(BQ) Part 2 book Pediatric and adolescent knee surgery has contents: Transarticular drilling of osteochondritis dissecans, meniscal allograft transplantation, salter harris distal femur and proximal tibia fractures, patella sleeve fractures,... and other contents.
SECTION Osteochondritis Dissecans CHAPTER Eric W Edmonds Henry G Chambers 21 Osteochondritis Dissecans: Overview, Epidemiology, Etiology, Classification, Assessment INTRODUCTION Although loose bodies within a joint were first described by Paget,1 König later suggested three methods by which loose bodies could be created: (1) direct trauma with acute fracture, (2) minimal trauma that develops into osteonecrosis and subsequent fragmentation, or (3) no trauma with spontaneous fragmentation The latter variety he coined osteochondritis dissecans (OCD).2,3 Although it should be pointed out that the exact pathophysiology remains unknown, it is agreed that OCD is likely an acquired lesion of subchondral bone Beyond this characterization, it is less clear There are degrees of osseous resorption, collapse, and sequestrum formation with possible involvement of the articular cartilage through delamination unrelated to an acute osteochondral fracture of normal cartilage (Fig 21.1).4,5 This understanding of the end point of the disease process has led to many etiologies of OCD being postulated (particularly concerning the knee) including trauma,6,7 inflammation,2,8 genetics,9 vascular abnormalities,10,11 and constitutional factors.12 However, the etiology remains unknown, even though our veterinary medicine colleagues have made some leaps in understanding over recent years.13,14 Historically, there has been a distinction between juvenile-onset OCD and adult-onset OCD Many surgeons have suggested that skeletally immature patients (juvenile onset) have a better prognosis that has been inconsistently defined in the literature as either radiographic healing or merely resolution of pain.4,5,9,11,12,15 Despite the lack of an open physis at the time of diagnosis in an adult OCD, however, many authors suggest that the only true difference between juvenile- and adult-onset OCD is purely a reflection of patient age at the time of diagnosis A recent definition of human OCD lesions, proposed by the Research in Osteochondritis of the Knee (ROCK) study group, highlights the fact that these are (1) focal, (2) idiopathic, (3) involve subchondral bone, and (4) risk instability and disruption of articular cartilage with potential long-term consequences, such as premature osteoarthritis.16 This definition is the summary of epidemiology, etiology, classification, and assessment of OCD EPIDEMIOLOGY There are only three true epidemiology papers regarding knee OCD.10,17,18 The first was performed by Marsden and Wiernik18 in a review of 18,405 radiographs at a military hospital They found an incidence of symptomatic OCD of 2.3% of the radiographs and an overall incidence (including incidental discovery) of 4% OCD in their cohort A classic study by Linden10 in 1977 from Malmo, Sweden demonstrated an incidence of 29 per 100,000 boys and 19 per 100,000 girls More importantly, after he reviewed radiographs and obtained follow-up with many of these patients 33 years later, he discovered that there was an “accumulated risk of roentgenographic gonarthrosis in patients who have had osteochondritis dissecans.” If he assumed the risk of arthritis to be 0% at the start of life, this was unchanged at age 40 years with an OCD; but the risk increased to 70% at age 48 years and continued to increase to 95% at 70 years of age However, in those initially discovered with juvenile-onset OCD, he could not directly correlate any pathology such as gonarthritis with their OCD directly The only other study was published in 2014 and included a review of just over 1 million children aged 2 to 19 years within a closed health system.17 These authors found 192 children with 206 OCD lesions of the knee The majority (64%) of the lesions involved the medial femoral condyle, and the overall