Partial Humeral Head Resurfacing for Avascular Necrosis.
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ABSTRACT:
SUBMITTER: Bixby EC
PROVIDER: S-EPMC6993571 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background:Humeral head avascular necrosis (AVN) of differing etiologies may lead to shoulder arthroplasty due to subchondral bone collapse and deformity of the articular surface. There have been no large studies evaluating the complications for these patients after they undergo total shoulder arthroplasty (TSA). Questions/Purposes:The first objective of this study is to evaluate the complication rate after TSA in patients with humeral head AVN. The secondary objective is to compare the complication rates among the different etiologies of the AVN. Methods:Patients who underwent TSA were identified in the PearlDiver database using ICD-9 codes. Patients who underwent shoulder arthroplasty for humeral head AVN were identified using ICD-9 codes and were subclassified according to AVN etiology (posttraumatic, alcohol use, chronic steroid use, and idiopathic). Complications evaluated included postoperative infection within 6 months, dislocation within 1 year, revision shoulder arthroplasty up to 8 years postoperatively, shoulder stiffness within 1 year, and periprosthetic fracture within 1 year and systemic complications within 3 months. Postoperative complication rates were compared to controls. Results:The study cohorts included 4129 TSA patients with AVN with 141,778 control TSA patients. Patients with posttraumatic AVN were significantly more likely to have a postoperative infection (OR 2.47, P < 0.001), dislocation (OR 1.45, P = 0.029), revision surgery (OR 1.53, P = 0.001), stiffness (OR 1.24, P = 0.042), and systemic complication (OR 1.49, P < 0.001). Steroid-associated AVN was associated with a significantly increased risk for a postoperative infection (OR 1.72, P = 0.004), revision surgery (OR 1.33, P = 0.040), fracture (OR 2.76, P = 0.002), and systemic complication (OR 1.59, P < 0.001). Idiopathic and alcohol-associated AVN were not significantly associated with any of the postoperative evaluated complications. Conclusions:TSA in patients with humeral head AVN is associated with significantly increased rates of numerous postoperative complications compared to patients without a diagnosis of AVN, including infection, dislocation, revision arthroplasty, stiffness, periprosthetic fracture, and medical complications. Specifically, AVN due to steroid use or from a posttraumatic cause appears to be associated with the statistically highest rates of postoperative TSA complications. Given these findings, orthopedic surgeons should be increasingly aware of this association, which should influence the shared decision-making process of undergoing TSA in patients with humeral head AVN.
| S-EPMC5786582 | biostudies-literature
Project description:BackgroundSickle cell disease is the leading etiology for atraumatic humeral head avascular necrosis worldwide. Treatment of this condition is not standardized, with only few studies evaluating clinical outcomes after surgical interventions. The aim of this study was to review the available evidence on the results of surgical intervention for humeral head avascular necrosis in the sickle cell disease population.MethodsA systematic electronic search was conducted using PubMed (MEDLINE), EMBASE, and Cochrane Library databases. Relevant studies that reported the outcomes of surgical intervention for humeral head avascular necrosis for patients with sickle cell disease were reviewed. Outcome parameters were pain, range of motion, specific shoulder outcome scores, and complications.ResultsSix studies, three retrospective cohorts (2 level III and 1 level IV) and three case series (level IV), were included in this review. A total of forty-three patients with sickle cell disease, comprising forty-nine shoulders, underwent different surgical procedures. Surgical procedures were core decompression, arthroscopic intervention, humeral head resurfacing, shoulder hemiarthroplasty, and total shoulder arthroplasty.ConclusionSurgical intervention for humeral head avascular necrosis in patients with sickle cell disease is selected based on the osteonecrosis stage. In the precollapse stage, core decompression is regarded as the first surgical option. However, in the light of current evidence, it has not been confirmed to prevent or delay natural progression of the disease. Shoulder arthroplasty is reserved for late stages, which despite the fairly good outcomes, data for long-term implant survival and complications are not well documented.
| S-EPMC8178624 | biostudies-literature
Project description:Vascularised composite allotransplantation (VCA) represents an exciting and emerging field in plastic and reconstructive surgery. Despite the generally good functional and psychosocial outcomes, multiple complications can be associated with the procedure. The authors describe a case of avascular necrosis of the humeral head following successful upper extremity VCA.
