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Articular Cartilage Lesions of the Patellofemoral Joint in Dogs With Naturally Occurring Cranial Cruciate Ligament Disease

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Page 1: Articular Cartilage Lesions of the Patellofemoral Joint in Dogs With Naturally Occurring Cranial Cruciate Ligament Disease

Articular Cartilage Lesions of the Patellofemoral Joint inDogs With Naturally Occurring Cranial Cruciate LigamentDiseaseKimberly A. Agnello1, DVM, MS, Diplomate ACVS, Ian G. Holsworth2, BVSc, MACVSc, DiplomateACVS, Ana Vanessa Caceres1, DVM, Diplomate ACVR, Dorothy Cimino Brown1, DVM, MSCE, DiplomateACVS, Jeffery Runge1, DVM, Diplomate ACVS, Michael Schlicksup3, DVM, Diplomate ACVS, andKei Hayashi4, DVM, PhD, Diplomate ACVS1 Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania ,2 Veterinary Medical andSurgical Group, Ventura, California ,3 Veterinary Specialty Care, Mount Pleasant, South Carolina and 4 Department of Clinical Sciences, College ofVeterinary Medicine, Cornell University, Ithaca, New York

Corresponding AuthorDr. Kimberly A. Agnello, DVM, MS,Diplomate ACVS, Department of ClinicalStudies, School of Veterinary Medicine,University of Pennsylvania, 3900 DelanceyStreet, Philadelphia, PA 19104‐6010.E‐mail: [email protected]

Submitted November 2012Accepted May 2013

DOI:10.1111/j.1532-950X.2014.12107.x

Objective: To evaluate frequency, severity, and location of patellofemoral (PF)osteoarthritis (OA) in dogs with naturally occurring cranial cruciate ligament (CCL)disease.Study Design: Cross‐sectional observational study.Animals: Dogs (n¼ 40; stifles, 44).Methods: Stifle arthroscopic video recordings and radiographs were performed.Cartilage pathology was scored at 3 locations (proximal, middle, distal) in the trochleargroove and patella. A radiographic osteoarthrosis and synovial pathology score wereassigned. A Kruskal–Wallis test was used to determine if lesion severity varied by site,synovitis, and osteoarthrosis, and the Dunn’s test was used for pairwise comparisons.The variability of body weight was evaluated using 1 way ANOVA; P<.05 wasconsidered significant.Results: Cartilage pathology and synovitis was identified in all PF joints. Theproximal aspect of the trochlear groove had significantly higher cartilage scores than themiddle and distal sites and themiddle groove site was significantly higher than the distalsite. The distal aspect of the patella had significantly greater scores than the middle andproximal patellar locations. Higher synovitis scores were associated with increasedcartilage scores. Cartilage scores were significantly greater in stifles with higherradiographic osteophytosis, tibial sclerosis, and patellar enthesiophytosis scores.Higher body weights were significantly associated with greater synovial andradiographic scores.Conclusions: Dogs with CCL disease have a high incidence of PF cartilage pathologyand the severity of cartilage lesions varies depending on location within the joint.

Cranial cruciate ligament (CCL) disease is one of the mostcommon orthopedic conditions in dogs1,2 and is the leadingcause of degenerative change in the canine stifle joint.3 Themain weight bearing, femorotibial portion of the joint haslong been the major focus for examination of degenerativechange in the stifle4–6; however, limited information existson the alterations in the patellofemoral (PF) region in dogswith CCL disease. Osteoarthritis (OA) of the PF joint hasbeen reported in dogs with naturally occurring CCLdisease7 and in dogs with experimentally induced CCL

insufficiency.8,9 In 1 study, 34 of 40 canine stifles with CCLdisease had cartilage lesions in the PF joint.7 Similarly, dogswith experimentally transected CCLs had cartilage hyper-trophy in the PF joint in the early time period aftertransection.8,9

