Successful orthopaedic treatment of intraarticular fractures depends on avoidance of a mechanical environment that is deleterious to articular cartilage. Clinically, the conventional wisdom is that restoration of joint congruity is necessary for that purpose. However, there are many reports of cases or series where patients have done surprisingly well in the presence of substantial incongruity, provided that joint stability is maintained. Conversely, many minimally displaced or congruously repaired intraarticular fractures fare poorly in the presence of joint instability. The etiology, or etiologies, of posttraumatic arthritis have not been well defined, but there clearly is a pathomechanical component.
There are three major schools of thought as to specific causality: (1) direct impact damage sustained by cartilage and/or bone1,11,36,54; (2) chronic elevation of cartilage contact stress resulting from residual articular incongruity23,25,26; and (3) pathologic loading resulting from articular instability.10,22,27 However, which of these three very different considerations dominate(s), and under what circumstances, are essentially unknown.
Although clinical evidence linking incongruity to posttraumatic arthritis is inconclusive,10,18,28,46,52 there has been a consistently observed association of instability with posttraumatic arthritis.8,9,22,55,59 It is likely that instability and incongruity each can be important determinants of posttraumatic arthritis, but their relative contribution to abnormal stress has not been well characterized. More importantly, both pathologic conditions often coexist after a severe intraarticular fracture, and the presence of instability and incongruity may severely exacerbate chronic hazardous cartilage loading, compared with one or the other alone.
Many confounding factors, especially heterogeneity of injury, preclude systematic human clinical study of the relative importance of instability versus incongruity as causes of posttraumatic arthritis. However, if in fact instability per se is the more potent determinant of posttraumatic arthritis, then orthopaedic treatment ought to prioritize attaining suitable thresholds of joint stability, rather than its presently dominant strategy of attaining suitable thresholds of congruity. Treatment strategies remain a heatedly debated subject in orthopaedic trauma circles, but mainly so on empirical and sometimes even anecdotal grounds, because the current base of rigorous scientific information is sparse.
Most experimental models of articular surface incongruity have measured relatively mild increases in articular surface contact stress, even in the presence of large incongruities.3,5,19,35,40,41 However, the majority of these studies used static testing (loading across a joint in a fixed position and no motion). Static testing cannot detect potential transiently elevated stresses, cannot measure loading rates, and cannot integrate potentially hazardous loads that accumulate as the joint courses through its ROM. Static tests also cannot measure potential pathologic loads associated with instability.
We review the clinical and basic scientific evidence relating incongruity and instability to posttraumatic arthritis. Second, because of new methodologic advances, key technical barriers have been removed, opening the way for systematic dynamic investigations of incongruity and instability. Early results from a new dynamic ankle loading apparatus, using a new real-time pressure transducer to investigate combined effects of ankle incongruity and instability, are presented. Such testing systematically can elucidate articular surface incongruity versus global joint instability (separately and in concert) as determinants of aberrant mechanical stresses at the local cartilage level.
Clinical Studies of Intraarticular Fractures: Instability versus Incongruity
In the hip, several large series of patients sustaining acetabular fractures have showed that long-term results are closely related to the quality of articular reduction.24,30,31 These series have concluded that changes in articular contact stress correlate with the disappointing clinical results associated with poor reductions. In hips sustaining acetabular fractures, instability is tolerated poorly. In 492 patients, more than 50% of those with unstable reductions (loss of parallelism between the femoral head and acetabular roof reflecting an unstable, nonconcentric articulation) had poor outcomes, with 60% of that subset requiring total hip arthroplasty (THA).24 In another series of 262 patients sustaining acetabular fractures, good clinical outcomes were realized in 80% of patients when the femoral head was stable within the acetabulum. In contrast, 60% of patients with unstable reductions had poor outcomes.30 Therefore, it seems that incongruity and instability are tolerated poorly in the hip.
Instability clearly has been linked to posttraumatic arthritis in knees sustaining tibial plateau fractures.10,18,22,46 In a classic study of 204 tibial plateau fractures in patients followed up for at least 5 years, 87% had good outcomes regardless of articular surface reduction, provided that coronal plane stability was maintained.46 Twenty-year followup of 102 knees from that same set of patients revealed continuing good results in 90% of patients with as much as 1 cm articular surface depression, provided that their knees were stable.22 In contrast, patients with residual instability have poor outcomes regardless of the articular reduction. In a series of 46 patients with tibial plateau fractures, the outcome in stable knees was not affected by incongruity.52 Incongruity is well tolerated in the knee provided that stability is maintained. However, residual instability after intraarticular fractures of the knee is tolerated poorly.
