Posterior shoulder fracture-dislocation: A systematic review of the literature and current aspects of management

Purpose Posterior fracture-dislocation of shoulder is an infrequent traumatic event;however,most orthopaedic surgeons may face the challenge of treating it.The aim of this study is to review and summarise systematically the current principles of the management of this complex injury,and create a treatment algorithm.Methods Both PubMed and Scopus Databases were systematically searched for the terms“posterior shoulder fracture-dislocation”or“posterior glenohumeral fracture-dislocation”or“posterior glenoid fracture-dislocation”for articles written in English and published in the last decade.Results A total of 900 articles were identified,of which 13 were retained for analysis.A total of 153 patients(161 shoulders)were identified.These patients were treated either with open reduction and internal fixation,modified McLaughlin procedure,allograft/autograft humeral head reconstruction or shoulder arthroplasty.The mean age was 40.15 years.The mean postoperative Constant score in cases treated by open reduction and internal fixation was 86.45,whereas by bone graft was 84.18.Further,the mean postoperative Constant score was between 79.6 and 67.1 in those that were managed by modified McLaughlin and arthroplasty procedure,respectively.Conclusion The management of posterior shoulder fracture-dislocation may be challenging,and the best surgical option depends on many variables such as the chronicity of the injury,the presence of a fracture at the level of the surgical neck or tuberosities and the extend of the Hill-Sachs lesion if any.A treatment algorithm is proposed,based on the current literature in an effort to create a consensus for these injuries.For the acute shoulder fracture-dislocations,an open reduction should be performed.For the chronic fracture/dislocations in the elderly low-demand patients,conservative treatment should be performed.For the rest of the patients,depending on the severity of the Hill-Sachs lesion different surgical options are available such as the McLaughlin technique,the use of an allograft,osteotomy or arthroplasty.     

Impact of Maternal Food Restriction on Heart Proteome in Appropriately Grown and Growth-Restricted Wistar—Rat Offspring

Objective: Fetal growth restriction is associated with increased postnatal cardiovascular morbidity. The alterations in heart physiology and structure caused by in utero nutrient deprivation have not been extensively studied. We aim to investigate the impact of maternal food restriction on the cardiac proteome of newborn rats with normal (non-fetal growth-restricted (FGR)) and reduced (FGR) birth weight. Methods: On day 14 of gestation, 10 timed pregnant rats were randomized into two nutritional groups: (a) Standard laboratory diet and (b) 50% global food restriction. Pups born to food-restricted mothers were subdivided, based on birthweight, into fetal growth-restricted (FGR) and non-FGR, while pups born from normally nourished mothers were considered controls. Rat neonates were euthanized immediately after birth and the hearts of 11 randomly selected male offspring (n = 4 FGR, n = 4 non-FGR, n = 3 control group) were analyzed using quantitative proteomics. Results: In total, 7422 proteins were quantified (q < 0.05). Of these, 1175 were differentially expressed in FGR and 231 in non-FGR offspring vs. control with 151 common differentially expressed proteins (DEPs) between the two groups. Bioinformatics analysis of DEPs in FGR vs. control showed decreased integrin and apelin cardiac fibroblast signaling, decreased muscle contraction and glycolysis, and over-representation of a protein network related to embryonic development, and cell death and survival. Conclusion: Our study illustrates the distinct proteomic profile of FGR and non-FGR offspring of food-restricted dams underlying the importance of both prenatal adversities and birth weight in cardiac physiology and development.     

Marital status and educational level associated to obesity in Greek adults: data from the National Epidemiological Survey

Background  

Obesity is an important public health issue and its prevalence is reaching epidemic proportions in both developed and developing countries. The aim of the present study was to determine associations of overweight (OW), obesity (OB) and abdominal obesity (AO) with marital status and educational level in Greek adults of both genders based on data from the National Epidemiological Survey on the prevalence of obesity.     