incidence seen in the cohort was 18.1 per 100,000 boys and 3.9 per 100,000 girls The incidence of knee OCD varied by ethnicity: non-Hispanic white was 10.3 per 100,000 overall (17.3 and 3.0 per 100,000 for boys and girls, respectively), non-Hispanic black was 10.3 per 100,000 overall (17.3 and 3.0 per 100,000 for boys and girls, respectively), Hispanic was 8.6 per 100,000 overall (14.3 and 2.8 per 100,000 for boys and girls, respectively), and Asian was 4.7 per 100,000 overall (9.1 and 0.0 per 100,000 for boys and girls, respectively) These authors performed multivariable logistic regression analysis that revealed a 3.3-fold increased risk of OCD of the knee in children aged 12 to 19 years compared with those aged 6 to 11 years Moreover, boys had 3.8 times greater risk of OCD than girls Finally, there is the discrete possibility that knee OCD may occur in both knees In the literature, there is a relatively wide range of bilaterality noted with about a 3% to 30% chance of discovering it in both knees by x-ray.5,18–23 ETIOLOGY No definitive etiology has yet been determined for the origin of knee OCD There are, of course, many hypotheses that have been presented and tested primarily via ex vivo histology The potential etiologies include inflammation, spontaneous osteonecrosis and vascular deficiency, genetic predisposition, and repetitive trauma Each of these will be discussed As suggested by the name “osteochondritis,” the first description in 1888 by König,2 by definition was atraumatic and it was postulated to be a result of inflammation However, histologic studies have not supported this etiology7,24; instead, these works appear to highlight findings of necrosis within the OCD lesions rather than inflammation Based on their histology findings, Green and Banks12,19 proposed that ischemia was the primary etiology, and Milgram,22 identifying revascularization in partially detached OCD lesion, further promoted this concept of poor vascularity Yet, Yonetani and colleagues25 found no evidence of necrosis on biopsies Uozumi and colleagues26 discovered a discrete absence of subchondral bone in many of their biopsy samples and, in those who had an osseous component present, only two demonstrated no viable osteocytes The difference between the first two studies and the second two is state of the OCD lesion prior to biopsy When the lesion was unstable (or even a loose body) at the time of biopsy, then necrosis was found by microscopic evaluation However, if the lesion was fully intact and in situ, then there was less definitive evidence for avascular necrosis Another hypothesis of the etiology is familial inheritance of OCD lesions A mild form of skeletal dysplasia with associated short stature has even been proposed.9,23,27–29 Two different authors, via different family tree assessments, have identified what they believe to be an autosomal dominant inheritance pattern.9,28 In contrast, Petrie30 reported on a radiographic examination of firstdegree relatives of those patients with known OCD and discovered only 1.2% with OCD themselves This suggests that the majority of knee OCD does not follow a predictable inheritance pattern However, it does not exclude the possibility that genetics may still play a role in OCD etiology Whether the aforementioned etiologies are primary or secondary remains a question unto itself, and the concept of repetitive microtrauma is another distinct possibility For example, despite the original description by König, there could be a significant traumatic event leading to avascular necrosis or there could be repetitive traumatic events that progressively develop vascular disruption In 1933, Fairbanks31 proposed traumatic contact between the lateral aspect of the medial femoral condyle and the tibial spine; yet, this theory would only explain OCD lesions on the lateral aspect of the medial femoral condyle However, the idea of repetitive trauma still holds our attention for the other locations of OCD as well Aichroth6 demonstrated that 60% of the patients with knee