ABSTRACT
(1) Background: The purpose of this systematic review was to determine the prevalence of bone bruises in patients with anterior cruciate ligament (ACL) injuries and the location of the bruises relative to the tibia and femur. Understanding the relative positions of these bone bruises could enhance our comprehension of the knee loading patterns that occur during an ACL injury. (2) Methods: The MEDLINE, EMBASE, and the Cochrane Library databases were searched for studies that evaluated the presence of bone bruises following ACL injuries. Study selection, data extraction, and a systematic review were performed. (3) Results: Bone bruises were observed in 3207 cases (82.8%) at the lateral tibia plateau (LTP), 1608 cases (41.5%) at the medial tibia plateau (MTP), 2765 cases (71.4%) at the lateral femoral condyle (LFC), and 1257 cases (32.4%) at the medial femoral condyle (MFC). Of the 30 studies, 11 were able to assess the anterior to posterior direction. The posterior LTP and center LFC were the most common areas of bone bruises. Among the 30 studies, 14 documented bone bruises across all four sites (LTP, MTP, LFC, and MFC). The most common pattern was bone bruises appearing at the LTP and LFC. (4) Conclusions: The most frequently observed pattern of bone bruises was restricted to the lateral aspects of both the tibia and femur. In cases where bone bruises were present on both the lateral and medial sides, those on the lateral side exhibited greater severity. The positioning of bone bruises along the front-back axis indicated a forward shift of the tibia in relation to the femur during ACL injuries.
ABSTRACT
Apoptosis has historically been considered the primary form of programmed cell death (PCD) and is responsible for regulating cellular processes during development, homeostasis, and disease. Conversely, necrosis was considered uncontrolled and unregulated. However, recent evidence has unveiled the significance of necroptosis, a regulated form of necrosis, as an important mechanism of PCD alongside apoptosis. The activation of necroptosis leads to cellular membrane disruption, inflammation, and vascularization. This process is crucial in various pathological conditions, including intervertebral disc degeneration (IVDD), neurodegeneration, inflammatory diseases, multiple cancers, and kidney injury. In recent years, extensive research efforts have shed light on the molecular regulation of the necroptotic pathway. Various stimuli trigger necroptosis, and its regulation involves the activation of specific proteins such as receptor-interacting protein kinase 1 (RIPK1), RIPK3, and the mixed lineage kinase domain-like (MLKL) pseudokinase. Understanding the intricate mechanisms governing necroptosis holds great promise for developing novel therapeutic interventions targeting necroptosis-associated IVDD. The objective of this review is to contribute to the growing body of scientific knowledge in this area by providing a comprehensive overview of necroptosis and its association with IVDD. Ultimately, these understandings will allow the development of innovative drugs that can modulate the necroptotic pathway, offering new therapeutic avenues for individuals suffering from necroptosis.
