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    ‘SYMPOSIUM | — Applied Biomechanics in Articular Injuries: Perspectives in the Basic Investigation of Articular Injuries and Clinical Application Steven A. Olson, MD, FACS ‘Thomas D. Brown, PhD Kyriacos A. Athanasiou, PhD, PE Roman M. Natoli, MD, PhD Douglas R. Dirschi, MD Abstract Joins injury isan important caus of arthritis. Atiough the reatment of injury, in “general, has been widely studied, he contribution of injury tothe development of ‘posrrsomatc arthritis is sci a relatively understudied area. One ofthe most per- iplesing aspect of investigating articular injuries is the complex nature ofthe inju- ‘9 itself and the.mtipl facets ofthe injury mechanism that can potentially lead to the development of arthritis. ‘A symposium by the Orthopaedic Research Society and the American Academy of Orthopaedic Surgeons was designed 10 examine the spectrum of basic science 60 clinical investigation in the role of biomechanics in the study of int injury and subsequent posteraumatic arthritis, Four perspectives inthe clinical aspects of man- aging articular injuries were investigated, including the clinical applications of basic science findings, the challenges and advancements in measuring and model- ing articular fractures, the relationship of articular cartilage mechanical injuries and osteoarthritis, and the controlled ereation ofan inert-artcular fracture to per- mie obrervations ofthe natural hiory of postraumaticarcrits Instr Course Lect 2011;60:583-594. ‘De Olona en mame ay membres as aboard member, ur afer, a commie mre ofthe “South Euscrs Fare Cons Foundations i ember of peer! barn or ht mad ai preens ams lof Se vd has eid rach or intaconl npr fm Se. Dr Broo ai mei omy member ern pid cana oan empl of Smith Nephew. De Aahanson oF (oe immed aly mercer apd emean 0 0 an empleo Arie breed arch ‘or iaiconel appre fom Spring and es ack or sock opin tn ViaCire Disheice Salaions ‘De Dinh van smmede fly mbna a oard mas, our fer, ocomniee member af ‘he American Orcas Aneiaton dba rece ec fom Bias. Nether Dr Natl no an i mei oly member as ied ageing of sale fom res sack neem compo oni on related ety indie te abet of ti caper © 2011 AAOS Instructional Course Lectures, Volume 60 ‘The overall effect of the condition of the musculoskeletal system on health in the United States is increasing. Re- cently, a working group of the Bone and Joint Decade initiative has at tempted to quantify the burden of musculoskeletal discase in-the United Seates.' Two of the major contributors to this burden of disease include ar- thrieis and injuries. In adults, arthritis is the most common cause of disability in the United States and is among the leading conditions causing work lim tations." From 2003 to 2005, arthritis ‘was diagnosed in approximately 21% or slightly more than 46 million pa- tients in the United State. By the year 2030, ic is projected chat 25% of the US adule population will have physician-diagnosed arthritis, Injuries to the musculoskeletal system account for another large portion of overall dis cease in the United States. In 2004, ap- proximately 57 million musculoskele- tal injury epitodes were ceated in physician offices, emergency depart ments, clinies, and other medical inst- 583 Orthopaedic Medicine tutions, More than 33% ofall injuries overall outcome of the patient. Tadi- Clinical Applications of Basic ‘were reported as strains and sprains. tional investigative techniques that Science Findings Fractures represented nearly 25% of all study isolated mechanisms of disease Like much of orthopaedic practice, reported musculoskelecal injuries have been applied to these mecha- fracture surgery is ruled by tenets “The subgroup of patients with inju- nisms.57°"° Although these investiga- Common sense, the desire to serve pa. fies to the musculoskeletal system ions provide new information, they tients, and the substantial influence of (particularly major joint injuties) ia do not replicate the complex condi- the AO group and its educational net whom arthritis develops is less well de- tions of an articular fracture, making work have resulted in ideas that have fined. This population of patients with clinica translation less cerain. become “fracture dogma.” Two of the posttraumatic arthris is a distinct —Pethaps one of the most perplexing most closely and passionately guarded group of patients contributing to che aspects of investigating articular frac genets in managing articular Fractures, overall burden of musculoskeletal dis- tures is the complex navure of the in- are as follows: the objective of teat case? As 2 disease entity, posttrau- jury and che effects of the trestments ment is precise reconstruction of the matic archritis is elaively unstudied. designed co restore che displaced arti- anticular surface, and patient outcomes Although arthritis can develop after ular surface. Clinicians have inade- will vary based on the accuracy of ar- any injury to a major joint, it most quate tools to accurately and reliably ticular reduction. predictably and rapidly develops afer assess che effects of the various aspects A review of the published literature inerv-arcicular fractures. The tadi- of injury on the ultimate clinical out- shows that the necessary precision rec tional view of the development of at- come." The physical disruption of the ommended for articular reconstruction thricis after an articular fracture has joint, the physiologic response to in- has changed overtime. Inthe tibial pl been one of focal stress elevation relat- jury, and impaction of the articular teau, for example, the * ced 0 articular malreduction following surface are all inseparably related. For threshold for articular congruity has de- surgical or nonsurgical weatment of example, how can posttraumatic ar- creased over the past 20 years fiom the injury.