OCD in his cohort were involved in high-level, competitive sports Moreover, Linden11 showed an association between the incidence of OCD and the increased involvement in organized sports in Sweden between 1965 and 1974 A large multicenter study conducted by the European Pediatric Orthopaedic Society demonstrated that nearly 55% of those with OCD were regularly active in sports or performed “strenuous athletic activity.”20 Evidence to support repetitive trauma as an etiology for OCD is mostly conjecture and circumstantial at best Perhaps abnormal pressure on the cartilage anlage is a better way of describing “microtrauma,” as several studies have noted associations between lateral femoral condyle OCD lesions and discoid menisci.32–34 Moreover, there is an apparent association with poor mechanical axis alignment and the presence of knee OCD.35 In fact, the association between alignment shifts and location of OCD development was predictive, with varus malalignment predicting medial OCD lesions and valgus malalignment predicting lateral OCD lesions.35 These findings suggest that aberrant mechanical pressure on the condyles may be an etiology to the formation of OCD (at least in the knee) Perhaps the unifying theory can be found in the work by our veterinary colleagues on horse and pig comparative models They believe that the OCD lesions in these animals originate within the cartilage anlage of the subchondral bone.13,14 They have actually been able to create an animal model for OCD by description of the cartilage canals (which is the blood supply to the epiphyseal anlage cartilage) This further hints toward a possible traumatic injury that disrupts the blood supply They also suggest modifying the term osteochondritis to osteochondrosis given the complete lack of inflammation being seen as a possible etiology Furthermore, they would include the modifier “dissecans” when the articular cartilage becomes involved but recommend using the terms latens when there is only necrosis of the anlage cartilage or manifesta in the presence of focal failure of enchondral ossification to differentiate the timing of discovery In other words, these authors believe that by the time this pathologic process becomes clinically evident in the knee, it has already evolved through all three stages and is in the final necrotic form of OCD (Fig 21.2) This concept is not new to human physicians, but the concept of disrupted cartilage canals is novel to the previous hypothesis of Ribbing36 in 1937 His thesis was presented in a 107-page supplement to the journal Acta Radiologica discussing abnormalities of endochondral ossification of the epiphysis His hypothesis was then further modified by Barrie7,24 to further define possible etiologies of OCD formation via epiphyseal secondary growth Basically, at an index event, there is an insult (single or repetitive) to the endochondral epiphyseal growth plate or perhaps to the cartilage canals just deep to subchondral bone With skeletal development, the uninjured region of endochondral epiphyseal ossification continues to ossify unhindered, creating an ever enlarging OCD central to the normal growth Although the concepts of disrupted cartilage canals or endochondral epiphyseal growth plates are appealing etiologies, there remains a gap in the explanation regarding how and why these structures become injured in the first place All children are quite active, jumping, playing, running, and falling So why do some develop an OCD and some do not develop an OCD? This question is yet to be answered CLASSIFICATION The simplest form of knee OCD classification is that set forth by Hefti and colleagues20 that merely describes location of the OCD The most common site of OCD is the lateral aspect of the medial femoral condyle (51% involvement), with other sites being involved with less frequency: 19% central medial femoral condyle, 17% lateral femoral condyle, 7% medial side of the medial femoral condyle, and 7% patella It may be important to note that irregular ossification centers of