Ischemic Necrosis Of Bone Research Articles

Ayurvedic management of Asthimajja gata vatarakta (Avascular necrosis of head of the femur) – A case report

Avascular necrosis is a condition where the bone tissue starts degenerating due to interrupted blood supply to the bone tissue. It is also known as ischemic bone necrosis, aseptic necrosis or osteonecrosis. From the contemporary medicine the management of AVN goes by pain management and joint replacement surgery. There is no direct correlation for AVN in Ayurveda. But concepts like Asthi kshaya, Asthi majja gata vata, Asthi majja gata Vatarakta symptoms stands very close to this disease condition. A female patient of age 42 came to the OPD complaining of pain in the bilateral hip joints with difficulty in walking since 6 months. MRI of the hip reveled grade 2 AVN of bilateral femur head. Patient was diagnosed as a case of Asthi majja gata Vatarakta with physical examinations. Pancha tikta ksheera kashaya, Lakshaguggulu, was given. Sandhaneeya mahakashaya gana Ksheera basti (enema with medicines processed in milk) was given to the patient for 14 days after sthanika snehana ans swedan . Pancha tikta ksheera kashaya has tikta and kashaya rasa. Tikta rasa has ashraya asharee bhava with asthi dhatu. Hence it improves the quality of asthi dhatu. Laksha guggulu helps in reducing the pain and improving the quality of rakta (rakta). Medicines included in Sandhaneeya mahakashaya gana are either Tikta, Kashya , Madhura. These rasa helps in reducing the rakta dushti (impaired circulation) and improves microcirculation. Ksheera basti helps in improving the quality of Asthi and majja dhatu. It also helps in reducing the pain in the affected region.

BISPHOSPONATE INDUCED OSTEONECROSIS OF JAW – A CASE REPORT

Osteonecrosis of the jaw (ONJ), is the death or necrosis of a bone caused by an insufcient blood supply. It is also called as avascular necrosis, aseptic necrosis or ischemic necrosis of bone. It is a clinically devastating condition that can affect the quality of life of patients. ONJ can be induced by medication such as anti-resorptive agents such as bisphosphonates (BPs) and [1,2,3,4,8,9] antiangiogenic drugs, so is termed as medication related ONJ (MRONJ). The management of MRONJ can be conservative or invasive, [4,7] depending upon the stage of the disease, size of the lesions ,contributing drug therapy and presence of comorbidities. We report a case of bisphosphonate induced osteonecrosis of jaw managed successfully with conservative treatment.

Pharmacodynamics of PanchatiktaGugguluGhritain AsthimajjagataVatawith special reference to avascular necrosis of femoral head

Avascular necrosis (AVN), is a condition that occurs when there is loss of blood supply to the bone, also known as osteonecrosis, bone infarction, aseptic necrosis, or ischemic bone necrosis. Based on pathogenesis and clinical sign and symptoms, it can be compared with AsthimajjagataVata. One of the popular and frequently used medications in the Ayurvedic medical systemis PanchatiktaGugguluGhrita. Panchatikta Guggulu Ghritahas been described in AstangahrudyamVatavyadiChikitsaAdhayayamwhich is indicated in Asthimajjagata Vata. Here is an attempt made on pharmacodynamics of Panchatikta Guggulu Ghrita in respect ofAsthimajjagataVata.

Etiology of Femoral Head Avascular Necrosis in Patients: A Cross-Sectional Study.

Avascular necrosis (AVN), known as osteonecrosis, aseptic necrosis, or ischemic bone necrosis, results in the destruction of bone cells. In the present study, we aimed to report the most common causes of AVN in in patients referred to Isfahan educational and medical centers. This study is a cross-sectional study that was performed on all patients with AVN in medical educational centers in Isfahan during 2019 and 2020. We included all patients diagnosed with AVN. Patients' information including age, sex, cause of femoral head necrosis, medical history, and drug usage were collected. Finally, reliable data from 99 patients were recorded. We collected data of 99 patients in this study. The most prevalent cause of ANV was corticosteroids use (32.3%), and it was more prevalent among women (51.4%); the second prevalent cause of AVN in our study sample was trauma (28.28%), and it was more prevalent among men (32.8%). The most common cause of AVN was corticosteroids, which was consistent with previous studies. Other main causes of AVN were traumatic or idiopathic issues.

ROLE OF PANCHTIKTA KSHIRA BASTI IN MANAGEMENT OF AVASCULAR NECROSIS: A CASE STUDY

Avascular necrosis additionally referred to as osteo-necrosis or Ischemic bone necrosis is a condition that occurs when there is a loss of blood supply of bone. An interruption in the blood supply causes bone cells to die. AVN of femoral head is that the commonest sort of necrosis affecting the bone. In Ayurveda, It correlated with asthimajjagata vaat (musculoskeletal disorder). An effort has been made within the present study to gauge the efficacy of panchtikta kshir basti in conservative management of femoral head necrosis of the bone. In Modern medicine, no any unique remedy as opposed to surgical operation is available.

