Materiały źródłowe

• #1 Avascular Necrosis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537007/

  Osteonecrosis is a degenerative bone condition characterized by the death of cellular components of the bone secondary to an interruption of the subchondral blood supply. Also known as avascular necrosis, it typically affects the epiphysis of long bones at weight-bearing joints. The most common sites for AVN are the femoral head, knee, talus, and humeral head. The hip is the most common location overall. Advanced disease may result in subchondral collapse, which threatens the viability of the joint involved. Therefore, early recognition and treatment of osteonecrosis are essential. This activity discusses the etiology and pathogenesis of the disease, presentation, and treatment options of the most common forms of osteonecrosis. […] Osteonecrosis is a degenerative bone condition characterized by the death of cellular components of the bone secondary to an interruption of the subchondral blood supply. It is also known as avascular necrosis, aseptic necrosis, and ischemic bone necrosis. It typically affects the epiphysis of long bones at weight-bearing joints. Severe cases can lead to the destruction of subchondral bone or the collapse of an entire joint.

• #2 Avascular Necrosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/333364-overview

  Avascular necrosis (AVN) is defined as cellular death of bone components due to disruption of the subchondral blood supply. It results in pain, loss of joint function, and long-term joint damage. AVN is also known as osteonecrosis, aseptic necrosis, and ischemic bone necrosis. […] AVN usually involves the epiphysis (end part of a long bone), but small bones can also be affected. This condition most commonly occurs in the femoral head. […] AVN is associated with numerous conditions. Corticosteroid use, sickle cell disease, and allogeneic hematopoietic stem cell transplantation and kidney transplantation are high-risk factors for AVN. […] The use of steroids is the leading cause of nontraumatic osteonecrosis. […] Although the pathophysiology of AVN is not fully understood, the final common pathway is interruption of blood flow to the bone. AVN often affects bones with a single terminal blood supply, such as the femoral head, carpals, talus, and humerus. The earliest pathologic characteristics of osteonecrosis are necrosis of hematopoietic cells and adipocytes followed by interstitial marrow edema.

• #3 Avascular Necrosis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537007/

  The widely accepted view in the literature is that a reduction in subchondral blood supply is responsible for osteonecrosis. However, numerous risk factors and theories exist on the development of this vascular impairment. Shah et al. succinctly categorizes these into six groups. […] A reduction in subchondral blood supply induces a state of hypoxia, leading to loss of integrity of cell membranes and necrosis of cells. The pathological appearances of necrosis marked by the appearance of neutrophils and macrophages will predominate. Macroscopically, this induces subchondral collapse and subsequent joint degeneration. […] Osteocytes undergo apoptosis, and phagocytosis cannot occur. Thus, the osteocytes are not replaced. This process leads to poor bone remodeling and osteosclerosis. […] There are several identified risk factors for osteonecrosis, but the exact pathogenesis remains unestablished. More likely, a combination of different factors and conditions leads to the destruction of bone cells.

• #4 Pathophysiology and risk factors for osteonecrosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4596210/

  Osteonecrosis, also known as avascular necrosis or AVN, is characterized by a stereotypical pattern of cell death and a complex repair process of bone resorption and formation. […] Most likely, a common pathophysiological pathway exists involving compromised subchondral microcirculation. […] Understanding the pathophysiology and risk factors of ON is limited by the unavailability of longitudinal studies in humans and the lack of a bipedal mammalian model. […] Nevertheless, the best evidence suggests a common pathophysiological pathway involving compromised subchondral microcirculation. […] A unifying concept of the pathogenesis of ON has been presented that emphasizes the central role of vascular pathology and ischemia leading to osteocyte necrosis. […] Decreased femoral head blood flow can occur through three pathogenic mechanisms: vascular interruption by fractures or dislocation, intravascular occlusion from thrombi or embolic fat, or intraosseous extravascular compression from lipocyte hypertrophy or Gaucher cells.

• #5 Avascular Necrosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/333364-overview

  Interruption of the vascular supply and resultant necrosis of marrow, medullary bone, and cortex are theorized to be caused by the mechanisms listed below. However, individual patients usually have more than one risk factor; this indicates that the pathogenesis of AVN is likely multifactorial. […] Mechanisms of AVN may include the following: Vascular occlusion: This is characterized by the interruption of the extraosseous blood supply via factors such as direct trauma (eg, fracture, dislocation), nontraumatic stress, and stress fracture. […] Altered lipid metabolism: Animal studies have led to the hypothesis that increased levels of serum lipids leads to lipid deposition in the femoral head, causing femoral hypertension and ischemia. […] Intravascular coagulation: Disorders of the coagulation system have been implicated in the pathogenesis of AVN.

• #6 Avascular Necrosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1247804-overview

  Interruption of the vascular supply and resultant necrosis of marrow, medullary bone, and cortex are theorized to be caused by the mechanisms listed below. However, individual patients usually have more than one risk factor; this indicates that the pathogenesis of AVN is likely multifactorial. […] Mechanisms of AVN may include the following: Vascular occlusion: This is characterized by the interruption of the extraosseous blood supply via factors such as direct trauma (eg, fracture, dislocation), nontraumatic stress, and stress fracture. […] Altered lipid metabolism: Animal studies have led to the hypothesis that increased levels of serum lipids leads to lipid deposition in the femoral head, causing femoral hypertension and ischemia. […] Intravascular coagulation: Disorders of the coagulation system have been implicated in the pathogenesis of AVN.