Cartilage damage and associated PF pain is a frequentlyencountered problem in people presenting for knee com-plaints.10,11 PF pain is both complex and multifactorial withnumerous proposed causes and risk factors.11–13 It is acondition seen alone or associated with other knee prob-lems.14–16 Anterior cruciate ligament injury is a wellrecognized risk factor for developing PF pain and OA inpeople, is reported in patients with conservative, medicaltreatment for anterior cruciate ligament injuries, and is one of

All work was performed at the University of Pennsylvania,Matthew J. Ryan Veterinary Hospital, 3900 Delancey Street,Philadelphia, PA 19104‐6010.

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the most common complications after surgical reconstruc-tion.14–18

Abnormal PF contact and tracking (dynamic PF alignmentthroughout range of motion) is a commonly recognized theoryfor the development of PF osteoarthritis and pain.19–22 In thedog, contact mechanics and alignment of the PF joint have beenexamined ex vivo in canine cadaveric limbs with transection ofthe CCL.23 After transection of the CCL ligament, the peakcontact area was located more proximally in the trochleargroove and there was an increase in the patellar tilt angle whencompared to the CCL intact cadaver stifles.23

It is our clinical impression that PF cartilage lesions arefrequent. Therefore, our purpose was to evaluate the incidenceand severity of PF osteoarthritis in dogs with naturallyoccurring CCL disease. This included examination of thelocation and severity of articular cartilage pathology on botharticular surfaces of the trochlear groove and the patella.Associations with synovial inflammation, radiographic signsof OA, competence of the CCL, meniscal injury, andsignalment were examined. We hypothesized that dogs withnaturally occurring CCL disease will have a high incidence ofPF OA and the distribution of cartilage lesions will mimic thechanges in retropatellar contact mechanics and malalignmentobserved in an ex vivo cadaveric biomechanical study.23

MATERIALS AND METHODS

Dogs

Forty dogs admitted for treatment of CCL disease byarthroscopic exploration and surgical stabilization werestudied. Owner consent was obtained for arthroscopicexploration and surgical stabilization. Method of surgicalstabilization was determined by surgeon and owner preference.

History and Physical Examination

Dogs had no prior history of other orthopedic disease orsurgery performed on the affected stifle. Age, breed, gender,and weight were recorded. Each dog was examined forlameness, stifle joint effusion, stifle pain, cranial drawer,and tibial thrust. If cranial drawer and tibial thrust were notappreciated, CCL pathology was diagnosed at the time ofarthroscopic exploration. CCL competence was based onthe ability to palpate gross instability of the stifle (i.e.,presence of cranial drawer and tibial thrust). Dogs withpalpable cranial drawer and tibial trust were consideredincompetent, even if intact fibers of the CCL were identifiedduring arthroscopy, whereas, a competent ligament referredto partial tears of the cranial cruciate ligament withoutdetectable gross instability.

Radiography

Two orthogonal digital radiographic projections (cranial–caudal and medial–lateral) of the affected stifle joint were

obtained before surgery to rule out any concurrent orthopedicabnormalities and for radiographic assessment scoring. Allradiographic assessment and scoring were performed by a singleboard certified radiologist (AVC). Radiographic osteoarthrosisscoringwasmodified using a previously reported scoring system(Table 1).6 Stifle radiographs for each dog were given a globalosteoarthrosis score (0–3): 0¼ no signs of osteoarthrosis;1¼ barely visible or mild signs; 2¼moderate osteophytosisobserved on some of the stifle joint bones (predominantly thetibia); and 3¼ stifle had severe signs with marked osteophytosiswith all bones of the stifle joint (femur, tibia, patella, and fabella)affected. A stifle joint effusion score (0–2) was assigned to eachstifle: 0¼ no radiographic evidence of stifle joint effusion;1¼mild or 1/3 obliteration of the infrapatellar fat pad; and 3¼ 1/2 obliteration of the infrapatellar fat pad with caudal bulging ofthe joint soft tissues. An osteophytosis score (0–3) was assignedto each stifle joint: 0¼ no radiographic osteophytes identified;1¼minimal or questionable osteophytes identified; 2¼ defini-tive identification of osteophytes (mild to moderate in amount);

