Differential knee joint loading patterns during gait for individuals with tibiofemoral and patellofemoral articular cartilage defects in the knee.

OBJECTIVE: To determine compartment-specific loading patterns during gait, quantified as joint reaction forces (JRF), of individuals with knee articular cartilage defects (ACD) compared to healthy controls (HC). METHODS: Individuals with ACDs and HC participated. Individuals with ACDs were divided into groups according to ACD location: PF (only a patellofemoral ACD), TF (only a tibiofemoral ACD), and MIX (both PF and TF ACDs). Participants underwent three-dimensional gait analysis at self-selected speed. TF joint reaction force (TF-JRF) was calculated using inverse dynamics. PF joint reaction force (PF-JRF) was derived from estimated quadriceps force (FQUAD) and knee flexion angle. Primary variables of interest were the PF- and TF-JRF peaks (body weight [×BW]). Related secondary variables (gait speed, quadriceps strength, knee function, activity level) were evaluated as covariates. RESULTS: First peak PF-JRF and TF-JRF were similar in the TF and MIX groups (0.75-1.0 ×BW, P = 0.6-0.9). Both peaks were also similar in the PF and HC groups (1.1-1.3 ×BW, P = 0.7-0.8), and higher than the TF and MIX groups (P = 0.004-0.02). For the second peak PF-JRF, only the HC group was higher than the TF group (P = 0.02). The PF group walked at a similar speed as the HC group; both groups walked faster than the TF and MIX groups (P < 0.001). With gait speed and quadriceps strength as covariates, no differences were observed in JRF peaks. CONCLUSIONS: The results suggest the presence of a TF ACD (TF and MIX groups), but not a PF ACD (PF group), may affect joint loading patterns during walking. Walking slower may be a protective gait modification to reduce load.

Biological and physiological role of reactive oxygen species--the good, the bad and the ugly.

Reactive oxygen species (ROS) are chemically reactive molecules that are naturally produced within biological systems. Research has focused extensively on revealing the multi-faceted and complex roles that ROS play in living tissues. In regard to the good side of ROS, this article explores the effects of ROS on signalling, immune response and other physiological responses. To review the potentially bad side of ROS, we explain the consequences of high concentrations of molecules that lead to the disruption of redox homeostasis, which induces oxidative stress damaging intracellular components. The ugly effects of ROS can be observed in devastating cardiac, pulmonary, neurodegenerative and other disorders. Furthermore, this article covers the regulatory enzymes that mitigate the effects of ROS. Glutathione peroxidase, superoxide dismutase and catalase are discussed in particular detail. The current understanding of ROS is incomplete, and it is imperative that future research be performed to understand the implications of ROS in various therapeutic interventions.

Mesenchymal stem-cell potential in cartilage repair: an update.

Articular cartilage damage and subsequent degeneration are a frequent occurrence in synovial joints. Treatment of these lesions is a challenge because this tissue is incapable of quality repair and/or regeneration to its native state. Non-operative treatments endeavour to control symptoms and include anti-inflammatory medications, viscosupplementation, bracing, orthotics and activity modification. Classical surgical techniques for articular cartilage lesions are frequently insufficient in restoring normal anatomy and function and in many cases, it has not been possible to achieve the desired results. Consequently, researchers and clinicians are focusing on alternative methods for cartilage preservation and repair. Recently, cell-based therapy has become a key focus of tissue engineering research to achieve functional replacement of articular cartilage. The present manuscript is a brief review of stem cells and their potential in the treatment of early OA (i.e. articular cartilage pathology) and recent progress in the field.

M1/70 attenuates blood-borne neutrophil oxidants, activation, and myofiber damage following stretch injury.