* More recent studies sug- thritis be prevented in a patient with a § mm co 2 mm." Outcomes follow- gest that elements of posttraumatic at- comminuted articular fracture? Should ng care, however, appear to be largely thrits serve as components ofthe over- prevention efforts be focused on re- unchanged."*"™ It appeats chat the all mechanism of disease and may alter storing articular reduction, mitigating chreshold for acceptable reduction has chondrocyte viability, incite an acute the effects of impaction injury to the more closely followed improvements inflammatory response, and conceib- cartilage, enhancing a combination of jn the’ technical abilities of surgeons ute eo altered mechanical wear*® ——_Jocal and. systemic physiologic te- rather than improvementsi outcomes. Many factors contribute to the'reli- sponse to the injur’ or shotlé'll of Another important factor is that 3 sur tive lack of knowledge concerning these areas be addressed? To improve _ geon's ability to reliably measure articu- posceaumatic arthrtis® From a re patient functioning following a dis Jarincongruiy (even ava la surface lke search perspective, posttraumatic ar- placed articular injury; itis critical to he tibial plateau) is rather poor, with a thritis is a difficul ropic to seudy. The develop research strategies to investi- 9596 confidence interval of +12 mm for overall spectrum of disease that can gare the role oF injury mechanisms that quantifying articular step-off." lead to clinical arthritis after injury is will allow the development of new extensive, ranging from articular frac- therapies to limit or prevent posetau- duction in a simple, low-energy frac tures to injuries wich ligamentous dis- matic osteoarthritis (OA). ture will result in significant pain and ruption to joint contusion without The material presented in this extremely poor function. In contrast, fiacture.”® Arccular fractures are ex- chapter is based on a combined Ortho- chere are other cases i which a poor amples of worst-case scenarios, with paedic Research Society and American reduction in highly comminuted physical disruption of the articular sur- Academy of Orthopaedic Surgeons fracture results in litle pain and good face, blunt impaction of the articular (AOS) symposium designed to &- function. Despite the desire to follow surface, and local hemarthrosis; these amine the spectrum of basic science © esrablished fracture tenets and princi- fractures are often associated with a clinical investigation in the role of In numerous instances, a perfect re: pls, observations indicate that the re systemic inflammatory response. Each biomechanics in the study of joint |arionship between articular reduction of these aspects of injury represents 4 injury and subsequent posttraumatic and outcome is neither as direct nor a8 unique physiologic and biomechanical archrits. fhanism that can contribute ro the braeietecbehsttet 584 © 2011 AAOS Instructional Course Lectures, Volume 60 [SE os Applied Biomechanics in Articular Injuries The simple bur nonincuitive truth is chat articular congruity is not the only factor thac influences outcomes after fraccure. An array of confounding variables, many of which are poorly understood, have & profound impact fon the patients outcome following an articular injury. Some of these fac- tors include the magnitude and type of articular injury, the magnitude of the soft-tissue injury, the patient's re- sponse co the injury, morphologic and mechanical differences becween joints, subtle but pronounced effects of joint kinematics and dynamic insta- bility, cartilage biology and its response ‘co injury, the patient's age and is effect on injury response, and the effects of load distribution chat is not restored with the restoration of articular con- sgruity Current research is helping clini- fans understand these factors. Appre- ciating the value of this new research and incorporating i into clinical prac- tice requires chat clinicians challenge their traditional thinking about articu- lar faccures. For example, articular ccongruitys injury to the articular cari- lage; and other Factors such as limb alignment, joint stability, and kine- matics can independently and in com- bination have an impact on patient iutcomes. Mose orthopaedic fracture surgeons focus on the primacy of artic- ular reduction in improving outcomes, ‘This approach is overly simplistic and does not take into account other fac- tors that have a profound impact on ‘outcomes. To overcome this bia, ici important to recognize several truths (1) All of the factors affecting out- comes are inextricably linked; there is no rational or realistic way to separate the effeets of one from the others (2) There is much evidence (new and cold) in the literature co indicate that articular reduction may not be the ‘most important factor in determining ‘outcomes. (3) The appropriate weight of various factors is nor yet known. If these truths are accepted, the clinician ‘ean acknowledge factors other than ar- ticular reduction as critically impor- tant to patient outcomes and can begin to incorporate these ictors in the cl ical care of patients with fractures. In science, only what ean be mea sured can be known. As medical scien- tists, orthopaedic feaecure surgeons should embrace work that cries co im- prove methods to measurably charse- terize articular injury; the body's 1e- sponse to it; and the mechanical, kinematic, and biologic effects of teat- ment. Research currently in progress includes finice element modeling ofin- jured and reconstructed joints,"7 methods for quantifying injury sever- methods for measuring cartilage health and response to injury" methods for measuring dynamic me- 1.21 methods for cor- chanical seresses, relating measurements with out- comes,” and methods for predicting outcomes and guiding treatment. The goals of these and other research stud- ies should be to better determine the relationships berween articular cart- lage injury, articular