Anterior knee pain independently alters landing and jumping biomechanics.

Background Biomechanical effects of anterior knee pain are difficult to distinguish from effects of other factors also related to knee injury (e.g., joint effusion). The purpose of this study was to evaluate independent effects of anterior knee pain on landing and jumping biomechanics. Methods Thirteen healthy participants performed a land and jump movement task, under three experimental conditions (pre-pain, pain, and post-pain), during one data collection session. One 1-ml injection of hypertonic saline into the infrapatellar fat pad was used to induce experimental anterior knee pain during the pain condition. Participant-perceived anterior knee pain was measured every 2 min throughout data collection. Landing and jumping biomechanics were measured and compared between the experimental conditions using a functional statistical approach. Findings The aforementioned injection increased mean participant-perceived anterior knee pain, from zero during the pre-pain condition to 2.6 ± 0.71 cm during the pain condition. Vertical ground reaction force, knee flexion angle, and internal knee extension moment decreased by approximately 0.100 body weights, 3°, and 0.010 Nm/body weight × body height, respectively, between the pre-pain and pain conditions. Conversely, hip flexion angle and internal hip extension moment increased by approximately 3° and 0.006 Nm/body weight × body height, respectively, between the pre-pain and pain conditions. Several biomechanical changes persisted after anterior knee pain abatement (the post-pain condition). Interpretation Anterior knee pain alters landing and jumping biomechanics, independent of other injury-related factors. These altered biomechanics likely change knee joint loading patterns and might increase risk for chronic knee joint injury and/or pathology.

Effects of Experimental Anterior Knee Pain on Muscle Activation During Landing and Jumping Performed at Various Intensities.

CONTEXT: Although knee pain is common, some facets of this pain are unclear. The independent effects (ie, independent from other knee injury or pathology) of knee pain on neural activation of lower-extremity muscles during landing and jumping have not been observed. OBJECTIVE: To investigate the independent effects of knee pain on lower-extremity muscle (gastrocnemius, vastus medialis, medial hamstrings, gluteus medius, and gluteus maximus) activation amplitude during landing and jumping, performed at 2 different intensities. DESIGN: Laboratory-based, pretest, posttest, repeated-measures design, where all subjects performed both data-collection sessions. METHODS: Thirteen able-bodied subjects performed 2 different land and jump tasks (forward and lateral) under 2 different conditions (control and pain), at 2 different intensities (high and low). For the pain condition, experimental knee pain was induced via a hypertonic saline injection into the right infrapatellar fat pad. Functional linear models were used to evaluate the influence of experimental knee pain on muscle-activation amplitude throughout the 2 land and jump tasks. RESULTS: Experimental knee pain independently altered activation for all of the observed muscles during various parts of the 2 different land and jump tasks. These activation alterations were not consistently influenced by task intensity. CONCLUSION: Experimental knee pain alters activation amplitude of various lower-extremity muscles during landing and jumping. The nature of the alteration varies between muscles, intensities, and phases of the movement (ie, landing and jumping). Generally, experimental knee pain inhibits the gastrocnemius, medial hamstring, and gluteus medius during landing while independently increasing activation of the same muscles during jumping.

Ambulation speed and corresponding mechanics are associated with changes in serum cartilage oligomeric matrix protein.

Because serum cartilage oligomeric matrix protein (COMP) has been used to reflect articular cartilage condition, we aimed to identify walking and running mechanics that are associated with changes in serum COMP. Eighteen subjects (9 male, 9 female; age=23 ± 2 yrs.; mass=68.3 ± 9.6 kg; height=1.70 ± 0.08 m) completed 4000 steps on an instrumented treadmill on three separate days. Each day corresponded to a different ambulation speed: slow (preferred walking speed), medium (+50% of slow), and fast (+100% of slow). Synchronized ground reaction force and video data were collected to evaluate walking mechanics. Blood samples were collected pre-, post-, 30-minute post-, and 60-minute post-ambulation to determine serum COMP concentration at these times. Serum COMP increased 29%, 18%, and 5% immediately post ambulation for the fast, medium, and slow sessions (p<0.01). When the speeds were pooled, peak ankle inversion, knee extension, knee abduction, hip flexion, hip extension, and hip abduction moment, and knee flexion angle at impact explained 61.4% of total variance in COMP concentration change (p<0.001). These results indicate that (1) certain joint mechanics are associated with acute change in serum COMP due to ambulation, and (2) increased ambulation speed increases serum COMP concentration.

Body weight independently affects articular cartilage catabolism.

