HARVEY, J.B. KNIGHT, DOUGLAS P. HANEL, M.D., AND ALLAN F. TENCER, PH.D.

Figure 1: Drawing of the dorsal side of the hand showing the scapholunate ligament (SLL) and threebone-ligament-bone graft replacements, DPR (dorsal periosteal retinaculum), 2MT (2nd metacarpal-trapezoid), and 3MC (3rd metacarpal-capitate) (adapted from Netter FH, Ciba-Geigy, Summit, NJ, Vol8).

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42 1998 ORTHOPAEDIC RESEARCH REPORT

SLL 2MT 3MC DPR0

50

100

150

200

250

300

stiffnessstrength

Stif

fnes

s (N

/mm

) or

Str

engt

h (N

)

SLL strength

SLL stiffness

RECOMMENDED READING

Augsberger S, et al, J Hand Surg17A:360-9, 1992.

Kleinman WB, et al, J Hand Surg,15A:408-14, 1993.

Weiss A, Trans AAOS 213:169, 1996.

Svoboda SJ, J Hand Surg, 20A:980-5,1995.

Figure 2: Stiffness and strength of potential bone-ligament-bone substitutes for the scapho-lunate ligament available through the same incision used for therepair (SLL-scapho-lunate ligament, 2MT-2nd metatarsal-trapezoid, 3MC 3rd metacarpal-capitate, DPR-dorsal periosteal retinaculum).

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1998 ORTHOPAEDIC RESEARCH REPORT 43

T reatment of post-traumaticelbow stiffness secondary toheterotopic ossification (HO) is

controversial. This is especially trueregarding timing and post operativemeasures to prevent recurrence. Manysurgeons delay treatment until serumalkaline phosphatase and bone scansnormalize, processes which may take 2years post injury to occur. Afterexcision of the HO and release of thecontractures, various prophylacticmeasures have been proposed includingradiation and/or non steroidalantiinflammatories (NSAIDS). Wewish to present our approach to thisproblem which includes early surgicalrelease and 5 days of NSAIDS postoperatively as a measure to preventrecurrence of HO.

METHODS

Sixteen patients (18 elbows) weretreated at Harborview Medical Centerwith early excision of post-traumaticelbow HO in the past 4 years. Eachpatient was treated with open surgicalrelease alone or with open release anddistraction arthroplasty. The criteriafor operative release were: (1) functionlimiting elbow stiffness, (2) fractureunion, (3) heterotopic bone on plainradiographs, (4) preservedulnohumeral articular surfaces and (5)resolved traumatic brain injury. Eachelbow was classified accordingHastings: class I (0), class IIA (7) , classIIB (1), class IIC (5), and class III (5).Delayed cubital tunnel syndrome wasdocumented in 7 patients. The averagetime from injury to release was 31weeks. Alkaline phosphatase and bone

scans were not obtained.Postoperatively, CPM was used for fivedays. A daily program of aggressiveactive and active-assist motion exerciseswas continued for six weeks. Radiationwas not used. Indomethacin wasprescribed for the first five days postoperatively. The average duration offollow-up was 26 months.

RESULTS

Preoperatively, the mean flexion/extension and pronation/supinationarcs were 33 and 75 degrees,respectively. The correspondingfollow-up values were 117 and 155degrees. Cubital tunnel syndromeresolved in all patients. There were nooperative complications. Three post-operative complications occurred intwo patients. 3 months after release, theskin over the olecranon in one patientbroke down as range of motion andactivity improved. This was correctedwith free tissue transfer. The other twocomplications occurred in one patient:a pin tract infection from a hingedfixator which cleared with pin removaland oral antibiotics. In addition thispatient went on to develop avascularnecrosis of the capitellum. The patienthas pain with heavy lifting butcontinues to work as a carpenter. Therewere no recurrent contractures or lossof motion resulting from contracture

Early “Simple” Release of Post-Traumatic Elbow ContractureAssociated with Heterotopic Ossification

RANDALL W. VIOLA, M.D. AND DOUGLAS P. HANEL, M.D.

release.

