SAS weekly rounds: avascular necrosis.
Ontology highlight
ABSTRACT:
SUBMITTER: Hamilton TW
PROVIDER: S-EPMC2744745 | biostudies-other | 2009 Sep
REPOSITORIES: biostudies-other
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Project description:Large chondral lesions of the humeral head are often treated with total shoulder arthroplasty, but this may not be an ideal option for young, active patients. Humeral head resurfacing is another option, which better preserves the native biomechanics. This article and the accompanying video present the surgical technique of partial humeral head resurfacing, which further preserves the remaining healthy cartilage. It is described for a chondral lesion due to avascular necrosis, but the method has been successfully used to treat chondral lesions from a broad range of causes.
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Project description:Avascular necrosis (AVN) of the hip is a devastating disease that affects middle-aged adults with poor outcomes if not treated in its early stages. In recent years, subchondroplasty with calcium phosphate solution has shown promising results. Concomitant intra-articular pathologies, including femoroacetabular impingement and chondral lesions, have been described in hips affected by AVN. These should be addressed at the time of surgery to lower the risk of failure. In this Technical Note, we describe an arthroscopic approach to femoral head subchondroplasty with precollapse lesion in AVN affected hip, combined with labral reconstruction and acetabular chondral treatment.
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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.
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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:BackgroundThis study was conducted to assess whether patient-reported outcomes (PROs) differ by the underlying diagnosis (rheumatoid arthritis (RA)/inflammatory arthritis, osteoarthritis (OA), avascular necrosis of bone (AVN), other) in patients undergoing primary total hip arthroplasty (THA).MethodsWe used prospectively collected data to assess the association of diagnosis with index hip function and pain. Moderate-severe activity limitation and moderate-severe pain were assessed at two- and five-year follow-up after primary THA using multivariable-adjusted logistic regression analyses. Odds ratios (OR) and 95% confidence intervals (CI) were calculated.ResultsThere were 5,707 primary THAs at two-years and 3,289 at five-years, 51% were women and the mean age was 65 years. The underlying diagnosis was RA in 3%, OA in 87%, AVN in 7% and other in 3%. In multivariable-adjusted analyses, compared to RA, diagnoses of OA and AVN were significantly associated with lower odds of moderate-severe activities of daily living limitations with an OR (95% CI) of 0.5 (0.3 to 0.8) (P = 0.01) and 0.4 (0.2 to 0.8) (P = 0.01), respectively, at two-years, but not at five-years, 0.7 (0.4 to 1.4) (P = 0.36) and 0.9 (0.4 to 1.8) (P = 0.78), respectively. At two-years, neither OA nor AVN were significantly associated with higher odds of moderate-severe pain (1.6 (0.6 to 4.5) (P = 0.40) and 2.8 (0.9 to 8.5) (P =0 0.06)), respectively. At five-years, AVN was associated with higher odds of moderate-severe pain with OR 4.1 (1.2 to 14.1) (P = 0.02), but not OA, 2.1 (0.7 to 6.5) (P = 0.22).ConclusionsWe found that patients with OA and AVN had better functional outcomes and those with AVN worse pain outcomes after primary THA, compared to patients with RA/inflammatory arthritis. Insights into mediators of these relationships are needed to better understand these associations.
