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Related Concept Videos

Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Bone Remodeling01:40

Bone Remodeling

Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
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Blood and Nerve Supply to the Bones

Bones are dynamic organs that require a rich supply of oxygen and nutrients. Around 5% to 10% of the cardiac output supplies blood to the bones. A typical long bone has three main sources: the nutrient artery, the metaphyseal and epiphyseal arteries, and the periosteal arteries.
Nutrient Artery
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Bone Disorders01:29

Bone Disorders

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Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during bone...

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Related Experiment Video

Updated: Jun 30, 2026

Tension-Free Weight-Bearing Model of Steroid-Induced Osteonecrosis of Femoral Head in Rats
05:55

Tension-Free Weight-Bearing Model of Steroid-Induced Osteonecrosis of Femoral Head in Rats

Published on: September 27, 2024

Avascular Necrosis (Aseptic Osteonecrosis).

E M Camporesi, V Zanon, G Vezzani

    Undersea & Hyperbaric Medicine : Journal of the Undersea and Hyperbaric Medical Society, Inc
    |June 28, 2026
    PubMed
    Summary

    Avascular necrosis (AVN) is bone death due to poor blood supply, often affecting the femoral head. Early detection and treatments like hyperbaric oxygen therapy may help preserve the joint, but advanced stages may require total hip arthroplasty.

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    Published on: September 27, 2024

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    10:31

    Surgical Angiogenesis in Porcine Tibial Allotransplantation: A New Large Animal Bone Vascularized Composite Allotransplantation Model

    Published on: August 13, 2017

    Area of Science:

    • Orthopedics
    • Vascular Biology
    • Radiology

    Background:

    • Avascular necrosis (AVN), or aseptic osteonecrosis (AO), affects various bones, most commonly the femoral head (AVNFH).
    • This condition results from compromised blood supply to bone tissue, leading to hypoxic conditions.
    • The Ficat classification system stages AVN of the femoral head based on radiographic findings.

    Purpose of the Study:

    • To review the etiology, pathogenesis, and staging of avascular necrosis, particularly of the femoral head.
    • To discuss the role of hyperbaric oxygen therapy in managing AVN.
    • To outline treatment strategies, including joint preservation and surgical interventions like total hip arthroplasty.

    Main Methods:

    • Literature review of avascular necrosis (AVN) and aseptic osteonecrosis (AO).
    • Analysis of the Ficat classification system for staging femoral head osteonecrosis.
    • Discussion of treatment modalities for AVN, from conservative to surgical.

    Main Results:

    • AVN is caused by vascular compromise, leading to bone cell death and potential joint collapse.
    • The Ficat classification stages AVN from I (pain, no radiographic changes) to IV (femoral head collapse).
    • Hyperbaric oxygen (HBO₂) may aid in hypoxic condition management, while advanced stages necessitate total hip arthroplasty (THA).

    Conclusions:

    • Avascular necrosis of the femoral head is a progressive condition requiring timely diagnosis and management.
    • Treatment aims for joint preservation, but surgical intervention (THA) is often required for advanced stages.
    • Understanding AVN pathogenesis and staging is crucial for effective patient care.