ABSTRACT
Oxidative stress has emerged as a significant contributor to skeletal muscle atrophy, influencing cellular processes that underlie muscle wasting. This review article delves into the intricate interplay between oxidative stress and muscle atrophy, shedding light on its mechanisms and implications. We begin by outlining the fundamental concepts of oxidative stress, delineating reactive oxygen species (ROS) and reactive nitrogen species (RNS), their sources, and the ensuing oxidative damage to cellular components. Subsequently, we delve into skeletal muscle atrophy, elucidating its diverse forms, molecular pathways, key signaling cascades, and the role of inflammation in exacerbating muscle wasting. Bridging these concepts, we explore the connections between oxidative stress and muscle atrophy, unveiling how oxidative stress impacts muscle protein synthesis and breakdown, perturbs cellular signaling pathways, and contributes to mitochondrial dysfunction. The review underscores the complexity of quantifying and interpreting oxidative stress markers, highlighting the challenges posed by the dynamic nature of oxidative stress and the presence of basal ROS levels. Addressing the specificity of oxidative stress markers, we emphasize the importance of selecting markers pertinent to muscle tissue and considering systemic influences. Standardization of experimental protocols emerges as a critical need to ensure consistency and reproducibility across studies. Looking ahead, we discuss the implications of oxidative stress in diverse scenarios, encompassing age-related muscle loss (sarcopenia), muscle wasting in chronic diseases like cancer cachexia, and disuse-induced muscle atrophy. Additionally, we delve into potential therapeutic strategies, including antioxidant supplementation, exercise, pharmacological interventions, nutritional approaches, and lifestyle modifications, as avenues to mitigate oxidative stress-driven muscle atrophy. The review concludes by outlining promising future directions in this field, calling for deeper exploration of specific oxidative stress markers, understanding the temporal dynamics of oxidative stress, validation through translational studies in humans, and the development of targeted therapeutic interventions. By advancing our understanding of the intricate relationship between oxidative stress and skeletal muscle atrophy, this review contributes to paving the way for innovative strategies to address muscle wasting and improve muscle health.
ABSTRACT
Chondroblastoma considered a rare form of osseous neoplasm contributes less than 1% of all bone tumours. It is typically found in young patients with chief complaints of moderate pain with joint stiffness. It develops as a lytic lesion in the epiphysis of long bones which might spread to the metaphysis. We report a case of an 18-year-old patient who presented with progressive right knee pain which aggravated with movements. Investigations included X-ray, magnetic resonance imaging (MRI), and biochemical assessment. A focal, well-defined, lesion in the upper end of the tibia with surrounding marrow oedema was observed and diagnostic arthroscopy was taken for management. Histopathology of specimen observed chondroblasts proliferation with areas of mature cartilage, and giant cells confirming intrasynovial chondroblastoma. Usually, surgery is the treatment of choice; however, possibilities of the secondary bone cyst, haemosiderin deposition on the joint, etc., make treatment approaches uncertain. Diagnostic arthroscopy is a rare but essential modality in such cases due to better visuals, complete tumour excision, and combination with adjuvant therapies. Chondroblastoma, if untreated, proves detrimental, hence, a thorough evaluation is critical for overall better outcomes.