| S-EPMC5532758 | biostudies-other
Project description:Autophagy serves as a stress response and may contribute to the pathogenesis of avascular necrosis of the femoral head induced by steroids. Statins promote angiogenesis and ameliorate endothelial functions through apoptosis inhibition and necrosis of endothelial progenitor cells, however the process used by statins to modulate autophagy in avascular necrosis of the femoral head remains unclear. This manuscript determines whether pravastatin protects against dexamethasone-induced avascular necrosis of the femoral head by activating endothelial progenitor cell autophagy. Pravastatin was observed to enhance the autophagy activity in endothelial progenitor cells, specifically by upregulating LC3-II/Beclin-1 (autophagy related proteins), and autophagosome formation in vivo and in vitro. An autophagy inhibitor, 3-MA, reduced pravastatin protection in endothelial progenitor cells exposed to dexamethasone by attenuating pravastatin-induced autophagy. Adenosine monophosphate-activated protein kinase (AMPK) is a key autophagy regulator by sensing cellular energy changes, and indirectly suppressing activation of the mammalian target of rapamycin (mTOR). We found that phosphorylation of AMPK was upregulated however phosphorylation of mTOR was downregulated in pravastatin-treated endothelial progenitor cells, which was attenuated by AMPK inhibitor compound C. Furthermore, liver kinase B1 (a phosphorylase of AMPK) knockdown eliminated pravastatin regulated autophagy protein LC3-II in endothelial progenitor cells in vitro. We therefore demonstrated pravastatin rescued endothelial progenitor cells from dexamethasone-induced autophagy dysfunction through the AMPK-mTOR signaling pathway in a liver kinase B1-dependent manner. Our results provide useful information for the development of novel therapeutics for management of glucocorticoids-induced avascular necrosis of the femoral head.
| S-EPMC5900057 | biostudies-literature
Project description:BackgroundANFH is a major health problem, to which long lasting and definitive treatments are lacking. The aim of this study is to study RNA alterations attributed to cortisol-induced ANFH.MethodsRat models were stratified into three groups: in vitro group (n = 20) for molecular biological assays, control group (n = 3), and ANFH group induced using lipopolysaccharide and dexamethasone (n = 3). Bone marrow-derived endothelial progenitor cells (BM-EPCs) were extracted from the rats. An RNA expression array was performed on BM-EPCs, and enriched genes were subject to pathway analysis. In vitro studies following findings of array results were also performed using the isolated BM-EPCs.ResultsSignificant alterations in mammalian target of rapamycin (mTOR) and HIF signaling pathways were identified in BM-EPCs of ANFH. By applying cortisol and dexamethasone to BM-EPCs, significant changes in mTOR and HIF elements were identified. The alteration of HIF pathways appeared to be downstream of mTOR signaling. Glucocorticoid receptor (GR) expression was related to glucocorticoid-dependent mRNA expression of mTOR/HIF genes. mTOR-dependent angiogenesis but not anabolism was the target of GR in ANFH. Inhibition of mTOR signaling also induced apoptosis of BM-EPCs via CHOP-dependent DR5 induction in response to GR stimulation.ConclusionDecreased mTOR signaling in response to GR stimulation leading to downregulated HIF pathway as well as increased apoptosis could be the pathophysiology.
| S-EPMC5648506 | biostudies-literature
Project description:Avascular necrosis of the femur head (AVNFH) is a debilitating disease caused due to the use of alcohol, steroids, following trauma or unclear (idiopathic) etiology, affecting mostly the middle aged population. Clinically AVNFH is associated with impaired blood supply to the femoral head resulting in bone necrosis and collapse. Although Homocysteine (HC) has been implicated in AVNFH, levels of homocysteine and its associated pathway metabolites have not been characterized. We demonstrate elevated levels of homocysteine and concomitantly reduced levels of vitamins B6 and B12, in plasma of AVNFH patients. AVNFH patients also had elevated blood levels of sodium and creatinine, and reduced levels of random glucose and haemoglobin. Biophysical and ultrastructural analysis of AVNFH bone revealed increased remodelling and reduced bone mineral density portrayed by increased carbonate to phosphate ratio and decreased Phosphate to amide ratio together with disrupted trabeculae, loss of osteocytes, presence of calcified marrow, and elevated expression of osteocalcin in the osteoblasts localized in necrotic regions. Taken together, our studies for the first time characterize the metabolomic, pathophysiological and morphometric changes associated with AVNFH providing insights for development of new markers and therapeutic strategies for this debilitating disorder.