CONCLUSIONS

These results suggest that theconventional delay of surgery untilnormalization of both the patient’sbone scan and serum alkalinephosphatase may be unnecessary.Furthermore, this series documents alow complication rate anddemonstrates that good results may beachieved without postoperativeradiation and with less than one weekof Indomethacin.

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44 1998 ORTHOPAEDIC RESEARCH REPORT

A Prospective Multicenter Functional Outcome Study ofArthroplasty in Glenohumeral Inflammatory Arthritis

DAVID N. COLLINS, M.D., DOUGLAS T. HARRYMAN, II, M.D., AND MICHAEL T. WIRTH, M.D.

Patients with intractable shoulderpain and dysfunction frominflammatory glenohumeral

arthritis are often treated with shoulderarthroplasty to improve their shouldercomfort and function. While thisprocedure yields predictable pain relief,improvements in active motion are lessconsistent. Persistent functional deficitsmay be related to rotator cuffpathology, loss of glenohumeral jointarchitecture and the severity of thissystemic disease.

The purpose of this study was tocompare and contrast the functionaloutcomes of hemiarthroplasty (HA)and total shoulder replacementarthroplasty (TSA) for end-stageglenohumeral inflammatory arthritis.

METHODS

The study cohort included 59 casesof hemi (35) or total shoulder (24 )

arthroplasty performed by multiplesurgeons using a single prosthesissystem (GlobalTM, DePuy). Thesepatients had at least 24 months of postoperative follow-up (mean 39 months(range 24 to 73)). Standardized formswere used to record clinicalobservations as well as pre and postoperative self-assessment of comfort(Visual Analogue Scale (VAS)) andfunctional inventories using the SimpleShoulder Test and a 48-item activity list.Physical examination documentedmotion, strength and stability beforeand after treatment. Pre andpostoperative anteroposterior andaxillary lateral radiographs were alsoreviewed by the three authors.

The authors reviewed thepreoperative radiographs to determinewhether they thought the shoulders hadadequate bony architecture to supportthe prosthetic components in anatomic

position. Criteria for inadequate boneincluded:

1) Glenoid erosion to the base ofthe coracoid (AP view).

2) Head migration to less than 3mm from the inferior acromion. (APview).

3) Greater tuberosity inadequate tocover prosthetic template. (AP view).

4) Loss of > 40% of theglenoid.(Axillary view).

5) Missing acromion orclavicle.(Axillary view).

Post-operatively, glenohumeralalignment was determined from therelationship of the humeral headposition relative to the glenoid on APand axillary radiographs. Criteria forinadequate alignment were:

1) Humeral head dislocation orsubluxation of > 3 mm from glenoidcenter line on either view.

2) Improper head height relative totuberosity (<0 or >10 mm).

3) Acromiohumeral interval < 3mm.

4) Glenoid angulation on AP oraxillary view of > 15° from normalglenoid axis orientation.

RESULTS

No statistical differences wereidentified between the patients treatedwith HA and those treated with TSAwith respect to their pre-operative pain,comfort, extremity related function,quality of life or by total SST score orrange of motion (Student’s two samplet-test corrected if unequal varianceswere present between groups usingSatterthwaite’s adjustment, significancelevel p<0.05).

Full thickness rotator cuff tears werepresent in 19 (54%) of the 35 HA and8 (25%) of the 24 TSA cases. In thepresence of a full thickness rotator cufftear, the HA group reported greaterpain at rest and during sleep.

An average overall improvement onSST of 4.4 “yes” responses was observed.Range of motion improved for both HAand TSA but much better improvementin active elevation was achieved forthose who underwent TSA (50°

Figure 1A: AP view immediately following prosthetic hemiarthroplasty replacement. Note 15 mm ofhumeral head offset between the medial coracoid base and humeral head articular surface and 7mm of gap between the coracoid and the glenoid articular surface.

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1998 ORTHOPAEDIC RESEARCH REPORT 45

increase to an average of 118°, p<0.05)relative to those after HA (15° increaseto an average of 89°).