reduction, ocher ‘mechanical factors, and patient out comes. The support of orthopaedic cli- nicians is needed to continue this type of research. In daily interactions with col- leagues, staf, and patients, surgeons should indicate that they understand that factors other than articular align- ment are important to patient out- comes. Surgeons should be willing to recommend treatment other than open reduction and internal fixation when it is not clear chat articular re- duction will change the patient's out- come, Cartilage biology, joint and limb mechanies, and articular congru- ity should be considered when making treatment decisions and counseling pa- © 2011 AAOS Instructional Course Lectures, Volume 60 Chapter 45, Challenges and Advancements in Measuring and Modeling Articular Fractures Despite the need to objectively charac- terize articular injury, quantify injury response atthe tssue and whole-joint al and level, and measure the mecha biologie effects of treatment, few appropriate techniques to achieve these goals. Developing or refining as- sessment tools 10 yield reliable me- chanical data on joint injuries poses substantial biomechanical technical challenges. Although joint injuries are “global” events, the resulting patho- physiology originates locally at the tissue and cell levels the efficacy of therapeutic interventions (surgical and nonsurgical) depends on achieving fa- vorable local effects, One of the classic challenges has bocen co measure chronic cartilage in- sult caused by residual incongeuiies following imprecise reduction of intra- arsicular Fractures? Empirical clinical experience has shown that different joints and different specific fractures of these joints produce different tolerance levels fot atticular incongruity. Trying to reach agreement on specific accept- able tolerance levels has often resulted in controversy among leading sur geons. Corresponding aberrations of cartilage stress, either quasi-scatic stess concentrations locally near sites of sur- face irregularity or abrupt transients of cartilage stress associated with joint in- sability events, probably consticute much of the unifying explanation of why different joints behave or respond. so differently ‘Two distinct measurement method- clogies using Fuji lm (Sensor Products, Madison, NJ) or Tekscan pressure map- ping (Tekscan, South Boston, MA) have been developed for measuring cartilage contact sees. The Fujifilm method in- volves mechanockemical transduction 585 Orthopaedic Medicine process based on pressure-dependent rupture of populations of microcapsules (containing a phororeactive liquid) de- posited on the surface of paperlike ace- tate sheets. The sheets can be easily cut by hand to fit the articular anatomy of interest. The higher the contact pres- sure, the greater the fraction of micro- capsules chat rupture and the more in- tense the resulting (red) stain.” The intensity of the Fuji staining is nor- ‘mally quantified using laser scanning and digital image analysis. Accucacies in the range of 10% to 15% are the generally accepted norm. Because of the size scale of the microcapsules, for practical purposes the resulting stain pattems are essentially continuous, thus providing excellent spatial resolu- tion for assessing local details of pres- sure aberrations into the submillimeter range. The primary limitation of this method is thar che date capcures are necessarily static, reflecting the high- water mark of pressure experienced at any given site on the film. Despite this limitation, che Fuji film method has been useful in answering many prag- matic surgical questions concerning al- ternative fracture reconstruction tech~ niques and dose-response relationships between incongruity and the resulting pressure abnormality at various ana- omic sites #5 ‘The Tekscan transduction modality uses an entirely diferent methodology. Ie involves pressure-dependent changes in the electrical resistance berween lange numbers of intersection sites be- ‘ween rows and columns of conduc- tors, scparated by a thin layer of pi- exoresistive elastomer. This system enables transient recordings, although the spatial resolution of such record- ings i limited by the row-column den- sity of the conductor grid. Because trimming the sensors would destroy the electrical circuitry, che Tekscan sys- tem lacks the versatility of Fuji film to 586 be easily cur to fit the anatomy of in- terest, Past biomechanical applications have usually involved general purpose sensor geomesties designed for indus- trial purposes; therefore, this system ‘may provide suboptimal coverage of an anatomic joint surface, or it may be difficult accommodate the necessary (fragile) connecting cables. Recently, there have been several varieties of cus- tom biomechanical sensors developed for specific anatomic locations (the ence, the ankle, and the hip), provid- ing for well-conforming articular sut- face coverage and anatomically cogni- ant cable protection.** Currently, ‘maximum dara caprure rates exceed 100 frames per second, and available spatial resolutions are on the order of 0.5 mm? per sampling site. A major advantage of transient data collection is that a loaded joint can be studied throughout its range of motion, thereby providing information about habitual cartilage loading, rather than just snapshot information at specific in- stants that may notbe representative of the duty cycle and may not identify worst-case situations. Recent Tekscan measurements focusing on bial plafond fractures have identified incongruity-dependent abnormalities of local comtace stress magnitude and con- tac stress rates of change, shfis of glob- al load transmission patterns, and the occurrence of seemingly dramatically deleterious fluctuations of loading un- der conditions of joint insabiliey””** Computational advancements in articular joint contact mechanics have greatly reduced the need for