the distal femoral condyle tend to be found more posteriorly on the condyle (although they can be anywhere on the condyle) and are associated with younger age Cahill12 wrote a review of OCD and identified multiple other authors who have similarly classified knee OCD by location, but he makes no mention of classifying the lesions in any other method (stability, outcomes, etc.) De Smet and colleagues37 took things to the next level and classified the OCD either stable or unstable and correlated their magnetic resonance imaging (MRI) findings with arthroscopic findings They reported that a high signal interface between the OCD lesion and the normal femoral bone was indicative of instability by arthroscopy This same author then later improved his assessment by MRI and added three other signs of instability that are discussed in the following text (Fig 21.3).38 The arthroscopic classification of OCD lesions is the gold standard in understanding the lesion, yet even here, we do not have associated outcomes Guhl39 was the first to set an arthroscopy classification and it has been used as a template for other authors: (1) intact lesions, (2) lesions showing signs of early separation,( 3) partially detached lesions, and (4) crater with loose bodies (salvageable or unsalvageable) (Fig 21.4) To this point, no correlation with outcomes has been made ASSESSMENT Most authors20,40 suggest that treatment for knee OCD should be based on skeletal maturity and lesion stability A number of classification systems mentioned earlier includes these two principles.12,37–39 Therefore, it is important to identify OCD, identify skeletal maturity, and identify OCD stability Children with OCD may have two different presentations, either the OCD is an incidental radiographic findings or it may be thought to be the cause of their symptoms.41,42 Cahill and Ahten43 reported that 80% of the children had mild pain and limp for a mean of 14 months prior to presentation—suggesting that the symptoms associated with knee OCD may not differ greatly from idiopathic adolescent knee pain However, there may be substantial symptoms associated with the OCD lesion, such as mechanical symptoms of locking and popping Effusion is present in less than 20% at presentation.20 Wilson53 described a test on physical examination to diagnose OCD: The knee is flexed to 90 degrees, the tibia is externally rotated, and the knee is gradually extended to 30 degrees of flexion A positive test is characterized by pain over the anteromedial aspect of the knee as the knee is extended to 30 degrees with relief of pain with internal rotation of the tibia Anatomically, this maneuver is believed to cause impingement of the tibial spine on the lateral aspect of the medial femoral condyle (and therefore would only be positive on those particular OCD lesions) The Wilson test is of limited diagnostic value with a reported positive test in only 16% of knees with radiographically proven OCD lesions.20 The diagnosis of OCD is truly dependent on imaging rather than history or physical examination Especially considering that many OCD lesions may be asymptomatic until separation or dislodgment occurs resulting in significant effusion and pain—this is considered a late finding in the treatment of these lesions Most lesions can be identified by plain radiographs and will usually not be missed as long as four views are obtained, including anteroposterior (AP), lateral, tunnel (notch), and Merchant (sunrise) views To date, there is no historical literature assessing the sensitivity or specificity of radiographs to identify OCD lesions, and the American Academy of Orthopaedic Surgeons (AAOS) clinical pathway guideline task force recommended that there was only limited evidence to support obtaining initial plain radiographs in the assessment of knee OCD (and inconclusive evidence to obtain contralateral films at initial evaluation).40 In the assessment of children with an OCD lesion, it appears to be clinically acceptable to obtain contralateral films to evaluate for