Anatomic reconstructability waspredicted in 53% of cases with HA andachieved in only 22% of those. It wasnot predicted in 46% of HA but wasachieved in 29% of those.Reconstructability was predicted in70% of TSA and was achieved in 69%of those; whereas it was not predictedfor 30% of TSA but was achieved in27% of those.

Glenohumeral alignment wasanatomically restored in 27% of thecases of HA and 51% of the cases ofTSA. Significantly better VAS scoreswere noted when the glenohumeralalignment was achieved as opposed towhen alignment was not achieved. Thisincluded overall pain, sleep comfort,work and play usage and overall qualityof life (all p=0.05, two-sample Student’st-test).

For all cases in which alignment hadbeen restored, active total elevationsignificantly improved by a mean of 21°(p=0.068). TSA significantlyoutperformed HA in this category withpost-operative elevation of 131° versus

85° (p=0.004). Active external rotationand passive elevation were better forTSA than HA, 48° versus 29° (p=0.023)and 144° versus 104° (p=0.006),respectively. The presence of a fullthickness rotator cuff tear at the timeof operation did not influence postoperative VAS, SST, ROM, orradiographic alignment.

Progressive glenoid erosion wasnoted in 12% of HA (Figure 1A and 1B)and there were two TSA cases of glenoidcomponent loosening. VAS, SST, orROM did not change significantly withtime.

CONCLUSIONS

In this series of patients withglenohumeral inflammatory arthritis:

1) The most favorable outcomes forimplant arthroplasty appear to occur inthe presence of an intact rotator cuffand sufficient bony architecture tosupport humeral and glenoid implants.Factors mitigating against glenoidresurfacing include rotator cuff deficitsand glenoid erosions.

2) Both hemi and total shoulderarthroplasty improved the VAS pain

scores, SST scores, activities of dailyliving, and range of motion. Activeelevation was significantly better for theTSA group (118° versus 89°).

3) Pain relief and functionalparameters were better whenglenohumeral alignment was restored.

4) Progressive glenoid erosions canoccur following hemiarthroplasty,potentially resulting in pain, instability,and functional loss.

RECOMMENDED READING

Barrett W, Thornhill TS, Thomas WH,Gebhart EM, Sledge Cb.Nonconstrained total shoulderarthroplasty in patients withpolyarticular rheumatoid arthritis. JArthroplasty. 1989; 4:91-96.

Boyd AD Jr, Thomas WH, Scott RD,Sledge CB, Thornhill TS. Totalshoulder arthroplasty versushemiarthroplasty. Indications forglenoid resurfacing. J Arthroplasty.1990; 5:329-361.

Figgie MP, Inglin AE, Figgie HE III,Sobel M, Burstein AH, Kranny MJ.Custom total shoulder arthroplasty ininflammatory arthritis. Preliminaryresults. J Arthroplasty. 1992; 7(1):1-6.

Franklin JL, Barrett W, Jackins SE,Matsen FA. Glenoid loosening in totalshoulder arthroplasty. J Arthroplasty.1988; 3:39-46.

Friedmann RJ, Thornhill TS, ThomasWH, Sledge CB. Nonconstrained totalshoulder replacement in patients whohave rheumatoid arthritis and class IVfunction. J Bone Joint Surg AM. 1989;71A:494-498.

Stewart MPM, Kelly IG. Total shoulderreplacement in rheumatoid disease: 7 -13-year follow-up of 37 joints. J BoneJoint Surg. Br. 1997; 79(B):68-72.

Figure 1B: AP view of hemiarthroplasty 36 months following prosthetic hemiarthroplasty replacement.Note medial erosion of approx. 10 mm and the narrow gap between the coracoid and the glenoidarticular surface. The humeral head offset is now only 5 mm (medial coracoid base to humeral headarticular surface minus magnification).