The Cadaverous Carnage- Aseptic Bone Necrosis

Aseptic necrosis is a commonly discerned degenerative condition of the bone characteristically constituted of deteriorated cellular components. Generally, the condition arises secondary to discontinuity of subchondral vascular effusion. The disorder is additionally designated as avascular necrosis, osteonecrosis or ischemic bone necrosis and no bone is exempt. Specific sites incriminated are the tibial tuberosity as encountered in Osgood-Schlatter’s disease or proximal femoral epiphysis as denominated in Legg-Calve’-Perthes disease.

Tarsal Navicular Osteonecrosis in Children

Osteonecrosis (avascular, aseptic or ischemic bone necrosis) of the tarsal navicular in children may develop either spontaneously (primary, idiopathic, atraumatic or non-traumatic) or secondary to trauma (post-traumatic) and osteochondrosis. In both groups, of primary and secondary osteonecrosis, the clinical findings as well as the radiographic abnormalities are self-limited and usually resolve spontaneously irrespective of weight-bearing and immobilization treatment modalities. Köhler’s disease has been defined either as atraumatic navicular osteonecrosis or as an osteochondrosis process, based on the similar radiographic appearance of increased sclerosis and flattening detected in both asymptomatic and symptomatic children. Post-traumatic tarsal navicular osteonecrosis in children may follow microtrauma or overuse injuries, stress fractures, acute fractures, osteochondritis dissecans and severe foot injuries. This editorial aims to present the primary and secondary causes of osteonecrosis of the tarsal navicular in children and to describe the difficulties of the clinical and radiological evaluation in order to define an accurate diagnosis.

Ostéonécroses aseptiques, une revue générale des ostéonécroses de la hanche, et au-delà

Avascular necrosis is an ischemic or cytotoxic necrosis of epiphyseal bone, responsible for joint pain, altered life quality and frequently affecting young patients. Avascular necrosis can be unifocal or multifocal, underlining the possibility of a systemic origin. Avascular necrosis involves the femoral head in more than 75% of cases. Although avascular necrosis is irreversible, many risk factors must be sought, including corticosteroid treatment, hypercholesterolemia, sickle cell disease or alcohol abuse. MRI imaging is the main exploration for the diagnostic and staging of the disease, and should be performed in unexplained hip pain in young patients with normal X-rays. In the earlier stages of the disease (stage I and II of the Arlet and Ficat classification), joint surface is preserved, and conservative treatment is recommended. In the more advanced stages (III and IV of the Arlet and Ficat classification), the articular surface collapses and joint arthroplasty is the main treatment. However, there are some recent therapeutic advances, based on mesenchymal stem cells, which may contribute, in the future, to improve the bad functional prognosis of the disease.

Integrated Approach of Naturopathy And Physiotherapy in Patient With Post Operative Hip Arthroplasty-A Case Report

TamilNadu, Abstract: Avascular Necrosis (AVN) of the bone, aseptic necrosis and ischemic bone necrosis, is a relatively common disease characterized by death of the cellular elements of bone and marrow due to the interruption of the blood supply. Patients tend to suffer from post surgical pain, limitataion of motion with stupping gait along with aggravating of pain, numbness & spasm in gluteal region. This condition has a number of charactertics clinical and radiographic signs that differentiate it from other osteonecrotic conditions. 'Mitchell's GRADE A' with marrow edema in head & neck regions of femur being the first charactertics of diagnostic feature. This is a case report of single post surgical issues with history of severe pain and difficulty in walking.

Steroid-induced ischemic bone necrosis of femoral head: Treatment strategies.

Fat hypertrophy, intravascular coagulation, and fat emboli are important risk factors of steroid-induced ischemic bone necrosis (SI-IBN) which may develop during the initial one year after commencing the use of steroids. This pathology is best studied by MRI, particularly for its staging. The cautious strategies such as low dose, oral route, short duration of steroid usage, use of steroid sparing agent, and alcohol avoidance should be followed as a traditional therapy. The objective of this review article was to recognize and evaluate various Treatment strategies for steroid-induced ischemic bone necrosis of femoral head.Literature Search:Various electronic databases including PubMed, Google and Cochrane library were comprehensively searched for articles on steroid-induced ischemic bone necrosis of femoral head and its treatment strategies. Ninety four articles were reviewed, examined and importantly appraised and the most appropriate 32 papers were used to write this review article.Conclusion:Bisphosphonates, alendronate, and hyperbaric oxygen (HBO) treatments have been reported to be effective against IBN. To recommend the regular use of bisphosphonate in IBN patients, more evidences with a larger number of patients are required to verify its therapeutic effectiveness. Core decompression, osteotomy, bone graft and tantalum rod are the surgical approaches for the management of IBN. Advance form of IBN (bone tissue collapse) is advised to be treated with arthroplasty which should be durable, particularly in young patients.