Patients sustaining ligamentous injuries in the knee without fracture-associated incongruity also have a significant incidence of posttraumatic arthritis.8,12,21 Patients sustaining ACL tears followed up prospectively for greater than 5 years had a significantly increased incidence of posttraumatic arthritis.8 In a review of ACL tears, injured knees had a 10-fold increase of degenerative changes, compared with uninjured limbs.12 Similarly, in knees with PCL injuries, approximately ½ of the patients having PCL reconstruction for chronic laxity had posttraumatic arthritis.7
Ankle degeneration seems to be particularly linked to instability. Patients sustaining rotational ankle fractures with talar instability clearly have better outcomes with operative stabilization.29,44,58 Patients with residual ankle instability, resulting from fracture or chronic ligamentous injury, in the absence of articular surface incongruity, have a substantial incidence of posttraumatic arthritis.29,57,58 Pilon fractures particularly are severe injuries. Compared with intraarticular fractures of the knee, pilon fractures have a much higher incidence of posttraumatic arthritis.2,28,42,53 Although thought to be related to soft tissue injury and articular surface damage, the specific mechanical reasons for the particularly aggressive course of posttraumatic arthritis associated with pilon fractures are not known.
Intraarticular fractures of the lower extremity affect the hip, knee, and ankle differently. Incongruity is tolerated poorly in the hip, yet well tolerated in the knee provided that alignment and stability are preserved. Instability is tolerated poorly by all three joints.
Laboratory Studies of Articular Incongruity and Instability
Static single-leg stance tests of the hip have shown that large posterior wall acetabular defects result in only a 25% decrease in contact area throughout the entire acetabulum.40,41 In such situations, the mean contact stress increased only 10% to 15% in the posterior, superior, and anterior acetabulum. Using similar testing methods, transverse acetabular fractures through the weightbearing dome with 2–4 mm step-offs led to 50% increases in mean contact stress, with a 100% increase in peak contact stress in the superior acetabulum, and to minimal changes in anterior or posterior contact stresses.16 In the acetabulum, little is known of the local mechanical effects of global instability.
As with the hip, mechanical investigations at the knee have concentrated almost entirely on static articular surface contact stress changes associated with incongruity. In static contact pressure studies of knees from human cadavers, articular surface step-offs as much as 5 mm on the tibial plateau resulted in 50% to 75% increases in peak pressures, with substantially lower increases in mean pressures.3 In a canine cadaveric model, statically loaded cartilage defects as much as 7 mm in diameter in the medial femoral condyle showed mean contact stress increases of only 10% to 30%, compared with normal knees.5 In a similarly conceived canine defect repair model, 6-mm defects showed minimal degenerative changes at 11 months after injury, with no appreciable increase in static contact stress compared with the contralateral normal knee.35 Instability induced in knees in canines by division of the ACL consistently produced posttraumatic arthritis, and dogs with ACL injuries modified their gait apparently to minimize instability.9,38,56
Compared with the hip and knee, little is known on how incongruity affects contact stress in the ankle. In contrast, several studies have investigated ankle instability. In the classic Ramsey-Hamilton model, shortening of the distal fibula caused lateral shifting of the talus, with substantial rises in contact stress.45 However, two additional studies of fibular shortening using more physiologically realistic, less constrained loading have detected only minimal increases in contact stress statically.4,43 The talus self-centers under the distal tibia, even with unstable ankle fractures and fibular shortening as much as 5 mm. Although these and other laboratory data suggest that static contact stress increases are minimal with unstable ankle fractures in the absence of incongruity, the overwhelming weight of clinical evidence shows that unstable ankle fractures left untreated have poor outcomes.20,48,58,59 Together, these two complementary sets of observations strongly suggest that, rather than static contact stress elevation, it is the dynamic pathomechanical effects of instability that most directly cause posttraumatic arthritis in the ankle.
Interestingly, mechanical testing has shown that the knee and ankle accommodate similar articular incongruities differently, in terms of epiphyseal load transmission. In static testing, articular surface defects in the distal tibia cause marked increases in strain in the trabecular bone underlying the defect, in stark contrast to decreases in trabecular bone strain in bone underlying similar defects in the tibial plateau.32 Plausibly, differences in joint geometry, osteoarticular stability, and/or cartilage compliance explain these diametrically opposite changes in trabecular bone strain adjacent to a cartilage defect.