Table 1 Radiographic Assessment Scoring System6 of the CanineStifle Used to Evaluate Cranial–Caudal and Medial–Lateral RadiographicViews of Stifles With Naturally Occurring Cranial Cruciate LigamentDisease

Global osteoarthritis score (0–3)0 No signs of

osteoarthrosis identified1 Barely visible or mild

signs of osteoarthrosis2 Moderate amount of osteophytosis

visualized on some of the stiflebones (predominantly the tibia)

3 Severe signs with marked osteophystosisinvolving all bones of the stifle

Effusion score (0–2)0 No effusion identified1 1/3 obliteration of the infrapatellar fat pad2 1/2 obliteration of the infrapatellar fat pad

and caudal bulging of joint soft tissuesOsteophytosis score (0–3)0 No radiographic osteophytes identified1 Minimal or questionable osteophytes

visualized2 Definitive identification of osteophytes

with a mild moderate amount3 Marked osteophytes on all bones of

the stifle jointIA mineralization score (0–2)0 No mineralization identified1 Minimal or questionable mineralization

visualized2 Definitive mineralization visualized

Tibial sclerosis score (0–1)0 None identified1 Tibial sclerosis visualized

Patellar osteophytosis score (0–1)0 None identified1 Patellar osteophytes visualized

Trochlear groove osteophytosis score (0–1)0 None identified1 Trochlear groove osteophytes visualized

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and 3¼marked osteophytes on all bones in the stifle joint. Astifle intra‐articular mineralization (0–2) score was given to eachstifle: 0¼ no mineralization; 1¼ questionable or mild minerali-zation; and 2¼ definitive mineralization identified. Patellarenthesiophytosis, trochlear ridge osteophytosis, and tibialsclerosis were independently scored for each stifle (0–1): 0¼ thevariable of interest was not present and 1¼ the variable waspresent.

Arthroscopic Stifle Exploration

A systematic and complete stifle joint exploration wasperformed in all dogs by a single board certified surgeon(KAA). High definition video recordings (Stryker1, San Jose,CA)were obtained of the proximal joint capsule synovium, andthe patella and trochlear groove cartilage. All synovial andcartilage scoring was performed on the video recordings at alater time period by a single observer (KAA). A previouslydescribed synovial pathology scoring system was used(Table 2).4 A score of 0 was given to the normal jointsynovium that was opal white, semitranslucent, and had asmooth surface, along with sparse well defined blood vessels.A score of 1 represented slight changes consisting of focalinvolvement with slight discoloration, visible proliferation,fibrillation, and thickening, along with a notable increase invascularity. A score of 2 was associated with mild changes withdiffuse involvement, slight discoloration, consistent notableproliferation, fibrillation, and thickening with notable increasein vascularity. A score of 3 signified moderate diffuseinvolvement, severe discoloration, consistent notable prolifer-ation, fibrillation, and thickening with a moderate increase invascularity. A score of 4 represented marked changes,consisting of diffuse involvement, severe discoloration,consistent and marked proliferation, fibrillation, and thicken-ing with diffuse hypervascularity. Finally, a score of 5 denoted

a synovium with severe diffuse involvement, severe discolor-ation, consistent and severe proliferation, fibrillation, andthickening along with severe hypervascularity.