bilateral bilaterality of, 184 cartilage and, 221 classification, 185–187, 186f, 187f, 200 epidemiology, 183–184 etiology, 184–185, 186f example, 183, 184f history and physical exam, 199 imaging, 199–200, 200f inflammation and, 184–185 juvenile versus adult, 183 microtrauma and, 185 ORIF with metal compression screws arthroscopic case, 203, 203f, 204f, 205f cases, 202–205 complications, 205 CPM machine, 204 defect preparation, 201, 201f equipment used, 203 fragment reduction and fixation, 202 open case, 200f, 201f, 202–203, 202f, 203f overview, 200 patient positioning and setup, 200–201 postoperative rehabilitation, 204–205 technique, 200–202 overview, 1, 183, 184f, 199 retroarticular drilling aftercare, 197, 198f author’s preferred treatment, 195–197, 196f, 197f, 198f complications, 197 equipment, 195–197, 196f, 197f indications and contraindications, 195 Micro Vector pin guide, 195, 196f overview, 195 transarticular drilling compared with, 190–191 transarticular drilling authors’ preferred treatment, 191–193 complication avoidance, 193 operative, 190–191, 192t, 193f rehabilitation, 192–193, 193f retroarticular drilling compared with, 190–191 studies assessing, 192t surgical technique, 191–192 treatment indications, 190 treatment, 200, 201f veterinary research on, 185, 186f OT See Over-the-top femoral reconstruction Outside-in anterior horn repair, 238–239, 238f, 239f Over-the-top (OT) femoral reconstruction, 15–16 Paley multiplier method, 314 Partial meniscectomies, 244 Partial transphyseal (hybrid) technique ACL drilling guide, 63, 63f author’s preferred treatment, 62–64, 63f, 64f, 65f, 66f equipment list, 65 FlipCutter, 63–64, 64f graft choice and preparation, 63 indications and contraindications, 61–62 operative technique and outcomes, 62 overview, 61 preoperative setup, 62 reconstruction, 63–64, 63f, 64f, 65f, 66f rehabilitation, 65 treatment, 61–62 Patella dislocation, 135f growth plate and, 306–307, 307f IMGG and, 330–331 mobilization for ACL, 34, 34f, 80 Patellar instability rehabilitation advanced strengthening and function phase cardiovascular fitness, 168 guidelines, 173, 178 plyometrics, 169 gait phase gait/ambulation, 165, 165f guidelines, 171, 176 neuromuscular control and proprioception, 165–166, 166f precautions, 166 quadriceps, 166 ROM, 166 standing posture, 164 strength, 166 symptom control, 164 therapeutic exercise, 165–166 guidelines, 170–179 overview, 162, 163f preoperative phase activity modification, 163 ambulation, 162–163 cryotherapy, 163 expectations, 162–163 foundation building, 162 protective phase, 163–164 guidelines, 170, 175 RTP phase, 169 guidelines, 174, 179 strengthening phase balance and proprioception, 167, 167f guidelines, 172, 177 patience, 167 precautions, 168 proximal, 168 quadriceps, 167–168, 168f ROM, 168 therapeutic exercise, 167–168 Patellar sockets, 143, 144f Patella sleeve fractures anatomy and function, 284 epidemiology, 284 etiology, 284 evaluation, 284–285, 285f, 286f imaging, 285, 285f K-wires and, 286 overview, 284 pathomechanics, 284 pearls/pitfalls, 287 rehabilitation, 286 schematic representation of, 285f treatment authors’ preferred, 286 indications/contraindications, 285–286 nonoperative, 285 operative, 285–286 Patellofemoral instability (PFI) See also Hamstring MPFL reconstruction technique; Medial patellar tendon transfer with proximal realignment; Quad tendon MPFL technique; Tibial tubercle osteotomy authors’ preferred treatment, 133–134, 134f Beighton test, 131, 131f causes, 140 CD index, 129, 129f clinical assessment, 128 conclusions, 132 crossing sign, 129, 129f, 130f double contour, 129–130 early-onset, 127–128 epidemiology, 128 first-time dislocation, 128–131, 129f, 130f hyperlaxity syndromes and, 128 Insall-Salvati index, 129, 129f literature review regarding, 133 major studies on, 141t miserable malalignment and, 128 nontraumatic, 128 osteochondral fractures and, 130 overview, 1, 127 pathomechanics, 127–128 physical exam, 129 radiographs, 129, 129f, 130f recurrent, 131–132, 131f risk factors, 128, 128t supratrochlear