The combined effects of incongruity and instability were investigated using an established incongruity model in a rabbit knee.27 Initial work showed that medial femoral condyles subjected to coronal plane step-offs of 0.5 mm healed with no posttraumatic arthritis. Knees in rabbits subjected to identical coronal plane step-offs and concomitant division of their ACL had severe degenerative changes. Furthermore, rabbits with no incongruity but with transection of their ACL had greater cartilage fibrillation than rabbits with step-offs in stable knees. These data suggest instability is a potent determinant of posttraumatic arthritis in knees in rabbits.
Several studies of static mechanical testing suggest that incongruities seldom lead to seemingly consequential elevations in static contact stress, especially in the knee. In contrast, consistent experimental evidence shows instability leads to posttraumatic arthritis in several animal models.9,38,56 However, potentially deleterious mechanical signals caused by incongruity may be masked completely by static testing. Static tests cannot measure potentially important transient elevated peak stresses, loading rate effects, or cumulative stress integration over the functional ROM of a joint.
Dynamic Ankle Testing
In a pilot study, the concurrent effects of incongruity and instability on contact mechanics in the ankle from a human were tested using a new dynamic ankle testing system. Ankles from cadavers were subjected to a coronal plane step-off of the distal tibia and axially loaded during normal plantar flexion and dorsiflexion motion. A posteriorly directed force was increased incrementally on the tibia, until the talus was observed to subluxate anteriorly from beneath the distal tibia during motion. Articular surface contact pressure was measured using a new dynamic pressure transducer.
Fresh-frozen ankles from cadavers with normal motion were screened for radiographic abnormalities, severe osteopenia, or evidence of prior trauma. Soft tissue was removed to allow access to the anterior and posterior ankle joint, preserving the syndesmosis and major ligaments. The hindfoot, forefoot, and tibial diaphysis were potted into PMMA blocks designed to mate with a loading fixture, maintaining unrestrained motion in the ankle, hindfoot, and midfoot. The PMMA blocks of the hindfoot and forefoot mated with an A1 plate designed to mount onto the load-cell of an MTS loading machine (MTS Systems Corporation, Eden Prarie, MN). The PMMA block on the tibial diaphysis mated with the load actuator on the MTS machine.
Specimens were secured to a novel ankle motion applicator for quasiphysiologic loading and motion delivery. This device was mounted into and controlled by an MTS Bionix material test station. Axial loading and plantar flexion and dorsiflexion motion were under the control of the MTS. Anteroposterior forces were applied independently to the tibia through a pneumatic actuator. Ankle motion and loading therefore could be coordinated to simulate the stance phase of gait (Fig 1).
Dynamic Contact Stress Measurements
Contact stresses between the articulating surfaces of the tibia and talus were measured using TekScan (TekScan Inc, Boston, MA), a real time pressure transducer. The TekScan sensor has intersecting arrays of parallel electrical conductors whose resistance changes instantaneously with local contact stress. A custom sensor was designed specifically for the ankle, allowing measurement of pressure at approximately 1500 discrete points (sensels) on the distal tibia articular surface, at a frequency of 132 Hz. The sensor was inserted into the ankle through a small anterior and posterior arthrotomy.
The test was designed to investigate the concurrent effects of incongruity and instability on dynamic contact pressure, in a pilon fracture model. Initially, specimens were loaded intact with a 300-N axial load, and coursed through a normal motion cycle (ranging from 15° plantar flexion to 15° dorsiflexion) at 0.5 Hz. The anterior 50% of the distal tibial articular surface then was osteotomized, displaced proximally 3 mm, and then rigidly secured with internal fixation, thereby creating a fixed incongruity with a potentially unstable ankle. Loading cycles were repeated with a 300-N axial load, whereas a posteriorly directed force was applied to the tibia, and increased in 2-N increments. The posterior force incrementations were repeated until the talus was observed to transiently subluxate anteriorly from beneath the tibia during motion. The talus first was observed to subluxate anteriorly from beneath the tibia when the posterior force applied to the tibia reached 20 N. The trial immediately preceding the initial subluxation, with a posterior force of 18 N, had no tibiotalar subluxation. This allowed contact pressure to be measured in each specimen just before (preinstability trial) and concurrent with the initial instability event (instability trial).
