Comparison of loading rate‐dependent injury modes in a murine model of post‐traumatic osteoarthritis

Post‐traumatic osteoarthritis (PTOA) is a common long‐term consequence of joint injuries such as anterior cruciate ligament (ACL) rupture. In this study we used a tibial compression overload mouse model to compare knee injury induced at low speed (1 mm/s), which creates an avulsion fracture, to injury induced at high speed (500 mm/s), which induces midsubstance tear of the ACL. Mice were sacrificed at 0 days, 10 days, 12 weeks, or 16 weeks post‐injury, and joints were analyzed with micro‐computed tomography, whole joint histology, and biomechanical laxity testing. Knee injury with both injury modes caused considerable trabecular bone loss by 10 days post‐injury, with the Low Speed Injury group (avulsion) exhibiting a greater amount of bone loss than the High Speed Injury group (midsubstance tear). Immediately after injury, both injury modes resulted in greater than twofold increases in total AP joint laxity relative to control knees. By 12 and 16 weeks post‐injury, total AP laxity was restored to uninjured control values, possibly due to knee stabilization via osteophyte formation. This model presents an opportunity to explore fundamental questions regarding the role of bone turnover in PTOA, and the findings of this study support a biomechanical mechanism of osteophyte formation following injury. © 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 32:79–88, 2014.     

Post‐traumatic osteoarthritis: Improved understanding and opportunities for early intervention

Even with current treatments of acute joint injuries, more than 40% of people who suffer significant ligament or meniscus tears, or articular surface injuries, will develop osteoarthritis (OA). Correspondingly, 12% or more of all patients with lower extremity OA have a history of joint injury. Recent research suggests that acute joint damage that occurs at the time of an injury initiates a sequence of events that can lead to progressive articular surface damage. New molecular interventions, combined with evolving surgical methods, aim to minimize or prevent progressive tissue damage triggered by joint injury. Seizing the potential for progress in the treatment of joint injuries to forestall OA will depend on advances in (1) quantitative methods of assessing the injury severity, including both structural damage and biologic responses, (2) understanding of the pathogenesis of post‐traumatic OA, taking into account potential interactions among the different tissues and the role of post‐traumatic incongruity and instability, and (3) application of engineering and molecular research to develop new methods of treating injured joints. This paper highlights recent advances in understanding of the structural damage and the acute biological response following joint injury, and it identifies important directions for future research. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 29:802–809     

Inflammatory and degenerative phases resulting from anterior cruciate rupture in a non‐invasive murine model of post‐traumatic osteoarthritis

Joint injury is the predominant risk factor for post‐traumatic osteoarthritis development (PTOA). Several non‐invasive mouse models mimicking human PTOA investigate molecular mechanisms of disease development; none have characterized the inflammatory response to this acute traumatic injury. Our aim was to characterize the early inflammatory phase and later degenerative component in our in vivo non‐invasive murine model of PTOA induced by anterior cruciate ligament (ACL) rupture. Right knees of 12‐week‐old C57Bl6 mice were placed in flexion at a 30° offset position and subjected to a single compressive load (12N, 1.4 mm/s) to induce ACL rupture with no obvious damage to surrounding tissues. Tissue was harvested 4 h post‐injury and on days 3, 14, and 21; contralateral left knees served as controls. Histological, immunohistochemical, and gene analyzes were performed to evaluate inflammatory and degenerative changes. Immunohistochemistry revealed time‐dependent expression of mature (F4/80 positive) and inflammatory (CD11b positive) macrophage populations within the sub‐synovial infiltrate, developing osteophytes, and inflammation surrounding the ACL in response to injury. Up‐regulation of genes encoding acute pro‐inflammatory markers, inducible nitric oxide synthase, interleukin‐6 and interleukin‐17, and the matrix degrading enzymes, ADAMTS‐4 and MMP3 was detected in femoral cartilage, concomitant with extensive cartilage damage and bone remodelling over 21‐days post‐injury. Our non‐invasive model describes pathologically distinct phases of the disease, increasing our understanding of inflammatory episodes, the tissues/cells producing inflammatory mediators and the early molecular changes in the joint, thereby defining the early phenotype of PTOA. This knowledge will guide appropriate interventions to delay or arrest disease progression following joint injury. © 2018 The Authors. Journal of Orthopaedic Research® Published by Wiley Periodicals, Inc. on behalf of the Orthopaedic Research Society. J Orthop Res 36:2118–2127, 2018.     