• #7 Osteonecrosis of the femoral head: pathophysiology and current concepts of treatment in: EFORT Open Reviews Volume 4 Issue 3 (2019)

  https://eor.bioscientifica.com/view/journals/eor/4/3/2058-5241.4.180036.xml

  Osteonecrosis (ON), also defined as avascular necrosis or aseptic necrosis, is characterized as bone cell death that follows an impairment of the blood flow to the bone from a traumatic or non-traumatic origin. ON most often happens in the hip joint (femoral head) but may also occur in other anatomical locations (e.g. shoulder, knee and ankle). The aim of this article is to present the pathophysiology of the ONFH and understand its underlying causes. Most theories point towards an alteration in the intravascular blood flow as the potential mechanism of ON initiation. These alterations may occur either from a traumatic or a non-traumatic cause or be a consequence of some well-accepted risk factors. […] Intravascular coagulation can occur as the end result of local vascular impairment; vascular occlusion occurs because of thrombus formation due to abnormally shaped red blood cells as seen in sickle cells anaemia or fat or nitrogen embolism. Extravascular compression may arise secondary to damaged femoral head vessels that permit the accumulation of fat and blood in the extravascular space which leads to alterations in blood flow through local compression.

• #8 Pathogenesis of Osteonecrosis | Orthopaedic Articles & Publications | Dr Jason Lance Crane

  https://www.capetownorthopaedic.co.za/pathogenesis-of-osteonecrosis.php

  The Pathogenesis of Osteonecrosis […] James Russell first described osteonecrosis in 1794, and a full description of the entity followed in 1930 by Phemister et al. Since then many researchers have been trying to determine the pathogenesis of osteonecrosis, but this seems only to have succeeded in creating more questions. […] The treatment of osteonecrosis is considerably more successful at early stages of the disease. The early diagnosis of osteonecrosis depends upon the identification of individuals at risk. Understanding the pathogenic factors leading to osteonecrosis enables the early investigation of at-risk individuals and facilitates prompt diagnosis. […] Osteonecrosis is defined as cell death of bony tissue (marrow and mineralized tissue) due to ischaemia. It represents the final common pathway of several disease entities, which result in impaired blood supply to the bone tissue, causing necrosis of the bone. […] Although many theories and multiple causes for osteonecrosis have been suggested, until recently little has been known about its pathophysiology or the pathogenic mechanisms involved in its various forms. Today it is most appropriate to consider osteonecrosis as a multifactorial group of disorders that lead, possibly by a common pathway, to bone necrosis. […] Trauma is thought to play a role. […] Jones has postulated that intravascular coagulation activated by a variety of underlying diseases may be the missing link that joins several seemingly unrelated risk factors and leads to the final ischaemic insult producing intraosseous thrombosis and bone necrosis. […] Current evidence suggests that intravascular coagulation, an intermediary mechanism, is the most likely final common pathway by which intraosseous fat embolism causes nontraumatic osteonecrosis. […] Osteonecrosis has been associated with several autoimmune diseases most notably Systemic Lupus Erythematosus (SLE) and Rheumatoid arthritis. […] The pathogenesis of osteonecrosis in relation to alcohol use seems to be similar to that of corticosteroid use, with fat emboli produced by the liver occluding vessels in the subchondral bone. […] Several haemoglobinopathies, especially sickle-cell disease, are common causes of osteonecrosis. […] The pathogenic mechanism seems to be embolic, with air bubbles causing occlusion and ischaemia, although rapidly expanding nitrogen can cause secondary injury to adipocytes within the marrow and cause vessel collapse. […] The accumulation of lipid-laden Gaucher cells in the bone marrow can increase intraosseous pressure, influence coagulation and occlusion of intraosseous vessels leading to osteonecrosis. […] Osteonecrosis in HIV-infected patients was first reported in 1990. […] The pathogenesis of osteonecrosis is still an enigma, which remains to be solved. Understanding the pathogenesis of osteonecrosis will have a significant impact on the prevention and treatment of this debilitating disease. […] Most of the evidence points to the existence of a final common pathway (coagulopathy) regardless of the etiological factors involved.

• #9 :: JKMS :: Journal of Korean Medical Science

  https://jkms.org/DOIx.php?id=10.3346/jkms.2021.36.e65

  There are sufficient data to support such a pathophysiologic cascade: fat cell hyperplasia; intra-osseous hypertension; vascular compression and thrombosis; ischemia; marrow and bone necrosis; subchondral fracture; and collapse of the femoral head, particularly in corticosteroid – and alcohol- associated ONFH, while other risk factors may work through different mechanisms. […] This leads to subsequent secondary arthritis of the hip; the end-stage of ONFH. […] In the presence of thrombophilia/hypofibrinolysis and/or impaired angiogenesis, prolonged damage due to ischemia occurs and definite ONFH develops. […] After complete ischemia, osteocytes start to disappear within 24 to 72 hours and a focal sequestrum is formed. […] Once a sequestrum is formed, the course of the disease is irreversible. […] The exact pathogenesis of ONFH is still unknown. Most investigators agree that ONFH has a multifactorial etiology but progression of the disease occurs through one final common pathway, which is decreased blood flow to the femoral head that leads to ischemia and cell death.