spur, 129, 130f surgical treatment indications and contraindications, 133 traumatic, 128 TT-TG distance, 130–131, 130f type A dysplasia, 129, 129f type B dysplasia, 129, 130f type C dysplasia, 129–130 type D dysplasia, 130 PD See Proton density Peanut plate, 329t PediPlates, 329t PEP See Prevent Injury and Enhance Performance Performance pyramid, RTP, 104, 104f PFI See Patellofemoral instability PGA See Polyglycolic acid Physial techniques, ACL, 47 Physis bridging and, 291, 292f diagnostic imaging computed tomography, 294–295, 295t MRI, 295–299, 296f, 296t, 297f, 298f, 299f overview, 291 radiography, 294, 294f, 295f fracture categorization type 1, 291, 292f type 2, 291, 292f, 293f type 3, 292, 292f, 293f type 4, 292, 292f type 5, 292, 292f gender and, 21 layers of, 319f overview, 1 skeletal growth assessment and, 311, 312f Plank, 35, 35f Platelet-rich fibrin matrix, 240 PLB See Posterolateral bundle PLLA See Polylevolactic acid Plyometric training, 36–37, 36f, 95, 95f, 118, 119f, 169 Polyglycolic acid (PGA), 208, 209t, 210t Polylevolactic acid (PLLA), 207, 208, 209t, 210t Popping knee syndrome See Discoid meniscus Posterolateral bundle (PLB), 13 elongation patterns of, 14, 14f Posterolateral corner injury, genu valgum and, 333, 334f Postoperative ACL rehabilitation advanced activity phase agility training, 89–90, 93f motor learning strategy, 89 neuromuscular training, 90, 92 overview, 87, 89t plyometric progression, 89, 91f, 92f running progression, 92–93 strengthening, 87, 89, 90f treatment recommendations, 87, 89–93 considerations for athletes, 78–79 functional strengthening and corrective movement phase leg dominance correction, 86 neuromuscular imbalances: risk factor reduction, 83, 84f, 85, 85f, 86f overview, 83, 83t ROM and flexibility deficits addressed, 83, 84f squat, 86–87, 88f, 89f strengthening, 83, 85–86, 86f, 87f strengthening for dynamic valgus correction, 85, 86f strengthening for trunk dominance correction, 85–86, 87f treatment recommendations, 83–87 graft selection effect on, 78 intermediate protection phase bracing and ambulation, 81 flexibility, 83 modalities, 81 neuromuscular training, 82–83, 83f overview, 81, 81t ROM, 81, 81f strengthening, 81–82, 82f treatment recommendations, 81–83 overview, 78 protection phase bracing and ambulation, 79 neuromuscular training, 80–81, 80f overview, 79, 79t pain and effusion modalities, 79 patella mobilizations, 80 ROM, 79–80, 80f strengthening, 80 treatment recommendations, 79–81 RTP clearance phase dynamic cutting, 97, 97f overview, 95–97, 97t sport-specific exercises, 95, 96f, 97 RTP preparation phase agility and plyometric training, 95, 95f assessment, 94 muscular coactivation for dynamic stabilizers, 94, 94f overview, 93–94, 94t reaction time training, 95, 95f Postural Stability Analysis, 103 Prevent Injury and Enhance Performance (PEP), 120, 120t Primary spongiosa, 305 Proliferating growth cartilage, 303f Proliferative zone, 304, 305f Prone quad stretch, 34 Proprioception training, 117, 118f, 118t, 166f, 167, 167f Proton density (PD), 297–298 Proximal metaphysis, 303f Proximal tibia, fractures anatomy, 278–279, 278f classification, 275f, 279, 279f diagnosis, 279–280 epidemiology, 279 imaging, 280–281, 280f mechanism of injury, 279 nerve damage and, 279 outcomes, 281 overview, 278 treatment, 281 vascular injury and, 278, 278f Proximal tibial physis, 255 Proximal tibia metaphyseal fracture, 281, 282f Psychology, RTP and, 102–103 Pyle, S I., 312 Pyramid See Performance pyramid, RTP QSI See Quadriceps Strength Index Quadriceps dominance, 83, 112, 113f, 114f patellar instability and, 167–168, 168f Quadriceps Strength Index (QSI), 104 Quad sets, 33, 33f Quad stretch, prone, 34 Quad tendon MPFL technique authors’ preferred treatment, 133–134, 134f indications and contraindications, 133 literature review regarding, 133 overview, 133 surgical technique complication avoidance, 137–138 conclusion, 138 equipment, 138t goal, 134 graft illustrations, 134f OSI flat-top table, 134, 134f pitfalls, 138 preoperative planning, 134–135, 