Evaluation of articular cartilage with quantitative MRI in an equine model of post‐traumatic osteoarthritis

Chondral lesions lead to degenerative changes in the surrounding cartilage tissue, increasing the risk of developing post‐traumatic osteoarthritis (PTOA). This study aimed to investigate the feasibility of quantitative magnetic resonance imaging (qMRI) for evaluation of articular cartilage in PTOA. Articular explants containing surgically induced and repaired chondral lesions were obtained from the stifle joints of seven Shetland ponies (14 samples). Three age‐matched nonoperated ponies served as controls (six samples). The samples were imaged at 9.4 T. The measured qMRI parameters included T₁, T₂, continuous‐wave T_1ρ (CWT_1ρ), adiabatic T_1ρ (AdT_1ρ), and T_2ρ (AdT_2ρ) and relaxation along a fictitious field (T_RAFF). For reference, cartilage equilibrium and dynamic moduli, proteoglycan content and collagen fiber orientation were determined. Mean values and profiles from full‐thickness cartilage regions of interest, at increasing distances from the lesions, were used to compare experimental against control and to correlate qMRI with the references. Significant alterations were detected by qMRI parameters, including prolonged T₁, CWT_1ρ, and AdT_1ρ in the regions adjacent to the lesions. The changes were confirmed by the reference methods. CWT_1ρ was more strongly associated with the reference measurements and prolonged in the affected regions at lower spin‐locking amplitudes. Moderate to strong correlations were found between all qMRI parameters and the reference parameters (ρ = ?0.531 to ?0.757). T₁, low spin‐lock amplitude CWT_1ρ, and AdT_1ρ were most responsive to changes in visually intact cartilage adjacent to the lesions. In the context of PTOA, these findings highlight the potential of T₁, CWT_1ρ, and AdT_1ρ in evaluation of compositional and structural changes in cartilage.     

Is elevated contact stress predictive of post‐traumatic osteoarthritis for imprecisely reduced tibial plafond fractures?

Despite the widely held belief that residual incongruities from intra‐articular fractures subject the joint to contact stresses that predispose to post‐traumatic osteoarthritis (PTOA), objective evidence has been lacking. This study tested the hypothesis that a metric of elevated contact stress exposure would predict the onset of PTOA. The ankles of 10 tibial plafond fracture patients were treated initially using a spanning fixator, with subsequent screw fixation of the articular surface. Following up on an earlier report of finite element computed post‐operative contact stress distributions in these patients' ankles, Kellgren–Lawrence (KL) scores were assessed from minimum 2‐year follow‐up radiographs to characterize the presence/severity of PTOA. At that time point, seven patients had developed PTOA (KL ≥ 2). Five different metrics of contact stress exposure were calculated, all of which exhibited excellent concordance with KL scores, ranging from 88% to 95%. When time of stress exposure was included, one metric was able to predict PTOA development (KL ≥ 2) with 100% reliability, and all metrics exhibited >94% prediction reliability. These findings, albeit in a small population, support the existence of a contact stress exposure threshold above which incongruously reduced tibial plafond fractures are highly likely to develop PTOA. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29:33–39, 2011     

New surgical model of post‐traumatic osteoarthritis: Isolated intra‐articular bone injury in the rabbit

Osteoarthritis (OA) is a leading cause of disability worldwide. We hypothesized that inflammation following isolated intra‐articular bone injury can stimulate post‐traumatic OA and developed a rabbit model to test that concept. Sixty female New Zealand White Rabbits were used. Twenty‐six experimental animals had two holes drilled into their right femoral‐notch, 18 rabbits had sham surgery, and 16 were un‐operated controls. Rabbits were euthanized in subgroups at 72 h, 3, 6, 9, and 52 weeks. Knees were assessed grossly and tissues collected. Cartilage and synovium were analyzed with histology and qPCR and subgroups compared statistically. All surgical joints showed gross and histological (modified Mankin score) cartilage damage after surgery, with experimentals worsening with time (p < 0.05). Cartilage qPCR showed fivefold increases in TGFβ (p < 0.05) expression at 72 h and 3 weeks with sixfold increases in MMP13 (p < 0.025) expression at 72 h. By 6 weeks, expression of these markers was similar to baseline levels. Synovial membrane thickening with increased cellularity was seen at both 9 and 52 weeks (p < 0.05). Short‐term synovial inflammatory marker (IL‐1β, IL‐Ra, IL‐6, and IL‐8) expression was three‐ to fourfold increase in experimentals at 72 h (p < 0.01) returning to baseline levels by 3 weeks. Intra‐articular bone injury creates early joint inflammation with some chronic synovial changes and progressive cartilage damage consistent with OA in adult rabbits. This model provides an exciting new avenue to potentially explore some relevant inflammatory drivers of OA without major mechanical variables. © 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31: 914–920, 2013     