Periodontal disease is associated with higher levels of C-reactive protein in non-diabetic, non-smoking acute myocardial infarction patients

Objectives

A link between periodontal disease (PD) and cardiovascular events has been proposed, but confounding by shared risk factors such as smoking and diabetes remains a concern. We examined the prevalence of PD and its contribution to C-reactive protein (CRP) levels in acute myocardial infarction (AMI) patients and in subjects without AMI and with angiographically nonobstructive coronary disease in the absence of these confounding risk factors.

Methods

Periodontal status and admission CRP levels were evaluated in 87 non-diabetic and non-smoking subjects undergoing cardiac catheterization. The study group comprised of 47 patients with documented AMI, and 40 subjects without AMI and with angiographically nonobstructive coronary disease (ANCD group).

Results

Both the prevalence of PD and CRP levels were significantly higher in AMI patients compared with ANCD subjects (38.3% vs. 17.5%, p = 0.03 and 44.3 vs. 8.5 mg/L, p < 0.001 respectively). PD was associated with higher CRP levels in AMI patients (52.5 vs. 36.1 mg/L, p = 0.04) as well as in ANCD subjects, however, in this group this was not significant (12.6 vs. 7.6 mg/L, p = 0.5). Multivariable regression analysis confirmed two separate measures of PD as strong and independent contributors to elevated CRP levels in AMI patients (R² = 0.28, R² = 0.30, p = 0.001).

Conclusions

PD contributes to elevated CRP levels in non-diabetic, non-smoking AMI patients, independently of other confounding factors. These findings imply that periodontitis may emerge as a novel target for reducing future risk in AMI survivors.     

Association of LRRK2 exonic variants with susceptibility to Parkinson's disease: a case-control study

Background

Background The leucine-rich repeat kinase 2 gene (LRRK2) harbours highly penetrant mutations that are linked to familial parkinsonism. However, the extent of its polymorphic variability in relation to risk of Parkinson's disease (PD) has not been assessed systematically. We therefore assessed the frequency of LRRK2 exonic variants in individuals with and without PD, to investigate the role of the variants in PD susceptibility.

Methods

LRRK2 was genotyped in patients with PD and controls from three series (white, Asian, and Arab–Berber) from sites participating in the Genetic Epidemiology of Parkinson's Disease Consortium. Genotyping was done for exonic variants of LRRK2 that were identified through searches of literature and the personal communications of consortium members. Associations with PD were assessed by use of logistic regression models. For variants that had a minor allele frequency of 0·5% or greater, single variant associations were assessed, whereas for rarer variants information was collapsed across variants.

Findings

121 exonic LRRK2 variants were assessed in 15?540 individuals: 6995 white patients with PD and 5595 controls, 1376 Asian patients and 962 controls, and 240 Arab–Berber patients and 372 controls. After exclusion of carriers of known pathogenic mutations, new independent risk associations were identified for polymorphic variants in white individuals (M1646T, odds ratio 1·43, 95% CI 1·15–1·78; p=0·0012) and Asian individuals (A419V, 2·27, 1·35–3·83; p=0·0011). A protective haplotype (N551K-R1398H-K1423K) was noted at a frequency greater than 5% in the white and Asian series, with a similar finding in the Arab–Berber series (combined odds ratio 0·82, 0·72–0·94; p=0·0043). Of the two previously reported Asian risk variants, G2385R was associated with disease (1·73, 1·20–2·49; p=0·0026), but no association was noted for R1628P (0·62, 0·36–1·07; p=0·087). In the Arab–Berber series, Y2189C showed potential evidence of risk association with PD (4·48, 1·33–15·09; p=0·012).

Interpretation

The results for LRRK2 show that several rare and common genetic variants in the same gene can have independent effects on disease risk. LRRK2, and the pathway in which it functions, is important in the cause and pathogenesis of PD in a greater proportion of patients with this disease than previously believed. These results will help discriminate those patients who will benefit most from therapies targeted at LRRK2 pathogenic activity.

Funding

Michael J Fox Foundation and National Institutes of Health.