A modified Outerbridge classification system was used tograde the cartilage of the patella and the trochlear groove.4,10,24

Three regions along the articular surface (proximal, middle,distal) of the trochlear groove and the patella were scoredindependently (Fig 1). A Modified Outerbridge score of 0represented a smooth articular cartilage surface; a score of 1meant the articular cartilage surface was fibrillated and/or had aroughened surface; a score of 2 represented a fibrillated surfacewith focal and partial thickness cartilage lesions; a score of 3was identified as cartilage lesions that were full thickness, andhad deep defects to the subchondral bone with surrounding

Table 2 Synovial Arthroscopic Pathology Scoring System4

Gross Characteristics Score

Normal Opal white, semitranslucent, smooth,with sparse well defined blood vessels 0

Slight Focal involvement, slight discoloration,visible proliferation/fimbiation/thickening,notable increase in vascularity 1

Mild Diffuse involvement, slight discoloration,visible proliferation/fimbiation/thickening,moderate vascularity 2

Moderate Diffuse involvement, severe discoloration,consistent notable proliferation/fimbiation/thickening, moderate vascularity 3

Marked Diffuse involvement, slight discoloration,consistent and marked proliferation/fimbiation/thickening, diffusehypervascularity 4

Severe Diffuse involvement, slight discoloration,severe proliferation/fimbiation/thickening,thickening to the point of fibrosis,severe hypervascularity 5

Figure 1 Illustration of the locations within the patellofemoral jointwhere cartilage scoring was performed. Three locations (proximal,middle, and distal) were examined on the articular cartilage surface of thetrochlear groove and the underside of the patella. TP, trochlear grooveproximal; TM, trochlear groove middle; TD, trochlear groove distal; PP,patella proximal; PM, patella middle; and PD, patella distal.

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damage; and finally a score of 4 represented large areas of full‐thickness cartilage loss (eburnation).

Data Analysis

Descriptive statistics were calculated. Continuous data wereexpressed as mean� SD, unless not normally distributed, inwhich case median values and ranges were reported.Categorical data were expressed as frequencies. Because ofnonnormality of the data, Kruskal–Wallis tests were used toevaluate the severity of the cartilage lesions by (1) location ofthe lesions, (2) synovitis score, and (3) radiographic features ofthe joint (joint effusion score, global osteophytosis score, intra‐articular mineralization score, tibial subchondral sclerosisscore, and patellar and trochlear ridge osteophytosis scores).The Dunn procedure was used to compare specific pairs if theKruskal–Wallis test was significant. One‐way ANOVA withBonferroni adjustment for multiple comparisons, was used toevaluate the variability of body weight by those same variables(lesion location, synovitis score, and radiographic findings).P<.05 was considered statistically significant. Statisticalanalyses were performed with software (Stata version 11,StataCorp, College Station, TX).

RESULTS

This study included 44 stifles (19 left, 25 right) of 40 dogs (24females [22 spayed, 2 intact], 20 males [18 castrated, 2 intact])with naturally occurring CCL disease. Mean body weight was36.2 kg (range, 6.4–81.8 kg) andmedian age, 5 years (range, 2–9 years). Breeds were: Labrador Retriever (n¼ 10), mixedbreed (n¼ 9), Newfoundland Mastiff (n¼ 2), Boxer (n¼ 2),and 1 each of Beagle, English Bulldog, Doberman Pinscher,Yorkshire Terrier, Rottweiler, Cane Corso, Cairn Terrier,Golden Retriever, Bernese Mountain Dog, German Short-haired pointer, Great Dane, Shiloh Shepard, Portuguese WaterDog, and German Shepherd Dog (Table 3).

Cartilage lesions were identified in all 44 stifles (Fig 2).Cartilage scores varied depending on location within the PFjoint (P<.001; Fig 3). The proximal trochlear groove site (TP)had significantly higher cartilage scores than the middle (TM)and distal (TD) trochlear groove locations (P<.001). TM wassignificantly greater than TD (P<.001). TP was alsosignificantly greater than all of the patella sites (proximal,middle, and distal; P<.001). When examining cartilagelesions identified on the articular surface of the patella, the

distal aspect of the patella (PD) had significantly greater scoresthan the middle (PM) and proximal (PP) patellar locations(P<.001).