Metabolomic serum profiling after ACL injury in rats: A pilot study implicating inflammation and immune dysregulation in post‐traumatic osteoarthritis

ACL rupture is a major risk factor for post‐traumatic osteoarthritis (PTOA) development. Little information exists on acute systemic metabolic indicators of disease development. Thirty‐six female Lewis rats were randomized to Control or noninvasive anterior cruciate ligament rupture (ACLR) and to three post‐injury time points: 72 h, 4 weeks, 10 weeks (n = 6). Serum was collected and analyzed by ¹H nuclear magnetic resonance (NMR) spectroscopy and combined direct injection and liquid chromatography (LC)‐mass spectrometry (MS)/MS (DI‐MS). Univariate and multivariate statistics were used to analyze metabolomic data, and predictive biomarker models were analyzed by receiver operating characteristic (ROC) analysis. Topological pathway analysis was used to identify perturbed pathways. Two hundred twenty‐two metabolites were identified by ¹H NMR and DI‐MS. Differences in the serum metabolome between ACLR and Control were dominated by medium‐ and long‐chain acylcarnitine species. Further, decreases in several tryptophan metabolites were either found to be significantly different in univariate analysis or to play important contributory roles to multivariate model separation. In addition to acylcarnitines and tryptophan metabolites, glycine, carnosine, and D‐mannose were found to differentiate ACLR from Control. Glycine, 9‐hexadecenoylcarnitine, trans‐2‐Dodecenoylcarnitine, linoelaidyl carnitine, hydroxypropionylcarnitine, and D‐Mannose were identified as biomarkers with high area under ROC curve values and high predictive accuracies. Our analysis provides new information regarding the potential contribution of inflammatory processes and immune dysregulation to the onset and progression of PTOA following ACL injury. As these processes have most commonly been associated with inflammatory arthropathies, larger‐scale studies elucidating their involvement in PTOA development and progression are necessary. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:1969–1979, 2018.

     

Acute and late changes in intraarticular cytokine levels following anterior cruciate ligament injury

Surgical reconstruction of the anterior cruciate ligament (ACL) does not necessarily decrease the risk of developing osteoarthritis (OA). The inflammatory response and relative changes in pro‐ and anti‐inflammatory cytokines could participate in triggering the development of OA. To test this hypothesis we measured the concentrations of IL‐1β, IL‐1ra, IL‐6, IL‐8, IL‐10, and TNF‐α at different times after ACL rupture. The sample population consisted of 48 patients with ACL tear which were assigned to different groups according to the time elapsed from the injury: 22 acute (A), 7 early sub‐acute (ESA), 11 late sub‐acute (LSA), and 8 chronic (C). In group A, there were high levels of IL‐1β, IL‐6, and IL‐8, whereas levels of IL‐1ra and TNF‐α were significantly lower than usually reported. IL‐1β and IL‐8 concentrations returned with time to normal levels in the ESA group. Interestingly, IL‐1ra levels remained always significantly lower than normally reported levels, and TNF‐α levels did not increase after trauma. Our data show increased level of pro‐inflammatory cytokines (IL‐6 and IL‐8) in the acute phase of inflammation which could be responsible for triggering cartilage catabolism and suggest that prompt neutralization of IL‐6 and IL‐8 accumulations in synovial fluid could help prevent development of OA in ACL‐injured knees. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31: 315–321, 2013     

Influence of secondary damage to menisci and articular cartilage on return to sports after anterior cruciate ligament reconstruction