• #10 Osteonecrosis of the femoral head: pathophysiology and current concepts of treatment in: EFORT Open Reviews Volume 4 Issue 3 (2019)

  https://eor.bioscientifica.com/view/journals/eor/4/3/2058-5241.4.180036.xml

  Moreover, it is nowadays admitted that the pathophysiological mechanism arises from an interaction between vascular impairment, altered bone-cell physiology, risk factors as well as genetics. Vascular impairment appears as the end result of coagulation disorders seen in hypercoagulable conditions such as sickle cell anaemia, hereditary thrombophilia, antiphospholipid antibodies, malignancy and inflammatory bowel disease. An altered cell-bone physiology is often proposed as being part of the osteonecrotic process and the hypothesis is that ON appears secondary to impaired mesenchymal differentiation which leads to a damage of the bone structure. […] Whatever the underlying cause, all forms of ON of the femoral head are related to blood flow impairments. After the onset of ischaemia, histological signs of marrow necrosis and osteocyte death become apparent within 24 to 72 hours. Then, a saponification of free fatty acids appears within the extracellular matrix as well as a calcium ion expression that leads to an inflammatory response. Finally, the acellular trabecular bone is replaced by inferior woven bone that does not tolerate normal loading and collapse may occur.

• #11 Avascular necrosis – Wikipedia

  https://en.wikipedia.org/wiki/Avascular_necrosis

  Avascular necrosis (AVN), also called osteonecrosis or bone infarction, is death of bone tissue due to interruption of the blood supply. […] The hematopoietic cells are most sensitive to low oxygen and are the first to die after reduction or removal of the blood supply, usually within 12 hours. […] Experimental evidence suggests that bone cells (osteocytes, osteoclasts, osteoblasts etc.) die within 12-48 hours, and that bone marrow fat cells die within 5 days. […] Upon reperfusion, repair of bone occurs in two phases. First, there is angiogenesis and movement of undifferentiated mesenchymal cells from adjacent living bone tissue grow into the dead marrow spaces, as well as entry of macrophages that degrade dead cellular and fat debris. […] Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts. […] Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue.

• #12 Diagnosis of Acute or Subacute Avascular Necrosis | CDA-AMC

  https://www.cda-amc.ca/diagnosis-acute-or-subacute-avascular-necrosis

  Although the natural history of AVN has not been completely determined, it is recognized that delayed diagnosis of AVN can seriously affect patient morbidity and quality of life. For example, the average age of diagnosis for AVN of the femoral head is less than 40 years, making preservation of the joints a priority. Steinberg et al. have devised a quantitative system for staging AVN of the femoral head. Their evaluation of more than 1,000 hips during a period of 12 years provides evidence that early diagnosis and treatment can greatly improve prognosis and reduce morbidity. Once radiographic changes occur (stage II), most joints will collapse within six to 24 months, if untreated. By the time the patient has reached stage IV, the changes are irreversible. Replacement of the femoral head may be considered at stage IV, but by stage V, total hip replacement is required.

• #13 Avascular Necrosis: Bone Death Symptoms, Causes, Stages, Treatments & Cure

  https://www.emedicinehealth.com/avascular_necrosis/article_em.htm

  Avascular necrosis is a localized death of bone as a result of local injury (trauma), drug side effects, or disease. […] This is a serious condition because the dead areas of bone do not function normally, are weakened, and can collapse. […] Avascular necrosis ultimately leads to destruction of the joint adjacent to the involved bone. […] While the precise mechanism for the development of avascular necrosis is not known, it is suspected that interruption of the blood supply to the affected bone plays some role. […] There are many causes of avascular necrosis, but the vast majority of avascular necrosis is caused by either traumatic injury to the affected bone (such as fracture and dislocation), steroid medication usage (glucocorticoid medications such as prednisone and prednisolone, particularly when given in high doses), or excessive alcohol consumption.

• #14 Avascular necrosis (osteonecrosis) – Symptoms & causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/avascular-necrosis/symptoms-causes/syc-20369859

  Avascular necrosis is the death of bone tissue due to a lack of blood supply. Also called osteonecrosis, it can lead to tiny breaks in the bone and cause the bone to collapse. The process usually takes months to years. […] Avascular necrosis occurs when blood flow to a bone is interrupted or reduced. Reduced blood supply can be caused by: […] Sometimes the cause of avascular necrosis not brought on by trauma isn’t fully understood. Genetics combined with overuse of alcohol, certain medications and other diseases likely play a role. […] Untreated, avascular necrosis worsens. Eventually, the bone can collapse. Avascular necrosis also causes bone to lose its smooth shape, possibly leading to severe arthritis.

• #15 Pathophysiology and risk factors for osteonecrosis

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4596210/

  Elevated intraosseous pressures have been measured within ON femoral heads associated with venous outflow obstruction and venous stasis. […] Elevated intraosseous pressures can be found in osteoarthritis as well as ON and can also be produced by elevations in intra-articular pressure. […] Risk factors that are strongly implicated as causal for ON seem to converge through mechanisms of vascular impairment to produce subchondral or segmental ischemia and marrow and osteocyte death. […] A repair process follows that usually results in resorption of subchondral bone that exceeds formation, leading to structural compromise and fracture. […] Understanding risk factors and pathophysiology has therapeutic implications since several treatment regimens are available to optimize femoral head circulation, to prevent bone resorption and to preserve the subchondral bone.