Morphological aspects of the pathogenesis of arthroses

The morphological changes in human osteoarthrosis are compared with those occurring in the ankle joints of old rats. Chondrocytic necrosis, proteoglycan loss, cartilage fibrillation and loss of cartilage and bone are similar in both species. It is concluded that osteoarthrosis of the ankle joints in old rats may be a model to study the mechanisms leading to cartilage destruction. In contrast to the process in rats the human disease is "complicated" by secondary events as ischemic bone necrosis and debris synovitis. The latter two processes are of importance for the understanding of the clinical symptoms of osteoarthrotic joints.

Predictive value of magnetic resonance imaging in avascular necrosis following talar fractures.

Ischemic bone necrosis following talar fractures is a problematic complication and its early diagnosis is important. Patients with Hawkins Type II and III talar fractures received internal fixation using titanium alloy screws, and chronological bone changes were observed with Magnetic Resonance Imaging (MRI). With the Type II patient, Hawkins' sign was radiographically confirmed 2 months after the surgery. Furthermore, there were no changes of MR images for 2 years and a good clinical outcome was obtained. However, in the Type III patient, Hawkins' sign was negative and MRI revealed a low signal-intensity band on the talus 2 months after the surgery and then necrosis was radiographically confirmed; pain appeared 10 months later. These 2 cases suggest that MRI is a useful means for detecting bone necrosis with talar fractures in the early post-operative period.

The Vascularization of the Os Calcaneum and the Clinical Consequences

This study was conducted to analyze extraosseous and intraosseous vascularization of the os calcaneum and to elucidate possible clinical manifestations. The arteries of 13 lower leg and foot specimens of human cadavers were injected with a polymer and subjected to maceration or were embedded in plastic. The examination revealed that 45% of the bone is vascularized via medial arteries and 45% via lateral arteries, whereas the remaining 10% is supplied by the sinus tarsi artery. From the medial side, two or three vessels branch off the posterior tibial artery, penetrate the calcaneus below the sustentaculum, and supply the medial part of the posterior joint. The lateral calcaneal artery normally is a branch from the posterior tibial artery. In two of 13 specimens, this lateral supply comes from the peroneal artery. The medial and lateral intraosseous arterial supply for the calcaneus is equal. Inside the bone there is a water-shed zone where the medial and lateral arterial supply meet in the midline. Only 10% of the blood flow is supplied by vessels in the sinus tarsi. Clinically, interruption of the lateral calcaneal artery during the conventional lateral surgical approach for a calcaneus fracture may result in ischemic bone necrosis. The lateral calcaneal artery could supply a local microvascular flap to cover soft tissue defects of the heel. A compartment syndrome after a calcaneus fracture may be caused by bleeding from the medial calcaneal arteries into the quadratus plantae compartment.

Hypercoagulability and Hypofibrinolysis in Primary Osteoarthritis

Histologic evidence of venous thrombosis and lipid abnormalities have previously been reported in osteoarthritis. Hypofibrinolysis has been recorded in patients with ischemic necrosis of bone, and it has been proposed as a major cause of osteonecrosis. This study determines whether systemic evidence of coagulation and lipid abnormalities could be detected in osteoarthritis. Global and specific tests were used to assess coagulability and fibrinolysis in 44 patients with degenerative osteoarthritis of the hip and 52 matched control subjects. In patients with osteoarthritis, an increase in factor VIIlc, increased platelet sensitivity over a range of adenosine diphosphate concentrations (0.05 micromol/L-4 micromol/L) and elevated D dimer levels were found. Euglobulin clot lysis time was prolonged in this group and plasminogen activator inhibitor Type 1 activity was increased. Relative hyperlipidemia was observed in the osteoarthritis group, with increased cholesterol, low density lipoprotein cholesterol, and triglyceride levels. It is concluded that there is a hypercoagulable and prothrombotic condition in osteoarthritis, with hypofibrinolysis and indirect evidence of increased fibrin generation. The possible contribution of lipid abnormalities to hemostatic imbalance in osteoarthritis is discussed.