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46 1998 ORTHOPAEDIC RESEARCH REPORT

Department of Orthopaedics Faculty

Frederick A. Matsen III, M.D.Professor and Chair

Stephen K. Benirschke, M.D.Associate Professor

Stanley J. Bigos, M.D.Professor

James T. Bruckner, M.D.Assistant Professor

Howard A. Chansky, M.D.Assistant Professor

Jens R. Chapman, M.D.Associate Professor

Randal P. Ching, Ph.D.Assistant Professor

John M. Clark Jr., M.D., Ph.D.Associate Professor

Ernest U. Conrad III, M.D.Professor

Mohammad Diab, M.D.Assistant Professor

David R. Eyre, Ph.D.Professor

Theodore K. Greenlee, Jr., M.D.Associate Professor

Douglas P. Hanel, M.D.Associate Professor

Sigvard T. Hansen, Jr., M.D.Professor

Douglas T. Harryman II, M.D.Associate Professor

Children’s Hospital andMedical Center4800 Sand Point Way NESeattle, WA 98105(206) 526-2000

Harborview Medical Center325 Ninth AvenueSeattle, WA 98104(206) 731-3462

University of WashingtonMedical CenterBone and Joint Center4245 Roosevelt Way NESeattle, WA 98105(206) 548-4288

VA Puget Sound Health Care System1660 South Columbian WaySeattle, WA 98108(206) 764-2215

Department of OrthopaedicsUniversity of Washington1959 N.E. Pacific StreetBox 356500Seattle, Washington 98195-6500

Phone: (206) 543-3690Fax: (206) 685-3139

Affiliated Institutions

M. Bradford Henley, M.D.Associate Professor

Roger V. Larson, M.D.Associate Professor

William J. Mills, M.D.Assistant Professor

Sohail K. Mirza, M.D.Assistant Professor

Vincent S. Mosca, M.D.Associate Professor

Sean E. Nork, M.D.Assistant Professor

John O’Kane, M.D.Assistant Professor

Milton L. Routt Jr., M.D.Associate Professor

Bruce J. Sangeorzan, M.D.Professor

John A. Sidles, Ph.D.Professor

Peter T. Simonian, M.D.Associate Professor

Douglas G. Smith, M.D.Associate Professor

Kevin L. Smith, M.D.Assistant Professor

Kit M. Song, M.D.Assistant Professor

Lynn T. Staheli, M.D.Professor Emeritus

UNIVERSITYOF WASHINGTON

SCHOOL OFMEDICINE

Michael D. Strong, Ph.D.Research Professor

Carol C. Teitz, M.D.Associate Professor

Allan F. Tencer, Ph.D.Professor

Thomas E. Trumble, M.D.Professor

Jiann-Jiu Wu, Ph.D.Research Associate Professor

Adjunct FacultyBasia R. Belza, R.N., Ph.D.

Associate Professor, Physiological Nursing

Anne-Marie Bollen, Ph.D.Assistant Professor, Orthodontics

Charles H. Chesnut, M.D.Professor, Nuclear Medicine

Gregory C. Gardner, M.D.Associate Professor, Rheumatology

Thurman Gillespy, M.D.Associate Professor, Radiology

Daniel O. Graney, Ph.D.Associate Professor, Biological Structure

John C. Hunter, M.D.Assistant Professor, Radiology

Frederick A. Mann, M.D.Professor, Radiology

Susan M. Ott-Ralph, M.D.Associate Professor, Division ofMetabolism

Wendy Raskind, M.D., Ph.D.Associate Professor, General InternalMedicine

Michael L. Richardson, M.D.Professor, Radiology

Robert Schoene, M.D.Professor, Medicine

Peter A. Simkin, M.D.Professor, Medicine

Tony J. Wilson, M.D.Professor, Radiology

Joint FacultyJohn E. Olerud, M.D.

Professor, Division of Dermatology

Nicholas B. Vedder, M.D.Assiociate Professor, Plastic Surgery

Affiliate FacultyDavid A. Boone, C.P.

Director and Co-Principal Investigator,Prosthetics Research Study

Sarah E. Jackins, R.P.T.Rehabilitation Medicine

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1998 ORTHOPAEDIC RESEARCH REPORT 47

Mohammad Diab, M.D.

1998 Department of OrthopaedicsIncoming Faculty

Randy Ching, Ph.D.