• #16

  https://www.omim.org/entry/608805

  Some ANFH previously considered idiopathic may actually represent a feature of hereditary thrombophilia (an increased tendency for intravascular thrombosis) or hypofibrinolysis (a reduced ability to lyse thrombi). […] Deficiency of activated protein C (PROC; 612283) or protein S (PROS1; 176880), resulting in thrombophilia (176860; 612336), has been reported to be associated with osteonecrosis of the hip in adults and with LCP in children. […] Hypofibrinolysis, mediated by high levels of plasminogen activator inhibitor (PAI; 173360), has been cited as a major cause of idiopathic osteonecrosis.

• #17 Treatment of non‑traumatic avascular necrosis of the femoral head (Review)

  https://www.spandidos-publications.com/10.3892/etm.2022.11250

  Non-traumatic osteonecrosis of the femoral head (NONFH) is the result of impaired blood supply to the femoral head and structural and functional disruption of local articular cartilage, subchondral bone and blood vessels, which culminate in subchondral osteonecrosis, femoral head collapse and hip joint pain. […] Studies have shown that femoral head necrosis is associated with several underlying diseases, including trauma or surgery of the hip joint, excessive corticosteroid production, hyperlipidemia, abnormal blood pressure, autoimmune diseases, endotoxin poisoning, smoking, excessive alcohol consumption and blood hypercoagulability. All of these pathological changes can eventually lead to vascular damage, bone marrow infarction and avascular necrosis. […] Long-term steroid use is the most common cause of NONFH, as it can lead to microthrombosis and impede blood and oxygen supply to the femoral head, resulting in osteonecrosis. […] Alcohol abuse is one of the main risk factors of bone deterioration. Ethanol impairs the proliferation of human bone mesenchymal stem cells and induces their differentiation into adipocytes, which eventually leads to bone loss and structural damage.

• #18 Risk Factors and Mechanism for Steroid Induced Avascular Necrosis of the Femoral Head

  https://www.ebmconsult.com/articles/mechanism-risk-factor-steroid-avascular-necrosis-femoral-head

  Evidence suggests a multifactorial process that results from an imbalance in bone resorption and repair, compromise of vasculature, and both direct and indirect bone cell apoptosis. […] As such the mechanisms of steroid-induced AVN can be classified into 3 broad categories which exist in a complex interplay: an imbalance of bone resorption and repair, impairment of vasculature within the bone, and apoptosis. […] Differentiation of bone marrow cells becomes skewed towards adipogenesis rather than osteogenesis in the presence of steroid therapy. This is due to an upregulation of the transcription factor peroxisome proliferator activated receptor- (PPAR-), which promotes adipogenesis, and down regulation of Runx2/core-binding factor a1 (Cbfa1), which regulates osteoblast differentiation and maturation. This mechanism directly reduces the number of bone precursor cells, which ultimately leads to a decrease in bone remodeling. Existing adipocytes have also been noted to hypertrophy. Adipogenesis and adipocyte hypertrophy have been implicated in vascular impairment and apoptosis as discussed below. Bone homeostasis is further disrupted by increasing Dickkopf-1 concentrations, which agonize the activity of osteoclasts and antagonize the activity of osteoblasts.

• #19 Risk Factors and Mechanism for Steroid Induced Avascular Necrosis of the Femoral Head

  https://www.ebmconsult.com/articles/mechanism-risk-factor-steroid-avascular-necrosis-femoral-head

  Vascular endothelial growth factor, responsible for angiogenesis and bone repair, is decreased by up to 45% in the presence of steroids. Vascular impairment has also been noted due to fat emboli and direct compression of arteries due to increased intraosseal pressure from adipogenesis and adipocyte hypertrophy. Thrombi may also cause occlusion of the vasculature due to increased thrombin production and decreased fibrinolytic activity. Finally, hypertension, a well-known effect of steroid therapy, may lead to epiphyseal artery constriction and damage, ultimately reducing or eliminating blood supply to the femoral head. […] Apoptosis, or programmed cell death, of osteoblasts and osteocytes is mediated both directly through steroid interactions with the glucocorticoid receptor and indirectly through vascular compromise leading to ischemia and cell compression due to adipogenesis and increased intraosseal pressure. Death of mature bone cells and their progenitors further drives the imbalance of bone remodeling.

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

  https://www.mdpi.com/1660-4601/19/12/7348

  The most common non-traumatic causes are corticosteroid treatment and alcohol abuse. Corticosteroids alter adipocytes’ differentiation, increasing the size and number of adipocytes. This process leads to the intracellular accumulation of lipids. As a result of increased pressure inside the bone cells, vascular endothelial cells become damaged, leading to local coagulopathy, vascular thrombosis, and ischemia. […] Alcohol abuse is reported by 20–30% of the patients with AVN. The potential mechanism of induction of AVN is unknown. Alcohol may provoke osteocyte death through several pathways, e.g., by increasing intracellular deposition of triglycerides, which leads to pyknosis of osteocytes similarly to corticosteroids, and by decreasing osteogenesis through promoting stromal cell differentiation into adipocytes.