The purpose of this study was to determine the role of the CD11b-dependent respiratory burst in neutrophil oxidant generation and activation, interleukin-8 (IL-8) production, and myofiber damage after muscle stretch injury by using the monoclonal antibody M1/70 to block this pathway. Twelve male New Zealand White rabbits were randomly assigned to a treatment group: M1/70 (n = 6), IgG isotype control (n = 3), or saline control (n = 3). After intravenous injection of the assigned agent under gas anesthesia, a standardized single-stretch injury was created in the right tibialis anterior, whereas the left tibialis anterior underwent a sham surgery. Blood-borne neutrophil oxidant generation and CD11b receptor density and plasma IL-8 levels were measured pre- and 24 h postinjury. Damage was assessed histologically at the hematoma site by counting torn myofibers. M1/70 group demonstrated decreased blood-borne neutrophil oxidant generation (P < 0.05) and CD11b receptor density (P < 0.05), an increase in plasma IL-8 concentration (P < 0.01), and less torn myofibers (P < 0.01) compared with IgG isotype or saline control groups. These data indicate that 1). CD11b-dependent respiratory burst is a major source of oxidants produced by the neutrophil, and that treatment with M1/70 2). attenuates neutrophil activation status, 3). increases plasma IL-8 concentration, and 4). minimizes myofiber damage 24 h postmuscle stretch injury.

Oxidant production and immune response after stretch injury in skeletal muscle.

PURPOSE: This study investigated oxidant production and associated immune response after acute muscle stretch injury. METHODS: A standardized single stretch injury was performed on the tibialis anterior (TA) muscle of 36 male New Zealand white rabbits while contralateral control limbs underwent a sham surgery. Animals were sacrificed 0, 4, 12, 24, 48, and 72 h after injury. Potential sites of oxidant production, measured with a dichlorofluorescein (DCF) probe, were evaluated using two separate buffers. RESULTS: Nonmitochondrial oxidant production measured under basal buffer conditions (0.1 M potassium phosphate) was increased in both injured and control limbs at 24 h (P < 0.01) and was greater in the injured limb at 12 and 48 h (P < 0.01). There was also an interaction of time and injury (P < 0.05). Maximum oxidant production by neutrophils and macrophages, stimulated by the induced buffer (including 1.7 mM ADP, 0.1 mM NADPH, 0.1 mM FeCl3), was increased in both injured and control limbs at 4 h (P < 0.01) and was greater in the injured limb at 48 h (P < 0.01). Myeloperoxidase (MPO) activity, indicating the presence of activated neutrophils, was higher in the injured limb at 4 and 48 h (P < 0.01). The activities of superoxide radical producing and quenching enzymes, xanthine oxidase (XO) and superoxide dismutase (SOD), were elevated at 24 (P < 0.01) and 4 h (P < 0.05), respectively, but showed no difference between injured and control limbs. CONCLUSION: We conclude that acute muscle stretch injury and the required surgeries to generate the injury result in a biphasic increase in oxidant production in both injured and control limbs, suggesting a systemic immune response. The increase in oxidant production at 4 h may be caused by an increase in activated neutrophils, whereas XO activity may contribute to oxidant generation at 24 h.

Free radical activity, antioxidant enzyme, and glutathione changes with muscle stretch injury in rabbits.

The present study investigated changes in rate of free radical production, antioxidant enzyme activity, and glutathione status immediately after and 24 h after acute muscle stretch injury in 18 male New Zealand White rabbits. There was no change in free radical production in injured muscles, compared with noninjured controls, immediately after injury (time 0; P = 0.782). However, at 24 h postinjury, there was a 25% increase in free radical production in the injured muscles. Overall, there was an interaction (time and treatment) effect (P = 0.005) for free radical production. Antioxidant enzyme activity demonstrated a treatment (injured vs. control) and interaction effect for both glutathione peroxidase (P = 0.015) and glutathione reductase (P = 0.041). There was no evidence of lipid peroxidation damage, as measured by muscle malondialdehyde content. An interaction effect occurred for both reduced glutathione (P = 0.008) and total glutathione (P = 0.015). Morphological analysis (hematoxylin and eosin staining) showed significant polymorphonuclear cell infiltration of the damaged region at 24 h postinjury. We conclude that acute mechanical muscle stretch injury results in increased free radical production within 24 h after injury. Antioxidant enzyme and glutathione systems also appear to be affected during this early postinjury period.