Peak Dynamic Contact Pressures
Peak pressures from a single representative specimen for intact, preinstability, and instability trials are shown in Figure 2. The 3 mm step-off in the preinstability and instability trials caused peak pressures to increase approximately 300% throughout the majority of the motion cycle. At the instability event, peak pressures increased approximately 400% to 500% compared with the intact trial, and 75% to 100% compared with the preinstability trial.
Maximum Contact Stress Loading Rates
Measuring contact stress throughout the entire motion cycle allowed temporal gradients (loading rates) to be measured. Temporal gradients characterize how local contact stresses change with time. Measuring temporal gradients is important because bone and cartilage biophysical response are highly load rate dependent.6,14,17,37,49 The maximum temporal gradients from one representative specimen were calculated throughout the entire motion cycle for the intact, preinstability, and instability trials (Fig 3). Throughout the majority of the loading cycle, the step-off (preinstability and instability trials) caused mild increases (approximately 50% to 100%) in temporal gradients compared with the intact trial. However, the instability event increased maximum temporal gradient approximately 250% compared with the preinstability trial and approximately 800% compared with the intact trial.
Maximum Contact Stress Spatial Gradients
Spatial gradients measured the maximum rate of contact stress change over the surface of the distal tibia. Elevated spatial gradients could lead to excessive hazardous shear stresses and inhomogenous interstitial fluid flow within the substance of the cartilage. During the majority of the motion cycle, the step-off resulted in increases of approximately 100% to 150% in spatial gradients in a single representative specimen. At the instability event, spatial pressure gradients were increased approximately 80% in the instability trial compared with the preinstability trial and approximately 250% to 300% compared with the intact trial (Fig 4).
Although it long has been assumed that articular incongruity leads to posttraumatic arthritis, clinical and basic science evidence to support such a stance is lacking. Some orthopaedic surgeons think that articular surface incongruity leads to deleteriously high chronic cartilage contact stress, therefore justifying aggressive surgical reduction and fixation of intraarticular fractures.30,33,41 Complications of aggressive open procedures to repair intraarticular fractures are among the worst in orthopaedic surgery.10,42,53 As complications have accumulated, a push toward limited open procedures and percutaneous procedures to treat intraarticular injuries has evolved.2,28,51 Unfortunately, little mechanical evidence exists to help in formulating any treatment plan for these difficult injuries. Developing a clear understanding of the pathomechanical signals resulting from intraarticular injuries and the pathobiologic transduction of such signals by the cartilage hopefully will eventually unlock the secrets of posttraumatic arthritis.
The majority of articular contact studies have measured changes in static contact stress in the face of an articular incongruity. Several series of static tests in the lower extremity showed at best modest rises in peak and mean contact stresses, even in the face of substantial incongruity.3,5,19,23,35,40 These data called into question the importance of articular surface congruity in the pathoetiology of posttraumatic arthritis. However, static tests cannot detect peak transient stresses that occur during motion, cannot measure loading rates, and necessarily ignore potential pathologic insults that may accumulate throughout the entire ROM of a joint. Therefore, it is likely that potential deleterious pathomechanical signals associated with surface incongruities cannot be detected with static testing.
Cartilage is a complex material that transmits load by deformation of its solid matrix constituents, and through hydrostatic pressurization of the interstitial fluid permeating the solid matrix.34 Because of its biphasic nature, stresses developed within cartilage are highly time-dependent.15,34,39 Static testing arguably poorly replicates the biphasic nature of cartilage load transmission. The transient loads physiologically conducted through interstitial fluid flow are absent in static testing, thereby subjecting the solid matrix constituents to perhaps misleadingly high loading and deformation. In static testing, increased deformation of cartilage surrounding an incongruity therefore allows more cartilage to be recruited into contact than occurs physiologically, thereby potentially accounting for the modest elevations in contact stress detected with large incongruities. Measuring dynamic loads also is important in cartilage, because it is likely that cartilage metabolism is more sensitive to load rate than to load magnitude. In multiple studies done on animals and humans, proteoglycan (PG) synthesis and DNA synthesis in cartilage explants increased in samples loaded dynamically, yet decreased in samples subjected to static loads.6,14,17,50
Substantial clinical evidence has shown that instability is extremely deleterious. Consistent experimental evidence shows that the intrinsic biophysical responses of bone and cartilage at the local tissue and cellular level are very sensitive to load rates, perhaps even more so than to load magnitude.13,15,37,49 Coupling these scientific observations, there is a compelling need for dynamic testing of incongruous and unstable joints. In the current series, ankles with identical incongruity and negligible differences in loading had substantial elevations in contact pressure, in temporal pressure gradients, and in spatial pressure gradients, when the talus transiently subluxated from beneath the distal tibia. The greatest percentile increases in this isolated trial were increases in loading rate. This suggests that instability events may result in serious transient pathologic loads. However, it must be stressed that these are preliminary data from one specimen. Therefore, the mechanical and clinical significance of these observations is not known. It should also be emphasized that the mechanical abnormalities measured occurred with simultaneous instability and incongruity. The sharp increases resulting from the subluxation event may be substantially different in specimens without an associated incongruity.