The influence of secondary damage to joint structures (menisci and articular cartilage) on return to sports activities following anterior cruciate ligament (ACL) reconstruction was investigated. Two hundred and sixty athletes who had undergone ACL reconstruction with the Leeds-Keio artificial ligament and had achieved satisfactory joint stability and range of motion were involved in this study. The follow-up period was 7–50 months (mean, 23.4 months). There was a clear correlation between the severity of damage to the joint structures (the menisci and articular cartilage) and the level of return to sports. The most common reason for not being able to return to the original level of sports activity was “pain”. Thus, it was concluded that irreversible secondary damage to joint structures was an important factor hindering return to sports after ACL reconstruction. This study showed that the incidence of meniscal injury and cartilage damage increased with the passage of time after ACL injury, and that, once meniscal injury develops, the incidence of cartilage damage increases. Since sports activity is a factor that accelerates or promotes processes that give rise to this meniscal injury and cartilage damage, it was concluded that it is vital to perform ACL reconstruction before irreversible secondary damage to joint structures occurs in athletes with ACL injuries who hope to continue their sports activities.     

Risk factors for radiographic joint space narrowing and patient reported outcomes of post‐traumatic osteoarthritis after ACL reconstruction: Data from the MOON cohort

The Multicenter Orthopaedic Outcomes Network (MOON) is an NIH‐funded prospective, longitudinal cohort of over 3,500 patients who have undergone anterior cruciate ligament reconstruction (ACLR) by 14 sports medicine surgeons at 7 academic medical centers. Patient reported outcome questionnaires (PRO's) are completed at baseline and multiple timepoints after surgery, and a nested cohort of patients return for radiographs to assess the development of joint space changes. We review the risk factors for worse patient reported outcomes, the predictors of clinically significant symptoms of post‐traumatic osteoarthritis (PTOA), and the factors associated with more radiographic joint space narrowing. Baseline PRO's were highly predictive of follow‐up scores. Factors associated with worse PRO's at 2 and 6 years included female sex, higher BMI, smoking, less education, allograft, medial meniscectomy, or repair, and chondral injury. Partial lateral meniscectomy was unexpectedly associated with better PRO's. Factors associated with clinically significant symptoms of PTOA at 2 and 6 years included subsequent surgery, meniscal pathology, and chondral injury. Factors associated with narrower medial compartment joint space width included medial meniscectomy, medial meniscus repair, and increased age. Medial joint space width was slightly wider overall for the ACLR knees compared to the contralateral normal knees. Future studies will evaluate PRO's and radiographs at 10‐year follow‐up. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:1366–1374, 2017.

     

Single intra‐articular injection of fluvastatin‐PLGA microspheres reduces cartilage degradation in rabbits with experimental osteoarthritis

Statins are cholesterol‐lowering drugs that inhibit 3‐hydroxy‐3‐methylglutaryl‐coenzyme A (HMG‐CoA) reductase, a rate‐limiting enzyme of the mevalonate pathway. The anti‐inflammatory effect of statins has been reported in recent years. The present study investigated therapeutic effects of the local administration of statin in osteoarthritis (OA). We assessed clinically used statins and selected fluvastatin for further experimentation, as it showed potent anabolic and anti‐catabolic effects on human OA chondrocytes. To achieve controlled intra‐articular administration of statin, we developed an intra‐articular injectable statin using poly(lactic‐co‐glycolic acid) (PLGA) as a drug delivery system (DDS). The release profile of the statin was evaluated in vitro. Finally, therapeutic effects of fluvastatin‐loaded PLGA microspheres (FLU‐PLGA) were tested in a rabbit OA model. Rabbit knees were divided into four subgroups: group 1‐A, PLGA‐treated group; group 1‐B, PLGA contralateral saline control group; group 2‐A, FLU‐PLGA‐treated group; and group 2‐B, FLU‐PLGA contralateral saline control group. Histological analysis 5 weeks after intra‐articular injection revealed that OARSI scores were lower in group 2‐A. No significant differences in OARSI scores were observed between groups 1‐A, 1‐B, and 2‐B. This study indicates that a single intra‐articular injection of fluvastatin‐loaded PLGA microspheres could be a novel therapeutic approach for treating patients with OA. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:2465–2475, 2017.

