What causes knee osteoarthrosis: are different compartments susceptible to different risk factors?
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Biomedical subjects
Publications and source records attributed to E L Radin.
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The efficacy of treatment of overuse patellofemoral pain with an elastic knee sleeve with a silicone patellar ring was compared with a simple elastic sleeve and with no treatment in a prospective study of 395 army recruits. During 14 weeks of basic training, 84 knees were diagnosed as having overuse patellofemoral pain. Recruits treated with a simple elastic knee sleeve had a statistically significant better comfort score and more had their pain resolved by the end of training than those treated with elastic knee sleeves with a silicone patellar ring. The mean pain score at the end of training decreased more among recruits who were treated with a simple elastic knee sleeve than among recruits who received no treatment, but this difference was not significant. Among the treatment options tried, the simple elastic knee sleeve was no more effective than no treatment at all, but it was more effective than the more elaborate patellar brace.
Dynamic finite element analysis is used to elucidate the manner in which juxtaarticular stress distributions depend on the transitional mechanical properties of the calcified cartilage layer. A finite element model is used to study how these stresses change in response to the thinning of the articular cartilage layer associated with tidemark advancement. The finite element results indicate that shear stress levels within the deepest layer of articular cartilage are increased when tidemark advancement with concomitant cartilage-thinning and calcified cartilage/subchondral plate thickening is modeled. The cartilage-thinning associated with tidemark advancement, observed both clinically and experimentally, may be an explanation for what has previously been considered wear-related thinning.
We sought to determine whether synovial leukocytic inflammation is a primary event in mechanically induced osteoarthrosis. Repetitive impulse loading (50 ms duration at 60 Hz for 40 minutes each day) was applied to the right hindlimbs of 24 New Zealand white rabbits for 3, 6, or 9 weeks. The synovial membrane from the medial suprapatellar area was examined qualitatively using transmission electron microscopy and quantitatively using light microscopic morphometry. The results indicate that synovial inflammation is not a primary event in this mechanically induced osteoarthrosis, but synovial hyperplasia occurs prior to histologically evident cartilage destruction at 6-9 weeks.
To test the hypothesis that appropriate and timely neuromuscular control of limb motions plays an important role in the preservation of joint health, we kinematically and kinetically examined the behavior of the legs of young adult subjects at heel strike during natural walking. We compared a group of 18 volunteers, who, we presumed, were preosteoarthrotic because of mild, intermittent, activity-related knee joint pain, with 14 age-matched asymptomatic normal subjects. The two groups of subjects exhibited similar gait patterns with equivalent cadences, walking speeds, terminal stance phase knee flexion, maximum (peak) swing angular velocity, and overall shape of the vertical ground reaction. However, our instrumentation detected statistically significant differences between the two groups within a few milliseconds of heel strike. In the knee pain group, the heel hit the floor with a stronger impact in this brief interval. Just before heel strike, there was a faster downward velocity of the ankle with a larger angular velocity of the shank. The follow-through of the leg immediately after heel strike was more violent with larger peak axial and angular accelerations of the leg echoed by a more rapid rise of the ground reaction force. This sequence of events represents repetitive impulsive loading, which consistently provoked osteoarthrosis in animal experiments. We refer to this micro-incoordination of neuromuscular control not visible to the naked eye as "microklutziness."
The joint is an organ and functions as a mechanical bearing created of biological materials. In the joint, as in all connective tissues, there is a relationship between mechanical factors and tissue behavior. Therefore, it is not surprising that joint health and osteoarthrosis are reflections of both mechanical and biological factors. Osteoarthrosis is not a disease, but organ failure caused initially by mechanical factors. The biological changes follow. There is no habitual pathophysiological cascade. Osteoarthrosis is best thought of not as a common final pathway, but as a common end stage. The hypotheses that in osteoarthrosis substructural disorganization of the matrix proceeds chondrocytic enzyme production, that impulsive loading is an essential factor in the progressive cartilage destruction, and that tidemark advancement and horizontal cartilage splitting are the primary mechanisms in progressive cartilage loss are discussed.