depen- dence on physical experimentation. Fi- nite element techniques have spear- headed those developments. Previous limitations, which have recently been overcome, ate the ability to simulace cartilage contact under physiologically realistic joint-loading magnitudes and the rates of change of joint-loading iagnitudes in the presence of local in- congruities2” Another important de- velopment has been the use of numer- ical techniques to study the interaction ‘of solid and fluid components of eart- lage matrix for situations involving ar- ticular surface contact. This is an im- portant consideration in evaluating cal incongruities because of the heightened ease for fluid egress from rupcured cartilage surfaces. Another class of developments has been the ability to realistically simulate cartilage impaction events, both for impulsive loadings beeween native joine surfaces and for laboratory impaction events involving platen loading of exposed joint surfaces or of specialty osteo- chondral explant preparations. Proba- bly the most important current im- provement in articular contact finite clement analysis has been the develop- rent of novel meshing techniques to accommodate arbitrary derangements of joine surface geometry.**™ These improvements have allowed the study of actual clinically occurring fractures rather than geometrically idealized st- uations, such as straight-edged step- offs. These meshing techniques can be applied to prospective clinical scudies to quantify risk factors for degenera- tive change” ‘Assessing injury severity has been another fertile area for computational innovation. It was intuitively accepted thar joint fractures resulting from high-energy mechanisms had a greater risk for posttraumatic OA than low- energy fractures; however, a method £0 direcely quantify the involved energy did not exist. A fundamental rene oF engineering fracture mechanics of brit tle solids holds thae the kineric energy absorbed duzing the fracture event is transformed into fice-wurface energy of the resulting fragment fracture suf faces, In human clinical fractures, in- formation on fragment free-surface =~ ergy is available postfacto from CT mages ofthe fracture bed and is based © 2011 AOS Instructional Course Lectures, Volume 60 Applied Biomechanics in Articular Injuries con segmentation (edge delineation) of all individual fragments, a process that is well suited to automated computa- tional analysis. This has allowed “back- ing out” a measurement of the me- chanical. energy absorbed in bone fracture events. A series of laboratory computational/experimental studies has documented the quantitative accu- racy of the essential concept.>°** After several computational developments to streamline and expedice the analysis, ithas now been applied to human pro- spective studies,'” allowing objective identification of the relative risk of posttraumatic OA to individual pa- Another new area of computational development is the identification of anatomically correct reconstructions of displaced comminuted articular fiac- tures. Surgical reduction of such frac- tures must be done piece by piece, with Limited visibility, and with no way of knowing in advance ifthe reassem- bled fragments will result in gaps (espe- cially periarticularly) because of missing cor compacted fragments. An analogous | process of three-dimensional puzzle solving performed computationally pro- vides advanced information about ap- cit aerate nse propriate geometric reassembly of indi- vidual fragments and identifies any region(s) of void that will necessarily result? To implement this process, the puzale-solving algorithm begins with aucomated segmentacions of the © bony fragments, with their respective surface facets identified as being native periosteal surface, native subchondral plate, or de novo Fracture surface. Na- tive fragment surface facets are compu- tationally matched to geometrically corresponding sectors on a. surface remplate that is defined by misror im- aging of the intact contralateral limb. Successive fragment facets are then computationally “locked into place” using an iterative closest point algo- rithm in a manner that minimizes their topographic disparity with corre sponding sectors on the template sur- face. Homogencous surrogates with biofidelty, which were Fractured under controlled laboratory conditions, were initially used to tune the puzzle solver toachieve fragment reassembly accura- cy im the range of a few cenths of 1 mm. After porting this computational procedure (with appropriate modifica tions) co cadaver material, submilime- ter accuracies in fitting the template surfaces were maintained. Facilitated by new computational procedures to expedite fragment segmentation and an advanced surgeon-friendly graphic interface to manipulate fragments, the procedure has been applied to “puzzle- solve” a clinical case series of commi- rnuted tibial plafond fractures, 10 com- pare geometrically ideal versus surgically obtained reconstructions, and to help understand the practical difficulties in obsaining fully anatomic reconstructions (especially of the artic- ular surface) on a case-by-case bass, ‘A large-animal survival model of incra-artcular fracture that allows or- thopaedic interventions analogous to those for human clinical cases i also being developed. This model comple- ments the capabilities of a recently de- veloped mouse model, whose primary strengths were the abiliry to under- stand the pathophysiology and natural history of intra-articular fractures, es- pecially in concere with geneticlevel assessments and interventions. The large-animal model involves evaluating the hock joint of the adult Yucatan minipig after Fractures with controlled morphology (for example, replicable fracture line location on the articular surface) are achieved by a specially de- veloped offset impaction technique. ‘The investigator has knowledge and control