Avascular Necrosis of Femoral Head—Overview and Current State of the Art

Abstract

Avascular necrosis (AVN) of the femoral head is caused by disruption of the blood supply to the proximal femur. The alterations in the blood supply may occur following a traumatic event or result from a non-traumatic cause. Femoral neck fracture and hip dislocation and associated surgical procedures, corticosteroid therapy, and alcohol abuse frequently lead to AVN development. Type of fracture (displaced or undisplaced) and time between injury and surgery are the most critical factors in assessing the risk of developing AVN. Diagnosis of AVN can be established based on patients’ complaints, medical history, and radiographic findings. There is no consensus on the treatment of patients with AVN to date. Non-surgical methods are dedicated to patients in the early pre-collapse stages of the disease and consist of pharmacotherapy and physiotherapy. Surgery is recommended for patients with advanced disease.

Does Diabetes Mellitus Increase the Risk of Avascular Osteonecrosis? A Systematic Review and Meta-Analysis

“…Only the study based on the Taiwanese registry diagnosis was made based on plain film, nuclear scan, or MRI. MRI is useful in the early diagnosis of AVN and can identify patients at risk of femoral head fracture [ 15 ].…”

“…AVN of the jaw is a debilitating disease that occurs predominantly in people using bisphosphonates, which are medications that inhibit bone resorption [ 13 , 14 ]. The treatment of early-stage AVN primarily involves physiotherapy, whereas late-stage disease often requires surgery [ 15 , 16 , 17 ].…”

“…AVN may be caused by trauma, such as fracture, particularly displaced fractures [ 18 ], or it can be non-traumatic. The pathogenesis of non-traumatic osteonecrosis is unclear, but there are several established risk factors such as corticosteroid treatment, alcohol abuse, rheumatic diseases, bone-marrow transplantation, or antiretroviral treatment [ 15 , 19 , 20 , 21 , 22 , 23 ]. Diabetes mellitus (DM), which causes disease of both large vessels (macroangiopathy) and small vessels (microangiopathy) [ 24 ], can also increase the risk of avascular osteonecrosis [ 25 , 26 , 27 ].…”

The Antagonism of Neuropeptide Y Type I Receptor (Y1R) Reserves the Viability of Bone Marrow Stromal Cells in the Milieu of Osteonecrosis of Femoral Head (ONFH)

“…In view of the decreased BMSCs in the ONFH femoral head, the application of BMSCs over the osteonecrotic lesion sites seems to be a reasonable revenue. Clinical trials of autologous BMSCs therapy for ONFH have shown promising results in early-stage cases [ 10 , 25 ]. However, the compromised regenerative potentials of BMSCs harvested from ONFH patients remain a problem.…”

Autologous Marrow Mesenchymal Stem Cell Driving Bone Regeneration in a Rabbit Model of Femoral Head Osteonecrosis

“…Osteonecrosis of the femoral head (ONFH), also known as avascular necrosis, is a progressive degenerative disease characterized by a disruption in blood flow to the femoral head (FH) [ 1 ]. ONFH is a multifactorial disease caused by traumatic (e.g., interruption of the ligament of teres) or non-traumatic events (e.g., chronic use of alcohol, smoking, or as a result of steroids, radiotherapy, and chemotherapy) [ 2 ].…”