Lumbar intervertebral disc herniation is thought to be related to senescent changes in the nucleus pulposus except in rare instances of trauma. This investigation provides the first in vitro model of disc prolapse that reliably ruptures discs under physiologically reasonable stress. Fourteen vertebral motion segments with intact posterior elements were loaded repetitively at 1.5 Hz in a combination of flexion (7 degrees), rotation (less than 3 degrees), and compression (1,334 N) for an average of 6.9 hours (range, 3.0-13.0 hours) in a materials testing machine. Loading was terminated when reaction force leveled off for more than 1 hour. Ten discs failed through annular protrusions, and four failed by nuclear extrusion through annular tears, supporting the hypothesis that intervertebral disc prolapse is peripheral in origin. The annulus fibrosus is the site of primary pathologic change.
A dynamic contact finite element formulation was used to study transient stresses in the impulsively loaded rabbit knee, an established experimental model of mechanically induced osteoarthrosis. The computations were used to test the hypothesis that stress wave propagation and reflection, from juxtarticular interfaces of material property discontinuity, could be responsible for markedly increased levels of transient local cartilage stress. The finite element results demonstrated intuitively credible stress wave propagation and interfacial reflection phenomena. However, the magnitude of these waves was not nearly large enough to appreciably alter the quasi-static stress distributions otherwise prevailing. Thus, local stress wave reflection from interfaces of modulus discontinuity (for example the cartilage/subchondral plate) probably does not contribute appreciably to the heightened tissue sensitivity to impulsive loading experimentally observed in this animal model.
The purpose of this work was to determine whether subchondral bone changes are an integral part of the development of osteoarthrosis of the knee following experimentally created tibial angulation. Thirty degree varus or valgus proximal tibial osteotomies were created in female New Zealand white rabbits. Bone and cartilage changes were assessed grossly, radiologically, and histologically. Thirty-four weeks following osteotomy, severe cartilage changes, including osteophytes, fibrillation, derangement of cell columns, and cloning, were evident on the overloaded condyle, accompanied by increased subchondral bone density. The pattern of cartilage deterioration was different from that found in other experimental, mechanically induced arthroses. We conclude that osteoarthrosis is a final common pathway for mechanically induced joint failure, and that progressive cartilage change is associated with increased subchondral bone density.
Fatigue behavior of compact bone at physiological strain ranges was examined in vitro. Standardized specimens of bovine compact bone were cyclically loaded in uniaxial tension of 0-1200 or 0-1500 microstrain for up to 13-37 million cycles to study the long-term fatigue properties. All specimens exhibited fatigue during the first several million cycles of loading, evidenced by a gradual decrease of specimen modulus during this initial loading period; mean modulus loss for all specimens was approximately 6%. After this initial stiffness loss, specimen modulus stabilized and did not change again for the duration of the loading. Osteonal bone specimens lost significantly more stiffness than primary bone specimens during the early loading history, but neither microstructural type progressed to fatigue failure. These data suggest that some fatigue of compact bone is a realistic expectation of the normal loading environment, but this fatigue does not progress to fatigue failure within a physiologically reasonable number of cycles when tested in vitro at strain magnitudes like those measured in living animals. Implications for fatigue/stress fractures in vivo are discussed.
A dynamic nonlinear finite element model was developed to study juxtarticular stresses in the splinted rabbit knee, an established laboratory model for creating osteoarthrosis due to impulsive loading. Plane strain finite element results were validated by comparison with corresponding experimental data. Parametric effects studied included the input tibial displacement speed, the local bone density distribution, and the modulus of cartilage and subchondral bone. While the computed resultant contact force magnitude was sensitive to a number of model parameters, the stress patterns, when normalized to a given resultant force magnitude, were not. Despite comparable force peaks, the finite element results showed approximately six-fold higher effective strain rate levels for a severely impulsive loading protocol known to induce rapid osteoarthrosis, versus those for a mildly impulsive loading protocol not usually associated with cartilage damage. A propensity for elevated shear in the deep cartilage layer near the contact periphery, observed in nearly all computed stress distributions, is consistent with previous experimental findings of fissuring at that level in the impulsively loaded rabbit knee.