     

Cartilage‐on‐cartilage versus metal‐on‐cartilage impact characteristics and responses

A common in vitro model for studying acute mechanical damage in cartilage is to impact an isolated osteochondral or cartilage specimen with a metallic impactor. The mechanics of a cartilage‐on‐cartilage (COC) impact, as encountered in vivo, are likely different than those of a metal‐on‐cartilage (MOC) impact. The hypothesis of this study was that impacted in vitro COC and MOC specimens would differ in their impact behavior, mechanical properties, chondrocyte viability, cell metabolism, and histologic structural damage. Osteochondral specimens were impacted with either an osteochondral plug or a metallic cylinder at the same delivered impact energy per unit area, and processed after 14 days in culture. The COC impacts resulted in about half of the impact maximum stress and a quarter of the impact maximum stress rate of change, as compared to the MOC impacts. The impacted COC specimens had smaller changes in mechanical properties, smaller decreases in chondrocyte viability, higher total proteoglycan content, and less histologic structural damage, as compared to the impacted MOC specimens. If MOC impact conditions are to be used for modeling of articular injuries and post‐traumatic osteoarthritis, the differences between COC and MOC impacts must be kept in mind. © 2013 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31: 887–893, 2013     

Coefficients of friction,lubricin, and cartilage damage in the anterior cruciate ligament‐deficient guinea pig knee

The coefficient of friction (COF) of articular cartilage is thought to increase with osteoarthritis (OA) progression, and this increase may occur due to a decrease in lubricin concentration. The objectives of this study were to measure the COF of guinea pig tibiofemoral joints with different stages of OA and to establish relationships between COF, lubricin concentrations in synovial fluid, and degradation status using the Hartley guinea pig model. Both hind limbs from 24 animals were harvested: seven 3‐month‐old (no OA), seven 12‐month‐old (mild OA), and 10 that were euthanized at 12 months of age after undergoing unilateral ACL transection at 3 months of age (moderate OA). Contralateral knees served as age‐matched controls. COFs of the tibiofemoral joints were measured using a pendulum apparatus. Synovial fluid lavages were analyzed to determine the concentration and integrity of lubricin using ELISA and Western blot, and the overall articular cartilage status was evaluated by histology. The results showed that the mean COF in the ACL‐deficient knees was significantly greater than that of the no OA (p < 0.01) and mild OA knees (p < 0.01). Lubricin concentrations in the ACL‐deficient knees were significantly lower than that in both of the other groups (p < 0.01). No significant differences in COF or lubricin concentration were found between the no OA and mild OA knees. Histology verified the extent of cartilage damage in each group. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:231–237, 2008     

Affective personality type,post‐traumatic stress disorder symptom severity and post‐traumatic growth in victims of violence

The current study explored the differential association between affective personality type, post‐traumatic stress disorder (PTSD) symptom severity, and post‐traumatic growth (PTG) in victims of violence (N = 113). Relying on previous research, median cut off‐scores on the Positive and Negative Affect Schedule Short Form were used to classify participants as high affective [i.e. high positive affectivity (PA) and high negative affectivity (NA)], self‐actualizing (i.e. high PA and low NA), self‐destructive (i.e. low PA and high NA) and low affective (i.e. low PA and low NA). Results indicated that the self‐destructive and high affective personality styles were strongly associated with increased PTSD symptoms severity. High affective personality type was found to be the only significant predictor of PTG. Results, study limitations and directions for future research were discussed. Copyright © 2010 John Wiley & Sons, Ltd.     

The pattern of cartilage damage in antero‐medial osteoarthritis of the knee and its relationship to the anterior cruciate ligament

Within antero‐medial gonarthrosis (AMG) of the knee, there is a spectrum of damage seen in the functionally intact anterior cruciate ligament (ACL). Our aim was to correlate the degree of ACL damage to the geographical extent and degree of cartilage loss on the tibial plateau. Ninety tibial plateaus resected during unicompartmental arthroplasty were photographed and digitally mapped. The ACL damage was graded (0: normal, 1: synovium loss, 2: longitudinal splits), and dimensions of full thickness cartilage loss and damage recorded. The percentage of full thickness loss in patients with a normal ACL was compared to those with a damaged, but functionally intact ligament. All specimens showed similar elliptical loss of cartilage in the antero‐medial part of the tibial plateau. A total of 45(50%) patients had a macroscopically normal ACL, 21(23%) had synovial loss, and 24(27%) had longitudinal splits. An increase in the area of cartilage damage was seen with progressive ACL damage (p < 0.001). The area of macroscopically normal cartilage found posteriorly did not change. This study demonstrates that phenotypic distribution of cartilage damage in AMG is highly reproducible with a pattern of increasing cartilage erosion associated with increasing ACL damage. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31: 908–913, 2013     

Attenuation of cartilage pathogenesis in post‐traumatic osteoarthritis (PTOA) in mice by blocking the stromal derived factor 1 receptor (CXCR4) with the specific inhibitor,AMD3100