• #21 Osteonecrosis | UW Radiology

  https://rad.washington.edu/about-us/academic-sections/musculoskeletal-radiology/teaching-materials/online-musculoskeletal-radiology-book/osteonecrosis/

  The mechanism outlined here helps to explain the overwhelming distribution of osteonecrosis toward the convex side of the joint. […] Chronic steroid use causes fat cells to grow. […] As the patient spends more and more time on steroids and the intramedullary fat cells grow larger and larger, the baseline intramedullary pressure begins to rise. […] However, as the pressure continues to rise, the intramedullary veins on the convex side of the joint finally become occluded all of the time.

• #22 SciELO Brazil – Osteonecrosis of the Femoral Head: Update Article Osteonecrosis of the Femoral Head: Update Article

  https://www.scielo.br/j/rbort/a/nfqMzLfXzPDSg7Zg8T4NqPf/

  As for the use of corticosteroids and alcohol abuse, both have been proven to be dose-dependent, with an increase in the risk with the use of more than 20 mg a day of corticosteroids and an almost 18-fold increase in the risk with an intake of more than 1,000 mL a week of alcohol. […] Other less common pathologies, such as Gaucher disease, Caisson disease, dysbarism from deep water diving, as well as HIV, radiation therapy, pregnancy, smoking and gout can also lead to ONFH. A current study has shown that, in idiopathic cases, acetabular alterations with less coverage of the femoral head may be related to ONFH. […] Treatment of ONFH is perhaps the most controversial point involving this pathology. Due to numerous peculiarities regarding the etiology and pathophysiology, clinical presentation, and difficulty in defining an exact prognosis, the treatment varies greatly in the literature and, therefore, among hip surgeons, especially in cases in which there is still no involvement of the articular surface and no subchondral fracture in the femoral head. In these cases, the following therapeutic options are described:

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

  https://www.mdpi.com/1660-4601/19/12/7348

  Posttraumatic AVN occurs when the blood supply to the femoral head is disrupted due to a fracture or dislocation of the femoral head. In most cases, AVN is related to fractures in the sub-capital region of the femoral neck. Injury in this region disrupts the anastomosis between the lateral epiphyseal vessels, limiting the blood supply to the femoral head. […] Many authors have described cases of AVN after a femoral neck fracture surgery. DHS was shown to be associated with a high risk of osteonecrosis. Some studies have demonstrated that it might be even higher than that with other hip-preserving techniques, such as cancellous screws. […] Using large implants for fixation (such as those used in DHS) of femoral neck fracture is associated with a disruption in blood supply to the femoral head.

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

  https://www.mdpi.com/1660-4601/19/12/7348

  The time between surgery and injury appears to be crucial in assessing the risk of bone ischemia—a time interval between injury and surgery greater than 24 h was associated with an increased risk. […] AVN cases in children require separate discussion. In the pediatric population, the incidence of AVN may be higher than that in adults. […] The diagnosis of AVN is mainly based on both clinical and radiographic findings. Typical clinical presentation includes increasing pain, stiffness, and crepitus, usually proceeded by a period of minimal symptoms. […] MRI is the gold standard for osteonecrosis diagnosis and allows differentiating AVN from other diagnoses that may mimic it, such as bone bruises or transitioned osteopenia. […] Conservative treatment of AVN aims to improve hip function, prevent the femoral head from collapsing, provide pain relief, and delay necrotic changes. Nonoperative management is mainly reserved for the early stages of disease in patients without a history of trauma.

• #25 Osteonecrosis (avascular necrosis) in HIV: A Case-Control Study

  https://www.natap.org/2000/sept/osteonecrosis010101.htm

  Osteonecrosis (also known as avascular necrosis [AVN] or aseptic necrosis) results in cell death of various bone components, including hematopoietic fat marrow and mineralized tissue. […] Most osteonecrosis patients in our series had risk factors known to be associated with this condition, most commonly hyperlipidemia (32%), alcohol abuse (20%), and corticosteroid use (12%). […] Corticosteroids are a known risk factor for osteonecrosis and are frequently prescribed in HIV-infected patients. […] Altered lipid metabolism has been recognized in patients with HIV infection. […] Thromboembolic disease and hypercoaguable states are well described risk factors for osteonecrosis. […] Alcohol abuse is prevalent in our clinic population. […] In our study, a similar number of cases and controls received PIs.

• #26 Osteonecrosis (avascular necrosis) in HIV: A Case-Control Study

  https://www.natap.org/2000/sept/osteonecrosis010101.htm

  Most of our patients were receiving PIs; however, an equal proportion of our controls were too. […] Delay in the diagnosis of osteonecrosis was common in our cohort. […] Most patients diagnosed with osteonecrosis had one or more risk factors, suggesting that the increased incidence of osteonecrosis in HIV/AIDS may be due to an increased frequency of risk factors previously associated with osteonecrosis.