The hip, knee, and ankle respond differently to intraarticular injuries of similar magnitude.2,22,28,30 Although residual incongruity in displaced acetabular fractures has been linked to poor outcome, tibial plateau fractures seem to tolerate substantially greater incongruities without degeneration, provided they remain stable.10,22,24,30 Although differences in natural stability, congruity, and cartilage thickness may explain clinical observations, the reasons for these differences essentially are unknown. Multiple clinical studies try to correlate outcome with postoperative congruity.24,30,33 However, measuring residual incongruity on postoperative radiographs is difficult and inaccurate, especially in the acetabulum.33,47 Therefore, correlating outcome with postoperative radiographic congruity is difficult. Studies relating congruity to outcome also are complicated by the fact that the great majority of these studies do not control for injury severity. Perfectly repaired articular fragments may be irreversibly damaged by impact at the time of injury.
The pathomechanical etiology of posttraumatic arthritis is unclear. Previous static tests have failed to show substantial increases in articular contact stresses caused by surface incongruities. However, these tests are limited by their static nature. A new dynamic approach to measuring contact abnormalities across joints under pathologic loading conditions is reported here. Measuring the relative contribution of incongruity and instability to pathomechanical loading therefore becomes possible for the first time. Determining dynamic articular surface contact characteristics under physiologic loading conditions plausibly will aid in understanding the etiology of posttraumatic arthritis.
1. Atkinson PJ, Haut RC: Injuries produced by blunt trauma to the human patellofemoral joint vary with flexion angle of the knee. J Orthop Res 19:827–833, 2001.
2. Bone L, Stegemann P, McNamara K, Seibel R: External fixation of severely comminuted and open tibial pilon fractures. Clin Orthop 292:101–107, 1993.
3. Brown TD, Anderson DD, Nepola JV, et al: Contact stress aberrations following imprecise reduction of simple tibial plateau fractures. J Orthop Res 6:851–862, 1988.
4. Brown TD, Hurlbut PT, Hale JE, et al: Effects of imposed hindfoot constraint on ankle contact mechanics for displaced lateral malleolar fractures. J Orthop Trauma 8:511–519, 1994.
5. Brown TD, Pope DF, Hale JE, Buckwalter JA, Brand RA: Effects of osteochondral defect size on cartilage contact stress. J Orthop Res 9:559–567, 1991.
6. Buschmann MD, Gluzband YA, Grodzinsky AJ, Hunziker EB: Mechanical compression modulates matrix biosynthesis in chondrocyte/agarose culture. J Cell Sci 108:1497–1508, 1995.
7. Clancy Jr WG, Shelbourne KD, Zoellner GB, et al: Treatment of knee joint instability secondary to rupture of the posterior cruciate ligament: Report of a new procedure. J Bone Joint Surg 65A:310–322, 1983.
8. Daniel DM, Stone ML, Dobson BE, et al: Fate of the ACL-injured patient: A prospective outcome study. Am J Sports Med 22:632–644, 1994.
9. Dedrick DK, Goldstein SA, Brandt KD, et al: A longitudinal study of subchondral plate and trabecular bone in cruciate-deficient dogs with osteoarthritis followed up for 54 months. Arthritis Rheum 36:1460–1467, 1993.
10. Delamarter RB, Hohl M, Hopp Jr E: Ligament injuries associated with tibial plateau fractures. Clin Orthop 250:226–233, 1990.
11. Ewers BJ, Dvoracek-Driksna D, Orth MW, Haut RC: The extent of matrix damage and chondrocyte death in mechanically traumatized articular cartilage explants depends on rate of loading. J Orthop Res 19:779–784, 2001.