134f, 135f rehabilitation, 137 steps, 135, 136f, 137, 137f, 138t surgical approach, 135, 135f Radiography of complete transphyseal hamstring autograft, 76f PFI, 129, 129f, 130f physis and, 294, 294f, 295f Range of motion (ROM) ACL phase 1 exercises, 34, 34f phase 2 exercises, 34, 34f, 35 ACL postoperative rehabilitation functional strengthening and corrective movement phase, 83, 84f intermediate protection phase, 81, 81f protection phase, 79–80, 80f patellar instability rehabilitation gait phase, 166 strengthening phase, 168 Research in Osteochondritis of the Knee (ROCK), 183 Reserve zone, 303–304, 305f Retroarticular drilling, 190–191 Return to play (RTP) ACL conclusions, 107 controversies, 101–107 decision making current models, 103–104 decision modifiers step, 105f, 106 evaluation of health status step, 104, 105f evaluation of participation risk step, 104–105, 105f general model, 104–106, 105f HSS, 106, 106f, 107f overview, 101 performance pyramid, 104, 104f psychological factors, 102–103 rates of, 102, 102t risk of reinjury, 101–102 risk of second injury factors, 103 single leg hop, 107f single limb stance, 106f clearance phase dynamic cutting, 97, 97f overview, 95–97, 97t sport-specific exercises, 95, 96f, 97 patellar instability and, 169 preparation phase agility and plyometric training, 95, 95f assessment, 94 muscular coactivation for dynamic stabilizers, 94, 94f overview, 93–94, 94t reaction time training, 95, 95f ReUnite, 209t Reverse tensioning (RT) button, 54 Rickets See Hypophosphatemic rickets Right and left backbiters, 236, 237f Right and left side biters, 236, 237f Ring of LaCroix, 304–305 ROCK See Research in Osteochondritis of the Knee ROM See Range of motion Roux-Goldwait, Galeazzi, Nietosvaara technique, 155 RT See Reverse tensioning button RTP See Return to play Salter-Harris distal femur fractures anatomy, 274–275 classification, 275, 275f complications, 278 diagnosis, 275 distal femoral physis widening and, 276, 276f epidemiology, 275 fixation, 277, 277f growth arrest and, 318, 319f imaging, 275–277, 276f, 294f, 296, 297f mechanism of injury, 275, 276f outcomes, 278 overview, 274, 275f proximal tibia fractures classification and, 275f, 279, 279f treatment and, 281 skeletal growth assessment case, 315–317, 316f, 317f SPGR imaging of, 294f, 296, 297f Thurston-Holland fragment, 274, 275, 275f treatment, 277, 277f Saucerization, discoid meniscus, 236, 239f SBA See Shorthand bone age assessment Sharpey-like fibers, 16 Shell technique, 218 Shorthand bone age (SBA) assessment, 312–313, 313f Sinding-LarsenJohansson syndrome, 284 Single leg hop, 107f Single limb stance, 106f Skeletal growth assessment case study, 315–317, 316f, 317f clinical application of information, 315 conclusions about, 317 Greulich and Pyle atlas method, 312, 312f leg length determination Anderson-Green method, 314, 315f arithmetic method, 314 overview, 314 Paley multiplier method, 314 straight-line method, 314 overview, 311 physes and, 311, 312f SBA method, 312–313, 313f Tanner-Whitehouse method, 312 Slack length, 12 SmartNail, 208, 209t SmartScrew, 209t Snapping knee syndrome See Discoid meniscus Snowman technique, 218 Sockets technique See All-epiphyseal sockets technique Spoiled gradient recalled (SPGR) imaging, 224 for baseline, 297 conclusions, 299 ligamentous injuries and, 299 limitations, 296–297, 298f of metaphyseal intrusions, 296, 297f of osseous bar, 296, 296f PD and, 297–298 for postoperative damage, 297, 298f qualitative and quantitative analyzing of, 298 of Salter-Harris fracture, 294f, 296, 297f software and, 298–299, 299f usefulness of, 295–296 Sportsmetric ACL Prevention Program, 118–120, 120t Squats, 36, 36f, 37, 86– 87, 88f, 89f Stationary bike, 34 Stem cell/collagen-scaffold, 240 Straight-leg raise to the front, 33, 33f Straight-line method, 314 Supratrochlear spur, 129, 130f Tanner stages of maturity, 31, 31t, 40 Tanner-Whitehouse method, 312 Tegner score, 39 Tendon See also Medial patellar tendon transfer with proximal realignment; Quad tendon MPFL technique adductor