Although obesity is associated with osteoarthritis, it is unclear whether body weight (BW) independently affects articular cartilage catabolism (i.e., independent from physiological factors that also accompany obesity). The primary purpose of this study was to evaluate the independent effect of BW on articular cartilage catabolism associated with walking. A secondary purpose was to determine how decreased BW influenced cardiovascular response due to walking. Twelve able-bodied subjects walked for 30 minutes on a lower-body positive pressure treadmill during three sessions: control (unadjusted BW), +40%BW, and -40%BW. Serum cartilage oligomeric matrix protein (COMP) was measured immediately before (baseline) and after, and 15 and 30 minutes after the walk. Heart rate (HR) and rate of perceived exertion (RPE) were measured every three minutes during the walk. Relative to baseline, average serum COMP concentration was 13% and 5% greater immediately after and 15 minutes after the walk. Immediately after the walk, serum COMP concentration was 14% greater for the +40%BW session than for the -40%BW session. HR and RPE were greater for the +40%BW session than for the other two sessions, but did not differ between the control and -40%BW sessions. BW independently influences acute articular cartilage catabolism and cardiovascular response due to walking: as BW increases, so does acute articular cartilage catabolism and cardiovascular response. These results indicate that lower-body positive pressure walking may benefit certain individuals by reducing acute articular cartilage catabolism, due to walking, while maintaining cardiovascular response. Key pointsWalking for 30 minutes with adjustments in body weight (normal body weight, +40% and -40% body weight) significantly influences articular cartilage catabolism, measured via serum COMP concentration.Compared to baseline levels, walking with +40% body weight and normal body weight both elicited significant increases in articular cartilage catabolism, while walking with -40% body weight did not.Cardiovascular response (HR and RPE) was not significantly different during walking with normal body weight and when compared to walking with -40% body weight.

The influence of experimental anterior knee pain during running on electromyography and articular cartilage metabolism.

OBJECTIVE: To determine whether anterior knee pain (AKP), during running, acutely affects lower-extremity electromyography (EMG) and articular cartilage metabolism. METHODS: A within-subjects design was used. Each of 12 able-bodied subjects ran on a treadmill for 30 min for three different sessions: control (no infusion), sham (0.9% NaCl infusion into the involved-leg infrapatellar fat pad), and pain (5.0% NaCl infusion into the involved-leg infrapatellar fat pad). Bilateral surface EMG was monitored for the vastus medialis (VM), vastus lateralis (VL), and gastrocnemius (GA). Serum cartilage oligomeric matrix protein (COMP) concentration was determined before, after, and 60 min after the run. A functional analysis approach was used to compare EMG amplitude, across the entire stance phase, between sessions and legs. Mixed-model analysis of covariance was used to compare serum COMP concentration between sessions, across time. RESULTS: Relative to the uninvolved leg, greater involved-leg VL and GA EMG amplitude existed during midstance for the sham and control sessions (P < 0.01). During the painful session, however, involved-leg VM, VL, and GA EMG amplitude was 5-10% less than for the uninvolved leg. COMP concentration immediately post-run was 14% and 21% greater than pre-run (P = 0.01) and 60 min post-run concentrations (P < 0.01), respectively. Session, however, did not significantly influence COMP. CONCLUSION: During a 30-min run, AKP acutely alters midstance VM, VL, and GA EMG amplitude. AKP during a 30-min run does not, however, acutely influence articular cartilage metabolism.

Induction of protective cytotoxic T-cell responses by a B-cell-based cellular vaccine requires stable expression of antigen.

B-cell-based cellular vaccines represent a promising approach to active immunotherapy of cancer complementing the use of dendritic cells, especially in pediatric patients and patients with low bone marrow reserves. B cells can be easily prepared in large numbers and readily home to secondary lymphoid organs, the primary site of induction of cytotoxic T lymphocyte (CTL) responses. However, most B-cell-based vaccines tested so far failed to induce functional and protective CTLs in in vivo models. Here, we show that B-cells activated through the toll-like receptor-9 (TLR-9) and CD40 up-regulate surface expression of major histocompatibility complex and costimulatory molecules, produce IL-12, and exhibit potent antigen-presenting properties in vitro. Importantly, although administration of peptide-coated or transiently transfected B cells fails to induce immune responses, therapeutic immunization with low numbers of genetically modified B cells stably expressing antigen results in an induction of functional CTLs and protection against the growth of tumor in an animal model. After activation, B cells partially loose their ability to home to organized lymphoid tissue because of the shedding of CD62L; however, this property can be restored by expression of protease-resistant mutant of CD62L. In summary, the data presented in this report suggest that genetically modified activated B cells represent a promising candidate for a cancer vaccine eliciting functional systemic CTLs.