of the delivery energy and im- paction force. At the whole-joint level, the fracture patterns closely resemble those of human tibial pilon fractures. © 2011 AAOS Instructional Course Lectures, Volume 60 Slee Chapter 45 At the cellular and tissue levels, che patcerns of matrix damage and cell death (and its temporal and spatial progression after impaction) closely re- semble those seen for impaction frac- tures of fully viable normal human an- Kle specimens obtained from above- knee tumor amputation patients Minipigs are clinically toleranc of both plate and screw internal fixation and spanning external fixation of the hock jing, the pigs shortly resume non weight-bearing protected limb usage. This model offers exciting promise for evaluating the efficacy of novel chera- peutic interventions screened in vitro and in small-animal (nonrecon- structible) fracture models and isa key laboratory testing step before cransla- tion to human clinical eral. Articular Cartilage Mechanical Injuries and OA Mechanical injuries of articular carti- lage can eesule from events such as mo- tor vehicle crashes, falls, and spores injuies. Such injuries can lead to pose traumatic OA, although the patho- physiologic processes are not filly understood.” Arcicular cartilage. responds 0 injury by two separate processes that are linked to each other through — mechanotransduc- tion.™*° During che injurious event, the tissue responds mechanically by deforming according t0 the applied load. Subsequentl, the biologic re- sponse starts when the mechanical forces applied to che tissue activate in- tracellular signaling OA can be thought of as a condi- tion that develops as a result of the overloading of healthy tissue (acute trauma) or from normal loading of ab- normal tissue. Overloading of healthy cartilage can immediately cause surface fissuring, cell death, and damage to the extracellular matrix from which the tis- sue cannot recover. Alternatively, over- loading of normal cartilage may cause 587 Orthopaedic Medicine subcritical damage that leads to less chanical properties of articular carti- entation. Each method radially con. fobust tissue, Subsequent loading of lage are che macroscopic result ofits strains surrounding tissue diferent this abnormal casilage, even at physi- underlying organization and biochem- Some studies have included preinjury ologic levels, can resul in chronic in- ical content. The collagen network of tise processing steps including the jury and damage accumulation that the issue governs tensile behavior, use of fallhickness cartilage versus vrentually manifest as OA. Artcular whereas proteoglyeans are necessary cartilage with the superficial zone te- Carlage does not heal well:® At- for resisting compression. The ten- moved, "* and equilibrating issue in « tempted selErepai results in the for- sie stiffness of articular cariage posi- culture medium before loading * mation of mechanically inferior tively correlates tissue collagen content These factors must be considered fibcocarilagelike issue, which has and collagen cros-linking, Within car. when comparing studies more collagen type Tand contains less lage collagen is atanged in a depth. flycovaminoglyean than normal aie- dependent manne. Collagen isparlel Early Postinjury Biology tar carilage”°® These biochemical to the articular surface in che superfi- and Treatment Changes lead o changes inthe disues cial zone, oriented randomly in the Following the mechanical response of tnechanical properties, preventing not- middle zone, and is perpendicular in cartilage co injury, biologie response smal function 2”? the deep zone as it anchors into the occurs. Within the tissue, mechanical Changes in the physical properties calcified eariage ayer. Inthe superti loading generate streaming potential, ofarticular cartilage concribuce signifi- cial zone, collagen also follows pre- stessstrain fields, and hydrostatic fantly tothe development of OA. Be- freed directions known as split lines. pressure, The biologic response stars Cause of damage and los of extracella-- The rssue is stiffer when pulled in the _ when chondrocytes experience the me- Jar matrix, the compressive and tensile direction of spic ines when compared chanical forces applied to the tissue triffness decreases and permeability in- with offaxis pulling. The proteoglycan and intracellular signaling cascades ae creases" Cartage ftom osteoarthritic contencof the tissue gives articular car- activated through stretch activated joines is chinner and more hydrated tilage its aby co rsse compresive channels and integfns locted in he wpa healthy issue. For example, are- loads because ofthe electrostatic repulr eel membrane."*"**° Following ths view by Knecht et aM? reported chat sion of the negitively charged l)~ mechanotransduetion, the biologic re the compressive stifiess of articular cosaminoglycans when forced into sponse to injury evolves over time cartilage decreases by 20% in early close proximity Injuries to arccular_Time-point for investigation afer am Sages of the disease, a change that catlage chat fect collagen or protco- in vitro mechanical injury have ranged probably would be undeecred by eur glheansalter the biomechanical behav- fiom 3 hours co 2 week. Sever cll rent clinical assessment methods, The ior ofthe disue. matrix adhesion molecules have shown decrease in compreaive stiffness cocre- The mechanical features ofthe ex- decreased expression as early as 3 hous fares with increased scores on the ternal system used for in vitro study of after injury.