| S-EPMC3850929 | biostudies-literature
Project description:The underlying mechanisms of glucocorticoid (GC)‑induced avascular necrosis of the femoral head (ANFH) have yet to be fully understood, in particular the mechanisms associated with the change of gene expression pattern. The present study aimed to identify key genes with a differential expression pattern in GC‑induced ANFH. E‑MEXP‑2751 microarray data were downloaded from the ArrayExpress database. Differentially expressed genes (DEGs) were identified in 5 femoral head samples of steroid‑induced ANFH rats compared with 5 placebo‑treated rat samples. Gene Ontology (GO) and pathway enrichment analyses were performed upon these DEGs. A total 93 DEGs (46 upregulated and 47 downregulated genes) were identified in GC‑induced ANFH samples. These DEGs were enriched in different GO terms and pathways, including chondrocyte differentiation and detection of chemical stimuli. The enrichment map revealed that skeletal system development was interconnected with several other GO terms by gene overlap. The literature mined network analysis revealed that 5 upregulated genes were associated with femoral necrosis, including parathyroid hormone receptor 1 (PTHR1), vitamin D (1,25‑Dihydroxyvitamin D3) receptor (VDR), collagen, type II, α1, proprotein convertase subtilisin/kexin type 6 and zinc finger protein 354C (ZFP354C). In addition, ZFP354C and VDR were identified to transcription factors. Furthermore, PTHR1 was revealed to interact with VDR, and α‑2‑macroglobulin (A2M) interacted with fibronectin 1 (FN1) in the PPI network. PTHR1 may be involved in GC‑induced ANFH via interacting with VDR. A2M may also be involved in the development of GC‑induced ANFH through interacting with FN1. An improved understanding of the molecular mechanisms underlying GC‑induced ANFH may provide novel targets for diagnostics and therapeutic treatment.
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Project description:Musculoskeletal disorders, standing as the fifth leading cause of disability-adjusted life years globally, present significant challenges in orthopedics. Osteochondritis dissecans (OCD) and avascular necrosis (AVN) are distinct but closely related conditions within this spectrum, impacting patients' quality of life with pain, limited mobility, and dysfunction. OCD, involving cartilage and bone detachment in joints, predominantly affects young athletes, but its exact etiology and optimal management remain subjects of ongoing research. Conversely, AVN, marked by bone tissue death due to compromised blood supply, is linked to systemic factors like corticosteroid use and traumatic injuries. Diagnosis for both conditions relies on radiography and magnetic resonance imaging. Conservative treatment for AVN includes the use of a cane or crutches, pharmacological therapy, or physical therapy. On the other hand, in OCD, the primary approach is activity/sports restriction. Surgical treatment options for AVN patients encompass core decompression, bone grafting, or, in the most advanced cases, total hip arthroplasty. OCD may be surgically treated through subchondral drilling or fixation of unstable lesions. Advanced cases of OCD involve cartilage salvage with resurfacing techniques. The presentation of differences between these conditions enhances our understanding, facilitating improved diagnosis and management strategies.
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Project description:HIV-infected individuals have an increased risk of avascular bone necrosis (AVN). Antiretroviral therapy (ART) and particularly protease inhibitors (PI) have been implicated as a risk factor. We aimed to study the associations of ART with the occurrence of AVN among Swiss HIV Cohort Study participants (SHCS).We used incidence density sampling to perform a case control study within the Swiss HIV Cohort Study (SHCS) comparing prospectively collected AVN cases and controls by conditional logistic regression analysis. To evaluate the effect of ART, multivariable models were adjusted for HIV transmission risk group, age, alcohol consumption, use of corticosteroids, CD4 nadir, maximum viral load, and pancreatitis.We compared 74 AVN cases and 145 controls. Associations with AVN were shown for heterosexual HIV acquisition (odds ratio [OR], 3.4; 95% confidence interval [CI], 1.1-10), alcohol consumption (OR, 2.7; 95% CI, 1.3-5.7), and hyperlipidemia (OR, 3.6; 95% CI, 1.4-9.6). After adding ART substances to the multivariable base model, there was evidence of an association for treatment with tenofovir (TDF) >1 year (OR, 4.4; 95% CI, 1.4-14) with AVN. Neither exposure to specific frequently prescribed ART combinations or ART drug classes nor cumulative ART exposure showed any associations with AVN.In the HIV-infected population, a combination of risk factors such as heterosexual HIV acquisition, moderate to severe alcohol intake, and hyperlipidemia seem to contribute to AVN. ART does not seem to be a relevant risk factor for AVN. The association of prolonged TDF exposure with AVN needs to be confirmed.
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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