Treatment of Experimental Avascular Necrosis of the Femoral Head with Hyperbaric Oxygen in Rats: Histological Evaluation of the Femoral Heads during the Early Phase of the Reparative Process

Introduction: The treatment of avascular necrosis of the femoral head (AVNFH) is based on invasive (e.g., core decompression) and non-invasive methods (e.g., hyperbaric oxygen therapy – HBO2). The purpose of the present study is to evaluate the effect of HBO2 on the quality of life (QoL) of patients with AVNFH. Methods: This was a prospective observational non-controlled study of patients with AVNFH treated by HBO2. It was conducted, with the use of Steinberg scale, on 73 patients with AVNFH Stage I or II who were treated with HBO2. Patients’ QoL was assessed with EuroQol-5D-5L (EQ), Harris Hip Score (mHHS), MAHORN (MHOT), and VAS, in three different phases: before HBO2; after the completion of the first phase (20 HBO2 sessions, up to two months); and after the completion of the second phase (20 HBO2 sessions, up to two months after the first phase). A reassessment was made on the completion of each phase. Ratings were also made after the completion of each phase, over the first five months of follow-up. Results: All 73 patients (67.1% males, 32.9% females, mean age: 40.34, SD ± 9.99) participated in the study. Steinberg scale, mean EQ (F (1, 57) = 25.18, η2 = .306 and F (1, 43) = 43.402, η2 = .502); mHHS (F (1, 61) = 67.13, η2 = .524) and F (1, 43) = 31.84, η2 = .425); MHOT (F (1, 61) = 11.68, η2 = .161) and F (1, 43) = 98.01, η2 = .695); and VAS (F (1, 53) = 24.11, η2 = .313) and F (1, 39) = 45.61, η2 = .539), improved between the first and second measurements and between the second and third measurement accordingly (p < .01). Conclusions: HBO2 treatment does not induce alteration of quality of life and is well tolerated and accepted by patients.

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The outcome of hyperbaric oxygen therapy versus core decompression in the non-traumatic avascular necrosis of the femoral head: Retrospective Cohort Study

Annals of Medicine and Surgery ◽

10.1016/j.amsu.2021.01.084 ◽

2021 ◽

Vol 62 ◽

pp. 450-454

Author(s):

Isam Moghamis ◽

Abduljabbar A. Alhammoud ◽

Osama Kokash ◽

Ghalib Ahmed Alhaneedi

Keyword(s):

Cohort Study ◽

Femoral Head ◽

Avascular Necrosis ◽

Hyperbaric Oxygen ◽

Retrospective Cohort Study ◽

Hyperbaric Oxygen Therapy ◽

Retrospective Cohort ◽

Oxygen Therapy ◽

Core Decompression

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Hyperbaric oxygen therapy as a treatment for stage-I avascular necrosis of the femoral head

Journal of Bone and Joint Surgery - British Volume ◽

10.1302/0301-620x.85b3.13237 ◽

2003 ◽

Vol 85-B (3) ◽

pp. 371-375 ◽

Cited By ~ 60

Author(s):

N. D. Reis ◽

O. Schwartz ◽

D. Militianu ◽

Y. Ramon ◽

D. Levin ◽

...

Keyword(s):

Femoral Head ◽

Avascular Necrosis ◽

Hyperbaric Oxygen ◽

Hyperbaric Oxygen Therapy ◽

Oxygen Therapy ◽

Stage I

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Atorvastatin Upregulates microRNA-186 and Inhibits the TLR4-Mediated MAPKs/NF-κB Pathway to Relieve Steroid-Induced Avascular Necrosis of the Femoral Head

Frontiers in Pharmacology ◽

10.3389/fphar.2021.583975 ◽

2021 ◽

Vol 12 ◽

Author(s):

Yusong Zhang ◽

Limin Ma ◽

Erhai Lu ◽

Wenhua Huang

Keyword(s):