12. Gillquist J, Messner K: Anterior cruciate ligament reconstruction and the long-term incidence of gonarthrosis. Sports Med 27:143–156, 1999.
13. Goldstein SA, Matthews LS, Kuhn JL, Hollister SJ: Trabecular bone remodeling: An experimental model. J Biomech 24(Suppl 1):135–150, 1991.
14. Gray ML, Pizzanelli AM, Grodzinsky AJ, Lee RC: Mechanical and physiochemical determinants of the chondrocyte biosynthetic response. J Orthop Res 6:777–792, 1998.
15. Guilak F: The deformation behavior and viscoelastic properties of chondrocytes in articular cartilage. Biorheology 37:27–44, 2000.
16. Hak DJ, Hamel AJ, Bay BK, Sharkey NA, Olson SA: Consequences of transverse acetabular fracture malreduction on load transmission across the hip joint. J Orthop Trauma 12:90–100, 1998.
17. Hall AC, Urban JP, Gehl KA: The effects of hydrostatic pressure on matrix synthesis in articular cartilage. J Orthop Res 9:1–10, 1991.
18. Honkonen SE: Degenerative arthritis after tibial plateau fractures. J Orthop Trauma 9:273–277, 1995.
19. Huber-Betzer H, Brown TD, Mattheck C: Some effects of global joint morphology on local stress aberrations near imprecisely reduced intra-articular fractures. J Biomech 23:811–822, 1990.
20. Hughes JL, Weber H, Willenegger H, Kuner EH: Evaluation of ankle fractures: Non-operative and operative treatment. Clin Orthop 138:111–119, 1979.
21. Kannus P, Jarvinen M: Postraumatic anterior cruciate ligament insufficiency as a cause of osteoarthritis in a knee joint. Clin Rheumatol 8:251–260, 1989.
22. Lansinger O, Bergman B, Korner L, Andersson GB: Tibial condylar fractures: A twenty-year follow-up. J Bone Joint Surg 68A:13–19, 1986.
23. Lefkoe TP, Trafton PG, Ehrlich MG, et al: An experimental model of femoral condylar defect leading to osteoarthrosis. J Orthop Trauma 7:458–467, 1993.
24. Letournel E: Acetabulum fractures: Classification and management. Clin Orthop 151:81–106, 1980.
25. Llinas A, McKellop HA, Marshall GJ, et al: Healing and remodeling of articular incongruities in a rabbit fracture model. J Bone Joint Surg 75A:1508–1523, 1993.
26. Lovasz G, Llinas A, Benya PD, et al: Cartilage changes caused by a coronal surface step-off in a rabbit model. Clin Orthop 354:224–234, 1998.
27. Lovasz G, Park SH, Ebramzadeh E, et al: Characteristics of degeneration in an unstable knee with a coronal surface step-off. J Bone Joint Surg 83B:428–436, 2001.
28. Marsh JL, Bonar S, Nepola JV, DeCoster TA, Hurwitz SR: Use of an articulated external fixator for fractures of the tibial plafond. J Bone Joint Surg 77A:1498–1509, 1995.
29. Marti RK, Raaymakers EL, Nolte PA: Malunited ankle fractures: The late results of reconstruction. J Bone Joint Surg 72B:709–713, 1990.
30. Matta JM: Fractures of the acetabulum: Accuracy of reduction and clinical results in patients managed operatively within three weeks after the injury. J Bone Joint Surg 78A:1632–1645, 1996.
31. Mayo KA: Open reduction and internal fixation of fractures of the acetabulum: Results in 163 fractures. Clin Orthop 305:31–37, 1994.
32. McKinley TO, Bay BK: Trabecular bone strain changes associated with cartilage defects in the proximal and distal tibia. J Orthop Res 19:906–913, 2001.
33. Moed BR, Willson Carr SE, Watson JT: Results of operative treatment of fractures of the posterior wall of the acetabulum. J Bone Joint Surg 84A:752–758, 2002.
34. Mow VC, Kuei SC, Lai WM, Armstrong CG: Biphasic creep and stress relaxation of articular cartilage in compression?: Theory and experiments. J Biomech Eng 102:73–84, 1980.
35. Nelson BH, Anderson DD, Brand RA, Brown TD: Effect of osteochondral defects on articular cartilage: Contact pressures studied in dog knees. Acta Orthop Scand 59:574–579, 1988.
36. Newberry WN, Garcia JJ, Mackenzie CD, Decamp CE, Haut RC: Analysis of acute mechanical insult in an animal model of post-traumatic osteoarthrosis. J Biomech Eng 120:704–709, 1998.