| S-EPMC5587540 | biostudies-literature
Project description:The early and accurate diagnosis of steroid-induced avascular necrosis of the femoral head (SANFH) is appealing considering its irreversible progression and serious consequence for the patients. The purpose of this study was to investigate the metabolic change of SANFH for its early detection. Two stages were designed in this study, namely discovery and verification. Except the biochemical index anomaly and the accidental death, 30 adult healthy adult Japanese white rabbits were used for screening out the potential metabolites in discovery experiment and 13 rabbits were used in verification experiment. The femoral heads were assessed with magnetic resonance imaging and transmission electron microscopy. The metabolomic profiling of serum samples were analysis by UHPLC-MS/MS. Metabolomic cluster analysis enable us to differentiate the rabbits without and with injection of the glucocorticoid in 1 week even when there is no obvious abnormal symptom in behaviors or imaging diagnosis. The majority of differential metabolites were identified as phospholipids which were observed significant change after injection of glucocorticoid in 1, 2, 3 weeks. And the results obtained in verification experiment of 6 weeks showed that these differential metabolites exhibited consistent trends in late progression with that in early-stage. At the end of 6 weeks the damage of SANFH could be verified by pathological imaging. Therefore the finding of serum metabolite profile links to the progression of SANFH and provides the potential of early detection of SANFH.
| S-EPMC5814275 | biostudies-literature
Project description:Avascular necrosis (AVN) of the femoral head is a progressive disease affecting young adults that results in collapse of the femoral head and subsequent degenerative joint disease. Although precollapse stages of AVN can be successfully treated with core decompression, making the diagnosis is often difficult given alternative sources of hip pain in this age group. We propose that arthroscopic-assisted core decompression of the femoral head offers an effective method of addressing AVN of the femoral head as well as coexistent hip disorders in the same operation. This article describes in detail the technique used to perform an arthroscopic-assisted core decompression of the femoral head, and a companion video demonstrating the procedure is included. Our experience suggests that arthroscopic-assisted core decompression can be used as an alternative to open core decompression, while simultaneously addressing other sources of hip pain, with successful outcomes.
| S-EPMC3882712 | biostudies-literature
Project description:Avascular necrosis of the femoral head (ANFH) is a debilitating disease that commonly leads to destruction of the hip joint in adults. The etiology of ANFH is unknown, but previous studies have indicated that heritable thrombophilia (increased tendency to form thrombi) and hypofibrinolysis (reduced ability to lyse thrombi), alcohol intake, and steroid use are risk factors for ANFH. We recently identified two families with ANFH showing autosomal dominant inheritance. By applying linkage analysis to a four-generation pedigree, we excluded linkage between the family and three genes related to thrombophilia and hypofibrinolysis: protein C, protein S, and plasminogen activator inhibitor. Furthermore, by a genomewide scan, a significant two-point LOD score of 3.45 (recombination fraction [theta] = 0) was obtained between the family with ANFH and marker D12S85 on chromosome 12. High-resolution mapping was conducted in a second family with ANFH and replicated the linkage to D12S368 (pedigree I: LOD score 2.47, theta = 0.05; pedigree II: LOD score 2.81, theta = 0.10). When an age-dependent-penetrance model was applied, the combined multipoint LOD score was 6.43 between D12S1663 and D12S85. Thus, we mapped the candidate gene for autosomal dominant ANFH to a 15-cM region between D12S1663 and D12S1632 on chromosome 12q13.
| S-EPMC1216065 | biostudies-literature
Project description:BACKGROUND: The results of studies on association between ABCB1 gene polymorphisms and glucocorticoid-induced avascular necrosis of the femoral head (GANFH) are controversial. This study aimed to assess the association of ABCB1 gene polymorphisms with the risk of GANFH by conducting a meta-analysis. MATERIAL AND METHODS: The PubMed, Cochrane Library, and Embase databases were searched for papers that describe the association between ABCB1 polymorphisms and GANFH risk. Summary odds ratios and 95% confidence intervals (CI) were estimated based on a fixed-effects model or random-effects model, depending on the absence or presence of significant heterogeneity. RESULTS: A total of 5 studies and 833 patients were included in the final analysis. Significant differences were found for rs1045642 polymorphism in the comparisons of CC vs. CT+TT (OR, 1.462; 95% CI, 1.066-2.007; P=0.019), and rs2032582 polymorphism in the comparisons of GG vs. G(TA)+(TA)(TA) (OR, 1.548; 95% CI,1.063-2.255; P=0.023). CONCLUSIONS: The study demonstrated that the ABCB1 polymorphisms (rs1045642 and rs2032582) significantly reduced the risk of GANFH.
| S-EPMC4285923 | biostudies-literature