• #27 Avascular Necrosis of the Hip | Musculoskeletal Key

  https://musculoskeletalkey.com/avascular-necrosis-of-the-hip/

  A so-called multiple-hit theory was proposed as a pathophysiologic mechanism directly through bone homeostasis alteration and cell injury and indirectly through blood flow impairment. […] In addition, there have been reports of several biomarkers and genes that may play a role in osteonecrosis development. […] Dysfunction of endothelial progenitor cells, which participate in vasculogenesis, has been demonstrated. […] Other research has focused on inherited thrombophilia and hypofibrinolysis as risk factors for blood flow impediment. […] Additionally, aberrant lipid metabolism has been reported, along with corticosteroid-induced extravascular fat deposition, adipocyte hypertrophy, and lipotoxic effects or oxidative stress. […] Direct cellular insult may result from irradiation, chemotherapy, or oxidative stress.

• #28 :: JKMS :: Journal of Korean Medical Science

  https://jkms.org/DOIx.php?id=10.3346/jkms.2021.36.e65

  The second theory considers only intravascular coagulation as the pathway to ischemia. […] The third theory promotes ONFH as having a multifactorial etiology. […] In most cases, ONFH is associated with multiple factors including genetic predispositions as well as the exposure to risk factors. […] The progression is generally dependent on the restoration of vascular perfusion and the creeping substitution of dead bone by new bone. […] However, unlike the coronary artery, the lateral epiphyseal vessels are housed within the closed chamber of the femoral head, which is filled with marrow cells. Therefore, femoral head osteonecrosis should be considered as a compartment syndrome of the femoral head due to intra-osseous hypertension rather than as a vascular obstructive disease, although this is debatable.

• #29 Avascular Necrosis of the Hip | Musculoskeletal Key

  https://musculoskeletalkey.com/avascular-necrosis-of-the-hip/

  Lee et al. observed that osteogenic differentiation of mesenchymal stem cells derived from the proximal femur was significantly reduced in patients with osteonecrosis compared with patients with osteoarthritis. […] Osteonecrosis or avascular necrosis of the femoral head can cause structural failure of bone with collapse and dysfunction of the hip. […] Collapse of the femoral head was observed in 75% of cases of avascular necrosis of the femoral head within 3 years of presentation by Merle dAubign et al. and in 80% within 4 years of onset of hip pain due to avascular necrosis by Ohzono et al. […] The evaluation and treatment of avascular necrosis continues to be controversial. Despite many potential causes of osteonecrosis of the femoral head, the pathophysiology remains uncertain.

• #30 Angiogenesis of Avascular Necrosis of the Femoral Head: A Classic Treatment Strategy

  https://www.mdpi.com/2227-9059/12/11/2577

  Avascular necrosis of the femoral head (ANFH) is a type of osteonecrosis due to the cessation of blood supply, characterized by persistent local pain and collapse of the joint. […] A large number of studies have shown that vascular injury is the initial factor in the onset of ANFH. […] Ischemia resulting from various conditions is considered the primary pathogenesis. […] Vascular injury is the initial factor in the onset of ANFH, and impaired angiogenesis is an important pathway in the occurrence of ANFH. […] Promoting angiogenesis and restoring the formation of blood vessels in the necrotic area to rebuild the blood supply in the necrotic area is beneficial to the collateral circulation and repair of the necrotic area. […] The occurrence of ANFH is intimately associated with vascular injury.

• #31 Avascular Necrosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/333364-overview

  Healing process: Necrotic bone triggers a process of repair that includes osteoclasts, osteoblasts, histiocytes, and vascular elements. […] Primary cell death: Osteocyte death without other features of AVN has been seen in kidney transplant recipients, as well as in patients receiving steroids and those who consume significant amounts of alcohol.

• #32 Avascular Necrosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1247804-overview

  Healing process: Necrotic bone triggers a process of repair that includes osteoclasts, osteoblasts, histiocytes, and vascular elements. […] Primary cell death: Osteocyte death without other features of AVN has been seen in kidney transplant recipients, as well as in patients receiving steroids and those who consume significant amounts of alcohol.

• #33 Avascular Necrosis: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/1247804-overview

  Avascular necrosis (AVN) is defined as cellular death of bone components due to disruption of the subchondral blood supply. It results in pain, loss of joint function, and long-term joint damage. AVN is also known as osteonecrosis, aseptic necrosis, and ischemic bone necrosis. […] AVN is associated with numerous conditions. Corticosteroid use, sickle cell disease, and allogeneic hematopoietic stem cell transplantation and kidney transplantation are high-risk factors for AVN. […] Although the pathophysiology of AVN is not fully understood, the final common pathway is interruption of blood flow to the bone. AVN often affects bones with a single terminal blood supply, such as the femoral head, carpals, talus, and humerus. The earliest pathologic characteristics of osteonecrosis are necrosis of hematopoietic cells and adipocytes followed by interstitial marrow edema.

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

  https://www.mdpi.com/1660-4601/19/12/7348

  Avascular necrosis (AVN) of the femoral head is a type of aseptic osteonecrosis, which is caused disruption of the blood supply to the proximal femur, which results in osteocyte death. AVN may occur due to ischemia developing on a traumatic or non-traumatic background. The most common etiological factors include treatment with corticosteroids, fractures, dislocation of the hip joint, and alcohol abuse. […] The exact pathomechanism of AVN is often unclear. Each case is probably determined by different factors, including underlying conditions or medication that increase the likelihood of vessel obstruction, alteration of the osteocyte’s metabolism, and genetic factors. […] Obstruction of the subchondral microcirculation, particularly retinacular vessels, leads to bone necrosis. Bone cell necrosis is linked with a high risk of developing secondary osteoarthritis and restrictions in the hip range of motion through an accumulation of microfractures in the osteonecrosis area.