All 44 stifles had synovitis. Higher synovitis scores wereassociated with increased cartilage lesion severity (P<.001).Stifles with a score of 3 (P<.003) or 4 (P<.001) hadsignificantly higher cartilage scores in the PF joint. Cartilagescores were significantly higher in stifles with higherradiographic osteophytosis (P<.001), tibial sclerosis(P<.001), and patellar enthesiophytosis (P<.001) scores.Dogs with synovitis scores of 3 (37.4� 17.0 kg) or 4(45.0� 14.9 kg) had a significantly higher body weight thanthose with synovitis scores of�2 (21.3� 16.0 kg;P¼.047 andP¼.006, respectively). Body weight was significantly greaterin dogs with stifles that had tibial sclerosis (31.8� 15.9 kg vs.51.4� 16.6 kg; P<.002), and patellar (22.8� 15.3 kg vs.38.8� 17.4 kg; P<.03) and trochlear ridge (28.6� 16.6 kg vs.41.5� 17.1 kg; P<.02) osteophytosis evident on radiographs.An increased body weight was also significantly associatedwith higher cartilage scores (P<.001). Dogs with severityscores of 1 (39.8� 16.9 kg), 2 (40.2� 17.1 kg), and 3(50.0� 19.1 kg) had significantly higher bodyweights(P<.001 in all cases) than dogs with a severity score of 0(26.7� 15.0 kg).

Six of 44 stifles (13.6%) explored had competent partialCCL tears. None of the competent stifles had gross meniscaltears requiring a partial meniscectomy and 12 of theincompetent stifles (27.2%) had gross meniscal tears with asubsequent partial meniscectomy.

DISCUSSION

In this group of dogs with CCL disease, articular cartilagelesions in the PF joint were commonly identified. We foundsome degree of cartilage pathology in all 44 PF jointsexamined. The severity of the cartilage lesions varied based onthe location within the joint. In the trochlear groove, severity ofcartilage lesions decreased from proximal to distal, whereas inthe patella the most affected site was the distal location. Theproximal aspect of the trochlear groove was the most severelyaffected location in the joint and pathology was noted in allstifles at this location.

Cartilage changes have been reported previously in the PFjoint of dogs with CCL disease,7 although the frequency ofoccurrence was higher in our study. Voss et al.7 reported 34 of40 stifles (85%) had cartilage lesions in the PF joint, whereaswe found all 44 stifles had pathology. One possible differenceis that Voss et al.7 did not specify the location of scoring andonly 1 score was given to the entire PF joint. Therefore, lesionsmay not have been identified because all surfaces were notconsistently examined or an “average” score was give to thejoint as a whole. We expanded on the evaluation of PF jointwhere we observed both joint surfaces (patella, femur) and at 3locations along each of the surfaces (proximal, middle, distal).

PF joint biomechanics have been studied in caninecadaveric stifles with CCL transection.23 This ex vivo studyidentified that the CCL deficient stifle had a proximal shift in

Table 3 Arthroscopic Articular Cartilage Scoring System4,10

Gross Characteristics Score

Smooth surface 0Slightly fibrillated/roughened surface 1Fibrillated surface with focal partial thickness lesions 2Deep lesions with surrounding damage 3Large areas of severe damage 4

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the peak pressure location in the trochlear groove and anincreased patellar tilt when compared with nontransected CCLstifles.23 The biomechanical changes identified in the cadaverPF joints23 are consistent with the locations where we identifiedthe most severe pathology in dogs with naturally occurringdisease. Alterations from the normal mechanical loading acrossjoints have been associated with the onset and progression ofOA25,26 suggesting that the inciting cause in the PF joint with aCCL tear may be mechanically induced. Guerrero et al.23 didnot identify an increase in the peak pressure across the joint withCCL transection, but rather a change in the pressure location. Inthe CCL intact or nonaffected stifle, the cartilage at this moreproximal site does not normally incur these forces and thereforethis altered mechanical environment may initiate cartilageinjury.We found examining this site, that in addition to cartilagelesions, there was marked hypervascularity of the proximal

adjacent joint capsule and in some cases pannus extended overthe damaged proximal trochlear articular cartilage. Thesignificant change in patella alignment with an increasedpatellar tilt allows for abnormal contact or forces not normallyexperienced by cartilage in the distal aspect of the patella.23