R andy Ching, Ph.D. is anAssistant Professor ofOrthopaedics at the University

of Washington. Dr. Ching received hisresearch training at the OrthopaedicBiomechanics Laboratory atHarborview Medical Center where henow serves as Assistant Director. Heearned both his Masters degree (1988)and Ph.D. (1992) from the Departmentof Mechanical Engineering at theUniversity of Washington.

Dr. Ching’s main area of research ison the biomechanics of the spine.Beyond the more traditional approachto evaluating spinal stability bymeasuring its load-carrying capacity, hehas explored the ability of the spine toprotect the neural elements both duringand immediately following traumaticevents. This paradigm of “neuralstability” has had importantimplications for spinal-injuryprevention as well as the post-traumaticmanagement of patients with spinalinjury. Current projects with NHTSA(National Highway Traffic SafetyAdministration) and the U.S. Air Forcehave allowed Dr. Ching to focus hisresearch towards developing spinalinjury threshold criteria for both the

pediatric and adult spine subjected todynamic loading environments.

Outside of his research, Dr. Chingand his wife, Joan, are busy raising theirtwo daughters Megan and Erin (ages 10and 4). In between the softballpractices, swimming lessons, and soccergames, he enjoys trail running and anoccasional round of golf.

William J. Mills, M.D.

Upon completion of his one yearPediatric OrthopaedicFellowship at Boston

Children’s Hospital Mohammad Diabwill be rejoining the University ofWashington as an Assistant Professor atChildren’s Hospital and MedicalCenter. Dr. Diab was a resident herefrom July 1993 to June 1997.

Dr. Diab was born in Cairo, Egypt.He went to Dollar Academy in Scotlandfrom 1976 to 1979. He received his B.Sc.in Biology as well as a B.A. in Classicsfrom Stanford University, graduatingsumma cum laude in both fields. Hereceived the Fairclough Scholarship inClassics. Dr. Diab was also elected to PhiBeta Kappa while at Stanford. He stayedat Stanford to attend Medical School.

After working for a number of yearsas a reasearch and teaching assistant atStanford, he joined the U.S. NavalMedical Research Unit #3 in Cairo,Egypt as a Guest Investigator.

Following this he interrupted hisresearch career to work as a volunteerfor the victims of the Afghanistan Warin Pakistan for a month. Years later, afterbeginning his internship at theUniversity of Washington, he workedat Casa de Columbia, Hospital San Josede Buga in Columbia as a volunteer.

Dr. Diab has also received a numberof awards, honors, and recognitions,including the United States Navy YoungInvestigator Grant in 1987-88, theVictor H. Frankel Award at theUniversity of Washington, the BestResident Paper (IntermedicsOrthopedics) at the American Academyof Orthopaedics Surgeons annualmeeting of February 1994, and mostrecently the Von L. Meyer Fellowshipat Children’s Hospital in Boston for1997-1998.

William J. Mills, M.D. joins theUniversity of WashingtonDepartment of

Orthopaedics as an Assistant Professor.Dr. Mills will be joining the HarborviewMedical Center Trauma team. Hisprevious position was as anOrthopaedic Staff Physician at theNaval Medical Center in San Diego, CA.

Bill Mills began his collegeeducation at the University ofMichigan, where he received hisBachelor’s of Science degree. He wenton to get his Masters at the Universityof Minnesota and his Medical Degreeat the University of Colorado.

He was an intern here at theUniversity of Washington Departmentof Surgery and he stayed here for hisresidency in Surgery from 1990-1991before his Orthopaedic residency herefrom 1991-1995.

Dr. Mills was appointed Ensign inthe United States Naval Reserve in Mayof ‘86. He has been promoted twicesince then. He joined the staff at theNaval Hospital in San Diego in July1995.

In his career he has won numerous

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48 1998 ORTHOPAEDIC RESEARCH REPORT

John O’Kane, M.D.

medicine training with the Universityof Washington OrthopaedicDepartment, and he is currentlyworking in Orthopaedics as a memberof the Sports Medicine staff. Oneaspect of his job he especially enjoys ishis current role as a Husky teamphysician, a job combining generalmedical care and orthopaedics in aunique population of young adults.

