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Background: Proximal tibial epiphysiolysis (PTE) can have debilitating consequences for young athletes. The mechanism and predisposing factors for this lesion have yet to be determined. To find a common denominator and a biomechanical explanation for PTE, we were using a retrospective analysis of 15 cases in combination with a systematic review of literature.Methods: A retrospective review of medical charts was performed to identify all PTE between 2003 and 2012. Records were screened for patient age and gender, sports activity, mechanism of injury, and treatment protocols. Additionally, a literature review (MEDLINE/PubMed database, the Cochrane Library, online search engines) was conducted.Results: Medical charts of 14 adolescents (15 Salter-Harris I and II fractures) were analyzed. The literature review revealed additional 75 fractures. The predominant mechanisms were landing from a jump, takeoff for a jump, stop and go movements, and eccentric muscle contraction with the knee in flexion. The main sports-activities implicated in these injuries were basketball.Conclusions: Landing from a jump with a decreased knee and hip flexion movement increases tensile forces on the proximal tibia epiphysis. During physiological epiphysiodesis, the growth plate displays an increased vulnerability and such increased tensile forces can lead to a growth plate failure. Neuromuscular fatigue can alter coordination and proprioceptive accuracy during landing from a vertical jump and thus perturbs sagittal shock absorption. In our opinion, trainers should instruct young athletes in techniques that help avoiding uncontrolled high impact landings.Level Of Evidence: Level IV. [ABSTRACT FROM AUTHOR]

Purpose: Muscle atrophy is a commonly encountered problem in osteoarthritis (OA). The aim of this study was to estimate the amount of muscle atrophy and fatty degeneration of the lower leg muscles related to ankle OA by magnetic resonance imaging (MRI). Methods: Twenty-one patients with unilateral ankle OA were included in this cohort study. Calf circumference of the affected and healthy lower leg was documented. The degree of OA was classified in conventional radiographs. The cross-sectional areas and fatty degeneration of the muscles of the lower leg were measured in bilateral MRI. Results: We found a significantly reduced calf circumference of the affected vs. healthy leg ( p = 0.016). MRI showed a significantly lower cross-sectional area of the entire lower leg musculature in OA ( p = 0.013). Sub-analysis of muscle groups revealed that only the M. soleus had a significant cross-sectional area decrease ( p < 0.01). All muscles showed a significant fatty degeneration ( p < 0.01). Conclusions: We conclude that unilateral ankle joint osteoarthritis leads to an overall lower leg muscle atrophy, but significant atrophy of the M. soleus. All muscles of the affected leg undergo a fatty degeneration. [ABSTRACT FROM AUTHOR]

We have previously shown that ES-62, a phosphorylcholine (PC)-containing glycoprotein secreted by the parasitic filarial nematode Acanthocheilonema viteae targets dendritic cell (DC) responses, specifically by suppressing TLR4 signalling to inhibit Th1/Th17-driven inflammation. We have now investigated the molecular mechanisms underpinning such immunomodulation and show here that ES-62-mediated downregulation of protein kinase C-δ (PKC-δ), a TLR4-associated signalling mediator required for full activation of LPS-driven pro-inflammatory responses, is associated with induction of a low level of autophagic flux, as evidenced by upregulation and trafficking of p62 and LC3 and their consequent autophagolysosomal degradation. By contrast, the classical TLR4 ligand LPS, strongly upregulates p62 and LC3 expression but under such canonical TLR4 signalling this upregulation appears to reflect a block in autophagic flux, with these elements predominantly degraded in a proteasomal manner. These data are consistent with autophagic flux acting to homeostatically suppress proinflammatory DC responses and indeed, blocking of PKC-δ degradation by the autophagolysosomal inhibitors, E64d plus pepstatin A, results in abrogation of the ES-62-mediated suppression of LPS-driven release of IL-6, IL-12p70 and TNF-α by DCs. Thus, by harnessing this homeostatic regulatory mechanism, ES-62 can protect against aberrant inflammation, either to promote parasite survival or serendipitously, exhibit therapeutic potential in inflammatory disease. [ABSTRACT FROM AUTHOR]