tendon pedicle graft, 141, 142f growth plate anatomy and, 307–308, 307f, 308f Thermal ablation, 237 Three screw technique, 264, 267f Thurston-Holland fragment, 274, 275, 275f Tibial spine/ACL avulsion fractures authors’ preferred treatment, 268–270, 269f, 270f, 271f, 272f fixation overview, 269, 269f preparation, 268–269 type III high-strength suture fixation, 270, 271f type IV high-strength suture fixation, 270, 271f, 272f classification and, 268 pitfall avoidance, 272 rehabilitation, 272 treatments, 268 Tibial spine avulsion fractures anatomy related to, 261 classification, 262–263, 268 complications, 266–267 evaluation history and physical examination, 261–262 imaging, 262, 262f, 263f, 264f genu valgum secondary to, 331, 331f, 332f management, 263 mechanism and epidemiology, 261 operative technique diagnostic arthroscopy, 263, 265f equipment, 265t reduction, 263–264 screw placement, 264–265, 266f three screw technique, 264, 267f overview, 261 rehabilitation, 265–266, 266f, 267f surgical management modalities, 263 Tibial tubercle anatomy, 255, 336, 337f apophysis, 255 avulsion fractures anatomy and function and, 255 classification, 256, 258 epidemiology, 255 history, 256 imaging, 256, 257f, 258f management, 258 mechanism of injury, 256 operative technique, 258–259, 259f overview, 255 physical examination, 256 postoperative care, 259 risk factors, 256 Tibial tubercle osteotomy (TTO), distal realignment authors’ preferred treatment, 156–161 complication avoidance, 161 contraindications, 155 evaluation, 156 greenstick fracture, 159, 159f indications, 154–155 K-wire placement, 158, 158f landmark topography, 157, 157f lateral capsulotomy, 157–158, 157f lateral displacement measurement, 155 operative techniques, 155 osteotomes used in, 159, 159f overview, 154 pictorial representation, 160, 160f preparation for procedure, 156–157 rehabilitation, 161 shingle length marking, 158, 158f surgical technique, 156–160, 157f, 158f, 159f, 160f treatment, 154–155 Tibial tubercle–posterior cruciate ligament (TT-PCL), 155 Tibial tubercle–trochlear groove (TT-TG), 155 age and, 141 distance, 130–131, 130f Tibial tubercle transfer (TTT) See Patellar instability rehabilitation TigerStick, 64 TigerWire, 270 TightRope ABS, 64 TightRope RT device, 54 Toe region, 12, 12f Towel stretch, 34, 34f Transepiphyseal ACL reconstruction postoperative rehabilitation for, 50–51 technique, 47–49, 48f, 49f Transphyseal techniques, ACL, 46 Trephination, 240 Trunk dominance, 85–86, 87f, 114, 117f TTO See Tibial tubercle osteotomy TTPCL See Tibial tubercle–posterior cruciate ligament TTT See Tibial tubercle transfer TT-TG See Tibial tubercle–trochlear groove Type A dysplasia, 129, 129f Type B dysplasia, 129, 130f Type C dysplasia, 129–130 Type D dysplasia, 130 UEFA See European Football Associations Upward-going biter, 236, 237f Valgus moment, 10, 11f Varus malalignment, 245 Varus moment, 10, 11f Varus–valgus malalignment, 246 Vastus medialis obliquus (VMO) medial patellar tendon transfer, with proximal realignment, 149–150, 150f, 152, 152f pathomechanics, 127 tearing, 129 Walking lunges, 36, 36f Watson-Jones classification, 256 Women’s National Basketball Association (WNBA), 102, 102t Wrisberg variant discoid meniscus, 232, 232f Zone of provisional calcification, 304, 305f ... of osteochondritis dissecans of the knee in children and adolescents Am J Sports Med 20 14; 42( 2): 320 – 326 18 Marsden C, Wiernik G The incidence of osteochondritis dissecans J R Army Med Corps 1956;1 02( 2): 124 –130 19 Green WT, Banks HH... Orthopaedic Surgeons clinical practice guideline on: the diagnosis and treatment of osteochondritis dissecans J Bone Joint Surg Am 20 12; 94(14):1 322 –1 324 41 Glancy GL Juvenile osteochondritis dissecans Am J Knee Surg 1999; 12: 120 – 124 42 Kocher MS, Micheli LJ, Yaniv M, et al... Sports Traumatol Arthrosc 20 10;18: 723 –730 26 Uozumi H, Sugita T, Aizawa T, et al Histologic findings and possible causes of osteochondritis dissecans of the knee Am J Sports Med 20 09;37 :20 03– 20 08 27 Kozlowski K, Middleton R