The hypothesis that training with viscoelastic orthotics may lower tibial stress fracture morbidity was studied using an animal model. No difference was found in the incidence of tibial stress fractures between groups trained with and groups trained without viscoelastic orthotics. The results in the animal model do not support the need for a clinical trial.
The damaging effect of transient loads on joints has been observed in vitro and in vivo, and may be an aetiological factor in osteoarthrosis. The events around heel strike, when the velocity of the foot is brought rapidly to zero, may be a source of such loads in normal activity. By modifying the rate at which the limb descends to the ground, quadriceps action influences the magnitude of the heel strike transient. Experiments were carried out to analyse the occurrence of these transients, and a two-dimensional mathematical model of the knee joint and lower leg was used to calculate the forces developed at the knee in response to them. Paralysis of the quadriceps resulted in a large increase in the heel strike transient.
We have shown that stress fractures can be induced in the tibial diaphysis of an animal model by the repeated application of non-traumatic impulsive loads. The right hind limbs of 31 rabbits were loaded for three to nine weeks and changes in the bone were monitored by radiography and bone scintigraphy. The presence of stress fractures was confirmed histologically in some cases. Most animals sustained a stress fracture within six weeks and there was a positive correspondence between scintigraphic change and radiological evidence. Microscopic damage was evident at the sites of positive bone scans. The progression, location, and time of onset of stress fractures in this animal model were similar to those in clinical reports, making the model a useful one for the study of the aetiology of stress fractures.
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Ultra high molecular weight polyethylene (UHMPWE) is now the material of choice for total joint replacement prostheses, in combination with a metal surface against which the polymer articulates. As this material has now been in use in this application for approximately three decades and other limiting factors (e.g. loosening of the prosthesis) have been improved upon, it is appropriate to attempt a long-term prognosis.
Compact bone specimens were cyclically loaded in uniaxial tension for one million cycles; loading was performed at either of two physiological strain rates (0.01 s-1 or 0.03 s-1) and a physiological strain range (0-1200 microstrain). Microdamage in loaded and nonloaded control specimens was then assessed histomorphometrically. Fatigue, evidence by stiffness loss, was observed at both strain rates and was significantly greater in specimens loaded at the high experimental strain rate than in specimens loaded at the low strain rate. Morphologically, this fatigue corresponded to increased numbers of microcracks in the bone. These data show that fatigue and resultant microdamage are realistic expectations of cyclic loading within the physiological strain range. The rate at which strains are developed influences the fatigue behavior of compact bone, suggesting that cyclic loading at high physiological strain rates, characteristic of vigorous activities, is more damaging to compact bone than loading at lower physiological strain rates.
This study defines the alteration in bone tissue kinetics responsible for the "adaptive remodeling" response to altered strain environments. Adult beagle dogs were separated into three experimental groups: ulnar osteotomy, ulnar osteotomy with fracture fixation plate spanning the gap and sham surgery. Four sets of double fluorochrome labels were administered. Prior to sacrifice at 1, 3, and 6 months, strains were measured through rosette strain gages on the cranial and caudal surfaces of the intact radius. Histomorphometric analysis indicated that the increased bone mass in response to elevated strain results from increased activation frequency of modeling with more sites undergoing formation processes than resorption processes on periosteal and endocortical surfaces. Increased remodeling activation did not lead to increased bone mass. There was no evidence that elevated strain changes the individual vigor of osteoclasts or osteoblasts, or that the sigma period was altered by elevated strain.