“ With the exception of Manin histologic scoring system for cartilage mechanical injury ae also im- SOX9, a transcription factor promos articular ertlage increased tisue hy- portant because the e7pe of loading, ing collagen sype Ul there i generally dation, and deceased sulfated gly- boundary condivions, and preinjury upregulation of gene expresion from onaminoglycan content. Te fice that sue processing al affect expeimen- 4 024 hows afer injury” ® Exam: Changes in tisue occur 40 early sug- ta outcome. Loading regimens have ples of uprgulated genes include ma gots thae timely intervention needed varied and include injurious compres. tix’ metalloproccinases (MMPS). a to alter the course of OA. Sion, single impacts, and cyclical grecanases, and inhibitors of MMPs loads:*-*” Different load magnitudes These enzymes break down type Il cok Mechanical Considerations and rates have been used with each of lagen and aggrecan, Further study has for In Vitro Studies of these regimens. Experimental setup suggested chese changes in gene o% Cartilage Injury (boundary conditions) must also be pression normalize by 2 wecks after in- Beene the Rest sponse of articular considered, Different serups with re- jury and MMP-3 expression switches Cartage to injury is mechanical, ic spectro the presence or absence of un- from, inreased co decresed api eae aivlewtand the intense derlying bone and loading methods son,” suggesting thar MMP-3 cosld snechanical characteristics ofthe essue have been used.’ The loading be marker for time after injury: and the mechanical features ofthe ex- methods include confined compres Articular cartilage degradarion © ternal sytem enising injury, The me- son, unconfined compression, and in- mediated by several factors such a ell 588 © 2011 AOS Instructional Course Lectures, Volume 60 OO ‘Applied Biomechanics in Articular injuries death, matrix degrading enzymes, and inflammation. In attempts to mitigate some of these changes, the poloxamer 188 has been used to decrease cel death. P188 is an 8.4 kDa nonionic surfactant txiblock copolymer of poly- coxyethylene and polyoxypropylene thar inserts into lipid membranes.” PPostinjury, promising results have been reported with P1883 in bot and in vivo rabbit models scudy by Phillips and Haus,”? P188 (6 mg/mL) was delivered in the culture medium following a 25-MPs load to cartilage explants. Wich P188 reat ment, chere were more viable cells in the superficial zone at | hour and in all zones at 24 hours but only if the ex- planes were manually compressed ‘Compression presumably aided P188 entry into the tissue. In a 4-day in vivo seudy, a one-time intra-articular injec- tion of P188 was effective at reducing cell death in impacted retropatellar cartilage A more recent study re- é ported that P188 reduced cell death in tibiofemoral cartilage 6 weeks after in- | jury” Navoli and Achanasiou”® evalu- ated P188 (8 mg/mL) following «wo levels ofimpact loading (1.1 and 2.8 J) using continuous treatment. They re ported a 759% decrease in cell death at 1 week following the 1.1 J impact, In contrast to the study by Phillips and Haur, no compression protocol was needed to achieve this benefit, perhaps because of the adoption of a continu- ‘us treatment regimen compared with a one-time treatment. A recent 2009 study showed chat PI88 treatment was more effective at decreising cell death in human ankle cartilage after impact than inhibition of caspase 3 or 9 (cwo cenaymes that drive apoptosis)” Fu- ture research should investigate com- bining teatments for apoptotic and necrotic cell death to further chondro~ cyte preservation after injury. Osreourthrtic chondrocytes do not behave like native, healthy chondro- Aimee ee RCTER ES ceytes.”® Because traumatic injury may shife the phenotype of chondrocytes remaining in the tissue toward cata- bolic processes, che previously de- scribed studies of eeatment to decrease cell death should be interpreted cau- tiously. The catabolic nature of these cells (for example, the production of -matrix-degrading enzymes and inflam- matory signals) is evident based on the continued degradation of articular car- tilage afer the inciting event. Al- though chondrocyte survival postin- juny is necessary for tissue healing, ic ‘may nor be sufficient. Future research must also address the behavior of via~ ble chondrocytes after injury and should include measurements of tissue mechanical properties to assess tissue functionality. Researchers should also seek interventions thac promote a heal- ing response. In addition to preventing cell death, research has been directed at decreasing extracellular matrix degra- dation and inflammation after me- chanical injury with methods such as pharmaceutical therapy.”” Controlled Creation of an Intra-Articular Fracture: Observations on the Natural History of Posttraumatic Arthritis “The mechanisms leading ro the pro- gression of posttraumatic arthritis fol- lowing articular fracrure are not well understood, After injury, several fac- tors may affect the development of posttrzumacic arthritis, including dis- ruption of the arvicular surface, vari able amounts of impaction ofthe at ular cartilage, residual displacement of the articular surfices, and exposure of blood and marrow products to the ar- ticular surface and synovium.’ Because these predisposing factors are insepara- bly clinically linked with che injury, vestigations of traumatic joint injury thar focus on a single aspect of the acute injury, such as blunt trauma to © 2011 AOS Instructional Course Lectures, Volume 60 ee Chapter 45 the articular surface, are t00 limiced. Traditional models of investigating 2 single aspect of injury trade simplicity for the complexity of 2 more realistic injury model system. To gain a broader perspective on the effects of intea-articular fracture, it is necessary to understand ehe natural history of che development, over time, of posteraumatic arthritis in a dis- placed articular injury. A model was developed to create a closed joint in- jury in 2 relatively reproducible fash- ion thar was usable ina survival animal model. Furman er al® described work to prove the concept that established the abiliey to create a closed fracture of the tibial plateau with varying degrees of severity. A single hind limb fracture was created in strain C57/BL6 mice. The fracture was allowed to heal wieh- ‘out attempts at fracture reduction or fixation, thus allowing the natural his- tory of posttraumatic arthritis to be studied; the contralateral limb served as an internal control. Faxitron imag- ing, micto-CT at the time of limb har- vest, and histologic analysis were used to assess the joints 6f both extremities from cach specimen. In che C57/BL6 mice, ehis injury reliably resulted in the development of a tricompartmen- tal arthritis a4 and.8 weeks afte injue ry, with complete loss of articular carti- lage by 50 weeks after injury.