SDF‐1 was found to infiltrate cartilage, decrease proteoglycan content, and increase MMP‐13 activity after joint trauma. In this study, we tested the hypothesis that interference of the SDF‐1/CXCR4 signaling pathway via AMD3100 can attenuate pathogenesis in a mouse model of PTOA. We also tested the predictive and confirmatory power of fluorescence molecular tomography (FMT) for cartilage assessment. AMD3100 was continuously delivered via mini‐osmotic pumps. The extent of cartilage damage after AMD3100 or PBS treatment was assessed by histological analysis 2 months after PTOA was induced by surgical destabilization of the medial meniscus (DMM). Biochemical markers of PTOA were assessed via immunohistochemistry and in vivo fluorescence molecular tomography (FMT). Regression analysis was used to validate the predictive power of FMT measurements. Safranin‐O staining revealed significant PTOA damage in the DMM/PBS mice, while the DMM/AMD3100 treated mice showed a significantly reduced response with minimal pathology. Immunohistochemistry showed that AMD3100 treatment markedly reduced typical PTOA marker expression in chondrocytes. FMT measurements showed decreased cathepsins and MMP activity in knee joints after treatment. The results demonstrate that AMD3100 treatment attenuates PTOA. AMD3100 may provide a viable and expedient option for PTOA therapy given the drug's FDA approval and well‐known safety profile. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:1071–1078, 2015.     

Single intra‐articular dexamethasone injection immediately post‐surgery in a rabbit model mitigates early inflammatory responses and post‐traumatic osteoarthritis‐like alterations

Despite surgical reconstruction of the anterior cruciate ligament, a significant number of patients will still develop post‐traumatic osteoarthritis (PTOA). Our objective was to determine if mitigating aspects of the acute phase of inflammation following a defined knee surgery with a single administration of a glucocorticoid could prevent the development of PTOA‐like changes within an established rabbit model of surgically induced PTOA. An early and late post‐surgical time‐point was investigated in this study (48 h and 9 weeks post‐surgery) in which the following groups were repeated (each n = 6, for a total of 24 rabbits per time‐point, and 48 rabbits used in the study): control (age/sex matched), sham (arthrotomy), drill injury (arthrotomy + two drill holes to a non‐cartilaginous area of the femoral notch), and drill injury + single intra‐articular (IA) injection of dexamethasone (DEX). At 48 h post‐surgery, DEX treatment significantly lowered the mRNA levels for a subset of pro‐inflammatory mediators, and significantly lowered the histological grade. Nine weeks post surgery, DEX treatment significantly lowered the histological scores (presented as effect size) for synovium (3.8), lateral femoral condyle (3.9), and lateral tibial cartilage (5.1) samples. Thus, DEX likely acts to prevent injury induced inflammation that could contribute to subsequent joint damage. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:1826–1834, 2015.     

Tibiofemoral cartilage contact biomechanics in patients after reconstruction of a ruptured anterior cruciate ligament

We investigated the in vivo cartilage contact biomechanics of the tibiofemoral joint in patients after reconstruction of a ruptured anterior cruciate ligament (ACL). A dual fluoroscopic and MR imaging technique was used to investigate the cartilage contact biomechanics of the tibiofemoral joint during in vivo weight‐bearing flexion of the knee in eight patients 6 months following clinically successful reconstruction of an acute isolated ACL rupture. The location of tibiofemoral cartilage contact, size of the contact area, cartilage thickness at the contact area, and magnitude of the cartilage contact deformation of the ACL‐reconstructed knees were compared with those previously measured in intact (contralateral) knees and ACL‐deficient knees of the same subjects. Contact biomechanics of the tibiofemoral cartilage after ACL reconstruction were similar to those measured in intact knees. However, at lower flexion, the abnormal posterior and lateral shift of cartilage contact location to smaller regions of thinner tibial cartilage that has been described in ACL‐deficient knees persisted in ACL‐reconstructed knees, resulting in an increase of the magnitude of cartilage contact deformation at those flexion angles. Reconstruction of the ACL restored some of the in vivo cartilage contact biomechanics of the tibiofemoral joint to normal. Clinically, recovering anterior knee stability might be insufficient to prevent post‐operative cartilage degeneration due to lack of restoration of in vivo cartilage contact biomechanics. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:1781–1788, 2012