• #35 Avascular Necrosis – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537007/

  Osteonecrosis is a degenerative bone condition characterized by the death of cellular components of the bone secondary to an interruption of the subchondral blood supply. Also known as avascular necrosis, it typically affects the epiphysis of long bones at weight-bearing joints. The most common sites for AVN are the femoral head, knee, talus, and humeral head. The hip is the most common location overall. Advanced disease may result in subchondral collapse, which threatens the viability of the joint involved. Therefore, early recognition and treatment of osteonecrosis are essential. This activity discusses the etiology and pathogenesis of the disease, presentation, and treatment options of the most common forms of osteonecrosis. […] Osteonecrosis is a degenerative bone condition characterized by the death of cellular components of the bone secondary to an interruption of the subchondral blood supply. It is also known as avascular necrosis, aseptic necrosis, and ischemic bone necrosis. It typically affects the epiphysis of long bones at weight-bearing joints. Severe cases can lead to the destruction of subchondral bone or the collapse of an entire joint.

• #36 Summary of the various treatments for osteonecrosis of the femoral head by mechanism: A review

  https://www.spandidos-publications.com/10.3892/etm.2014.1811

  The development of ONFH is accompanied by the apoptosis of osteocytes and osteoclasts. Zaidi et al reported that ACTH plays a role in preventing osteonecrosis by promoting osteoblastic support and the expression of VEGF. Early ONFH reveals medium or strong staining of fibroblast growth factor 2 and VEGF, which may promote osteogenesis and bone reconstruction. […] Bisphosphonates, such as alendronate, promote osteoclast apoptosis through several mechanisms, including inhibiting protein prenylation and blocking mevalonate metabolism. Bisphosphonate reduces edema and the rate of remodeling, which contracts the remodeling spaces and prevents the progression of bone collapse. Bone formed during alendronate treatment is histologically normal and the treatment appears to offer the greatest protection against fracture.

• #37 15. Avascular Necrosis (Aseptic Osteonecrosis) – Undersea & Hyperbaric Medical Society

  https://www.uhms.org/?view=article&id=1455:15-avascular-necrosis-aseptic-osteonecrosis&catid=18&highlight=WyJhdmFzY3VsYXIiLCJuZWNyb3NpcyJd

  Avascular necrosis (AVN), also referred to as aseptic osteonecrosis (AO), can develop in several osseous districts of the body. […] Pathology is chiefly caused by a reduced vascularization of a terminal vascular bed, such as the one perfusing the femoral head, or similar vascular distributions such as femoral condyles, humeral head, the talus, the calcaneus, the navicularis, and other bony structures. […] Hypoxic conditions mediate the condition and can improve with a course of hyperbaric oxygen (HBO2). […] All bones can develop an osteonecrotic lesion, but the segments most frequently affected are undoubtedly the terminal portions of the long bones (epiphyses), especially that of the femoral head. […] This pathology usually affects the age range of the most active population (40-50 years old), with repercussions both on the patients quality of life (as it is often progressively disabling, leading to femoral head collapse if left untreated and eventual surgery) and on the general economy as well (due to its reduction in the ability and work performance of those affected).

• #38 Avascular Necrosis: Bone Death Symptoms, Causes, Stages, Treatments & Cure

  https://www.emedicinehealth.com/avascular_necrosis/article_em.htm

  Avascular necrosis occurs more frequently in patients with certain underlying diseases, including systemic lupus erythematosus, diabetes mellitus, vasculitis, and inflammatory bowel disease. […] It is currently suspected by some researchers that intravenous bisphosphonate medications, including zoledronate (Zometa) and pamidronate (Aredia), which are used to reduce elevated calcium levels in patients with cancer and to treat osteoporosis, may increase the risk of avascular necrosis of the jaw bone. […] The treatment for avascular necrosis includes avoiding injury to a bone that is affected by avascular necrosis. […] Treating any underlying cause of avascular necrosis (stopping smoking and alcohol intake, etc.) and management of underlying diseases are essential to minimize the progression of the disease and prevent the involvement of other bones. […] Joint-preservation operations that delay the need for total joint replacement include measures that allow improved blood supply to the affected bone. […] The underlying cause as well as the amount and location of bone affected by avascular necrosis to some degree determine the outcome.

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

  https://www.mdpi.com/1660-4601/19/12/7348

  Surgical treatment of AVN includes joint preserving procedures. These are mostly reserved for young patients in the pre-collapse stage of the disease. THA is indicated for patients with advanced disease. […] AVN of the femoral head is a common cause of disability in patients aged between 20 and 40 years. AVN may be a complication of surgical treatment of femoral head fractures. AVN risk following such procedures is diverse and depends on several factors: the type of internal fixation, type of fracture, Garden classification, preoperative traction, and the time interval between injury and surgery.