®” ‘Application of this method to the MRL/Mp} strain of mice proved en lightening. Clark et al®* was the First to describe the unique healing character istics of MRL/MpJ mice. Because these mice were able to spontancously regenerate tissue in ear punch holes ‘without searting, the stain was called the “super-healen.” The creation of similar types of closed tibial plateau fractures in the MRIMp] mice did not resule in the development of articular degeneration, despite articular Fracture and displacement.®? The observation that a displaced fracrure results in ar- 589 Orthopaedic Medicine = obtain adequate amounts of DNA to I generate reliable daca, Histologic anal lL — . | yas allows assessment of proteoglycan staining of cartilage and synovial cllu- lar response to fracture.*” Determining the cellular viability and immunohis- tochemistry of the joints allows assess ‘ment of the variation of response, over time, following articular fracture The inital focus of research has been on understanding the initial events in the development of tricom- partmental arthitis after fracrure in the C57/BL6 mouse strain, Early ef Energy of Fracture (i) fects of injury in the C57/BL6 strain ——— show that the loss of cellular viability Figare'1” Graph iusvatog the vlatonship between applied load (as repre- of chondrocyesparalicls he suc FIoMES by indenter displacement) and eneray of fracture inthe creation of a damage of the articular surface a de- Sa eciculer fracture in a murine model. (Reproduced with permission om termined by the modified Mankin his- core ABD, strand J, Hembree WC, Ward BD, Gullak F, Olson SA: Join de- —cologic scoring system for articular cat- generation folowing closed intraarticular fracture in the mouse knee: A model : Of postiraumatic artis. J Orthop Fes 2007;25(5)578-592,) Indenter Displacement (mm) (int tilage ® Additionally, changes in the synovium wich increasing cellularity are proportional co the increasing en- thrtis in one strain but nor in the model of tibia plateau fracture, then- ergy of fracture. cher suggests altering physiologic re- ergy of fracture hasan excellent corre- Preliminary results of comparisons Sponse to injury isa porenil interven- lation with che libersed fracture of early events following articulat fac- tion strategy. area®* ture in the C57/BL6 and MRL/Mp] Assessing the severity of injury is Interest in the physiologic response strains indicate important difference. challenging. Three methods of injury following articular fracture in the The severity of injury and the basic Severity assesment were applied inthis C57/BL6 and the MRL/Mp] mice fracture characteristics are similar be- rode (1) A modification of the strains stimulated che development of _cween mice strains, as is che initial in- AOIOTA classification for clinical novel techniques of assessing the re- crease in the cellularity ofthe synovial fractures wis applied to daca from fax- sponse. Standard serum analysis of cy- layer; however, local gene activation, iivon imaging and mieroCT® The ba- rokines and biomarkers is a valuable synovial fluid levels, and serum levels efor chanson system is,in pare, technique. Howeret, serum levels of ojtokines differ berwocn sins to suatfy discrete events ino varying alone reflect incomplete information In che C57/BL serain theres signif Categories of severity. (2) The applied abour physiologic response co injury. A icancly more robust inflammatory *= nergy and the energy ofinjury atime novel technique was developed for sponse to injury compared with se Sf feccure are boch known.” A plot quantitatively assessing cytokines and MRL/Mpj stain. One example ofthe showing the relationship benween ap- biomarkers in synovial fluid of the effec ofthis response is 2 marily n> plied energy andthe energy of facture knee of mice following injury. Using creased presence of activated macty shown in Figure 1 This relationship small amounts of a calcium sodium al- phages in the synovial lining of the allows the energy offraceue to becon- ginate compound 10 absorb synovial CS7/BL6 mice that persists wesks Troll. (3) Mieeo-CT from both con- fluid with conrolled lyase digestion al-_ after injury, whereas a cansiene blush trol and experimental limbs were used lows quantitative analysis.” Gene ac- of activated macrophages occurs int to determine the liberated fracture sur- tivation following injury can be as- cally in the synovium and then returns fhe as a thied severity measure. Au- sessed from synovial tisue.®® The to levels of the control limb in the thors have described che assessment of small amount of synovil tissue avail MRL/Mp] mice." Iberated faceare as a means of asset- able From this technique in mice eypi- This simple observation provides ing injury seve?” Tn che marine cally requires pooling of specimens tothe bass for new hypotheses regading 590 © 2011 AAOS Instructional Course Lectures, Volume 60 | Applied Biomechanics in Articular Injuries Chapter 45 mechanisms beyond the waditional tion, an improved ability to predict. 