Objective. To compare the knee joint loading patterns in individuals with differing radiographic grades of knee osteoarthritis (OA) for characterization of the mechanical implications of different structural states, and to compare the knee adduction angular impulse, a measure of gait complementary to the commonly used peak knee adduction moment.Methods. Asymptomatic subjects (those without knee OA) having a Kellgren/Lawrence (K/L) radiographic severity grade of 0 or 1 (n ‫؍‬ 28) and subjects with symptomatic knee OA having K/L grades of 2 (n ‫؍‬ 66) or 3 (n ‫؍‬ 23) were recruited. Gait analysis was used to calculate the peak external knee adduction moment and the external knee adduction angular impulse for the whole stance and for the 4 subdivisions of stance.Results. Both the peak knee adduction moment and the knee adduction angular impulse increased with K/L radiographic grade (P < 0.05). However, only the knee adduction angular impulse differed between subjects with moderate (grade 3) and those with mild (grade 2) radiographic knee OA (P < 0.05).Conclusion. The differences between mild and moderate symptomatic radiographic knee OA are not only structural but also functional, based on the magnitude of load in the medial knee joint. Moreover, knee adduction angular impulse provides additional information beyond that available from the peak knee adduction moment, and may therefore be an important gait parameter to include in OA research. These findings are important for our understanding of the pathophysiologic mechanisms of OA.The peak external joint moments determined by gait analysis are surrogate markers of the effects of contact load on an individual's joints. In particular, in the knee, the external adduction moment is the primary predictor of load distribution across the tibial plateau (1) and is a main determinant of clinical outcomes following surgical intervention to correct varus deformity (2). Individuals with symptomatic radiographic knee osteoarthritis (OA) have higher-than-normal peak external knee adduction moments during walking (3-8).The peak external knee adduction moment has been implicated in progression of radiographic OA (9) and has been identified as a marker of disease severity (8,10), when individuals with OA radiographic severity grades Յ2 are compared with those with grades Ն3, using the Kellgren and Lawrence (K/L) scale (11). In addition, when the first and second peak external knee adduction moments, occurring during midstance and terminal stance, respectively, were compared in healthy controls and in individuals with less or more severe OA, the first peak was higher than normal regardless of disease severity, whereas the second peak was higher than normal only in those with more severe OA (8).As a measure of knee load, the peak external knee adduction moment reflects only a single time point during stance and is independent of the duration of the stance phase of gait. Because individuals with OA ambulate at slower speeds (3) and exhibit a prolonged stance phase as compared with hea...

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Objective. To verify the biologic links between progressive cellular and structural alterations within knee joint components and development of symptomatic chronic pain that are characteristic of osteoarthritis (OA), and to investigate the molecular basis of alterations in nociceptive pathways caused by OA-induced pain.Methods. An animal model of knee joint OA pain was generated by intraarticular injection of monoiodoacetate (MIA) in Sprague-Dawley rats, and symptomatic pain behavior tests were performed. Relationships between development of OA with accompanying pain responses and gradual alterations in cellular and structural knee joint components (i.e., cartilage, synovium, meniscus, subchondral bone) were examined by histologic and immunohistologic analysis, microscopic examination, and microfocal computed tomography. Progressive changes in the dynamic interrelationships between peripheral knee joint tissue and central components of nociceptive pathways caused by OA-induced pain were examined by investigating cytokine production and expression in sensory neurons of the dorsal root ganglion and spinal cord.Results. We observed that structural changes in components of the peripheral knee joint correlate with alterations in the central compartments (dorsal root ganglia and the spinal cord) and symptomatic pain assessed by behavioral hyperalgesia. Our comparative gene expression studies revealed that the pain pathways in MIA-induced knee OA may overlap, at least in part, with neuropathic pain mechanisms. Similar results were also observed upon destabilization of the knee joint in the anterior cruciate ligament transection and destabilization of the medial meniscus models of OA.Conclusion. Our results indicate that MIAinduced joint degeneration in rats generates an animal model that is suitable for mechanistic and pharmacologic studies on nociceptive pain pathways caused by OA, and provide key in vivo evidence that OA pain is caused by central sensitization through communication between peripheral OA nociceptors and the central sensory system. Furthermore, our data suggest a mechanistic overlap between OA-induced pain and neuropathic pain.

