Medial patellofemoral ligament injury patterns and associated pathology in lateral patella dislocation: an MRI study

BACKGROUND: Lateral Patella dislocations are common injuries seen in the active and young adult populations. Our study focus was to evaluate medial patellofemoral ligament (MPFL) injury patterns and associated knee pathology using Magnetic Resonance Imaging studies. METHODS: MRI studies taken at one imaging site between January, 2007 to January, 2008 with the final diagnosis of patella dislocation were screened for this study. Of the 324 cases that were found, 195 patients with lateral patellar dislocation traumatic enough to cause bone bruises on the lateral femoral trochlea and the medial facet of the patella were selected for this study. The MRI images were reviewed by three independent observers for location and type of MPFL injury, osteochondral defects, loose bodies, MCL and meniscus tears. The data was analyzed as a single cohort and by gender. RESULTS: This study consisted of 127 males and 68 females; mean age of 23 yrs. Tear of the MPFL at the patellar attachment occurred in 93/195 knees (47%), at the femoral attachment in 50/195 knees (26%), and at both the femoral and patella attachment sites in 26/195 knees (13%). Attenuation of the MPFL without rupture occurred in 26/195 knees (13%). Associated findings included loose bodies in 23/195 (13%), meniscus tears 41/195 (21%), patella avulsion/fracture in 14/195 (7%), medial collateral ligament sprains/tears in 37/195 (19%) and osteochondral lesions in 96/195 knees (49%). Statistical analysis showed females had significantly more associated meniscus tears than the males (27% vs. 17%, p = 0.04). Although not statistically significant, osteochondral lesions were seen more in male patients with acute patella dislocation (52% vs. 42%, p = 0.08). CONCLUSION: Patients who present with lateral patella dislocation with the classic bone bruise pattern seen on MRI will likely rupture the MPFL at the patellar side. Females are more likely to have an associated meniscal tear than males; however, more males have underlying osteochondral lesions. Given the high percentage of associated pathology, we recommend a MRI of the knee in all patients who present with acute patella dislocation

Rottlerin inhibits (Na+, K+)-ATPase activity in brain tissue and alters D-Aspartate dependent redistribution of glutamate transporter GLAST in cultured astrocytes

The naturally occurring toxin rottlerin has been used by other laboratories as a specific inhibitor of protein kinase C-delta (PKC-d) to obtain evidence that the activitydependent distribution of glutamate transporter GLAST is regulated by PKC-d mediated phosphorylation. Using immunofluorescence labelling for GLAST and deconvolution microscopy we have observed that D-aspartateinduced redistribution of GLAST towards the plasma membranes of cultured astrocytes was abolished by rottlerin. In brain tissue in vitro, rottlerin reduced apparent activity of (Na?, K?)-dependent ATPase (Na?, K?-ATPase) and increased oxygen consumption in accordance with its known activity as an uncoupler of oxidative phosphorylation (``metabolic poisonÿÿ). Rottlerin also inhibited Na?, K?-ATPase in cultured astrocytes. As the glutamate transport critically depends on energy metabolism and on the activity of Na?, K?-ATPase in particular, we suggest that the metabolic toxicity of rottlerin and/or the decreased activity of the Na?, K?-ATPase could explain both the glutamate transport inhibition and altered GLAST distribution caused by rottlerin even without any involvement of PKC-d-catalysed phosphorylation in the process

Rottlerin inhibits (Na+, K+)-ATPase Activity in brain tissue and alters d-Aspartate dependent redistribution of glutamate transporter GLAST in cultured astrocytes

The naturally occurring toxin rottlerin has been used by other laboratories as a specific inhibitor of protein kinase C-delta (PKC-delta) to obtain evidence that the activity-dependent distribution of glutamate transporter GLAST is regulated by PKC-delta mediated phosphorylation. Using immunofluorescence labelling for GLAST and deconvolution microscopy we have observed that D-aspartate-induced redistribution of GLAST towards the plasma membranes of cultured astrocytes was abolished by rottlerin. In brain tissue in vitro, rottlerin reduced apparent activity of (Na+, K+)-dependent ATPase (Na+, K+-ATPase) and increased oxygen consumption in accordance with its known activity as an uncoupler of oxidative phosphorylation ("metabolic poison"). Rottlerin also inhibited Na+, K+-ATPase in cultured astrocytes. As the glutamate transport critically depends on energy metabolism and on the activity of Na+, K+-ATPase in particular, we suggest that the metabolic toxicity of rottlerin and/or the decreased activity of the Na+, K+-ATPase could explain both the glutamate transport inhibition and altered GLAST distribution caused by rottlerin even without any involvement of PKC-delta-catalysed phosphorylation in the process