6. Martin JA, McCabe D, Walter M, njury patterns and patient char. BuckwalterJA, MeKinley TO: é N-acetyleysteine inhibits post- impact chondroeyr death in ox- view of residual displacement of thear- what ticular surface as the cause of arthritis acteristics are at a true high risk for | following fracture. Recent work in joint degeneration is needed to stu t eae teochondral explants. J Bone Joine eng seer tach pe lmrveoneathny bse - le. Sing om 2009°91(8)1890-1897 fence of necrotic material, macro- The need for prospective registries phages become activated or primed to with longitudinal follow-up is impor- 7 Borrell} J, Ricci WM: Acute produce more inflammatory cyto- tant ro identify these acrisk patient Orthop Relat Res 2004:423:33-39. | kines Disruption of the aricular populations. Approaching postau- y surface inherently produces necrotic matic arthritis from these varied per- © McKinley TO. Rudere MJ. chondrocytes and other cell types. Is spectives will contribute o a berter un- iy oona Ince In hu ate this a signal that can result in activa- derstanding of how articular injury ogy of posteraumatie arthritis tion of synovial macrophages? The contributes to this condition and will Clin Orthop Relat Res 2008; © question suggests 2 shift in perspective improve patient eat. 40334451 © from postraumatc archi asa con- 9. Llinas A, MeKellop HA, Mar- © sequence of injury tothe articular sur- shall GJ, Sharpe F, Kischen M, F face wo chat ofan organevel response ACknowledgments Sarmiento A: Healing and remod | oinjuryin which ehere is physiologic THe authors wish to acknowledge che ling of articular incongruiis n= | Ganaling beeveen arcu earalage CoMibutions of Farshid Guilak, PhD, rabbit fracture model. / Boe int | indore isuswithinthejoine New 264 Bridgewe Furman, BA, 0 this Sg4m 1993,75(10:1508-1528 H methods of investigating the effects of | ChPtE. 10. Baline L, Park SH, BellyeiA, © injury that consider the organ level re- ee 7 vise G: Repair of steps and gaps : sponse of the joint may offer new in- References in articular fracture models. Clin | Sights into this importa area. Orthop Relat Ret 20053130 i 1, Jacobs J: The Buren of Mesculor 208-218. / Summary ‘eleaal Diseases in the United Ser ade FB Injury tothe arcular sutace coneib- Suter Rosermon, IL American 11" Barta AE TE Nepal [esto che development ofthe clinical Academy of Orthopaedic Sur- ter TA: Radiographic faceure © condition recognized 2s posttraumatic «0+, 2008 assessments: Which ones can we © arbritis in a large number of patients 2, Brown TD, Johnston RC, Salz- reliably make? J Orshop Trauma © each year. The basic mechanisms by man CL, Marsh JL, Buckwal BONES P08 © which articular injury contributes co tet JA:Postraumatic osteoarthri- 12, Luche U, PlgeardS: Fractures of the development of joint degeneration tA Firs esimate of incidence, the tibial condyles. eta Orchop reamainy tmeomplerchy chersererized, prevalence, and burden of disease Scand 1971;43(4)366-376 Raat J Orohop Trauma 2006;20(10): 13, Ratmassen PS: Tibial condylar Currently, che clinical treatment of the Oaseee fracture itself is the primary form of fractures: Impairmene of knee intervention in attempting to prevent 3 Olion SA, Gulla F: From aricu- inne abit aan ncn fr the development of posttraumatic ar- theiti "Abb bow: ala ‘Surg Am 1973;55(0): 1331-1350. thritis. There sso nicole teopaned J Ontup Thuume ia anloge Obey Ke tervevions or other therapies aalable—2995;20(103651-662, ner L, Andeesson GD: Tibial con- at can prevent ot delay the onset o ae ee posttraumatic arthritis. Several lines of 4 Marsh JL, Buclewalte J, Gelber- follow-up. J Bone Joint Surg Am aman R, etal: Articular fractures ongoing research discussed in this Dauitsaaimaleraiesen rly 1986,68(1):13-19, chapter have the potential ro add to change the result? Bone Joint 15. Koval KJ, Sanders R, Borel J, the knowledge of posttraumatic arthi- Surg Am 2002:84-8(7)1259- Helfer D, DiPasquale T. tis, with the potential co identify fu 1271, ‘Mast JW: Inditecr reduction and percutaneous screw fixation of | ture eagets for intervention. 5. Bocelli J: Chondrocyte apopto- Aisplaed bil placeauf splaced tibial plateau fraceures Although patients with articular in- auc osetia arog, J Ons Tae 1992560) jury generally have an increased isk J Orthop Traum 2006;20(10): 340-346. for the development of joint degenera 726-731 © 2011 AAOS Insiructional Course Lectures, Volume 60 591 Ste ‘Orthopaedic Medicine 16, Honkonen SE: Indications for Increased peak contact stress after highly fragmented bone fractures, surgical treatment of tibial con- incongruent reduction of trans- SPIE Medical Imaging 200736512: Ale Fractures. Clin Orchop Relat verse acetabular fractures A ca- 6512(1P1)-6512(1P10). Res 1994;302:199-2 daveric model. J Trauma 2001; 35, Chrisman OD, Ladenbauer Bellis 17. Anderson DD, Mosqueda T, BUCTORTID: IM, Panjabi M, Goeltz S: The ‘Thomas T, Hermanson EL, 25. Moed BR, Ede DE, Brown TD: relationship of mechanical trauma Brown TD, Marsh JL: Quanify- Fractures of the olecranon: An and the early biochemical reac- ing tibial plafond fracture severity in vitro seudy of elbow joint tions of osteoartritc cartilage. “Absorbed energy and fragment secesses after tension band wire (Clin Orchop Relat Res 19815161: Sipsenent ae ink Eon res prosimal face 275-284, rank ordering. J Orthop Res 2 fragment excision. J Trauma ; 26(8):1046-1052. 3002:53(6):1088-1093. 34, Wang JH amp BEA 7 18, Hembree WC, Ward BD, Fur- 26, Brown TD, Rudert MJ, Gro- robiology. Biomech Model Mecha- rman BD, et al: Vibilty and sland NM: New methods for s- nobiol 2006;5(1):1-16. apoptosis of human chondrocytes sessing cartilage contact stest after 35. Knobloch TJ, Madhavan S, in osteochondral fragments fol- articular fracture. Clin Orthop ST Asal S is eres ian eerie font — ‘ela By 2004S SLB Nan Ags San: re ep0799(1051389-1395. 27, Gonham-Voss CM, Me- fea oe alae 19. Anderson DD, Goldsworthy JK, Kinley TO, Brown TD: A finite nals. Crit Rev Eukaryot Gene Expr Shivanna K, etal: Intra-arcicular clement exploration of cartilage 2008;18(2):139-150. onsacr ses disbutions a the Sue nearan area ncongrty : Y 36, Hunker EB Arcular cat

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