• #40 SciELO Brazil – Osteonecrosis of the Femoral Head: Update Article Osteonecrosis of the Femoral Head: Update Article

  https://www.scielo.br/j/rbort/a/nfqMzLfXzPDSg7Zg8T4NqPf/

  Core decompression: performance of one or multiple perforations of the subchondral bone close to the region of the lesion, in order to provide relief of symptoms and seek an improvement in local blood circulation by reducing intraosseous pressure. It presents best results in small injuries located outside the weight-bearing area. […] Total hip arthroplasty: for cases in which there is already joint involvement, such as the presence of subchondral fracture, flattening of the femoral head and/or joint narrowing, in addition to acetabular changes, the most common treatment is total hip arthroplasty.

• #41

  https://journals.lww.com/annals-of-medicine-and-surgery/fulltext/2025/05000/knowledge_mapping_of_core_decompression_in.27.aspx

  Core decompression is a surgical technique aimed at alleviating bone pressure and fostering the growth of new blood vessels. By creating a channel in the femoral head, core decompression enhances blood flow, reduces pain, and promotes the body’s natural healing processes. […] The synergistic application of MSCs transplantation and core decompression has emerged as a pivotal advancement in the treatment of ONFH, as evidenced by a collection of seminal studies. […] The complexity of signaling pathways in MSCs-mediated treatment has unveiled multiple targets to enhance core decompression therapy’s effectiveness in ONFH. […] Treating ONFH with MSCs and core decompression therapy presents multiple challenges. […] Addressing the current therapeutic challenges in ONFH requires a comprehensive research approach. Future research should prioritize personalized treatment strategies, utilizing genomics and biomarker discovery to customize therapies according to individual patient profiles. […] These insights collectively pave the way for a comprehensive gene-based strategy to enhance MSCs reparative potential in ONFH.

• #42 Osteonecrosis of the Hip – OrthoInfo – AAOS

  https://orthoinfo.aaos.org/en/diseases–conditions/osteonecrosis-of-the-hip/

  It is not always known what causes the lack of blood supply, but doctors have identified a number of risk factors that can make someone more likely to develop osteonecrosis. […] Osteonecrosis develops in stages. Hip pain is typically the first symptom. This may lead to a dull ache or throbbing pain in the groin or buttock area. As the disease progresses, it becomes more difficult to stand and put weight on the affected hip, and moving the hip joint is painful. […] Although nonsurgical treatment options such as anti-inflammatory medications, activity changes, and using crutches can help relieve pain and slow the progression of the disease, the most successful treatment options are surgical. […] Core decompression prevents osteonecrosis from progressing to severe arthritis and the need for hip replacement in some cases. This depends upon the stage and size of the osteonecrosis at the time of the procedure.

• #43 Osteonecrosis of the Hip – OrthoInfo – AAOS

  https://orthoinfo.aaos.org/en/diseases–conditions/osteonecrosis-of-the-hip/

  When osteonecrosis is diagnosed after collapse of the bone, core decompression is not usually successful in preventing further collapse. In this situation, the patient is best treated with a total hip replacement. Total hip replacement is successful in relieving pain and restoring function in the majority of patients with osteonecrosis.

• #44 Angiogenesis of Avascular Necrosis of the Femoral Head: A Classic Treatment Strategy

  https://www.mdpi.com/2227-9059/12/11/2577

  Researchers are now concerned with ways to promote vascular regeneration and repair following vascular injury brought on by a variety of causes in order to restore the femoral head’s local blood supply. […] Angiogenesis is a process in which endothelial cells are activated from the long-term dormant quiescent state after receiving local ischemia, hypoxia, or other stimuli, which starts the angiogenesis process. […] The interaction between the molecular pathways affected by these angiogenic factors promotes angiogenesis and bone repair in necrotic areas through an angiogenesis–osteogenesis coupling and ultimately promotes the healing of femoral head necrosis. […] HIF-1α is involved in the local repair response of ANFH, which demonstrates the key role of HIF-1α in the disease of ANFH. […] The exact pathophysiological mechanism behind ANFH is not always clear and is generally considered to be multifactorial, but no matter what the inducing factor is, the result is basically the death of bone cells and bone marrow due to insufficient blood flow of the proximal femoral subchondral bone. […] Early diagnosis and timely regulation of angiogenesis of the femoral head play an important role in the treatment and prevention progression of ANFH.

• #45 Avascular Necrosis (Osteonecrosis) and Stem Cell Therapy – Dr. Dennis Lox Stem Cell Therapy

  https://www.drlox.com/avascular-necrosis-osteonecrosis-stem-cell-therapy/

  Avascular Necrosis (AVN), sometimes referred to as osteonecrosis, ischemic necrosis, bone infarction or aseptic necrosis, is a troubling condition. […] Basically, avascular necrosis (AVN) refers to a situation in which the blood supply to a region of bone has been disrupted. This loss of blood supply known as ischemia or avascular, leads to bone cell death (necrosis) as the loss of blood supply results in loss of cellular nutrition which causes cell death of the bone(s). This can result in joint collapse and rapid secondary arthritis. […] There is a surgical method of delivering stem cells, though not originally known that it worked by this mechanism, called core decompression. […] A simpler method is to simply extract the stem cells from adipose tissue (fat) and perform a joint injection of stem cells. There is no downtime associated with surgery and the total stem cell count is much higher. As regenerative medicine continues to expand the use of therapies such as Platelet Rich Plasma (PRP) and Stem Cell Therapy will be a viable option for patients with AVN and other musculoskeletal conditions.

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