Similarly, we found this to be the most severely affected site onthe patella in dogs with naturally occurring CCL disease.

The triggers for induction of PF OA, in CCL insufficientstifles, is suggested by these alterations identified in themechanical loading of the PF joint23,25,26; however, the trueinciting cause of OA is unknown. Debate exists aboutmechanical versus biochemical versus structural changes asthe initiating event in development of OA; however, themultifactorial nature of the disease suggests all are likelycontributing factors.25–28 In CCL deficient stifles, although thecontact mechanics and alignment are altered, the overall totalretropatellar force is decreased in the PF joint.23,29–31 This isthought to be because of the decreased extensor force acting onthe PF joint when the CCL is incompetent.23,31–33 Any changein the loading mechanics of a joint can be posed as a risk factorfor development of OA. Interestingly, unloading a joint is manytimes used as a treatment to decrease pain in patients where OAis already present.34 Advancement of the tibial tubercle wasdescribed in people to decrease the retropatellar forces andtherefore decrease pain from PF OA and malalignment.32,33,35–40 In dogs, the tibial tuberosity advancement (TTA) procedureis a common method used for stabilization of the stifle afterCCL injury.41–43 The contact mechanics and alignment of thePF joint in the CCL transected stifle with the TTA stabilizationtechnique closely restores that of the nontransected CCL stifle,but with continued reduction in retropatellar force.23 Guerreroet al.23 suggested that restoration of the contact mechanics ofthe PF joint may be advantageous in cases with significant PFOA, to potentially decrease the rate of OA progression. Theyalso suggested that TTA could be beneficial in dogs with PFOA because of its effects on retropatellar force,23 and thepotential clinical benefits of unloading joints with OA.34

However, caution must be taken into consideration whenextrapolating these speculations with clinical cases. Theretropatellar forces, contact mechanics, and alignment of thePF joint have also not been examined in other surgicalstabilization techniques commonly used for CCL diseasetreatment in dogs.

Figure 2 Arthroscopic images of the patellofemoral joint of dogs with cranial cruciate ligament disease. (A) Articular cartilage of the proximal trochleargroove with minimal change; and (B) a trochlear groove with deep cartilage lesions and a modified Outerbridge score of 3. (C) Articular cartilage of thedistal patella with no abnormalities; and (D) a distal patella with severe fibrillation, deep cartilage lesions, and a modified Outerbridge score of 3.

Figure 3 Box and whisker plots of the modified Outerbridge cartilagescores of the trochlear groove and the patella in the patellofemoral joint.The bold line within the box represents the median cartilage score (50thpercentile) and the box represents the 25th and 75th percentiles.Whiskers above and below the box indicate themaximum andminimumdata scores. The symbol & represents a significant difference betweenthe proximal and middle locations, # represents a significant differencebetween the proximal and distal locations, and $ represents a significantdifference between the middle and distal locations (P< .05).

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Synovitis was identified in all stifle joints examined.Inflammation of the synovium is a well‐known component ofOA and CCL disease in dogs44–46 and likely plays a key role indevelopment and progression of OA.47 In people, the presenceof synovitis in patients with OA is associated with increasedpain and joint dysfunction and may be a predictive factor ofincreased rates of cartilage loss.48–52 Our results support thisidea that higher degrees of synovitis are associated with moresevere cartilage lesions, and again that inflammation is animportant contributor to both development and progression ofOA.