Oxidative Stress ◽

Femoral Head ◽

Avascular Necrosis ◽

Molecular Mechanisms ◽

Cell Damage ◽

Lipid Lowering ◽

Histological Evaluation ◽

Active Components ◽

Pathway Inhibition

Steroid-induced avascular necrosis of the femoral head (SANFH) is caused by the death of active components of the femoral head owing to hormone overdoses. The use of lipid-lowering drugs to prevent SANFH in animals inspired us to identify the mechanisms involving Atorvastatin (Ato) in SANFH. However, it is still not well understood how and to what extent Ato affects SANFH. This study aimed to figure out the efficacy of Ato in SANFH and the underlying molecular mechanisms. After establishment of the SANFH model, histological evaluation, lipid metabolism, inflammatory cytokines, oxidative stress, apoptosis, and autophagy of the femoral head were evaluated. The differentially expressed microRNAs (miRs) after Ato treatment were screened out using microarray analysis. The downstream gene and pathway of miR-186 were predicted and their involvement in SANFH rats was analyzed. OB-6 cells were selected to simulate SANFH in vitro. Cell viability, cell damage, inflammation responses, apoptosis, and autophagy were assessed. Ato alleviated SANFH, inhibited apoptosis, and promoted autophagy. miR-186 was significantly upregulated after Ato treatment. miR-186 targeted TLR4 and inactivated the MAPKs/NF-κB pathway. Inhibition of miR-186 reversed the protection of Ato on SANFH rats, while inhibition of TLR4 restored the protective effect of Ato. Ato reduced apoptosis and promoted autophagy of OB-6 cells by upregulating miR-186 and inhibiting the TLR4/MAPKs/NF-κB pathway. In conclusion, Ato reduced apoptosis and promoted autophagy, thus alleviating SANFH via miR-186 and the TLR4-mediated MAPKs/NF-κB pathway.

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Spontaneous resolution of avascular necrosis of femoral heads following cure of Cushing’s syndrome

Endocrinology Diabetes and Metabolism Case Reports ◽

10.1530/edm-16-0015 ◽

2016 ◽

Vol 2016 ◽

Cited By ~ 1

Author(s):

A Pazderska ◽

S Crowther ◽

P Govender ◽

K C Conlon ◽

M Sherlock ◽

...

Keyword(s):

Femoral Head ◽

Avascular Necrosis ◽

Cushing’S Syndrome ◽

Cushing's Syndrome ◽

Leg Pain ◽

List Type ◽

Rapid Weight Gain ◽

Free Cortisol ◽

Femoral Heads ◽

Adrenal Disease

Summary Avascular necrosis (AVN) is a rare presenting feature of endogenous hypercortisolism. If left untreated, complete collapse of the femoral head may ensue, necessitating hip replacement in up to 70% of patients. The majority of the described patients with AVN due to endogenous hypercortisolaemia required surgical intervention. A 36-year-old female, investigated for right leg pain, reported rapid weight gain, bruising and secondary amenorrhoea. She had abdominal adiposity with violaceous striae, facial plethora and hirsutism, atrophic skin, ecchymosis and proximal myopathy. Investigations confirmed cortisol excess (cortisol following low-dose 48h dexamethasone suppression test 807nmol/L; 24h urinary free cortisol 1443nmol (normal<290nmol)). Adrenocorticotrophic hormone (ACTH) was <5.0pg/mL. CT demonstrated subtle left adrenal gland hypertrophy. Hypercortisolaemia persisted after left adrenalectomy. Histology revealed primary pigmented micronodular adrenal disease. Post-operatively, right leg pain worsened and left leg pain developed, affecting mobility. MRI showed bilateral femoral head AVN. She underwent right adrenalectomy and steroid replacement was commenced. Four months after surgery, leg pain had resolved and mobility was normal. Repeat MRI showed marked improvement of radiological abnormalities in both femoral heads, consistent with spontaneous healing of AVN. We report a case of Cushing’s syndrome due to primary pigmented nodular adrenocortical disease, presenting with symptomatic AVN of both hips. This was managed conservatively from an orthopaedic perspective. Following cure of hypercortisolaemia, the patient experienced excellent recovery and remains symptom free 4 years after adrenalectomy. This is the first report of a favourable outcome over long-term follow-up of a patient with bilateral AVN of the hip, which reversed with treatment of endogenous hypercortisolaemia. Learning points AVN of femoral head can be a presenting feature of hypercortisolism, both endogenous and exogenous. Rarely, treatment of hypercortisolaemia can reverse AVN without the need for orthopaedic intervention. Primary pigmented nodular adrenal disease is a rare cause of ACTH-independent Cushing’s syndrome.

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