Objective. The relationship between knee pain and radiographic evidence of knee osteoarthritis (OA) is notoriously imperfect. In particular, conditions that distinguish individuals with symptoms from those with comparable radiographic involvement who remain asymptomatic are unclear. We investigated dynamic loading across the knee in individuals with mild radiographic OA who were distinguished by the presence or absence of knee pain. Methods. Subjects were recruited into 3 groups: symptomatic with a Kellgren/Lawrence (K/L) grade of 2 (n ‫؍‬ 52), asymptomatic with a K/L grade of 2 (n ‫؍‬ 19), and asymptomatic with a K/L grade of 0 or 1 (n ‫؍‬ 37), the latter representing a normal comparator group. Dynamic knee loading was assessed with gait analysis, and both the peak external knee adduction moment and the knee adduction angular impulse were determined. Results. Peak knee adduction moment and knee adduction angular impulse were 19% and 30% higher, respectively, in symptomatic K/L grade 2 individuals than in asymptomatic individuals with the same radiographic grade (P < 0.05). Conversely, the asymptomatic K/L grade 2 group did not differ from the K/L grade 0 -1 normal comparator group (P ‫؍‬ 1.00). Conclusion. Among individuals with mild radiographic knee OA (K/L grade 2), those who are symptomatic have significantly higher medial compartment loads than those who are asymptomatic, whereas those who are asymptomatic do not differ from normal controls (asymptomatic K/L grade 0 or 1). These findings suggest a biomechanical component to the distinction between asymptomatic and symptomatic radiographic OA, which may be pathophysiologically important.

In osteoarthritis, one postulate is that changes in the mechanical properties of the subchondral bone layer result in cartilage damage. The goal of this study was to examine changes in subchondral trabecular bone properties at the calcified tissue level in the early stages of cartilage damage. Finite element models were constructed from microCT scans of trabecular bone from the proximal tibia of donors with mild cartilage damage and from normal donors. In the donors with cartilage damage, macroscopic damage was present only in the medial compartment. The effective tissue elastic moduli were determined using a combination of finite element models and mechanical testing. The bone tissue modulus was reduced by 60% in the medial condyle of the cases with cartilage damage compared to the control specimens. Neither the presence of cartilage damage nor the anatomic site (medial vs. lateral) affected the elastic modulus at the apparent level. The volume fraction of trabecular bone was higher in the medial compartment compared to the lateral compartment of tibiae with cartilage damage (but not the controls), suggesting that mechanical properties were preserved in part at the apparent level by an increase in the bone volume fraction. It seems likely that the normal equilibrium between cartilage properties, bone tissue properties and bone volume fraction is disrupted early in the development of osteoarthritis. © 2001 Orthopaedic Research Society. Punlished by Elsevier Science Ltd. All rights reserved.

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Severe loss of bone related to stress-shielding is one problem threatening the long-term integrity of noncemented total hip arthroplasty. It is widely accepted that this phenomenon is caused by adaptive bone remodeling according to Wolff's law. Recently, quantitative bone-remodeling theories have been proposed, suitable for use in computer-simulation models in combination with finite-element codes, which can be applied to simulate the long-term effect of the remodeling process. In the present paper, the results of such a computer simulation are compared with those in an animal experiment. A three-dimensional finite-element model was constructed from an animal experimental configuration concerning the implantation of a fully coated femoral hip prosthesis in dogs. The simulation results of the adaptive bone-remodeling process (geometric adaptations at the periosteal surface and density adaptations within the cancellous bone) were compared with cross-sectional measurements of the canine femurs after 2 years of follow-up. The detailed comparison showed that long-term changes in the morphology of bone around femoral components of total hip replacements can be fully explained with the present quantitative adaptive bone-remodeling theory.