Understanding the causality of the post-traumatic osteoarthritis (PTOA) disease process of the knee joint is important for diagnosing early disease and developing new and effective preventions or treatments. The aim of this review was to provide detailed clinical data on inflammatory and other biomarkers obtained from patients after acute knee trauma in order to (i) present a timeline of events that occur in the acute, subacute, and chronic post-traumatic phases and in PTOA, and (ii) to identify key factors present in the synovial fluid, serum/plasma and urine, leading to PTOA of the knee in 23–50% of individuals who had acute knee trauma. In this context, we additionally discuss methods of simulating knee trauma and inflammation in in vivo, ex vivo articular cartilage explant and in vitro chondrocyte models, and answer whether these models are representative of the clinical inflammatory stages following knee trauma. Moreover, we compare the pro-inflammatory cytokine concentrations used in such models and demonstrate that, compared to concentrations in the synovial fluid after knee trauma, they are exceedingly high. We then used the Bradford Hill Framework to present evidence that TNF-α and IL-6 cytokines are causal factors, while IL-1β and IL-17 are credible factors in inducing knee PTOA disease progresssion. Lastly, we discuss beneficial infrastructure for future studies to dissect the role of local vs. systemic inflammation in PTOA progression with an emphasis on early disease.
Inflammation plays a central role in the pathogenesis of knee PTOA after knee trauma. While a comprehensive therapy capable of preventing or delaying post-traumatic osteoarthritis (PTOA) progression after knee joint injury does not yet clinically exist, current literature suggests that certain aspects of early post-traumatic pathology of the knee joint may be prevented or delayed by anti-inflammatory therapeutic interventions. We discuss multifaceted therapeutic approaches that may be capable of effectively reducing the continuous cycle of inflammation and concomitant processes that lead to cartilage degradation as well as those that can simultaneously promote intrinsic repair processes. Within this context, we focus on early disease prevention, the optimal timeframe of treatment and possible long-lasting sustained delivery local modes of treatments that could prevent knee joint-associated PTOA symptoms. Specifically, we identify anti-inflammatory candidates that are not only anti-inflammatory but also anti-degenerative, anti-apoptotic and pro-regenerative.
Background: Turner syndrome (TS), also known as 45,X, is a genetic disorder caused by the partial or complete lack of an X chromosome. TS can cause a variety of medical and developmental conditions. We aimed to investigate TS mosaicism and variants pattern and research the presence of a correlation between the different variant’s factors and TS occurrence. Methods: From 1984-2018, 100,234 patients referred to the Farhud Genetic Clinic, Tehran, Iran, for karyotyping were studied. TS was determined by the chromosomal assay, and the patients’ karyotype was obtained from amniotic fluid and blood samples. Different variants of the TS diagnosed patients were investigated, including maternal and paternal age at pregnancy, parental consanguinity, and the presence/absence of a family history of the disease. Results: Overall, 261/100,234 (0.26%) were diagnosed with TS. These, 150 cases were identified to have the classical 45,X karyotype and 111 cases were identified to have either TS mosaicism or other less common variations of TS karyotyping. Higher parental age at pregnancy and TS data suggested that the occurrence of TS is significantly higher. Conclusion: Data suggest parental age at pregnancy is an important factor for TS occurrence. Hence, prenatal screening in these groups of parents recommended. This study also implicates early medical diagnostic testing before the onset of puberty or as soon as symptoms arise is essential for early treatment.
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