In their spare time, he and his wifecontinue to enjoy skiing, hiking, biking,and other outdoor pursuits. He alsoenjoys playing guitar.

honors and awards such as: VandenbergScholar in 1979 at the University ofMichigan, the James J. Waring Awardof Nu Sigma Nu in 1988 and the GeorgePackard Award for outstanding recordin surgery in 1989 at the University ofColorado School of Medicine, theVictor H. Frankel Award for ScientificPaper in 1995 at the University ofWashington’s Resident Research Days,and the Orthopaedic Residents’ StaffTeaching Award in 1995-96 at the NavalMedical Center in San Diego.

Dr. Mills is a member of theAmerican Medical Association, theAmerican Academy of OrthopaedicSurgeons, the Western OrthopedicAssociation, and the Society of MilitaryOrthopaedic Surgeons. He has givenscientific presentations on open tibiafractures , streptococcal infections, aswell as other topics. And, he haspublished work on the effects of thetopical use of anesthetic, shivering andother forms of tremor, differentapproaches to fracture treatment as wellas cold injuries and abduction stress.

Sean E. Nork, M.D.

S ean E. Nork, M.D. has beenappointed Assistant Professor atHarborview Medical Center. He

has previously worked for theDepartment as an Acting Instructor.

Dr. Nork did his undergraduatestudies at the University of Californiaat Berkeley in Bioengineering. He wentto medical school at the University ofCalifornia at San Diego and he was aresident at the University of Californiaat San Francisco.

His major field of interest isorthopaedic traumatology. He hasworked in particular on fractures of thepelvis and acetabulum as well as lowerextremity periarticular fractures.

His published papers include workon outcomes after instrumentedposterior spinal fusions fordegenerative spondylolisthesis, therelationship between ligamentouslaxity and the site of upper extremityfractures in children, and externalfixation versus skeletal traction forpediatric femoral shaft fractures.

Dr. Nork is currently investigatingthe treatment of U-shaped sacralfractures with iliosacral screws. Othercurrent research topics include:

biomechanical evaluation of fixation offracture dislocations of the sacroiliacjoint, results of iliosacral screw fixationwithout SSEP’s, biomechanicalevaluation of fixation of U-shapedsacral fractures, and CT evaluation ofsacral dysmorphism and safe screwplacement.

Dr. John O’Kane is currently anActing Instructor and will bejoining the Sports Medical

Center as Assistant Professor, July 1,1998.

Dr. O’Kane spent his childhood inVermont enjoying small town life andwinter sports. He went to DartmouthCollege where he played football anddirected the ski school. He met his wife-to-be in college, then they both movedon to University of Vermont MedicalSchool.

Through college and medical schoolhe blended his interests in sports andteaching through coaching andeventually directing summer ski campsin Switzerland. Dr. O’Kane and his wifecame to Seattle together as residents inthe University of Washington Dept. ofFamily Practice. She is currentlyworking in the UWP Family Practiceclinic in Issaquah.

Dr. O’Kane completed an additionalyear of orthopaedic and sports

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1998 ORTHOPAEDIC RESEARCH REPORT 49

Graduating ResidentsClass of 1998

Donald Ericksen, M.D., his wife, Sara,and their children will be staying inSeattle while Don does a six month footand ankle fellowship at HarborviewMedical Center. The family will moveto Kalispell, MT where Don will bejoining the Flathead ValleyOrthopaedics and Sports MedicineClinic following his fellowship.

David Belfie, M.D., his wife, Barbara,and their two children will be going toAlbuquerque, New Mexico, for fouryears where David will assume activeduty status in the United States AirForce.

Oriente DiTano, M.D., will bereturning to the east coast where he willparticipate in a hand and upperextremity fellowship in Pittsburgh,Pennsylvania.

Colin Poole, M.D., his wife, Louise, andtheir two children are going to SanDiego, California, where Colin will bepartaking in a one year adultreconstruction fellowship at the ScrippsClinic and Research Foundation.