Another interesting finding was that increasing bodyweight was associated with higher cartilage severity scores,synovitis, and some radiographic scores. The significance ofthese associations is unknown and may suggest that largerbreed dogs have more severe detectable disease. A limitation ininterpretation of this information is that we only examinedbody weight and did not take into account body condition scoreor body mass index. These measurements would most likelyprovide a more complete understanding in determining if dogsize or overweight conditioning is the result of more severedisease.

Six stifles included in this study had competent partialCCL tears. Although this is a small number, they all hadsimilar patterns of cartilage damage as the incompetent PFjoints and did not have any significant differences in any of thevariables examined when compared with incompetent stifles.This suggests that potential micromotion or microinstabilitymay exist in the femorotibial joint of stifles with partial tears,which can not be palpated grossly. Therefore, this micro-instability may result in similar alterations in the biomechanicsseen with an incompetent stifle. However, this is onlyspeculation and alternatively all joints examined had synovitispresent, which may be the contributing factor to thedevelopment of the cartilage pathology observed. Also, thereis a limited number of partial tears in the study and a lack ofdata on contact and pressure changes in stifles with partialtears.

Radiographic examination of the entire stifle and PF jointhad some associations with the degree of cartilage damage inthe joint. Tibial sclerosis, an overall stifle osteophytosis score,and enthesiophytosis of the patella were associated with highercartilage lesion scores in the PF joint. Patellar enthesiophytosiswas the only change specific to the PF joint and may be anindicator of more severe PF cartilage damage. However, not allstifles with cartilage lesions in the PF joint had radiographicpatellar enthesiophytes. Therefore, cartilage lesions may bepresent without radiographic changes. Although, not examinedin this study, patellofemoral joint space in a flexed medial–lateral radiographic projection has been shown to increase afterCCL stabilization in dogs.53 This increase in joint space wasspeculated to be because of changes to articular cartilagethickness and the development of OA; however, this was notconfirmed by gross examination of the articular cartilage.53

Alternative radiographic projections, such as the dorsoprox-imal‐dorsodistal or “skyline” view of the patella and trochleargroove may be beneficial in diagnosing PF disease. However,in people there is variable data showing the benefit of the

skyline view in diagnosing PF OA.54–56 Magnetic resonanceimaging (MRI) is the preferred noninvasive imaging modalityused in people for detection and evaluation of articular cartilagelesions.57–59 Unfortunately, in dogs, poor delineation of thearticular cartilage on MRI has been reported, making thepresence and degree of cartilage damage difficult todetermine.60,61

An important limitation of our study is that, although thecartilage and synovitis scoring were performed at a later timethan the arthroscopic surgery, the observer was not blinded tothe clinical presentation and radiographs of the dog. This mayhave allowed for bias in the scoring of the cartilage andsynovitis abnormalities.

In people, patellofemoral OA and pain have beenobserved in patients in both short and long term outcomeperiods after ACL injury.14–18 In long term follow‐upexamination of patients ranging from 2 to 15 years afterACL injury, PF OA was identified in both the ACLreconstructed knees and the conservative, medically managedpatients.14–16 Also, patients who developed PF OA experi-enced worse overall final outcomes for knee function andcomfort.16 We identified that PF OA exists in dogs with CCLdisease, but there is no information on the clinical con-sequences of PF cartilage pathology in dogs.

Summarily, we identified a high incidence of PF OA indogs with naturally occurring CCL disease and propose that theabnormal mechanical loading and joint malalignment identi-fied by Guerrero et al.23 in an ex vivo canine cadaveric model,most likely contributes to development of PF joint OA. Furtherstudies are needed to determine the clinical consequence andsignificance of PF OA in the dog.

ACKNOWLEDGMENT

We would like to thank John Doval from the University ofCalifornia, Davis for his contribution of the graphic artwork design.

DISCLOSURE

The authors report no financial or other conflicts related to thisreport.

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