37. O’Connor JA, Lanyon LE, MacFie H: The influence of strain rate on adaptive bone remodeling. J Biomech 15:767–781, 1982.
38. O’Connor BL, Visco DM, Rogers PI, Mamlin LA, Brandt KD: Serial force plate analyses of dogs with unilateral knee instability, with or without interruption of the sensory input from the ipsilateral limb. Osteoarthritis Cartilage 7:567–573, 1999.
39. Oloyede A, Flachsmann R, Broom ND: The dramatic influence of loading velocity on the compressive response of articular cartilage. Connect Tissue Res 27:211–224, 1992.
40. Olson SA, Bay BK, Chapman MW, Sharkey NA: Biomechanical consequences of fracture and repair of the posterior wall of the acetabulum. J Bone Joint Surg 77A:1184–1192, 1995.
41. Olson SA, Bay BK, Pollak AN, Sharkey NA, Lee T: The effect of variable size posterior wall acetabular fractures on contact characteristics of the hip joint. J Orthop Trauma 10:395–402, 1996.
42. Ovadia DN, Beals RK: Fractures of the tibial plafond. J Bone Joint Surg 68A:543–551, 1986.
43. Pereira DS, Koval KJ, Resnick RB, et al: Tibiotalar contact area and pressure distribution: The effect of mortise widening and syndesmosis fixation. Foot Ankle Int 17:269–274, 1996.
44. Pettrone FA, Gail M, Pee D, Fitzpatrick T, Van Herpe LB: Quantitative criteria for prediction of the results after displaced fracture of the ankle. J Bone Joint Surg 65A:66–77, 1983.
45. Ramsey PL, Hamilton W: Changes in tibiotalar area of contact caused by lateral talar shift. J Bone Joint Surg 58A:356–357, 1976.
46. Rasmussen PS: Tibial condylar fractures: Impairment of knee joint stability as an indication for surgical treatment. J Bone Joint Surg 55A:1331–1350, 1973.
47. Rice J, Kaliszer M, Dolan M, et al: Comparison between clinical and radiologic outcome measures after reconstruction of acetabular fractures. J Orthop Trauma 16:82–86, 2002.
48. Rowley DI, Norris SH, Duckworth T: A prospective trial comparing operative and manipulative treatment of ankle fractures. J Bone Joint Surg 68B:610–613, 1986.
49. Rubin CT, Lanyon LE: Regulation of bone formation by applied dynamic loads. J Bone Joint Surg 66A:397–402, 1984.
50. Sah RL, Kim YJ, Doong JY, et al: Biosynthetic response of cartilage explants to dynamic compression. J Orthop Res 7:619–636, 1989.
51. Starr AJ, Reinert CM, Jones AL: Percutaneous fixation of the columns of the acetabulum: A new technique. J Orthop Trauma 12:51–58, 1998.
52. Stevens DG, Beharry R, McKee MD, Waddell JP, Schemitsch EH: The long-term functional outcome of operatively treated tibial plateau fractures. J Orthop Trauma 15:312–320, 2001.
53. Teeny SM, Wiss DA: Open reduction and internal fixation of tibial plafond fractures: Variables contributing to poor results and complications. Clin Orthop 292:108–117, 1993.
54. Thompson Jr RC, Oegema Jr TR, Lewis JL, Wallace L: Osteoarthrotic changes after acute transarticular load: An animal model. J Bone Joint Surg 73A:990–1001, 1991.
55. Tornetta III P: Non-operative management of acetabular fractures: The use of dynamic stress views. J Bone Joint Surg 81B:67–70, 1999.
56. Vilensky JA, O’Connor BL, Brandt KD, Dunn EA, Rogers PI: Serial kinematic analysis of the canine hindlimb joints after deafferentation and anterior cruciate ligament transection. Osteoarthritis Cartilage 5:173–182, 1997.
57. Weber BG, Simpson LA: Corrective lengthening osteotomy of the fibula. Clin Orthop 199:61–67, 1985.
58. Yablon IG, Leach RE: Reconstruction of malunited fractures of the lateral malleolus. J Bone Joint Surg 71A:521–527, 1989.
59. Yde J, Kristensen KD: Ankle fractures: supination-eversion fractures of stage IV: Primary and late results of operative and non-operative treatment. Acta Orthop Scand 51:981–990, 1980.