Jay Crary, M.D., his wife, Jennifer, andtheir two children, will be going toDetroit, Michigan, where Jay willparticipate in a one year foot surgeryfellowship.

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50 1998 ORTHOPAEDIC RESEARCH REPORT

Incoming Residents

Timothy DuMontier: Tim graduatedmagna cum laude from the Universityof Southern California in 1993 with aB. A. degree in Biology. Tim went onto attend the University of WashingtonMedical School where he received hisM.D. in 1997. Activities enjoyed outsideof medicine include weight lifting,hunting, hiking and horseback riding.

Scott Hacker: Scott graduated magnacum laude from the University ofCalifornia - San Diego in 1990 with aB. S. degree in Bioengineering. This wasfollowed by a M.S. degree inBioengineering from UCSD in 1991.Scott attended UC-Irvine MedicalSchool where he received his M.D. in1997. Interests enjoyed outside ofmedicine include mountain biking,hiking, diving and running.

Timothy Rapp: Tim received his B. S.with honors in Biochemistry from theUniversity of Iowa in 1993. Tim wenton to attend the University of Iowawhere he received his M.D. in 1997.Tim’s personal interests are competitiveathletics, running, tennis, skiing, traveland cooking.

William Sims: Bill received his B. S. inZoology from the University of Idahoin 1993. Bill went on to attend theUniversity of Washington MedicalSchool where he received his M. D. in1997. His extracurricular activitiesinclude cycling, weight training andskiing.

Carla Smith: Carla received her B. A.magna cum laude in Biochemistry fromRice University in 1989. Carla attendedBaylor College of Medicine where shewas accepted into a combined M.D./Ph.D. program in 1989. Carla receivedher Ph.D. in immunology in 1995followed by receiving her M.D. in 1997.She enjoys sports which includecompetitive cycling.

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1998 ORTHOPAEDIC RESEARCH REPORT 51

MAY 1997 THROUGH APRIL 1998

Friends of Orthopaedics

Sarah AdlerJeffrey W. AkesonEdward AlmquistFranklin and Marilyn AlvineAmerican Orthopedic Foot & Ankle SocietyDavid and Jean AndersonCarl A. AndrewsTheresa AntonettiCraig ArntzArtro CareAllan and Carol BachSamuel BakerWilliam BarrettTimothy BealsStephen BenirschkeCarol BennMonte L. BennGary BergmanBioelectronDavid BishopJohn C. BrownJames D. BrucknerJames D. Bruckner (Steven Sitcov)Ernest BurgessSusan CeroHoward ChanskyHerbert Clark (NW Ortho Clinic)Todd ClarkeErnest ConradVernon CooleyJames CrutcherJerome H. Debbs IIDavid DenekaDePuy, Inc.Catherine Ann DeserannoRichard Dimond

We express our appreciation to all who have contributed to the work of the Department of Orthopaedics over the past year.Your assistance makes possible special research activities, educational programs, and other projects that we could not facilitatewithout this extra support from our alumni, faculty, and friends in the community. We owe a special thanks to the Universityof Washington Resident Alumni who have made significant contributions to help further the education of our currentresidents.

Contributors to Departmental Research and Education

E. Anne ElliottKimberly A. ElliotDavid R. EyreEdward FarrarThomas FischerJim Fletcher (Howmedica)Jonathan Franklin (Ortho Consultants)James FriendKen FujiJoy D. GarnerJames GhiglioneBenjamin H. GillPark GloydJean GoehringThomas GreenTheodore and Sandra GreenleeWilliam A. GuinnMarian HamptonDouglas P. HanelSigvard HansenNova Sue HarrisonDoug T. HarrymanLinda S. HempelJanet HenryScott HormelJohn HunterTom Hutchinson (W.W. Med Group)Innovasive DevicesSarah JackinsCathy KeatingCarleton KeckDavid KierasRichard KirbyBetty E’Drene KilloranEdith D. Klep

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52 1998 ORTHOPAEDIC RESEARCH REPORT