The pathogenesis of joint destruction in chronic polyarthritis

Joint destruction, a hallmark of rheumatoid arthritis, is described with respect to different mechanisms: destruction by inflammatory cells of the synovial fluid, pannus tissue and even ischemic bone necroses. Destruction via the synovial fluid is due to polymorphonuclear neutrophils (PMN) that can invade the pannus-free cartilage surface. In the absence of anti-proteases as a result of direct contact between the PMN and cartilage, enzymatic degradation can occur. Pannus tissue usually develops from the synovial insertion. Increased cellular proliferation in this area leads to a superficial pannus tissue that covers the cartilage (Fig. 4b); granulation tissue from the synovial insertion can destroy cortical bone and invade the subchondral tissue. The problem of isolated subchondral inflammatory foci is briefly discussed. The effector cells of cartilage destruction are identified as macrophages, PMN, and mast cells -cells that produce or activate destructive enzymes. Bone destruction is due to osteoclasts and even macrophages. Acute destruction via the granulation tissue may be followed by defect healing-scar tissue or chondroid metaplastic tissue can be present in the final stages of the disease. Ischemic bone necrosis leading to pseudocysts may also contribute to joint destruction.

Intraosseous thrombosis in ischemic necrosis of bone and osteoarthritis

It has been proposed that nontraumatic ischemic necrosis of bone (INB) is a result of lipid associated intraosseous thrombosis. A histological study of 15 patients with INB confirmed the presence of intravascular lipid and thrombosis in the vessels of the femoral head. A similar analysis of 11 patients with primary osteoarthritis (OA) showed similar changes at lower levels. These changes were not observed in seven control femoral heads. The possibility that both INB and OA result from intraosseous thrombosis is discussed.

Marrow infarction in sickle cell anemia: Correlation with marrow type and distribution by MRI

Ischemic necrosis of bone is believed to occur exclusively in areas of predominantly fatty marrow. Sickle cell disease is unusual in that marrow infarction occurs in areas of active hematopoiesis. MR images of long bone obtained in ten patients with sickle cell anemia (SCA) were analyzed to correlate the distribution and appearance of marrow infarction with the type of marrow. While the hematopoietic marrow predominated in metaphyseal and diaphyseal regions of femurs and tibias, the fatty or mixed marrow was the most common pattern in epiphyses. Infarcts occurred in fatty as well as hematopoietic marrow. Marrow infarcts were isointense or minimally hyperintense on T 1 weighted images with the hematopoietic marrow and therefore difficult to detect. On T 2 weighted images, the infarcts showed very high signal. T 2 weighted images are essential for detection of marrow infarction. Soft tissue changes seen as low signal on T 1 and high signal on T 2, may be secondary to intramuscular injections of analgesics or muscle ischemicia occurring during sickle crisis.

The early diagnosis of ischemic necrosis of bone.

One hundred sixty-nine patients with radiographic or histologic evidence of ischemic necrosis of bone (INB) were evaluated. Ninety-nine (59%) of the 169 patients had multiple sites of INB, with 310 bones affected. Two hundred sixty-three (85%) of the 310 ischemic bones were symptomatic. Routine radiography produced negative findings in 58 (20%) of the bones with histologically confirmed INB. Results of hemodynamic studies, including baseline bone marrow pressure, saline stress test, and/or intraosseous venography, were abnormal in 243 (94%) of 259 ischemic bones so evaluated. Most importantly, hemodynamic studies detected 51 (93%) of the 55 bones that were radiographically normal but had histologically confirmed INB.

The intravertebral vacuum phenomenon.

An intravertebral vacuum phenomenon was observed within 19 vertebrae of 17 patients. It represents a non-healing vertebral fracture. Three possible pathologic mechanisms are discussed: ischemic bone necrosis, trauma with ensuing ischemic necrosis, and intraosseous disc prolapse. The intravertebral vacuum phenomenon was found in two patients with multiple myeloma and thus does not exclude the presence of malignancy in the affected bone. Radiographs obtained during traction or extension may be of diagnostic value.

Corticosteroid therapy associated with ischemic necrosis of bone in systemic lupus erythematosus

In this prospective study, 28 (52 percent) of 54 patients with systemic lupus erythematosus (SLE) had ischemic necrosis of bone in 93 sites. All but two of the patients had multiple sites of involvement, with hips, knees, and shoulders affected in decreasing order of frequency. Demographic, clinical, and laboratory features were comparable in patients with and without ischemic necrosis of bone except for cushingoid changes in 24 (86 percent) of the 28 patients with ischemic necrosis of bone versus four (15 percent) of the 26 patients without ischemic necrosis of bone (p <0.0001). The duration of steroid therapy, total cumulative steroid dose, and the mean daily prednisone dose for the first one, three, six, and 12 months of therapy were not significantly different between the two groups. Mean daily prednisone dose for the highest single month as well as the highest consecutive three, six, and 12 months of therapy was significantly higher in patients with ischemic necrosis of bone. The mean daily dose of prednisone for the highest month of therapy was greater than 40 mg per day in 93 percent and greater than 20 mg per day in all patients with ischemic necrosis of bone. In patients with ischemic necrosis of bone, there was a statistically significant correlation between higher mean prednisone dose at all time intervals and increased number of bony sites involved. A lower mean dose of prednisone was required to produce ischemic necrosis of bone in patients with Raynaud's phenomenon.