Experimental impact injury to the cervical spine: relating motion of the head and the mechanism of injury.

The purpose of this study was to analyze, with use of an impact model, the relationships among motion of the head, local deformations of the cervical spine, and the mechanisms of injury; the model consisted of the head and neck of a cadaver. Traditionally, the mechanisms of injury to the cervical spine have been associated with flexion and extension motions of the head and neck. However, the classification of the mechanisms is not always in agreement with the patient's account of the injury or with lacerations and contusions of the scalp, which indicate the site of the impact of the head. Eleven specimens were dropped in an inverted posture with the head and neck in an anatomically neutral position. Forces, moments, and accelerations were recorded, and the impacts were imaged at 1000 frames per second. The velocity at the time of impact was on the order of 3.2 meters per second. The angle and the padding of the impact surface varied. Observable motion of the head did not correspond to the mechanism of the injury to the cervical spine. Injury occurred 2.2 to 18.8 milliseconds after impact and before noticeable motion of the head. However, the classification of the mechanism of the injuries was descriptive of the local deformations of the cervical spine at the time of the injury. Accordingly, it is a useful tool in describing the local mechanism of injury. Buckling of the cervical spine, involving extension between the third and sixth cervical vertebrae and flexion between the seventh and eight cervical vertebrae, was observed. Other, more complex, buckling deformations were also seen, suggesting that the deformations that occur during impact are so complex that they can give rise to a number of different mechanisms of injury.

Incomplete, intrasubstance strain injuries of the rectus femoris muscle.

Rectus femoris muscle strain injuries commonly occur at the distal muscle-tendon junction of the quadriceps tendon. However, we have recently recognized a pattern of strain injury that consists of an incomplete intrasubstance tear at the muscle-tendon junction formed by the deep tendon of the muscle's indirect head and those muscle fibers originating from this tendon. These injuries are found more proximally within the thigh than the "classic" distal rectus femoris muscle strain. We reviewed 10 athletes with these intrasubstance tears, all of whom had diagnostic imaging performed using computed tomography or magnetic resonance imaging or both. Two of these patients required surgical intervention. The mechanism of injury usually involved kicking or sprinting. All patients had chronic thigh pain or an anterior thigh mass or both. Physical examination revealed thigh asymmetry and a nontender to mildly tender intrasubstance muscle mass. Magnetic resonance imaging demonstrated abnormal signal intensity centered about the intramuscular tendon of the indirect head of the muscle. Surgical findings included a mass of fibrous scar and fatty tissue encasing the deep tendon. Surgical removal of this fibrous mass appears curative. We contrast this injury from distal strains of the rectus femoris muscle, as well as from soft tissue neoplasms.

Posterior cruciate ligament reconstruction by transfer of the medial gastrocnemius tendon.

A retrospective study to determine the efficacy of medial gastrocnemius tendon transfer for symptomatic PCL instability is presented. Results from a group of 31 patients undergoing this procedure were compared with a group of 8 patients managed conservatively while awaiting surgery. The mean injury to follow-up interval was 82 months in the operated group and 104 months in the nonoperated group. The mean surgery to follow-up interval was 53 months. Sixty-nine percent of surgical patients were subjectively improved; however, 29 (91%) continued to have pain and 19 (59%) continued to experience giving way. Thirteen patients from the operated group who had associated procedures performed were significantly better subjectively than those with no associated procedures (P less than 0.05). Physical examination demonstrated no difference in clinical laxity between the operated and nonoperated groups. Medial gastrocnemius transfer did not result in any significant reduction in anterior-posterior translation (KT-1000 assessment) when reconstructed knees were compared with control posterior cruciate deficient knees. Surgery, combined with subsequent immobilization, may have also been responsible for the significant reduction in lower limb function observed in the reconstructed patients. We do not recommend this procedure as a primary PCL reconstruction.