Friends of Orthopaedics

Harvey W. KlepJonathan KnightPhilip KregorWally KrengelRonald KristensenDennis KvideraAlbert LarsonRoger LarsonLaurie A. LeeDavid LevinsohnTim LovellJoan MalmassariMaxine MalmassariFrederick A. MannRebecca & Steve MarshFrederick A. Matsen IIIKeith MayoJulia C. McCloudDaniel J. McClureJoseph MezistranoSohail MirzaPeter MitchellMichael MorrisVincent S. MoscaCarol MyersDavid NankJohn NeufeldWade Alan NewmanEd NorthNorthwest Ortho PhysiciansNorthwest Spine Surgeons (Bach, Krengel, Dales)William OppenheimJohn Orr (Zimmer)Orthopedic Physician Associates (Knight, R)Lawrence PageArnold PetersonEli PowellLane PremoDonna M. PresleySteve RatcliffeSteven ReedAlberta M. ReganReiff (Northwest Biomet)

John Sack, M.D. (Seattle Hand Surgery)Michael SailerSaint Frances Med TechRonald SandlerBruce J. SangeorzanRichard SemonPeter T. SimonianCindy SmithKevin SmithKit M. SongLyle SorensenDon StriplinIlene M. SwansonJames M. SwansonMarc SwiontkowskiCarol C. TeitzSteven ThomasMichael ThorpeGayle C. ToneyThomas E. TrumbleValley Orthopedic Associates (Arntz, Barrett, Hendrickson)Eric VanderhooftNicholas VedderRobert VeithJanet L. VietTheodore WagnerPamela WalkerRobert Watkins, Jr.Amy WeisnerJohn D. WestRichard WilliamsonBeverly A. WilsonJay WinzenriedNancy M. Anderson WiresBrodie WoodJoseph D. Zuckerman

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1998 ORTHOPAEDIC RESEARCH REPORT 53

NATIONAL RESEARCH GRANTS

DEPARTMENT OF ORTHOPAEDICS

National Institutes of Health (NIH)

Collagens of Cartilage and the Intervertebral DiskDavid R. Eyre, Ph.D.

Imaging of Molecules by Oscillator-Coupled ResonanceJohn A. Sidles, Ph.D.

Regulation of Gene Expression in CartilageLinda J. Sandell, Ph.D.

Pathology of Inborn Skeletal DiseasesDavid R. Eyre, Ph.D.

Skeletal DysplasiasDavid R. Eyre, Ph.D.

Salvage vs. Amputation Following Limb Threatening InjuryMarc F. Swiontkowski, M.D.

Veterans Affairs Medical Center Review Grants

Rehabilitation Research and Development Center for Prosthetics andAmputation

Bruce J. Sangeorzan, M.D.

Biomechanics of Foot Deformities and Alternatives for Surgical CorrectionBruce J. Sangeorzan, M.D.

Synthesis and Function of Cartilage Matrix MoleculesLinda J. Sandell, Ph.D.

Centers for Disease Control

Low Speed Cervical Whiplash InjuryAllan F. Tencer, Ph.D.

Orthopaedic Research and Education Foundation (OREF)

Bristol-Myers Squibb/Zimmer Institutional GrantFrederick A. Matsen III, M.D.

Randomized Multicentered Clinical Trial of Distal Radius Fracture TreatmentDoug P. Hanel, M.D.

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54 1998 ORTHOPAEDIC RESEARCH REPORT

NATIONAL RESEARCH GRANTS

DEPARTMENT OF ORTHOPAEDICS

Orthopaedic Research and Education Foundation (OREF)

Predictable Spine and Occupational Health DataStanley J. Bigos, M.D.

The Shoulder Function and Health Status of Individuals with DocumentedRotator Cuff Tears Before and After Treatment: A MulticenteredProspective Study

Douglas T. Harryman II, M.D.

A Prospective Field Trial to Assess the Reliability, Validity, and Responsivenessof the Short Form Musculoskeletal Function Assessment Instrument(SMFA)

Marc F. Swiontkowski, M.D.