Hip arthroscopy after periacetabular osteotomy for acetabular dysplasia - incidence and clinical outcome.

BACKGROUND: The periacetabular osteotomy (PAO) is the treatment of choice for acetabular dysplasia and has demonstrated improvement in patient reported outcomes measures (PROMs) as well as acceptable long-term survival. However, acetabular dysplasia is also associated with intra-articular lesions that can negatively impact clinical outcome. This study aimed to analyse the incidence, operative findings, and outcomes of hip arthroscopy after PAO. METHODS: This is a single center retrospective study by querying our hip preservation prospectively collected database from 2006 to 2020. All patients having undergone hip arthroscopy after a PAO, with a minimal follow-up of one year, were identified. 202 PAOs were done with a mean age of 28.3 years (12.7 - 53.6) including 39 males and 167 females. Failure was defined as conversion to hip replacement. Demographics, surgical findings, reoperations, and PROMs (pre and post operatively at the last follow-up point only for hips not converted to hip replacement). RESULTS: Fifteen hips in 15 patients (7.4%) out of 202 PAOs underwent a hip arthroscopy at a mean time of 3.9 years (0.3-10.3) after PAO. There were 2 males, 13 females and the mean age was 29.8 years (18.5-45). 12 hips had no radiological osteoarthritis (Tönnis 0) and 3 hips had early osteoarthritis (Tönnis 1). At time of arthroscopy, all hips had a labral tear, 9 had a chondral damage ≥ Beck 4. Eight hips had labral debridement, 7 had labral repair, 2 had resection of adhesions and 4 underwent a femoral osteochondroplasty. Four hips (27%) were converted to a hip replacement at a mean time of 1.8 years(0.5-3.2) after hip arthroscopy. Patients converted to hip replacement were significantly older (p = 0.01), had a lower post-PAO LCEA (p = 0.01) and a higher post-PAO Tönnis angle (p = 0.02). There were no significant improvements in PROMs. CONCLUSION: This study reports a hip arthroscopy reoperation rate after PAO of 7.4%. All three types of dysplasia (uncovered anteriorly, posteriorly, or globally) were present in this cohort. Twenty seven percent of patients were converted to hip replacement and PROMs were not significantly improved by hip arthroscopy. Therefore, this procedure should be approached with some caution.

Putting Together the Pieces: A Metabolic Model of Viral Infection and the Subsequent Development of Asthma.

While the prevalence of asthma and atopic disease continues to rise over the past half a century, the exact mechanism behind this remains elusive. Of late, the role of metabolic dysfunction in disease is becoming more clearly classified. The part of metabolic dysfunction in respiratory viral infections is studied, which reopens the debate in the role of infection on asthma development in childhood. During infection, there is a rapid shift in nutrients available for immune cells to metabolize. Exploring these metabolic changes and the resulting immune cell function, a striking pattern emerges. In asthma development following viral infection, it is proposed there is a transient state of impaired glucose tolerance resulting in a sudden increase in glucose for lymphocytes to metabolize, triggering them to enter a state of increased aerobic glycolysis. Reviewing this outcome, along with previous work, a new working metabolic model of asthma development is proposed by suggesting a new step between a healthy immune system and asthma.

The Effects of Viral Infection on Lymphocyte Metabolism: A New Perspective on Disease Characterization.

Over the past decade, metabolic dysfunction has been re-examined as an area of interest in a variety of atopic, malignant, and autoimmune conditions. The unique immune and, specifically, lymphocyte metabolic dysfunctions in disease are starting to be more clearly classified. Exploring the lymphocyte metabolic profiles of these diseases in the current literature, we characterize these diseases into two distinct metabolic groups. The influence of viral infection on immune metabolic dysfunction is explored. During an acute or chronic infection, there is a varied rapid shift in nutrients available to immune cells. This article explores the effect of these changes in nutrient availability and the resulting outcome on immune cell function. From this, a new hypothesis is proposed that these two groups of conditions, characterized by two unique immune profiles, are caused by either acute or chronic viral infections. The physiology behind this is explored, which proposes a new step between a healthy immune system and that of disease, in a unique working model.